text:
CO2 availability to phytoplankton in oceans and climate change impacts
I learned through research that increasing levels of atmospheric CO2 was increasing the acidity level of ocean waters. I then was looking into how this was affecting the phytoplankton and read that warmer water was actually decreasing the amount of CO2 in the water for the phytoplankton to use.
I am now confused as to why many sources claim that greater atmospheric CO2 is making ocean waters more acidic but at the same time CO2 is decreasing in availability to phytoplankton. How does all of this relate to climate change? Would you be able to explain to me what is happening or direct me to sources that explain it?

One of my students in my Environmental Science class asked me this question, and it seemed very much worthwhile to post the Q&A to Bio.SE!  [Note: the student never got back to me with her sources of information, so unfortunately I cannot include them here].

Is all the ocean water becoming more acidic or is it only in certain areas and how are those areas moved by currents? Same question as regards temperature. The use of averages often hides important detail...

@SolarMike yup, of course there must be huge variability in both space and time. However, the student originally asked the question in a broad, global perspective (as do many individuals when asking about global change), and so I have copied their question and responded to it from this fairly global viewpoint. Notice in my answer that I hint toward more localized impacts, but I did not go into much detail given the already global scope of my biogeochemical answer (and its formidable length!!)

https://earthscience.stackexchange.com/search?tab=relevance&q=acidification

 Short Answer
I do not believe that CO2 will become less available to phytoplankton on a global scale in the foreseeable future. Instead, I believe that rates of increasing concentrations of CO2 (and resulting chemical products) will not remain sustained at their current levels.
There are two global change phenomenon occurring that are relevant:

increasing concentrations of atmospheric CO2 and
increasing global temperature.

As CO2 concentration increases in the atmosphere, diffusion will lead to higher concentrations in ocean waters as well. The rate of diffusion is related to the relative concentrations of CO2 in both air and water.
Increasing temperatures can impact this diffusion rate as well in two ways:

Increased atmospheric temperatures result in higher surface water temperatures, which leads to less mixing of water (i.e., ocean stratification). This functionally reduces the volume into which CO2 can diffuse and therefore will slow the diffusion rate. (but not decrease the amount of dissolved CO2).

Increased temperatures often decrease solubility of gasses in water, and this decreased solubility may result in offgassing of CO2. However, decreased mixing of strata may result in less upwelling and therefore less offgassing.

As long as global ocean temperatures don't get too warm and atmospheric CO2 doesn't get too low, it seems that the above will result in a net global slowing down of CO2 absorption into oceans but not a reversal (i.e., loss of CO2). In other words, I do not believe absolute CO2 availability to phytoplankton will decrease, but that only the rate of further increased availability will decrease.

Though perhaps such decreases could be experienced as local phenomena?

 Long Answer
It's not immediately clear to me what you're referring to. I'll try to react with some things that come to mind. My response is mostly biogeochemical in nature, so I invite others to address this physiologically if appropriate.
Are you sure you didn't misread something and it's really the declining CO32- that you read about?  (see here). Assuming that's not the case, read on...
Raising Temperatures may decrease the absorption rate of CO2
Alternately, maybe you read that as oceans warm, the water can absorb less CO2 (as in the rate of absorption will decline).
This is due to warm water not mixing as well with cooler lower water, so you end up with unmixing layers (called stratification). Eventually, the surface layer saturates with CO2 and can't absorb more from the atmosphere. It's not that this top layer of water has less CO2, but rather that it gets so saturated that it can't absorb any more (causing the rate of absorption to decline).

Under less warm conditions, the "layers" of water aren't so different in temperature, and so more mixing of layers can happen. As a result, all that CO2 that is being absorbed at the surface level can be exchanged to lower layers of water where it will be stored longer. In other words, with cooler surface temperatures (and therefore greater mixing of layers), the volume of water that can hold CO2 is no longer just the surface, but a much "thicker" layer of water. Result: more CO2 absorbed.

So... raising temps can cause less mixing of water due to more stratification (layering), which results in less water in the ocean available to absorb and hold the CO2. This means that as atmospheric CO2 continues to increase, the non-mixing surface layer of ocean water (which will become saturated with CO2 at some point) won't be able to keep up with more and more and more CO2 in the air. As a result, the ocean will decline (and eventually potentially fail) in its ability  to "buffer" the ever increasing CO2 in the air. This would mean that the rate of CO2 in the air will start increasing more rapidly (since less and less of it is being absorbed by the oceans).
As for the phytoplankton (which are in this top layer of water), this stratification will not directly result in less CO2 availability to them. As atmospheric CO2 increases, so will the amount in this top layer of water. The rate of increase in CO2 concentration will just slow until a saturation point is reached, but absolute levels will not decline.

Though, note, however, that phytoplankton tend to thrive in areas of high nutrients (i.e., upwelling zones). Less mixing of waters will decrease the upwelling of nutrient-rich, cooler subsurface water. So less mixing (i.e., more stratification) likely would lead to declines in phytoplankton abundance due to decreased nutrients availability. (See here). Perhaps this decreased nutrient availability (which would include loss of carbon sources) is related to what you're referring to?

Read here for some more thoughts: https://earthobservatory.nasa.gov/features/OceanCarbon
Raising Temperatures may decrease CO2 solubility
However, given all this, the solubility of CO2 in water does decline with increasing temperature (see here for raw data). This suggests that some rise in global temps may impact CO2 concentration in ocean waters.

The cause for this decreased solubility with increased temperature is due to the imbalance of an equilibrium state of free energy required for dissolving/off-gassing gasses in/out of water. Since the dissolution of CO2 into water is an exothermic reaction (i.e., one that releases heat), any addition of heat will lead to a greater favoring of the opposite endothermic reaction (release of dissolved gasses in this case). In more chemical terms, added heat to the solution provides energy to overcome attractive forces between the CO2 and the solvent (i.e., water) molecules. The result is decreased solubility. See here and here for further explanation.
(The partial pressure of gasses are also impacted with increased temperatures, so investigating Henry's Law might also be pertinent to your research. (This link I found quickly explains a bit of the phys/chem).)

However, to further complicate all of this, not all of the CO2 absorbed by ocean water remains as carbon dioxide. Much of it undergoes reactions to become carbonic acid, carbonate, etc. (see here). This means that the equilibrium state is more complex to model or understand vs simply examining these effects on CO2 in water in a controlled lab setting.

This solubility fact, in combination with the mixing of layers above, are why polar waters tend to absorb more CO2 and equatorial waters tend to give off more CO2.
From http://www.carboeurope.org/education/CS_Materials/CO2solubility.pdf:

In the world oceans, the northern Atlantic and the southern Oceans act as major sinks of CO2 because they are colder. Adding to this, cold water is denser than warm water, causing it to sink. The carbon dioxide taken up in the surface can be effectively transported to the deeper waters by convection hence the CO2 is stored in the bottom layers of the ocean.

On the other hand, warm equatorial waters tend to release CO2 into the atmosphere. In these regions upwelling of CO2-rich deep waters occurs. When the water reaches the surface, it is warmed decreasing gas solubility leading to the degassing of CO2 .

However, note that if there is greater stratification of water (i.e., less mixing) as described above, such upwelling could actually decline. This would result in trapping more CO2 in cooler waters instead of warming those waters as they rise to the surface and offgassing that CO2 back into the atmosphere. (We won't even begin to discuss how ocean currents in general will be impacted by changes in temperature...).

To add even more complication, as waters warm, ice will melt leading to (at least temporary) increased mixing of ocean waters!! (see here). If temperature decline from ice melt is great enough to combat the increased surface temperature, then perhaps for some period greater mixing and offgassing could occur.

End results
What does this all mean for climate change?
Well, as atmospheric CO2 increases, it's going to make the oceans more acidic (due to carbonic acid). In other words, if we kept temperature constant, more atmospheric CO2 means more ocean CO2. (You can see that from my previous two links -- again, here (showing ocean CO2 concentration on Y axis) and here).
However, as the earth warms up, water temps will warm up. This means less mixing and therefore less net CO2 absorption. It also means that the warmest surface waters will not hold as much CO2 due to its reduced solubility, which will result in greater "off gassing" of some CO2. The combination of these two things means essentially that the rate of CO2 increase in the atmosphere will likely accelerate.
But what is the net impact on oceans? (and therefore on plankton)
Well, in regards to the oceans themselves, there is probably some calculable "tipping point"  in which the higher concentration of CO2 in the atmosphere (and therefore greater diffusion pressure) doesn't outweigh the reduced solubility of CO2 (due to higher temps and less mixing). At whatever temperature that tipping point occurs, then I assume that the CO2 in the oceans can/will decline instead of increase. In reality, though, gasses are constantly moving back and forth between atmosphere and ocean, so it's unlikely the ocean water will get so warm that there is a net movement out of the water, but probably just a decrease in the rate of further absorption.
On a more local level, if the phytoplankton are living in an especially warm region of ocean, it is possible that off-gassing of CO2 increases in those regions due to the decreased solubility as described before. However, again, if the concentration of CO2 in the atmosphere and the temperature of the atmosphere both keep increasing, then these effects would (at least partially) negate the increased offgassing from reduced CO2 solubility. Again, modelling when this would occur is much too complicated for me to figure out for this post, but I'm sure we have experts working on calculating this "tipping point" as we speak.

Again, the bigger issue for the phytoplankton is probably the reduced upwelling of nutrient-rich water due to greater climate-mediated stratification of the ocean column.

Final Thoughts
Given all of this explanation, ice-core research by Pedro, Rasmussen and van Ommen (2012)  (summarized here) suggests that after only a few hundred years of warming, CO2 concentrations seem to decline in ice cores. This may suggest that perhaps a net release of CO2 is possible within a hundred years or so. Again, this "tipping point" is likely calculable, but it's too complicated for me to figure out for a stackexchange post ;p.
Further readings:
Basu, S. and Mackey, K.R., 2018. Phytoplankton as key mediators of the biological carbon pump: Their responses to a changing climate. Sustainability, 10(3), p.869.
Hülse et al. (2017) Understanding the causes and consequences of past marine carbon cycling variability through models. Earth-science reviews, 171, pp.349-382.


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Could someone help me identify this insect?
Does anyone know what this insect is? I put a rubber ball on my lawn, and within seconds a bunch of these insects (maybe 15 or 20) landed on it. I took a look around and saw that there were lots of them flying low near the grass or sitting on the grass (they were not as obvious on the lawn as on an orange ball :).
Location: Massachusetts (USA).

Could you provide an estimated size of your specimen?

Looks like a Bibio, sometimes referred to as "March flies" and one species in particular known as "St Mark's Fly". Yours seems unlikely to be that one because it is found in England and it seems like nowhere else.
Most likely I think yours is a Bibio vestitus from the picture below (unfortunately I wasn't able to find multiple sources corroborating this, though, so take it with some caution), and although I had trouble finding definitive distribution data, it looks like the one in your picture has the copper-colored legs, and in addition the first image below claims to be from Massachusetts. There are many many species of Bibio though so I can't be certain of species.

Bibio vestitus
Reference

This is certainly some species of fly (order Diptera) and appears to be a species of march fly (Bibionidae)

 Bibio anglicus
Bibionidae (march flies) characteristics [Source]:

Dark colored
Eyes usually meet along the top of the head
Front legs often have strong spines on the tibia
Often with dark spots or “stigma” on the wings.
Wing patterns (from Wikipedia):

The wings have two basal cells (posterior basal wing cell and basal wing cell), but are without a discoidal wing cell. R4+5 is simple or branched; at most, only three branches of R developed. The leading edge wing veins are stronger than the weak veins of the trailing edge.

The march flies are known to hover close to the ground like you saw [Source].
Although IDing to species is difficult with the low quality of the photo, I would think that Hardy et al 1958 would be a good start for you to use:

Hardy, D.E. et al., 1958. Guide of the insects of Connecticut PartVI. The Diptera or true flies of Connecticut Sixth Fascicle: March flies and gall midges. Bibionidae, Itonididae (Cecidomiidae). Conn. Geol. Nat. Hist. Surv. Bull. 87, 218 pp., 15 pl., 29 figs.

Your specimen is likely in the genus Bibio (march flies or St. Mark's flies).
You can tell it's not a robber fly (family Asilidae) because the eyes of your specimen come together at the top of the head (like most march fly species [Source]), while according to here

All robber flies have a characteristic divot on top of the head, which is located between their especially prominent compound eyes.

source: Stack Exchange

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Name and Behaviour of Arthropods near a Cactus
Background Story
I have a small, old cactus on my sunny, south-facing window sill in southern Germany. Since a few years, small black dots gathered around its pot. At first, I thought the dots were dust or sand and wiped them away. But the dots appeared again and again, so I had a closer look at them and saw that they were tiny insects or arachnids, probably lice or mites. We just call them arthropods from now on.
More information
The following picture shows my cactus with some of the arthropods around the pot. Click here for higher resolution.

Here are some close-ups.

The arthropods seem rather dead. They do not move and most of them lie on their back. However, they are not dead. Once they are picked up and set on a paper towel they start to move. If they get on their legs (with a little help) they walk around, which can also been observed by the naked eye.
I inspected some individuals using a detached camera objective as a magnifying glass. The arthropods are brown, shiny, somewhat translucent, and have 8 legs. I could recognize a small head without a neck (like most bugs have) but couldn't recognize a mouth or eyes – probably because of the size.
I couldn't take a picture, but tried to draw what I saw:

Later I got hold of a cheap microscope and took a few videos. The video quality is miserable. In reality, the arthropods are not that dark, see my drawing and the photographs.
Here's on individual laying on its back, flipping over, and walking away.

Here's another individual walking.

The Strange Part
As said, the arthropods keep on re-appearing around the plant pot. But in all those years, I never saw any of them on the pot, inside the pot, or on the cactus. I also have other cacti right next to the "infected" cactus, but their pots were never surrounded by the arthropods.

Question
What are these arthropods, where do they live, and why do they leave their habitat?
My Theory
I suspect the arthropods to live inside the dead and cracked part of the cactus. They could walk on the spikes of the cactus and jump from the ends of the spikes to the ground. If they land on their backs, they cannot get up and stop moving after some time.
I don't think that the arthropods live inside the soil. Two reasons for that:

The arthropods could have drowned often. From time to time I put too much water in the pot, such that all soil is fully covered by water, often for more than 8 hours (yes I know that can't be good for a cactus *cough*).
In order to get to the window sill, the arthropods would have to walk quite a while. Over time, I should have seen at least some of the arthropods on their way to the outside world.

There are some kind of ticks according to 8 legs and lack of segmentation.  And they can live in the soil despite the drowning and damage the cactus roots.

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Size of the glycan chain in a glycosylated protein
I would like to know where I can find the (experimental/estimated) distribution of glycan sizes attached to proteins.

Uniprot includes glycosylation info if known...

@MattDMo I was expecting something more "digested". Anyway, thank you I will check uniprot.


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Why do I see different hues of colors between each of my eyes?
Frequently, I see colors with a slightly different hue when looking through my eyes individually. The right eye is more red-tinted ('warmer' hued) and the left is typically more blue-tinted ('cooler' hued). However, sometimes I can't notice any difference in hue between the eyes (even when closing the other) and on a very rare occasion the warm/cool differentiation is switched (left is warm hued, right is cool hued). Numerous others have confirmed they've experienced similar patterns.
My questions:

What causes this differentiation between eyes?
What would cause the hues from being sometimes clearly noticeable and other times non-existent? Is the cause potentially environmental, behavioral, physiological, chemical, etc?
I wonder if this is occurring at the eyeball level (e.g., cone physiology) or somewhere in my brain (e.g., PVC in the occipital lobe)?

Red + Blue is what gives me 3D vision!! :p

If I had to guess, I would say maybe it's related to cone fatigue/neural adaptation, with each eye experiencing slightly different stimuli and ending up with different temporary adaptations.

@CactusWoman seems like a fair guess,  but I've never heard of this effect influencing perception of color hues. Further, the difference in hue perception can last for hours, even under changing visual stimuli

This is an interesting phenomenon which I have been aware of for several years, but I haven't yet come across any official description of it or explanation for it.
Nonetheless, the phenomenon is easy to explain. It is a result of light adaptation in your retina responding to different levels of light being received by each eye.
Background
The level of ambient light present over the course of the day varies by as much as 10 orders of magnitude, and our visual systems have evolved to account for this. The human retina and later visual processing centers have a number of ways to adapt to the light level present in the environment. They are constantly doing this, but these adaptation mechanisms take a little bit of time to adjust to a different light level, usually on the order of fifteen seconds to a few minutes. This is why when you step out of a dark room into the sunshine, you are momentarily blinded by the (relatively) bright light.
Some of these adaptation mechanisms are color-specific, such as those that occur in the cone cells themselves.
Explanation
TL;DR-ers, just read this section
Most of the time, both of your eyes experience roughly the same levels of light intensity, both in general and for each color of light. But this is not always the case.
If you have one eye covered for a period of time, such as when you've been laying down, then your two eyes will be adapted to two different sources of light. If you then uncover that eye, then for a short period of time that eye will perceive the world to be brighter than the other eye. If the light level present in the environment has a tint to it as well, then the just-uncovered eye will perceive that tint more strongly than the other eye.

DIY Science Time
You can verify this yourself, like I have been doing over the past hour, with nothing more than a makeshift eyepatch and nothing better to do.

First, check your initial state by closing one eye and then the other and switching back and forth rapidly while looking at something white. If you've been awake and active, the images from each eye should appear to have roughly the same hue and intensity.
Cover one eye completely (without pressing on it) for a period of about five minutes, while leaving the other eye open.
Then, remove the eyepatch and alternate closing each of your eyes again.

If my hypothesis and explanation is correct, the previously-covered eye should see the world as slightly brighter and more strongly tinted than the uncovered eye does (the hue of this tint should depend on your light source).
If you guys actually do this, you should report your results in the comments, especially if your results demonstrate a flaw with my hypothesis. Let's do some science, people.

I appreciate the effort you put into writing your answer and the enthusiasm you have for running your experiment, but I'm ultimately looking for existing evidence cited from one or more reputable sources. If you have any such source(s), please add them . Thanks! :)

Your crystalline lenses are different colors.  You are developing cataracts.
I have noticed this too.  I assumed it was early cataract in the yellow eye and this is the opportunity to do the back reading.  A cataract is the lens of the eye which has yellowed and to some degree opacified with age.
from http://vsri.ucdavis.edu/research/psychophysics

Changes occur slowly and so unless you compare one side to the other you don't perceive everything is getting yellower.  But after cataract surgery everything is much bluer.  The squares in the image below show regular white light and then how yellow it appears through a cataract.  Same source.

I assume your red tinted eye is the cataract eye.  But do not be worried.  Cataract surgery is not a big deal.
I do not have an explanation for the switching back and forth / normalization.

Thanks for the interesting post. However, I would think cataracts is certainly not the culprit in this case given the switching back and forth.

@theforestecologist I wouldn't be so quick to dismiss this. The key finding here is the fact of a difference. The subjective experience of an occasional switch in hue could certainly occur at the cortical level. Cataracts are extremely common.

While cataracts is a possible explanation, the much more likely explanation is this answer about light adaptation.
There's a significant amount of literature about perceptional hue shifts with varying adaptation to brightness. While these experiments were not done with monocular variants, it's reasonable to believe that the effects measured can affect eyes individually.
Stabell et al. 2003 describes the effects of light and dark adaptation of rods on specific hue thresholds:

Specific-hue threshold as a function of absolute rod threshold was measured with long-, middle-, and short-wavelength monochromatic test lights presented 17 deg extrafoveally. The measurements were obtained both during the rod phase of long-term dark adaptation and under conditions where the rod receptor system was gradually light adapted from a dark-adapted state by a scotopic background field of increasing retinal illumination. The results show that change in specific-hue threshold with change in absolute rod threshold is not, in general, identical for light and dark adaptation of the rod receptor system.

Ambler 1974 also describes a similar effect linked to brightness adaptation:

Rod interference is a possible factor contributing to the elevation of chromatic threshold in peripheral vision. It was found that light adaptation lowered peripheral chromatic thresholds. This result was interpreted as being due to the lowering of rod sensitivity. It was also found that light in the photochromatic interval appeared blue, indicating that rods may add a blue component to peripheral color vision.

Additionally, the Purkinje effect can also contribute to shifts in the hues observed when the eyes are differentially adapted to brightness. This effect has also been shown in Wolfe et al. 2015 to affect monocular vision, further supporting the hypothesis that perceptional hue shifts can be caused by light adaptation.

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Pink growth (aka pink slime) in bathtub or shower
I was wondering if anybody had studied or was knowledgeable about the pink growth that people often find around water fixtures in their homes, especially bath tubs and showers?
My understanding is that this pink growth is actually a bacteria and not a fungus as many assume (source1,source2). Supposedly, the bacteria, Serratia marcescens is airborne and thrives in areas of retained moisture and fatty residue.
My main questions are:

How ubiquitous is this bacteria? What is the bacteria's geographical range of occurrence?

For example, is this species more prevalent in more humid environments?

Are there other species of Serratia that can create similar pink biofilms in tubs? (Are the sources of "pink" separated by geographic location?)

Is S. marcescens even forming a biofilm in these pink stains??

What likely introduces S. marcescens into a bathroom?

I ask, because I've seen this bacteria both present or absent from similarly clean or dirty bathrooms, and thus far have not really seen any consistent patterns in the bacteria's spatial occurrence.
Any other interesting facts or sources on S. marcescens would be great!

I think that it may be well be inorganic calcium-deposits, or other salts. Tap water is often rich in calcium-salts and the reddish color I've seen pretty often down under too. I don't know where you are located, but in Oz there's a lot of iron in the ground, perhaps explaining the reddish hue. All guesses though.

Is the film slimy ? Try checking with a swab

@WYSIWYG Sometimes but not always. I don't have this in my own home, so I don't get to check too often...

Also @Christiaan: the deposits I'm talking about are  more pink and therefore indicative of S. marcescens. Iron deposits would be more dark reddish (or reddish yellow if also associated with heightened aluminum). Calcium deposits would typically be white.

I live in St. Louis, MO and get this in my bathtub over time, but not in my other sinks. I actually think @Christiaan is correct here, but with a few additional observations:

I don't think it's bacteria. When dry, it's not slimy, nor does it grow back quickly when wiped away. It feels much more like a mineral deposit.
It was no longer pink when using a different shampoo. Upon returning to an older brand, the color returned to pink.
It's only directly around the drain, it isn't on the walls or anywhere else.

These lead me to think it's a mix of mineral deposits from the hard water and potential reactions with certain soaps/shampoos, at least in my case. These are only based on my own observations though, there very well could be a pink bacteria/fungi that tends to inhabit damp areas.

No it's definitely bacteria. They like to grow wherever water pools with organic matter or certain  soap deposits. You typically have water around your drain long enough for the chlorine or other treatment chemicals to evaporate off to allow the bacteria to live. Coming or going with different soaps just means that one of the soaps had more of the ingredients (fats and /or phosphorous) they prefer

Well, I guess at least you know that geographically it's present in the midwest as well. For what it's worth, I also live in a basement apartment, so it's likely more humid than most.

It could be Haloarchaea

so @theforestecologist not Bacteria but Archaea!

https://en.wikipedia.org/wiki/Haloarchaea

Thanks for the post, but this is very unlikely since salt water is not used in plumbing. Your proposed organism is halophilic, meaning it likes to live in salty conditions!


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Is Zika suspected of causing birth defects only if contracted during pregnancy?
There seems to be growing evidence that a recently spreading strain of Zika virus is in fact linked to microencephaly and other birth defects in newborns (see here, here, and here for examples).
I understand that this is currently an active area of research and a number of questions remain unanswered. However, even given the current uncertainties, I feel any discussion about when a mother gets infected has been largely ignored by all of the news/media/science outlets I've seen.
My question is: does the virus lead to birth defects only if the mother gets infected during pregnancy, or can a previous (or latent) infection lead to similar birth defects? If the former, does timing of infection during different trimesters matter?

sources suggesting support for either case would be nice, too, in the absence of yet published rigorous support...

Related http://biology.stackexchange.com/questions/43050/how-long-do-viruses-such-as-zika-stay-in-the-body

As you mentioned, there is evidence that mother-child transmission of Zika virus causes congenital anomalies like microencephaly.
Now your question, if a cleared infection before the pregnancy could affect it? In principle, no. Once the virus is cleared, it should not reactivate, unless there is reinfection. Here's a quote from the Zika article from Uptodate.com:

Women of childbearing potential — It is uncertain how long women of childbearing potential should wait between Zika virus exposure/infection and conception. Most pregnant women with Zika virus exposure give birth to normal infants [111]. Zika virus usually remains in the blood of an infected person for a few days to a week, and thus far there is no evidence that a fetus conceived after the virus has cleared from the blood would be at risk for Zika infection [94,112]. However, information regarding the persistence of Zika virus following infection is not known. It has been suggested that infection due to other flaviviruses such as West Nile virus may persist years after initial infection [113-115]; these data are controversial. Pending further study, healthcare providers should encourage women to make such decisions based on their individual circumstances, values, and preferences.
Daniel J Sexton, MD
  Editor-in-Chief — Infectious Diseases Section
  Editor — Bacterial Infections
  Professor of Medicine
  Duke University Medical Center

Citing whole sections is discouraged.

@Christiaan Except all of it is relevant, and answers directly the question

There are citations to unmentioned sources and its better to synthesize an answer rather than reproducing it. The info is good,  it's just the way it's presented.

Could you also provide a link to the article and expand on points it makes

@rg255 I would like to, but the article is not accessible for free, I can only access it because of my University affiliation. But here's the link: http://www.uptodate.com/contents/zika-virus-infection


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How many species of mites live on the human body?
How many known species of mites regularly live on the human body?
I've always heard that most people have eyebrow mites. This source  mentions 2 species of face mites, Demodex folliculorum and D. brevis,  that also regularly live on humans, but I'm wondering if there are in fact other species of mites that also call human bodies home. If so, how many? And where do they live?
Note: I'm not talking about disruptive mites such as scabies,  but mites that go less detected.

Mites like all living things require an energy source. Demodex and lice are parasite. Other mites can be ectoparasites but are not permanent residents of the human body

The answer is 2-3 human mites.
This page says that 2 mites specialize on humans:
http://www.bbc.com/earth/story/20150508-these-mites-live-on-your-face
https://link.springer.com/article/10.1007/s10493-009-9272-0
Another page I found said there are 3 common human mites, adding scabies to the list.
This page talks about bites from a variety of dust and house mites:
https://link.springer.com/article/10.1007/s10493-009-9272-0
My biology lecturer from university of Edinburgh told us that we have hundreds of species of detrital nematodes living on and inside us and that nematodes can be a few microns long. About 800 million humans have a 30cm large nematode inside them according to the WHO.


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Does variation in human gut length vary predictably with diet of ancestors?
Background: Numerous online searches, textbooks and other sources seem to pin the average length of the human gut from mouth to anus (oroanal) between about 5-10m in length. To pick a reputable example, this page from Harvard suggests that the small intestine is typically 2.91m and the average large intestine is 1.90m. The paper they cite (Helander & Fändriks, 2014) suggests this makes up most of the ~5m of the average human gut. Helander & Fändriks (2014) performed a lit review to come to these numbers, so their average lengths are probably some of the best estimates we have. (Other sources can be seen here and here, and Raines et al. 2014 seem to suggest that intestines of living people are much longer).
Regardless, Helander & Fändriks (2014), similar to Raines et al. (2014) and other sources, comment that there is "considerable variation between individuals" throughout the literature they reviewed.
My question: is the length of a given human gut predictable by the diet of their ancestors? In other words, are gut lengths between individuals more similar between family members and their ancestors than for others whose ancestors lived elsewhere in the world (and presumably had an alternative diet)?

For example: Are the guts of people of western European descent more similar to each other than the gut lengths of those of East Asian descent (or Sub-saharan descent, etc.).

Reasoning: Gut length (& complexity) of different animals varies based on digestive needs (which are a result of the typical diet of the animal). The general assumption (with support) is that diets high in food with indigestible material results in increased gut dimensions.

See Naya et al., 2009 for a general discussion about "gut flexibility", list of review citations, and results indicating correlation of population (diet) with gut length in toads.
Davis et al. (2013) found strong evidence that diet and intestinal complexity were linked in terapontid fishes -- specifically, more complex guts seemed to be associated with shifts away from carnivorous diets.
Gut plasticity does not seem to be immediate. For example  Ferraris & Diamond (1993) found (unsurprisingly) that intestinal length was independent of diet in a week-long mouse study.
Discussion of variation in human diet can be found here.

I haven't been able to find any sources discussing this "gut flexibility" phenomenon in humans.


text:
When and why did humans start disliking the way we naturally smell?
Like many animals, humans produce a myriad of scents from sweating, bacteria, possibly pheromones, etc. Many of these scents are used throughout the animal kingdom for mate choice, recognition of individuals, or signifying presence or territory.
I know that humans subconsciously react to some scent cues (see here, here, or here for examples), but it seems many humans find natural human scent to, well, smell. Interestingly, this article suggests that humans' smell is worse than that of other animals.
My question is: if these scents hold so much information, how/why did humans develop an aversion to the natural scent of other humans?
Further, when did this occur? -- recently or long ago in human culture? I know Egyptians made perfumes thousands of years ago, so this is not a fully recent trend. Perhaps someone could comment on the ubiquitousness of this aversion across modern cultures as well.

I don't believe this question is opinion based. It is fairly well known and demonstrated in my links (and countless other sources) that people find the body odor of others repugnant at times. The question asks for a historical /evolutionary explanation of why that is. That falls well in the range of accepted questions on this SE site. I feel those that voted to close nitpicked details in my text instead of focusing on the actual question, which is valid here.

I think that the "humans produce pheromones" part is problematic, you might want to remove that. To my knowledge no human pheromone (a specific molecule) has ever been identified, although some behavioral studies have suggested that there is information in smell. But this is really not so relevant to the question in the title anyway, so you could take out this part. Just the question of why our "natural" odor is repugnant to us is interesting in itself, regardless of what "information" it might carry,

@Roland I've modified this portion. I've now included the phrase "possibly pheromones" and included a link to a TED talk by one of the world's experts on the subject, Tristram Wyatt, who gives a good summary of the pheromone subject (which I believe is pertinent to this question). Please vote to reopen if you see no additional issues with this question.

I don't think there is a general aversion against other people smells. In fact, smells seem to me to be a very important part of a romantic relationship.

@Remi.b but there is a general aversion: that's ultimately why the deodorant industry exists (and arguably why perfumes and soaps exist as well...).  For further discussion, for example, see here

I think it's not human smell per se, just sweat. Probably because of association with bad hygiene and therefore risk of infection as you mention yourself - disgust as part of the behavioural immune system. I'd guess we gave up on smell in favour of social cognition and language, which we use for some social functions for which other animals use smells. So it wouldn't surprise that we find a different use for smell.

Hunting... if you smell bad, animals smell you better.  Go take bath.  Also, clean people get less diseases, go take bath.  Etc.  Therefore, smelly people are gross, weak hunters who get people sick.  Also, if you like smelling bad, you die more.


text:
Why plant tissues end in -enchyma?
Many plant tissue types end in the affix -enchyma.

Etymology: enkhyma "infusion," from en- "in" + khein "to pour"

Examples are parenchyma, collenchyma, and sclerenchyma.

(meaning "to pour beside," "glue infusion," and "hard infusion.")

My question: Where did this usage of -enchyma meaning "infusion" for plant tissues come from?

I'm curious from a biological more so than a historical perspective. I.e., why was this word choice chosen for plant tissues?

The best explanation I've found is from Plant Systematics by Michael Simpson:

Para, beside + en-chein, to pour; in reference to the analogy that parenchyma is poured beside other tissues to fill up space.

So far I haven't been able to corroborate this or expand upon it...

According to Wikipedia, Originally, Erasistratus and other anatomists used [parenchyma] to refer to certain human tissues. Later, it was also applied to plant tissues by Nehemiah Grew. so perhaps further investigation from a human anatomy perspective will be informative

I'm also interested to learn more about the difference between the Greek roots for chyme vs -chyma (khūlos vs khéō) and how their origins inform this question further...


text:
Chemistry of phosphodiester bond formation by DNA polymerase
As I'm teaching General Biology to my college students, I realized that I don't fully understand how a 3-P nucleotide like ATP is broken down to be incorporated into DNA during replication. How does this work??
In other words, what is the actual mechanism/reaction pathway for the following:

What I know:
I understand that ATP is typically hydrolyzed to become dephosphorylated in other contexts. I also understand that a phosphate of one nucleotide is bonded to a deoxyribose of an adjacent nucleotide via dehydration synthesis from the joining of their hydroxyl groups to form DNA.
However, I cannot seem to find a good resource (online or in any of my [admittedly simple] general bio textbooks) that demonstrate how exactly both of these reactions take place during replication...
I'm assuming that DNA polymerase is taking advantage of the released phosphates from ATP (and the appropriate forms of GTP, CTP, TTP) to become activated?
Overall, what does this whole process look like on a chemical/molecular level?
I'd love a visual (especially a video) if you could provide such a resource in addition to a thorough explanation of what's going on here.

Molecular Biology of the Gene is a good book if you have access to it.

I am unclear what you want to know. Is your question about the enzyme reaction mechanism or the thermodynamics? Your use of the word "power" in the title suggests energetically but the body of your question seems concerned with mechanistics. This and other statements about DNA polymerase "taking advantage of…" seem to indicate a basic ignorance of enzyme catalysis. Have you read the appropriate chapter in Berg et al ?

@David I want to know both and all of the above.

If you want to know all then your thirst for knowledge admirable, but your question too wide to answer on SE Biology. I would read the appropriate chapters in Berg or Lodish etc. As regards your college students, what you focus on depends on their background and the time you have. The chemical aspects require a chemical background but don’t seem particularly interesting to me, except that the dNTP substrates drive the reaction energetically and pyrophosphatase makes it irreversible. Conceptual problems — proofreading, initiation and Okazaki fragments etc.  — may be better.

@David. Thanks for the suggestions. I don't actually plan to teach them the specifics I'm asking about in this post -- these details are just for me to more fully understand the process as I explain to them a simplified version. Could you also more specifically indicate which texts you refer to? Is there a specific edition of Berg's or Lodish's texts?

This post seems helpful as a quick explanation of the reaction I'm asking about in my question: http://virtuallaboratory.colorado.edu/Biofundamentals-web/lectureNotes-Revision/Topic3-2_NucleicAcids.htm

Also relevant: https://www.biosyn.com/tew/What-is-a-Phosphodiester-bond.aspx

I have edited your title so that it is now an agnostic question, rather than one that (incorrectly) assumes a particular answer about the role DNA polymerase. I have not touched the body of the question, but after reading my answer (and that of @Nicolai) I would suggest your remove or replace the incorrect figure.

@David I've updated my image to try to better demonstrate that the arrow you've questioned is meant to be conceptual and not chemical. The image is meant to demonstrate that I'm asking about the bonding of a tri-phosphate molecule to an existing nucleic acid in such a way that a phosphodiester bond is formed and 2 phosphates are released.

theforestecologist, I found Biochemistry by  Jeremy M. Berg, John L. Tymoczko, and Lubert Stryer, to offer a great explanation of the mechanism. idk if you are still looking for reference material but its still one of my favorite all time undergrad text books

I found this paper, which goes very deep into the molecular details of the individual steps of this reaction and also discusses how this is coupled to nucleotide selectivity.
The 'basic' details about the reaction (quoted from this section, which also has a nice figure):

The polymerization reaction proceeds by a simple nucleophilic attack
  of the 3'OH of the primer on the α-phosphate of the incoming dNTP
  followed by the elimination of pyrophosphate [...] The reaction uses a
  "two metal ion" mechanism in which metal ion A activates the 3'OH as a
  metal hydroxide while both metals A and B stabilizes the developing
  negative charge on the α-phosphate in the transition state.

The metal ions are Magnesium (Mg$^{2+}$) and are properly positioned by the enzyme structure and some additional amino acid side chains also help with the activation of the reaction.

Apologia
The answer given by @Nicolai is essentially correct (and I have upvoted it). However I feel that the question embodies certain mistaken assumptions that should be challenged so that naïve readers of the question are not misled in to accepting them. (I refer to these below as ‘problems’.) I also feel that illustrations — not included in the answer provided by  @Nicolai — are needed in this respect.)
Supporting authority
I have used a 2016 paper in Science by Gao and Wang as my authority, quoting from it and reproducing part of one of its figures for those who have not library access to this journal. The authors actually propound a ‘three-metal ion’ mechanism, rather than the ‘two-metal ion’ mechanism mentioned by @Nicolai. This, however does not affect the basic points I am making, although it serves to illustrate that the details of the enzyme mechanism are of a complexity that is unsuitable for teaching at an introductory level.
Here are two key frames from Fig. 1 of that paper:

Problem 1

“I'm assuming that DNA polymerase is taking advantage of the released phosphates from ATP (and the appropriate forms of GTP, CTP, TTP) to become activated?”

An enzyme is not ‘activated’ by the products of the reaction it catalyses. The binding of the substrate may result in a conformation change that results in more favourable state for catalysis — and which might be referred to as ‘activation’‡ in a discussion of that topic; but the use of that word can only confuse at the level at which the current question is asked. This is because one of the key concepts in enzyme catalysis is ‘activation energy’ — the energy required to achieve the transition state. Activation energy refers to the activation of the reactants — not the enzyme. To quote from the paper:

Enzymes increase the rate of chemical reactions, which is thought to occur by a reduction in the activation energy required to reach the transition state (Fig. 1A)

Chemical reactions which result in a decrease in (Gibbs) Free Energy (the ‘Energy’ axis in Fig. 1A) are thermodynamically favourable. They occur slowly because they proceed through a transition state of higher energy. The role of an enzyme catalyst is to lower the energy to get to that transition state (the activation energy). As the figure shows, this reaction is thermodynamically favourable. The released pyrophosphate has no function, except to be hydrolysed by pyrophosphatases to prevent the polymerization being reversed.
Problem 2
It is unclear what the arrow at the left of the figure in the question (from the α-phosphate of the dNTP to the primer OH) is meant to represent†. Normally one would assume that this would be an electron, however here this does not make sense. As @Nicolai says

“…reaction proceeds by a simple nucleophilic attack of the 3'OH of the primer on the α-phosphate of the incoming dNTP”

i.e. the arrow should be from the oxygen electrons of the OH to the nucleophilic phosphate. This is shown in Fig. 1B (where the nascent DNA chain is on the left and the dNTP on the right). The latter figure actually shows the transition state, which allows one to see in a general way how this could be of lower energy than for the uncatalysed non-enzymic reaction. It is stabilized by the two metal ions (Mg2+), which themselves are held in the appropriate position by acidic side-chains at the active site of the enzyme.
Footnotes
‡As @user1136 points out, the expression ‘enzyme activation’ is also used to describe action of positive allosteric effectors — small molecules that increase the activity of the active site by a structural change initiated by their binding at a site distal from the active site — the allosteric site. This is a further potential cause of confusion as it has no relevance here.
†In a comment, the poster writes “The arrow in the… picture… represents conceptual movement of molecules and not ‘real-world’ chemical interactions”. If this is what was intended (I am not familiar with the source), in my opinion the authors should have used a different style of arrow (e.g. a wider one, ➡ rather than ➛, and not drawn it from the phosphate to the OH. It betrays a lack of either knowledge or concern for chemical conventions, and is particularly misleading for the student who wishes to understand biology at a chemical level. I find it inexcusable in a publisher with a reputation like that of Benjamin.

My plan is actually not to teach at as advanced level as you describe. My hope is (as a forest ecologist) to better understand the true molecular/biochemical workings of this process so that I -- being then more properly informed -- could simplify the material in such a way that I wasn't actually perpetuating/teaching pseudo-truths. Thanks for providing some clarifications.

@theforestecologist OK. I'll remove my last para.

The image that you mention under "Error 2" is from Starr et al.'s (2013) textbook "Biology: The Unity & Diversity of Life." Being an introductory biology textbook, the image is not trying to depict movement of atoms or subatomic particles. Rather, the arrow you've criticized is simply meant to be conceptual: it shows that the incoming tri-phosphate nucleotide bonds to the 3' hydroxyl group of the existing nucleic acid backbone.

I've updated the picture to be slightly clearer. There's still an arrow that you'd likely consider dubious for the same reasons mentioned in your post. The arrow in the new picture still represents conceptual movement of molecules and not "real-world" chemical interactions. However, the picture best represents my conceptual understanding of the process in question, and as such, I need to keep such a "simplified" (conceptual) image. The whole point of my question was to get a more detailed biochemical/molecular response from others like yourself more experienced in this branch of biology.

@theforestecologist — I question your arguments for retaining the illustration, but at least it allows me to address this sort of misleading content in biology texts. I have commented on it at more length in a footnote. If I had bought a copy of the text I would have pointed out the error either on the publisher's site or that of Amazon or whoever sold it. Text books are written by mortals like me. I can make mistakes, and other authors can and do. Good publishers put major texts out for critical review, but reviewers can only spot errors in areas of their own expertise.

I have edited my answer, as mentioned in other comments, but also replaced "error" by "problem". I suspect that that may have been poor psychology. (Must remember to go round the lab and replace all "poison" labels by "substance the non-toxicity of which cannot be guaranteed".)

@user1136 — I have added a footnote about the use of the term in relation to positive allosteric effectors.


text:
What makes/breaks the hydrogen bonds between DNA and RNA during transcription?
So I know that RNA polymerase catalyzes the phosphodiester bonds that hold the sugar backbones of a growing mRNA molecule together during transcription. However, I'm less sure about the hydrogen bonds between the nitrogenous bases of the forming RNA and the template DNA strands.
I do assume that hydrogen bonds are forming, but they must be short-lived.
Their existence are confirmed here:

ribonucleotides containing 3 phosphate groups hydrogen bond through the process of complementary base pairing with the exposed deoxyribonucleotides on the unwound strand that is to be transcribed

and represented in this gif:

Is RNA polymerase responsible for creating the hydrogen bonds between DNA and RNA? Is it, then -- I assume -- also responsible for breaking these bonds? Are the breaking bonds driven by chemical reactions or more due to the physical movement of the polymerase along the DNA template?
This site mentions the transient H-bonds formed by holoenzyme at promoter sites, but I haven't been ale to fnd a reputable source discussing the transient H-bonds between nucleic acid strands.
I'd appreciate if someone can provide a clearer molecular description of what's going on here. Pictures/animations are a plus!

Be careful with animations. The one you present indicates an unwound stretch of DNA with RNApol (not shown) somehow moving along it. Misleading at the very least if RNApol is causing the DNA to unwind. I'd remove it. The formation of a transient heteroduplex of at least one bp is fundamental. It seems to me that the crux of your question should be 1. How does RNApol melt the dsDNA, 2. How does it process along the DNA duplex, and 3. What causes the transient heteroduplex of the growing RNA chain to dissociate?  The answer is presumably to be found in a recent review paper.

David, thanks for the comment. I think you're right that all those components are an important part of the process, but I am most interested in the construction/breakdown of the H bonds themselves. I'd welcome an answer that addresses the H-bonds in the context you indicate. Do you have a citation or title for the review paper you have in mind? I'll allow your comment to provide the caution regarding the unwound nature of my animation, but I think I'll leave it as part of my "evidence" that H-bonding occurs and as a quick indication of the H-bond to which I'm referring. Thanks!

I am away with just my phone at the moment which is not really the thing for literature searches etc. If nobody else has done so by next week I'll either do a Papers search for reviews and/or look at recent PDB entries for RNApol. However remember that hydrogen bond formation is driven by thermodynamic considerations at a rate that is governed by kinetic factors.  If RNApol makes additional interactions with the rNTP and binds it so it is in the right position and configuration to base pair with the DNA this will allow it to speed up the kinetics — catalyse the reaction.

Finally done it. Perhaps a bit over the top for a non-chemical biologist (as I assume from your bio) or for teaching at certain levels (as you mentioned previously). However as you have made frequent contributions to SE Biology your question deserves a thorough answer.

I wouldn't really say RNA polymerase is "creating" the hydrogen bonds so much as it's thermodynamics that creates them. When we talk about an enzyme "creating" a bond, what we're generally referring to is an enzyme facilitating a reaction by lowering its activation energy so that it can proceed.
However, in the hydrogen bonding between base pairs, there's not really much activation energy to overcome. Before the formation, the nucleotide is just floating around in the cell (solvated by water), and forming a base pair is more energetically stable than not being paired. When a ribonucleotide happens to diffuse into contact with the unpaired DNA strand, the hydrogen bond will spontaneously form because it's energetically favorable. The thing about hydrogen bonds, though, is they're fairly weak, so there's an equilibrium between formation and breaking. When a mismatched nucleotide diffuses into that space, the hydrogen bonding isn't as strong, and it might be in an improper orientation, so it'll diffuse out again. When the correct nucleotide enters, the hydrogen bonds will form spontaneously, hold it there longer, and orientate it properly. This properly places the phosphates for backbone formation, which allows RNA polymerase to proceed with making the backbone.
As for the breaking of the hydrogen bonds, it's the energy released from the phosphodiester bond formation that causes the bonds to break at the other end of the RNA-DNA hybrid. To simplify things a lot, it's kind of like a zipper, where forward translocation of RNA polymerase along the DNA strand is driven by phosphodiester bond formation, which breaks the hydrogen bonds of the RNA-DNA hybrid somewhat mechanically, as the nascent RNA strand leaves through a different channel than the DNA does.
References:
Structural Model of RNA Polymerase II Elongation Complex with Complete Transcription Bubble Reveals NTP Entry Route
Transcription elongation: Heterogeneous tracking of RNA polymerase and its biological implications

Although the answer provided by @StephenB is essentially correct, I’d like to supplement this with more visual illustrations — including a link to an animation which the poster requested — as well as reiterating the important points he makes about enzymes. This is a question about enzymology and structural biology and is essentially chemical in nature.
Enzymes and Chemistry
To answer the specific question posed:

No. Enzymes are not responsible for creating any sort of bond.

The creation of bonds — including the hydrogen bonds of base-pairs — is governed by the thermodynamics. Enzymes are catalysts and only affect the speed of reactions that are thermodynamically favourable. In brief:
1. Reactions only occur which result in a decrease in Gibbs free energy.
We are always comparing two alternative situations. In the case of nucleic acid hybridization, for example,  we may at different stages of transcription have to consider ssDNA v. dsDNA, ssDNA and ssRNA v. RNA-DNA heteroduplex, DNA-DNA homoduplex v. RNA-DNA heteroduplex. The problem with transcription is not why rNTPs bind to DNA, but why different hydrogen-bonded structures, of necessity, occur at different stages in the cycle.
2. Reactions involve an equilibrium between the forward and reverse direction.
Unless a reaction product is removed, there is generally no conceptual difficulty about the reaction also occurring in the reverse direction. The extent to which this happens will depend on the position of the equilibrium. For transcription such reversal is important because stretches of RNA, initially hydrogen-bonded to DNA, need to be released from it, and stretches of DNA have to alternate between being double-stranded and single-stranded.
3. Enzymes speed up reactions (in both forward and reverse direction). They have no effect on whether or not a reaction is thermodynamically favourable.
As @StephenB mentioned, enzymes speed up reactions by affecting the activation energy — generally raising the ground state or lowering the activation energy by facilitating an alternative reaction sequence. In the case of the binding of the an rNTP we know from chemistry that the strength of a hydrogen bond depends on its directionality. Hence many random collisions will be unproductive. Without knowing anything about the real situation, we can speculate that weak bonds to residues on the rNTP binding-site of RNA polymerase may facilitate a reorientation to the optimal position for base pairing.
This material is covered more fully in textbooks of biochemistry, e.g. Berg et al. Ch. 8.
Transcription — The Movie
In a Cell Perspectives article in 2012, Cheung and Cramer described a movie of mRNA transcription by RNA polymerase II and other factors based on published structures of various intermediates. Although this was produced by interpolating between static ‘snapshots’ of structures, it is a comprehensive attempt using three-dimensional structures to address different stages of transcription — melting of the dsDNA, movement relative to the DNA duplex, and dissociation of the transient heteroduplex. This is illustrated in a figure from the paper:

I have  constructed my own composite of screen shots of that section of the movie (from about 3.00 min) that deals with binding of rNTPs. In  contrast to the figure above, it shows only a small section of RNA polymerase in order to focus on the dynamic changes that occur in two sections of this protein on binding the substrate (another feature of many enzymes).

The rNTP-binding step
The depiction of rNTP-binding in the movie is summarized as:

…an NTP substrate first binds to an open active center conformation, adopting a preinsertion state…. The NTP then moves slightly to occupy the insertion site as the trigger loop folds to close the active center…. Closure of the active site around the NTP generates contacts that are required for correct NTP selection and leads to catalytic nucleotide incorporation and RNA extension ….

This is based on the work of Vassylyev et al. who describe the molecular interactions in more detail. I quote an extract from their paper to illustrate that the supposition about interaction of the substrate with residues on the enzyme is borne out, but also that the complexity of the interactions is such that it is not possible to make a simple summary:

In the ttEC/AMPcPP complex, AMPcPP forms a Watson–Crick base pair with the acceptor template sandwiched between the 39 end of the RNA/DNA hybrid on one side and the protein residues from the TH and BH on the other. Met b91238 (TH) and Thr b91088 (BH), which stack directly on the substrate and template bases, respectively, seem essential for the positioning and selection of the substrate (Fig. 2); the corresponding RNAPII residues Leu 1081 and Thr 831 seem to have similar functions in the yeast EC13. In agreement with modelling and biochemical studies1,4,15, Asn b9737 forms hydrogen bonds with both O39 and O29 of the substrate ribose, thereby permitting discrimination against the non-cognate dNTPs lacking either or both of these atoms (Fig. 2b, c).

The interested reader will need to study the paper himself. I restrict myself to reminding him that the structures of enzymes are dynamic because there may be an equilibrium between different possible structures and the position of this equilibrium can be changed by the binding of other molecules to the enzyme. It’s still chemistry — not magic!
Coda — Why no straight answer?
The reader accustomed to having reaction mechanisms of enzymes presented in dogmatic form may wonder why there are so many ifs and buts and molecular dynamics involved in working out how the rNTP gets to the correct conformation to bind to the DNA template. The answer is that although the structure of the binding site (actually there appear to be two alternatives) is known in detail, the successive positions of the rNTP are not, because there is no way of ‘freezing’ it at these different stages. Generally one captures intermediates in a reaction by making derivatives of them that will bind but not react, for example. So it is relatively easy to get structures for the rNTP bound and hydrogen-bonded, but not on its way in. A 2017 paper in the Journal of Biophysics indicates that mathematical methods are still being used as the basis of arguments about the detailed binding mechanism.


text:
Looking for realistic representation of angiosperm sperm cells during pollination
I've scoured Youtube, google, and a handful of my botany textbooks for a cellular-scale photo, animation, or video illustrating an angiosperm sperm cell during pollination/fertilization.
Unfortunately, other than an unclear glimpse of one in this video I've had essentially no luck.
Ideally, I'd like a microscope recording or a realistically-animated video demonstrating the accurate shape and movement of sperm along the pollen tube and into the ovary.
I think a video will better allow my botany students to visualize this process.
Please let me know if you can find or are aware of any such video or animation from any textbook supplemental materials, journal supplement, or via some reputable online resource.


text:
What is the function of the Hyoepiglottic ligament?
The hyoepiglottic ligament (ligamentum hyoepiglotticum) is an elastic band that connects the epiglottis to the hyoid bone.
Although I can find information about the clinical significance of this ligament (mentioned here), I have not been able to find a definitive or reputable description of its actual physiology/function.
Can anyone provide a reputably-supported description of the function (physiology) of the hyoepiglottic ligament?

My thought was that the hyoepiglottic ligament might act as a see-saw during swallowing. Specifically, my assumption was that as the hyoid is raised during swallowing (thus raising the hyo- end of the ligament), the opposite end of the hyoepiglottic ligament (attached to the epiglottis) is pushed down, forcing the epiglottis to cover the glottis to prevent food stuffs from getting into the trachea. Is this possibly right?

Note: I would be (almost) equally happy if someone can find a reputable source that claims we don't actually know its function (if that is indeed the case).

Have you read this paper? It has a brief review in the introduction of the proposed function of the hyoepiglottic ligament during swallowing, and the Discussion suggests a few mechanisms of function during phonation, respiration and swallowing. This paper which is older is also worth reading for a discussion of a model of its role in deglutition. Were you looking for something more evidence-based?

I'm not sure about the validity of your proposal - a ligament is quite 'stretchy' and I'm not aware of any central attachment point of the hyoepiglottic ligament, so I can''t visualise it being able to act as a 'seesaw'.

@anon yes, my proposal seemed not entirely likely to me, but I had not come up with anything better :p. Your linked abstracts are both interesting and much more on the topic of physiology than anything I had found. I'd say if you draw up an answer detailing/summarizing the main points of the actual full papers, I wouldn't mind accepting this as an answer worth awarding. Of course, I still welcome others to respond :)

It's an interesting question. This 2010 paper contains some discussion of the function of the hyoepiglottic ligament. The following is a quote from the introduction:

The epiglottis is connected to the
  hyoid bone by the hyoepiglottic ligament (ligamentum
  hyoepiglotticum), which is a connective tissue structure that
  serves as the roof of the paraglottic space and the
  preepiglottic space. Anatomically, the hyoepiglottic ligament
  separates the supraglottic larynx from the base of the
  tongue. Some clinical studies have shown that this
  ligament inhibits the spread and invasion of carcinoma... The hyoepiglottic ligament is elongated by
  approximation of the thyroid to the hyoid during swallowing.
  Tension on the ligament results in a “snap” retroversion
  of the epiglottis. Thus, the folded epiglottis represents a
  state of higher energy than that represented by the unfolded
  epiglottis; relaxation of the tension on the hyoepiglottic
  ligament releases the cartilage to automatically return to its
  normal resting position [emphasis mine].

In the study, the authors demonstrate histologically that the hyoepiglottic ligament is bipartite, with a part they call the pars hyoideus connecting the anterior epiglottis to the hyoid, and a part they call the pars lingualis connecting the epiglottis to the root of the tongue (they claim that this attachment to the tongue was previously unreported). Another quote from the paper follows:

It is suggested that the pars lingualis plays an
  important role in active mechanisms such as upward
  movement of the epiglottis during phonation associated
  with tension of the lingual muscle and supraglottic airway
  patency during respiration.

To get some idea of how tension in a ligament anterior to the epiglottis can cause posterior movement (i.e. closure of the epiglottic 'flap'), I found this 1979 paper useful. They used cinefluorography to investigate the biomechanics of the epiglottis. The following lengthy quote should help to clarify the proposed model:

The radiographic observations indicate that
  at the peak of the deglutitional excursion of the
  hyoid bone and the larynx the following circumstances
  prevail:
(1) Forward translation of the hyoid bone in
  conjunction with extreme thyroid-hyoid approximation
  causes extreme elongation and
  tension on the hyo-epiglottic ligament at its attachment
  to the margins of the epiglottic
  tubercle.
(2) The compression of the median thyrohyoid
  fold, secondary to extreme thyroidhyoid
  approximation, tends to make the epiglottic
  tubercle bulge backward transversely
  as well as vertically.
The principle of the mechanism of folding
  deduced from these observations is demonstrated
  in a working model that can be set up
  in a few seconds. All that is needed is a rectangular
  piece of fairly stiff paper. The piece
  of paper represents the complete epiglottic
  cartilage (epiglottis and tubercle). A $\Lambda$-shaped
  crease is applied at the center (Fig. 4) to simulate
  the groove on the back of the cartilage,
  between the epiglottic tubercle below and the
  epiglottis proper above. One next applies stress to the model from the opposite side, at
  the site of attachment of the hyo-epiglottic
  ligament. This is done by grasping the paper
  lightly at the edges, below the level of the
  crease, whereupon the part above the crease,
  representing the epiglottis, immediately begins
  to fold down.
  Each limb of the crease functions as the
  directrix of a cone; the apex of the crease is
  the vertex of the cone. When the paper is
  gripped the directrices rotate towards each
  other and pull the attached paper after them,
  giving it a conical shape.

I've attached the figure 4 from the paper to illustrate better (I'm not sure if that's allowed on SE; please delete it if that's appropriate):
$\hskip 2 in$
The authors of this paper and this paper argue that the model just given does not fully explain the motion of the epiglottis during swallowing. The latter paper describes the existence of distinct lateral hyoepiglottic ligaments attaching to the ends of the greater horns of the hyoid bone. These, they argue, transmit the biomechanical forces generated by the movements of the hyoid and thyroid cartilage to the epiglottis to cause downfolding, although their full argument is too long to reproduce here.
Hopefully all of that has shed a little light on the possible function of this ligament. It seems to be quite complex, but there appears to be a relative consensus that the transmission of tension via this ligament is important in causing the folding down of the epiglottis during swallowing.


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Does the humeroradial joint move medially/laterally?
The humeroradial joint is a ball-and-socket joint that, if unrestricted, would allow for movement around all possible axes. However (as succinctly stated from Wikipedia):

the annular ligament, by which the head of the radius is bound to the radial notch of the ulna...prevents any separation of the two bones laterally.

As a result of the annular ligament, the proximal radioulnar joint and -- quite honestly -- the humeroulnar joint, the humeroradial joint is considered to be "limited." In other words, the humeroradial joint is typically considered only to be capable of taking part in flexion/extension of the elbow and lateral/medial rotation of the forearm.
However, although no internet/textbook search I've conducted mentions it, I'm wondering does the humeroradial joint allow any movements at all in the frontal plane (i.e., adduction/abduction)?
Here's a visual:

It seems unlikely, but at least a slight "jittering" seems possible.
Although just barely related, the knee (a hinge joint) comes to mind because of its somewhat unexpected (based on classification, not structure) ability to "slightly rotate" when unlocking.

Adduction is highly unlikely because of the restriction provided by the crest in the articular surface of humerus. Also there are no muscles for voluntary abduction and adduction.


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Squirrel nest construction
I've often wondered how squirrels -- specifically, eastern grey squirrels (Sciurus carolinensis) make their nests. Specifically, I've been curious about how they "weave" everything together to make these so called "dreys" stay together (and stay in the tree).

According to this site:

[squirrel nests are] constructed from various twigs, leaves, moss and other material. To start, twigs are loosely woven together to make up the floor of the nest. Next, squirrels create more stability by packing damp leaves and moss on top of the twig platform to reinforce the structure. Then a spherical frame is woven around the base, which creates the outer shell. The final touches include stuffing in leaves, moss, twigs and sometimes even paper to build up the outer shell of the new home.

I've tried finding a video (preferably time-lapse) of a squirrel nest being built to better understand/appreciate this animal home. However, I've thus far been unable to find such a video on the internet.
Does anybody have such footage or know where I can find some?

Ideally, close-up and even internal shots would be included.
Additional notes about tree-branch drey construction would be appreciated, too!

https://www.youtube.com/watch?v=BcTweYHQ-II
It seems like they just pile the leaves on.


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Are "sympathetic nerves" the same as "cardiopulmonary splanchnic" nerves?
I've gathered from a number of sources (e.g., Patel (2015), Wikipedia, and here) that the sympathetic nerves leaving the sympathetic trunk to innervate the heart and lungs are called "cardiopulmonary splanchnic nerves".
However, I've noticed that both the 14th and 15th edition of Tortora & Derrickson's A&P textbook seem to suggest that these nerves are simply called "sympathetic nerves," even though they make reference to abdominopelvic and adrenal splanchnic nerves more specifically.  See below from Tortora & Derrickson (2013):

...Then, the axons of the postganglionic neurons leave the trunk by forming sympathetic nerves that extend to visceral effectors in the thoracic cavity (Figure 15.4). Sympathetic nerves provide sympathetic innervation to the heart and lungs.

Here are subsets of images from Patel (2015) [LEFT] vs Tortora & Derrickson (2013) [RIGHT] (my emphasis):

My question: Are "Sympathetic nerves" the same as "cardiopulmonary splanchnic" nerves?

Are these names interchangeable? I can't find further evidence supporting Tortora and Derrickson's usage of this phrase in such a specific manner to refer to postganglionic neurons leaving the trunk to innervate the heart and lungs. Are they acting rogue? Are they simplifying? Any insight would be appreciated.

Cited works:
Patel, T. R. 2015. "Chapter 36 - Anatomy of the Sympathetic Nervous System." Pages 495-506 in Tubbs, R.S., Rizk, E., Shoja, M.M., Loukas, M., Barbaro, N. and Spinner, R.J. eds. Nerves and Nerve Injuries: Vol 1: History, Embryology, Anatomy, Imaging, and Diagnostics. Academic Press.
 Tortora, G. J. and B. Derrickson. 2013. Principles of anatomy and physiology, 14th edition. John Wiley & sons, Inc.

You might consider cross-posting to SE Medical sciences who know more about this stuff.
I think that they are simply using a more general term than other authors. In the same way, most people call crabs crabs, but some people might occasionally refer to them as crustaceans.
Based on wikipedia, it seems that cardiopulmonary splanchnic nerves are a subset of sympathetic nerves. The sympathetic nervous system innervates a large number of organ systems of the body (see image), such that the cardiopulmonary splanchnic nerves are simply the sympathetic nerves that innervate the heart and lungs.
Looking further at the wikipedia for splanchnic nerves, it seems that this is a technical term relating to the fashion in which organs are innervated by the sympathetic nervous system; e.g. in my crude understanding they are organ hookups to the sympathetic nervous system.
In other words, all cardiopulmonary splanchnic nerves are sympathetic nerves, but most sympathetic nerves are not cardiopulmonary splanchnic nerves.

thanks for the answer. However, -1 b/c I feel like it doesn't answer my question. I know what the sympathetic nervous system is, and I know that the cardiopulmonary splanchnic nerves are the part of the sympathetic system that go to the heart/lungs. I also know that all nerves carrying sympathetic signals are considered "sympathetic nerves". I indicated all of this in my post. It appears to me, that everything you've mentioned in this answer repeats points made in my question, so I don't think this is actually an answer to my question. Could you clarify your post if this isn't the case?

IMO you did not indicate all of that. It was not clear that you understood that the sympathetic nervous system could be a superset of nerves of which splanchnic nerves was a subset, and that the authors in question could be substituting a more general term. I am happy to delete the answer if you do not feel that it addresses your question. But if you knew all of that in the first place I am not sure why you are even asking the question? It seems you have answered it yourself before even posting it.

Cardiopulmonary splanchic nerves consist of:

sympathetic nerves
the vagus nerve (a part of parasymathetic system)


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True anatomical/physiological explanation for "metaphysis" etymology
The anatomy textbook1 I use for my students states that the prefix meta- means "between:"

The metaphyses (me-TAF-i-sez; meta = between; singular is metaphysis) are the regions between the diaphysis and the epiphysis.   [my emphasis added]

This sounds reasonable given the explanation. However, I have never seen meta- applied in this manner; more generally, the suffix meta- usually seems to refer to "after."
In fact, Dr. Toby Arnold's Glossary of Anatomy provides the following etymology of the word metaphysis:

metaphysis: Greek meta = after, and physis = growth; hence, the end of the shaft of a bone alongside the epiphysial or growth cartilage  [again, my emphasis added]

The latter explanation is somewhat underwhelming, but the etymological usage fits more with my prior experience with meta-.
So, which is it?
Can someone find a reputable source definitively indicating a clear anatomical/physiological explanation for why meta- was used in the case of "metaphysis"?

A webpage on EnglishLearner.com reports that our earliest usage of the term "metaphysis" came from an obstetrician named William Dorland (1864–1956) in the early 20th century. I couldn;t find additional info.

1. Tortora, G. J. and B. Derrickson. 2014. Principles of Anatomy & Physiology, 14th edition. John Wiley & Sons, Inc., USA.

meta-:

word-forming element of Greek origin meaning 1. "after, behind; among,
  between," 2. "changed, altered," 3. "higher, beyond;" from Greek meta (prep.) "in the midst of; in common with; by means of;
  between; in pursuit or quest of; after, next after, behind," in
  compounds most often meaning "change" of place, condition, etc. This
  is from PIE *me- "in the middle" (source also of German mit, Gothic
  miþ, Old English mið "with, together with, among"). Notion of
  "changing places with" probably led to senses "change of place, order,
  or nature," which was a principal meaning of the Greek word when used
  as a prefix (but also denoting "community, participation; in common
  with; pursuing"). (Etymonline)

physis:

The growth plate, or physis, is the translucent, cartilaginous disc
  separating the epiphysis from the metaphysis and is responsible for
  longitudinal growth of long bones. (The Royal's Children Hospital Melbourne)

Anatomically and physiologically, meta- in metaphysis means next after physis (growth plate or epiphyseal plate) and refers to the changing (growing) part, which is in between the non-growing parts of a long bone (diaphysis and epiphysis):

The metaphysis is the wider portion of a long bone adjacent to the
  epiphyseal plate. It is this part of the bone that grows during
  childhood; as it grows, it ossifies near the diaphysis and the
  epiphyses. (Orthopaedicsone)

Picture: Parts of the bone (Radiopedia, Creative Commons license)

Thanks for the answer, @Jan. I was surprised to see meta referring to "between", but I now know it's not unprecedented. A comment on your last point though... So -physis is actually the part of the word referring to "growing" (changing), but you got me to thinking: the epiphyseal plate (associated with the metaphysis) is all about growing the bone's length (i.e., "beyond"), so I wonder if this is the physiological explanation for the etymology??

Again, I appreciate you finding the linguistic source, but could your try to provide a source that supports your last paragraph directly? Makes sense to me too, but I'm curious to see a reputable indication of Dorland's reasoning  (or modern physiological interpretation thereof)

consider metaphase, between-phase.

@theforestecologist, I made it simpler: anatomically and physiologically, meta- in metaphysis means "next after" physis and "between" diaphysis and epiphysis.

@John duhhh. Wow, you just made me realize I've explored this very question before but focused on metaphase previously. Of course, meta is between in that context! Oy I knew that! (I need more sleep before I post questions :p). Thanks, Jan, for the updates!

Bones grow for a long time.(teenage? adolescence?)
what does the suffix "-physis" mean? "Growth", so bone is longer and longer. We know the vital part of bone is metaphysis, but let's suppose that we are ingorant, simply observing that the bone shaft growing after the LINE between the bone shaft and "骺".
(both ends of bones are called “骺” in Chinese)
Bone's length is the diaphysis itself, growing INSIDE it.
Bone's length is following the metaphysis, growing AFTER it.
Bone's length is not influenced epiphysis (both ends of bones are called “骺” in Chinese), growing BELOW it, and “骺” is OVER the shaft.
This is why we use prefixes "dia-" "meta-" and "epi-", because this is how the components relate to the length.


text:
What kind of spider is this and is it poisonous?
 A brown furry diamond shape on its back and brown joints all on black body. Caught entering my house in Trinidad (small island off South America) -- killed the first one, this is the second.

Can you provide any information about where it was observed and if it was wild?

All spiders are venomous. I suspect you mean deadly. We would need the location too.

It's in Trinidad, small country off South America. It is wild and I think it was regularly feeding on me.

It's a Mygalomorph spider, of the sort which are usually called Tarantulas.  This is told by the two long, upcurved spinnerets and the large, dish-shaped carapace, with the eyes clustered in a clump - looking rather like the disk of the USS Enterprise from Star Trek, if the command bump was placed near the front edge.  I'm not sure which species it would be, but the good news is that like almost all spiders, it's pretty much harmless to humans.  These guys do have large fangs, though, so if you got bitten by one, you'd feel it.  As far as I'm aware, the venom of South American species is no big deal, so the feeling of being poked by a big needle is likely to be the worst effect.  Presumably they were entering your house to hunt for the small animals which share your home with you - large insects, small mammals and lizards, maybe.  I'd post an image, but I'm not sure which tarantula this would be (not really being a tarantula guy), and you could probably do as good a job of searching the internet as I could.  However, here is a resource I was able to turn up with a short search:
ttfnc.org/livingworld/index.php/lwj/article/download/479/462
As I said, I'm not really a tarantula guy, and so am not confident as to a specific ID of this spider.  However, having been pressed for an image, there are in this article some images of a spider which may or may not be yours.  The images are, however, tarantulas from Trinidad.  You will need to page through to the end of the article to see them:
http://sciencepress.mnhn.fr/sites/default/files/articles/pdf/z2017n2a5.pdf

Please provide evidence/support/citations for claims made as answers. Otherwise, we're no different from yahoo answers, which nobody should trust :p.

This is Holothele longipes (Trinidad dwarf pink tarantula) (formerly named Holothele sanguiniceps). It is found in a number of countries, including Trinidad and Tobago.

It is one of the smaller tarantulas, just a few inches long at full size.

(photos and map from GBIF: https://www.gbif.org/occurrence/gallery?taxon_key=2153490 )
It is identified by having no markings, black legs and palps which can shine blue, and red-to-brown thorax and abdomen with many red-to-brown hairs.


text:
Identification - hornet
It has around 3cm. Does it look like a European or Asian Hornet?
The place where I found it is Central Europe/Romania but, after the wikipedia picture for Asian Hornet's head .. it looks exactly the same.
Thank you!


text:
Is it normal for corn to have multiple ears in one place?
I have (out of a mistake) one corn plant in my greenhouse and it made 4 cobs in one place. Is that normal?! I never saw something like this before.

Google 'corn bouquet' and ignore floristry e.g. https://u.osu.edu/mastercorn/bouquet-ears/

This is an example of "bouquet ears", or, what Rob Nielsen coined in his 1999 paper2 as "MESS Syndrome" (Multiple Ears on Same Shank).
Although not a regular occurrence, MESS syndrome is not unusual. According to Nielson in an online article in 2014 [my emphasis included]:

The fact that multiple ears sometimes develop from a single ear shank is not, in and of itself, physiologically unusual. Ear shank development essentially replicates the developmental pattern of the main stalk of the plant.

The ear shank is comprised of nodes and internodes just like the main stalk (Fig. 7).
Each node of an ear shank develops a leaf just like the main stalk, although we add the adjective "husk" to describe them.
The ear shank terminates with a reproductive organ (the female ear), akin to the main stalk terminating with a reproductive organ (the male tassel).
Secondary ear shoots can develop from individual nodes of the ear shank just like secondary ear shoots develop from individual nodes of the main stalk.

Normally, hormonal apical dominance exhibited by the primary or apical ear on an ear shank (or simple competition for photosynthates) suppresses the initiation or development of secondary ears at lower shank nodes. However, under certain conditions or with certain genetic backgrounds, one or more secondary ear shoots not only initiate successfully, but also continue to develop to the point that their presence is clearly noticeable. While the appearance of one or more additional ear shoots with silks emerging from lower husk leaves may not be attractive, I do not believe there is any real detriment to the plant by their existence as long as the primary ear is "normal".

Bonnet (1966)1 described this phenomenon in the 1960s and reports of occurrences happen periodically. In 2006, Nielson3 coined the "bouquet" terminology to describe multiple reports of out-of-proportional growth of multiple ears from single shanks in numerous midwestern farms.

According to Nielson:

The common factor in affected fields was some sort of damage to the development of the primary ear prior to or during silking that seemed to "set loose" the continued development of the secondary ears on the same ear shank.

An Ohio State University article suggests that the cause of this phenomenon is unknown, but Nielson is probably the expert:

Some hybrids may be genetically prone to developing multiple ears on a single ear shank. A threshold genetic trait may be triggered by particular stress events that occur during primary ear formation. Dr. Bob Nielsen at Purdue University has proposed that more than one external “trigger” may enable the development of multiple ears to occur on these hybrids. He has observed that the “bouquet” effect is more prevalent and severe in late plantings where silk clipping by rootworm beetles prevented kernel set on the primary ear (i.e., possibly minimizing or negating apical dominance against secondary ears).

You can see an image of a bouquet from one of Nielson's studies below:

 Source: Purdue Dept of Agronomy; Credit: Bob Nielson (2014)

1  Bonnet, O.T. 1966. Inflorescences of Maize, Wheat, Rye, Barley, and Oats: Their Initiation and Development. Univ. of Illinois, College of Ag., Agricultural Expt. Sta. Bulletin 721.
2  Nielsen, R.L. 1999. What A MESS! (aka Multiple Ears on a Single Ear Shank). Corny News Network, Purdue Univ. http://www.kingcorn.org/news/articles.99/990823b.html
3  Nielsen, R.L. 2006. A Problem with “Bouquets”. Corny News Network, Purdue Univ.  http://www.kingcorn.org/news/articles.06/Bouquets-0912.html.


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Why do bumble bees run repeatedly into walls?
I have noticed on dozens of occasions that bumble bees will run repeatedly into a wall. Usually between 1 - 5 times before clearing the obstacle or flying away.

 Credit: Spine Films
This source suggests that this might be due to "unpredictable, unsteady airflow ... [that results in them being] buffeted back and forth by wind."
However, I've seen this occur in very clear, calm weather.
Further, I do not see other genera of bees colliding into things with anywhere near the frequency of bumble bees.
So what's going on here?
(FYI: their eyes, though primitive, are not likely the reason. Nor is their intelligence).

Stubbornness? If they have so many positive traits (like advanced navigation or emotions) like your links say, why shouldn't they have developed some of the more... mixed traits that exist?

Crall et al., 2015, studied bumblebee collision avoidance (note the senior authors are the same from your link). It seems that, contrary to popular belief and experience, bumblebees are actually quite good at avoiding collisions, but they are also in an environment that has a lot of obstacles, so collisions still happen frequently.
There is a lot of interesting content in that paper, but one of the interesting discussions was about types of collision avoidance by body size. The authors note that for larger animals, collision avoidance strategies tend toward reversal/slowing down to reduce impact, whereas in smaller animals, strategies tend toward direction-change. This might be because collisions at high speeds are more dangerous for larger animals, so slowing down is the priority. Accelerating in a lateral or vertical direction, instead, would result in a full-force collision if the acceleration was insufficient to avoid the object (I have to admit, though, your gif doesn't seem to show any deceleration).
Larger individuals in their study performed more slowly on their obstacle course than smaller ones, but it seemed like all the bees were pretty good at avoiding obstacles.
Based on this study, I don't know that we can conclude definitively why bumblebees repeatedly run into walls, but given how well they navigate an obstacle course like this I am guessing it isn't simply because they are incapable, but rather has to do with a few things:

Walls are somewhat unexpected obstacles; bumble bees are probably best evolved for navigating around foliage that has a limited horizontal size, and once headed home they are expecting a direct route to be most efficient. A good transit strategy in that case would be to fly slightly laterally in the event of a collision to find a new opening, but not deviate too much from the original path of travel.
Speed/collision tradeoff. Getting home fast can have some obvious advantages because it increases the effective foraging potential. If collisions can be mitigated or aren't damaging, it might make sense to fly at high speed and just deal with the collisions as they come.
Bumblebees are big. Therefore, it's harder for them to stop, and they might use a strategy for collision avoidance that reduces impacts rather than avoids impacts altogether.
Cognitive biases in humans. Bumblebees make quite the racket when they run into things. You're going to hear it each and every time if you are nearby. The same isn't necessarily true for other bees or other insects.

References
Crall, J. D., Ravi, S., Mountcastle, A. M., & Combes, S. A. (2015). Bumblebee flight performance in cluttered environments: effects of obstacle orientation, body size and acceleration. Journal of Experimental Biology, 218(17), 2728-2737.


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Understanding the concept of a "Place Field" and the difference between place cells and grid cells
I have 3 questions that are interrelated:

After reading the proper literature on the subject, my understanding of the place field is that it's a place in space to which an animal's place cell reacts by firing. Then there might also be another place in field to which the same place cell reacts by firing. Is this understanding correct?
1.1 Why is it called place "field," what does the "field" actually imply, etymologically speaking?
1.2. The Wikipedia Grid Cell Page says that:

By contrast, if a place cell from the rat hippocampus is examined in the same way (i.e., by placing a dot at the location of the rat's head whenever the cell emits an action potential), then the dots build up to form small clusters, but frequently there is only one cluster (one "place field") in a given environment, and even when multiple clusters are seen, there is no perceptible regularity in their arrangement.

So then what are those "clusters", i.e. I guess the place fields, are they the ones I highlighted in red on this picture (sorry, I am a very visual learner!) and also, why do they fire in clusters?

The Wikipedia Page has the following description of this picture but I am still not sure I am understanding it correctly:

Spatial firing patterns of 8 place cells recorded from the CA1 layer of a rat. The rat ran back and forth along an elevated track, stopping at each end to eat a small food reward. Dots indicate positions where action potentials were recorded, with color indicating which neuron emitted that action potential.

The first question stems from the second and the main one I am confused about: what is actually the difference between the place cells and the grid cells, in a layman terms (beyond the obvious structural differences, i.e. that the place cells are pyramidal neurons and the grid cells fire in a hexagonal pattern)?
In terms of their functional differences, is the difference mainly in the fact that the grid cells are theoretically responsible for path integration, whereas "The place cells are thought, collectively, to act as a cognitive representation of a specific location in space, known as a cognitive map" ( O’Keefe John, 1978 ).

What is the physiological or anatomical difference between.... Available from: https://www.researchgate.net/post/What_is_the_physiological_or_anatomical_difference_between_place_cells_and_grid_cells_in_the_hippocampus [accessed Aug 16, 2017].
O'Keefe, John (1978). The Hippocampus as a Cognitive Map. ISBN 978-0198572060.

Yes, that's correct. Mostly, place cells fire in different places in different contexts, and they don't necessarily share the same spatial relationship in different contexts (like in your picture, the "yellow" cell comes right before a "cyan" cell; those place fields wouldn't necessarily be adjacent in a different context.

1.1. "Field" is just a term that refers to a region of space. I'd say the Merriam-Webster definition closest is #6:

a region or space in which a given effect (such as magnetism) exists

1.2 The picture you have is probably a schematic, but what it depicts is a recording from several different cells. Each cell is assigned a color. Every time the cell fires a spike, there is a dot placed at the location in space where the animal was at the time of the spike. You let the animal run through the maze and get a record of lots of these points, and you see that they cluster together into place fields.
2&3 - These questions are getting to be a bit too broad and also you are only supposed to ask one question per submission, so I'll be very brief here. Grid cells are located in an entirely different part of the brain, the entorhinal cortex (part of neocortex), although this part does project to the hippocampus where place cells are found.
Grid cells fire in regular patterns in a spatial field, like in this image:
https://en.wikipedia.org/wiki/Grid_cell#/media/File:Autocorrelation_image.jpg
They also keep their relationship of firing locations relative to each other constant across contexts. You can think of them like a nested coordinate system.
Place cells do not do this. For a given environment, they seem to be somewhat randomly arranged relative to each other. Most likely, what actually happens with place cells is that if you could record from all of them, there would be a unique combination of cells active at any location, and this location could then be associated with other information like "I found food here."
Perhaps you could think about grid cells like a GPS location, but place cells are like a map marker.

the picture you've attached is the autocorrelation heatmap, and I have always been wondering, how are those maps usually generated for grid cells? I heard they use something like Gaussian process? But the what is correlated with what in that plot?

@Jen The x- and y- axes are space. It's an autocorrelation, so the process is that you iterate through each spike you observe, and call the place the animal is when that spike is fired (0,0); then you look at where the animal is when every other spike is fired, and mark an event at each spatial coordinate relative to that first spike. Then you do that for all the other spikes. A gaussian filter is just used to filter the data a bit, so you see blotches rather than just a bunch of dots.