Musings: January 2019 to ?? (current posts)

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

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   Introduction (separate page).
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Current posts -- 2019 (January - ??)
   New items Posted since most recent e-mail; they will be announced in next e-mail, but feel free... !
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   January 16 (Current e-mail)
   January 9

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New items

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


How to preserve dead mice so they stay fresh and edible

January 18, 2019

Modern humans rely largely on refrigeration to preserve food for later use.

A new article reports that one type of beetle may use antibiotics for that purpose. Antibiotics from its gut microbiome.

Part A shows photographs of two pieces of mouse carcass. They are labeled "Untended carcass" (UC) and "Tended carcass" (TC). Tended by whom? By a pair of beetles. Burying beetles, Nicrophorus vespilloides.

Compare the two... the TC is in much better condition. The UC shows considerable signs of degradation, including having a white mold growing on it. That is, the beetles have kept the mouse carcass in good condition.

Why? That's easy. The carcass is food for their offspring, beetle larvae. Preventing the natural degradation of the carcass is good for the survival of the beetles. They preserve the meat for use by their family.

How? Part B of the figure gets us started. The diagram at the right shows a piece of carcass, in blue. Just inside that, in yellow, is a feeding cavity, which is "installed" by the beetles. You can see a couple of beetle larvae feeding. More importantly, there are all those little black things in the feeding cavity, on the surface of the carcass tissue. Those represent bacteria. The story that the authors develop is that the parent beetles establish the feeding cavity and inoculate it with bacteria from their own gut. These bacteria make antibiotics, which help preserve the carcass -- thus keeping it as good food for the larvae.

   This is slightly modified from Figure 1 in the article. I have added the labels UC and TC at the top of part A. (The authors use those abbreviations extensively in the article.)


Does it matter? Here are some data for how the larvae grew...

The graph shows the weight of the larvae under two conditions. One is the normal condition of a tended carcass; this is labeled "matrix control". For the other condition, the bacterial layer (or "matrix") in the feeding cavity was removed.

The larvae gained about 40% more weight in the control condition, with the normal tended carcass. Removal of the bacterial layer reduced larval growth.

Note that the two conditions here are not the same as in the top figure. The current figure shows that the beetles have enhanced the food value of the carcass. It does not directly show the value of preventing decomposition per se.


   This is Figure 5A from the article.


Above we have shown two parts of the story: that the beetles reduce carcass degradation and that the tended carcass has higher food value. There is more to the work... In particular, the authors show that the bacteria in the feeding cavity come from the beetles' gut, and that these beetle-bugs inhibit the microbes responsible for deterioration of the carcass. It is inferred, but not shown directly, that the effect is, at least in part, due to antibiotics made by the beetles' bacteria inoculated into the feeding cavity.

Whatever the details, it is an interesting story about how mature works -- how these beetles preserve meat for their kids.


News story: How beetle larvae thrive on carrion -- Burying beetles rely on their gut symbionts in order to transform decaying carcasses into nutritious nurseries for their young. (Science Daily, October 15, 2018.)

The article, which is freely available: Microbiome-assisted carrion preservation aids larval development in a burying beetle. (S P Shukla et al, PNAS 115:11274, October 30, 2018.) Much of the article is quite readable, especially for the parts relating to how the organisms interact. (The parts on the composition of the microbial communities get rather detailed.)

A recent post about an insect microbiome: Glyphosate and the gut microbiome of bees (October 16, 2018).

Among posts on beetles...
* An armadillo the size of a beetle (April 8, 2016).
* Polystyrene foam for dinner? (October 19, 2015).
* How to fly a beetle (April 27, 2015).
* Dung beetles follow the Milky Way (February 24, 2013).

More on antibiotics is on my page Biotechnology in the News (BITN) -- Other topics under Antibiotics. It includes an extensive list of related Musings posts.



January 16, 2019 (Current e-mail)


Briefly noted...

January 16, 2019


Pasta that is stronger than steel. Ten billion times stronger. This pasta -- more specifically, lasagna -- is in neutron stars; the term is used for the material in the inner crust. How did scientists measure this? They didn't. It's all computer simulation. (The figure legend for Figure 1a is: "Tensile deformations pulling lasagna sheets apart."
* News story: Meet the strongest material in the universe: nuclear pasta. (T Puiu, ZME Science, September 20, 2018.) Links to the article. (A freely available preprint is available at ArXiv.)



A flexible system for making small batches of pharmaceutical-quality proteins

January 15, 2019

Making drugs is complicated. There are many steps, including synthesis and purification. Each step must be done according to established standards, ensuring product quality and safety. It is a major effort to develop, test, and document a process. No wonder that drug manufacturers want high-volume drugs.

What if it were practical to make drugs in small quantities? A recent article offers an approach.

The basic idea is to have a simple generic production system. Plug in a gene for the desired protein, and let the system make it.

The following figure shows the manufacturing facility...

That's it. The full system shown above is less than two meters across, and about a meter high -- on a bench top.

The modules include production (synthesis) and purification, as noted above. The final module, at the right, is formulation: packaging into the final form.

   This is Figure 1b from the article.


The scientists report results for producing three proteins, all of which are approved drugs. In each case, the product from the new system meets established specifications.

The article includes much data... multiple production runs for those three protein products. There is information on process details, and on characterizing the products to show that they are satisfactory. We could show some of those results here, but that would miss the point. The big picture is the collection of results, which show that their system works well overall, for a variety of products.

In general, it takes them a few weeks to tune the process for a new product, and a few days to do a single production run. The scale is making 100-1000 doses.

The system may be suitable for making drugs needed for rare conditions. That's a niche not well served by drug manufacturers at present. It may also be useful for making small quantities of experimental or variant drugs.

There is no claim that the proposed system will work for everything. First, it focuses on drugs that are single proteins -- made from a single gene. Then, the process uses common modules. Proteins with special or more complex requirements won't work here. That's okay; the system described here is a start. Many proteins are made in similar processes, and a system that works using common steps is a big step toward being able to make small amounts of high-quality pharmaceutical proteins.

The authors call their system InSCyT, for Integrated Scalable Cyto-Technology.


News stories:
* Manufacturing small batches of biopharmaceuticals on demand -- Portable biopharmaceutical drug manufacturers could be the future method of producing the drugs on demand for outbreaks of disease. (I Farooq, European Pharmaceutical Review, October 1, 2018.)
* A new way to manufacture small batches of biopharmaceuticals on demand. (A Trafton (MIT), Phys.org, October 1, 2018.)

The article: On-demand manufacturing of clinical-quality biopharmaceuticals. (L E Crowell et al, Nature Biotechnology 36:988, October 2018.)



Provision of milk and maternal care in a spider

January 13, 2019

Milk (more specifically, mammary glands) is a defining feature of mammals. However, milk (in some general sense) occurs in a few non-mammals. A new report describes the role of milk -- and maternal care -- in a spider; it may be the most advanced example of milk among non-mammals.

The spider here is Toxeus magnus, a jumping spider. The scientists noticed that some nests had one adult female and several juveniles. That's an unusual situation for a spider. They investigated further...

On the left is Mom.

On the right is a higher magnification picture of what her abdomen looks like after you press on the red square.


Does she look like an ant? Indeed, this spider is considered an ant mimic. But count the legs!

   This is Figure 2 from the article. Note the red scale bars, 1 millimeter, at the lower right of each part.


The figure above shows milk. Does it matter? The following figure shows what happen when the baby spiders are deprived of milk.

The figure shows survival curves for four groups of spiderlings, under different conditions related to milk.

Curve #1 is a control, with ordinary maternal behavior. That gives the highest survival curve.

Curve #4 shows what happens if spidermom's milk is blocked at day 1. All the baby spiders die within a few days.

Curve #2 shows what happens if milk is blocked at day 20. This curve is about the same as the control curve (#1). Comparison with curve #4 shows that blocking the milk early is very bad, but blocking it at day 20 has little effect.

Curve #3 is about another way to stop the milk supply. In this case, Mom was removed from her babies at day 20. Survival is a little worse than for simply blocking milk (curve 2). The comparison of curves 2 and 3 provides some evidence for maternal care beyond supplying milk.


How does one block milk? By painting over the body opening it comes from. With "correction fluid."

This is modified from Figure 3A from the article. I added numbering for the conditions, both in the key at the top and on the corresponding curves. I also labeled the x-axis (which is labeled in the article at the bottom of the full Figure 3).


What is spider milk like? It's full of nutrients -- more nutrient-dense than cow milk.

The work uncovers some novel findings. Not just the milk, but the extensive maternal care, which extends into young-adulthood. Nothing like this has been seen in spiders before.


News stories:
* Jumping Spiders Produce Milk to Feed Their Young. (D Kwon, The Scientist, November 29, 2018.)
* Spider milk is a thing, and it's 4 times more nutritious than cow's milk. (T Puiu, ZME Science, November 30, 2018.)

The article: Prolonged milk provisioning in a jumping spider. (Z Chen et al, Science 362:1052, November 30, 2018.)

More milk... Cockroach milk (August 21, 2016).

A recent spider post: The spider with the mostest ... (and such) (January 2, 2018).

More about parenting: The earliest known example of maternal care? (May 2, 2016).



Treating a heart attack using a microneedle patch

January 11, 2019

Mammalian hearts do not recover well after injury. Multiple approaches to improving recovery are being explored.

A recent article makes use of a type of device we have noted before, and repurposes it to promote heart recovery.

Here's the idea...

The figure shows a microneedle patch attached directly to an injured heart.

The patch contains heart cells ("cardiac stromal cells"), which release growth factors into the heart via the microneedles.


   This is Figure 1A from the article.

Some results...

The graphs show a measure of heart function at two times following an artificial heart attack in lab rats. In each graph. the four bars are for different treatments.

In the key, for the treatments... MI = myocardial infarction; MN = microneedle patch; CSC = cardiac stromal cells. MN-CSC means MN with CSC.

The left-hand graph shows the results shortly following the heart attack. The four bars are all about the same. That's not surprising, since there has been almost no actual treatment time.

The right-hand graph shows the results after three weeks of recovery and treatment. The right-hand (red) bar is for the full treatment, using a patch with the cells. Heart function is considerably higher than in the control condition (black bar at the left, labeled simply MI). It is also a little better than the baseline value. (In contrast, function has decreased compared to baseline for some conditions.)

The middle two bars are for two more conditions, each of which has only one part of the treatment. The results with the patch alone (without cells) are not significantly different from the untreated control. The results with the cells alone (without patch) are somewhat higher than the untreated control, but not as high as the full treatment, which allows the cells to gradually release their products over time.

   This is part of Figure 4 from the article.


Taken at face value, the results shown above are encouraging. They suggest that a continual supply of the needed factors can be good. The novel aspect of using the patch here is the inclusion of cells, which supply the factors over an extended time.

The article also contains some early work with pig hearts.

There has been controversy over the years about methods for promoting heart recovery. We need not get into that here. The current article can be taken as preliminary work, which needs to be followed up. It may be that the improved delivery system, using the microneedle patches, will finally allow cell-based therapy based on secretion of factors to become effective.


News stories:
* Cardiac cells integrated into microneedle patches to treat heart attack. (EurekAlert!, November 28, 2018.)
* Microneedle patch heals heart attack damage. (H Siaw, Physics World, December 19, 2018.) It's interesting that this physics-oriented source picked up this article.

The article, which is freely available: Cardiac cell-integrated microneedle patch for treating myocardial infarction. (J Tang et al, Science Advances 4:eaat9365, November 28, 2018.)

More on microneedles:
* Treating obesity: A microneedle patch to induce local fat browning (January 5, 2018).
* Clinical trial of self-administered patch for flu immunization (July 31, 2017).
* A smart insulin patch that rapidly responds to glucose level (October 26, 2015).

Previous post about dealing with heart problems: Pig hearts can sustain life in baboons for six months (January 7, 2019). Just a little below.

Another post about a patch for the heart: Fixing the heart with some glue and light (July 27, 2014).



January 9, 2019


Briefly noted...

January 9, 2019


Pancreas cell size and lifespan. Scientists observed that in mice the pancreas grew primarily because the cells got larger. In contrast, in humans the increase in pancreas size is primarily due to an increase in cell number. This contrast led them to look further -- at 24 mammalian species. There was a correlation: animals with large pancreas cells had shorter lifespan. Interesting.
* News story: Pancreatic cell size linked to mammalian lifespan, finds zoo animal analysis. (EurekAlert!, June 18, 2018.) Links to the article.



Pig hearts can sustain life in baboons for six months

January 7, 2019

A new article reports progress in heart transplantation from pig to primate.

The following figure summarizes the results -- and shows the hearts...

Part a (top) shows survival curves for three groups of baboons that received heart transplants from pigs.

Quick inspection shows that the results got better and better going from group I to II to III. This was, it seems, due to improved procedures. We'll comment on the procedural development later.


The survival curve for group III is a little more complex than it may seem. There are three "tic" marks on the curve: one at about 100 days, and two near the end. Those marks indicate that animals that appeared to be healthy were removed and euthanized for testing. Two animals were removed at the time of the first tic mark (three months). That was the originally-planned end of the experiment, but two animals were maintained for another three months. Those final two animals, still apparently healthy, were euthanized at 182 and 195 days. That is, it is true that only one animal in this group of five died for health-related reasons. But it is not true that 80% survived to the end.

Part e (bottom) gives an example of a donor pig heart (left) and a normal baboon heart (right). There is no scale bar, but other parts of the full Figure include a ruler. The heart sizes here are presumably a few inches.

For part a, each group contained 4-5 animals.

   This is part of Figure 1 from the article.


A reasonable view is that the survival in groups I and II was "poor", but that the survival in group III was "very encouraging." All recipients in the first two groups died with health problems within two months; that is consistent with earlier work. Most of the recipients in group III survived in good health until they were sacrificed for testing, at 3-6 months.

What did the scientists do differently that allowed the group III animals to do so much better? The changes were in two main areas:
- They used an improved procedure for maintaining the organs while they were out of an animal. Traditional procedure is simply to keep the organs ice-cold. However, the use of more biological conditions, including oxygenation, improves survival.
- Steps were taken to keep the pig heart from growing to its normal full size in the baboon recipient, which is somewhat smaller. This size-match issue is less important for pig-to-human transplants, but still needs to be considered. Controlling organ growth also interacts with immunosuppression procedures.

The details are fairly technical; we'll skip them here. What's important is that the scientists think they understand why the procedural changes led to better survival.


This work, in a primate model, showed survival, in good health, of most recipients of a pig heart for as long as they were followed, up to six months. Work will continue. How close are they to doing such a test with a human recipient? What criteria must be met before one would try such a transplantation with a human recipient? The success of the current work suggests that it is time to address those questions seriously.


News stories:
* Progress made in transplanting pig hearts into baboons. (B Yirka, Medical Xpress, December 6, 2018.)
* Pig Hearts Provide Long-Term Cardiac Function in Baboons. (R Williams, The Scientist, December 5, 2018.)
* Expert reaction to study looking at long-term function of genetically modified pig hearts transplanted into baboons. (Science Media Centre, December 6, 2018.) Several comments from experts in the field.

* News story accompanying the article: Medical research: Success for cross-species heart transplants. (C Knosalla, Nature 564:352, December 20, 2018.)
* The article: Consistent success in life-supporting porcine cardiac xenotransplantation. (M Längin et al, Nature 564:430, December 20, 2018.)

A post about earlier work on pig hearts in baboons: Long term survival of a pig heart in a baboon (April 30, 2016). In this earlier work, the baboons kept their own heart. In the new work, the pig heart replaced the baboon heart.

Also see:
* Added January 11, 2019. Treating a heart attack using a microneedle patch (January 11, 2019).
* Laika, the first de-PERVed pig (October 22, 2017). Another development toward making pig donors better: the removal of their endogenous retroviruses. This feature was not included in the current work.
* Organ transplantation: from pig to human -- a status report (November 23, 2015). Perspective.

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



Games genes play -- Alzheimer genes, in your brain

January 4, 2019

Genes are regions of DNA that code for protein. The genes are transcribed (copied) into messenger RNA (mRNA), which is then used to dictate protein production. The genes themselves remain in the DNA, unchanged. So we are told.

A recent article extends a story that has been developing... Some people with Alzheimer's disease (AD) have extra copies of a key AD gene in their brain cells. Further, those copies carry diverse mutations; some of the mutations are of a type likely to enhance the disease.

It's a startling claim -- one that could turn out to be important.

There are many questions...
- What's the evidence?
- How does it happen?
- Why does it happen?
- Does it matter?
- What might we do about it?


What's the evidence?

Here is one type of evidence: direct visualization of the mutant genes...

Part j (left) shows pictures of brain cell nuclei that have been stained for a particular type of mutant AD gene. Specifically, the nuclei were stained with a DNA probe -- a small piece of DNA -- that can bind only if two parts of the gene, not normally together, are now together: exons 16 and 17. (In the normal gene, there is an intron between them.)

The reddish specks show places where the probe bound. The top frame of part j shows many such specks. In the bottom frame, the specks are (largely) gone. Why? The sample was treated to destroy any such DNA, using a restriction enzyme (RE). (The top and bottom parts are labeled ‑RE and +RE. Remember, ‑RE is "normal" here; the test for the mutant gene. Adding the restriction enzyme, the +RE condition, is intended to destroy the mutant gene, and eliminate the signal. It's one type of control, to see if the probe is binding to what we intend.)

Part k is a quantitation of those results, showing the number of specks seen in each case. The result for ‑RE is set to 1; you can see that the number is greatly reduced by the +RE treatment.

The next two parts (l and m) show the results of another such test. Same AD gene, different mutation. In this case, exons 3 and 16 are directly together. The observations are about the same as for the first mutation.

Part n (right side) is a control to see whether the probe results found in the earlier parts are associated with normal genes. That is, is the mutation part of an otherwise normal gene (a gene with some normal features, as well as the mutation) -- or distinct from it? Two probes were used together. The red probe is for a feature of a normal gene (the boundary between intron 2 and exon 3). The green probe is for one of the two mutations tested earlier. It's hard to see the actual specks, but hopefully the red and green arrows are shown fairly. You can see that the two types of probe light up at quite different places in the nuclei. This control suggests that the probes for mutant genes are lighting up distinct structures -- different copies of the gene; extra copies.

DISH (in the figure headings)? That's DNA in situ hybridization.

   This is part of Figure 2 from the article. The scale bars are 10 µm.


That is some of the evidence for the presence of mutant forms of the AD gene. The probing in parts j and l provides evidence for gene copies that have two exons joined together. The probing in part n suggests that these are from extra copies of the gene.

If you have reservations about the conclusions above, that's fine. The claims are indeed quite extraordinary, and require extraordinary evidence. What's shown above are pieces of the evidence. The controls, too, are only small pieces of the story. I hope you can see the logic: how the evidence is consistent with the claims. But accepting the claims requires far more. Indeed, the article provides much more, as do the earlier articles it builds on.

Overall, the case is getting strong: people have extra copies of an AD gene in their neurons, and those extra copies carry diverse mutations.

One further important result... These mutant genes are more prevalent in brain samples from people with AD than from AD-free controls of similar age. That is, there is some connection between the presence of extra and mutated AD genes and the AD disease. However, there is no actual evidence what that connection is. In particular, there is no evidence at this point that what is found here is causal to the disease.

No evidence. But if you are suspicious or at least wondering, you are not alone.


How does it happen?

In general terms, it is fairly clear what the process is. The new gene versions lack introns. This suggests that the genes have gone through a stage of being like messenger RNA. The mRNA copy of the original gene is then reverse-transcribed back into DNA and recombined into the genome; somewhere along the line in that process mutations -- major ones -- get introduced.

Reverse-transcribed? That's what happens with retroviruses. In fact, the reverse transcriptase (RT) enzyme that makes the new gene copies reported here almost certainly comes from one of the retroviruses that is part of the human genome.


Why does it happen?

The short answer is that we don't know.

There are at least two specifics issues here. One is why RT is present in neurons; the other is why the AD gene is particularly subject to the process of expansion-with-mutation. We don't really have much to say about either part.


Does it matter?

Ultimately, this is the key question. How is this newly-recognized process relevant to the disease process? In particular, is it a cause of AD? One can easily imagine how it could be. Importantly, at this point there is no information. A new phenomenon has been discovered. It involves an AD gene, but we do not have any evidence that the new process actually matters. There is no evidence it doesn't matter. It's just that, for now, we don't know.


What might we do about it?

Studying AD is not easy. It is a disease that develops slowly, perhaps over decades. It is likely that considerable disease development has occurred before symptoms are evident, thus complicating intervening early in the disease -- or even observing the early stages. No animal model is accepted as definitive.

So, how do we proceed here, testing a new idea about the development of AD? The good news is that the nature of the process suggests a treatment.

The proposed process has a key role for the enzyme RT. Hey, we have drugs that inhibit that enzyme -- drugs that have been tested and approved for use on humans (in particular, for the treatment of HIV). Is it possible that RT inhibitors would be effective in preventing (or slowing) AD?

The article includes some use of an RT inhibitor, in cell culture experiments. It does reduce the accumulation of defective copies of the AD gene in such experiments. The authors also note that AD is uncommon in those who have received RT inhibitors for long periods.

I suspect that AD and retrovirus experts are considering how to test an RT inhibitor for its effect on AD in humans.


In any case, it is a fascinating story -- and one that might be important. It is a story of how the retroviral debris in our genome is really doing something -- very likely not for the better. But we also must wonder what if any role there is for the lower level of such activity in healthy people. Is this an aspect of normal brain function, maybe even good?


News stories:
* HIV drugs may help Alzheimer's, says study proposing an undiscovered root cause. (B J Fikes, Medical Xpress, November 23, 2018.)
* Could Rogue APP Variants Invade Genome of Individual Neurons? (ALZFORUM, November 21, 2018.)

* News story accompanying the article: Alzheimer's disease: A mosaic mutation mechanism in the brain. (G Chai & J G Gleeson, Nature 563:631, November 29, 2018.) Excellent.
* The article: Somatic APP gene recombination in Alzheimer's disease and normal neurons. (M-H Lee et al, Nature 563:639, November 29, 2018.)

Previous post about AD: Alzheimer's disease: What is the role of ApoE? (November 6, 2017).

Previous post about endogenous retroviruses: A connection: an endogenous retrovirus in the human genome and drug addiction? (October 29, 2018). Links to more. Note that the current story and this earlier story about possible effects of our endogenous retroviruses are very different. In the current case with AD, the suggestion is that a gene product from the retrovirus, the RT, is relevant. In the previous case, it was the presence of a viral sequence within a gene that seems relevant.

My page for Biotechnology in the News (BITN) -- Other topics includes a section on Alzheimer's disease. It includes a list of related Musings posts.



Why did many bees in the United States stop buzzing mid-day on August 21, 2017

January 2, 2019

The Moon did it.

Seriously. Bees fly in daylight. And on August 21, 2017, the Moon blocked the Sun's light from reaching the surface during part of the day. A swath of the Untied States was in total darkness for a few minutes during this solar eclipse. Scientists took advantage of the opportunity to see what the bees did. They stopped flying.

To be more precise, what the scientists measured was that the bees stopped buzzing. That's ok... most bee buzzing is due to wing motion during flying. And it is easier to measure buzzing than flying (especially when it is dark). The scientists had prepared for the event by installing microphones -- near flowers -- along the eclipse path.

From page 22... "Microphones were protected with wind screens (Movo WS10n Universal Furry Outdoor Microphone Windscreen Muffs; Los Angeles, CA)... "

The following graph summarizes the key results...

The graph shows how many buzzes were recorded (per minute) during three time periods: before, during, and after total darkness.

The pattern is clear: buzzing -- and hence flying -- pretty much stopped during the period of totality.

The graph shows some statistics -- and they are not properly done. The y-axis is a bounded measure: the lowest possible value is zero. However, the statistical analysis failed to deal with this properly. Visual inspection suggests that the conclusion from the data is fine. However, this should also be a little lesson in statistics. Not good.

   This is Figure 2 from the article.


The result is not a surprise. But it is good to see that someone has tested a prediction with quantitative data.

The article is of special interest because it involved a team of about 400 people, including elementary school teachers and their students. It is a nice example of "citizen science", including outreach to local schools. (It would have been better if the adult academics had provided proper data analysis in the formal presentation.)


News story: Bees Stopped Buzzing During the 2017 Total Solar Eclipse. (Entomology Today (Entomological Society of America), October 10, 2018.) Includes a field photograph that shows the microphone -- with its furry wind screen. It also includes some artwork drawn by a fifth-grader; there is more in the article itself.

The article: Pollination on the Dark Side: Acoustic Monitoring Reveals Impacts of a Total Solar Eclipse on Flight Behavior and Activity Schedule of Foraging Bees. (C Galen et al, Annals of the Entomological Society of America 112:20, January 2019.)

More about this eclipse: Solar energy: What if the Moon got in the way? (August 16, 2017).

Among recent posts on bees:
* Glyphosate and the gut microbiome of bees (October 16, 2018).
* The advantage of living in the city (July 27, 2018).

More citizen science: Finding Planet 9: You can help (March 13, 2017). Links to more.



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