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Musings: January-April 2016 (archive)

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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   Introduction (separate page).
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2016 (January-April)
   April 30    April 27    April 20    April 13    April 6    March 30    March 23    March 16    March 9    March 2    February 24    February 17    February 10    February 3    January 27    January 20    January 13    January 6
      Also see the complete listing of Musings pages, immediately below.

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2010:    January-June    July-December
2009
2008

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Archive items may be edited, to condense them a bit or to update links. Some links may require a subscription for full access, but I try to provide at least one useful open source for most items.

Please let me know of any broken links you find -- on my Musings pages or any of my regular web pages. Personal reports are often the first way I find out about such a problem.

April 30, 2016

Los Angeles leaked -- big time!

April 29, 2016

Another story of a leak of natural gas (methane). A big event, a disaster, one that was headline news in California for several months. (And one that was only about ten miles up the road from a place I lived long long ago.)

The leak in this case was in a storage container for natural gas. That storage container was an old oil field. Yes, the gas company stored gas underground, in the Earth. It's a common practice, and it usually works ok. But this gas field sprang a leak, associated with a particular well. The leak spewed natural gas into the air in northern Los Angeles (LA) for several months.

Here are some numbers...

Numbers. What do they mean?

The event is the second largest known accidental release of methane in the US. During the time of the event, it approximately doubled the methane release rate in the LA area.

On the other hand, such large releases are uncommon. Although the release doubled the LA area methane emission over that time period, it would be only a blip when looked at over a long time period.

Will such releases continue to be uncommon? If a similar event occurred, would we do a better job of containing it? Have we learned something from this event and others that would help reduce the risk in the future? Those are the types of questions we should be asking. Certainly, scientists are asking the questions. But implementing the answers is a political matter, too.

In addition to being a report on the Los Angeles leak, the work shows the value of using small airplanes carrying instrumentation for monitoring. The results from airborne monitoring were quickly made available to relevant parties, and guided what needed to be done on the ground.

News stories:
* California gas well blowout caused nation's largest methane release, study finds. (Phys.org, February 25, 2016.)
* Study: California's Aliso Canyon blowout led to largest U.S. methane leak ever. (NOAA, February 25, 2016.) From one of the government agencies involved in the work.

The article: Methane emissions from the 2015 Aliso Canyon blowout in Los Angeles, CA. (S Conley et al, Science 351:1317, March 18, 2016.) Check Google Scholar for a freely available preprint. (In the news media, the event was commonly described as being near Porter Ranch, the nearby community.)

Among previous leak reports: Boston is leaking (February 13, 2015).

A previous post about understanding and dealing with the leak problem: Methane leaks -- relevance to use of natural gas as a fuel (April 7, 2014).

Also see... Emissions from gas stoves, even when 'off' -- air pollution implications (February 21, 2023).

There is more about energy issues on my page Internet Resources for Organic and Biochemistry under Energy resources. It includes a list of related Musings posts.

An interesting story about a natural leak: Underwater "lost city" explained (July 25, 2016).

By the way, not all leak reports are about methane... Europa is leaking (February 10, 2014).

More from Los Angeles...
* Earthquakes induced by human activity: oil drilling in Los Angeles (February 12, 2019).
* DNA evidence in restaurants: is the fish properly labeled? (June 5, 2017).

April 27, 2016

Measuring brain injury after head trauma?

April 25, 2016

A person gets hit in the head. Is there a brain injury, such as a concussion? It's a question that is getting much attention, particularly in the context of athletes. And it's not easy to tell.

What about a blood test for brain injury? Perhaps the level of certain proteins in the blood would indicate the status of brain injury. These might be proteins released as a result of injury, or proteins induced by the injury as part of a repair response.

A new article reports some encouraging results; the following figure is an example. It is a real-world test, monitoring a couple of candidate proteins that had been identified previously.

The results are encouraging. It may be that a simple blood test immediately following a trauma could provide quick information about whether the person has suffered a brain injury. Further, the test can still be very useful even if the person is not examined for a few days after the trauma. That's also important, because it is common for brain symptoms to be delayed, and for people to not seek immediate treatment after seemingly minor trauma.

News stories:
* Concussions In Sports: Simple Blood Test Could Diagnose Traumatic Brain Injury In 7 Days, Help Prevent CTE. (J Caba, Medical Daily, March 29, 2016.)
* Simple blood test can detect evidence of concussions up to a week after injury -- Biomarker released by the brain during injury found to stay in the bloodstream for 7 days. (Science Daily, March 28, 2016.)

The article: Time Course and Diagnostic Accuracy of Glial and Neuronal Blood Biomarkers GFAP and UCH-L1 in a Large Cohort of Trauma Patients With and Without Mild Traumatic Brain Injury. (L Papa et al, JAMA Neurology 73:551, May 2016.)

A post on the problem of evaluating brain injury... Early detection of brain damage in football players? A breakthrough, or not? (September 14, 2015). This and the current post address different parts of the problem. The new post is about immediate evaluation of possible brain injury following a trauma. The earlier post is looking for accumulated damage in the brain.

... and on doing something about it ... Role of a receptor for HIV in stroke recovery (March 23, 2019).

More about trauma: Studying concussions in egg yolks (February 28, 2021).

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

Blood vessels from dinosaurs?

April 22, 2016

Look...

That's the heart of the story from a recent article. Samples from a dinosaur fossil have identifiable proteins, consistent with them being from dinosaur blood vessels. The figures above show the evidence for myosin; the full figure includes similar evidence, using antibodies, for three other proteins. The article also includes analysis of the proteins by mass spectrometry.

It is a startling claim, because scientists have been skeptical that proteins can survive that long -- on the order of a hundred million years.

This is not a completely new story. It is part of an ongoing effort to identify proteins in dinosaur fossils. Musings has noted earlier work [link at the end].

Work with ancient DNA went through a time of serious skepticism. In fact, some of the early work was wrong. The problem is not the measurements per se. It's clear that the dinosaur sample above stains for myosin. The concern is sample integrity. Is the sample really what is claimed, or has it -- somehow -- been contaminated with other materials, either in the field or in the lab? Over time, the ancient DNA scientists have worked out procedures and standards for such work; the ancient protein scientists are trying to follow. Much of the current article discusses the integrity issue.

The current work is framed around a rather modest issue. Some have suggested that the protein material in the dinosaur fossils is from bacterial biofilms. The work in the article provides good evidence that these are animal proteins, not bacterial proteins. But there is much more to wonder about.

What's the take home lesson? I suggest that we simply note it. A team of scientists reports that structures and proteins in dinosaur fossils appear to be from blood vessels. Others will work on this, addressing every possible concern. Perhaps we will see independent confirmation. Perhaps someone will identify fatal flaws in the work. Perhaps finding flaws will lead to improved procedures. For now, all we can do is report what has been claimed, and await further developments. Science in progress.

News stories:
* Paleontologists Find Mineralized Blood Vessels in 80-Million-Year-Old Hadrosaur Fossil. (E de Lazaro, Sci.News, December 1, 2015.)
* Dinosaur Blood Vessels Survived 80 Million Years Without Fossilizing. (L Geggel, Live Science, December 9, 2015.)

The article: Mass Spectrometry and Antibody-Based Characterization of Blood Vessels from Brachylophosaurus canadensis. (T P Cleland et al, Journal of Proteome Research 14:5252, December 4, 2015.)

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

Most recent post about dinosaurs... What caused the extinction of the dinosaurs: Another new twist? (January 26, 2016).

Posts about blood vessels include... Peripartum cardiomyopathy -- a heart condition associated with pregnancy (June 30, 2012).

Some posts about the ancient DNA field...
* Ancient DNA: an overview (August 22, 2015).
* Chromosomes -- 180 million years old? (April 18, 2014). The claim here is based on visible features; there is no claim of old DNA.
* The oldest DNA: the genome sequence from a 700,000-year-old horse (August 4, 2013). I think this still stands as the oldest DNA that has been sequenced.

More mass spec: Hydride-in-a-cage: the H₂₅^- ion (January 22, 2017).

April 20, 2016

Huntington's disease: Mutant human protein disrupts singing in birds

April 18, 2016

Huntington's disease (HD) is a progressive neurodegenerative disease. It is caused by mutations in the gene for a protein called huntingtin (HTT). Interestingly, the mutations involve expansions of a three-base (triplet) repeat, leading to repeats of the amino acid glutamine in the protein. How the mutant protein causes disease is not understood.

What if we put the mutant huntingtin gene into a songbird?

Let's look at what was reported in a recent article...

In this experiment, zebra finches with various forms of the huntingtin protein were studied. The key variable is the number of consecutive glutamines in the protein. This is shown by a number such as 4Q, meaning a repeat of 4 glutamines. (Q is the code for glutamine.) In the test here, the birds learned their song by three months of age. They were then followed to see (hear?) how well they remembered it later. This is shown as a similarity score (y-axis), plotted against time (x-axis). You can see that the 4Q and 23Q birds remembered their songs rather well, but the 145Q birds performed poorly over time.    This is Figure 3C from the article.

The results show that birds with mutant HTT protein, with a large Q repeat, have song defects. Much of the article elaborates on this story.

Let's fill in some details... First, the birds naturally have a HTT gene, which is quite similar to that in humans. In fact, the birds labeled 4Q are normal, wild-type (WT) birds, with that normal bird HTT gene. (That is, 4Q is the normal repeat for these birds.) The birds with 23Q have the human wild-type HTT gene added. (23Q is about normal for humans, but it varies.) The birds with 145Q have an added HTT gene from a human with the disease.

HD is a dominant disorder. Thus, adding the human HTT gene to the birds (not replacing their natural copy) is appropriate.

The experiment described above shows that adding the wild-type human HTT has little effect. (Some of the experiments reported do show some effect of adding 23Q.) Adding the form of the HTT gene that causes disease in humans disrupts song in the birds.

Interestingly, the song birds with the 145Q HTT protein are generally normal, except for their problems with song. In fact, the authors note that their birds are "the first experimentally created, functional mutant songbirds" (abstract).

What does one do with this finding? That's not clear yet. Might it be useful in studying the nature of Huntington's disease? Might it be useful in studying bird song? For now, it is an intriguing new finding.

Why study HD in songbirds? The birds, like humans but unlike other common lab animals, make vocalizations that are learned.

News stories:
* Songbirds Could Be Used as Valuable Tool to Study Brain Neurodegeneration, Huntington's Disease. (M Ammam, Huntington's Disease News, October 7, 2015.)
* Finches offer researchers a new tool to study Huntington's disease. (Rockefeller University, October 5, 2015. Now archived.) From the lead institution.

The article: Human mutant huntingtin disrupts vocal learning in transgenic songbirds. (W Liu et al, Nature Neuroscience 18:1617, November 2015.)

Previous post about HD: Huntington's disease: Is it an amino acid deficiency? (October 4, 2014).

and more...
* An "antidote" for Huntington's disease? (February 29, 2020).
* Triplet-repeats: Do they act through the RNA? (September 24, 2017).

More about songbirds...
* The oldest known syrinx (December 4, 2016).
* Are urban dwellers smarter than rural dwellers? (August 2, 2016).
* Bird brains -- better than mammalian brains? (June 24, 2016).

My page for Biotechnology in the News (BITN) -- Other topics includes a section on Brain (autism, schizophrenia). It includes a list of brain-related posts.

It's CRISPR vs HIV -- and HIV might win

April 17, 2016

The heart of the CRISPR system is a nuclease, Cas9, which cuts DNA at a target site. The targeting is achieved by a guide RNA. The use of an RNA for targeting is what makes CRISPR so easy to use; it is easy to make an RNA complementary to any DNA region of interest. What happens after the cut depends on how the system is being used.

A simple use of CRISPR is to restrict the growth of a virus, such as HIV. In this case, the guide RNA targets a critical region of the viral genome; Cas9 cuts at the targeted site. It is left to normal cellular processes to repair the cut; the expectation is that such repair will make the virus unable to grow.

Maybe. Here is an example of what happens, as reported in a new article...

The graph shows HIV virus produced vs time of infection, for three conditions. (Actually, the scientists measured the amount of one viral enzyme, the reverse transcriptase (RT).) The cellular host contained the Cas9 nuclease; the three conditions differed in what the targeting guide RNA was.

In the control ("Ctrl"), there was no guide RNA. In effect, this is a normal virus infection. There is a peak of virus production at 10-12 days. For the other two conditions, there was a guide RNA targeted to a critical region of the virus. You can see that normal virus production was indeed stopped. Testing two different guides, targeted to different critical sites, helps to show that the result is of some generality. However, keep looking, and something else happens. Ten days later, there is a burst of virus. It is as if the HIV has overcome the CRISPR, and finally made virus.    This is Figure 2A from the article.

That's the basic observation. Given some time, HIV seems to overcome CRISPR. The rest of the article explores why this happened.

The short version of the story is that, while most events repairing the Cas9 cut inactivated the virus, a few made a virus that could replicate. Those viruses, by the way, were no longer susceptible to the original guide RNAs.

What's the big message? CRISPR is a new tool, and we are still learning about it. For some uses of CRISPR, we carefully test what the result is before putting the resulting cells into a live organism. That helps protect against undesired events such as seen here. For direct use of CRISPR in organisms, we will need to think carefully about what unexpected consequences might happen.

News stories:
* HIV overcomes CRISPR gene-editing attack -- Virus can quickly develop mutations that resist attack by DNA-shearing enzymes. (E Callaway, Nature News, April 7, 2016.)
* How HIV Can Escape an Experimental CRISPR Therapy. (T Lewis, The Scientist, April 7, 2016.)

The article, which is freely available: CRISPR/Cas9-Derived Mutations Both Inhibit HIV-1 Replication and Accelerate Viral Escape. (Z Wang et al, Cell Reports 15:481, April 19, 2016.)

A CRISPR post, which includes a complete list of all Musings CRISPR posts... CRISPR: an overview (February 15, 2015).

Next HIV post: Should we make antibodies to HIV in cows? (November 14, 2017).

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

The genetics of being a "morning person"?

April 15, 2016

You've probably heard the terms. Someone says they are a "morning person"; another is a "night person". Are these real characteristics? Are they determined, even in part, by our genes?

A new article reports finding some genes that may be associated with being a morning person. It's an interesting story. As usual, it is very preliminary.

The article is from a company that does "personal genomics", namely 23andMe. You send the company some cells and some money; they test your DNA, and send you back a report. Companies such as 23andMe collect vast amounts of human genome information. They also ask their customers to provide some information, so they are in a position to see if there is any correlation between certain genome sequences and certain characteristics.

Analysis of the company database suggests there is a correlation between certain sequences and being a morning person.

Here is how the results are presented...

That's it. There are several red points, above the cutoff line. There appears to be a correlation between having these genome sequences and being a morning person.

Now what? Each of those candidates needs to be tested, to see if the association is real. If so, what is the mechanism? Some of them will prove to be false positives, but some may prove interesting. That's the nature of GWASes; they can only offer hints, but they are very good at doing that.

There is a little more information than that, but be careful about reading too much into it at this point. The scientists can look at the regions of the genome where those candidate sequences occur. Sometimes we know a little about the genetic region, sometimes not. For some of these candidates, there is already some reason to suspect they have some relationship to sleep or to circadian rhythms.

News stories:
* Genetic links to being a 'morning person', says 23andMe study. (B Czub, BioNews, February 8, 2016.) (This story says that morning people are more likely to sleep soundly; they got that backwards.)
* Can Your DNA Determine If You're a Morning Person or Night Owl? (GEN, February 3, 2016. Now archived.)

The article, which is freely available: GWAS of 89,283 individuals identifies genetic variants associated with self-reporting of being a morning person. (Y Hu et al, Nature Communications 7:10448, February 2, 2016.)

The principle behind what companies such as 23andMe do is sound. There is some controversy about the information they send back to the customers, and the company has been challenged by the FDA. The issue is not the hard facts, but how much interpretation they do, and how much "medical advice" they offer. At least the better of the companies do good science, and are trying to learn how to build an acceptable business based on personal genomics.

The work here is a research activity of the company, not something they are reporting to the customers.

* * * * *

A recent post on sleep and circadian rhythms: How caffeine interferes with sleep (December 11, 2015). It mentions the idea of morning people.

Also...
* Daylight savings time: night-owls have more difficulty adapting (August 1, 2021).
* Evening light: how it affects our sleep (July 30, 2019).
* Circadian rhythms and class time? (June 10, 2018).
* What if a lion came into your hotel room while you slept? (July 20, 2016).
* Sleepy teenagers (July 23, 2010).

More circadian rhythms: Why growing sunflowers face the east each morning (November 8, 2016).

A post about personalized medicine... Personalized medicine: Getting your genes checked (October 27, 2009). This includes an extensive list of related posts.

Previous GWAS post... A gene that reduces the chance of successful pregnancy: is it advantageous? (May 18, 2015).

More from 23andMe: Ear lobe genetics: more complicated than you thought (March 23, 2018).

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.

April 13, 2016

Upgrading ethanol?

April 11, 2016

Making ethanol from biomass is a well-known process. However, hydrocarbons are generally considered a better transportation fuel than ethanol.

A recent article addresses how to make hydrocarbon fuels from ethanol. It raises some interesting issues.

The following figure shows a key result...

The general nature of the experiment is that ethanol is treated under conditions to convert it to hydrocarbons. For convenience, the scientists divide the hydrocarbon products, a complex mixture, into two types, depending on the number of carbon atoms per molecule: C2 and C3+. C2 includes ethylene, a well-known product of simply dehydrating the ethanol molecule. C3+ refers to all larger hydrocarbons (with three or more C atoms). It is a simplification, but for the current context... the more C3+, the better.

The graph shows the percentage of the C3+ products (y-axis) vs the temperature of treatment (x-axis). The various curves are for various catalysts. The first observation is that all the curves have the same general shape: the percentage of C3+ products increases with temperature (T), up to around 360 °C. It then declines some with higher T. Next, we see that one curve shows the best results. The curve with blue diamonds is highest, or very nearly so, at all T. In fact, one key finding from the work is that the catalyst used for the blue-curve test is the best catalyst so far. Some chemistry detail... All the catalysts have ZSM-5 in the name. That refers to a class of zeolites. The front part of the name identifies the added elements. The best catalyst is the InV one -- which is better than In or V alone. The InV catalyst contains both indium and vanadium; it is a heterobimetallic catalyst, as identified in the article title.    This is the right-hand side of Figure 2 from the article.

The results above show that a new catalyst helps in making a larger hydrocarbon product, which is useful for transportation fuels.

The scientists also address the mechanism of the reaction. It is well known that ethanol can be dehydrated to make ethylene. In chemical terms... CH₃CH₂OH --> H₂C=CH₂ + H₂O. In that process, the H of the alcohol group goes to the water, and does not end up in the hydrocarbon product.

In the current work, the scientists test this mechanism, by using alcohol with the isotope deuterium (D) replacing ordinary hydrogen in the alcohol group. To their surprise, the D got incorporated into the hydrocarbon products. This suggests that dehydration is not the first step in their process. The result has implications for how development proceeds, but for now, it is rather murky what is going on.

News stories:
* Energy-efficient reaction drives biofuel conversion technology. (Science Daily, November 3, 2015.)
* ORNL team discovers mechanism behind direct ethanol-to-hydrocarbon conversion; implications for energy efficiency and cost of upgrading. (Green Car Congress, November 4, 2015.)

The article, which is freely available: Heterobimetallic Zeolite, InV-ZSM-5, Enables Efficient Conversion of Biomass Derived Ethanol to Renewable Hydrocarbons. (C K Narula et al, Scientific Reports 5:16039, November 3, 2015.)

Some of the authors are involved in a start-up company that is working to develop the process described here.

A post about catalyst development, in the context of biomass: Turning lignin into a useful product (April 11, 2015).

Another post about zeolites: Upsalite: a novel porous material (September 6, 2013). Zeolite is a term for a broad group of chemicals; there is no connection between the functions in the two zeolite posts.

More: A better catalytic sponge: degrading plastics, and more (August 11, 2020).

More vanadium: A better membrane for vanadium-based flow batteries (March 11, 2022).

There is more about energy issues on my page Internet Resources for Organic and Biochemistry under Energy resources. It includes a list of some related Musings posts.

An armadillo the size of a beetle

April 8, 2016

Here is the armadillo:

A fossil glyptodont. This is reduced from a figure on a web page from the American Museum of Natural History: Glyptodonts.

If you don't know how big a beetle is, go check the Volkswagen web site.

Glyptodonts were armored animals that lived over many millions of years in South America; they probably became extinct about 10,000 years ago. The largest ones fit in with the age of megafauna. The fossils have been known for nearly two centuries; Charles Darwin may have been one of the first to note them. It has long been suspected that the glyptodonts were closely related to armadillos, but classifying fossils is always hard.

A new article reports recovery of DNA from a glyptodont fossil. about 12,000 years old. Sequencing showed that it is indeed an armadillo.

News stories, which will let you see the tail:
* Extinct glyptodonts really were gigantic armadillos, ancient DNA shows. (Phys.org, February 22, 2016.)
* Researchers Sequence Mitochondrial Genome of Glyptodont. (N Anderson, Sci.News, February 22, 2016.)

The article: The phylogenetic affinities of the extinct glyptodonts. (F Delsuc et al, Current Biology 26:R155, February 22, 2016.) The article itself, only two pages, is largely sequencing and its analysis; as typical of genome papers, it is not easy reading. You can look at the family tree, if you want.

Other posts about armadillos...
* An armadillo's distress call (October 15, 2019).
* Leprosy: the armadillo connection (May 14, 2011).
* Twins (April 30, 2009).

Among many posts on beetles... How to preserve dead mice so they stay fresh and edible (January 18, 2019).

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.

April 6, 2016

Biodegradation of an implant in the brain

April 5, 2016

Is that a good idea? It might be if you don't need the implant anymore. It might be better than having a second surgery to remove it.

A new article reports such a device -- an implant that will disappear. It follows on much work learning what happens to materials in the body.

Here is a test...

The test shown above establishes the principle of a device that can disappear, but it is a quite artificial test. It is an accelerated test. The lab may be able to relate it to natural conditions; the test itself is artificial -- but fast.

Here is some testing under more relevant conditions...

In this test, individual materials used to make devices were incubated in artificial cerebrospinal fluid (ACSF) at 37 °C. The y-axis reports h/ho, the relative thickness of the material, over time (x-axis). The ratio starts at 1, by definition, and declines to zero when the material is gone. You can see that each material tested "disappears" over the time course of the observations. That's the main point.

The materials are: Si NMs: silicon nanomembranes; np-Si: nanoporous Si; Mg foil: magnesium foil; SiO2: silicon dioxide.    This is Figure S16 from the "Supplementary Information" accompanying the article.

Most of the article is about the performance of the devices, in rats. Not surprisingly, they perform well. The more interesting part of the work, perhaps, is the ability of the material to disappear, in a safe manner. The materials used have been tested before. The two graphs shown above are examples of data on device stability from the new article.

In the title I used the term biodegradable. That term is questionable, if you think about how we commonly use it. I use it more loosely to mean "degrades in the body". The authors use the term bioresorbtion, which may be fine if you understand it -- and if that is what happens. In fact, it's not entirely clear what happens to all the material -- except that it "disappears", in the body. Don't worry much about the details of how for now.

The story is that we are closer to having devices that can be implanted in the body, even in the brain, to take measurements, and which will somehow disappear without ill effect when no long needed.

News story: Tiny electronic implants monitor brain injury, then melt away -- Eliminate the need for additional surgery to remove monitors and reduce risk of infection and hemorrhage. (Kurzweil, January 19, 2016.)

The article: Bioresorbable silicon electronic sensors for the brain. (S-K Kang et al, Nature 530:71, February 4, 2016.)

More on electronics that can disappear when no longer needed...
* Using wood-based material for making biodegradable computers (July 21, 2015).
* Silk-clothed electronic devices that disappear when you are done with them (October 19, 2012). Earlier work from the same lab.

My page for Biotechnology in the News (BITN) -- Other topics includes a section on Brain (autism, schizophrenia). It includes a list of brain-related posts.

At what wind speed do trees break?

April 2, 2016

42 meters per second.

Here are some data, reported in a new article. The data are based on a major storm, called Klaus, in France in 2009.

The figure shows the percentage of trees that were broken (y-axis) as a function of wind speed (x-axis). You can see that the percentage of broken trees is low at low wind speed. It then rises -- with increasing steepness -- as the wind speed increases. The midpoint of the curve is at about 42 m/s (90 miles per hour).    This is the inset from Figure 2b in the article.

The scientists were intrigued by the seemingly simple curve. After all, trees vary in both diameter and height, and there are different kinds of wood structures.

They then did some experimental work in the lab, measuring the breaking point of logs. They could measure the effects of diameter and height. Most real trees, it seems are in the range where these effects tend to cancel out. That is, most real trees have similar sensitivity to breaking.

What does this mean? I wonder... Perhaps it means that trees have adapted to the environment over the ages. They survive common winds well, but not extreme winds. If this is so, then it might be that similar work in other places would yield different critical values. That is testable.

Don't go away from this with just "the answer". (Admittedly, there is some appeal to "The answer is 42.") It's a nice story of how some good observations in the field can lead to interesting exploratory lab science. And maybe to more.

Why does this matter, beyond being fun? Wood strength matters. Climate change will probably lead to more severe storms. Can we understand storm damage better? Further, mankind uses wood, in part for its strength.

This is not a new field of inquiry. The reference list goes back over 500 years, to a work by L da Vinci [ref 13]. In fact, the reference list includes several items dating back to the 18th century or earlier, some from familiar names. Remember Hooke's Law?

News stories:
* Trees break at fixed wind speed, irrespective of size or species. (I Randall, Physics World, February 10, 2016.)
* Oddly enough, all trees regardless of size break at the same wind speed. (T Puiu, ZME Science, February 9, 2016.)

The article: Critical wind speed at which trees break. (E Virot et al, Physical Review E 93:023001 February 2, 2016.) Check Google Scholar for a copy.

Posts about wind include...
* Atmospheric rivers and wind (May 9, 2017).
* What is the proper length for eyelashes -- and why? (March 16, 2015).
* How rocks travel (November 14, 2014).

Posts about trees include...
* The quality of citizen science: the SOD Blitz (September 28, 2015).
* More from the artificial forest with artificial trees (August 31, 2015).
* Why do koalas hug trees? (June 13, 2014).

More about wood and such:
* The strongest bio-material? (May 30, 2018).
* Making wood stronger (March 19, 2018).

March 30, 2016

Progress toward a practical brain-computer interface: self-calibrating software

March 28, 2016

A brain-computer interface (BCI) allows a person to control mechanical operations using their thoughts. During training, the computer learns what brain signals mean. It can then act on the user's thoughts.

The principle of the BCI is now well-established. Musings has noted an example of a basic BCI [link at the end], as well as other examples of using the information content of brain waves.

However, BCI devices do not work very well -- yet. The dream of a disabled person being able to carry out activities by thinking about them is not yet fulfilled. One of the problems is that the device is not very robust, and requires frequent re-calibration.

A new article takes a useful step. Re-calibration occurs continually during normal use of the device.

The following figure shows some results.

The best typing speeds seen here are 2-3 times the best previously reported. Importantly, they can be sustained, without outside intervention (from lab staff).

The nature of the continual re-calibration is not particularly novel. It's an extension of the original calibration, just based on data while the person is doing real typing. What's important is they have implemented it, and it helps.

News story: Self-calibration enhances BrainGate ease, reliability. (Science Daily, November 11, 2015.)

The article: Virtual typing by people with tetraplegia using a self-calibrating intracortical brain-computer interface. (B Jarosiewicz et al, Science Translational Medicine 7:313ra179, November 11, 2015.) Check Google Scholar for a copy available from the authors. Caution... it is not easy reading.

More on BCI:
* Brain-computer interface -- without invasive electrodes (December 28, 2016).
* Brain-computer interface: Paralyzed patients control robotic arm by their thoughts (June 16, 2012). From the same lab as the current post.

My page for Biotechnology in the News (BITN) -- Other topics includes a section on Brain (autism, schizophrenia). It includes a list of brain-related posts.

An unusual hydrogen bond, involving boron

March 26, 2016

A familiar example of a hydrogen bond is that between two molecules in liquid water; such bonds are responsible for some of the remarkable properties of water. (And very similar hydrogen bonds are responsible for how information is stored in DNA and for some aspects of the structures of proteins.)

Here is how we might draw such a hydrogen bond, in simple text:

H-O-H^δ+ --- ^δ-OH₂

We have two water molecules there; they are shown differently to facilitate lining them up for a hydrogen bond. The dashed line is the hydrogen bond between the two molecules (intermolecular). We've also shown the basis for the bond: the two atoms have small opposite charges, and thus attract. (The δ, the lower case "delta", is usually interpreted as meaning "slightly".) Why do those atoms have slight charges? O atoms hold electrons more tightly; we say that the O atom is more electronegative.

In general, hydrogen bonds occur when an H is between two atoms that are highly electronegative (and quite small).

Here is another hydrogen bond, as reported in a new article.

The dashed line in the figure shows a hydrogen bond between a H atom in diborane, B2H6, and the side of a benzene ring. That's different. Let's deal with the benzene ring first. That aspect is actually not new. The side of a benzene ring has a slight negative charge; think about those π electrons. It's the other end of this hydrogen bond that is quite novel. It is an H attached to a B; in fact it is an H attached to 2 B atoms. B? 2 B? B is not a highly electronegative atom. In fact, it is more positive than H. One might expect a B-H bond to be polarized Bδ+- δ-H.

Why, then, is this H δ+? Because there are two B atoms pulling electrons away from the H. That in itself makes compounds such as this unusual; the whole field of B-H chemistry is full of things that came as quite a surprise given our basic understanding of bonding.    This is from the "graphical abstract" accompanying the article at the journal web site.

That's the idea. What do the authors do? They do theoretical calculations and experimental measurements. Together they support the story above: an H bonded to two B atoms can be δ+, and capable of serving as a hydrogen bond donor. The resulting bond is similar in strength and length to a common H bond between water molecules.

News story: New type of hydrogen bond discovered. (D Bradley, Chemistry World (RSC), March 9, 2016.)

The article: B-H...π Interaction: A New Type of Nonclassical Hydrogen Bonding. (X Zhang et al, Journal of the American Chemical Society 138:4334, April 6, 2016.)

As noted above briefly, boron chemistry gets quite fascinating. Those who think that chemical bonds contain two shared electrons will not be able to make sense of the diborane structure shown above. Hint... The five bonds in the middle, between the two B atoms, contain a total of four electrons.

A post about hydrogen bonding: Life's newest DNA base pair: 5SICS-NaM (June 4, 2014).

More about boron... Paleobioboron (January 26, 2011).

More unusual bonding: How many atoms can one carbon atom bond to? (January 14, 2017).

March 23, 2016

Sliced meat: implications for size of human mouth and brain?

March 23, 2016

Man has a large brain, compared to other animals (taking size into account). However, our overall energy expenditure is about the same. It follows, therefore, that we must spend less energy on some other activity in order to fuel the energy-intensive brain. A good candidate is digestion. Man has a smaller digestive system than other animals. That includes a smaller mouth and teeth.

How can we get by with less of a digestive system? By eating food that is more easily digested. It has been proposed that the invention of fire was important in this regard. Cooked meat is more easily digested than raw meat. Moving toward cooked meat would have allowed ancient hominids to divert energy resources away from gut toward brain.

A new article offers another possibility.

To get an idea of the main results from the new work, we look at what is in the mouths of the participants.

That's it. Slicing meat, as well as cooking it, can make meat more digestible. It is a clever lab experiment.

So, which was it? Which innovation for improving meat played the key role in allowing humans to develop larger brains -- if indeed that is the correct model? The work here does not address that; it merely offers the possibilities. What actually happened is some historical fact, and requires some historical evidence to solve.

The authors suggest that the tools for slicing meat were available earlier than the tools for cooking it. But it's not at all conclusive.

If some ancient hominids had tried using their stone knives on their meat, would they have realized any benefit? The results above show that slicing made the meat easier to chew, so they might have liked it even if they did not measure energy expenditure.

From this work, it becomes plausible that learning to slice meat contributed to the development of human intelligence -- and to the development of a smaller mouth. It is now time for the archeologists to get more facts -- but that will not be easy.

News stories:
* How sliced meat drove human evolution. (L Wade, Science magazine, March 9, 2016.)
* The benefits of food processing: Processing food before eating likely played key role in human evolution. (Science Daily, March 9, 2016.)

The article: Impact of meat and Lower Palaeolithic food processing techniques on chewing in humans. (K D Zink & D E Lieberman, Nature 531:500, March 24, 2016.)

More about the history of meat-eating...
* Carnivory in human ancestors: when did it start? (April 2, 2022).
* Did Lucy butcher a cow? (February 11, 2011).

More meat: Growing meat without an animal? (April 11, 2018).

More about the brain size-gut size problem:
* The metabolic rate of humans vs the great apes: some data (August 1, 2016). This post challenges the assumption that the overall energy expenditure of humans is at the same level as the other apes.
* Fish with bigger brains may be smarter, but ... (January 25, 2013). This is more directly relevant to the current post than you might guess.

More about brain size: A possible genetic cause for the large human brain (March 25, 2017).

My page for Biotechnology in the News (BITN) -- Other topics includes a section on Brain (autism, schizophrenia). It includes a list of brain-related posts.

More about chewing: A robot that can chew gum (March 30, 2021).

More about goats: Q     or     Beware of goats bearing infections     or     It's one health. (February 20, 2010).

Also see: Can we distinguish monkey tools and human tools? (April 17, 2023).

Why do elephants have a low incidence of cancer?

March 20, 2016

Elephants are big, and they live a long time. Those are both risk factors for cancer. However, their incidence of cancer is similar to that of other mammals. Why do elephants have a relatively low incidence of cancer, given their large size and lifespan?

A recent article offers a clue.

The idea developed in the new work is that elephants are better at dealing with DNA damage. They do this by killing off damaged cells better, by a process known as apoptosis. One important protein controlling apoptosis is called p53. Elephants have more p53, so they are better at killing off damaged cells -- so says the argument. In fact, elephants seem to have 40 copies of the p53 gene, an odd finding in itself.

Apoptosis is sometimes called programmed cell death. It is easy to understand that some cells may die because they are damaged so they can't grow anymore. But that's not apoptosis. In the present case, the cells have been damaged so they grow too well, uncontrollably-- with the potential to cause cancer. Apoptosis is an active process to kill cells that are identified as harmful or somehow unwanted.

Here are some results for one part of the story. In this experiment, various types of cells were damaged with radiation. The cells differed in how many copies of the p53 gene they have. The amount of apoptosis was measured.

The y-axis shows the amount of apoptosis. The x-axis shows the three types of cells used here: * In the middle are normal human cells, with two copies of TP53, the gene that codes for p53. * At the left are some human cells with only one copy of TP53; they are from people with a genetic disease called Li-Fraumeni syndrome. (The details of the samples for this disease are shown in the inset; we can ignore all that, since they all gave similar results.) * At the right are elephant cells, with 40 copies of the TP53 gene.

Look at the results... the more copies of TP53, the more apoptosis there is.    This is Figure 4 from the article.

That is one piece of evidence for the story: the more p53, the more of the irradiated cells die. That death is presumably a way to weed out damaged cells, and thus reduces cancer. Elephants have more p53 than we do; that reduces their cancer incidence.

It's all reasonable. p53 has long been recognized as important for preventing cancer. The mutant cells with reduced p53 are from people who have a high incidence of cancer. There have even been attempts to develop p53-based therapies. However, the story is complex and incomplete. For example, you can see in the figure above that going from one copy of TP53 to two copies doubles the response, but going to the 40 copies of the elephant only doubles it again. That may be ok, but we don't understand it. (For one thing, it isn't clear that all 40 copies are active.)

The bottom line? We have a model for why elephants have a low incidence of cancer. It's a plausible model building on ideas of damage and repair that make sense. Data in the new article lend support to the model, which can now be tested further.

News story: How elephants avoid cancer -- Pachyderms have extra copies of a key tumour-fighting gene. (E Callaway, Nature News, October 8, 2015.) This story also links to a second, related article; to my knowledge, it has not yet been formally published.

* Editorial accompanying the article: Evolutionary Adaptations to Risk of Cancer Evidence From Cancer Resistance in Elephants. (M Greaves & L Ermini, JAMA 314:1806, November 3, 2015.)
* The article: Potential Mechanisms for Cancer Resistance in Elephants and Comparative Cellular Response to DNA Damage in Humans. (L M Abegglen et al, JAMA 314:1850, November 3, 2015.) Check Google Scholar for a copy.

Follow-up: More about elephants, cancer, and p53 (August 30, 2022).

Why are size and long life risk factors for cancer? Because it means that there are more cell divisions. At least one source of mutation for cancer is cell division. This was discussed in the following post. The focus article of the post was challenged, but the general point that cell divisions are risky holds. Why are some types of cancer more common than others? (February 6, 2015).

Another post about an animal with a low incidence of cancer: A clue about cancer from the naked mole rat? (January 18, 2014).

Another post about apoptosis, also in the context of cancer: A cancer drug with a switch: it acts only in a cancer cell (September 26, 2010).

More about apoptosis and p53: A treatment for senescence? (June 4, 2017).

More p53: CRISPR connections: p53? cancer? (October 6, 2018).

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

* Previous post about elephants and such... Did the First Americans eat gomphothere? (July 29, 2014).
* Next... Carbon-14 dating of confiscated ivory: what does it tell us about elephant poaching? (February 10, 2017).

March 16, 2016

Good news on the coffee front: Coffee is good for you

March 15, 2016

Briefly noted...

A major study now reports that coffee does not increase the risk of death. In fact, it seems to lower it a bit (10% or so). Some effect is seen even with consumption of one cup of coffee per day, and it is probably maximal by about three cups per day. Importantly, the effect continues with higher levels of coffee consumption. The effect holds for both regular and decaffeinated coffee.

The one big exception is for smokers. The conclusions stated above are for never-smokers. For smokers, there seems to be some interaction, with higher levels of coffee consumption leading to higher mortality for smokers. Sorting out the effect of smoking was the big step forward here, compared to earlier such studies.

The study followed about 200,000 people for as long as 30 years, as part of large ongoing studies. During the course of the study, about 15% of the participants died. The current work involved statistical analysis of the data about the subjects. Isolating single variables, such as coffee consumption, is a tool of statistics. The findings are statistical correlations, and provide no information about causes.

I doubt that anyone drinks coffee to extend their life. Further, the effects seem small. So the main point is that a large study shows no evidence for adverse effects of coffee. That's for non-smokers. For smokers, there may be a complex interaction at high doses.

News story: Moderate coffee drinking may be linked to reduced risk of death. (Science Daily, November 16, 2015.)

Both of the following may be freely available:
* Clinical Summary accompanying the article: Association of Coffee Consumption With Total and Cause-Specific Mortality in 3 Large Prospective Cohorts. (Circulation 132:2287, December 15, 2015.) The file is a collection of summaries for several articles; scroll down to this item.
* The article: Association of Coffee Consumption With Total and Cause-Specific Mortality in 3 Large Prospective Cohorts. (M Ding et al, Circulation 132:2305, December 15, 2015.) The article comes as a 66 page pdf file; 55 of those pages are the supplement, consisting almost entirely of tables. Only dedicated statisticians will delve far. But you can get the main ideas from the abstract and introduction (pages 1-2), and perhaps Figure 1 (on page 5).

For more on coffee (or caffeine)...
* A thermotolerant coffee plant, with high quality beans (June 8, 2021).
* Why you should freeze the coffee beans before grinding them (May 29, 2016).
* How caffeine interferes with sleep (December 11, 2015).
* Brain-computer interface: Paralyzed patients control robotic arm by their thoughts (June 16, 2012).
* Your desire for caffeine: It may be in your genes (May 31, 2011).

Zika virus can infect and inhibit neural progenitor cells

March 14, 2016

The disease of the moment is Zika. Zika virus has been known for several decades, but has attracted little attention. Zika has been considered a mild viral infection. In areas where it is endemic, people presumably become immune, so that even mild Zika becomes uncommon in adults. A few outbreaks in new areas have been noted in recent years, but even those seemed of no great consequence.

In 2015 Zika got to Brazil, and something new happened. We started getting reports of a high incidence of microcephaly in babies born to women who had contracted Zika during pregnancy. Microcephaly literally means small head; it's actually a poorly defined term, but at least some of those born with microcephaly will have serious deficiencies in brain development.

Now there is something serious about Zika.

Here is a new article that offers a clue about the role of Zika virus in microcephaly. We must caution that it is only a clue. The Zika-microcephaly story has many mysteries, and the new work is incomplete. Nevertheless, it is worth noting, as a small step, a possible piece of the puzzle.

The work started with human stem cells; they were differentiated in the lab to develop as cells of the nervous system. Cells at various stages of differentiation were tested to see if they could be infected with Zika virus. The heart of the new work is summarized in the following graph.

The figure shows the infection rate of various cell lines with Zika virus. The two high bars, with 70-80% infection, are for hNPC, which stands for human neural progenitor cells. The four low bars, with about 20% infection, are for two types of stem cells (hESC = human embryonic stem cells; hiPSC = human induced pluripotent stem cells) and neurons.    This is Figure 1C from the article.

The results show that Zika virus infects different kinds of cells with different efficiency. Further, the best infection is with the cells most like those of the early developing brain. The scientists go on to show that the virus inhibits the growth of those cells, and may even kill some of them.

There is no proof here. There are many limitations of the work -- starting with the fact that the Zika virus used here is not the same strain as the one currently circulating in Brazil. What the work does is to get us started with a line of inquiry that could yield information about how Zika promotes microcephaly.

News story: Zika Infects Neural Progenitors -- Scientists provide a potential biological link between Zika virus infection and microcephaly. (R Williams, The Scientist, March 4, 2016.) Good overview.

* News story accompanying the article: Understanding How Zika Virus Enters and Infects Neural Target Cells. (J J Miner & M S Diamond, Cell Stem Cell 18:559, May 5, 2016.)
* The article: Zika Virus Infects Human Cortical Neural Progenitors and Attenuates Their Growth. (H Tang et al, Cell Stem Cell 18:587, May 5, 2016.)

I have added a new section on Zika to my page Biotechnology in the News (BITN) -- Other topics. There isn't much there yet, but there are links to good sources of information, both background and current news. I will maintain a list of Musings post on Zika there.

Next post on Zika... Zika: An estimate of the risk of microcephaly, outside Brazil (March 30, 2016).

There is more about stem cells on my page Biotechnology in the News (BITN) for Cloning and stem cells. It includes an extensive list of related Musings posts.

What can we learn by giving a praying mantis 3D glasses while it watches a movie?

March 12, 2016

Mantises are adept at catching flying insects. How do they do it? There is evidence that they use stereopsis, or 3D vision, but the experimental systems used previously are difficult. The use of 3D glasses makes it easier to test mantises for 3D vision. With 3D glasses, different images can be presented to the two eyes.

With the test system, a mantis is shown a movie of a flying "insect". If the mantis is fitted with the 3D glasses, the insect appears to be floating in front of the screen. If the separate images shown to each eye are designed to provide a 3D image, the mantis strikes at the "prey".

Study of 3D has been almost entirely restricted to vertebrates. Development of this test system will allow detailed study of 3D vision in an invertebrate for the first time.

News stories:
* Bug Eyed: Tiny 3D Glasses Help Confirm 3D Vision in Insects. (Neuroscience News, January 8, 2016.)
* Bug eyes: Tiny glasses confirm 3D vision in insects. (Newcastle University, January 7, 2016.) From the lead institution. It's about the same story as above (which is derived from this university press release), but it has more pictures. Includes a slide show just below the main text. Recommended.

The article, which is freely available: Insect stereopsis demonstrated using a 3D insect cinema. (V Nityananda et al, Scientific Reports 6:18718, January 7, 2016.)

Posts about vision in (non-human) animals include:
* A see-shell story (February 21, 2016).
* How to seat a spider in front of the computer (September 28, 2010).
* Octopus will only pay attention to television if it is "high definition" (August 20, 2010).

A post about the advantages of seeing things in 3D: 3D printing: Sculplexity -- and a printed model of a forest fire (December 29, 2013).

More about predation by mantises:
* Can an insect catch fish for its dinner? (October 8, 2018).
* A "flower" that bites -- and eats -- its pollinator (December 27, 2013).

Also see: The ogre-faced spider, with massive eyes but no ears, detects the sound of prey using its legs (February 9, 2021).

March 9, 2016

Why Salmonella Typhi doesn't infect mice: a challenge to a previous post

March 9, 2016

Original post: Why mice don't get typhoid fever (November 26, 2012).

In that post, evidence was presented to show that mice had a component of the innate immune system that recognized Salmonella Typhi and allowed the mice to resist infection.

A number of labs now report that they disagree with some of the findings in the article discussed there. The authors of that article respond; they defend some of their original findings, but also note that they have had trouble repeating some findings. Interestingly, there is some speculation -- but little real evidence -- that differences in the gut microbiota may be responsible for some of the differences in results.

There is no resolution at this point.

I have attached this update, with the new references, to the original post.

Why do many tarantulas have blue hair?

March 7, 2016

Some tarantulas are quite pretty, at least as judged by color. Some are a nice blue. For example...

A recent article explores blue tarantulas. The blue color is due to reflections off crystals in the hairs, not absorption by pigments. However, the details of those reflecting structures are quite diverse. Interestingly, the blues of different blue tarantulas are very similar, despite the structural differences. Is there some reason for this convergence?

The work suggests that the color is not something the animals themselves sense. In fact, they seem rather colorblind. (They have only one kind of photoreceptor, and generally poor vision -- despite having eight eyes.) The colors do not change during the mating season, suggesting that a role in mating is unlikely. Another possibility is that the color is to protect them from others. For now, there is no evidence on that point.

The big conclusion? We still don't know why many tarantulas are blue -- a very specific blue.

News story: Study suggests blue hue for tarantulas not about attracting a mate. (B Yirka, Phys.org, November 30, 2015.) More pictures.

The article, which is freely available: Blue reflectance in tarantulas is evolutionarily conserved despite nanostructural diversity. (B-K Hsiung et al, Science Advances 1:e1500709, November 27, 2015.)

More on tarantulas:
* Tarantulas in the trees (November 11, 2012). Also features a picture.
* What else are feet good for? (August 8, 2011).

More hair: Could smelling a piece of wood improve the growth of your hair? (November 5, 2018).

More blue animals: Big blue sticks (July 19, 2019).

More about such iridescence or "structural color": How to "dye" carbon fiber -- with titanium dioxide (January 20, 2018).

More about reflectance: Earth is not as bright as it used to be (October 9, 2021).

A drug for heart hypertrophy?

March 4, 2016

You've heard the stories... Young athlete drops dead after a workout, and is found to have a mutation that leads to excessive growth of heart muscle, which somehow leads to defective function -- and sudden death.

The condition is called hypertrophic cardiomyopathy (HCM). It is caused by mutations in a gene for a heart muscle protein. In some people, the condition is silent until the sudden death.

Mutations most commonly lead to reduced function. One might think that HCM involves loss of heart muscle function, and that the excessive growth (hypertrophy) is a compensatory response. However, that may not be true here. It seems that HCM involves over-activity of a muscle function; that leads to the excessive growth. If so, it might be possible to have a drug that inhibits the activity.

There is such a drug under development. Here are some results -- in a mouse model of HCM...

In this experiment, one manifestation of the disease was measured: the left ventricular wall thickness (LVWT). That is the thickness of (one part of) the heart wall. The measurement was made for four conditions. There are two kinds of mice -- normal and mutant. Each was tested with and without the drug.

Quick analysis... You can see that one curve is high, and the other three are low and similar. The high curve is for the untreated mutant mice. The three lower curves are for the wild type mice, treated and untreated, and for the treated mutant mice. In more detail... The two black curves are for the normal mice. The dashed black curve is for untreated mice; the solid black curve is for mice treated with the drug the same way as for the mutant strain. The similarity of those two curves shows that the drug has no ill effect on the normal mice (as judged by this criterion). The red and blue curves are for the mutant mice. The red curve is for untreated mutant mice. The blue curve is for mutant mice treated with the drug. You can see that the mutant mice develop heart wall thickening. The thickening reaches about 50%, compared to the normal mice. The increase in thickness is substantially reduced by the drug treatment. R403Q in the lower right corner identifies the specific mutation studied in this experiment. The coding means that the amino acid R (arginine) at position 403 has been changed to a Q (glutamine). That is in the β-cardiac myosin heavy chain. That change is a known mutation causing the condition in humans. Here, it has been moved into the corresponding mouse gene. The mice are heterozygous for the mutant form of the gene: they carry one copy each of the mutant and normal alleles. The drug was given throughout the time shown. (The article also contains some results for experiments in which the drug was given only after considerable thickening had developed. Those experiments gave mixed results.) Heart wall thickness was measured in live animals by echocardiography. This is Figure 2B from the article. I have added labeling on the axes. (The original labeling was lost when I trimmed this part from the larger figure.)

The figure above shows that the drug substantially reverses one effect of the mutation. The article contains other work on other effects.

Such drug experiments play two roles. First, they help us understand the disease process. The scientists understand what the drug does (or at least think they do). The results are best explained by the model that the mutation leads to an increased activity, which the drug can inhibit, thus restoring normal growth. Of course, it is far more complicated than just the one experiment shown above, but the use of drugs to help understand diseases is important.

Second, it is possible that this is a useful drug. However, it is much too early to know. The work here is with mice, and an artificial test system in the mice. Even if the basic story about the disease process carries over to humans, there is no assurance that the drug will be effective -- and safe -- there.

The article is, in part, from the company that makes the drug. The company plans to take the drug to clinical trials in humans. That's fine. However, only a small percentage of drugs that go to clinical trials lead to useful drugs. For now, this is more about using a drug as a tool to help us understand a disease than about having a clinically useful drug.

News story: MyoKardia Publishes Article in Science Demonstrating That MYK-461 Prevents and Reverses Disease in Genetic Mouse Models of Hypertrophic Cardiomyopathy. (MyoKardia, February 4, 2016.) A press release from the company. It is posted here at Globe Newswire, at NASDAQ. It is more business than science, but it is good as far as it goes.

* News story accompanying the article: Heart disease: Throttling back the heart's molecular motor. (D M Warshaw, Science 351:556, February 5, 2016.)
* The article: A small-molecule inhibitor of sarcomere contractility suppresses hypertrophic cardiomyopathy in mice. (E M Green et al, Science 351:617, February 5, 2016.)

Recent heart-related posts include...
* Increased risk of congenital heart defects in offspring from older mothers: Why? and can we do anything about it? (July 18, 2015).
* The opah: a big comical fish with a warm heart (July 13, 2015).
* Can we pinpoint a specific molecular explanation for tissue damage following a heart attack? (March 24, 2015).

March 2, 2016

Help design a new alphabet

March 1, 2016

How do we choose items for Musings? Sometimes an article seems important, sometimes interesting, sometimes provocative -- or sometimes just fun. Sometimes a picture is striking, and serves as the starting point for developing a story.

This post starts with a figure. I'm still not sure I get much from the article, but the figures in it are irresistible. The following is typical of a large set of figures that dominate a recent article and its news stories:

The figure shows ten characters of a proposed new alphabet.    This is part of Figure 7Ai from the article. It is the middle example from the top row.

What is the story around this figure? Well, the figure is part of a challenge, and you can play... Your task is to provide more characters. How about ten more?

The rules? Just what is above.

You can take a break here, and spend some time developing your set of characters. But before you do, you should be aware that the authors of the article don't care much about your efforts. They know what humans can do with such a challenge.

What the authors care about is how computers deal with the challenge. Many of the character sets shown in the article were created by a computer, after being given a prompt such as the one shown above. The authors imbed questions for you: can you tell which character sets were offered by a human, and which by a computer? If you can't tell, that's good. It means they have succeeded. And they claim the computer is getting more efficient

So we now have computers that can generate new alphabets? Why? It is an example of improving the ability of computers to analyze concepts, and that is important.

It's a story of artificial intelligence (AI), if you want to get into it. Otherwise, it is just a rather odd collection of pictures. The news stories will give you the idea.

News stories:
* When machines learn like humans -- Probabilistic programs pass the "visual Turing test". (Kurzweil, December 10, 2015.)
* Scientists teach machines to learn like humans. (Phys.org, December 10, 2015.) Check out the videos.

The article: Human-level concept learning through probabilistic program induction. (B M Lake et al, Science 350:1332, December 11, 2015.) Check Google Scholar for a copy.

More on alphabet design... The nano-alphabet (June 29, 2012).

Another Turing test: Eugene Goostman and his Turing test (June 17, 2014).

More AI: Is AI ready to predict imminent kidney failure? (August 24, 2019).

The collision of Theia with Earth: head-on?

February 29, 2016

The common view is that the Moon was formed in a collision of another body, called Theia, with the early Earth. The energy of the collision led to the ejection of a big chunk; it became Moon.

However, as evidence has become available, we have come to recognize that one common prediction of the basic model seems incorrect. The model predicts that Earth and Moon should differ in details of their chemical composition. That assumes that the two colliding bodies were different; since most Solar System bodies are different, that has generally been considered likely. There have been several comparative analyses of Earth and Moon, based on measurements of isotopes of various elements. Most of the evidence says that the composition of the Moon is very similar to that of Earth. This has led some to consider whether it is realistic that the two colliding bodies might have been similar. That suggestion and other background is in previous Musings posts [link at the end].

A new article presents another way to resolve the apparent contradiction that there was a collision of two dissimilar bodies giving rise to two similar bodies. What if the collision was so violent that the two bodies mixed thoroughly before one portion was ejected? Then the two resulting bodies would be similar to each other -- but different from both parents. Remember that we have no evidence about the parent bodies; we can only look at the current Moon and Earth -- and they seem similar.

The work here is largely computer simulation. With computer simulation of collisions, the authors show that such a scenario is possible. According to this article, we should consider the possibility that Theia and Earth met "head-on", a collision of maximum violence, which would give thorough mixing of the material from the two bodies. This contrasts with previous models, which generally suggested more of a glancing blow that preserved the identity of the two bodies.

If you are trying to envision the collision... The authors even suggest that Theia might have been about the same size as Earth.

There is experimental work in the current article. It includes further analyses, which support that the Earth and Moon are similar. In particular, the authors refute one recent article claming to find small differences of possible significance. The main interest in the new article is the model that is presented.

A reminder, of course, that the computer simulations -- and the model -- don't tell us what happened. Instead, they help to define what the possibilities are. The work here and in the background post show distinct scenarios that are plausible. Perhaps further evidence will distinguish them.

News story: Moon was produced by a head-on collision between Earth and a forming planet. (S Wolpert, UCLA, January 28, 2016.) From the lead institution.

The article: Oxygen isotopic evidence for vigorous mixing during the Moon-forming giant impact. (E D Young et al, Science 351:493, January 29, 2016.)

Background post on how the Moon was formed: Birth of the Moon: Is it possible that Theia was similar to Earth? (June 20, 2015). Links to more.

More... Formation of the moon: was the Earth surface molten? (June 16, 2019).

My page of Introductory Chemistry Internet resources includes a section on Nuclei; Isotopes; Atomic weights. It includes a list of related Musings posts.

Another Musings post with a February 29 date: An "antidote" for Huntington's disease? (February 29, 2020).

How intestinal worms benefit the host immune system

February 27, 2016

The hygiene hypothesis proposes that the lack of infections that used to be common is adversely affecting our immune systems. That is, we are -- in some ways -- worse off now because we are cleaner. It is an intriguing idea, and there is plenty of circumstantial evidence to support the broad idea. However, specifics are generally lacking.

A recent article develops a rather detailed story of how an intestinal worm interacts with the host immune system to reduce inflammation. The work here is with mice.

Here is an example of the findings...

The y-axis shows the level of a molecule called interleukin-5 (IL-5); it is a marker for inflammation. The IL-5 level is measured under various conditions. The left-hand bar is the control (Ctrl).

The next two bars show the IL-5 level (inflammation) after exposure to "HDM". That is an extract from house dust mite; it is an irritant, which can lead to inflammation. You can see that it induces IL-5 in one case, not the other. What's the difference? The tall bar (middle) is for just that: the effect of HDM. For the right-hand bar, the mice had been infected with a helminth worm (Hpb), then given the irritant HDM. You can see that the worm completely prevented the IL-5 increase due to the HDM. The worm used here, labeled Hpb, is Heligmosomoides polygyrus bakeri. (The mice not infected with the worm are called "naive".)    This is Figure 1D from the article.

Of course, that is just one piece of evidence. After many experiments, the authors suggest the following scenario...
* Infection with the worms leads to changes in the gut microbiome.
* The worm-adapted microbiome makes a higher level of short chain fatty acids (SCFA).
* The SCFA interact with a specific protein of the immune system.
* As a result, there is less inflammatory activity mediated by the immune system.

The major new point from the current article is the role of the microbiome in mediating the effect of the worm on the immune system.

The reduced inflammation presumably benefits the worms. It also helps protect the host from excessive inflammation, such as seen in asthma.

The basic work in the new article focuses on a particular worm and a particular host (mice). However, it appears that the conclusions hold for a range of helminth worms and a range of mammalian hosts. Thus the article offers a detailed model of how the hygiene hypothesis plays out.

News story: Intestinal worms 'talk' to gut bacteria to boost immune system. (Science Daily, October 27, 2015.) The word "boost" in the title is a poor choice. Note that the authors use "modulate" in the article title.

The article, which is freely available: The Intestinal Microbiota Contributes to the Ability of Helminths to Modulate Allergic Inflammation. (M M Zaiss et al, Immunity 43:998, November 17, 2015.)

More on the hygiene hypothesis:
* Treating asthma with a hookworm protein? (December 2, 2016).
* Are lab mice too clean to be good models for human immunology? (May 21, 2016).
* Reducing asthma: Should the child have a pet, perhaps a cow? (November 28, 2015).
* Are girls too clean? (February 26, 2011).

A post about treating worm infections: How to administer Bt toxin to people? (May 16, 2016).

More asthma: Is Helicobacter pylori good for you or bad? (April 10, 2012). The "good" is that Helicobacter may help prevent asthma, by its effect on the immune system. This has some similarity to the hygiene hypothesis in that it involves our microbiome affecting our immune system. It is different in that Helicobacter infection is not considered related to hygiene.

A recent post about the microbiome: Breastfeeding and obesity: the HMO and microbiome connections? (November 14, 2015).

More on the gut microbiome...
* Possible role of gut bacteria in Parkinson's disease? (March 17, 2017).
* A robot that can feed itself (February 3, 2017).

Also see: What can the mites on your face tell us about your ancestry? (May 31, 2016).

Regional changes in sea level: evidence from gravity measurements

February 26, 2016

As the Earth warms, sea level rises. That is often noted. However, it is more complex. There are multiple factors that affect sea level, and the overall effect varies by region.

A new article provides more analysis of the details of sea level change than ever before.

In general, there are two types of reasons for sea level rising. First, water expands when it warms. That is, the existing water has an increased volume. Second, water may be added to the oceans, for example by melting of glaciers and ice sheets (most famously from Greenland and Antarctica).

How can we distinguish these? One way is gravity measurements: changes in gravity at a location are commonly interpreted as changes in the amount of water. A key part of the new article is using the extensive gravity measurements over the entire Earth in the last decade (actually 2002-2014).

Some of the above ideas have been introduced in earlier posts [links at the end].

The following figure summarizes much of the findings from the new article.

The contribution of the "steric" effect is the focus of the article. The authors show that previous estimates of ocean warming have underestimated it.

That gives you the idea. The article represents a very detailed analysis of how the oceans are behaving -- and why they are doing so. That is our main point.

News story: Climate change: Ocean warming underestimated -- Researchers at Uni Bonn: Ocean warming plays a bigger role than previously believed. (EurekAlert! (University of Bonn), January 25, 2016.)

The article: Revisiting the contemporary sea-level budget on global and regional scales. (R Rietbroek et al, PNAS 113:1504, February 9, 2016.) The article is not easy reading, in part because of excessive jargon (and odd things such as negative pies). But you can get the ideas by browsing it.

Background posts...
* Sea level: 2011: There was less water in the oceans (November 25, 2012).
* Using gravity measurements to measure water: Evaluating the world's water resources (August 11, 2015). Links to more.

More about sea level: Climate change and sea level (October 2, 2017).

More about climate change: Is the weather getting better or worse? (May 23, 2016).

More about gravity: Which is older, the center of the Earth or the surface? (September 7, 2016).

February 24, 2016

Pregnancy in males: It's similar to pregnancy in females

February 22, 2016

Humans are viviparous, meaning that they give birth to live young. (In contrast, birds lay eggs.) Viviparity seems to have arisen independently over 150 times among the vertebrates, over 20 times in fishes alone. It is interesting to compare the process of pregnancy in diverse animals in which viviparity arose independently.

A recent article examines pregnancy in a fish, and then compares it to pregnancy in humans and more generally in mammals.

The scientists measured the level of gene expression at various stages during pregnancy. About 3000 genes showed some difference in expression during pregnancy. The scientists found that the genes could be grouped into nine clusters based on the pattern of gene expression. The following figure illustrates this, summarizing results for two of those clusters.

That's the basic framework: there are groups of genes with specific patterns of expression during pregnancy in this fish.

The authors then go on to look at the lists of genes with known function. The patterns of gene expression observed here are similar to those for mammals. The general picture they develop is that pregnancy in this fish seems rather similar to that in mammals. The pregnant parent provides similar functions in both cases, and many of the same genes are involved, presumably in similar ways.

The article provides mostly qualitative discussion of the genes. It makes the comparison and finds considerable similarity in the nature of the pregnancies.

Except for one thing... In the fish studied here, it is the male that gets pregnant and carries the brood during internal development. The fish is Hippocampus abdominalis, commonly known as the seahorse.

It's unusual for males to get pregnant; it seems to happen only in the seahorse and some closely related fishes. How that got started is not known. But it is interesting that, once the animal took the course of developing pregnancy in males, the nature of that pregnancy is rather like other pregnancies.

If you don't know what a seahorse looks like, go look for a picture. They are rather silly-looking things. And if the belly looks distended, don't jump to conclusions. They look like that normally. (There is a good picture in the news story listed below, but you can probably find better.)

We should be clear... The work here does not mean that pregnancy is the same in the diverse animals. Pregnancy seems to have originated independently many times. Each case is different. However, there appears to be a basic tool-kit of pregnancy genes that tends to get used over and over once the animal embarks on viviparity. There is much more to be learned about all this, in diverse animals.

News story: Male seahorse and human pregnancies remarkably alike. (Science Daily, September 2, 2015.)

The article: Seahorse brood pouch transcriptome reveals common genes associated with vertebrate pregnancy. (C M Whittington et al, Molecular Biology and Evolution 32:3114, December 2015.)

Other posts about pregnancy include...
* A gene that reduces the chance of successful pregnancy: is it advantageous? (May 18, 2015).
* Cannibalism in the uterus (May 31, 2013). Another fish.
* Light-dark (day-night) cycles affect pregnancy (August 10, 2012).
* An advanced placenta -- in Trachylepis ivensi (October 18, 2011).

Another silly-looking fish... CO₂ emissions threaten clowns (September 20, 2010).

A see-shell story

February 21, 2016

What is a see-shell? It is a shell you can see with. A chiton shell. (A chiton is a mollusk, the same phylum as clams.)

Chiton shells have eyes. Lots of eyes. A new article investigates the optical properties of the eyes. Here is an example...

The top frame shows a fish, side view. The middle frame shows the image of the fish that is obtained using a lens from a chiton shell eye. The measurement here is in a lab situation, using an isolated lens. It is equivalent to what would be found with a "20-cm-long fish that is 30 cm away" [p 954, right column]. The bottom frame shows what the scientists think the animal may actually perceive. It's not as good as the direct image itself. That is, the lens is not limiting. (What is limiting? The spacing of the photoreceptors, in the "retina" layer below the lenses.)    This is Figure 3B from the article.

The shell of the chiton is made of calcium carbonate. It is designed for strength. At least, most of it is. But there are hundreds of specks on the shell. These also contain calcium carbonate, but arranged differently. In fact, they look like little lenses. Their physiological relevance has been uncertain. The present work adds to the argument that the eyes in the shell are part of the sensory system of the animal. The calcium carbonate crystals are the lens part of these eyes.

The authors also discuss the phenomenon of the shell containing two distinct regions, based on the same material, but optimized for different purposes. The eyes do weaken the shell, but they improve the vision.

News story: Chitons See with Ceramic Eyes, New Research Shows. (E de Lazaro, Sci.News, November 23, 2015.) Features a close-up picture of a chiton shell. The dark bumps are the eyes. (As the caption there notes, you can also see other sensory organs -- of unknown function. There is more to learn about these shells!)

* News story accompanying the article: Biomaterials: Crystalline eyes of chitons inspire materials scientists -- Mollusk makes hundreds of eyes from shell mineral. (E Pennisi, Science 350:899, November 20, 2015.)
* The article: Multifunctionality of chiton biomineralized armor with an integrated visual system. (L Li et al, Science 350:952, November 20, 2015.) Check Google Scholar for a preprint freely available from the authors.

Other examples of unusual eyes include...
* An eye that forms an image using a mirror (February 13, 2018).
* Where are the eyes? (August 19, 2011).

The chiton eyes are called ocelli. So we might make note of the following post: Is the warnowiid ocelloid really an eye? (October 12, 2015).

More about animal vision: What can we learn by giving a praying mantis 3D glasses while it watches a movie? (March 12, 2016).

A post about the optical properties of calcium carbonate: An ancient navigation device? (April 16, 2013).

A post about the structural properties of calcium carbonate: Armor (February 5, 2010).

What happens when a lithium ion battery overheats?

February 19, 2016

It may catch on fire, a well-known risk with this battery type. But what if it sensed the heat and just shut down?

A new article reports a design for lithium ion batteries that does just that. It is based on a simple principle: most things expand when they are heated. What if the expansion of a warmed battery caused it to break a contact, and shut down? What the scientists have done is to develop a practical implementation based on that idea. And it is reversible. When the battery cools down, contact is re-established, and battery function resumes. That is, they have built a fuse for the battery -- a fuse that is reversible.

The fuse is based on a tape-like material, which can be installed somewhere in the battery circuit. For example, the tape may cover an electrode.

The bulk of the tape is a plastic polymer, such as polyethylene. Embedded in the polymer are spiky nanoparticles, which are conductive. At low temperature (T), the particles form a conducting network, and the battery functions. At high T, the particles are further apart, and the conducting network is broken; the battery stops.

The following figure illustrates, in cartoon form, how the fuse works.

The blue rectangle shows the polymer. The conductive nanoparticles are shown as spiky yellow blobs, labeled as GrNi (for graphene and nickel). Upon heating, the polymer material expands, and the conductive particles become farther apart. At low T (top frame), the conductive particles are largely touching, making the tape as a whole conductive. At high T (bottom), the conductive particles don't touch much; the tape as a whole is no longer conductive. The dashed lines within the polymer area show pathways that electrons might follow. Each red X marks a blockage in the pathway, due to polymer expansion. The authors use the term percolation to refer to the conduction process. (Ignore the dashed lines at the left side; they relate this frame to a previous part of the full figure.) This is Figure 1c from the article. (The right-hand side of Figure 1a of the news story in the journal is essentially the same figure.)

The following figure shows the fuse in action, in an artificial test situation.

The authors show that they can make various forms of the fuse material, which will melt at various specific temperatures between 50-100 °C. The general requirement is that the fuse material breaks the circuit before overheating cases structural loss of the battery material. That happens a little above 150 °C, and can lead to a fire.

The change in resistance when heated is about 10⁸-fold. The fuse has minimal effect on the battery performance during normal use, but responds quickly to T changes when needed.

It looks like a promising way to improve the safety of the ubiquitous lithium ion battery. It will be particularly important to see how well the system scales up to large batteries.

News story: A battery that shuts down at high temperatures and restarts when it cools. (Kurzweil, January 11, 2016.)

Video: Safe & reliable lithium-ion battery. (YouTube, 2 minutes.) Narrated by the senior author; good diagrams of how it works, and an example.

* News story accompanying the article: Batteries: Polymers switch for safety. (K Amine, Nature Energy 1:201518, January 2016.)
* The article: Fast and reversible thermoresponsive polymer switching materials for safer batteries. (Z Chen et al, Nature Energy 1:20159, January 2016.) Check Google Scholar for a copy from the authors. The article is from the first issue of a new journal.

Previous post on batteries: A flow battery that uses polymers as the redox-active materials (January 8, 2016).

Previous post on lithium batteries: Fast charging batteries (March 13, 2009).

More...
* A low-temperature battery (July 29, 2018).
* Making lithium-ion batteries more elastic (October 10, 2017).

Previous post on lithium: Quiz: What is it? (March 6, 2012).

There is more about energy issues on my page Internet Resources for Organic and Biochemistry under Energy resources. It includes a list of some related Musings posts.

Also see... In the aftermath of gun violence... (January 8, 2018).

February 17, 2016

Gravitational waves

February 16, 2016

The photo at the right shows two pipes lying on the ground near Hanford, Washington. The pipes are each about four kilometers long and one meter in diameter.    This is reduced from the first figure in the Quanta news story.

Imagine that we wanted to know the exact length of one of the pipes. We could measure it by shining a laser beam down the pipe, and seeing how long it takes to reach the other end. (Or, we could put a mirror at the far end, and measure how long it takes for the light beam to make a round trip.) Since we know the speed of light, we could calculate the length of the pipe. We'll make this more complicated a little later, but that's the idea for now.

Now imagine that we make such measurements continuously. Suddenly we notice that the pipe length starts changing, in a rhythmic fashion.

While we are making these measurements, another team is measuring the length of a similar pipe 3000 km away near Livingston, Louisiana. At "exactly" the same time we notice those changes in length of the Hanford pipe, the other team observes exactly the same changes in length of the Livingston pipe.

That all really happened -- on September 14, 2015, at 09:50:45 UTC. The results, after careful analysis, were announced last week. Here is what the results look like...

The graph shows the fluctuations in the lengths of the two pipes vs time. Each of the colored lines is for one pipe. The y-axis is labeled "strain". 1 on this scale means that the pipes changed length by 1 part in 1021. That is about 4 attometers (for the 4 km pipe).

You can see that there is some background noise. At about 0.35 seconds, the fluctuations in length become noticeably larger, and are the same at both sites. Another tenth of a second... it's all over. This is reduced from a figure in the Quanta news story. It is probably the equivalent of the upper right part of Figure 1 from the article. Why does it say "shifted" in the labeling for the Hanford data? The data have been corrected for the distance between the two sites. This is also why I put "exactly" in quotation marks above.

Why are two pipes 3000 km apart fluctuating in length -- in exactly the same way? Because the structure of space is changing. A gravitational wave passed by -- a gravitational wave perhaps from the collision of two black holes.

Einstein predicted such gravitational waves a century ago, as part of the theory of general relativity. The results shown above are the first observations of such gravitational waves. They are from a project called the Laser Interferometer Gravitational-Wave Observatory (LIGO).

Scientists have long wondered how they might measure the gravitational waves that Einstein predicted. Einstein himself thought it might not be possible to measure them. Over recent decades, sensitive instruments have been built to try to make the measurements; we now have a success.

Why is it so difficult? Look at those numbers with the graph. The change in length is one part in a billion trillion. An infinitesimal change in the length of a 4 km-long pipe. The change is a tiny fraction of the size of the nucleus of an atom.

At the start we suggested how one might determine the length of the pipe by measuring how long a laser beam takes to travel its length. That's sort of what the scientists did, but that simple measurement would not be nearly good enough.

Recall that there are two pipes at each site, at right angles to each other. Because the pipes are at right angles, an encounter with a gravitational wave would affect the two pipes differently. What the scientists really did was to measure the difference between the lengths of the two pipes. They allow the light beams from the two pipes to interact with each other. This interaction, called interference, is extremely sensitive to tiny changes; that is what they measure.

Recent upgrading of the LIGO observatory led to reducing background noise by about 3-fold. While the scientists were testing the upgraded LIGO, a gravitational wave just happened to pass by that September morning. Without the improved (reduced) noise level, they would not have seen it.

If the current story is really all true, we should expect more reports of gravitational waves, from LIGO and from other gravitational wave observatories that are being developed. We are, it would seem, at the beginning of the era of using gravitational waves as a tool for observing the universe.

News stories. A lot has been written about this story, an indication of its perceived importance. At some level, it is easy to understand, but it also gets very technical. I've included multiple news stories, in approximate order of their level. Videos, both interviews and animations, are in some of them. Browse!
* Einstein's gravitational waves 'seen' from black holes. (P Ghosh, BBC, February 11, 2016.)
* Gravitational waves detected 100 years after Einstein's prediction. (Science Daily, February 11, 2016.)
* Gravitational Waves Discovered at Long Last -- Ripples in space-time have been detected a century after Einstein predicted them, launching a new era in astronomy. (N Wolchover, Quanta, February 11, 2016.) Includes an animation of what gravitational waves do to space-time. It's mesmerizing, whether you understand it or not.
* LIGO detects first ever gravitational waves -- from two merging black holes. (T Commissariat, Physics World, February 11, 2016.)

* News story in the publisher's news magazine; it is freely available: Viewpoint: The First Sounds of Merging Black Holes. (E Berti, Physics 9:17, February 11, 2016.) Includes a video describing the measurement system.
* The article, which is freely available: Observation of Gravitational Waves from a Binary Black Hole Merger. (B P Abbott et al, Physical Review Letters 116:061102, February 11, 2016.)

The article authorship includes the LIGO team as well as collaborators from other gravitational wave teams around the world. The list of authors and their affiliations takes 5 of the 16 pages of the article; three of the authors are dead.

There is a second article, focusing on the black hole merger that is thought to be the source of the gravitational waves observed here. That article is also freely available. The Physics World news story, above, links to it.

* * * * *

Follow-up: Gravitational waves: II (July 12, 2016).

and ... Gravitational waves: What caused them, and how do we know? (November 1, 2016).

and ... Gravitational waves: a challenge to the announced discovery (July 19, 2017).

Posts about gravity include...
* Which is older, the center of the Earth or the surface? (September 7, 2016).
* Does anyone know how strong gravity is? (September 16, 2014).
* A galaxy far, far away: the story of MACS 1149-JD (October 12, 2012). Includes gravitational lensing.

Another post that notes interference of light waves: Graphene bubbles: tiny adjustable lenses? (January 15, 2012).

Posts about black holes include: Mayhem at the center of the Milky Way (August 23, 2011).

On my page of book suggestions, this work is noted in the listing for the book: Gribbin & Gribbin, The Cat in the Box -- A history of science in 100 experiments (2017).

The man who established the (US) National Academy of Sciences

February 12, 2016

It is his birthday today. We note the event with a 272-word speech.

Why 272 words? Why do we even note the length? Because that man gave a famous 272-word speech -- in the same year he established the National Academy of Sciences (NAS). Many of our American readers have memorized all or part of that speech; many do not know that the author was also the man behind one of the most prestigious science institutions in the world.

In 2013, the 150th anniversary of the speech, a number of Americans, from various walks of life, were asked to commemorate the occasion -- in their own 272 words. One of the resulting speeches recently surfaced as an editorial in Science. It tells the story, and links to a video of the author delivering his speech.

The editorial, with video of the speech, is freely available: America's science legacy. (N d Tyson, Science 350:891, November 20, 2015.) The page includes his editorial describing the situation, a link to the video of the speech, and the text of the speech, "The Seedbed", at the bottom.

We also have some music. It includes some of the text of the original 272-word speech. Music (YouTube, 16 minutes).

Most recent post based on an article from the NAS journal: Do oil dispersants work? Is biodegradability bad? (January 9, 2016).

My page Internet resources: Miscellaneous contains a section on Science: history. It includes a list of related Musings posts. It also includes a list of books that deal with science history. Of particular relevance here may be books that deal with science and American leaders, such as Shachtman (2014), Tanford (1989), and Thomson (2012).

That page also has a section on Art & Music. It includes a list of related Musings posts.

This post is 318 words (between the horizontal lines).

* * * * *

Text here and below was added later, and is not included in the word count shown above.

More about national academies of science: Women in science: How about at the highest level, the national academies? (April 12, 2016).

February 10, 2016

BRCA1 (the breast cancer gene) and Alzheimer's disease?

February 8, 2016

BRCA1 is a gene well known for its effect on breast cancer. Women with one copy of the mutant allele are at increased risk for breast cancer.

A new article makes a connection between the BRCA1 gene and Alzheimer's disease (AD).

Here are the basic results that got the story started...

This test involves two kinds of mice. One is normal; the other also has hAPP -- the gene for the human amyloid-beta (Aβ) protein that is a feature of AD. Mice with hAPP are a model system for studying AD.

The absence or presence of hAPP is shown by - or + in the top row of the figure. The rest of the figure shows the amounts of various proteins present in brain tissue from the two kinds of mice. The intensity of a band is a measure of how much protein is present. The proteins from each kind of mouse were separated by electrophoresis, and identified with antibodies. This is a procedure known as a Western blot. For presentation here, the bands of interest have been cut out and shown together in a single montage. The labeling at the right side shows the size of each protein, in kDa (kilodaltons). The bands can be measured quantitatively, but you can just eyeball them. (The quantitative results are in the article, in part b of the figure. The important results are clear by eye, though.) The first protein shown is BRCA1. You can see that there is less of it when hAPP is present. That's the key result. Most of the other proteins shown are about the same in the two strains. (Me2H3 is present in larger amounts with hAPP; that is beyond our discussion here.)    This is Figure 1a from the article.

This experiment makes a connection between the BRCA1 protein and AD... At least in this mouse model, there is less BRCA1 in the AD mice. That's intriguing, but, by itself, says nothing about why -- or about human AD.

The article goes on to look further. Among the findings...
* Reducing the level of BRCA1 by other means causes damage to the nervous system in mice. This result suggests there is some functional relevance of the BRCA1 reduction.
* Examination of post-mortem brain samples from some AD patients suggests that they, too, had reduced levels of BRCA1. This result begins to make the connection between the mouse model and the human disease.

How can a single gene affect two diseases as different as breast cancer and AD? It is now known that BRCA1 is involved in DNA repair. Perhaps DNA repair is somehow involved in both diseases. That a DNA repair gene is involved in cancer is reasonable; we know that cancer involves the accumulation of mutations. There is evidence for DNA damage in AD and other neurodegenerative diseases, but how DNA repair is involved is not clear at this point.

The results here suggest there is a role for BRCA1 in AD; they deserve to be followed up.

News stories:
* Alzheimer's Linked to Protein that Repairs DNA -- Researchers find low levels of BRCA1 in brains of Alzheimer's patients. (M Ammam, Alzheimer's News Today, December 4, 2015.)
* Breast Cancer Gene Implicated in Alzheimer's. (G D Zakaib, ALZFORUM, December 4, 2015.)

The article, which is freely available: DNA repair factor BRCA1 depletion occurs in Alzheimer brains and impairs cognitive function in mice. (E Suberbielle et al, Nature Communications 6:8897, November 30, 2015.)

Are people who carry BRCA1 mutations at increased risk for AD? The evidence currently available suggests that they are not. This is an issue that will need to be resolved.

* * * * *

More on BRCA1:
* Distinguishing pathogenic and benign BRCA1 mutants: a high-throughput test (January 26, 2019).
* A gene for breast cancer: what does it do? (May 4, 2010).

Next cancer post: Is glyphosate (Roundup) a carcinogen? (March 6, 2016).

Recent post on AD: Transmission of Alzheimer's disease in humans? (September 27, 2015).

More about cancer and AD: What's the connection: Alzheimer's disease and cancer? (October 31, 2022).

My page for Biotechnology in the News (BITN) -- Other topics includes sections on Alzheimer's disease and Cancer. Each includes a list of related posts.

Did selenium deficiency play a role in mass extinctions?

February 5, 2016

There have been five mass extinctions through the history of life on Earth. Musings has discussed the possible causes of some of them. The most recent event, 66 million years ago including the dinosaurs, has gotten the most attention. As a recent post made clear, our understanding of any extinction is incomplete. [Background links at the end.]

A new article raises an intriguing point, the significance of which is hard to judge. So we just note it. A team of scientists suggests that deficiency of the trace nutrient element selenium may be related to extinctions.

Here is an example of what they find...

It's not an easy graph! Let's go slowly... The x-axis is a time scale. Ma means millions of years ago; here, time runs the right way -- and the numbers run backwards. Just above the numeric scale are some labels for geological periods. In particular, note the Triassic and Jurassic, with a vertical line between them, at about 201 Ma. In some form, that line extends upward through the entire graph; it marks the extinction event. In fact, it is labeled ETE, which means end Triassic extinction.

Just to the left of that ETE line is an arrow, pointing downward, labeled "rapid Se drop". That refers to a curve, purple with red diamonds, near the arrow. That curve shows the amount of Se found in rocks of various ages. You can see that the curve indeed falls dramatically just before the ETE line. In the two points before the extinction line, the Se level falls from its highest value to near its lowest value.    This is Figure 6 from the article.

That's the key point: there was a dramatic drop in selenium just before the extinction. The rest is filling in details. Since we now have your attention -- that this might be interesting -- let's look at some of those details.

The Se decline was more than 10-fold. The Se levels are shown using the left-hand scale, labeled "Se pyrite (ppm)"; the unit ppm means parts per million. It is a log scale. Also, there is a horizontal line, labeled "Current Se level"; it is just above 10². The low part of the Se curve, at the extinction, is about 100-fold lower than the current level.

The graph also shows O₂ and CO₂ levels. These use the scale on the right side, which is not a log scale. I don't think we need to go through those here. We do note that there was an O₂ decline, but the timing does not match the extinction very well. Their point in the article is that it is the Se level that matches the extinction.

The graph above focuses on one extinction event. In their full analysis, the scientists find a major Se decline associated with three of the five mass extinction events.

Selenium is an interesting trace nutrient. Is it possible that it plays such a critical role that it influences life on the scale of mass extinctions? The authors argue that the Se levels fall below what many organisms need.

There is a geology connection, too. Geological activity, such as volcanoes and earthquakes, affect selenium levels.

It is also possible that the Se is not the key component, but simply correlates with it. In fact, the article shows changes in other trace minerals. The Se effect was the largest and clearest, but that doesn't mean it was the most important. It could be that it is a "marker", but not the key variable. The graph above shows a correlation; causation is a separate question.

Finding the correlation -- between selenium levels and mass extinctions -- is an interesting novel finding. The biology, chemistry, and geology of Se are all complex; it is hard to know where this will go.

News story: Tiny Molecules May Have Caused Ancient Mass Extinction Events, Says New Theory. (A Laguipo, Tech Times, November 5, 2015.) This is somewhat awkwardly written in some parts, but overall gives a reasonable overview of the work.

The article: Severe selenium depletion in the Phanerozoic oceans as a factor in three global mass extinction events. (J A Long et al, Gondwana Research 36:209, August 2016.)

Background posts about mass extinctions include:
* What caused the extinction of the dinosaurs: Another new twist? (January 26, 2016).
* What caused the mass extinction 252 million years ago? Methane-producing microbes? (October 12, 2014).
* The 6th mass extinction? (April 4, 2011).

More selenium biology: Selenium and neurodegenerative diseases? (June 25, 2022).

This is the first Musings post from the journal Gondwana Research. If you don't remember what Gondwana was, check the post How were the Gamburtsevs formed? (December 7, 2011).

February 3, 2016

A ninth planet for the Solar System?

February 2, 2016

Big news story! A new planet for our Solar System.

Predicted. It hasn't been found; the pictures you see of it are "artist's conceptions".

There is nothing new about predicting the existence of a planet, because the observed orbits of known bodies don't seem quite right. One can predict that there must be some other body, not yet known, whose gravity is affecting the observed orbits. Neptune was first predicted, using such an argument; later it was found.

Many such predictions have been made; only Neptune was found. Caltech planetary scientist Mike Brown recently said of such a prediction, "If I read this paper out of the blue, my first reaction would be that it was crazy." That's from the news story in Nature, listed below. The paper he was referring to is the one that is the subject of this post -- and he is a co-author. He goes on, "But if you look at the evidence and statistics, it's very hard to come away with any other conclusion." Perhaps, but we'll believe it when we see it -- the planet.

The following figure gives an idea of the basis for the prediction.

The figure legend is: "Orbital clustering in physical space." That's the point. Even without the details, you can see that the orbits that are shown cluster off to one side. The figure is a diagram of part of the Solar System. There are two circles in the figure, a small one and a big one. The big one has a scale bar to the right: 250 AU. (1 astronomical unit (AU) is the distance from Earth to Sun; Pluto is about 40 AU from the Sun.) I'm not sure what the smaller circle is; it may be near the orbit of Neptune, about 30 AU from the Sun, and marking the beginning of the Kuiper belt. The Sun would be in the middle -- a tiny dot.

The ellipses are the orbits of known bodies in the outer part of the Solar System. They are clustered. Why? That is the question the authors address. Planet Nine is their proposed answer. A massive object off to the other side; its gravity is a major determinant of the distribution of objects "out there".    This is the right-hand frame of Figure 2 from the article.

That's the idea. I caution you that the article is much more complex. The prediction may seem like hand-waving here, but is based on detailed mathematical analysis, which leads to a specific prediction about the orbit.

The article is exciting because of its prediction. Not only a ninth planet, but a big one -- and way out there in that mysterious region of the Kuiper Belt. But be cautious. Until someone finds it, it is just a prediction -- and most predicted planets don't show up. (It would be nice to get back to having nine planets, wouldn't it?)

What are the prospects of finding it? We know the orbit, but we don't know where it is in the orbit -- which is big. It's a faint object. The good news is that it is within the range of some telescopes, with better ones coming online soon. The astronomers think there is a good chance of finding Planet Nine within a decade. If it is there.

News stories:
* Evidence grows for giant planet on fringes of Solar System -- Gravitational signature hints at massive object that orbits the Sun every 20,000 years. (A Witze, Nature News, January 20, 2016.) This news story contains a version of the above figure -- with the proposed orbit of Planet Nine also shown. The story also includes a listing of some other planetary predictions; look at the section, partially hidden, called "Solving for X".
* Astronomers say a Neptune-sized planet lurks beyond Pluto. (E Hand, AAAS, January 20, 2016.)

The article, which may be freely available: Evidence for a distant giant planet in the solar system. (K Batygin & M E Brown, Astronomical Journal 151:22, February 2016.) Not easy reading!

More about Planet 9:
* Briefly noted... Cataloging the outer solar system (April 27, 2022).
* Finding Planet 9: You can help (March 13, 2017).

The planet Neptune was predicted because of the odd orbit of Uranus. The following post notes the discovery, but does not talk about the prediction. Discovery of Neptune: The one-year anniversary (July 12, 2011).

More about planetary orbits: A planet that may be only ten years old? (March 8, 2016).

More planets: Another Solar System planet -- revealed by its diamonds? (May 22, 2018).

Author Mike Brown played a key role in the developments a few years ago about the status of Pluto. I list his book on the Pluto story on my page of Book Suggestions: Brown, How I Killed Pluto -- and why it had it coming. The listing there notes another Musings post about his work.

Another book about predicting planets: Levenson, The Hunt for Vulcan -- And how Albert Einstein destroyed a planet, discovered relativity, and deciphered the universe.

Facultative endothermy: a lizard that is warm-blooded in October

February 1, 2016

We maintain our body temperature (T) at about 37°C, regardless of the environmental T. That's called endothermy, or warm-bloodedness. Mammals and birds are common examples. Some animals don't maintain their body T, which is then about that of the environment. That's called ectothermy, or cold-bloodedness. Reptiles and fishes are common examples.

But is it that simple? And in any case, how and why did endothermy arise?

There is debate about whether dinosaurs were warm- or cold-blooded. Since we have no direct measurements, it is something to be inferred from evidence that survives -- in fossils. And at least one fish is warm-blooded, contrary to the norm for its group. Musings has noted these topics before [links at the end].

Lizards are reptiles -- ectotherms. A new article reports a lizard that is... Well, let's look.

The lizards are Salvator merianae, known as black and white tegu lizards. They are apparently native to Argentina. The work reported here was done in Brazil; the first results we will examine are for June -- the beginning of winter. Here are those results...

Why is this of interest? It's an example of an animal on the borderline of endo- vs ecto-thermy. It is a lizard-like ectotherm most of the time, but does a little endothermy when that seems of benefit. It tells us that even an individual species can be both. We must wonder if what this lizard does might relate to the origins of endothermy.

The endothermy is related to reproduction. We know that reproduction requires a higher level of energy production, but that alone is not sufficient to explain the heat rise. It seems likely that the heat rise itself is of benefit. Is this a clue to the origin of endothermy?

We've opened up a lot of speculation in the last two paragraphs. Remember, the graph above is data. That is what the animal does. What it means is open.

The lizard is now described as a facultative endotherm. Facultative in this context means that it is optional.

To be clear... We are not suggesting that humans are derived from tegu lizards. What we suggest -- or at least wonder about -- is whether what this lizard did is an example of an early step in developing "true" endothermy. If tegu lizards developed facultative endothermy, it is likely that other animals did, too. Some may still be around, waiting for us to do this test on them. Some may be extinct. It would be nice to study the genetic and biochemical basis of multiple facultative endotherms. For example, did different species develop facultative endothermy for the same "purpose"? Using the same mechanism?

News stories:
* Lizard found to heat itself during mating season. (B Yirka, Phys.org, January 25, 2016.)
* Tegus get hot and bothered during the breeding season. (Reptipage, January 22, 2016.)

The article, which is freely available: Seasonal reproductive endothermy in tegu lizards. (G J Tattersall et al, Science Advances 2:e1500951, January 22, 2016.)

Background posts about endothermy:
* The opah: a big comical fish with a warm heart (July 13, 2015).
* Were dinosaurs cold-blooded or warm-blooded? (August 23, 2014).

More... Failure to regenerate heart tissue: role of thyroid hormone (May 14, 2019).

Other posts about lizards include:
* How to clamp down to keep the partner from straying (December 15, 2020).
* A story of dirty toes: Why invading geckos are confined to a single building on Giraglia Island (November 12, 2016).
* Twenty percent of the females are genetic males (October 6, 2015).
* An advanced placenta -- in Trachylepis ivensi (October 18, 2011).

What's the latest in the field of odonatology?

January 29, 2016

The latest issue of the journal Odonatologica contains a single article. It is 230 pages. Surely, devoting an entire issue to one big article suggests that the article is important. So let's look.

Here are two of the findings...

Ceriagrion banditum, the band-eyed citril. The species name refers to its apparent mask, not to its behavior.	Zygonyx denticulatus, the pale cascader.
This is trimmed and reduced from Photo 21 of the article.	From Photo 76.
Size? Each is probably 3-4 cm long. (Some figures in the article have scale bars.)

You might recognize these as odonates: the dragonflies and damselflies. But you probably haven't seen these particular ones before. They are newly described species, reported in the current article -- along with 58 other new odonates.

And that's the story: 60 new species of dragonflies and damselflies, all from Africa. It's another step toward cataloging Earth's life.

One point the article makes is that it wasn't all that hard to find these.

Keep looking.

What's the difference between a dragonfly and a damselfly? Well, damselflies tend to have a skinnier body and to fold their wings behind them when not flying. Look at the two specimens above. The one on the left is a typical damselfly on these criteria; the one of the right is a typical dragonfly.

News story: The need to name all forms of life: 60 new species of dragonflies described from Africa. (Phys.org, December 10, 2015.) It briefly describes the work, and discusses the importance of the odonates, which depend on fresh water. The story is also a plea for support of work to find and classify life forms. The story here is based on a press release from the Naturalis Biodiversity Center.

The article, which is freely available: Sixty new dragonfly and damselfly species from Africa (Odonata). (K-D B Dijkstra et al, Odonatologica 44:447, December 2015.) The introductory section is very readable, and is an overview of the importance of the work. It starts: "Unnamed species are anonymous to conservation." The bulk of the article contains the formal taxonomic descriptions, but there are many pictures of both animals and habitats. Good browsing.

More about dragonflies:
* Black silicon and dragonfly wings kill bacteria by punching holes in them (January 28, 2014).
* Eating frog legs -- and why the hind legs taste better (July 16, 2009).

More about African insects: Why don't black African mosquitoes bite humans? (December 19, 2014).

January 27, 2016

What caused the extinction of the dinosaurs: Another new twist?

January 26, 2016

The common view has been that the dinosaur extinction was caused by a meteorite that slammed into the Yucatan peninsula of Mexico. Some have argued that the extreme volcanism in the Deccan Traps of India was a major cause. This was long a minority view; however, recent improved dating of the Deccan Traps has made that case more plausible. This was discussed in a Musings post a year ago [link at the end]; that is good background reading for the current post.

A recent article reports more analysis of the Deccan Traps volcanism. The work supports another suggestion: the meteorite impact may have "caused" the Deccan Traps volcanism.

That's a startling idea, isn't it? Let's elaborate.

The Deccan Traps volcanism occurred over a long time span. The claim is not that the impact caused the volcanism per se, but that it caused a huge increase. That is, the suggestion is that it greatly enhanced the volcanism, perhaps making it catastrophic. Sorting this out required a refinement in the dating of the Deccan Traps volcanism, coupled with information on the amount of volcanic activity over time.

Here is some of the data...

From what is above, you can see some trends. And you can see that there was an increase in volcanic activity around the KPB. That's interesting. And we must admire the work needed to generate all these results.

The analysis above does not establish a causal relationship between the KBP (for this purpose taken as the meteorite impact) and volcanism, and only hints at the exact timing. However, the scientists make further analysis. In particular, they think that the enhanced rate shown above is due to fewer but much larger eruptions. The larger eruptions have the potential to be catastrophic. Then they offer speculation. It's not so much that they claim to have shown a causal connection but that it becomes plausible. They have evidence that the Deccan magma system changed at about the time of the impact; it is plausible that the seismic effect of the impact caused that change.

Interestingly, geophysicists are not too surprised. They had predicted that such a connection might have occurred, with a time scale of perhaps thousands of years between the trigger and the effect.

The dinosaurs are gone, whatever the reason. Trying to understand what caused this mass extinction event has led to a series of fascinating findings. Finding that the two proposed causes of this extinction event may actually be linked -- not just coincident but mechanistically linked -- is just the latest twist. Surely, this is not the end of the story.

News stories:
* Double Catastrophe Wiped Out Dinosaurs: Deccan Traps Volcanism and Chicxulub Impact. (Sci.News, October 2, 2015.)
* Deccan Trap sprung by bolide? (S Drury, Earth-Pages, October 15, 2015.)

The article: State shift in Deccan volcanism at the Cretaceous-Paleogene boundary, possibly induced by impact. (P R Renne et al, Science 350:76, October 2, 2015.) Check Google Scholar for a copy.

Background post on the Deccan Traps system: What caused the dinosaur extinction? Did volcanoes in India play a role? (April 13, 2015).

More on the dinosaur extinction event:
* Briefly noted... Dinosaur extinction: What time of year was it? (May 10, 2022).
* How the birds survived the extinction of the other dinosaurs, why birds don't have teeth, and how those two points are related (July 30, 2016).
* A major algal bloom associated with the dinosaur extinction event? (May 13, 2016).

More extinctions: Did selenium deficiency play a role in mass extinctions? (February 5, 2016).

Next dinosaur post... Blood vessels from dinosaurs? (April 22, 2016).

More seismic waves... How seismic waves travel through the Earth: effect of redox state (June 8, 2018).

A MERS vaccine, for camels

January 22, 2016

The MERS outbreak continues. There is no good preventive or therapeutic treatment. About a third of the reported cases are fatal.

A new article reports some interesting progress: a vaccine against MERS -- for camels.

The vaccine is based on a poxvirus, a vaccinia strain commonly used for vaccine work. A gene from the MERS virus has been inserted into the vaccine strain. Previous work showed that the vaccine protected mice from MERS infection. Now we have a test in camels.

The following figure shows some results...

The figure shows the level of anti-MERS antibodies made by some camels that had received one or another vaccination. There are results for three time points following vaccination. Before getting into details, let's look at the key result. There are four points, upper right with red squares, that stand out as the highest points on the graph. These are the results for the antibody level found in four camels 7 weeks after receiving the vaccine. That's it; the camels getting the vaccine made antibodies against the MERS virus. All the rest of the graph is time points and controls.

Now that you know the graph shows something interesting, here is some detail... The y-axis is labeled VNT. That means virus-neutralizing titer. It is a measure of the amount of antibody -- against the MERS virus, as the label says. It is a log scale; each number is twice the preceding number. The horizontal dashed line is the detection limit. Most values are essentially zero. The x-axis is for camels; each column is for one camel. The label on the x-axis shows what the camel was vaccinated with. The first two got PBS, the buffer solution. The next two got MVA-wt; that is the poxvirus vector, with no MERS gene added. The last four (the four on the right) got MVA-S, the vaccine. (The S stands for the "spike" protein of the MERS virus, a protein on the virus surface that induces antibodies.) Results are shown for three time points, with symbols as shown in the key. None of the controls (buffer or poxvirus vector) showed any measurable antibodies to MERS at any time point. The four camels that got the vaccine showed increasing levels over time.    This is Figure 1A from the article.

The figure shows that the vaccine induces antibodies against the MERS virus. In other work in the article, the scientists showed that the vaccine reduced shedding of virus by the camels. It also reduced their runny noses, their main symptom of MERS infection.

MERS does not seem to cause serious problems for camels. The reason we would vaccinate camels against MERS is to reduce transmission to humans. (That is similar to vaccinating dogs against rabies to prevent the disease in humans.) That the scientists observed reduction in virus shedding is encouraging, but we don't know how useful that would be in reducing transmission.

The vaccine might have one more benefit. As noted above, the vaccine is based on a poxvirus. It induces antibodies to poxviruses, too -- including camelpox. It is possible that will be considered of some value; camelpox is a serious disease in camels.

The vaccine will also now be tested in humans.

News stories:
* MERS virus: Drying out the reservoir. (Science Daily, December 18, 2015.)
* New vaccine against MERS virus tested successfully on dromedary camels. (Universitat Autònoma de Barcelona, December 18, 2015.) From one of the institutions involved. It includes a video (2 minutes), narrated in Spanish (?). The video has some interesting footage, including showing some camels in the lab; it may be worthwhile even if you don't understand the narration.

* News story in the journal prior to print publication: Infectious disease: Camel vaccine offers hope to stop MERS -- Vaccinated animals shed less virus, but is that good enough to prevent human outbreaks? (K Kupferschmidt, Science 350:1453, December 18, 2015.)
* The article: An orthopoxvirus-based vaccine reduces virus excretion after MERS-CoV infection in dromedary camels. (B L Haagmans et al, Science 351:77, January 1, 2016.) Check Google Scholar for a copy.

Recent posts about MERS:
* How the MERS virus spread in Korea: role of super-spreaders (November 3, 2015). This is about the largest MERS outbreak outside the Middle East. No camels here.
* Camels and the transmission of MERS: blame the kids? (March 30, 2015).

A post more broadly about coronaviruses: Bats and the coronavirus reservoirs (July 25, 2017).

A non-MERS camel post... Cloning: camel -- update (June 11, 2012).

There is more about MERS on my page Biotechnology in the News (BITN) -- Other topics in the section SARS, MERS (coronaviruses). It includes links to good sources of information and news, as well as to related Musings posts.

That Biotechnology in the News (BITN) -- Other topics page also includes a section on Smallpox (poxviruses)

Also see: A better strategy for distributing rabies vaccine? (April 26, 2021).

January 20, 2016

Cheese-making and horizontal gene transfer in domesticated fungi

January 19, 2016

A recent article reports sequencing the genomes of ten strains of Penicillium fungi. Two of them were strains used in cheese-making: Penicillium roqueforti and P. camemberti. The genomes of the two cheese-making fungi contained some interesting surprises.

The genomes of both cheese-making fungi contained regions that were not typical of the species. Further, those regions carried genetic marks that suggested they had "jumped" there. That is, these regions appeared to be the result of horizontal gene transfer (HGT). As a reminder, HGT is inheritance by means other than from the parents; for example, it may be due to viruses or transposons carrying the genes from one organism to another.

Is there any significance to finding "foreign" genes in two cheese-making fungi? As a test, the scientists compared two strains of P. roqueforti which differed mainly in whether or not they contained two of those HGT-regions.

The following figure shows an example of what they found...

	The figure shows how two fungal strains grew under two different test conditions. The two strains are both P. roqueforti. One is W+C+ and the other is W-C-. W and C are two of those regions in the cheese-making genomes that seem to be from HGT. The two growth conditions are a common lab medium and the material used to make cheese.
Look at the results... On the medium used for making cheese (right side), the W+C+ strain (top) grew better than the W-C- strain. For the lab medium (left side, labeled MM), the opposite was true. The W-C- strain (bottom) grew better.    This is Figure 3A from the article.

The conclusion is that the W⁺C⁺ regions help the fungi grow in the cheese medium. That would explain why they are found in the two cheese-making strains.

What do we make of this? Here is what the scientists suggest might have happened... At some point in history, humans developed cheese-making. Certain fungi were useful for the process. The fungi did the job, but were not ideally adapted to grow on the cheese-making materials. With selection pressure applied by humans, strains that did better for cheese-making developed. Some of the genetic changes that improved the fungi came from other strains, by HGT. Overall, then, they suggest that mankind domesticated the fungi for cheese-making, and some of the changes along the way were due to HGT.

Remember, the article provides some data on the fungal genomes. The rest is building a story around the data. Over time perhaps we will find more data to support the story -- or not.

News story: The life and times of domesticated cheese-making fungi. (Phys.org, September 24, 2015.)

The article, which is freely available: Adaptive Horizontal Gene Transfers between Multiple Cheese-Associated Fungi. (J Ropars et al, Current Biology 25:2562, October 5, 2015.)

Previous cheese post: What's the connection: blue cheese, rotten coconuts, and the odorous house ant? (August 24, 2015). This may also be the previous post on a Penicillium.

Some cheese history... The oldest known piece of cheese (April 25, 2014).

More dairy: The nutritional value of yogurt? (September 28, 2018).

A recent post about HGT: Who's been genetically engineering the sweet potatoes? (June 28, 2015).

More about HGT in fungi: A gravity sensor in a mold: a story of horizontal gene transfer? (May 16, 2018).

More about domesticated fungi: The history of brewing yeasts (October 28, 2016).

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.

How to confuse a yeast -- a sensory illusion

January 15, 2016

You are probably familiar with optical illusions: you think you see something, but it turns out to be not real. Optical illusions are an example of sensory illusions.

We now have an example of a sensory illusion in yeast.

Osmotic stress occurs when yeast are switched to a medium with a high concentration of solutes. They can adapt, and then grow somewhat more slowly.

The following figure shows some examples of how yeast behave as the osmolarity of their growth medium is changed. (The osmolarity is a measure of how much stuff is dissolved in the growth medium.)

That's the finding. The yeast can adapt to fast or slow oscillations; they interpret either of those as high osmolarity, regardless of the period of the variation. Oddly, they cannot adapt to intermediate oscillations. They seem quite confused by that condition.

Explanation? What are the yeast thinking? The authors go on to study the mechanism of osmotic adaptation, at the level of gene control. They actually find what the problem is. With the intermediate oscillations, the cells are taking each increase as a new stress, but not responding to the decreases. Why they do that has to do with some details of gene regulation. Of course, this is an artifact of the unusual experimental conditions. Yeast do not normally get 8-minute oscillations of osmolarity in nature; if they did, they might have developed the ability to adapt to it. By exposing them to a non-natural stimulus, we create a sensory illusion, and confuse them. It's the same argument we make for why we can be confused by an optical illusion.

News story: A sensory illusion that makes yeast cells self-destruct. (Kurzweil, November 20, 2015.)

The article: Oscillatory stress stimulation uncovers an Achilles' heel of the yeast MAPK signaling network. (A Mitchell et al, Science 350:1379, December 11, 2015.)

Posts about optical illusions:
* How flies perceive optical illusions (November 30, 2020).
* Bright lights and pupil contraction (March 2, 2012).

And an acoustic illusion... Why bats fly into windows (December 3, 2017).

Among other posts on stress...
* How balloons burst (December 20, 2015). Physical stress.
* Are birds adapting to the radiation at Chernobyl? (August 3, 2014). Oxidative stress.

More about yeasts:
* What if yeast had only one chromosome? (August 26, 2018).
* On genome duplications (September 10, 2015).

January 13, 2016

Is a "dead" virus in the human genome contributing to the neurological disease ALS?

January 11, 2016

Mammalian genomes, including the human genome, contain debris from viruses and other "foreign" genetic elements. The simplest to think about are retroviruses, where the virus genome routinely integrates into the host genome. An occasional infection of the germ line can lead to the virus becoming a permanent part of the human genome. What are the consequences? It's commonly thought that, one way or another, the viral genome is rendered inactive or at least harmless. This may be done by the viral genome accumulating mutations that inactive it, or by the host genome developing regulatory mechanisms that keep the virus harmless.

As we learn more, from more sophisticated experiments, we may need to question that assumption.

Let's look at what was reported in a recent article. It deals with a particular retrovirus that is part of the human genome: human endogenous retrovirus K (HERV-K). And it deals with the neurological disease amyotrophic lateral sclerosis (ALS; also known as motor neuron disease -- and as Lou Gehrig's disease). Here is one result...

The figure compares two brain tissue samples, stained for a protein from the virus. The upper frame (part D) is for a sample from a person who died with ALS. The lower frame (part I) is for a control sample from a person who died with Alzheimer's disease. The cells from the ALS sample, but not from the control, show staining for the protein. The staining is in the membrane area, as would be expected for this protein. The scale bars are 50 micrometers. Ignore the box in part D. It is to show that a higher-magnification of this part is in the full figure (as part E).    These are parts of Figure 1 from the article.

That is, the person with ALS shows evidence for activity of a gene from one of those "dead" viruses.

Now, that doesn't prove much. We have a sample size of 1. Maybe the gene just, somehow, gets activated from time to time. It just happened to be in a person with ALS this time. However, the article goes on, and presents more evidence.

The additional evidence is along two lines, which we note just briefly... First, there is considerable evidence that the viral gene expression is specific for some people with ALS, and does not occur in controls, including those with other brain diseases. Second, experiments in lab cultures and in mice suggest that the protein can be neurotoxic.

What does this all mean? Is this protein from a "dead" endogenous retrovirus part of the ALS disease process? What is cause and what is effect here? The authors are cautious, and others are even skeptical. What the article does is to raise the question, and focus attention on the possibility that an endogenous retrovirus in our genome is important.

News story: Is an ancient virus responsible for some cases of Lou Gehrig's disease? (J Cohen, Science magazine news, September 30, 2015.) Includes a good discussion of the skepticism that scientists have about what this work means.

The article: Human endogenous retrovirus-K contributes to motor neuron disease. (W Li et al, Science Translational Medicine 7:307ra153, September 30, 2015.) Check Google Scholar for a preprint at arXiv.

More ALS:
* Effect of exercise on developing ALS (July 27, 2021).
* Triplet-repeats: Do they act through the RNA? (September 24, 2017).

A post on an ALS-like disease... How BMAA may cause motor neuron disease -- a clue? (July 1, 2014).

More about possible effects of endogenous retroviruses in humans: A connection: an endogenous retrovirus in the human genome and drug addiction? (October 29, 2018).

Concern about endogenous retroviruses is an issue in considering the possibility of using pigs as organ donors to humans. See the post: Pigs as organ donors for humans (February 16, 2010). More linked there.

New developments... How to do 62 things at once -- and take a step towards making a pig that is better suited as an organ donor for humans (January 17, 2016).

My page for Biotechnology in the News (BITN) -- Other topics includes a section on Brain (autism, schizophrenia). It includes a list of brain-related posts.

Do oil dispersants work? Is biodegradability bad?

January 9, 2016

Oil spill. To help get rid of it, we add what is called a dispersant. It is a type of detergent, which leads to break-up of the oil.

Is this a good idea? Where does the dispersed oil go?

A new article explores these issues. A caution... The results are confusing. Be careful about drawing conclusions.

Here is the general idea of the experiments... The scientists took a sample of ocean water. They added various things to it, such as oil (petroleum), a dispersant, or both. The microbes naturally in the ocean water were given time to work -- over about six weeks. The scientists measured what happened.

Some results...

There are three kinds of additions to the ocean water; these are labeled across the top. The left column is for oil (they call it "WAF"), the middle column is for dispersant, and the right column is for oil + dispersant (or "CEWAF"). Each row of the table is for a particular type of measurement. The first two (rows A and B) are measurements that reflect degradation of oil. The last two (rows C and D) are measurements that reflect total bacterial growth. Each box contains five bars, which show the measurements at five time points over six weeks. (You don't see five bars? Many are "zero".) This is part of Figure 3 from the article. I have added some labeling at the top. The full figure contains more rows and one additional column; the part shown here is enough to make all the main points.

Look at the first two rows (A and B) together. Both are intended to reflect oil degradation, and the results are qualitatively similar. In the first column, + oil, there is degradation of the oil at all time points past time zero. There is nothing in the column for + dispersant. That's fine; there is no oil present. Now look at the right-hand column, with oil + dispersant. Oil degradation is poor. There is less oil degradation with oil + dispersant than with oil alone.

Now, the last two rows (C and D). These reflect bacterial growth. It's good with oil alone or dispersant alone. It is reduced when both are added.

The primary result, then, is that use of the dispersant actually inhibits microbial degradation of the oil. In another part of the experiment, they show that the dispersant stimulates growth of bacteria that eat the dispersant. When both oil and dispersant are added, dispersant-eating bacteria grow well, but oil-eating bacteria do not.

Why the dispersant inhibits the oil-eating bacteria is not clear from this work. But the bottom line is that the effect of the dispersant is bad, at least as judged by this criterion.

In the title of the post, I posed two questions. Let's revisit them.
* Do oil dispersants work? That may depend on what you mean by work. They may disperse the oil, which was perhaps the original goal. But the new work says the dispersants may inhibit degradation -- and that's not so good.
* Is biodegradability bad? Well, that's not clear. We don't know why the dispersant inhibited oil degradation. However, one possibility is that the dispersant-eating microbes out-compete, or somehow inhibit, the oil-eating microbes. If so, then the biodegradability, in this sense, is bad.

The use of dispersants to help clean up oil spills is well-intentioned. The current article suggests that they are not working as intended. This work should lead to re-thinking the role of dispersants.

News stories:
* Study: Dispersants did not help oil degrade in BP spill. (S Borenstein, Phys.org, November 9, 2015.)
* Oil dispersants can suppress natural oil-degrading microorganisms, new study shows. (A Flurry, University of Georgia, November 9, 2015.) From the lead institution.

The story of the news stories... If you read both of the stories listed above, you will see that they are similar in many ways. That's mot a surprise; Phys.org tends to base their posts on the University news release. But what is interesting is that the Phys.org story completely misses a key point: that the dispersants stimulated growth of microbes that ate the dispersant.

The article, which is freely available: Chemical dispersants can suppress the activity of natural oil-degrading microorganisms. (S Kleindienst et al, PNAS 112:14900, December 1, 2015.) Caution... This paper is not easy to read, partly because of jargon.

Also see:
* The man who established the (US) National Academy of Sciences (February 12, 2016). A post about the journal.
* Oil in the oceans: made there by bacteria (January 3, 2016).
* A biodegradable agent for herding oil slicks (September 18, 2015). Herding agents and dispersants are different ways to deal with oil.

There is more about alkanes on my page Organic/Biochemistry Internet resources in the section on Alkanes. It links to a list of some related Musings posts.

A flow battery that uses polymers as the redox-active materials

January 8, 2016

In a recent post, we introduced the idea of a flow battery [link at the end]. That is a type of battery that stores the chemicals in holding tanks, separate from the electrode area. Flow batteries are thought to be suitable for use with large scale but intermittent energy sources, such as solar or wind.

Here we have another recent article on flow batteries. The point of this article is a particular design improvement.

The authors note some problems with their system. For example, the polymer solutions are more viscous and harder to pump. They suggest that further work will yield polymers that are more suitable. Nevertheless, the article illustrates work that is going on to develop flow batteries.

If you want more chemistry... Part b of the figure (bottom) shows the chemistry of the two redox reactions. "R" shows where these structures connect to the polymers. That is shown more in part a; the structures shown in the holding tanks give an idea of the chemical structures of the polymers, incorporating the groups shown in part b. (In previous flow batteries, the redox-active materials would be small molecules similar to those shown in part b, but with very small "R".)

News story: Chemists present an innovative redox-flow battery based on organic polymers and water. (Phys.org, October 21, 2015.)

The article: An aqueous, polymer-based redox-flow battery using non-corrosive, safe, and low-cost materials. (T Janoschka et al, Nature 527:78, November 5, 2015.)

Background post on flow batteries: Flow battery (January 4, 2016).

More about flow batteries: A better membrane for vanadium-based flow batteries (March 11, 2022).

More about batteries:
* Making lithium-ion batteries more elastic (October 10, 2017).
* What happens when a lithium ion battery overheats? (February 19, 2016).

More about viscosity... A better way to make chocolate, inspired by brake fluid (August 23, 2016).

There is more about energy issues on my page Internet Resources for Organic and Biochemistry under Energy resources. It includes a list of some related Musings posts.

January 6, 2016

Flow battery

January 4, 2016

Batteries do two things. They store energy in a chemical form, and they carry out reactions to convert that stored chemical energy into electrical energy. Rechargeable batteries also carry out the reaction to convert electrical energy into stored chemical energy.

A flow battery does all that, but there is a separation between where energy is stored and where it is converted. This provides more flexibility in battery sizing. The following figure illustrates the idea of a flow battery.

That figure was what caught my attention for this item. It is a good way to introduce the idea of flow batteries.

Flow batteries may find a role in storing energy from large scale intermittent energy sources, such as wind or solar. In fact, you can see those sources in the figure above, at the top. The ability to hold large amounts of energy in the holding tanks is important for that use.

If flow batteries are to become important for large scale energy storage, they must be low cost and robust. Commercialization of flow batteries is in the early stages; it's not clear that a really good solution is at hand. The current article offers some new choices for the chemistry. The authors argue that their flow battery would be lower cost and contain less toxic chemicals. We'll skip the details; the main purpose here is to present the idea of the flow battery.

News story: Alkaline flow battery charges up renewable energy storage. (M Gunther, Chemistry World (RSC), September 25, 2015.)

* News story accompanying the article: Batteries: Expanding the chemical space for redox flow batteries -- Flow batteries offer low-cost electricity storage for grid-scale renewable power sources. (M L Perry, Science 349:1452, September 25, 2015.)
* The article: Alkaline quinone flow battery. (K Lin et al, Science 349:1529, September 25, 2015.) Check Google Scholar for a preprint (manuscript-format) available from the authors.

More about flow batteries:
* A better membrane for vanadium-based flow batteries (March 11, 2022).
* A flow battery that uses polymers as the redox-active materials (January 8, 2016).

Among other Musings posts on batteries, illustrating their diversity...
* A battery for bacteria: How bacteria store electrons (May 2, 2015).
* A simple way to make a supercapacitor with high energy storage? (January 6, 2014).
* Fast charging batteries (March 13, 2009).

Alternatives:
* Storing energy from an intermittent source -- as compressed air under the sea (March 3, 2019).
* MOST: A novel device for storing solar energy (November 13, 2018).

There is more about energy issues on my page Internet Resources for Organic and Biochemistry under Energy resources. It includes a list of some related Musings posts.

Another post about oxidation and quinones... How the rain and cars in Seattle are killing the fish (January 26, 2021).

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