Musings -- May 2017 to ?? (current posts)

Musings is an informal newsletter mainly highlighting recent science. It is intended as both fun and instructive. Items are posted a few times each week. See the Introduction, listed below, for more information.

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New items

Posted since most recent e-mail; they will be announced in next e-mail, but feel free...

Peer review of scientific articles -- by crowd reviewing?

June 26, 2017

It's part of how science works... Before being published in a scientific journal, an article is read by other people in the field. These "peer reviewers" comment on the article, helping the editor decide whether the article should be published, and helping the author improve the article.

How well the peer review process works is the subject of debate. We need not get into the debate here, but simply note that many journals are experimenting with variations of the procedure.

A recent "Column" in Nature offers a new variation: letting a crowd have a chance to review the article. That's not just any crowd, but a collection of people in the field. Instead of the editor sending the article to three reviewers he or she chooses, the submitted article is posted and any of the journal's crowd of experts can contribute reviews. The author of the current item, who is the journal editor, claims it works rather well. For one thing, the reviewers are self-selected -- and they review articles they are interested in.

How well this procedure would work for larger and broader journals is open. It would probably be good to have pools of reviewers for different subject areas. In any case, it's an interesting idea, worthy of consideration. The one-page column is worth a browse, especially for those interested in how scientific articles get published.

Column, which is freely available: Crowd-based peer review can be good and fast. (B List, Nature News, May 30, 2017. In print edition 546:9, June 1, 2017)

My page for Biotechnology in the News (BITN) -- Other topics includes a section on Ethical and social issues; the nature of science. It includes a list of related Musings posts.

If an injured heart is short of oxygen, should you try photosynthesis?

June 25, 2017

Sure. Photosynthesis produces oxygen. If the heart is short of oxygen, doing photosynthesis should help the heart function.


The experiment here used a lab model of a heart attack (ischemia). Rats; open the chest; clamp the coronary artery. That blockage leads to an oxygen shortage in the heart muscle.

The graph shows the oxygen level in the heart tissue (y-axis), under different conditions at different times. The times are: before the ischemia ("baseline"), after the ischemia (the injury), and two times after the treatment.

You can see that the oxygen level dropped drastically upon injury. It then rose substantially after one of the treatments: the photosynthesis treatment. It remained low in the two treatments that did not provide photosynthesis.

We will come back to the nature of these treatments below.

   This is Figure 2A from the article.

You may have noticed... In the successful treatment, the oxygen level rose, but wasn't normal. But it was enough to significantly improve heart function...

This graph is similar in form to the one above, but the y-axis here is a measure of function: cardiac output. There is only one point after the treatment. Once again, the green line has the high value; the photosynthesis treatment significantly improved heart function.

There is a fourth line here. We'll come back to it in a moment after explaining the procedure further.

   This is Figure 2G from the article.

The graphs above, and much more in the article, provide evidence that photosynthesis helps restore heart function following an ischemic injury. It does so, presumably, by providing oxygen.

How did the scientists get the rats to photosynthesize? They injected bacteria into the heart. Photosynthetic bacteria -- the kind that make oxygen as a by-product. Cyanobacteria, Synechococcus elongatus. And then they shined light on the heart.

Note that "light" vs "dark" are listed in the key describing the treatments. The controls include no bacteria, or bacteria but no light. In the 2nd graph, the dotted line at the top shows the effect of the bacteria in a control with no injury. It had no effect. (The conditions are not clear, but that's the idea.)

Where is this going? Who knows. It's very preliminary work, illustrating that a treatment with photosynthetic bacteria could provide an immediate benefit to heart function.

The bacteria used here have been studied extensively. The authors note that it would be possible to modify their ability to provide glucose, too, which might also be helpful. Further, there are cyanobacteria that can use infrared (IR) light, which might allow light to be provided from outside the body.

It's an intriguing idea.

News stories:
* Scientists explore using photosynthesis to help damaged hearts. (Medical Xpress, June 15, 2017.)
* Bright Lights and Bacteria Treat Rats' Heart Attacks -- Injecting photosynthetic microbes into oxygen-starved heart tissue can improve cardiac function in rodents. (R Williams, The Scientist, June 14, 2017.)

The article, which is freely available: An innovative biologic system for photon-powered myocardium in the ischemic heart. (J E Cohen et al, Science Advances 3:e1603078, June 14, 2017.)

A recent post on repairing heart damage: Synthetic stem cells? (April 30, 2017). This work also uses a system of artificial heart attacks in rodents.

More about cyanobacteria and oxygen: A whiff of oxygen three billion years ago? (April 6, 2015).

More on animals using photosynthesis: Photosynthetic sea slugs; species vary (June 9, 2015).

RNA editing is a major contributor to protein diversity in cephalopod brains

June 23, 2017

Five years ago Musings noted an unusual finding. Octopus species that live in cold waters are, of course, adapted to the cold. One adaptation is to have an ion channel protein that is more flexible, and better able to function at low temperature. The surprising finding was that the cold-water octopus achieved this not by a mutation in the gene for the protein, but by modifying the messenger RNA. Such RNA editing is a well recognized process, but uncommon in animals. You may want to review that background post at some point along the way here [link at the end].

We now have a follow-up article. The scientists now find that RNA editing is a major process in some cephalopods. Specifically, it plays a major role in providing protein diversity in the nervous system for those cephalopods that we consider behaviorally "advanced". That includes the octopuses and squids.

Here is the basic data: how often RNA editing occurs...

The main graph shows how many examples of RNA editing the scientists found for each di-nucleotide sequence. Results are shown for six animals, using different colored bars, according to the key at the upper right.

The sites for RNA editing were identified by finding differences between the sequences of RNA molecules and the genes they were from.

You can see that there is one big peak, at the di-nucleotide sequence AG. There is little elsewhere. In particular, note that there is little at GA, the reverse di-nucleotide. This is evidence that what is being observed is specific; the enzyme that edits the RNA is known to be specific for AG.

There is another important observation. As we noted, the graph contains data for six animals. But there are only four high bars at AG. If you check the key, you will see that they are for the first four organisms listed: the behaviorally advanced cephalopods, such as squid and octopus. (Sepia is a cuttlefish.) The last two are "other" -- the nautilus, a less advanced cephalopod, and the sea hare, a non-cephalopod mollusc; they lack the massive editing.

The inset shows the same results plotted another way. In this case, they are presented as a fraction of the total -- for each organism. The conclusions are the same.

   This is Figure 1B from the article.

That's the big story. The octopus and its close relatives show a high degree of RNA editing, distinguishing them from other animals, including other cephalopods and other molluscs.

What more? The scientists show that the RNA editing occurs primarily in the nervous system, and that the editing sites are highly conserved from one species to another within the broad group of advanced cephalopods. They show that some of the editing leads to altered proteins.

These are fascinating organisms, starting with their appearance. More recently, we have come to understand that they are quite advanced organisms in some ways. The octopus may well be the most intelligent invertebrate. We now see that these are unusual organisms at the level of how their genes function -- their brain genes.

News stories:
* Science Reveals Yet Another Reason Octopuses and Squid Are So Weird. (Anna Vlasits, Wired, April 6, 2017.)
* Cephalopod Genomes Contain Thousands of Conserved RNA Editing Sites. (A Olena, The Scientist, April 6, 2017.)

The article: Trade-off between Transcriptome Plasticity and Genome Evolution in Cephalopods. (N Liscovitch-Brauer et al, Cell 169:191, April 6, 2017.)

Background post: How an octopus adapts to the cold -- by RNA editing (March 5, 2012). Links to more, including a delightful book about octopuses.

A recent post about another unusual feature of cephalopods: Chromatic aberration: is it how cephalopods see color with only one kind of photoreceptor? (October 14, 2016).

A recent post with another example of RNA-seq, the large scale sequencing of RNA molecules: Looking for genes for animal magnetism (June 11, 2017).

There is a section of my page Biotechnology in the News (BITN) -- Other topics on Brain (autism, schizophrenia). It includes a list of related Musings posts.

June 21, 2017 (Current e-mail)

Water loss from irrigated lawns

June 21, 2017

Much of Southern California is arid. The coastal city of Los Angeles (LA) gets only about 14 inches (35 cm) of rain per year. That's not enough to support a dense population. The secret to LA's growth is importing water. That imported water supply is now under stress. A recent multi-year drought highlighted the problem. The population of the LA area is far beyond what was envisioned when the water supplies were arranged. Further, others now want that water, too.

The situation in LA is not unusual. Water is becoming a scarce resource in many parts of the world. It forces us to look more carefully at how we use water.

A new article analyzes the LA water situation. Some of the results are not particularly surprising, but the article improves the robustness of the analysis. One conclusion is that LA "wastes" a lot of water on lawns.

The main issue addressed in the article is loss of water to the air -- from plants. It's a normal part of how plants grow: they take in water at the roots, and give off water through the leaves to the atmosphere. The process is called transpiration. It may be a normal part of what plants do, but look at the context: we import scarce water; plants take it up and release it to the air. Are we getting enough value to warrant this use of water?

It is an issue any time we irrigate plants. For agricultural use, we at least get some food back. Whether that is a good use of the water is a question for another time. But in LA, what we get is a green lawn that looks pretty.

Estimating water loss by plants in the real world is complicated. It is easy enough to measure such loss for an individual plant or a small area, but the real world contains a mix of plants under complex and varying conditions. In the current work, the scientists develop a model for overall transpiration based on the simple measurements combined with knowledge about the area.

The following graph summarizes some of the findings. The graph itself may or may not be very interesting; we'll comment on some of the findings below.

The graph shows estimated water loss due to transpiration over the course of a year.

The top frame shows the loss according to type of plant. Water loss peaks during the summer, as expected. Summer water loss is about three times winter water loss. The black part of the bars is for turfgrass -- that is, lawns. It is the major source of water loss due to transpiration. Flowering trees are second (gray bars); coniferous (and other) trees are negligible. (Did you know that there are over ten million trees in LA, most of them non-native?)

What are the numbers? Don't worry much about them, for now. They show the water loss, or evapotranspiration (ET), in millimeters per day. For the y-axis scale at the left, this is shown per area of land with vegetation. For the y-axis scale at the right, it is per area of total land.

The lower frame compares their modeled estimates of ET (gray bars -- same data as in the top frame) with values from two other sources. Suffice it to say that their values for ET agree well with one source, and are consistently higher than the other. If nothing else, this illustrates that we still have an incomplete understanding of the water loss problem.

   This is Figure 8 from the article.

The graphs above provide data. Of course, there is more in the article. What can we learn from the numbers?

How much water are we talking about? It's hard to relate to the numbers on the graphs. However, one can calculate that the summer rate of ET is about 100 gallons per day per person. That we can relate to. It's a lot. With a little effort, a person can reduce water use to 25 gallons per day for personal needs.

The top frame above shows that water loss is mainly from lawns, with trees second. That might reflect how much there is of each type of plant or the water efficiency of that plant. Turns out that both play a role. There are vast lawns in LA, and grass is inefficient with water. It is mostly leaf, and transpires rather freely. In contrast, trees transpire only from the leaf area, which is a small part of the tree. Further, trees regulate their water loss.

The rate of water loss is about the maximum expected for the plants -- all year long. This suggests that the lawns are over-watered -- all year long. Even if we think lawns are worthwhile when they require scarce water, they could get by just fine on less.

In an arid environment, the green lawn has become a symbol that we have conquered Nature. In fact, the authors show that water loss from plants correlates with income. ET is greatest in high income neighborhoods.

We need to think about our water usage. California, not just LA but most of the state, has just emerged from a major multi-year drought. Even a wet year such as we just had provides only temporary relief. Population continues to increase. And thus so does water demand, for personal use, agricultural use to feed us all, and recreational use such as lawns.

The article itself is a step forward in modeling water flow through plants in a complex urban environment. It discusses the improvements and limitations of the model. The practical output is better understanding of how one might reduce water usage. Even if some of the conclusions seem obvious, the modeling can provide good formal support, which helps to inform policy decisions.

News story: LA lawns lose 70 billion gallons of water a year. (P Gabrielsen, AGU blog, May 24, 2017.) "This post originally appeared as a press release on the University of Utah [the lead institution] website."

The article: Evapotranspiration of urban landscapes in Los Angeles, California at the municipal scale. (E Litvak et al, Water Resources Research 53:4236, May 2017.)

A post about one of those sources for LA water: Groundwater depletion in the Colorado River Basin (October 3, 2014).

More about transpiration: Plants and climate change (April 25, 2010).

A recent post about another problem in LA... DNA evidence in restaurants: is the fish properly labeled? (June 5, 2017).

Nuclear-mitochondrial interactions -- and the definition of a biological species

June 18, 2017

"Species" is an important idea in biology, yet there is much uncertainty about what it means. Biologists have many definitions of species; none of them are entirely satisfactory.

A classical idea of species is that two types of organisms are different species if they cannot interbreed. That idea requires sexual reproduction, and seems of no help when dealing with the vast numbers of organisms that lack this feature. Even with sexually reproducing organisms, we wonder what the basis of the separation is.

A recant article offers a new idea for what may cause organisms to be different species, that is, what may make them reproductively incompatible. It's an interesting argument, and certainly interesting biology.

The following cartoon lays the groundwork...

In this figure, the products of nuclear genes are shown in blue, and those of mitochondrial genes in green.

The top part of the figure shows, in cartoon form, complexes of the electron transport system (ETS). You can see that most of the complexes contain both "blue" and "green" pieces. That is, they contain proteins from nuclear genes and proteins from mitochondrial genes; these must all fit together in an integrated functional complex.

The bottom part shows that basic functions of the mitochondrial genome all require both nuclear and mitochondrial products.

   This is part of Figure 1 from the article.

So far, there is nothing new above. We know that nuclear and mitochondrial genes work together for some functions, most notably the ETS. That requires that certain nuclear and mitochondrial genes be compatible. The mitochondrial genome is very small: only 37 genes for birds, and only 13 of those code for proteins. The mitochondrial gene products must function cooperatively with nuclear gene products.

What's new is suggesting that this mitonuclear compatibility is a key issue is speciation.

Evidence? Well, not really. Nothing very definitive. But the author, Geoffrey Hill, notes how we are unable to explain speciation in birds, and offers that mitonuclear compatibility is a plausible alternative. In addition to the interdependence noted above, Hill notes the high mutation rate for mitochondria, which would help promote divergence.

An example he dwells on is two species of warbler, that are visibly very different. Perhaps oddly, members of the two species mate with each other readily, but the progeny are of low fitness. Analysis of their genomes shows that the nuclear genomes are very similar, but that there are substantial differences in the mitochondrial genomes.

Hill is clear that the proposal is on the table to be tested further. It makes some clear predictions. For example, if mitonuclear incompatibility is a key issue in speciation, then we should be able to find specific mutations in specific genes that explain specific speciation events.

Following the proposal takes some patience with biology, including some basic genetics. But it seems a good story -- worthy of the testing that the author suggests.

One of the news stories listed below is a reply by the author to a critique. Hill goes through much of the proposal step by step. It's very readable.

It is not important that we try to judge whether the proposal is "right". It's an interesting and provocative proposal; that is fine for now. It should stimulate further work on the nature of nuclear-mitochondrial compatibility. That may help us understand speciation.

News stories:
* New species concept based on mitochondrial & nuclear DNA coadaptation. (, March 8, 2017.)
* Defending the Mitonuclear Compatibility Species Concept. (G E Hill, Ornithologist's Blog, April 3, 2017.) This is by the author of the article. He responds to a critique of his proposal by a noted evolutionary biologist. Thus this page provides something of a pro/con on the proposal. In doing that, it serves to describe it well.

The article, described as a commentary (not a research article). It may be freely available: The mitonuclear compatibility species concept. (G E Hill, The Auk 134:393, April 2017.)

A recent post on mitochondrial function... The boy with three parents -- an article is now published (May 17, 2017).

A post on uniparental inheritance of mitochondria: How are mitochondria from the father eliminated? (September 20, 2016).

More about speciation: Making a new species in the lab (July 26, 2015).

Animal communities around bone-eating worms

June 16, 2017

The Osedax worm is a fascinating creature, both for what it does and how it does it. It is best known for eating whale bones. It does that without a gut; Osedax relies entirely on its bacterial symbionts for nutrition. Its appearance may fascinate, too; see the picture in the background post [link at the end].

A new article reports some interesting findings about what happens at a whale fall -- a dead whale on the sea floor. It is based on finding a whale carcass in an early stage of degradation. The article enhances our understanding of the ecological role of Osedax.

The authors made numerous observations on the whale carcass. The first observation was that one end of the vertebral column carried Osedax, and the other end did not. That observation served as the basis for most of what follows, which is a comparison of the animal communities on the two regions.

Animal abundance on several vertebrae was based primarily on detailed videos taken before the carcass was disturbed. Further work was done on the vertebrae in the lab. The scientists compared what was found depending on whether or not Osedax was present. The following figure is a summary...

Frame C (left) shows the number of species (y-axis) found. The left bar (red) is for vertebrae without Osedax; the right bar (blue) is for vertebrae with Osedax. It's a typical box-and-whiskers graph... the black line is the median; the main box shows the middle 50% of the distribution. It is clear that there are more species on the vertebrae with Osedax.

Frame D (right) is the same idea, but showing the number of individuals. The general pattern is the same.

Both y-axis parameters are per 100 cm3 of bone. The total number of vertebrae analyzed is 7; there are multiple samples.

   This is from Figure 6 of the article.

That's the big story. The animal communities are different with vs without Osedax. The authors suggest that is a causal relationship: that Osedax promotes diversity and abundance in the animal communities.

One can certainly imagine why that might be. Osedax attacks the bone, and releases nutrients. Its burrowing modifies the physical structure, creating more exposed surface; that provides access for other animals, and for water.

There are some limitations to keep in mind. To start, there is a sample size of one here. That's not a criticism; it is quite an achievement to have done one, and it gets us started. Beyond that, I wonder why the initial pattern was established, with the Osedax on one end. The authors explicitly say they do not know. Is it possible that something caused this distribution of the worms -- and also caused the other effects that were seen? All we can do is to ask such questions -- while admiring what the scientists have accomplished so far.

In any case, it is an interesting study, a detailed analysis of the degradation of a single whale carcass. It's an example of studying an ecological succession, in this case, one in an environment that is usually inaccessible. It suggests that the already-fascinating Osedax is an ecological engineer, playing an important role in modifying the environment and thus influencing the succession.

News story: Eating bones and building habitats: the life of an ecosystem engineer. (E McLean, oceanbites, May 30, 2017.)

The article: Bone-eating Osedax worms (Annelida: Siboglinidae) regulate biodiversity of deep-sea whale-fall communities. (J M Alfaro-Lucas et al, Deep-Sea Research Part II, in press.)

Background post... A quasi-quiz: The fate of bone and wood on the Antarctic seafloor -- and the discovery of new bone-eating worms (August 20, 2013). Includes -- even features -- a picture of an Osedax (a different species). Links to more -- about Osedax, other worms, and whales.

June 14, 2017

Building with wood: might it replace steel and concrete?

June 14, 2017

Concrete and steel are the common modern materials for constructing large buildings. They replaced wood. Is it possible that wood will make a comeback?

A recent news feature discussed work being done to re-examine the use of wood. Improved understanding of plywood greatly enhances its potential.

A potential advantage of wood is environmental. This is a complex issue, as it requires taking into account all steps of the material's production and use. Briefly, so long as wood is grown sustainably, wood is appealing. It's known how to grow wood sustainably, but there is a temptation to over-harvest.

The article is an interesting overview of a topic you may not have thought about. Worth a browse.

News feature, freely available: The wooden skyscrapers that could help to cool the planet -- Large timber buildings are getting safer, stronger and taller. They may also offer a way to slow down global warming. (In print edition, with a different title: Nature 545:280, May 27, 2017.)

More wood:
* Using wood-based material for making biodegradable computers (July 21, 2015).
* A quasi-quiz: The fate of bone and wood on the Antarctic seafloor -- and the discovery of new bone-eating worms (August 20, 2013).

More giant viruses, and some evidence about their origin

June 13, 2017

Viruses have long had a confusing status in the tree of life. Viruses are diverse. All mammals are presumably related to each other, and all bacteria are presumably related to each other. But viruses are not. They apparently have multiple origins, with various initial events of a virus forming.

One feature of viruses seemed clear: they are simple. Small, with small genomes -- and (nearly) free of some of the hallmarks of cells, such as enzymes.

Of course, some viruses are more complex than others. Pox viruses are remarkably complex -- for a virus, but they are unmistakably viruses, not cells.

The discovery of giant viruses a decade ago has confused things further. These viruses are not only bigger, but also more complex. They have genomes bigger than those of some bacteria, and they have quite extensive sets of enzymes. Nevertheless, their lifestyle is clearly virus-like, not cell-like. We might accommodate these giant viruses as outliers among the viruses. However, the complex protein component of these viruses led some scientists to suggest that the giant viruses reflect a totally new type of organism, a fourth domain of life. That's a provocative proposal; the scientific community has been skeptical.

A recent article reports more giant viruses. Further, analysis suggests a story for their origin that is perhaps disappointingly simple.

The new viruses are from sewage treatment plants in Austria, especially one in the town of Klosterneuburg -- which gave the viruses their name: Klosneuviruses.

The viruses were identified by metagenomic analysis. That is, the scientists analyzed the DNA in the sewage treatment plants, and inferred the presence of viral genomes. Complicated viral genomes, giant virus genomes.

The heart of the work is the comparison of these Klosneuvirus genomes. The scientists developed a family tree, showing the most likely ordering of the viruses. A part of it is shown in the following figure...

The figure shows the best-fit family tree for two groups of giant viruses. One is the Klosneuvirus group, discovered here; it is shown with a yellowish background. The other is the Mimivirus group, the original giant virus family.

The tree is based on several genes that are common to all these viruses.

The details are hard to read, even in the original, but we can make a few points to illustrate the main observations. We'll focus mainly on the Klosneuvirus group; it includes four species, one of which is called Klosneuvirus.

The black circles with numbers in them... The number is the number of gene families in that virus; the size of the circle reflects that number. You can see that the four most recent viruses, to the right, have the biggest numbers (and biggest circles); that is, they have the most diverse gene sets.

That statement is reinforced by some of the other numbers, though they are hard to read. Look at the upper right. The number for the Klosneuvirus is 1272. The virus just before it in the tree has 611 gene families. To get from that to the final Klosneuvirus, there was a gain of 724 genes, and a loss of 63 genes -- numbers shown above/below the line joining them.

The genes that are gained in the various virus lines look like they came from different sources.

   This is part of Figure 2 from the article.

In summary, if the scientists arrange the new viruses in the most likely family tree, using the usual tools of genetic analysis, it seems clear that these viruses started small, and gained genes -- from various hosts -- over time.

That pattern explains another feature: the gene sets in the various viruses are quite different from one to another. That makes sense if these viruses independently acquired multiple genes. We must note that we do not know why the viruses acquired the extra genes, or what the selective pressures are on them once acquired.

The results for the Mimivirus group are similar, but less dramatic.

Is this the end of the story? No. For one thing, the scientists here did not actually isolate any viruses. (They did see some pictures, which suggested the presence of large complex viruses.) These are hypothetical viruses, inferred from metagenomics. That is an established tool, but we are never quite sure what its limitations are. It would help if the scientists could find actual viruses -- and they plan to try to do just that.

It's still early in the story of giant viruses.

News stories:
* Klosneuviruses: New Group of Giant Viruses Discovered. (, April 11, 2017.)
* New Giant Virus Group Reported -- A genomic analysis of "Klosneuviruses" suggests that they evolved from small viruses that accumulated genetic material over time, but not all virologists are convinced. (D Kwon, The Scientist, April 6, 2017.)
* Novel group of giant viruses discovered. (, April 6, 2017.) A somewhat confusing news story, but it includes an animated gif file showing a virus going around acquiring genes from various host cells. It's cute, even if the main character doesn't look like a virus. (A green giant?)

* News story accompanying the article: Cell-like giant viruses found -- Pieced-together viral genomes contradict view that giant viruses represent a distinct branch of life. (M Leslie, Science 356:15, April 7, 2017.)
* The article: Giant viruses with an expanded complement of translation system components. (F Schulz et al, Science 356:82, April 7, 2017.)

Background post about giant viruses: The largest known virus (August 5, 2013).

The topic of giant viruses has long been on my page Unusual microbes in the section A huge virus. It includes information about the early work.

More sewage microbiology: Turning sewage into profit -- via rocket fuel (September 15, 2010).

More metagenomics: The Asgard superphylum: More progress toward understanding the origin of the eukaryotic cell (February 6, 2017).

There is more about genomes and sequencing on my page Biotechnology in the News (BITN) - DNA and the genome. It includes an extensive list of related Musings posts.

Looking for genes for animal magnetism

June 11, 2017

A recent article on a magnetic fish is interesting not because of the answers (there aren't any), but because of the approach.

It's known that a brief exposure to a strong magnetic field disrupts navigation in rainbow trout. They then recover.

The basic approach in the new work is to find which genes become more active after a magnetic pulse. The work here looks at the genes active in the fish brain. The method compares gene expression after the magnetic pulse vs the control. It does that by collecting all the RNA that is made and sequencing it, a method commonly called RNA-Seq. Brute force, and nowadays quite practical. The motivation for doing this is that it seems likely that genes whose expression is affected by the magnetic pulse include those involved in establishing (or repairing) the fish's magnetic response system. That is, the experiment offers candidate genes for further study.

Here are some results...

The graph may seem complicated, but the basic idea is simple: it shows the effect of the magnetic pulse on the level of expression of each gene (y-axis) vs the expression level of the gene (x-axis).

The details are somewhat cryptic, but it is not critical you follow them.

The y-axis scale uses the ratio of RNA found with the magnetic pulse to that in the controls. That is plotted on a log scale -- base 2 logs. The value 4 on the y-axis means 24, or 16, times greater expression with the pulse. The log scale is symmetric: +4 means the gene is 16 times more active with the pulse; -4 means it is 16 times more active in the control. (Although we earlier suggested that we are looking for genes that are more active with the pulse, it is possible that genes that are less active might also be of interest. The method per se yields both.)

The x-axis scale is a measure of how active the gene is. It's also on a log scale -- base 10 in this case. The value 4 means 104, or 10,000. A gene plotted at x = 4 is 10,000 times more active than one plotted at x = 0. The axis is labeled FPKM. That stands for fragments per kilobase of exon per million mapped fragments. In plain English, it is a measure of how much RNA they found for the gene.

Whether you follow all those details or not, you can see that there is a general pattern -- and a small number of points that may be outside the pattern. The points shown in red are calculated to be significantly outside the main pattern. Those are candidates for further study.

   This is Figure 1 from the article.

The work focuses attention on about 1% of the genes. We can describe those as genes whose expression level is significantly affected by a magnetic pulse. Many are genes involved in iron metabolism. It's not obvious that means these are genes involved in magnetism. After all, iron is magnetic, and it may be that anything involved with Fe will be affected by the magnetic pulse -- whether involved in magnetism or not.

No matter. The point for now is that the measurements lead to candidate genes for further study. It is an example of the "shotgun" approach, where the scientists look at "everything" and hope some candidates stand out. It is an approach that is becoming more common as costs of many molecular biology tools drop. The current work is apparently the first application to biomagnetism.

The authors plan to extend the work to other tissues and other organisms.

News stories:
* Candidate compass genes in fish. (B G Borowiec, oceanbites, May 31, 2017.) Good overview.
* Genes that help trout find their way home -- Study pinpoints genes to navigate by Earth's magnetic field. (Science Daily, April 26, 2017.)

The article: Candidate genes mediating magnetoreception in rainbow trout (Oncorhynchus mykiss). (R R Fitak et al, Biology Letters 13:20170142, April 2017.)

A recent post on bio-magnetism... The nature of a bio-compass? (June 10, 2016). Links to more.

Added June 23, 2017. Another example of RNA-seq, the large scale sequencing of RNA molecules: RNA editing is a major contributor to protein diversity in cephalopod brains (June 3, 2017).

On the spontaneous untying of shoe laces

June 10, 2017

A recent article from a group of engineers at the University of California, Berkeley, explores how it happens. The work uses high-speed video of normal walking and controlled lab experiments to provide evidence on how the shoe lace knot becomes untied. It is a two-step process.

The following figure looks at the first step. The experiment here involves an artificial system for studying shoe lace knots under controlled conditions. It uses a pendulum-like apparatus, with a tied shoe lace near the bottom. As the pendulum reaches the bottom of its stroke, it hits a solid barrier.

The apparatus is fitted with accelerometers. They record the acceleration in various directions.

From the figure legend (with format modified for clarity here)...

"The blue curve (labeled α) represents the accelerations experienced by the knot in the impact direction.

The green curve (labeled β) and red curve (labeled γ) represent off-axis accelerations in the vertical and lateral directions, respectively.

   This is Figure 5 from the article.

The blue curve shows spikes of acceleration of about 7 times gravity -- upon each impact. That serves to loosen the knot. The magnitude of the accelerations seen here with the apparatus were similar to those found with a person walking.

Detailed observation of knots that are becoming untied spontaneously shows that once the knot is a bit loose, the flapping ends promote slippage as the legs swing -- until all is lost. The first phase, where the impact loosens the knot, can be very slow. The second phase, where flapping causes the loose knot to become completely lost, can be very fast, occurring within a few steps.

Is there hope? A critical step is the initial loosening of the knot, due to repeated impact. A knot that is tied in a way that resists this initial loosening is less likely to become untied on its own. The authors show that a square knot would be better than the usual shoe lace knot; why it is better is not clear.

News story: Shoe-string theory: Science shows why shoelaces come untied. (, April 11, 2017.) Good overview.

The article: The roles of impact and inertia in the failure of a shoelace knot. (C A Daily-Diamond et al, Proceedings of the Royal Society A 473:20160770, April 2017.) The topic makes the article fun, but it is also good science, and the article is well-organized and well-written. I encourage you to at least browse it. This may be the first scientific article on the spontaneous untying of shoe laces, but knots are a big issue. The authors discuss knots and their applications. They express their hope that the work will lead to better theoretical modeling of shoe lace behavior. It is a good example of knots under dynamic stress.

Videos. There are two videos posted with the article as supplementary information. Each is about 2 minutes, with no sound. Caution... These are large files (122 & 175 MB). Here are direct links:
* Video 1. This is a video of a real shoe lace becoming untied, as the wearer runs on a treadmill. Slow motion.
* Video 2. This is a video of the pendulum apparatus.

More about the stresses on feet -- and therefore on shoes and shoe laces: Should you run barefoot? (February 22, 2010).

More about acceleronmeters The Quake-Catcher Network: Using your computer to detect earthquakes (October 14, 2011).

Also see: A shoe (August 9, 2010).

June 7, 2017

The new Ebola outbreak

June 6, 2017

The Ebola outbreak in West Africa, 2013-6, resulted in more cases and more deaths than all previous Ebola outbreaks combined. It also resulted in a burst of effort on Ebola treatment and prevention, including a vaccine. And it resulted in a critical examination of how the world looks as such outbreaks.

A new Ebola outbreak is in progress.

It is much more typical of previous outbreaks. It is in a remote region of the Democratic Republic of the Congo (DRC), a country familiar with Ebola.

Extensive testing was quickly implemented. The country has approved use of the new vaccine, to establish protection zones around contacts of those with Ebola (the "ring vaccination" strategy). It's good that the vaccine is available, and that the host country recognizes its possible value. Interestingly, the World Health Organization (WHO) has recommended against its use for now. Why? Well, the total number of deaths so far is three, and there have been no new cases in over two weeks. It is plausible that the outbreak has run its course. WHO says to prepare for vaccine use, but don't implement it. I don't see any point of trying to take sides for now; time will tell.

The big story here is that Ebola has our attention; even a small outbreak gets international attention. It's interesting to watch; have we learned our lessons?

With luck, there will be no follow-up to this post.

This post is based on a news story and a WHO report...

News story: DRC approves use of Ebola vaccine. (S Soucheray, CIDRAP, May 30, 2017.) CIDRAP notes news on the topic regularly. For updates, click on the Ebola link at the top of their page. The current page also includes more information on the vaccine, focusing on side effects.

Recent "Situation Report" from the WHO: Ebola virus disease -- Democratic Republic of the Congo -- External Situation Report 17. (WHO, May 30, 2017.) An 8 page pdf file summarzing the sitautoin and what WHO is doing. (This is one report more recent than the one noted in the news story above.)

Recent post about the Ebola vaccine: Update: Ebola vaccine trial (January 24, 2017).

There is more about Ebola on my page Biotechnology in the News (BITN) -- Other topics in the section Ebola and Marburg (and Lassa). That section links to related Musings posts, and to good sources of information and news.

DNA evidence in restaurants: is the fish properly labeled?

June 5, 2017

If you order your favorite cut of beef, and the waiter brings you a chicken leg, you would notice, and complain. Yet something logically similar is common. If you order fish, you may well get a different kind of fish -- and you usually can't tell. It's a well-known problem, and it isn't getting better.

That's the essence of a new article. The experimental work was straightforward, though making use of the most modern methods. The scientists went into several sushi restaurants and grocery stores in the Los Angeles area to get fish. They took samples of what they got back to the lab, and analyzed the DNA to identify the fish. They used the approach called DNA barcoding, in which they look at the sequence for specific genes that have been shown to be useful for the problem at hand.

The scientists analyzed samples from sushi restaurants over a four-year period, 2012-5. For each year, the DNA analysis showed that 40-50% of the samples were mislabeled. They also analyzed samples from "upscale" grocery stores for 2014; 42% were mislabeled.

Qualitatively, the results were not surprising. However, reports of the frequency of mislabeling of fish vary widely: from less than 2% to 79% mislabeling, according to a table in the current article. The reason for the variation has not been clear.

The authors suspected that the mislabeling varied between types of fish. Therefore, they subdivided their results by that criterion. The following figure shows the results.

The graph shows the percentage of sushi samples that were mislabeled, by type of fish.

The numbers on each bar show how many samples were mislabeled and the total. That is, for the bluefin (left bar), 0 of 11 samples were mislabeled. For the halibut (right), 43 of 43 samples were mislabeled. As those two bars show, the results varied from 0 to 100% mislabeling for various types of fish.

   This is Figure 2 from the article.

Overall, the article shows that about half of the fish are mislabeled, varying widely between types of fish. The four-year study from sushi restaurants suggests that the situation is not getting better, despite recent attention and the implementation of regulation.

Why does it matter? There are several reasons, starting with the basic point that you should get what you order. Issues beyond that include... Inexpensive fish may be passed off as more expensive fish, increasing someone's profits. Some fish, or even populations, are endangered, and mislabeling is a way to circumvent restrictions on harvesting some types of fish. In some cases, there may be health implications of having the fish properly identified.

The article concludes with discussions about the implications for conservation and policy. For example, the authors note that the current efforts in Los Angeles to reduce fish mislabeling seem ineffective.

News stories:
* Study Finds Significant Sushi Mislabeling, Part 1. (Slices of Blue Sky, February 12, 2017.)
* The Secret in Your Sushi. (A Yoon, Discover (blog), March 27, 2017.) Includes a flow chart of the general procedure used to identify the fish by DNA.

The article: Using DNA barcoding to track seafood mislabeling in Los Angeles restaurants. (D A Willette et al, Conservation Biology, in press.) The samples were collected by students in an undergraduate course in marine science.

The following post introduced the problem, and showed the potential usefulness of DNA analysis: Tracking illegal fish (June 15, 2012).

There is more about DNA sequencing on my page Biotechnology in the News (BITN) - DNA and the genome. It includes an extensive list of related Musings posts.

Previous post about sushi Sushi, seaweed, and the bacteria in the gut of the Japanese (April 20, 2010).

* Previous post from Los Angeles: Los Angeles leaked -- big time! (April 29, 2016).
* Added June 21, 2017. Next: Water loss from irrigated lawns (June 21, 2017).

A treatment for senescence?

June 4, 2017

An interesting development in the study of aging is the recognition that some cells go into a distinct stage called senescence. These senescent cells play a key role in the overall phenomenon of aging. Not only do these senescent cells fail to function properly, they interfere with normal functioning of other cells.

A recent article shows that a novel drug selectively kills senescent cells.

The following figure shows some results...

Part A (top) shows the basic effect, using lab cultures of the cells.

Two groups of cells were treated with increasing concentrations of the drug. The cells are control (Ctrl, black) or senescent (Sen, red).

The survival of the cells (y-axis) is plotted against the concentration of the drug, FOXO4-DRI (x-axis; micromolar).

It is clear that the Sen cells survive the drug poorly, compared to the Ctrl cells. For example, a concentration of 25 µM kills the senescent cells almost completely, with almost no effect on the control cells. A measure of the effect is the selectivity index (SI50), the ratio of concentrations needed to kill 50% of the two kinds of cells. The SI50 shown on the graph is 11.73; that is, it takes about 12 times more drug to kill the control cells compared to the senescent cells (as judged by the 50% points).

Part D (bottom) shows an experiment to help characterize the effect.

Three proteins are tested here. Each is tested at three concentrations (6.25, 12.5, and 25 µM); the little ramps at the bottom symbolize the increasing concentrations. The results for each protein are shown with a different color. The first bar (black) is a control (labeled "Mock"), and is set to 100% survival.

The bars vary. Look for bars with asterisks; they mark that the result is significantly different from the control. The only marked bars are the two red bars for the highest concentrations -- of FOXO4-DRI, the drug used above in Part A. That is, in this test, FOXO4-DRI again shows an effect that is consistent and dose-dependent. The other two proteins tested do not show a significant effect.

   This is from Figure 3 from the article.

What is this drug, and what is it doing? Those are both complex questions, since the work here is a small part of this emerging complex story of senescent cells. We can only hint at the answers here.

The drug is a peptide. It is a variant of part of the natural protein FOXO4. An interesting variant, one made up of mirror image amino acids arranged in reverse order. The suffix DRI stands for D-retroinverso. That may seem odd, but there is work suggesting that peptides made that way are sometimes useful. It's a lead, with no certainty of success. But that is what they used here; it worked.

What is FOXO4? It is a regulatory protein. Its level is elevated in senescent cells, and it helps the protein p53 to enter the nucleus. The variant of FOXO4 that the scientists used here was designed to specifically inhibit the interaction of the normal FOXO4 with p53, so that p53 can't enter the nucleus. The build-up of p53 in the cytoplasm leads to apoptosis, and the cells die. That is, the drug leads to apoptotic death of the senescent cells. At least, that is what they think is happening, and there is considerable evidence in the article to support that model. Regardless of the details, which are complicated, the FOXO4-DRI drug does seem to selectively kill senescent cells (as shown above), and the scientists at least partially understand why.

What are the other proteins in Part D, above? The second one (green) is the "normal" form of that same segment of FOXO4; "normal" means it was made with the regular L-amino acids. The right-hand protein (gray) is based on another member of the FOXO family, and made in the DRI form.

What happens in an animal? The scientists did some tests with mice, both a strain with accelerated aging and normal mice. They found that some physiological features associated with aging, such as kidney function, were improved by the drug. That is, the drug may promote healthier aging in some ways. It encourages them to study the system further.

The story of senescent cells is intriguing, but poorly understood at this point. The work here offers some understanding of part of the process of aging. It may seem to offer the hope that one might treat some aspects of aging by treating senescent cells with a drug, but this early lab work in mice is far too preliminary to make that anything but speculation.

News stories:
* Peptide targeting senescent cells restores stamina, fur, and kidney function in old mice. (Science Daily, March 23, 2017.)
* Modified protein promotes hair growth and fights aging in mice. (NHS Choices, March 24 2017.) This page emphasizes the animal studies, and, as usual for this source, emphasizes cautious interpretation.
* Expert reaction to study reporting the effect of a potential anti-ageing peptide therapy in mice. (Science Media Centre, March 23, 2017.)

The article: Targeted Apoptosis of Senescent Cells Restores Tissue Homeostasis in Response to Chemotoxicity and Aging. (M P Baar et al, Cell 169:132, March 23, 2017.)

A previous post about trying to modify aging... Extending lifespan by dietary restriction: can we fake it? (August 10, 2016).

More about apoptosis, including the role of p53: Why do elephants have a low incidence of cancer? (March 20, 2016).

My page for Biotechnology in the News (BITN) -- Other topics includes a section on Aging. It includes a list of related posts.

Coloring with graphene: making a warning system for structural cracks?

June 2, 2017

Some things have different colors when we look at them from different angles. We call that property iridescence. The basis of the color change is understood. It has to do with the physics of light. Consider a fish with thin scales -- thin, on the order of the wavelength of visible light. Light reflects off the fish, but exactly how varies with how we look at the fish. The layer of scales reflects different colors differently, and that is very sensitive to just how the scales are arranged and to our angle of observation.

What if we made bridges that were iridescent like fish?

A new article reports progress toward doing just that. Why? Iridescence might serve as a warning system for structural damage in a bridge. Iridescence for safety.

The idea is to coat the bridge with graphene nanoplatelets (GNP). If these are designed right, the layered coating is much like the fish scales: iridescent. In particular, changes in the structural material of the bridge, such as cracks, would distort the GNP -- and change the color of the bridge.

The following figure shows the idea and lays the groundwork.

The figure has two parts. The main part is a graph of some data. The inset is essentially a cartoon to show the idea.

The basic system involves a coating of graphene nanoplatelets. The coating is stressed, so that it becomes thinner. What is the effect on its color?

The inset cartoon shows three situations. As you go from left to right, you can see that the coating is thinner. Look at the colored arrows, and you can see, qualitatively, that which colors are reflected changes as the coating becomes thinner.

The graph? The x-axis is the strain on the coating, labeled εc. The value 5% (the right-hand end of the x-axis) means that the coating has been stressed so it is 5% thinner. Two measurements are plotted:
- d, the thickness of the GNP coating (left-hand scale);
- λr, the wavelength of the peak reflectance (right-hand scale).
You can see that both of these parameters vary with the strain. That is, the material deforms, and the deformation can be detected by the color change.

   This is Figure 3b from the article.

There is a little bonus in using the graphene-based system. Graphene conducts electricity. Crack the coating and it will lose its conductivity. Thus a pair of simple measurements, color and conductivity, should work in concert to monitor bridge integrity.

It's an interesting idea, and the scientists have shown, in lab-scale work, it might work. This isn't the first approach for making a self-diagnosing structure, but it seems to deserve consideration.

Amusingly, in the simple implementation of the proposal, the coating would change from red when safe to green when unsafe.

News story: Graphene coating that changes color when deformed or cracked. (B Yirka,, April 10, 2017.)

The article: Variable structural colouration of composite interphases. (Y Deng et al, Materials Horizons 4:389, May 2017.) It's an interesting article, but quite difficult.

A recent post about graphene: Water desalination using graphene oxide membranes? (April 29, 2017).

Posts about graphene are listed on my page Introduction to Organic and Biochemistry -- Internet resources in the section on Aromatic compounds.

The authors describe their work as bio-inspired, with the analogy to fish scales (and other materials). See my Biotechnology in the News (BITN) topic Bio-inspiration (biomimetics). It includes a listing of Musings posts in the area, and has additional information.

Another bridge post: Happy Birthday (May 27, 2012).

May 31, 2017

A step toward doing cephalosomatic anastomosis in humans?

May 31, 2017

A new article reports transplanting a head onto a rat, making a rat with two heads.

I'll skip the picture here. It is in the article, and in many of the news stories.

Actually, the picture is not particularly disturbing. But the story around the work might be.

There is nothing new about grafting a new head onto an animal. Scientists have been working on it for over a century. Making a two-headed animal is just one way of doing it, without removing the original. But this is now serious work, with a goal: doing a cephalosomatic anastomosis in humans. "Ceph" refers to head, "soma" to body, "anastomosis" to joining. In plain English, a head transplant.

Musings has recently noted work to develop embryos derived from three parents, in order to avoid mitochondrial diseases [link at the end]. That story has two parts. First, there is the science... understanding the problem and the approach to solving it, and then the testing to see how the new solution is working. Second, there are the ethical questions as the work progresses into humans. Do we, as a society, approve of such work? If so, how should it proceed? The ethical issues get highlighted when some scientists in the field seem to look for ways to avoid them, avoiding public debate and regulation.

So it is here, too. The new article indeed has technical advances that may interest some readers. The main development in this article is that the scientists used a third rat to help maintain the blood supply during the transplant.

However, the big story around the article is that the scientists have announced that a human head transplant is imminent (perhaps late this year). Are we ready for this? Is the science ready? And the ethical questions? Will the work be regulated appropriately -- whatever that means? Remember, establishing regulations, at least in countries such as the US, requires public debate.

I don't see any need to elaborate here. The issues are clear enough. I encourage you to look over some of the news stories. Some are listed below, as usual for Musings. If you want more, from a variety of sources, try searching on the article title, or on human head transplant, or on the name of the key scientist. (If you want to impress the people at Google who execute your searches, you can search on cephalosomatic anastomosis.)

How are the two-headed rats doing? They were euthanized within two days, so we will not get information on long-term effects. Up to that point, function seemed ok, though the information is limited.

News stories:
* Rat Head transplant test leading to human head transplant. (B Wang, Next Big Future, May 2, 2017.)
* Scientists Carry Out Rat Head Transplant. (H Osborne, Newsweek, April 28, 2017.) An item from the general news media. It's actually quite good.

The article: A cross-circulated bicephalic model of head transplantation. (P-W Li et al, CNS Neuroscience and Therapeutics 23:535, June 2017.)

The article contains a statement that the work was approved by the host institution. We should emphasize that there is no claim, so far as I know, that the scientists did anything illegal. The question may be whether that is a sufficient standard.

Most recent post in the story of tri-parental embryos: The boy with three parents -- an article is now published (May 17, 2017).

My page Biotechnology in the News (BITN) for Cloning and stem cells includes an extensive list of related Musings posts, including those on the broader topic of replacement body parts.

My page for Biotechnology in the News (BITN) -- Other topics includes a section on Ethical and social issues; the nature of science. And there is a section Brain (autism, schizophrenia). Each section includes a list of related Musings posts.

Was there a significant slowdown in global warming in the previous decade?

May 30, 2017

Global warming is a long-term phenomenon. Over a few years or even a decade, our weather varies, for various reasons. The effect of changes in greenhouse gases, such as CO2, is significant only over longer periods. The general prediction of most experts in the field is that the warming trend will continue for many decades, and will probably lead to an overall increase of more than two degrees (Celsius).

During the first decade of the 21st century, the global temperature (T) seemed to be leveling off. For those who were skeptical of the overall phenomenon of global warming, this was evidence that it had stopped.

The last three years have been the warmest on record. For those who want to press the panic button, what better evidence could there be?

A new article steps back, and looks at the big picture, the long-term trend.

The following graph shows the record of global T using five different data sets, going back well into the 19th century.

First, all five lines are fairly similar (at least, since about 1900). So, let's treat them as the same. (The article discusses some of the differences between the data sets, but that doesn't matter for us at the moment.)

The curves have long regions that are approximated by straight lines. There are three regions where the lines change direction. These are marked by (barely visible) vertical stripes on the graph, with the dates indicated. The most recent such change in direction is 1964-1982.

The current linear region extends right through the 2000-10 decade, which certainly does not look unusual on this graph. The authors also do statistical testing, and show that a group of low years, such as found shortly after 2000, is not at all unexpected given the observed variability.

The most recent points (2014-6) aim high, but there is no evidence -- yet -- that a new trend has begun.

   This is Figure 2 from the article.

That's it. A long-term perspective on global T. Over the short term, T fluctuates. We are interested in long-term trends, but it is hard to see what is significant over the short term.

We got through the 2000 decade, and the observed reduction in warming appears to not be significant. It is still fine to discuss factors that might have contributed to reduced warming in those years; that may be interesting or even useful. However, from the perspective of long-term trends, the short-term variations weren't significant. Recent years seem high. If one wants to suggest it is prudent to consider that these recent years might turn out to be significant, ok. But don't claim that there is evidence for a significance increase in the rate of warming. It will take a few years before we will be able to judge whether the recent increases are significant.

It's easy to see why the public can be confused. We tell people to look at the facts -- the data. They see the data, and then we try to explain that the data may not be significant.

News stories:
* Global warming trend with ups and downs, but without slowdown or speed-up. (Potsdam Institute for Climate Impact Research (PIK), April 25, 2017.) From the lead institution.
* Expert reaction to climate hiatus statistics. (Science Media Centre, April 25, 2017.) A collection of comments by some experts.

The article, which is freely available: Global temperature evolution: recent trends and some pitfalls. (S Rahmstorf et al, Environmental Research Letters 12:054001, April 25, 2017.) A quite readable article. There is some math, even some equations, but the authors explain what they do in plain English. I think that is their purpose, to explain the analysis.

A post about that low-T decade of the 2000s: Why the lull in global warming? (February 11, 2014). Links to more.

A recent post about global warming: Geoengineering: the advantage of putting limestone in the atmosphere (January 20, 2017).

Other posts about global warming include...
* How rice leads to global warming, and what we might do about it (September 2, 2015).
* Global warming (August 3, 2008).

There is more about statistics on my page Internet resources: Miscellaneous in the section Mathematics; statistics. It includes a listing of related Musings posts.

What if the caterpillars ate through the plastic grocery bag you put them in?

May 26, 2017

A beekeeper cleans up an infested hive, and puts the worms (caterpillars) in a plastic grocery bag. Later, she notices that the worms have eaten through the bag. The beekeeper happens to be a scientist, and realizes that the finding could be of interest. A new article reports some results.

Here is an example from lab testing of what these worms can do...

An ordinary plastic grocery bag. It contained 100 worms for 12 hours. This image focuses on a corner of the bag, including one handle.

   This is Figure 1B from the article.

Plastic grocery bags are made from polyethylene (PE), a plastic that is normally considered not biodegradable. PE has become a serious waste problem, and the use of such bags is restricted in many places. Finding a process for the biodegradation of PE would be of interest.

What makes the finding here of particular interest is the nature of the worms. They are the larvae of Galleria mellonella, and are commonly called wax worms. They eat the honeycomb of beehives. Not the honey, but the wax. (They are a pest, as hinted in the opening above.) Beeswax contains various chemicals, but some are very much like polyethylene -- basically a hydrocarbon chain. It is plausible that the wax worms eat PE just as they eat the beeswax. That is, it may be that Nature has indeed solved the PE problem, in the guise of beeswax.

The article here has limited evidence, but it is encouraging. The scientists see the degradation of the PE bag, and show that the process does not require intact worms; an extract, presumably containing enzymes, will do. A preliminary analysis suggests there is a chemical modification of the PE in a way that is consistent with biodegradation.

Let's assume that the basic finding holds up: wax worms degrade polyethylene. Could this be useful? That's a more difficult question. Could a pile of worms be the basis of a practical economic process for biodegradation of PE? We can guess that the process is carried out by microbes, by enzymes from those microbes. The more promising approach probably would be to look for those microbes, and for their enzymes. Can we develop them, the key players in what the worms are doing? The authors of the current work plan to pursue this project, so over time we may find out.

News stories:
* Caterpillar found to eat shopping bags, suggesting biodegradable solution to plastic pollution. (, April 24, 2017.)
* Plastic-eating worms could help wage war on waste. (I Sample, Guardian, April 24, 2017.)
* Plastic-eating bugs? It's a great story - but there's a sting in the tail. (P Ball, Guardian, April 25, 2017.) This page was written as a rebuttal to the one immediately above. It may be over-stated, but the main point is good. Ball emphasizes that using the worms would probably not be good for a practical process. However, he appreciates the interest in the work, and agrees that use of the microbes or enzymes might work. Read both of these and you get a good sense of what this is about.

The article: Polyethylene bio-degradation by caterpillars of the wax moth Galleria mellonella. (P Bombelli et al, Current Biology 27:R292, April 24, 2017.)

An earlier post on biodegradation of a plastic: Polystyrene foam for dinner? (October 19, 2015). Links to more.

More about polyethylene... Degradable polyethylene isn't (October 17, 2011).

More about beeswax... Bee history (February 13, 2016).

May 24, 2017

Trains, grains, and bears

May 24, 2017

The following figures show a problem...

Part c (left) shows a grizzly bear on the railroad tracks. Part b (right) shows one of the reasons. Trains, carrying agricultural products, leak and spill food on the tracks. Bears learn that the tracks may be a source of easy food.

These are trimmed from parts of Figure 1 from the current article. (In the figure legend in the article online, the descriptions of 1a and 1c are reversed; perhaps this will get corrected at some point.)

Trains kill bears. It is an increasing problem in parts of the Canadian Rockies. One might think the connection would be obvious, but it is just getting attention, and scientists are analyzing it.

The current article starts by measuring the amount of grain left on the tracks as trains cross through two national parks (Banff and Yoho) carrying shipments from the rich agricultural regions of central Canada. It is about 1.6 grams per square meter per day. That may not sound like much, but it totals about 110 tons over a year. That is about equal to the total needs of the entire population of grizzlies in the area. That doesn't mean it is their entire diet, but it shows that grain spillage from trains is potentially a significant contributor to the bears.

The authors did not find specific causes of grain loss from the trains, beyond the simple point that the hopper cars leak. I suspect that they may be over-filled, with a tendency to spill when the trains accelerate, including when they go around bends.

What do the authors suggest? First, fix the train cars to reduce grain spillage. That would seem simple in principle. Maybe the real first is to recognize the problem and give it full attention. The article is a step in keeping the bears off the train tracks.

News story: Following tracks to steer grizzlies from trains. (D Kobilinsky, Wildlife Society, February 17, 2017.) Includes some information and ideas beyond what is in the current article.

The article: Grain spilled from moving trains create a substantial wildlife attractant in protected areas. (A Gangadharan et al, Animal Conservation, in press.)

More on Banff wildlife...
* Why the bear used the overpass to cross the highway (May 11, 2014).
* Super Squirrel (September 19, 2009).

And locally... Berkeley wildlife (September 3, 2010).

The work here is part of the broader topic of the interaction of wildlife with humans.
* Musings has noted examples of such work with birds, e. g., Airport food: What do the birds eat? (May 24, 2014).
* And at a different level... Security fences at national borders: implications for wildlife (August 29, 2016).

We've noted before that we consider bears important... Bears (May 25, 2010). It's easy to poke a little fun at some aspects of the current work. But seriously, what's really important is that they are doing it. In California, we have immortalized the grizzly on our flag, but that's all we have left of that bear. The scientists doing this work may help save the grizzlies in the Canadian west.

Scientific curiosity -- and politics

May 22, 2017

A recent article explores an interesting connection hinted at in the title. It is hard to know what to make of the article. The authors provocatively put some issues on the table, but they are actually quite cautious in reaching conclusions. Let's look at some of the points they make.

The authors have recently developed a way to measure scientific curiosity. It is the Science Curiosity Scale (SCS). This in itself is something of an accomplishment, because it has been a rather vague idea in the past, with some claiming it couldn't be measured. Of course, developing a measurement doesn't tell us what it means -- or that it has any importance.

The current article explores what the SCS means. Here is an example...

In this test, the authors have viewers watch 10 minute segments of various movies. Two of the movies are science documentaries. One is a Hollywood gossip show.

The viewers are free to stop watching as they wish. That is what is measured here: how long they watch each movie. That is plotted (y-axis) vs the SCS (x-axis). Be careful with the x-axis; it is scaled oddly. It makes sense for something with a "normal" distribution. Don't worry much about that, though. The main point is to look for the general nature of any trends, and don't worry about the exact shape.

   This is Figure 5B from the article.

The basic observation from that graph is that those with greater scientific curiosity spend more time watching the science shows -- and less time watching the gossip show. The article includes other measures of the viewers' interest in the movies; they all give the same general pattern.

The following figure connects the SCS to politics...

A question is asked, shown at the top. Participants give their rating, using a common type of classification of risk. That risk rating is shown on the y-axis scale.

The responses for risk are then plotted two ways. In each case, the responses for "liberal democrats" and "conservative republicans" are shown separately. In one graph (right side), the two curves are parallel; in the other (left side), they show opposite effects.

What are these two graphs? On the left, risk scores are plotted against a measure of scientific intelligence (that is, knowledge); on the right, risk scores are plotted against the curiosity score -- the SCS.

   This is the top frame of Figure 8 from the article.

The authors suggest that scientific understanding, as measured here by the risk score, correlates with "curiosity" -- and does so across the political spectrum. Political views are still evident, but curiosity seems to have a consistent effect on top of that. In contrast, scientific understanding does not correlate with scientific "knowledge".

I noted at the start that I am not sure what to make of all this. I can think of many questions that I would want to ask before accepting the conclusions. The authors, too, are cautious. And I have presented here only parts of two figures, so you should be even more cautious.

That "curiosity" correlates with open-mindedness is plausible, but it may not be simple. That scientific curiosity may correlate with an openness on issues that are politically controversial is intriguing. More work is needed -- which is what the authors themselves say.

News stories. Both of the following are good overviews of the article. They are fairly low in overt hype, but they do lack skepticism and critique.
* How curiosity can protect the mind from bias. Neither intelligence nor education can stop you from forming prejudiced opinions - but an inquisitive attitude may help you make wiser judgements. (T Stafford, BBC, September 8, 2016.)
* Arousing Curiosity May Help Take the Politics Out of Science. (C Bergland, Psychology Today, February 1, 2017.)

The article, which is freely available: Science Curiosity and Political Information Processing. (D M Kahan et al, Advances in Political Psychology 38 Suppl. 1:179, February 2017.) If you're intrigued about the topic, I encourage you to look over the article. It's rather long, and not always easy. But for the most part it is well-written. (One of the authors may be known to some readers. Kathleen Hall Jamieson, from the University of Pennsylvania, is often on news shows as a commentator.)

Scientific curiosity has been invoked in many posts, such as... Ribosomes with subunits that are tethered together (October 5, 2015).

A post about the political spectrum: The political leapfrog (January 24, 2011).

My page for Biotechnology in the News (BITN) -- Other topics includes a section on Ethical and social issues; the nature of science. It includes a list of related Musings posts.

Is there food on Enceladus?

May 21, 2017

We now have about 30 seconds of evidence. Look...

The graph shows data collected by the Cassini spacecraft in its most recent -- and last -- fly-by of Enceladus.

The y-axis shows the amount of food. That is plotted against the time of the observation; zero on the x-axis is the time of closest approach of the spacecraft to the moon. The graph shows data from about 15 seconds before closest approach to 15 seconds after closest approach.

There is a zoo of data points. Perhaps you will see a pattern: quite a bit of food was detected from about -5 seconds to +5 seconds.

But the graph is more complicated, and actually rather interesting. This is high tech data for something not easily measured. And there isn't much of it. The scientists are carefully presenting the data in great detail. The green points (which seem to merge into short segments) are the background counts from the instrument. That is, the instrument sends back a small signal even when no food is actually present. The open circles are data points from the fly-by that are not significantly different from that background. Then there are blue circles; these are data points that are (more than) 1 standard deviation (σ) above background. And then there are some points marked as being 2σ or even 3σ above background; these points are almost all within 5 seconds of closest approach.

The y-axis scale is split. In the lower part, the scale is linear. In the upper part, it is a log scale. The split scale allows the authors to present the low points in detail, yet still show the full range of higher points.

   This is Figure 2 from the article.

What is this food, and how did the scientists measure it? Look at the label on the y-axis... it says "Mass 2". That is hydrogen gas, and the label might suggest they used mass spectrometry. (The label also says OSNB counts per IP. OSNB is the name for the method, and IP means integration period.)

Recall that Enceladus is the moon that sends out plumes of water [links at the end]. Cassini flew through the plumes; its mass spec, open to the outside, measured the gas it found. The graph shows the data for the amount of H2 found in the plumes during the few seconds of closest approach. There was some, though most of the measurements were barely above background.

H2? Not your idea of dinner? But it is a good energy source for some bacteria. We already knew Enceladus has water, probably even an ocean. That immediately started us thinking about the possibility of life. We now have some evidence for a food, a fuel. None of this is evidence for life on Enceladus; it only allows for life. It is intriguing.

There are more tidbits and much speculation here. The mass spec also shows there is CO2. The presence of H2 and CO2 together says that the system is not at chemical equilibrium. That's nice, and it allows for life processes, but it also raises questions about where these chemicals are coming from. There may be interesting geochemistry going on inside Enceladus. It is likely that the H2 is being made, on an ongoing basis, by the interaction between the ocean and the rock below.

Cassini has taught us much about Enceladus over recent years, but each answer raises new questions. For some scientists, Enceladus is now the #1 candidate for a body beyond Earth with life.

News stories:
* Scientists discover evidence for a habitable region within Saturn's moon Enceladus. (, April 13, 2017.)
* Hydrogen Gas Detected in Plume on Saturn's Moon Enceladus. (Deep Carbon Observatory, April 25, 2017.)
* Hydrothermal Activity in The Seas of Enceladus: Implications For Habitable Zones. (K Cowing, Astrobiology, April 11, 2017.) A good discussion of the implications.

* News story accompanying the article: Planetary science: Detecting molecular hydrogen on Enceladus. (J S Seewald et al, Science 356:132, April 14, 2017.)
* The article: Cassini finds molecular hydrogen in the Enceladus plume: Evidence for hydrothermal processes. (J H Waite et al, Science 356:155, April 14, 2017.)

Background posts about Enceladus:
* A water fountain for Saturn (October 23, 2011).
* Enceladus and its plume (November 17, 2009).

More about hydrogen as a food: The hydrogen economy -- in the mid-Atlantic (August 30, 2011). The work discussed here also involved mass spectrometry to measure H2.

A recent post involving mass spectrometry of unusual forms of hydrogen... Hydride-in-a-cage: the H25- ion (January 22, 2017).

A recent post about results from Cassini: Quiz: what is it? (April 5, 2017).

May 17, 2017

The boy with three parents -- an article is now published

May 17, 2017

Last Fall there were two Musings posts on tri-parental embryos [links at the end]. Briefly, tri-parental embryos involve the use of a third parent, who provides the mitochondria to the embryo. The method is also called mitochondrial replacement therapy (MRT). The purpose is to avoid mitochondrial disease carried by the mother. At some level, the method works, but there are considerable uncertainties. The first post discussed some recent lab studies with the method. The second, a week later, announced the birth of the first human baby from such a procedure. As discussed in those posts, the topic involves interesting scientific issues, and also involves ethical questions, about its application to humans.

The details have now been published in a regular scientific article. An editorial accompanying the article may be of particular interest.

Aside from the technical details, the article notes that the parents have decided that some medical testing of the child will be restricted, unless there are adverse symptoms. It is their right to make such a decision, but it does raise some questions about how the people were selected and informed about the procedure. The use of MRT is experimental. Is it reasonable to expect that the medical team would take great care that the family fully understands the experimental nature of the work, and the importance of the follow-up?

Comment... It may appear that I am expressing opinions about the work, here and in the previous posts on the topic. So I want to emphasize that the main intent is to raise questions, not to answer them. The questions here come up regularly with medical development, and it is good to think about them. They are not easy questions.

For now... The child is seven months old and healthy (as of the writing of the article). He has a measurable level of defective mitochondria, which currently is well below the level that would promote disease symptoms.

News stories. I've included multiple stories here, with a range of views, especially on the ethical questions. Some people may want to delve into the technical issues, but the ethical aspects of this may be of most interest for most readers. Those who have access are encouraged to read the editorial that accompanies the article. Otherwise, the news stories listed here will give you a good overview.
* Technique for 'Three-Parent Baby' Revealed. (Elsevier, April 3, 2017.) From the journal publisher.
* Method behind first successful mitochondrial replacement therapy revealed. (H Robertson, BioNews, April 3, 2017.) As usual with BioNews, this story links not only to the article (and editorial), but also to other news stories.
* It's a Boy: Ethical Implications of the First Spindle Nuclear Transfer Birth. (E Armstrong, Voices in Bioethics, March 2, 2017.) Armstrong refers to an item in the journal Fertility and Sterility from last Fall. That is only an abstract, for a meeting talk. The article listed below is the first full scientific publication of the work. By the way, Armstrong has an extensive list of references, including many news stories. One item, which she discusses briefly, is an article in a law journal; it apparently questions whether the procedure was in fact legal in the country where it was carried out. I have not checked this further.
* Expert reaction to study explaining technique behind first mitochondrial replacement therapy baby. (Science Media Centre, April 3, 2017.) A collection of comments by various people in the field. They are varied!

* Editorial accompanying the article: First birth following spindle transfer for mitochondrial replacement therapy: hope and trepidation. (M Alikani et al, Reproductive BioMedicine Online 34:333, April 2017.)
* The article: Live birth derived from oocyte spindle transfer to prevent mitochondrial disease. (J Zhang et al, Reproductive BioMedicine Online 34:361, April 2017.)

Background posts:
* Tri-parental embryos: the first human birth (October 1, 2016).
* Tri-parental embryos for preventing mitochondrial diseases (September 23, 2016).

Added June 18, 2017. More about mitochondria: Nuclear-mitochondrial interactions -- and the definition of a biological species (June 18, 2017).

Added May 31, 2017. Also see: A step toward doing cephalosomatic anastomosis in humans? (May 31, 2017).

My page for Biotechnology in the News (BITN) -- Other topics includes a section on Ethical and social issues; the nature of science. It includes a list of related Musings posts.

Information storage: One atom, one bit

May 15, 2017

Holmium atoms have one of two spin states, which we call up and down. In principle, we could store information using those spin states. In principle, each Ho atom, through its spin -- up vs down, could carry one bit of information.

To be useful, of course, we would need a way to "write" and "read" those Ho spin bits.

A recent article reports progress in doing exactly that. The following figure shows a memory device based on the use of Ho atomic spin. It is a 2-atom device.

Frame a (left) shows the setup. Two atoms of holmium and one atom of iron. The Ho atoms are the memory device, and the Fe atom is the sensor.

Note that the Fe atom is closer to one Ho atom than to the other. As a result, the HoA atom has more of an effect on the Fe.

Frame b (right) shows some measurements. They show a type of absorption spectra for the Fe, as influenced by the spins of the nearby Ho atoms. You can see that the four scans show peaks in four different places. The diagram to the right shows the spin states of the two Ho atoms responsible for each of the four curves. Each possible combination of spin states can be distinguished.

   This is Figure 3 from the article.

The conclusion? We can measure the spin states of individual Ho atoms. One atom, one bit -- and we can measure it.

The authors also note that the spin states are stable, at least over a period of a few hours. It is likely that the way the Ho atoms are attached to a surface, magnesium oxide in this case, helps promote the stability.

The work here is done in an atomic force microscope, in high vacuum and near absolute zero. The atoms are about a nanometer apart, but the equipment needed to operate the device would fill a small room. The authors conclude that they have shown that using one atom to store one bit of information is possible. They do not claim it is useful. Yet.

News story: IBM-led international research team stores one bit of data on a single atom -- Could lead to 1,000 times higher storage density in the future. (Kurzweil, March 9, 2017.)

* News story accompanying the article: Nanoscience: Single-atom data storage. (R Sessoli, Nature 543:189, March 9, 2017.)
* The article: Reading and writing single-atom magnets. (F D Natterer et al, Nature 543:226, March 9, 2017.)

More about data storage: Progress toward an ultra-high density hard drive (November 9, 2016). There are similarities between that and the present work. This post approaches the use of one atom per bit, by using the presence or absence of the atom at a particular site. It is also run with an atomic force microscope. The links there are also generally relevant here.

More on detecting magnetism... The nature of a bio-compass? (June 10, 2016).

Previous posts mentioning holmium: none.

However, there was a post about its neighbor in the periodic table... Penidiella and dysprosium (September 11, 2015).

An antibody treatment for Marburg virus disease?

May 14, 2017

A simple experiment. Four groups of animals were infected with Marburg virus. The survival curves for the four groups are shown in the following figure...

For two groups, survival was poor. All the animals were dead by 13 days after infection. These are the control groups, with no treatment.

For the other two groups, survival was better. In fact, for one group, all the animals were still alive by the end of the experiment (day 28). These groups were treated -- with one or another monoclonal antibody to the virus (#191 or 78, as labeled at the right side).

   This is modified from Figure 1A in the article. I added labels to identify the treatments.

Simple experiment. Simple result: the treatment works. So let's look at what this is about.

Marburg virus? It's a filovirus, a cousin of Ebola. As with Ebola, it is largely found in occasional outbreaks in Africa, there is no established prevention or treatment, and it is deadly.

Animals? The work shown above was done in guinea pigs as an animal model of the disease. The common Marburg virus doesn't grow in guinea pigs, so the scientists used a modified virus that had been adapted to that host.

Based on results such as those, the scientists conducted a similar test with rhesus macaques, using the better of those antibodies. The results were the same, with no survival of the controls and high survival of the treated animals. Treatment was initiated as late as 5 days after infection.

How many? One of those curves is suspiciously steep. For one of the control groups, the entire group died on day 10. One animal. The other control curve shows their "historical control" of animals without treatment. (The two treatment groups had five animals each.)

Survive? Those animals that survived -- are they actually ok? Yes, there is considerable data in the article suggesting that they are healthy. They gain weight normally, and they are virus-free.

The antibodies? They were derived from antibodies found in a survivor of Marburg infection. That source does not guarantee they are useful, but it seems to help. (Similar work has been done for Ebola.)

Specificity? Antibodies tend to be specific, and there is a strong selection for mutant viruses that can avoid them. Is that likely to be a problem here? In this work, the scientists also used a second virus, called Ravn; it is a strain of Marburg, but distinct. The same antibodies were as effective against Ravn as against Marburg. One treated macaque did die from the infection; why is not clear, but there was no evidence that it developed resistance. Those are encouraging points, but we don't know how much to make of them. Resistance to drugs or antibodies is probably inevitable; the real question is whether it is slow enough to be a manageable problem.

Problems? One of the simplest tests of an antibody is neutralization of the virus in the lab. Testing of the antibodies used here by that test did not agree with the ranking from the animal tests. It's not known why, but it does complicate screening for antibodies.

Bottom line? The recent Ebola outbreak made clear the need for a treatment against this type of virus. The use of antibodies is one possibility. Results to date have been mixed; the current work is encouraging. We need to be cautious about saying anything stronger. We can't do ordinary clinical trials with these viruses; testing in humans may well end up being done in the context of a real outbreak.

News stories:
* Monoclonal antibody cures Marburg infection in monkeys. (Medical Xpress, April 5, 2017.)
* Monoclonal antibody cures Marburg infection in monkeys. (NIH, April 5, 2017.) From one of the funding agencies.

The article: Therapeutic treatment of Marburg and Ravn virus infection in nonhuman primates with a human monoclonal antibody. (C E Mire et al, Science Translational Medicine 9:eaai8711, April 5, 2017.)

Previous post about Marburg virus: Ebola virus: ancient origins? (November 4, 2014).

Recent post about a filovirus: Update: Ebola vaccine trial (January 24, 2017). The vaccine trial was done in the context of the recent Ebola outbreak.

There is more about Marburg and the related Ebola on my page Biotechnology in the News (BITN) -- Other topics in the section Ebola and Marburg (and Lassa). That section links to related Musings posts, and to good sources of information and news.

Evidence for dinosaur protein extended by a hundred million years

May 12, 2017

Musings has discussed claims of finding dinosaur protein, from specimens as old as about 80 million years [link at the end]. A new article claims evidence for dinosaur protein from a specimen that is 195 million years old. The article uses some novel methodology and offers a suggestion for the remarkable preservation.

A caution... This is not easy to follow. The merit of work in this field is debated by experts; don't be surprised if you find yourself wondering about some of it. Fortunately, we can summarize some of the key ideas without being too technical, but let's start with some actual data.

The graph shows some infrared (IR) spectra for various materials.

The green curve (second from top) is for a bona fide sample of the protein collagen -- modern ("extant") collagen.

The red and blue curves (just above and below the known collagen) are for two samples from the dinosaur. The spectra are very similar to that for the known collagen sample in certain key places. For example, look at two peaks near 1600 on the x-axis. One is labeled amide I (1647) and one is labeled amide II (1545). Those two peaks are in the spectra for the known collagen and for the two dinosaur samples. Those two peaks are features we expect for collagen.

The other three curves are for various things that are not collagen -- not protein. They don't show those peaks.

   This is Figure 2 from the article.

The graph above, then, shows evidence for the protein collagen in the dinosaur sample. Whether you find that convincing or not doesn't matter much for now. As usual, we just say that the authors claim it is so, and this is some of the evidence.

There are other reasons why this particular report is of particular interest...

- They use novel methodology. In the current work, the spectra were measured on pieces of the fossil, rather than on material extracted into solution. There are probably advantages to both methods. The method here allows them to see the protein in the context of the overall structure. That's important. The collagen is seen in blood vessels, not in bone -- where it originally was most common.

- The specimen here is about 195 million years old. That's about a hundred million years older than the specimens for which dinosaur protein has been reported previously.

- Perhaps most intriguingly, the authors offer an explanation for the long term preservation of the protein. We noted that they find the collagen in blood vessels. Further, the preserved protein is associated with hematite, a form of iron oxide. That could derive from blood -- from the hemoglobin of the blood. They suggest a connection -- that the hematite is protecting the protein.

Previous reports of dinosaur protein have been met with considerable skepticism, even as the evidence grows -- slowly. Most of the work has been from one lab, and their collaborators. The work here seems to be independent, and it has some noteworthy aspects. Whether any of it is right remains to be seen.

Fascination with dinosaurs now extends to the molecular level.

News stories:
* More Dinosaur Proteins Found -- Evidence of Preserved Collagen in the Early Jurassic Dinosaur Lufengosaurus. (Everything Dinosaur, February 1, 2017.)
* Dino rib yields evidence of oldest soft tissue remains. (Phys.Org, January 31, 2017.)

The article, which is freely available: Evidence of preserved collagen in an Early Jurassic sauropodomorph dinosaur revealed by synchrotron FTIR microspectroscopy. (Y-C Lee et al, Nature Communications 8:14220, January 31, 2017.)

Background post: Dinosaur proteins (July 6, 2009). Links to more.

Previous post about dinosaurs... Red color vision in dinosaurs? (October 17, 2016).

More IR spectra: The real carbonic acid, at last? (January 10, 2015).

May 10, 2017

Atmospheric rivers and wind

May 9, 2017

Atmospheric river (AR) is a colorful term for an apparent channel of exceptionally high water content. Those who have been in a rain storm resulting from an atmospheric river know how appropriate the term is. Such storms are common in mid-latitude areas, including the western United States and Europe.

A recent article shows that ARs may bring not only extreme rain but also extreme wind. The following figure summarizes some of the findings...

Start with part d, on the right. It is a map of major wind storms. In particular, look at the ones marked by circles; the size of the circle reflects the economic loss from the storm.

If the circle is filled in with red, it means that the storm was associated with an atmospheric river.

You can see that six of the nine circles are red, including the two largest ones (the two with the largest damages).

The three graphs on the left side offer an explanation for that pattern. Start with the top graph (part a). It shows the probability of various levels of wind. The x-axis is cryptically labeled BWS; that stands for the Beaufort wind scale. Suffice it to say that BWS numbers of 8 or higher are for winds that might cause damage; 12 is hurricane-force winds.

There are two curves. One (blue) is for all conditions. One (red) is specifically for times when there is an AR in the area being measured.

Look at the results for high BWS numbers. You can see that the red curve is a little higher than the blue curve. A little? It's a log scale, and the red curve is actually about 10-fold higher. That is, winds high enough to cause damage are about 10-fold more common when there is in AR.

The three graphs on the left are for different areas: land, coast, and ocean. The big picture is similar for all of them.

   This is Figure 4 from the article.

Atmospheric rivers are important not only for their rain, but also their wind.

News story: Atmospheric rivers found to carry more wind than thought. (B Yirka,, February 22, 2017.) Don't spend much time trying to parse that title. The animated gif at the top of the page shows an AR in action; looks like it made a mess here.

An informational page from NOAA: Atmospheric River Q & A. (Earth System Research Laboratory, (US) National Oceanic and Atmospheric Administration.)

The article: Extreme winds and precipitation during landfall of atmospheric rivers. (D Waliser & B Guan, Nature Geoscience 10:179, March 2017.)

A recent post about rivers: When rivers (or streams) join, what is the preferred angle between them? (April 18, 2017).

More about winds:
* At what wind speed do trees break? (April 2, 2016).
* What is the proper length for eyelashes -- and why? (March 16, 2015).

More about floods:
* Flooding in The Netherlands: natural or manmade? (September 19, 2015).
* How to survive flooding by making a waterproof raft (May 27, 2011).

If you are talking with someone, how can you tell if they are paying attention?

May 8, 2017

You could scan both your brain and theirs, and see if they are synchronized. To do that, you both wear a headband equipped for functional near infrared spectroscopy (fNIRS). So reports a new article.

Let's start with something a little simpler. In this first experiment, two test subjects listened to stories. The scientists measured the correlation between the brains of the two listeners. Specifically, they measured the level of oxygenated hemoglobin (HbO) at various places in the brains, using the fNIRS method.

The results are shown on a map of the brain. Each little cross (+) represents the location of one sensor, called an optode. A black cross indicates that the brain activities of the two listeners were significantly correlated at that site.

A pattern is clear... In two of the tests, there are many black crosses. In the other two, there are no black crosses. What's the difference? For the two tests at the left, the stories were told in Turkish -- and are labeled with T. For the two tests at the right, the stories were told in English -- and are labeled with E. The listeners understood only English.

That is, in the E tests, the listeners understood the speaker. Activity in the two listeners' brains was correlated, because they were both doing the same thing at the same time. In contrast, they did not understand the stories in Turkish; whatever their brains were doing, they were different and not correlated.

The brain activities recorded here probably relate to language, though their precise role is not clear.

Why Turkish? The senior author is Turkish. (He is at an American university: Drexel, in Philadelphia.)

   This is the top part of Figure 1 from the article.

The results above show that the brains of two people listening to and understanding the same story are synchronized. The figure also shows the basic experimental design.

Now, let's look at an experiment comparing the brain responses of speaker and listener. This is more complicated. Why? Because the speaker and listener responses may not occur at exactly the same time. There might be a time lag between the speaker and listener. Therefore, looking for a possible time lag is part of the analysis.

In this case, the authors present the results with all the tests, both T and E, on a single graph -- a 3D graph...

The measurement is summarized by the z-axis, which shows the number of "significantly coupled optodes". (That is, it is like the count of the black crosses from the previous figure.)

The y-axis shows lines for individual stories, in T or E. The x-axis shows the time delay.

For the T stories, the count of significant correlations is zero. But for the E story, there is a high count if a time delay of about 5 seconds is included.

   This is the right-hand part of Figure 2a from the article.

The conclusion here is that the brain activities of the speaker and listener are correlated, but with a short time delay.

The conclusions about correlations between speaker and listener brains are not entirely new. Previous work had led to such conclusions -- using functional magnetic resonance imaging (fMRI). The real advance here is using a much simpler method, the fNIRS. fMRI requires that the subject lie still inside a complex machine. fNIRS uses a headband and relatively portable equipment. The new method, which the authors have been developing, may allow such brain measurements to be made on people during ordinary interaction. It also makes it practical to measure multiple people at the same time.

News stories:
* Brain-imaging headband measures how our minds mirror a speaker when we communicate. (Kurzweil, February 28, 2017.) Includes a picture of the headband device.
* Brain-synching: What Happens When You Converse with Other People . (J Rocheleau, nerve blog, March 1, 2017.) Short, but very nice.
* Brain imaging headband measures how our minds align when we communicate . (Science Daily, February 27, 2017.)

The article, which is freely available: Measuring speaker-listener neural coupling with functional near infrared spectroscopy. (Y Liu et al, Scientific Reports 7:43293, February 27, 2017.) A very readable article.

A recent post about advances in brain imaging: Imaging of fetal human brains: evidence that babies born prematurely may already have brain problems (March 10, 2017). fMRI.

More about listening... Speech: Are chimps good listeners? (July 25, 2011). I wonder, would the new method of the current post be a useful tool here?

There is a section of my page Biotechnology in the News (BITN) -- Other topics on Brain (autism, schizophrenia). It includes a list of related Musings posts.

Accumulation of deleterious mutations in the last mammoths

May 6, 2017

Two years ago, Musings noted the report of complete genome sequences for two woolly mammoths [link at the end]. One was from an animal about 45,000 years old; the other was from one about 4,300 years old. By that time, there were no mammoths on the mainland; only a few island populations survived. Extinction followed a few hundred years later.

The original report used the genome data to estimate the population sizes. The later population, on the island, was quite small.

A recent article reports further analysis of those two mammoth genome sequences. The basic question asked is: how many deleterious mutations did each animal have? The scientists examined the sequences, and looked for several types of mutation. They focused on types of mutation that, with high probability, would inactivate the gene.

The following table summarizes some of the results.

Mutation type Mammoth #1 (old)
   source: Oimyakon (Siberia)
age: 45,000 years
Mammoth #2 (recent)
   source: Wrangel Island
age: 4,300 years
   Ratio (recent/old)
Deletions 21,346 27,228 1.28
Retrogenes 2,130 2,853 1.34
Genes with exons deleted 1,115 1,628 1.46
Stop codons 503 819 1.63

The columns for the two mammoths show the number of mutations of each type, shown at the left. The final column, at the right, shows the ratio for the two genomes.

"Retrogenes" refers to genes that contain an insert from a transposable element. "Stop codons" refers to cases where a gene contains an extra stop codon that is early enough in the gene that it probably prevents formation of an active gene product.

The table shows some of the results from Table 1 of the article. I added the column showing the ratio. I omitted the footnotes clarifying what some of the numbers mean.

The last column gives the bottom line. The recent mammoth, one of the last of the species, had about 30-60% more deleterious mutations than the earlier mammoth. There is considerable uncertainty about exactly what the numbers mean, but the general picture seems clear enough.

The article also includes some discussion of specific gene losses. For example, the Wrangel mammoth has extensive loss of olfactory genes. One can imagine how that loss could have been detrimental to survival. However, it is also possible that it simply reflects that the island environment was different. The authors note loss of one particular gene that might have led to the coat providing less protection from the cold.

Do these numbers explain why the mammoths went extinct? That would be an over-statement. In fact, the authors would emphasize the other side of the story: small populations make it harder to eliminate deleterious mutations. What we can say, from this work and that in the background post, is that the last mammoths -- at least as judged by this one specimen -- had reduced genetic diversity and a higher level of mutations that are likely to be deleterious. Certainly, that's not good. It is plausible that unfavorable conditions, including isolation, led to smaller populations that were less able to adapt. There would then be a positive feedback loop, accelerating the decline. The decline in genetic diversity, which is now measurable, is one part of the story.

The work shows that animals from small populations may not represent the best of a species. This has implications for conservation work. It's not a new point, but the work here provides experimental evidence.

News story: Woolly mammoths experienced a genomic meltdown just before extinction. (, March 2, 2017.)

The article, which is freely available: Excess of genomic defects in a woolly mammoth on Wrangel island. (R L Rogers & M Slatkin, PLoS Genetics 13:e1006601, March 2, 2017.)

Background post: Comparing woolly mammoth genomes over time (June 1, 2015). The article of this post is reference 4 of the current article.

There is more about genomes on my page Biotechnology in the News (BITN) - DNA and the genome. It includes an extensive list of related Musings posts.

May 4, 2017

Watching ice form: new developments in nucleation

May 4, 2017

Well, watch... video of ice forming on a crystal of feldspar. (MP4 file. Movie S2 with the article listed below. 17 seconds; no sound.)

If that link doesn't take you directly to the movie file, try page for supplementary information for the article. Then scroll down to Movie S2.

If you can't get to the movie, the top figure in the news story is a good substitute.

That video is the reason for the post.

What's the story behind it? The freezing point of water is 0°C. Cool some water, and you night expect that it will freeze when it gets down to 0°C. But it's not that simple. In fact, it is easy enough to cool water below that without it freezing; the result is called supercooled water. Why? Because it is difficult to form the first ice.

One way to get the ice to form is to add a little piece of ice. That serves as a nucleus, or nucleation site, for further ice. However, other things can serve as nucleation sites, too, and it's not well understood how they work.

A recent article reports studies of ice nucleation on a mineral called feldspar. It's known that it is a good nucleation material for ice formation, but how it works has been unclear. It is important: feldspar contributes to ice formation in clouds, and hence to rainfall.

The movie above shows it in action.

The scientists do more, of course. The following figure summarizes some of the results...

The figure is a composite.

The basic underlying figure is an electron micrograph of one face of a feldspar sample.

That sample was allowed to serve as a surface for ice nucleation. In fact, that was done several times, allowing the ice to evaporate off in between.

The colored dots on the surface mark the sites where ice formation started. That is, the colored dots mark the nucleation sites. You can see that the nucleation sites are not random. They are on features, which turn out to be cracks and steps.

The colors of the dots reflect how long it took for ice to start forming at a site. There is a color code at the right side. But, frankly, the times don't matter much. Just seeing the overall pattern of where the dots are serves our purposes here.

   This is Figure 2A from the article.

And that's the point...There are specific atomic features that act as ice nucleation sites. They are not on ordinary surfaces, but at surface defects. The movie is fun; it is a reflection of the deeper understanding that follows.

News story: Cloud formation -- how feldspar acts as ice nucleus. (M Landgraf,, December 9, 2016.)

* News story accompanying the article: Atmospheric chemistry: Cracking the problem of ice nucleation -- Electron microscope data explain why feldspars are key to nucleating ice particles in clouds. (B J Murray, Science 355:346, January 27, 2017.)
* The article: Active sites in heterogeneous ice nucleation-the example of K-rich feldspars. (A Kiselev et al, Science 355:367, January 27, 2017.) There are four movie files posted with the article, as Supplementary Materials. One is linked at the start of this post. But you might enjoy watching all of them. Movie S4 is a close-up.

More on ice formation:
* An anti-freeze story: Why a tick carries a human pathogen (October 29, 2010).
* Ice nucleation -- by airplanes (September 24, 2010).
* Developing improved degradation of organophosphate pesticides (September 7, 2010).

A highly effective malaria vaccine -- follow-up

May 3, 2017

In 2013, Musings reported results from a small trial of a vaccine against malaria [link at the end]. The results suggested that the vaccine was extremely effective. In fact, in this small trial, it was 100% effective. The vaccine was novel, in that it made use of whole but irradiated malaria parasites -- injected directly into the bloodstream.

Scientists -- from the company Sanaria, which is behind the vaccine, and their collaborators -- have recently reported more results, with variations of the procedure. We note here one article with one approach. The vaccine uses ordinary -- and live -- malaria parasites, but is administered along with an anti-malaria drug. That is, the vaccine is effectively an attenuated infection, with the attenuation coming from the drug.

The results are encouraging, but complicated. At the highest dose used, a sequence of three injections over two months led to 100% protection -- with 9 subjects. (They were challenged with a lab infection ten weeks after the last vaccine dose.) A more accelerated schedule, which would be more convenient in the field, led to about 60% protection. That's respectable, and perhaps even better than the leading vaccine candidate now being tested. But perhaps they can do better; the procedure certainly has not been optimized.

As before, the results are intriguing. The optimistic view is that they may have a relatively simple vaccine and procedure that is highly effective. Infection with whole organisms allows exposure to all the antigens of the life cycle; that is undoubtedly good in establishing robust immunity. Giving live normal organisms is risky, though the use of a drug appears to effectively limit disease.

There is still only limited data, and the optimum procedure is still unclear. A longer term field trial is planned.

News stories:
* New malaria vaccine effective in clinical trial -- Researchers achieve protection of up to 100 percent using fully viable malaria parasites. (Science Daily, February 15, 2017.)
* Progress with Sanaria's Plasmodium falciparum sporozoite vaccines. (I van Schayk, Malaria World, March 17, 2017.) This news story discusses several recent related articles, including the focus article here.

The article: Sterile protection against human malaria by chemoattenuated PfSPZ vaccine. (B Mordmüller et al, Nature 542:445, February 23, 2017.)

Background post: A vaccine against malaria -- with 100% efficacy? (October 20, 2013).

Most recent post about malaria: Malaria history (January 18, 2017).

More on malaria is on my page Biotechnology in the News (BITN) -- Other topics under Malaria. It includes a listing of related Musings posts, including posts about mosquitoes.

Human heart organoids show ability to regenerate

May 2, 2017

Some things can regenerate following injury, some cannot. For vertebrates, we know that the zebrafish can regenerate heart tissue, whereas mammals generally cannot. However, newborn mice can.

What about blobs of heart tissue grown in lab culture? Heart tissue from human cells. Beating heart tissue. What if such a blob had a heart attack? Could it regenerate?

We're talking about organoids: small pieces of differentiated tissue developed in the lab from pluripotent stem cells. The organoids here are human cardiac organoids, or hCO.

A new article reports testing the ability of hCO to regenerate following injury.

Here is an example of the results...

Part A (top) outlines the plan. The hCO were injured at time zero. They were then tested twice: 6 hours and 14 days following the injury.

How do you injure an organoid? How do you give an hCO a "heart attack"? What the scientists did was to give the hCO a cryoinjury: they froze a bit of it. That killed cells, in a small area.

Each graph in Parts B and C shows the results for one type of organoid, at the indicated time. A "type" of organoid refers to the use of one particular stem cell line. The graph compares the force generated by an injured hCO (right bar in each graph; gray) vs an uninjured control (left; black).

Part B shows the results 6 hours after injury. In each case, the injured sample is considerably lower than the uninjured control. (The result for the middle hCO does not quite meet the usual test for statistical significance.)

Part C shows the results 14 days after injury for two of those types of hCO. Now, the injured sample has recovered, and is about the same as the uninjured control.

   This is part of Figure 4 from the article.

The full figure shows an additional test at 14 days, in Part D. That test was done with all three hCO types, and all showed normal force generation.

Overall, the work shows that human cardiac organoids can regenerate following an injury in the lab.

This is the early days of work on heart organoids. The authors note that there is currently no good model system for studying human heart development and regeneration in the lab. They also caution that there are clear differences between this system and real hearts in humans. For example, there is no immune system interacting with the hCO. Perhaps the work here will turn out to be part of a useful system. It does suggest that there is some innate ability to regenerate human heart tissue. Perhaps further study will reveal how that ability to regenerate is turned off in human hearts.

News story: Scientists create 'beating' human heart muscle for cardiac research. (Medical Xpress, March 17, 2017.)

The article: Development of a Human Cardiac Organoid Injury Model Reveals Innate Regenerative Potential . (H K Voges et al, Development 144:1118, March 15, 2017.) It's part of a special issue on organoids.

A recent post on natural heart regeneration: Zebrafish reveal another clue about how to regenerate heart muscle (December 11, 2016).

A recent post on repairing heart damage: Synthetic stem cells? (April 30, 2017). That is the previous post.

Posts on organoids include:
* An organoid for the gut: at last, a culture system for norovirus (October 30, 2016).
* Autism in a dish? (September 4, 2015).

There is more about regeneration on my page Biotechnology in the News (BITN) for Cloning and stem cells. It includes an extensive list of related Musings posts, including those on the broader topic of replacement body parts.

Older items are on the archive pages, starting with 2017 (January-April).

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Last update: June 26, 2017