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How is honey not toxic to our epithelial cells?
Being a supersaturated solution of sugar, honey pulls the water out of cells it comes in contact with via osmosis - killing the cells. It also contains the inactive enzyme glucose oxidase, which when diluted with water activates and then converts glucose into gluconic acid and hydrogen peroxide - both of which are bad news for cells.
Honey also likely contains an antibiotic protein Bee Defensin-1, which is also bad news for bacteria. I didn't yet look into how it works so I don't know if it affects our epithelial cells.
Then some honey types (manuka) contain Methylglyoxal. Damage by methylglyoxal to low-density lipoprotein through glycation causes a fourfold increase of atherogenesis in diabetics. [1] Methylglyoxal binds directly to the nerve endings and by that increases the chronic extremity soreness in diabetic neuropathy.[2][3]
How is it safe to eat?

Because the lining of the stomach guards the component cells from acid, osmotic stress, and all sorts of other nasty stuff, while digestive enzymes make short work of any food proteins that they encounter.

What about the esophagus and mucosa of the mouth?

I'll change my initial comment into a real answer.
The human digestive tract has evolved to allow us to be broadly omnivorous, safely consuming a wide range of vegetable, animal, and mineral-based foods. While honey can be damaging to exposed cells, the epithelial cells lining the digestive tract are not exposed like the endothelial cells that line the circulatory system. Eating honey is not the same as injecting it into your veins.
A layer of mucous covers the cells of the digestive tract from mouth to colon and provides both lubrication as well as protection to the cells underneath it. It is protective to varying degrees against such challenges as acid, osmotic stress, mechanical damage, and foreign microorganisms. Additionally, the cells themselves are layered and are continually being sloughed off and regenerated, so even if the mucosal lining isn't 100% effective, damaged cells will be replaced fairly quickly.
Food quickly travels from the mouth through the esophagus to the stomach, not allowing enough time for osmotic stress or enzymes to damage anything to any significant degree. (Obviously, if you swallow something extremely harsh like bleach, lye, or concentrated acid, that's a different story.)
Once in the stomach, a food like honey is diluted by the digestive juices and any other food or drink already present -- it's not like the stomach is totally empty and globs of honey can just sit in direct contact with cells for an extended period of time, allowing for osmotic or enzymatic damage. Digestive enzymes and the acidic environment quickly attack proteins and other substrates, so even if the glucose oxidase can become activated, it will be cleaved by proteases into inactive fragments long before damaging levels of H2O2 can build up.
Low-density lipoprotein (LDL) is found in the bloodstream, not in the digestive tract, so any methylglyoxal present in food would need to be actively transported into the blood to do any damage. The work in the paper you cited was done completely in vitro, with no evidence that MG-mediated glycation as a result of eating honey actually occurs in people.
Many foods we commonly eat would appear to be dangerous to our bodies in one way or another, yet we have evolved strong mechanisms to minimize harm. However, it's pretty clear that some foods are damaging in various ways over time, so we still need to moderate what we eat. I don't know if honey (or certain kinds of it) is one of those foods, so more research is needed.

What an answer. By the time I got through it, you answered several subsequent questions that popped up:) Amazing!


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Vertebrae looking bone found on beach in New Zealand
I found this bone on a beach in New Zealand. Does anybody have any idea which part of the body or which animal it’s from?

(click to enlarge)

Are you looking to identify it beyond just being a vertebra? It's a vertebra for sure, but beyond that, it's hard to identify beyond "probably a large mammal", which for New Zealand would likely be some kind of whale or dolphin, unless it's something non-native like a cow.

Welcome to Biology.SE. It would help if you could give some measurements for the vertebra — we can only get a very rough guess based on the hand size. My understanding is that the most probable answer for New Zealand is always going to be sheep, but I think these are too large ... I agree with kmm that these are likely to be from a marine mammal of some sort.

It would also help to know roughly where in NZ (e.g. Northland, BOP, West Coast, 'Naki, etc.), as the animals present vary quite widely from North to South and East to West.

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How is the Staverman's reflection coefficient in the Stirling equation determined?
The Stirling equation is expressed as follows
$J = Kf ([Pc-Pi] - σ [πc - πi])$
Here, capillary hydrostatic pressure (Pc) and Bowman's space oncotic pressure (πi) favor filtration into the tubule, and Bowman's space hydrostatic pressure (Pi) and capillary-oncotic pressure (πc) .
My questions:

What does σ, or Staverman's reflection coefficient, in this equation mean?
And by what logic or method is it determined?

References:

https://www.ncbi.nlm.nih.gov/books/NBK500032/
https://pcwww.liv.ac.uk/~petesmif/petesmif/why%20do%20we%20need%20kidneys/bowmans%20capsule.htm

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What kind of tree is this (Seattle, WA)?
This tree is a volunteer and I am hoping to find out what kind of tree it is.
Young tree

Leaf sample

Below is a more recent photo showing flowering.

Could you provide more information? Are there veins on the leaves? If so, how do they run? How big are the leaves (perspective with the camera is hard to tell how big the tree is in general)? Are there flowers? Anything budding? The more information, the better someone can identify the tree for you

The kind of leaf is typical of Fabaceae (https://en.wikipedia.org/wiki/Fabaceae).

It looks like a Laburnum. Probably a Common Laburnum Laburnum anagyroides, also known as a Golden Chain Tree. It is from central and southern Europe.
The seeds are poisonous.
https://en.wikipedia.org/wiki/Laburnum_anagyroides
Here is a photo of the leaves

From http://www.saps.org.uk/trees/laburnum.htm
And the flower

http://wildflowerfinder.org.uk/Flowers/L/Laburnum/Laburnum.htm

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Why does a lightsource postpone the time it takes for the leaves falling from a birch tree?
It is autumn and the leaves have already left their trees on all birch and other trees that has leaves, except one. This birch has a spotlight pointed to the tree and it is on 24/7. I have recognized that this birch have lost almost no leaves. And if we take a closer look at this birch, the back side of the birch, which is faced away from the spotlight have lost a noticeable amount more leaves than the front side which is directly hit by the light from the spotlight.
My conclusion is that having a lightsource pointing to a leafy tree will postpone the time from when it loses its leaves, relative to trees that does not have a lightsource pointerd at them.
 But I have no idea why this is happening. I do not know anything about trees, leaves, chloryphyll or the reason why trees drops their leaves in the autumn.
If any one is a expert in this field and might know why this is happening, or just have a hypothesis of why this is happening please provide it since I find this really interesting and I can't find anything on Google about this phenomenon.
You can make your anwer as complicated as you wish, I will understand it even if I might need to Google some of the things in the answer :).
Thanks!

Hi, first of all i higly recomment you to take a tour in our help center. Belive me, this provide you with lots of information about this site including valueble price.  About your question if i understod it right you would like know if light source can post pone the deatf of leaves on tree. I higly doubt it. First off all the light source is very dangerous and tricky energy source. So i think it rather be vice versa.

Yes, you have understood my question right. The thing is that I have had  this spotlight pointed at many different trees under many years, and I always get the exact same result. So I have started to see a pattern. Lets say you have 2 trees, X and Y. If i point the lightsource at X, that tree will lose its leaves much later than other trees of the same species, while Y will lose its leaves same time as all the others trees. If I then switch the lightsource to Y another year, Y will lose its leaves much later than the other trees and X will lose its leaves the same time as the other trees,

Don't really have time to write out a proper answer, but the basics is: tree's (as well as many other organisms/animals) are able to measure length of a day using light sensitive proteins combined with circadian/rhythmically expressed regulators. This allows trees (etc) to properly regulate physiological functions - like losing leaves -  according to the seasons. Since tree/plants are immobile targeting with a big spotlight will confuse their light sensors and disrupt this system (more than for animals which can/will move away at some point).

The leaves drop because of the sharp drop in temp.
your 'keeping a spot[heat]light on them 24/7'' ,isn't allowing the tree to 'feel' the drop in temp. Therefore keeping it's leaves longer[postponing falltime] .Trees appear to be sensitive to temp.change.
I dont believe trees are 'Photosensitive' that applies to cannabis.

It's to do with the chemistry taking place in the system, and then in turn the balance of energy resources.
Leaves contain chlorophyll, a molecule that traps light energy. It is large molecule containing a long carbon chain and a magnesium atom surrounded by 4 nitrogen atoms. In terms of a plants energy resources it is an 'expensive' molecule, but it is worth it as it is important to the plant.
The conversion of light energy by plants, using chlorophyll, is called photosynthesis. The chemistry of photosynthesis using chlorophyll is complex, but essentially Carbon Dioxide (CO2) from the air is combined with Water (H2O) from the roots to produce sugar and oxygen. Excess sugar is transported to the roots and stored as starch, and some sugar is used to keep the living cells throughout the plant alive. They need energy and this gained through respiration. Again, the actual chemistry is quite complex, but simply put the cells take in Oxygen from the air and 'burn' the sugar to release energy, this gives off Carbon Dioxide and Water. (There is plenty of resources and explanation on the actual mechanism - search for "ATP and ADP in plants")
Notice that it starts with carbon dioxide and water and ends with carbon dioxide and water, the energy is held within the chemical bonds.
When there is plenty of light (and water) the rate of photosynthesis, and therefore the rate of energy production, is high. The plant is producing excess energy, and the leaves are 'worth' the energy needed to keep them alive and functioning. Note that temperature also has an influence. The warmer the temperature (to a point) the greater the rate of photosynthesis.
So, in temperate climates with markedly different day lengths and temperatures between the summer and winter seasons some plants have evolved to be deciduous and shed their leaves in the autumn. The point at which this will start to happen will be when the day length shortens, and the temperature drops, and so when the amount of energy that the leaves are able to produce starts to balance the amount of energy being used to maintain the leaf.
If a plant has an artificial light source then the leaves will continue to be able to produce more energy than they use and so will be retained for longer.


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What is the name of this big tree with look of banyan branches?
Location is India, Tree is so huge & some branches are hanging like Banyan.

Its Hanging Branches look:

& Finally its leaf:

So what is it then?

Looks like a fig, it has large number of species.

Did you find any fruits of the same?

Looks like Ficus, maybe F. benghalensis

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Is this a young Ash Bud Moth (Prays fraxinella) caterpillar?
I am building up a my knowledge of organisms that live on trees (not necessarily as pests, but in the respect of the biodiversity that depend on different tree species) and their interactions.
Living on the underside of Fraxinus excelsior, in northern Europe (N. France), I have found these tiny caterpillars (end of May/start of June). They are eating small patches of the leaf, and excreting black frass.

The ash leaf in this photo is 70 x 35 mm, and so the caterpillar shown in approximately 1 mm in length, but there are others up to 2 mm.
The photo above also shows the mines in the leaf.
Under a hand lens, the body is an opal/beige colour and it has two black patches on the body above the head. The body is very shiny and glossy and it looks wet.

From my internet research it looks like a young caterpillar of the Ash Bud Moth (Prays fraxinella)?

I probably need to invest in a good macro lense for my camera

Since nobody seems to answer your question, I think you need to wait for another week or two. They will eventually mature and it will be easier to identify them.

Yes thanks, I am keeping an eye on them and will track their progress. I already have a photo of one twice the size which I can add to the post.

Every time you add a picture, your question is modified and it gets bumped up on top of other questions. If you have many pictures of you lovely green creature, don't post them all at once, add one picture per day. This way more people will be able to view your question and sooner or later somebody will be able to answer it.  Just a helpful tip.

Stereonychus fraxini (De Geer, 1775)

Well, that would explain why after returning from France to the UK, I haven't been able to find the larvae here. Perhaps this species has no yet made it across to the UK? I am familiar with ash bud moth, so I would have expected to find the larvae here. Interesting though how the Wikipedia Prays fraxinella caterpillar looks like an older version of the Hungary Forestry Institute images they name Stereonychus fraxini. I'd probably ere on the side of the latter, and agree with you. But yes as @theforestecologist says it would be good to provide some sources to back up your answer please.

I have been doing some further looking into this and came across a video of Prays fraxinella, feeding as a leaf-miner https://www.youtube.com/watch?v=LqL6LKEg05k&feature=youtu.be linked from this page http://www.ukflymines.co.uk/Moths/Prays_fraxinella.php so yes, this increasingly looks like Stereonychus fraxini


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Reformulation of Hamilton's rule
Who (and in which article) was the first to reformulate Hamilton's rule using the letters $B$ and $C$?. See below comments on this reformulation.
Hamilton, in his 1964's article gave a mathematical formulation to explain the direction of social traits. Below is its formulation. Note: Hamilton used quite a complicated formulation, I hope I am not misunderstanding its meaning. Please let me know if it is the case.
$$R\cdot\frac{dw(x,y,z)}{dx}>\frac{dw(x,y,z)}{dy}$$ where $R$ is the coefficient of relatedness which can itself be expressed as a correlation between the variables $x$ and $y$. $w(x,y,z)$ is the fitness function of a focal individual expressing trait $x$ and interacting with an individual draw from a subpopulation expressing trait $y$ (expected value of the probability distribution of trait expression of individuals in the subpopulation) in a population expressing trait $z$ (expected value again).
Most often this formula is expressed in the following form:
$$RB>C$$
$B$ and $C$ are called cost and benefit of the social trait. I believe that $B$ and $C$ are often not understood as a consequence of a change of the social trait but rather as a cost and benefit of carrying the social trait (compare to not carrying it).

Interesting question but since B and C basically strip the idea of a lot of mathematical content, isn't it possible that the first use was, say, in a graduate text for non-mathematicians to give a sort of quick idea? That would be hard to track down I bet.

@daniel Yes that's possible indeed! One thing that got me interested into this question is that $B$ and $C$ are usually conceptually understood a bit differently than $\frac{dw(x,y,z)}{dx}$ and $\frac{dw(x,y,z)}{dy}$ and I am wondering how the first guy has somehow argued for this new understanding of Hamilton's rule.

Tracing it backwards this was the earliest reference I found via google scholar, it's from 1988 and uses the $r B C$ notation in the format we are used to.

Hamilton's rule states that for a social
  action to be favored under natural selection, rb - c > 0, where c is the cost to the
  actor in terms of the effect on (usually a reduction in) his expected number of
  future offspring, bis the benefit to the recipient in terms of the effect on (usually
  an increase in) his expected number of future offspring, and r is the relatedness of
  the actor to the recipient

However, I've traced back a bit further by going through the references and found this Michod paper from 1978 where they defined terms $b_i$ and $c_i$ as the

"fitness effect of genotype $i$'s behaviour on others"

and,

"fitness effect of genotype $i$'s behaviour on self"

respectively, which was the first such notation I could find which could be interpreted as $b$ = benefit via the increased fitness of others and $c$ as a cost to self.
As far as I can tell this leaves a 14 year gap between Hamilton's long version and the beginnings of the current notation by Michod in 1978, with the first "rB - c > 0" type of notation appearing in 1988. Obviously my search is not exhaustive - many papers from this period will be hard to find and text search (e.g. using "rB" as a search term) - but it's a good start. If I find an older reference any time I will update.

(I will try to examine the papers further to try to find both "r = relatedness, b = benefit to recipient, c = cost to provider" and "altruism will evolve if rB>C" types of statements, but that will have to wait - It's quite laborious, even this much took over an hour, and I have a long list of jobs to do by Friday!)

Nice work. Thanks a lot Robert! Michod in his abstract talk about kin selection theory as the cost-benefit rule as if it was obvious to other people that kin selection theory is a cost-benefit rule. I should check Hamilton's paper to see if he himself used the word cost and benefit.


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Why are some housekeeping genes considered better?
Whenever a PCR is done, we have to use housekeeping genes like GAPDH, to self normalise the values to account for different starting cDNA/DNA. Now there are many different genes like GAPDH, ubiquitin, actin etc.
Now when dealing with cells, I can understand that due to their immortal nature and frankly shocking number of generations undergone by them, the expression of the housekeeping gene may change.
Assuming that I am not dealing with cells and instead with animal tissues, does it matter which house keeping gene I select? Or in other words is GAPDH going to give me the same consistency between samples as something like 18s Ribsomal RNA or am I missing something specific?

Yes, it does matter. Gene expression varies a lot thoughout tissues and living conditions, so you need to test a variety of genes and choose the ones with the smallest variation in the expression between sample and control.
If you don't find any, you have to test other genes for this purpose. This is important, as this can severly affect the outcome of your experiment, since you normalize to the housekeeping genes. If these are not constant, it will cause problems. Have a look into the references, this helped me a lot.
References:

Accurate normalization of real-time quantitative RT-PCR data by
geometric averaging of multiple internal control genes.
The normalization of gene expression data in melanoma: investigating
the use of glyceraldehyde 3-phosphate dehydrogenase and 18S
ribosomal RNA as internal reference genes for quantitative real-time
PCR.
Normalization of qRT-PCR data: the necessity of adopting a
systematic, experimental conditions-specific, validation of
references.

You need to watch out though. Some very used genes could be very uninformative as housekeeping genes in qPCR. ACTB and GAPDH have tons of pseudogenes (analogous genes not yielding proteins) that can interfere with the PCR. You can read more in this article (1).
To make it even worse, the PCR amplification fragments can be of the exact same length as the ACTB amplicon, making it impossible to differentiate.
In addition, you have to consider the specific cell type/application/treatment, because some mRNAs could be very constant through treatment A on cell type 1, but vary with treatment B or on cell type 2.
I think the best would be to use multiple housekeeping (3-5) and see how they behave relative to one another. You could also use the mean of these housekeeping.
(1) Sun, Yuan, et al. "Pseudogenes as weaknesses of ACTB (Actb) and GAPDH (Gapdh) used as reference genes in reverse transcription and polymerase chain reactions." PloS one 7.8 (2012): e41659.


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Is the male satin bowerbird's bower-building behavior innate?
The male satin bowerbird builds a stick structure, known as a bower (distinct from a nest), where courtship and mating take place.  They curiously decorate their bowers using blue or shiny objects.

(Image source: Wikimedia commons.)

When courting, the male satin bowerbird prances and struts around his bower. He offers the female items from his collection of blue objects, while making a series of hissing, chattering and scolding noises. Mating takes place in the avenue of the bower, and the male may mate with several females in a single season.  -- NSW Government Office Of Environment and Heritage

Question: Is the male satin bowerbird's bower-building behavior innate?
This is essentially a "nature vs. nurture" question.  E.g. If there were no other males around for him to learn it from, would he still build a bower?  If so, where did he get the idea from?  If there were no females around, would he still bother to build it?

Does your question allow for both possibilities simultaneously (nature and nurture)?

I guess it has to allow for both, as it could be the case.  (Mentioning nature vs. nurture was just to convey the spirit of the question; I'm not seriously suggesting these are the only two possibilities.)


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What do oxpeckers eat from thick-skinned hippopotamuses and rhinoceroses?
Noted for their thick skin are both rhinoceroses (1.5 to 5 cm) and hippopotamuses (6 cm).  They are further noted for their symbiotic relationship with bird called an oxpecker:

Both the English and scientific names arise from their habit of perching on large mammals (both wild and domesticated) such as cattle, zebras, impalas, hippopotamuses, or rhinoceroses, and giraffes, eating ticks, small insects, botfly larvae, and other parasites.
Oxpecker, Wikipedia

I feel like the thick skins of rhinoceroses and hippopotamuses would make them invulnerable to many parasites (such as those listed above), so I'm interested in finding out more specifically what oxpeckers eat from the skin of these two mammals.
Question: What do oxpeckers eat from thick-skinned hippopotamuses and rhinoceroses?
In the case of hippopotamuses, I feel like their semi-aquatic lifestyle would further impact many parasites.

I think you should (re)read that Wikipedia article — later on it says "They feed on ectoparasites, particularly ticks, as well as insects infesting wounds and the flesh and blood of some wounds as well. They are sometimes classified as parasites, because they open wounds on the animals' backs." There are also numerous references at the end of that article including at least one about rhinos ...

Thanks!  I admit it, I didn't read that part of the Wikipedia page prior to posting.  Although I'm still uncertain as to how oxpeckers use them as a source of ticks despite their thick skin, and, in the case of hippopotamuses, being submerged for large amounts of time.

That's the point — they appear to primarily use them as a source of blood. Think of them as little feathered vampires.

many is not the same as all


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Is this Weigela?
A work colleague found this growing in a Northumberland (UK) woodland (May 2018), took a photo and sent it to me.

It was in an area with non-native species, and this was growing as a shrub. It doesn't spring out as being native to the UK to me?
The leaves are hairy, not waxy. The photo shows a collection of, what I have confirmed, are buds.
If I had to compare it to anything I would say it looks like a Weigela?

Could you please post a different picture of a leaf and a flower up close and in better lighting? It's really hard to see.  It looks very similar to a bush that grows around there. Thanks.

Unfortunately, it's all I was given by a colleague. I'll ask her if she will ever be going to the location again, or can ask another to provide another sample.

The bush that looks like this one is one of the aronia varieties. If the picture was a bit lighter, I could have compared them better. The only difference is that the regular aronia is a shrub with clusters of berries/flowers, and the bush that grows here is very short and has only a few flowers. But I am sure they are related.


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What makes a bacterium move away from a neutrophil cell?
In this video we see a bacterium seemingly moving away from the neutrophil that is chasing it. What mechanism makes it "want" to avoid the neutrophil? It doesn't seem to mind being around other cells of the same organism. Why does it react differently to a neutrophil?

In the video doesn't it look like it's just moving passively in the solution? As the neutrophil moves around it displaces solution that has to go somewhere, and the third dimension is impeded on the microscope slide. Like when you try to scoop something from your soup and it gets pushed away by your spoon.

yes, it seems it does. This makes the question obsolete


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Identify brain junk - What are all the known intracellular and extracellular substances which build up with age and clog the brain?
What are the known junk substances which the body is unable to dispose of and which build up in the brain with age to eventually causes age related problems?
Starting with the most obvious ones:
Amyloid beta - https://en.wikipedia.org/wiki/Amyloid_beta
Lipofuscin - https://en.wikipedia.org/wiki/Lipofuscin

I'm voting to close this question as off-topic because a group effort to draw up a list is not a question in the terms of SE Biology.

@david it would be valuable info to have it all in one place, don't you think? I reworded the question

It may well be, but that place is not here — this is a site for answers to specific biological questions. I could perhaps also have voted to close on the basis that your question was too broad, but I thought your misunderstanding of the way SE works needed addressing.  Imagine there are reviews on this topic by people far more expert than those on this list.

Another example is the paired helical filament of Alzheimer's disease, so-called because neurofibrillary tangles have a ribbon-like structure when viewed under the electron microsocope.
It is now accepted that paired helical filaments consist of a single protein, microtubule-associated protein tau, in a polymerized and hyper-phosphorylated state. (see Lee and co-workers).
This old answer might also be of interest and contains a fuller reference list.
Neurofibrillary tangles are one of the two characteristic lesions of brain first described by Alzheimer, and are intracellular. The other characteristic lesion is the extracellular neuritic plaques caused by the build up of amyloid-beta (as the OP points out), which is itself part of a much larger transmembrane protein (of unknown function), the amyloid precursor protein or APP.

RNA-binding proteins TDP-43 and FUS form aggregates that accumulate in the cytoplasm, whereas these proteins would normally be predominantly soluble within the nucleus and shuttling to and from the cytoplasm. - https://www.ncbi.nlm.nih.gov/pubmed/23463272/


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Would a VR headset exacerbate myopia or could it be used to retrain the eyes?
I've learned that there are two primary hypotheses to explain myopia: not enough use of distance vision or not enough sunlight
If the distance between an eye and what it's focusing on is the primary cause, then having a VR screen inches away would seem like a recipe for exacerbating myopia.
However, since people with 20/20 vision can use VR headsets, while others need the maximum correction and still see everything out of focus, clearly there is something more than at play than simply focal distance between the eye and the screen.  Could this be used to help minimize, prevent, or possible reduce myopia?
Likewise, if the cause is primarily lack of sunlight, could sunny simulations be used to help minimize, prevent, or possible reduce myopia?  Or is the light produced too artificial?
Knowing that myopia is on the rise, and VR is going to be more prevalent in the near future, these seem like important relationships to understand.
Of course, it could be they are simply two factors of many; but they are extremely relevant to this question.
More recently, my ophthalmologist was adamant that I needed to follow the 20/20/20 rule, i.e. every 20 minutes focus on things more than 20 feet away for at least 20 seconds, which leads me to believe he at least subscribes to the distance hypothesis.

Personal medical and health questions are off-topic for this site.

This would make an interesting question when all reference to self would be removed. Voted to close but +1 for the question.

I made some edits to the phrasing of the question. Please check if this still reflects your intentions and rollback if required.

@MarchHo - Thank you.  That reflects my intentions perfectly!

When using VR headset your eyes focus on distant objects, not on the screen, that's the power of optics!

@szulat If you can find a citation for that, it would be a good answer. I am rather skeptical of that claim though.


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Drosophila grey / yellow
I am studying biology by myself via distance-learning. I have been trying to solve the following problem for a while now and hoped you could help me. As this is "homework" I would appreciate hints rather than solutions.

Drosophila has a gene "yellow body", $y$, on the X chromosome. The other, dominant, allele is "grey body", $y^+$.
When crossing female grey bodies  with male grey bodies we get 50% grey females, 22% grey males and 28% yellow males.
What is the genotype of the parents?

My work so far:
The genotype must be $Xy^+X?$ for the female and $Xy^+Y$ for the male.
There are two cases to consider: $?=y^+$ or $?=y$.
In the former we get $\frac{3}{8}$ grey females and $\frac{1}{8}$ yellow females and $\frac{2}{8}$ grey and yellow males each; that seems correct except for the yellow females.
In the latter, we get twice as many yellow females.
Perhaps the XXyy (yellow females) genotype is lethal but this doesn't help in determining the parents' genotypes.
If $? = y$ then cross-over from $Xy^+\mathbf{Xy} \; x \; \mathbf{Xy^+}Y$ would not eliminate yellow females.
I don't know of other effects to take into account, so I am stuck.
$ $
If you'd like to suggest resources (websites, textbooks $\ldots$) pertaining to this subject or on biology at this level in general, I would very much appreciate it.
Thank you.

Edit: I'd like to add an image for anyone having a similar problem.

Since Drosophila have the same system of sex chromosomes as human beings, (XY males and XX females).  Its clear that the sex determination is important - no females have yellow bodies. This is the key observation.
Amongst the males you have about 50%/50% Y/y phenotype.  This appears to be a classic sex chromosome related trait.  Does this help?  I can go further, but this should get you there.

Thank you for your answer, it did help. I made the problem more complicated than it is, the answer seems obvious now.

great to hear!  it takes some practice to get into this stuff !

@user34914 Although for your question, you can use the same system of sex chromosomes as human beings' , it actually is  more complicated. It also depends on autosomes. See this wikipedia article.

@user34914 Genetics - by Ursula Goodenough is an excellent book for studying classic genetics.


text:
What plant/tree is this?
Found this in a rural area next to the road last month and I wonder what is it?

From my searches I think it is a strawberry bush but I'm not sure and any help would be appreciated, thanks!

Add the site of your pictures? It might help you get a precise answer.

I took the pictures

Your pictures are a bit vague, but I think recognize Euonymus europeus, the spindle tree. So I assume the picture comes from Europe? The fruits are encapsulated in pink capsule, the fruit itself is bright orange.
https://en.m.wikipedia.org/wiki/Euonymus


text:
Identification of a bug in Vasai, India
Can someone please let me know what insect this is?
This may be something very common, but this is the first time I have seen them and that too suddenly in a large number.
They were mostly on plants, but the only clear image I got was of the one sitting on this bike. Image captured in Vasai, India

(Brought into Biology SE from https://i.sstatic.net/RHcrg.jpg)

It looks like Oides andrewesi.


text:
Where in this photo can I find archaea?
This photo is from Guide to the Six Kingdoms of Life under Archaebacteria:

It's not obvious to me where I can find archaea in this photo, although the website seems to indicate it's clear.
Question: Where in this photo can I find archaea?

It's probably the yellow bacterial mats, which are rich in life. The mats are a stratified ecology which varies with distance from the surface, so they are rich in many species of algea, procarote and eukariote. In Yellowstone,  the bacterial mats can range in color including brown, green, yellow and orange. They are different to precipitated minerals.
You can say "The photographer contains archaea"! So, no need to search very far.
Here is a pic of an bacterial mat habitat: https://www.sciencedirect.com/science/article/pii/S0717345817300738
You can see in some videos. Ideally we would have a a biology video demonstrating the stuff at Yellowstone to show if it's squishy, slimy, spongey, has growth rings, colord layers, cross sections... although it's only tourist videos for the moment.


text:
Dealing with Repetitive Bases in DNA?
I have been given a project involving a plasmid that contains long stretches of Adenine (60 or 120 bases each). These PolyA stretches are interrupted by the occasional G or C.
I understand that performing PCR, cloning, DNA synthesis, mutagenesis, and sequencing on repetitive sequences is difficult. What techniques and practices should I follow to improve the accuracy when dealing with these PolyA sequences?

What exactly are you trying to do with this plasmid (more spef. this PolyA tail). Do you need to amplify it, digest it etc... depending, different strategies can be implemented to minimize error with the polyA tail

@AdamRadekMartinez Let's say I wanted to replace those interrupting G's with an A. How does site directed mutagenesis work when you have more than 1 potential site? How do you sequence the DNA to verify that the mutation worked?

You can use much longer primers (up to 70bp or so), such that they span the repetitive region you want to change and some more specific sequence to anchor the primer (assuming your vector allows). If the multiple sites you want to change are within range of one another, you can order primers with 2 or more mutagenised sites - though expect your efficiency to drop. Your other option would be to do multiple rounds of mutagenesis, altering one position at a time.
I would then simply try these primers on a gradient PCR using a good enzyme like NEB's Q5. Trying to find a temperature for the correct size band will likely be key.
The real problem you're going to have though probably isn't the cloning, it'll be proving it. Homopolymer stretches are a real problem for sequencing, and the longer they get the worse it is. Automated sequencers find it difficult to tell between, for instance, 29 Adenines, and 30 adenines in a row. When your sequencing results are returned, if your sequencing is off by a base or two, it will be pretty much impossible to tell if your sequencing was wrong, or your construct was.

Okay, one of the main problems with polA tails is with PCR, which is a method commonly used in molecular cloning, specified mutagenesis etc...
One problem with PolyA tails and PCR is with the primers. Since A's only have 2 hydrogen bonds, instead of 3, this can make it hard to design good primers in this area. If you want to amplify this region using PCR, you may have troubles designing primers since it is recommended that you have a lot of G and C's (espically near the ends for stability). Thus, creating blunt ends, mutagenesis etc will be more difficult.


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Protein function and how it does not get affected with amino acid
How is it possible that a protein's function is not changed when an amino acid within it is replaced?

Good question. But it’s your homework, so you’re the one who is supposed to answer. Read the Tour and the Help on Homework questions.

The side chains of some amino acids are not reactive and therefore not involved in any covalent chemistry in enzyme active centers.
Isoleucine, an essential amino acid, is one of the three amino acids having branched hydrocarbon side chains. It is usually interchangeable with leucine and occasionally with valine in proteins.
Typical amino acids and their alternatives usually have similar physicochemical properties.
Amino acid replacement is a change from one amino acid to a different amino acid in a protein due to point mutation in the corresponding DNA sequence. It is caused by nonsynonymous missense mutation which changes the codon sequence to code for another amino acid instead of the original.
The effects of amino acid replacement may vary depending on how similar or dissimilar the replaced amino acids are, as well as on their position in the sequence or the structure.
References:
http://www.biology.arizona.edu/biochemistry/problem_sets/aa/Isoleusine.html
https://en.wikipedia.org/wiki/Amino_acid_replacement

Please do not answer obvious homework questions where the poster has made no attempt to answer himself.  That is against site policy and, in effect, you are helping the poster to cheat.

@david you seem to be on a mission when it comes to new users. I understand you have good intentions in mind but maybe your actions could be a double-edged sword which on one side cleans SE up but on the other side sterilizes if from new users. Is your subjective opinion that this is a homework post. I like the question so I answered. Did the question/answer set make SE a little bit richer place? You could have suggested to edit the question or something

— I do not normally respond to personal remarks: I just flag them to the moderators for deletion. However as you are a relatively new user, let me explain to you something about how SE works. It is regulated (for want of a better word) by its users, according to their status in the list. Elected moderators are the final adjudicators, and in this case I imagine one of them closed the question quickly. Users who have accumulated a certain number of points are asked to help by considering close votes, commenting to new users etc. That is what I was doing — my civic duty.

@David can be a bit cranky and blunt, and I do wish he would work on being more welcoming, but I think most of the time he's correct even if the message could be delivered differently. In this particular case, I think the question is a clear homework question, and unfortunately, people that ask a question like this are likely to just copy paste from your answer into the box on their quiz and not learn anything: that's why Biology.SE has a homework policy that differs from some other SE sites. Here's a good meta thread: https://biology.meta.stackexchange.com/questions/3377/homework-questions

@BryanKrause I understand and agree. However:) different biology enthusiasts are on different educational level. A layman or a teenager's question might come off as homework attempt. I realize that I won't change anyone's mind but since we are talking about it - Instead of making people feel unwelcome, how about answering all valid questions which don't contain "help, homework, urgent keywords" and then in the future close the obvious qeustions as duplicate. Having the obvious question/answer sets would bring a lot more search engine traffic and make this place bigger, richer.

@TardiGrade I think it's explained well in that meta thread, so I don't want to rehash it here, but tl;dr: because answering those questions does active harm. I consider it unethical to help people cheat, especially when the person they are cheating the most is themselves. We are happy to help people with their homework when they've demonstrated effort. If you want this policy to change you can make a case on Meta.


text:
What is this insect that I found under my bed

Found it under a hotel bed in Las Vegas, what is it?

That is a cockroach nymph. Don't worry, not a bedbug.

Added info about the city. Thanks Karl for the info, I started looking when I noticed a lot of what looked like bites on my legs and some on my arms and it reminded me of the time when I had a bedbug problem about 10 years ago. Couldn't find any in the beds though.

A size scale would be very helpful here

It is a Madagascar hissing  cockroach. They are native to Africa, particularly Madagascar. In the U.S. these roaches only invade homes when accidentally brought in via imported furniture or food, although some people do keep them as pets.
https://en.m.wikipedia.org/wiki/Madagascar_hissing_cockroach

-1. I don't think you're correct. Please provide additional support for your answer. I agree that the OP's specimen is a roach, but the appearance and size of the OP's specimen do not match a madagascar hissing roach. Further, finding a single, random MHR in Las Vegas is unlikely. Please update your answer with additional pieces of information that more definitively match your ID. Thanks.


text:
What's the meaning of the label MRE and a number like 162 or 600 in the names of bacteria?
I've stumbled across labels like E. coli MRE 162 or E. coli MRE 600 for different kinds of E. coli bacteria.
What's the meaning of MRE and the numbers like 162 or 600 in this context?

Interesting, I think it must be a strain/isolate designation, but I couldn't find any listing that mentions whatever collection "MRE" stands for ...

Have you checked out my answer? If it answers your question satisfactorily please accept it. If it does not, please indicate what is lacking.

MRE is an acronym for the Microbiological Research Establishment at
  Porton Down, UK.

It was applied to Escherichia coli strain MRE600 as that was where the strain was first deposited, according to this paper.
I tracked the answer down in an article by Chris Morris on the Culture Collection Page of Public Health:
“My association with Porton Down, the current location of the European Collection of Animal Cell Cultures (ECACC), started at an earlier date than the inception of ECACC, and was when the site was known as the Microbiological Research Establishment (MRE), part of the Ministry of Defence.”
The numeric portion of the strain designation (600 etc.) that follows MRE is presumably just a reference or accession number within the institute, with no biological meaning.
(As a matter of interest, Porton Down had a certain notoriety in Britain back in the ’60s as a secret military establishment.)


text:
Blood serum transfusions - could vaccines against the anti-A/anti-B etc. antibodies be derived, at least in theory?
People with the AB-positive blood type have all three of the A, B and RhD antigens present on their red blood cells, and no antibodies to these in their blood serum (aka blood plasma.)
This means that they cannot receive blood serum transfusions from people of other blood types, as their serum does contain these antibodies. In general, a person's blood serum contains antibodies for whichever of the A/B/RhD antigens are not on their blood cells, and no others.
Otherwise, an acute haemolytic reaction would occur.
The most-upvoted answer to another question on Biology.SE used a quote from Dean's "Blood groups and red cell antigens", chapter 5 to explain why these antibodies were present:

ABO antibodies in the serum are formed naturally. Their production is stimulated when the immune system encounters the "missing" ABO blood group antigens in foods or in micro-organisms. This happens at an early age because sugars that are identical to, or very similar to, the ABO blood group antigens are found throughout nature.

In a hypthetical future situation where the demand for blood serum transfusions was high, would it be possible to vaccinate young AB+ children against these antibodies? I'm thinking of injecting proteins similar to the antibodies, to train the immune system to produce "anti-antibodies". The memory-B cells would hopefully produce these fast enough and in large enough quantities to destroy the original antibodies and prevent ill-effects when a transfusion was given.
Would such a vaccine be feasible?
If not, would an immunisation relying on very small quantities of the actual antibodies (not enough to damage/agglutinate significant numbers of red cells) be viable?
I'm aware that if/when such antibodies pass through the placenta, they can lead to haemolytic disease of the newborn, so a newly-born child might be too young to receive such a vaccine. I'm imagining a situation where the number of such antibodies would not be high enough to cause these complications, or where the fake antibodies would not bond to the red cell antigens.
Source:
Dean, L. (2005). Blood groups and red cell antigens. 1st ed. Bethesda, Md.: NCBI.


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The emergence of Phengaris butterflies from ant nests
The butterflies of the Phengaris genus (also known as Maculinea) are known to be brood parasitic. During the fourth instar, the caterpillars leave their food plant and mimic ant larvae, causing the ants to take them back to their nest as if they were ant larvae that had escaped.
While in the nest, the caterpillars mimic ant larvae by means both of surface chemicals and acoustic mimickry (including, I understand it, mimicking sounds made by queens!) After pupating, the pupa continues to engage in acoustic mimickry, although I can't find any reference to whether it does (or even could!) engage in continued chemical mimickry.
But I can't find anything in the literature regarding the adult butterfly's emergence from the pupa and exit from the ant nest. A non-academic book and some web pages claim that the alcon blue (Phengaris alcon) and mountain alcon blue (Phengaris rebeli) adults are no longer engaged in any form of mimickry at this point, and may be attacked by the ants. These accounts differ as to how likely an attack is, how much danger the butterfly is in, and the level of protection afforded by the butterfly scales.
The webpages I mention belong to a University of Copenhagen researcher (Dr. David Nash) who has published work in this field. This suggests that the claim is probably correct.
That said, none of the peer-reviewed publications coauthored by him appear to mention it, and each of the two webpages creates a different impression as to the level of danger involved:
"If an ant tries to bite the butterfly it will only get a mouthful of scales." states one, suggesting that there is little the ants can do to harm or hinder the butterfly. But the other states "The adult has to get out of the ant nest quickly to prevent the ants killing it."
The book is written by someone else. It cites three papers, which do discuss the larvae/pupae and ants. But none of these have any information regarding this specific topic.
A paper by Elfferich provides some information in the case of Phengaris nausithous, the so-called "dusky large blue". The author states: "The butterflies always emerged between 00.00 and 06.00 and walked out of the nest ... During the night there was only a little ant activity and there was no real aggressive behaviour ... we may conclude that no pheromone to reduce aggression of the ants is produced by the butterfly."
Some published books (not from the academic literature) claim that the "large blue" (Phengaris arion) continues acoustical, and (according to one book) chemical mimickry. Far from being in danger, two of the books claim that they are escorted outside by ants as though they were acting as a bodyguard!
I believe that this is probably true. The reason for this is that two of the books (pub. 2008 and 2010 were describing discussions between the authors and Jeremy Thomas, an Oxford professor who has published research in this field. In fact, Professor Thomas's research identified the butterfly's dependence on ants, the reasons for its decline in the UK, and he was able to reintroduce the species after it became extinct in the UK. The other book (pub. 2014) mentioned Professor Thomas repeatedly, and described a book by him as "One of the essential wildlife books".
Even so, I don't have access to material in which Professor Thomas or any of his colleagues actually state this instead of just being mentioned by others. So it's still second hand information covering only one Phengaris species.
And to complicate matters further, in a paper that predates the three books, Thomas and other researchers stated that Phengaris arion and Phengaris teleius (scarce large blue) adults "show no interaction with ants after eclosion from pupae in the outer cells of Myrmica nests, from which they emerge while the ants are quiescent in the early morning".
Does anyone know of any peer-reviewed sources which confirm, for the various species, whether:

The adult butterfly continues to engage in mimickry?
Whether this is chemical, acoustic, or both?
The ants are more likely now to realise it's an intruder, and may attack it?
How likely this is?
How much danger are the butterflies in, if so?
Some accounts claim that the alcon/rebeli has scales which make it impossible for attacking ants to grasp them. Others refer to the scales protecting them from being bitten. If these attacks are a risk, how well is the butterfly protected and do attacks from angry ants still get through?

I've looked at too many papers to list here, but my sources include:
Non-paywalled:
Barbero F, Thomas JA, Bonelli S, Balletto E and Schönrogge K. (2009). Queen Ants Make Distinctive Sounds That Are Mimicked by a Butterfly Social Parasite. Science 06 Feb 2009: Vol. 323, Issue 5915, pp. 782-785. DOI: 10.1126/science.1163583
Thomas JA, Schönrogge K and Elmes GW. (2005). Specialization and host associations of social parasites of ants. In: Insect Evolutionary Ecology: Proceedings of the Royal Entomological Society's 22nd Symposium (Fellowes M.D.E., Holloway G.J. and Rolff J., Eds). 475–514
Als TD, Nash DR, and Boomsma JJ. (2001). Adoption of parasitic Maculinea alcon caterpillars (Lepidoptera : Lycaenidae) by three Myrmica ant species. Animal Behaviour, 62, 99-106. https://doi.org/10.1006/anbe.2001.1716
Akino T, Knapp JJ, Thomas JA and Elmes GW. (1999). Chemical mimicry and host specificity in the butterfly Maculinea rebeli, a social parasite of Myrmica ant colonies. 266 Proc. R. Soc. Lond. B. http://doi.org/10.1098/rspb.1999.0796
Elfferich NW. (1998). New facts on the life history of the dusky large blue Maculinea nausithous (Lepidoptera: Lycaenidae) obtained by breeding with Myrmica ants in plaster nests. DEINSEA 4: 97-102. ISSN 0923-9308
Paywalled:
Elmes GW, Thomas JA and Wardlaw JC. (1991). Larvae of Maculinea rebeli, a large‐blue butterfly and their Myrmica host ants: patterns of caterpillar growth and survival. Journal of Zoology, 224: 79-92. doi:10.1111/j.1469-7998.1991.tb04789.x
Elmes GW, Thomas JA and Wardlaw JC. (1991). Larvae of Maculinea rebeli, a large-blue butterfly, and their Myrmica host ants: wild adoption and behaviour in ant-nests. Journal of Zoology, 223: 447-460. doi:10.1111/j.1469-7998.1991.tb04775.x

One butterfly species at least, Liphyra brassolis, has been observed to use loose scales as a defence immediately after emerging from its chrysalis and while escaping the ant nest. See http://www.boic.org.au/files/Secrets%20of%20a%20Predatory%20butterfly.pdf and https://archive.org/details/butterflies02bingiala/page/456

I've been emailing some of the various researchers who worked on the papers I've cited. Jeremy Thomas and Judith Wardlaw both took time out of their (probably very busy!) schedules to reply, and they sent me very detailed replies as well as copies of papers I didn't have access to. Thanks to their replies, I'm in a position to post an answer to my own question.
Dr. Wardlaw, in the course of her research into the Phengaris rebeli (mountain alcon blue) species, had:

"looked after hundreds of rebeli caterpillars and reared them through pupation to adulthood. I watched their emergence from the ant nests in captivity where they were trapped in chambers together without means to escape. I also encountered many nests in the wild. In natural nests the caterpillars tend to crawl to upper chambers in preparation for pupation and eventual emergence and often these are narrow chambers which do not have huge numbers of workers in attendance. The ants do respond to the squeaks etc of the pupae and attend them; when emergence is imminent - much wriggling and increase in sounds emitted - my clear recollection is that the ants are almost stupefied and disperse away from the pupae - the emerging butterflies are not molested by the ants at all although they may revisit the pupal cases to lick any residual body fluids which may be ejected at the time of eclosion.  When they did encounter the emergent butterflies, I never witnessed any hostility shown to them so whether the scales act as protection or not, didn't seem to be an issue."

Professor Thomas had this to say regarding P. alcon, P. arion, and two non-Phengaris blues:

"The best and most natural film of the adult emergence in an ant nest is the Netflix film "From deserts to grasslands" in their 'Our Planet' series ... by David Attenborough (NB, some of the script they provided him with has minor inaccuracies so ignore the commentary: I was not shown the final script!). There's a sequence on Alcon large blues about 2/3 in. ... It shows the ants quite excited as the adult butterfly begins to break through the pupal case - but always benign and non-threatening - and then indifferent to it when it emerges and crawls to the surface to blow up wings, unaccompanied by ants. That's my observation of P. arion too (i.e. very different from Silver-studded blue which is tended throughout eclosion).   The behaviour with Large Blues is consistent with the possession of a stridulation organ on the pupal case, which produces sounds that mimic the queen ant's, and this will undoubtedly be broadcasting 'I belong here' sounds to the worker ants as the pupal case splits, but not thereafter. We have recordings of this from the Adonis Blue which has a similar organ to the large."

(The Silver-Studded Blue and Adonis Blue have mutualistic relationships with their ant hosts. They are not parasitic. I don't have Netflix so I can't provide a link to that video.)
In the case of Phengaris nausithous, note that the published research by Elfferich (which I quoted in my question) testifies to the same thing. There is no obvious defence mechanism on the newly emerged adult, but it isn't in any sort of danger from the ants, and doesn't need one. Note also the book quote in which Prof. Thomas states that the same is true for Phengaris teleius.
In a comment on my question, I mentioned Liphyra brassolis. This butterfly species also parasitises ants, and does rely on loose scales to defend itself from the ants after emerging. If you follow the PDF link in that comment, it includes photographs of the newly emerged butterfly with these scales. It also includes one photograph of an ant that has tried to attack the butterfly, and so become covered in scales as well.
Those scales are very conspicuous, both on the butterfly and the ant, and there was certainly nothing like them in any of the videos I saw of the Phengaris emergences:
"The Large Blue Butterfly Adopted By Ants" - BBC Earth. This one focuses on P. arion.
An extract from "Life in the Undergrowth", presented by David Attenborough.
Behind-the-scenes of the filming of ants-nest interiors for the Netflix "Our Planet".
I couldn't find a suitably licensed image of the L. brassolis covered in loose scales, so I can't include one in this answer. But as I say, you can just click on the PDF link to see it. In addition, there are some spectacular photos of the butterfly's underwings at:
https://the-butterfly675.blogspot.com/2009/05/another-re-discovery-for-singapore.html
https://www.ifoundbutterflies.org/sp/1094/Liphyra-brassolis
http://www.butterflycircle.com/checklist/showbutterfly/224
http://www.samuibutterflies.com/insects/butterflies/lycaenidae/liphyrabrassolisbrassolis/
The only credible evidence that the adult Phengaris are threatened by the ants is that one, unsupported statement on David Nash's University of Copenhagen webpage. I have emailed Dr. Nash, but have not received a reply. Nevertheless, I am convinced that the claim is not correct.
By contrast, we have a great deal of evidence that the various Phengaris species are not in any danger from the ants after emerging from their pupae, and neither have nor need a defence mechanism based on loose scales. I am confident enough in this that I am posting it as my answer.
As an aside, I also looked up the Ichneumon eumerus parasitoid wasp species, which lays its eggs in the caterpillars of P. rebeli (and maybe also P. alcon, I'm not sure.) After hatching and eating its pupated host from the inside, the adult wasp eventually emerges from the butterfly's chrysalis.
According to a 1993 paper (cited below), the emerging wasp is attacked by the ants! It emits an allomone which causes most of the ants to attack each other, but those closest to the wasp will still attack it. It relies on its armour plating to keep it safe from these as it leaves the nest.
The ants will later show some form of aggressive behaviour toward the empty chrysalis - something they don't do towards the ones that unparasitized butterflies emerge from.
Reference (paywalled):

Thomas JA and Elmes GW. (1993). Specialized searching and the hostile use of allomones by a parasitoid whose host, the butterfly Maculinea rebeli, inhabits ant nests. Animal Behaviour, Vol. 45, Issue 3, pp. 593-602. https://doi.org/10.1006/anbe.1993.1069


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What happens to human dopaminergic reward system once a teenager becomes adult?
I've recently heard a podcast which explained teenage impulsivity and novelty seeking in part by

"Lowering the baseline dopamine activity in the reward system"
"Increase in dopaminergic reward in response to novelty"

I assume that by reward system the author means mesolimbic and mesocortical dompaminergic pathways in the brain.
Here's an article that seems to state similar findings:

Starting in early adolescence and peaking midway through, this
  enhanced dopamine release causes adolescents to gravitate toward
  thrilling experiences and exhilarating sensations. Research even
  suggests that the baseline level of dopamine is lower—but its release
  in response to experience is higher—which can explain why teens may
  report a feeling of being “bored” unless they are engaging in some
  stimulating and novel activities.

The dopamine system here is being compared to the child's dopamine system. I'm interested in what happens to the dopaminergic system once a teenager/adolescent becomes an adult at around the age of 24-25?
I'm looking for insight along these lines - does the reward system of an adult "settle down" and no longer respond to novelty as strongly? Is the baseline dopamine level higher?

This may shed light on why the teenagers response to dopamine changes. Quote from reuniting website

There's much still to learn, but it looks like a number of reward
  circuitry events occur after climax that have the potential to
  desensitize us for a time. First, androgen receptors decline after
  ejaculation, and take up to seven days to normalize. (That means the
  effects of testosterone on the reward circuitry are probably blunted
  for a while, quite possibly affecting outlook.) In addition, opioids
  released during copulation hang around for a while, apparently causing
  lingering declines in oxytocin, which hamper sexual responsiveness. As
  noted above, there is also likely a drop in responsiveness to a
  neurochemical vital to our sense of well-being: dopamine. In effect,
  the brain has changed. It now requires more stimulation to get the
  same pleasure response as before, and sometimes no amount of
  stimulation will truly satisfy—until it recovers. Anecdotal evidence
  suggests that such changes affect both sexes.

The author further suggests that orgasm and ejaculation increase prolactin levels for up to 14 days, during which the brain is less responsive to pleasure and requires novel entertainment or partners to produce pleasure.
From the info on that site, it seems that the 14 day dopamine-affecting cycle following orgasm continues for as long as a person is sexually active (with orgasms). With this in mind, it appears that the adult response to dopamine release is the same as teenagers who are sexually active.


text:
How do I interpret this depiction of dopamine neuron signaling?
I am studying the work of Wolfram Schultz on reward signals. He depicts dopamine reward signals as shown below, which I do not know how to interpret. Each dot represents an action potential in a dopamine neuron, but is each row a different trial of the same neuron, or is each row the activation pattern of a different neuron? And are the bars at the top showing a sum of the count of the action potentials at each time step?
Schultz, W. (1999). The reward signal of midbrain dopamine neurons. Physiology, 14(6), 249-255.

Can you provide a reference? The bars at top are definitely a summed histogram. I suspect with ~90% certainty that the depictions are of one cell on multiple trials, though it is also possible to present simultaneous recordings from multiple cells this way.

From the figure caption for that figure:

Each line of dots shows one trial, the original sequence in each panel being from top to bottom.

The bars at top are a summed histogram. Dots mark the time of spikes (this is called a "raster"). Each line is a different single trial from the same neuron.
(also note: this type of paper is called a 'review' paper, i.e., it isn't original research, although the original research might have been done by the same author. That doesn't mean anything bad, reviews are an excellent place to start understanding a topic, but you should be aware that the figures here are just representative examples or in some cases schematic diagrams. There is a lot of other data behind the conclusions drawn besides these single examples)

Thanks! I was ~90% sure that's what it meant, but I needed confirmation.


text:
What is meant by "50% related to sibling" versus "95% related to chimpanzee"?
Obviously I am more related to my sister than to a chimpanzee, so what do these different percentages actually refer to?
Here is my preliminary research:
https://genetics.thetech.org/ask-a-geneticist/siblings-are-around-fifty-percent-related/
https://genetics.thetech.org/ask/ask395/

Related : https://biology.stackexchange.com/questions/61206/how-can-someone-share-50-of-their-dna-with-their-parents-yet-all-humans-share-9

Possible duplicate of How can someone share 50% of their DNA with their parents yet all humans share 99.9%?

The obvious answer is that the two sources you mention are using "% related" in different ways, and ones which are probably not clearly defined, althoug I cannot tell without a full quote (no, it's not up to us to read the references). On the one hand this site is concerned with questions to specific biological problems rather than correcting popular science on the internet, but, as two users have pointed out by their comments, this sort of confusing statement is widespread. A wider question with a more comprehensive answer would probably be useful, but it may take a little time.

50% related to sibling means that, out of the portion of the genome that vary in humans, you share half of them with your sibling. (if you compared total genetic match not just ones that actually vary in humans you are looking at something closer to  ~99.95% match)  Now because because variations are not evenly distributed and your parents likely came from the same source population you usually share more with a sibling, but recombinations has a random aspect, and sex chromosomes have a large effect as well. So 50% would be the average using the most common methods of comparison, and even then it is only shorthand. It is a calculation more than a conclusion, if you are 50% related to your parents and so is your sibling then the probability calculation is [0.5 X 0.5 = 0.25]  Note this is in humans, other animals use different chromosome distributions which can result in different numbers, bees for instance have haploid males making females siblings far more closely related.
95% identical to chimpanzee means out of all the genetic elements only 5% of human ones are unique to humans (or chimps) and not shared by chimps and humans while 95% is shared by both. 95% is a lower estimate because they are using the strictest comparison.
One important thing to consider is there are many ways to compare genetic variance, consider a book as an example, if I switch 2 chapters is that one change, two changes, or hundreds of changes (by the number of letters or words in the chapters). because criteria are different you get slightly different estimates of difference. In the case of the 95% estimate that would be using the "hundreds of differences" method of comparing. Deleting the sentence "Mary had a little lamb" would be 21 changes using this method. Other methods would consider it only one difference since it is the product of a single mutation.

What do you mean by "out of the genes that vary in humans"? As far as I am aware all genes vary (i.e. exhibit polymorphism) in humans. So it is the polymorphisms that you share, rather than the presence or absence of a gene. On which point, could you quote a reference to support your assertion that 5% of human genes are not present in humans — the article the poster cites refers to differences in DNA, not genes, and recent questions related to this suggest the percentage of unique genes is much lower.

No the vast number of genes in humans have no variation, at least ont ones that survive. The human species actually has remarkably little genetic variation. https://www.ashg.org/education/pdf/geneticvariation.pdf As for the 5% thats what the 95% similarirty means, it means 95% is shared and 5% is unique.

The article is not clear about what criteria they are using for comparison so I used the vaguest term available, genes which has both a laymen and more than one technical meaning. I will edit for clarity.

To your second comment — a vague answer is no good for this sort of question. The point is very confusing, given the number of questions about it, and any answer needs to be detailed and very precise. This is a list for "students of biology", not laymen.

You state the vast number (20,000) genes in humans have no variation. Perhaps you would care to comment on this explanation of single nucleotide polymorphisms (SNPs) from the NIH website, in which it states that there are 10 million in the human genome.

there are 3 billion nucleotides in the human genome, 10 million/3 billion = 0.003 that's less than 1%.

Blue eyes, rhesus A-ve, organ donor compatibility. 1 SNP every 300 bases, which is the length of an 100aa gene. No variation?

when did I say humans had no variation in genes or nucleotides? if you want to read more about the low genetic diversity in humans start here. https://www.ashg.org/education/pdf/geneticvariation.pdf

'Yesterday' (i.e. 10.09.18) John commented "No the vast number of genes in humans have no variation, at least ont ones that survive". Grammatically that means "all". It may be that you meant "most" or "the large majority", but, if so, I still dispute that. And you were talking about genes, not nucleotides, here and in the quotation "of the genes that vary in humans" originally queried. I do not "want to read more" but to have you clarify a point in your answer, the purpose of SE comments.  However the article only confirms my contention that most, if not all, human genes exhibit polymorphisms.

Vast number is not the same as all, It is important you understand the difference if you plan on continuing in the sciences, it is a common phrase. My comment is true for genes and nucleotides. I don't know how you could conclude the article says that, can you state what makes you believe this.

Enough. If you want me to explain the grammar, post that sentence on SE English Language & Usage.

Clarifying language is also a part of the process.  "vast number" is a common scientific phrase used in the source literature, understanding what it means is important. Contingent language is very important in scientific literature and if you are having difficulty with it it would explain why you are having trouble with my sources. Asking you to clarify were in a source you see a pece of information is completely normal, I suspect I know what part you are misinterpreting but it would be presumptuous to just comment on it  without clarification.

I said "enough".

The 95% comparison to chimpanzees is within the animal kingdom. That is, compared to other animals, human and chimpanzee genes have a 95% match. The ratio could be as high as 85% between humans and other mammals such as mice.
On the other hand, within the species, Homo Sapiens, you and your sibling may have only a 50% match of genes compared to other human beings. (That would be true if your parents were totally unalike, say European and African. Often, your parents may have some overlaps or even common ancestors. In that case, you and your sibling will have a better than 50-50 match.)
These percentages represent two different levels of "filter."


text:
Can anyone identify this queen ant?
I caught my first queen but I'm having trouble identifying her. Could anyone help me out? She has a reddish brown body and black legs.

It's important to get a clear picture and to have some sort of scale for species identification.

Probably not very accurately...

It's hard. I'll try to get a better picture tomorrow


text:
How does evolution eliminate problems that only cause diseases late in life?
Humans are vulnerable to heart attacks and strokes. Our modern diet leads to atherosclerosis, this already starts at a young age but it doesn't cause symptoms until an important artery is almost completely blocked or if a piece of plaque ruptures and causes a sudden shutdown of the blood supply to parts of the heart or brain.
However, if people eat like many indigenous people such as the Tsimané do, then they get far less atherosclerosis:

“Most of the Tsimané are able to live their entire life without developing any coronary atherosclerosis. This has never been seen in any prior research. While difficult to achieve in the industrialized world, we can adopt some aspects of their lifestyle to potentially forestall a condition we thought would eventually effect almost all of us.”

Similar results had been found previously, but this then relates to coronary heart disease not merely the presence of atherosclerosis, see e.g. here:

Williams and Jack Davies had shown clinically and pathologically that coronary heart disease was almost non-existent among the African population in Uganda, although Hugh Trowell had reported a single case of coronary heart disease in an African judge. In the Asian community of Uganda, on the other hand, coronary heart disease was extremely common, accounting for almost half of the male deaths in Kampala in 1956–1958.

The question is then how we could have evolved to be almost free of atherosclerosis when sticking to such a lifestyle, given that atherosclerosis doesn't cause symptoms until it has progressed quite a lot, which is typically late in life and that then in the developed world. For indigenous people like the Tsimané it's even less relevant, because they have a much lower life expectancy due to infections.
Nevertheless it does look like our ancestors did evolve such that they didn't get atherosclerosis.

"It does look like our ancestors did evolve such that they didn't get atherosclerosis" Do you have anything to support this peculiar statement?

@David If not, then it would be a massive coincidence that the diet that these indigenous people stick to just happens to yield extremely low levels of atherosclerosis. Note here that it's not just the Tsimané, we can read here: "In the African population of Uganda coronary heart disease is almost non-existent. This statement is confirmed by adequate necropsy evidence. In the Asian community, on the other hand, coronary heart disease is a major problem."

I don't think early man lived long enough to get atherosclerosis, even assuming his diet predisposed him towards this, which I doubt. We get it after reproductive age if our diet disposes us to it. I don't understand what you are on about.

@David The question is precisely about this problem. One the one hand they didn't live ling enough to get atherosclerosis. On the other hand, we now have evidence that sticking to their lifestyle prevents atherosclerosis, if you do live long enough.

I really don't understand you. Are you saying that the diet of native peoples (= prehistoric man) "evolved" to prevent atherosclerosis and you can't understand how selective pressures produced this? Because that's like saying that prehistoric man evolved to have an alcohol-free diet so that he didn't suffer from cirrhosis of the liver. You could argue that prehistoric man evolved to survive on the diet available to him (hence post-weaning lactose tolerance), but that has no relevance how a modern diet affects health.

Is atherosclerosis a specific interest, or just an example? If it's the latter, then Huntington's Disease seems like a good testament to the fact that crippling late-life diseases can definitely persist.

Please read The Blind Watchmaker by Richard Dawkins, it will give you the basic understanding how evolution works. That a certain diet protects against certain diseases does not have to do anything with evolution - it can be (and most probably is) just a random fact. It is possible that tomorrow we invent a completely new diet which by accident will make us highly resistant against let's say the encephalitis - and it will not be the result of evolution.

@HonzaZidek  How do you explain the astronomically low probability that the diet and lifestyle of these indigenous people (not just the Tsimané, also many tribes in Africa) who didn't choose their diet and lifestyles based on any scientific research, just happens to protect them against  atherosclerosis much better than the Mediterranean diet, which is the best scientifically designed diet? This is clearly not a random fact.

@HarrisWeinstein Not per se just atherosclerosis, it's simply that there is now a rigorous result about that. There were strong hints about low levels of atherosclerosis in indigenous populations who survive mainly on a plant-based diet supplemented by only small amounts of meat. Such a diet is likely also protective against bowel cancer, and colorectal cancer. There will of course be many diseases that do occur frequently, but the typical killers of Western people, things like cardiovascular problems, bowel cancer etc. can be prevented by sticking to an indigenous lifestyle.

@David Cirrhosis of the liver is not something that the medical community thought was something most people in old age would get. Atherosclerosis, on the other hand, is something that many doctors still believe is a normal part of a aging process. The Mediterranean diet yields good results compared to other diets, but it doesn't get you close to the results observed in the Tsimané population. And based on other results it would not be a surprise to see similar results in other indigenous groups, it's just a matter of bringing mobile CT scanners to other remote locations.

I am not interested in a discussion of the effect of diet on health, nor is that the purpose of comments on SE. I used the comment feature for what it explicitly says it is for, to try to get you to clarify your question. You did not respond directly to my enquiry, so I have voted to close your question as unclear.

@David Without evolution to not get atherosclerosis, the observation that indigenous lifestyles lead to extremely low levels of atherosclerosis, much lower than what most doctors would have thought possible using any lifestyle choice, would be a massive coincidence.

@CountIblis Just accept that if a diet has good influence on some potential disease, it is not necessarily related to evolution. Your premise is wrong. So your question "How does evolution eliminate problems..." is a nonsense from the beginning. The answer is simple: the evolution has (most probably) nothing to do with your topic.

@HonzaZidek Not necessarily, but that's extremely unlikely. I don't understand how you get to your "most probably" conclusion, given the typical nature of these plant-based indigenous diets. It's not that one has shifted through many thousands of different diets to find one that has good results against one of the many thousands of different illnesses. A typical result in that case would be some weird diet that would have a whole host of side effects that would have good results against a particular disease. Take e.g. the 500 Kcal diet designed to cure type-2 diabetes.

I guess the base question: "How does evolution eliminate problems that only cause diseases late in life?" is very good in general. However the specifics have problems, can you approach your general question with other less controversial example?

How does evolution eliminate problems that only cause diseases late in life?

This is a fantastic question, which still is the subject of intense research. One possibility might be that we age because there is no or little evolutionary selection against diseases late in life (as old people are less likely to produce offspring). As for any active area of research there are several subtleties. You might enjoy starting with the corresponding section on wikipedia: https://en.wikipedia.org/wiki/Evolution_of_ageing#Mutation_accumulation

If people eat like many indigenous people such as the Tsimané do, then
  they get far less atherosclerosis

This refers to another current research domain, which has only been published in the (really good) medical journal Lancet, where the authors themselves state that several questions remain open, see Kaplan et al. 2017.
Yet their paper already reaches to an important conclusion. While one could hypothesize that the difference in atherosclerosis was due to some genetically inherited property, the authors find support for (and hence favor) the alternative hypothesis, that those people generally live a very healthy lifestyle (e.g. normal BMI, no smoking, ...) which reduces the chance of some diseases.

Similar results had been found previously, but this then relates to
  coronary heart disease not merely the presence of atherosclerosis

Though it would be tempting that this observation could come from a healthy lifestyle, there could also be several alternate explanations (for instance one could hypothesize their genome contains something that only is under selective pressure within the region where they live, and that this something just happens to also help against coronary heart disease).

Heart attacks and strokes, and any other diseases that afflict humans after age 35 or so have absolutely no influence on natural selection because for the vast majority of our history, these diseases affect only post-reproductives. Evolution is not a state of advancement toward an ideal, but rather, a mechanism to put genes into the next generation. These genes lag behind our current situation by thousands of years because evolution acts slowly. So evolution still favors characteristics that would have been good for our Stone Age ancestors, who did not live long enough to be weeded out by diseases of old age.

Many of our stone age ancestors didn't survive long enough to reproduce. Those who did could live longer than more recent civilizations.

Heart disease, heart attacks and strokes do not only affect "post-reproductives". They have been known to affect young people too.

Yes, I agree. "Known to" is correct. How many heart attacks do you think happen before age 35? These are due to other problems. Evolution does not act on the elderly.

So, how then did we get adapted to not get atherosclerosis if we stick to the lifestyle of the indigenous people like the Tsimané people, as pointed out here?

Our ancestors did not evolve to not have atherosclerosis. The study you cited in the Lancet stated that it was the diet and lifestyle that protected the Tsimané from hardening of the arteries. Not adaptation, selection or evolution.

I have to disagree slightly about diseases after 35 or so not affecting selection.  There's what we might call social selection.  (Don't know if that's the proper term.)  That is, someone of reproductive age who has healthy older relatives to share the burden of child-raising is more likely to have surviving offspring.

The Lancet article also says that the levels atherosclerosis observed are much lower than the previous record low. Without evolution to not get atherosclerosis, the observation that certain indigenous lifestyles lead to extremely low levels of atherosclerosis, that are much lower than what most doctors would have thought possible using any lifestyle choice, would be a massive coincidence.

@jamesqf. Yes, I agree. The idea that grandparents can help their children and grandchildren survive makes sense. However, this phenomenon may not yet have had time to be fully imprinted on our genes.

The question is then how we could have evolved to be free of atherosclerosis when sticking to such a lifestyle.

If this is really is your question, here is the answer. The answer is not biological, it can be answered just by anyone educated in the basic logic.

It is not necessarily true that "we have evolved to be free of atherosclerosis when sticking to such a lifestyle".

The only fact which might be true (supposed the data are correctly interpreted) is that when sticking to such a lifestyle (and maybe also doing something else? or maybe having some enzymes which other population does not have?), these people are free of atherosclerosis. (There are still a lot of questions, e.g. taking into account that they do not live long and atherosclerosis usually does not occur in young age.)

Hence the question is based on an unproven assumption.
Hence the question does not make sense from the beginning.

The question should have been like this:

Is it caused by evolution, that sticking to a certain diet makes an animal free of a disease? How is it in the case of this specific disease and this specific diet?

Such a question would really be a valid question. However yours already assumes something which is not a proved fact and manipulates the answer.
It just sounds to me as one of the weird "arguments" of vegetarians that "humans are vegetarians by nature".

Ok. And I agree with your new answer, although I have no idea whether you are right about the poster's agenda.

1: Straw man, not literally 100% free but I gave the link where the details are given, and these details are non-trivial as also pointed out in the Lancet article. 2 Follows from 1, therefore based on your Straw Man argument therefore False and 3 does not even follow from 2 and/or 1, so it is totally wrong. Sounds like the argument that "humans are vegetarians by nature"? That's another rhetorical trick to smuggle in a Straw Man argument.

@CountIblis See my edit, straw man!

Important to note that a social species like ours has other sophisticated ways to ensure that its genes survive in the next generation alongside the obvious way of "passing down".
Even after our reproductive phase we can teach our children or even take care of their children, which highly rises their chance to thrive and reproduce.
It is also possible to ensure that some of your genes are safely passed, by helping your brothers and sisters to raise their children while sacrificing your direct reproduction, since you have similar genomes.
So even genes carried by infertile people can greatly affect how their identical or very similar instances in their blood relatives will pass through via advantageous social interactions.
Other:
That the Tsimané people have a low life expectancy now does not imply that it was always true. Maybe those infectious diseases were carried in by Western European explorers and conquerors.
You can research the grandmother hypothesis.
Here is a good paper to start.
Update:
The fact that the average life expectancy was low in the past, doesn't mean that nobody lived long. The infant mortality was very high, so relying solely on a average is not wise. Here is good publication on the subject. Mind the first table which shows the life expectancy of the ancient and medieval elite was close to the common life expectancy of the UK in the mid-20 century.

One of the ways a disease X that typically occur after reproduction can be eliminated is via individuals inheriting some other disease Y that cause health problems much earlier in life that interacts with X. Suppose that the vast majority of the population is genetically susceptible to X. Also, suppose that a small fraction of the population is prone to getting Y at a young age and that Y becomes a lot more severe if you are genetically susceptible to X.
Natural selection then already has led to Y to be suppressed via the genes that are directly responsible for that disease. It may that you only get that disease by inheriting the wrong gene from both parents. But the genes for X are also a factor, and mutations in the genes responsible for X would further lower the impact of Y on the population.
In case of X = atherosclerosis, Y could be familial hypercholesterolemia which can cause cardiovascular disease between the ages of 30 and 40 if one gene in inherited (in the modern Western population where almost virtually everyone eats an extremely unhealthy diet),  while it cause cardiovascular disease at childhood when two genes are inherited.


text:
What is this insect? 6 legs and black spots
What is this bug?

Details:
 - Georgia, (Southern) USA
 - Maybe 1-4cm in size
 - Seen near an open area/crack between an outer door-frame and door where it could have come from outside, or going from inside to outside since the temperature difference was noticeable in this area.
Thanks in advance!

Deffo isnt a grasshopper. A window louse?

It's almost certainly a harlequin ladybird (Harmonia axyridis). Well, that's the usual name for it in British English, I think Americans would refer to it as the Asian ladybeetle or Asian ladybug. The spot patterns for that particular ladybird species vary quite a bit so I'll need to do some googling to confirm.

(Note: I'm going to be using the British English "ladybird" instead of the US English "ladybug" in this answer.)
This is a clearly a species of ladybird. Going by the number of spots, their size and not-perfectly-round shape, the positioning of the four central spots relative to the others, and the fact that its background colour isn't bright yellow... I'm pretty sure it's Harmonia axyridis, the species that us Brits refer to as a "Harlequin ladybird". I think Americans refer to it as an "Asian ladybug" or "Asian ladybeetle".
The spot patterns for this particular species vary a lot, as to some extent do the colours, so I've googled for images to support this answer. The below picture was posted to:
https://en.wikipedia.org/wiki/File:Harmonia_axyridis01.jpg
and is the IP of a user or organisation called Entomart. On the Wikipedia page and on their homepage, Entomart grant permission for the use of the image as long as they are given proper attribution, so I'm able to include it in this answer:

For more pictures of the Harlequin (again, showing how much the spot pattern and colouration vary), see:
https://scx2.b-cdn.net/gfx/news/hires/2018/amechanismof.jpg
For pictures of other ladybird species to compare the Harlequin with - as also one more of the Harlequin:
https://www.naturespot.org.uk/taxonomy/term/19357
Thanks for posting this question! I didn't expect to see a ladybird on Christmas Day :-)


text:
What's the name of this bird species?

What's the name of this bird's species, please?

Welcome. By the looks of it, it's a species of sea eagle. To allow users to effectively ID this specimen, they need some additional information, most notably where (and perhaps when) the picture was taken (country, region, season), and what the approximate size of the animal is.

http://www.oiseaux-birds.com/article-fish-eagles-feeding-behaviour.html; guessing bald eagle because of habitat (north temperate?) and white restricted to head (not breast ...)

Is this your picture, or one you found on the web, like here?  Because it would probably be best to give attribution in the latter case.  Thanks!

Please [edit] your post with the location of the picture and an approximate size of the eagle. See [tag:species-identification] for guidelines for asking ID questions here. Thanks!

I would say that it is a bald eagle.  I did a search for similar birds but nothing quite matches the build and coloration.  The bird in question appears to be drying out after being in the water.  On the coast of British Columbia they often feed on fish caught from the water's surface and occasionally get a bit damper than they expect, they then have to dry out like the one in your image.  See the following sites: From Cornell University's site about birds

Welcome to Biology.SE! You are more likely to get a positive response to your answer if you explain in more detail why your identification is correct. Specifically, please edit your answer to add discussion of key features that allow you to distinguish this from the several other very similar species of sea eagle. Without this your answer is indistinguishable from opinion. ——— You may also wish to take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site. Thank you!

Sure looks like a Golden Eagle to me , white head and tail ( North America).

Golden eagle with a white head ?  If I saw this in N America I would say it was a bald eagle.

You are more likely to get a positive response to your answer if you explain why your identification is correct. Specifically, please edit your answer to add discussion of key features that led you to this conclusion and supporting references or at least validated images. Without this your answer is indistinguishable from opinion. In addition, please address the fact that this looks much more like a species of sea eagle. ——— You may also wish to take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site. Thank you!

I am absolutely wrong; don't know what I was thinking.

I may be uninvited from the Christmas bird count which will be in our area Saturday.

No big deal — we all have "brain farts" (or at least I doubt you and my entire family are the only sufferers). ——— You do know that you can [edit] (or if you don't think this question is worth the extra work delete) your post right?