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How do emus/ostriches/rheas have their upper leg connected to the rest of their body?
I'm working on a model for educational graphics of an emu in conjunction with other information, but there aren't a lot of great reference images. The thing that's most unclear is how the upper leg around the femur is connected to the rest of the body because it's always obscured by feathers.
Mainly, is the leg connected to the rest of the area around the hip only half way through the femur, at the distal joint of the femur, or past the distal joint of the femur to the tibia? Elephants seem to have the third option, while horses seem to have the second option, and wolves seem to have the first option, so there are many possibilities without a clear generalization.
Below are the three options with the red indicating how far up the body the leg is connected to the skin of the hip area.

Try typing "emu skeleton" into your search engine: https://www.google.com/search?q=emu+skeleton&sa=G&complete=0&hl=en&gbv=2&prmd=ivns&tbm=isch&tbo=u&source=univ&ved=0ahUKEwjy74zWsffYAhUC2WMKHWP9CQAQsAQIFA

I wish it was that brain-dead simple, but it would benefit you to know that bones aren't muscles and dermis tissue, so a skeleton doesn't tell someone how the muscles and dermis extend to connect to the rest of the body from the leg tissue, it's a supporting structure.

Well, googling for "featherless ostrich" does retry some results...

Tried that too, some of the first results were: a jumping featherless chicken, an owl chimera, a 3-headed camel, a t-rex, and an ostrich laying an egg.

@John Joe: Sorry, I wasn't clear on what you were asking.  Searching for "emu musculature" finds this: https://peerj.com/articles/716/ and this: http://onlinelibrary.wiley.com/doi/10.1002/(SICI)1097-4687(199810)238:1%3C23::AID-JMOR2%3E3.0.CO;2-O/full (which is paywalled, but you might find an online copy).


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What advantage do dogs have in clearly disclosing whether they are afraid or unafraid in a conflict?
Dogs are known to clearly show whether they are afraid or unafraid with the posture of their tails during a conflict.
How and why is this beneficial?
My limited understanding makes me feel that, in any social setting, disclosing whether an actor is afraid or unafraid would almost always be unfavourable for the actor. Is this incorrect?
Isn't it better for the less confident dog to try to bark out the stronger one and if it doesn't work then simply walk away, rather than broadcast that it is afraid of the stronger dog?

It is better for animals to broadcast their qualities, and size one-another up before risking injury in conflict. As pack animals, dogs are particularly sensitive to where they are placed in a hierarchy. So it is better for them to telegraph their qualities than to engage in conflict that may hurt them.

Dear Karl, Thanks for your answer. Isn't is better for the less confident dog to try to bark out the stronger one and if it doesn't work then simply walk away, rather than broadcast that it is afraid of the stronger dog?

it may be difficult to run away after you've just found out the hard way barking doesn't work...

I think that it is wrong to think that dogs do not have any emotions, or complex social strategies. However, it is a common mistake to think that dogs are like humans, only not quite as smart. We place our feelings and strategies on them, because they are our companions. But I don't think they engage in the kind of complex mental "chess" games that we do.

@JohnDvorak I understand. What seems surprising is that, rather than running away immediately, dogs continue barking even after broadcasting their low confidence.

@RiteshSingh I would presume that there might be some unconscious tradeoff game - bark might indicate that dog would fight if it is inevitable but the posture indicates it would rather not.

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

sort: votes


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Why do lychee seeds come in different shapes?
I've been eating lychee fruits recently and noticed that every once in a while (in about 1 of 10 fruits or so) the seed in the fruit is shriveled, while in other fruits from the same batch the seeds have regular ellipsoid shape:

Top: regular seed, bottom: shriveled seed
The fruits with the shriveled seeds don't look or feel or taste any different from those with the regular seeds.
It seems like a binary trait, i.e. seeds are not more or less shriveled, they are either shriveled or not.
Why are the seeds so different? Do they come from different cultivars, or it's some kind of Mendelian development, or maybe some kind of a plant disease?

The shrivelled seeds are aborted seeds, known as 'chicken tongues'. Some cultivars of lychees mainly produce fruits containing chicken tongues. These cultivars are usually considered more desirable, because they have more flesh.
Source: https://www.crfg.org/pubs/ff/lychee.html

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


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What kind of factors determine how someone looks according to their race or ethnicity?
From what I read, race is considered the biology, the physical traits inherited by ancestry. Ethnicity and nationality have to do with social construct and cultural identity. This is almost the same things as sex and gender, where the former means the biological characteristics, and the latter refers to the social identity.
So, is there any relationship between race, ethnicity, and nationality? For example, Asians have a different cuisine than Europeans, which consists of whole grain and wheat, which explains why they are generally shorter? What makes them have slanted eyes? Is it because they have been known to look up at the sun constantly that they developed that characteristic over time?
What makes Mexicans have black hair, brown eyes, and medium skin, or have higher foreheads? Again, does this have to do with the cuisine that they have, or something else?
The only explanation I have heard about race is that melanin affects the colour of the skin. It is always sunny in Africa, which is why Africans have really dark skin, despite the fact that all of humanity derived from Africa. Europeans lived in more cloudy weather, so their skin became paler. I'm sure there's more to these findings.

Concept of race
The concept of race often poorly represent the genetic structure of populations. There is therefore an important socio-cultural aspect to the concept of race. The first sentences from wikipedia > race make this point clear

Race is a concept used in the categorization of humans into groups, called races or racial groups, based on combinations of shared physical traits, ancestry, genetics, and social or cultural traits. Although such groupings lack a firm basis in modern biology, they continue to have a strong influence over contemporary social relations.

What explain why people of different race look different?
You should most definitely have a look at the post Why is a heritability coefficient not an index of how “genetic” something is?
Your question can therefore be rephrased as "What is the heritability of the phenotypic trait X in humans?", where trait X could be anything of interest such as hair colour for example.
The answer for such question is always the same. It goes in three points

It depends upon which phenotypic trait you are looking at
For whichever trait you consider, it will most certainly be a combination of both genetic and environmental factor.
The evolutionary reasons for the existence of such distinction among groups will again depend upon which trait you're looking at.

If there is one particular trait that is of interest to you, you might want to open a new post to ask what is the heritability of this trait and whether there is any selective reasons for why different ethnic group differ for this trait.

You might be interested in a short and easy intro course to evolutionary biology such as Evo101 by UC Berkeley


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What is this insect found in Malaysia?
Found in Malaysia, South East Asia. Small insect with wingspan of around 1 centimetre. Its back legs and abdomen are pointed away from the wall.
Front View:

Diagonal View:

That is a moth, (Lepidoptera), in the family Pterophoridae. It looks very much like Stenodacma wahlbergi.  https://en.wikipedia.org/wiki/Stenodacma_wahlbergi


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The total numbers of mutations on different branches of gene tree are independent or not?
I was reading Tajima's 1989 paper on his test for neutrality.
Tajima, Fumio. "Statistical method for testing the neutral mutation hypothesis by DNA polymorphism." Genetics 123.3 (1989): 585-595.
Here is the question:
Suppose we have three sequences labelled $C,D,E$, and their genealogy follows $\{\{CD\}E\}$  (i.e. $C$ and $D$ coalesce first before they coalesce with $E$). Let $B$ be the most recent common ancestor of $C$ and $D$.
Now, let the random variable $k_{ij}$ be the number of nucleotide differences between sequence $i$ and sequence $j$, then Tajima shows that $k_{BC}$ and $k_{BD}$ have a non zero covariance.
But aren't mutations in the branch $BC$ independent from mutations in the branch $BD$? I was thinking that the total numbers of mutations in the brand $BC$ and $BD$ are two independent identically distributed variables, so $k_{BC}$ and $k_{BD}$ are independent, then why they have a non-zero covariance?
============Update=============
Now I have some basic ideas, but haven't worked out the full answer.
Tajima's definition of $k_{ij}$ is neither independent of the sample size, nor for a fixed coalescent time. (See his 1983 paper: Tajima, Fumio. "Evolutionary relationship of DNA sequences in finite populations." Genetics 105.2 (1983): 437-460.)
For example, in a sample size of 3, if you pick 2 individuals, and condition on that the two coalesce first, their coalescent time will follow:
\begin{align*}
\mathbb{P}(t=T)=p(T)=\frac{3}{2N}e^{-\frac{3}{2N}T}
\end{align*}
Now conditioning on a fixed coalescent time $t$, the number of mutations under the infinite sites model in each branch either from $B$ to $C$ or from $B$ to $D$ will follow a poisson distribution with parameter $\mu t$, where $\mu$ is the mutation rate per sequence per generation. Let this poisson random variable be $\xi_t$ in branch $BC$ and $\eta_t$ in branch $BD$. Then
\begin{align*}
k_{BC}=\sum_{t=0}^{\infty}\xi_tp(t)\\
k_{BD}=\sum_{t=0}^{\infty}\eta_tp(t)
\end{align*}
If we only consider the partial sum of the above series,
\begin{align*}
k_{BC}^{(n)}=\sum_{t=0}^{n}\xi_tp(t)\\
k_{BD}^{(m)}=\sum_{t=0}^{n}\eta_tp(t)
\end{align*}
then $k_{BC}^{(n)}$ and $k_{BD}^{(n)}$ clearly have a zero covariance, because $\xi_t$ and $\eta_t$ are independent poisson variables, hence
\begin{align*}
\mathbb{E}(k_{BC}^{(n)}k_{BD}^{(n)})&=\mathbb{E}(\sum_{t=0}^{n}\xi_tp(t)\sum_{t=0}^{n}\eta_tp(t))=\sum_{i=0}^{n}\sum_{j=0}^np(i)p(j)\mathbb{E}(\xi_i\eta_j)=\sum_{i=0}^{n}\sum_{j=0}^np(i)p(j)\mathbb{E}\xi_i\mathbb{E}\eta_j\\
&=\mathbb{E}k_{BC}^{(n)}\mathbb{E}k_{BD}^{(n)},
\end{align*}
so their covariance is zero.
But as $n\to+\infty$, how $k_{BC}^{(n)}k_{BD}^{(n)}$ converges to $k_{BC}k_{BD}$ is questionable. It will not uniformly converge to $k_{BC}k_{BD}$ because otherwise we can first computing the expectation then take the limit, which gives us a zero covariance. Tajima didn't explicitly show us how he computed the covariance by summing together three infinite series (Line 7, Pg. 448, 1983's paper). I tried directly working on that series but failed in the last sum. His result is correct, though, I hope someone can give some hint on why there is inherent correlation between these seemingly independent random variables.
=======Update: a simple explanation has been posted==============

Could you please highlight where in the paper (which equation) is it claimed that $cov(k_{BC}, K_{BD}) ≠ 0$?

If the ancestor $B$ is not considered as a single sequence but as a population of sequences, then if B has many polymorphic sites $S$ and a high average heterozygosity $\pi$, then drift will have an important say in the values $k_{BC}$ and $k_{BD}$ and both values will be large. If the ancestor $B$, has $S=0$, then the only contributors to $k_{BC}$ and $k_{BD}$ are new mutations and hence both values will be small.

Hi Remi, the equation is at Pg. 586 at the middle right panel, roughly 5 lines above Equation (15). It is originally derived from His 1983 paper: Evolutionary relationships between DNA sequences in finite populations

But the coalescent process only considers the relationship among sampled individuals, so I think each label should be a unique sequence.

Hmmm.... Yes, I now agree with you. The graph makes it pretty clear that 'B','C', 'D' refers to individuals sequences. Would be worth going into this 1983 paper. +1 in the meantime. Good question!

Here is a simple answer to my question. The reason two numbers of total mutations accumulated in two divergent branches are not independent of each other is because they experience the same amount of coalescent time.
While the stationary Poisson mutation processes are independent from each other as long as they happen in different branches of a genealogy, they are likely to produce a similar number of mutations if two such processes happen together for a same amount of time. Thus, the non-zero part of the covariance between $k_{BC}$ and $k_{BD}$ is not from mutation processes themselves, but from the shared coalescent time $T$.


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Methane and wetlands
Some papers I have read show carbon accumulation (peat) in wetlands is reduced because of low methane emissions. Why is this the case?
Why does low methane emission reduce carbon accumulation in wetlands?

Welcome to Biology.SE! Could you provide the links to the papers you read?


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What is the "mucin net"?
From Giulia Enders, Gut: The Inside Story of Our Body’s Most Underrated Organ

Mucins are proteins that form the main constituent of mucus. They help provide hours of fascination and fun for young children who have just found out they can blow bubbles with their own spit. A more useful function is their ability to envelop our teeth and gums in a protective mucin net. We shoot them out of our salivary papillae like Spider-Man shoots webs from his wrists. These microscopic nets can catch bacteria before they have a chance to harm us. While the bad bacteria are caught in the net, antibacterial substances in our saliva can kill them off.

What is the mucin net the author refers to? No result is found when googling it.

From Wikipedia (emphasis mine):

Mucins are a family of high molecular weight, heavily glycosylatedproteins (glycoconjugates) produced by epithelial tissues in most animals. Mucins' key characteristic is their ability to form gels; therefore they are a key component in most gel-like secretions, serving functions from lubrication to cell signalling to forming chemical barriers.

The "ability to form gel" is the key here. Also from Wikipedia:

Gels are defined as a substantially dilute cross-linked system, which exhibits no flow when in the steady-state. By weight, gels are mostly liquid, yet they behave like solids due to a three-dimensional cross-linked network within the liquid.

So, a gel (and mucins are no exception) is composed of a liquid trapped in a 3D net, much like a sponge. This is the "mucin net" your book is referring to.


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What insect is this, large swarms?
I live in Brisbane, Australia and these creatures arrived a few weeks ago for a day or so and then they disappeared. There were thousands of them. I would love to know what they are.

That is some sort of ant. Many species of ants have this huge "nuptial" flights, particularly after rains, where winged males and females leave the nest in swarms. Males die shortly after, while females lose their wings and start a new nest in the soil. I'm not familiar with Australian species, but the fact thatyou can see a "waist" shows you that those are winged ants.


text:
Do neurons have agency with respect to modulation of spike timings?
I am aware of the mechanism of Spike Timing Dependent Plasticity (STDP) and its ability to cause Long Term Potentiation (LTP) and Long Term Depression (LTD). So far, I've been viewing neurons as input-output devices. However, there seems to be a problem with approximating neurons this way. If all they do is sum the inputs and produce an output, then it seems as if LTP and LTD as caused by STDP would be purely a function of the inputs from the environment. This would leave animals without any meaningful agency.
I would be much more comfortable with the idea that neurons actively try to optimize some parameters by competing with each other, perhaps by varying the timing of their spikes. Is this picture consistent with neuro-scientific findings?

I don't have time to look into this and form a proper answer, but if I were to guess at an answer, with regards to each individual neuron, they don't really have any 'agency', other than differences between their proteins, ion channel expression etc. However across a network of neurons, there would be some correlation of activity that drove patterns of excitation/inhibition that could be considered agency. You might look into developmental spontaneous activity that is important for formation of sensory circuits in the visual and audio systems to see if that fits with your idea.


text:
Power consumption of a ATP synthase in Watts
Considering the ATP synthase to be a rotating machine, does anybody know its power consumption and/or power production in Watts? At least roughly, e.g. based on the average chemical energy produced per time unit?

Watts? Science uses SI units. The joule is the unit of energy. Anyway, you are expected to demonstrate that you have done some of your own research before posting on this site. What have you done? What do you think the input is? What do you think the output is? We welcome you to SE Biology, but ask you please take the Tour read the Help before posting.

@David It's great that you want to help new posters write better questions, but in this case your comment is insulting for no reason. The Watt is the SI unit of power (1W=1J/s) and the question seems completely reasonable, just needing a pointer to the right literature.

@David Science routinely uses non-SI units.

@David I fully agree that SI-derived unit Joule [kg⋅m2⋅s−2] is the unit of energy, but I am interested in power and, therefore, used the SI-derived unit Watt [W] ([kg⋅m2⋅s−3]).

@VictorChubukov — You may not be aware that when you have achieved a certain SE Biology "reputation" you are expected to participate in the reviewing process, one aspect of which is reviewing posts by new users "This is the first question asked by a new user. Help them learn to use the site by reviewing their post." I indicated the particular parts of the Help that would allow him to see why his question — although interesting — did not conform to SE Biology guidelines, and gave concrete examples of points to research or mention in his question. I do not regard this as an insult.

There are tons of mechanistic studies of ATP synthase so you may be able to get a better answer from finding one of those. But here's a rough estimate based on thermodynamics and enzyme kinetics.
The $\Delta G$ of ATP synthesis/hydrolysis is about -50 kJ/mol. The $V_{max}$ is in the low hundreds (here is an estimate of 350 $s^{-1}$ for E. coli ATP synthase), giving you something like 17 MW/mol or 30 aW (3e-17 W) /molecule.
I did look briefly at some mechanistic studies, and found this reference of 80 pN * nM for the torque generated. That translates to almost exactly the same 50 kJ/mol (ATP synthase is very efficient). But of course you still need the $V_{max}$ (number of rotations per second) to get the power.

Thank you very much! This was exactly what I was looking for.


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Why did some animals evolve inward-slanted legs?
Something I noticed looking at reference images is some animals have legs that are slanted inward relative to the length of their body, like in the two images below. Why have animals evolved this instead of having their legs pointing more straight down like lions or elephants?

You picked the two habitual, upright, striding bipeds as examples.

So? The question remains the same.

I think @kmm is encouraging you to think critically about your question and giving a huge hint about the difference between the examples you came up with that have 'inward slanted' legs versus your counterexamples that do not.

No one teaches advanced mechanics until after calculus 3 or maybe 2, and frankly analyzing every possible force at every possible angle of three joints and a body with arbitrary self-locomotion and then guessing why something happened to coincidentally mutate that way is a nightmare for anyone, there's not much to critically think about unless you have a very accurate simulation set up. That's why the sources of answers to questions like these almost always originate from graduate researchers with extensive testing on live animals in motion or expensive robots.

Sorry no references other than illustrations for the moment.
If a running biped has it's feet further away from the line of gravity, then it's got less efficiency in forwards motion and more instability of the line of gravity falling left and right.
When you consider the kinetic downwards weight in kilos that goes into every step, a runner/sprinter who doesn't have aligned steps wastes a lot of energy.
here's are dinosaur footprints:
https://australianmuseum.net.au/Uploads/Images/7919/footprint%20comparisons_big.jpg
The hips joints tend to point sideways to give a strong musculature, lots of running muscle, and a wide base of more than 90 degrees, for a wide birth canal and other reasons.
So the tendency for efficiency of running bipeds is to have aligned footsteps and their hips tend to be a strong and wide base.
That's only the resting position, the walking angles actually vary a bit outwards and straight too, the knee goes outwards when it's rising.
https://cdn.pixabay.com/photo/2016/01/18/02/04/footprints-1145883_960_720.jpg
here is a comparison of ostrich and human bone angles: http://rsif.royalsocietypublishing.org/content/13/122/20160529


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What is a 1-flowered raceme?
PlantNET describes the inflorescences of Daviesia acicularis as:

Racemes reduced to 1 flower

How is a 1-flowered raceme different from a single flower?


text:
How long does it take a leech to attach?
How long does it take a hematophagous leech to attach?
Specifically, how dangerous is drinking water which might be infested with leeches?
Presumably, once the leach enters the stomach, it will be quickly dissolved, so the only danger is that it might attach in the mouth or esophagus. Can this actually happen?
(should I ask this elsewhere?)

Apparently, the leech won't wait for you to swallow it, but it'll attach in your aerodigestive tract as soon as it's in it. This case study of children who drank leech-infested water explains pretty well (and in a rather graphical way, in my opinion) what happened to them. I'll copy here just an excerpt (emphasis mine):

A seven year old girl was brought from a remote village (Kamardin Karaiz) with four days history of cough with blood stained sputum after drinking water from a pond. She also developed pain in her throat and was unable to swallow except for liquids. [...]
  Her coagulation profile was with in normal limits however her hemoglobin level was 9 g/dl. [...]
  On direct laryngoscopy a leech was found attached to the right pyriform fossa with its one end in the glottis which was removed immediately. The patient made a smooth postoperative recovery. On recovery the patient had no dyspnea, stridor or dysphagia and was discharged the next day on oral antibiotics.

This article also reports a historical case of a leech attached into the throat of a Pashtun man in India. The leech was removed with no consequences.
In short, leech ingestion will probably result in having a leech sucking your blood from inside your throat. Although removing it will probably grant a full recovery, it doesn't seem a pleasant experience.


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How did palaeontologists discover the age of the Tyrannosaurus rex named Sue?
I'm trying to understand how they discovered or speculated the age of Sue the Tyrannosaurus rex to be about 28–29 years old. How do they know exactly the age of Sue? Could it be wrong? Could it be possible that she is older then they thought — maybe 35 years old?

Dinosaur bones contain rings, similar to a tree, that can be counted to determine age. SUE was 28 when she died, making her the most geriatric Tyrannosaurus yet found. Her bones show signs of wear and even disease, including arthritis.
Paleontologists can make micron slices of bone and view the rings through polarized light, even on a microscope at 5-10x, similar to geologist mineral ID's.
https://mistralmtn.blogspot.fr/2013/03/bone-growth-rings.html

Wiki: Growth lines may be deposited in synchrony with endogenous biorhythms. For example, captive crocodilians exposed to constant temperature, diet, and photoperiod, still exhibit the periodic and cyclical skeletal growth banding of their wild counterparts.[4] Consequently, it is assumed by many paleontologists that the growth lines of dinosaurs reflect annual rhythms, and that they may be used to determine individual ages. However, in the large and long bones of many dinosaurian taxa, resorption of internal and external bone proceeds even as new cortical bone continues to be deposited, so that growth lines deposited early in development may need to be inferred.
http://tbrnewsmedia.com/wp-content/uploads/2015/05/Dinosaur-Growth-Rate-w.jpg

though could it mean sue might reach older age if yes how old im hoping 40yrs because most larger birds can reach over 30yrs

If you read about dinosaur longevity, It says that 29 is a fair old age for a T-Rex because they are related to eagles and ravens which live 20 to 30 years on average. The oldest wild bald eagle lived 38 years. 50 years in captivity. Because it has to hunt very actively, it must be in peak form every month of every year. Crocs can go 60 years but they are cold blooded. Other extinct genera than dinosaurs could manage 60-70 years perhaps.

The oldest wild tiger was 20 and the oldest bear was 39. If the T-Rex had the same health as a bird, at 32 years old, the probability that it can still catch prey with 15 tons to throw around, is slim. Spinosaurus could perhaps live to 40, because it's an agility predator too, same as an eagle, and you can imagine a 40 year old eagle fighting for territory, it would be doomed.

The oldest wild albatross is 67 years old, so perhaps a female Spinosaurus can live twice as long as a t-rex :) https://en.wikipedia.org/wiki/Wisdom_(albatross)

so trex cant live nearly 35-40yrs

so its not possible then?


text:
Is this silverfish? My apartment very dry
Can anyone please confirm whether insect below is a silverfish?  It looks a bit like the picture at our federal government pest control page.  It also moves with a wiggling motion, as described  at the Wikipedia Silverfish page.
I sprayed it with alcohol, and it seems to be dead.  I've seen this type of insect about once per month.  I don't know why they gravitate to my apartment, as the dehumidifier it set to maximum (35% relative humidity).
Sorry for the quality of the photo, but my iPhone SE does not have adjustable focus that I'm aware of. I can only tell the phone where the feature of interest lies within the picture.

Once per month is a healthy house. A biology teacher would tell you that they are pretty harmless human companions, with a cute name, and you probably won't see damage from them. I have them living under the linings of some old windows. I'm mostly bothered to disturb them. once a month is not worrisome.

Ick....!!!!  I could never....

you probably have a phobia of insects.

Now that you mention it, I can't think of a single insect that I would like to see inside the home.  Even ants, flies, lady bugs, bees, fruit flies.  They're fine outside (heck anything is fine outside), but if I see them inside, 9 floors up from the ground, I would immediately wonder how in they heck they got there.  I would naturally worry about an infestation.  So it's the circumstance that feeds the phobia.  Though I suspect that most people would react similarly.  Perhaps not those who study insects,though.

The reasons that the photo quality is poor are: it's a 0.1MP image, and you were too close. At 401x373 pixels (for the first image) it's obviously a cropped image (which is fine), since that camera is capable of 4032 x 3024 pixels (12 MP); you've cropped to 1/10th the size. Backing up a little will permit you to focus and you can still crop the image. Here is an example iPhone picture of a silverfish: http://sanxbile-blog.tumblr.com/post/44634480254/silverfish-are-cute-lookit-dat-little-eye-also - that was taken at low resolution setting, so you could improve on that.

Thanks for that suggestion, Rob!  I will try it the next time I need to photograph something very small.  Hopefully not for a while.

Remi is right that it's a silverfish, and here's some macrophotography of Lepisma Saccharina.

Thanks!  Up close, with the fur, they look almost cute.  (I said almost).

Yes if you compare that to a fly, I dunno why someone would be ickied about silverfish. flies are way worse. wheat and wool moths are worse. here's a guy that married a silverfish: https://www.youtube.com/watch?v=ErBgOTBenIA  forest people can live with tarantulas and snakes, I'm sometimes ickied by centipedes, which are garden animals. silverfish are cute and mysterious, they scratch paper and hide, rodents are far worse.

You're making me feel guilty about having ended my silverfish.  At least they went out with an alcoholic bang.

nice pictures, but you hardly answer the question. You should provide support for your answer and not just make a statement. Save for your up close pics, this really is more of a comment. Please consider updating with more info

The pictures are very low quality, but yes I think that is a silverfish.
You dehumidifier might affect your throat but will will likely not have much impact on silverfish. The number one rule is to clean. Also, if you live in an appartment building, silverfish can quite easily invade an appartment from another one. So, it might make it harder to fight against silverfish. If needed there are also traps and pesticides.

Silverfish are suppose to prefer humidity, so they should be flocking to other people's apartment rather than mind.  Maybe I got the ones that strayed.  I will try harder to clean, but things are quite clean already.  At least, compared to other apartments I've seen.  Thanks!


text:
Excess proteins in cells
Damaged proteins are broken down in cells by ubiquitin-proteasome pathway. Do cells experience excess of proteins? If yes,  how excess proteins are taken care of?


text:
Who were "Dawson and Wilson" (mentioned as authors of an embryonic postmortem examination method)?
A sentence from a Russian text I'm translating:

Following the drug administration period, the pregnant animals were euthanized in order to examine the embryos using the method developed by Dawson and Wilson.

That made me curious. Who were they? Google fails to bring up both these surnames at once in response to queries like "Dawson Wilson embryo necropsy" etc. Maybe one of them developed an embryo examination technique, and the other perfected it?

So this isn't a citation? Those surnames are not followed by a year, like Dawson and Wilson, 1972?

@LinuxBlanket - no, there is no reference, no footnote. There's another mention of Dawson several pages down the document - a mention of "embryos stained using the technique developed by Dawson".

I updated my answer. I couldn't find any specific reference to some article by Wilson, but I think I found out which Wilson is it.

This article (A Note on the Staining of the Skeleton of Cleared Specimens with Alizarin Red S) looks to be the one by Dawson.
Update: I think the Wilson your text is referring to is James G. Wilson, an important researcher on terathology. I can't find any reference to a single article, though.


text:
Would all the different species evolve to their respective next form of life eventually?
Would  all the different species evolve to their respective next form of life eventually? Like this generation apes to humans in next million years? Or does all the different species exist to only show how evolution happened to humans?
For example, it seems foxes can evolve into dogs by domestication, is that so?

There are a lot of misconceptions in your question. The better for you would be to simply start with an intro course to evolutionary biology such as Evo101 by UC Berkeley for example. I will answer your question directly in the text.

would all the different species evolve to their respective next form of life eventually?

You seem to have a very discrete conceputalization of what form living things can take. Current species won't all of a sudden change into a new one, like a "pokemon evolves". But all current lineages are still evolving. They keep changing gradually.

Like this generation apes to humans in next million years?

Humans have not "evolved from apes". Humans ARE apes. Humans and other apes have a common ancestor who already was an ape. The most closely related species to humans are chimpanzees and bonobos. The Most Recent Common Ancestor (MRCA) between humans and either chimpanzee or bonobos lived about 6 millions years ago.
See this answer for a short intro to phylogeny. You might also want to explore the tree of life by yourself on OneZoom.org. You'll find the human lineage here.

Or does all the different species exist alive now to only show how evolution happened, to humanz?

No, there is no intention. Nobody made evolution happen for humans to witness it. Evolution just happened and keeps happening. Nothing has stopped it and nothing (except extinction of all life on earth) can stop it.
If you follow a very short intro to evolutionary biology (such as the Evo101 suggested above), you'll understand what evolution is and why it always happens.

Though it seems foxes can evolve into dogs by domestication?

No. Some foxes are currently being domesticated and they manage to select for typical domestication traits (e.g. lower aggressivity). These domesticated foxes are not dogs and never will be. They are domesticated foxes. If those domesticated fox become different enough from wild foxes (typically if there is reproductive isolation), then we will eventually consider them as a new species and give a name to this species. But we should not call them dogs, they are not dogs (just like cats, cows, chicken or corn are different from dogs, yet all are domesticated).

Or even cats: domestication has made them different from the ancestral wild cat, just as dogs are different from the ancestral wolf, but few people would have trouble telling them apart.

I would say the first quote - specifically the "their respective next form of life" part - also implies the "ladder of evolution" misconception here.

to add, the foxes in question developed a couple of traits we associate with dogs, it  turns out these traits are linked to traits we select for, either consciously or unconsciously. basically it is showing that many of the unique physical traits of dogs may be just as much as result of domestication as behavioral ones.

You have so many misconceptions about evolution, it is impossible to give you a complete answer in a small text box
There is no "next form".  Populations change in response to their environment, and how that happens is in large part dependent on chance.
Foxes do not evolve into dogs.  Nothing the scientists did in that experiments was anything remotely like making foxes evolve into dogs.  All they did as put the population under enormous pressure by culling all but the friendliest animals.


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How to give a biological interpretation to this phase portrait?

Consider the following system and analyze its behavior.
$$\begin{array}{rl} \frac{dA}{dt} &= A \left( 2-\frac{A}{5000}-\frac{L}{100} \right)\\ \frac{dL}{dt} &= L \left(-\frac{1}{2}+\frac{A}{10000} \right)\end{array}$$

The analysis
It has $3$ equilibrium points. I know the stability of the three points but I am not sure if I interpret the meaning of them correctly according to the phase portrait. $x_1, x_2$ are saddle points and $x_3$ is stable point they are
$$\overline x_1=(0,0)$$
$$\overline x_2=(10000,0)$$
$$\overline x=(5000,100)$$
According to the phase portrait I think the behavior of the system is described as:
For every point $(A,L)$ given in the first quadrant, where $A$ is the number of aphids at time $t$ and $L$ is the number of lady-bugs at time $t$, we'll have that in the future, the maximum number of lady-bugs and aphids it's going to be $(5000,100)$ respectively. This also means that both population will never going to extinct.
Even in the case where there were just a few number (near 0) of lady-bugs, their population will grow and will be establish also.
My question
Did I miss something important in the biological description to the phase portrait?

You seem to once put bars over your equilibrum conditions and once not. I am not sure they are exactly the same. Also, I think you once meant $\bar x_3$ instead $\bar x$. Note that the usual is to use a hat rather than a bar for an equlibrium.

I don't think you missed anything important!
You could investigate the cyclic behaviour around the equilibrium. For example, looking at the variable aphid population size can start above its equilibrium point, then overshoot it and overshoot it again to finally reach the equilibrium point. If you zoom close to the equilibrium point, you might see long cyclic behaviour before ever reaching the equilibrium.
You sure could do all kind of further analyses such as a stability analysis or searching for cyclical equilibrium but it is easy to see with this simple model that nothing very complicated will arise. You could also investigate for what parameter values this classic pattern breaks up if it does.
Another option is to make the model more complex by introducing a carrying capacity (and then investigate under what aphid growth rate the behaviour becomes chaotic), or population structure, or whatever.
You might learn much from it but you might still want to have a look at the post What prevents predator overpopulation?.
I highly recommend the book A Biologist's Guide to Mathematical Modeling in Ecology and Evolution by Otto and Troy. It will show the typical kind of analyses that can be done for this kind of systems.

I don't see a cyclic behaviour. Cyclic means something circular ?

If you start at (15000, 300), you'll circle around the equilibrium. Maybe not a full circle though. I don't know. But both variables are going to overshoot the equilibrium at least twice.

You're right, haven't notice. Also you mention that I could make the model more complex by introducing a carrying capacity. Exactly how would be that term? I mean something like +1/k or -1/k

@Anneliset. Remember, when you are modeling biological data like this you are plotting means, but in the real world you are going to have some added noise. That means that even if you have a stable fixed point like in this phase diagram, if you actually simulate data rather than means you are going to oscillate a bit around it because a noise term keeps you in the 'cycle' and prevents settling to perfect stability.

Carrying capacity would typically like like an added $\frac{K-N}{K}$ term that multiply the rest. See logistic population growth. It is quite classic. You might want to read an intro book on the subject rather than having to reinvent the wheel by yourself. You might want to have a look at a population biology books. I had one in mind which is apparently very good but I can't remember the title or author right now.

You can ask for book recommendation on another post if you want. Here is a book recommendation post for population genetics.

I was wondering, time $t$ is measured in what units? days or months?

Typically measured in generation time. Your model must assume equal generation time (and non-overlapping generations) or must consider that the values are adjusted for differential generation time.

Oh ok, I was observing the model again and I've seen that there exist competence between aphids due this term $-\frac{A^2}{5000}$, why aphids compete in nature?

Sure.... there is always competition among individuals in pretty much any species.

But you are a biologist , you must know why they compete.Is it for food or ...? (I won't bother again, this is my last question:) So if you don't mind, answer me.

Well... I am not an aphid biologist! I am a theoretician (mainly numerical stuff, not much analytical) in population genetics. Also, it is the kind of question that would deserve its own post. I don't know the answer and I typically don't seek much in the literature for a follow-up question. I (or other users) might do it on another post. There is probably competition over habitat (incl. for leave where they make their galls), food, protection from ants, etc...

You can just go on Google Scholar > Aphid competition and you'll find some answers. Good luck @Annelise!

@Remi.b The model already has a logistic/carrying capacity component; the second term of the aphid equation can be rewritten as $-A^2/5000$, which could be interpreted as a carrying capacity of 5000 (or that $r/K = 1/5000$).


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Do archaea undergo the same horizontal gene transfer processes as bacteria?
Do archaea also undergo processes like conjugation, trasformation, etc.? If not, do they have their own horizontal gene transfer methods? Can bacteria conjugate with archaea?

Wagner A, Whitaker RJ, Krause DJ, Heilers JH, van Wolferen M, van der Does C, Albers SV (2017) Mechanisms of gene flow in archaea. Nat Rev Microbiol 15: 492-501.

The exchange of genetic material is a major driving force for genome
  evolution across the tree of life and has a role in archaeal
  speciation, adaptation and maintenance of diversity.

Soucy SM, Huang J, Gogarten JP (2015) Horizontal gene transfer: building the web of life. Nat Rev Genet 16: 472-482.

Horizontal gene transfer (HGT) is the sharing of genetic material between organisms that are not in a parent-offspring relationship. HGT
  is a widely recognized mechanism for adaptation in bacteria and
  archaea.

Fuchsman CA, Collins RE, Rocap G, Brazelton WJ (2017) Effect of the environment on horizontal gene transfer between bacteria and archaea. PeerJ 29: e3865.

Potential hotspots of horizontal gene transfer between archaea and
  bacteria include hot springs, marine sediments, and oil wells.

I think the OP was addressing the mechanics behind HGT of archaea, not just "is there such a thing".

@LinuxBlanket: My answer has both.

Your answer is "yes, there is HGT in archaea and it's important", not "archaea do HGT by conjugation and not by Y or Z". This information may be contained in one of the references, but not in your answer.

@LinuxBlanket: The references, and references therein, are also parts of the answer.


text:
Is DNase treatment necessary before RNA sequencing?
Is it necessary to treat total RNA with DNase before sequencing it? In particular, if the library prep relies on a poly-A enrichment, is it necessary to remove DNA, knowing that genomic DNA does not have as much polyA as mRNA?


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Mutations in organisms
I was researching mutations and came across an interesting question:
Do mutations occur in the DNA or mRNA of an organism? Is this more opinion that science?
Thanks in advance!

What do you mean by opinion?

DNA. mRNA is transcribed from DNA.

specifically I assume that the mRNA base changes are a result of the exons, correct?

A more complete answer would be great (I could write it myself but I just wanted to give you some ideas if you wanted to expand your answer). It could be stated for example that not all mutations will ever be transcribed and that of course if there is a mutation in a coding region that is being expressed, then you'll find the mutation in the mRNA also.

Simple questions are best answered with simple answers. You can have your opinions, but in my opinion, I am often annoyed by long winded answers.

@KarlKjer Fair enough. +1

From Wikipedia:

A mutation is the permanent alteration of the nucleotide sequence of the genome of an organism, virus, or extrachromosomal DNA or other genetic elements.

The key word here is genome. A mutation is defined as something occurring in the genome, and the genome of living beings is made of DNA. Hence, mutations arise in the DNA.
A special case concerns viruses (which, for the record, are often not considered living beings): they can have a RNA genome, so they can have mutations in the RNA.
BUT!
This does not mean that mRNA transcription is an error-free process! As an example, this link gives you a nice overview on the error rate in transcription and translation,which apparently are quite high. It's just that, by definition, mutations arise in the genome.


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ATP generation during respiration
How many ATP molecules are generated from oxidation of FADH2 formed during complete oxidation of 10 molecules of maltose?

40
60
80
20

My method-

As maltose is a disaccharide ( made up of two glucose molecules )and for one glucose molecule , 2 FADH2 are formed after complete oxidation.
Then for one maltose molecule 4 FADH2 will be formed (since maltose has 2 glucose molecules).
Such 10 molecules of maltose will give 40-FADH2.
1-FADH2 produces 2ATP during oxidative phosphorylation ,so total ATP formed =80

Try not to ask homework questions(direct option based questions) on this site. You'll get downvoted everytime. First, try to solve the question by yourself. If you encounter any problem in any step or can't understand something, then put forward your methods and ask the question(how should we do it and all). You can ask any conceptual problems related to particular topics but remember : NEVER post direct questions.

its not homework one it was asked in exam

look how i solved in  EXAM

as maltose is disaccharide made up of two glucose molecules and for one glucose molecule 2-FADH2are formed after complete oxidation then for one maltose molecules 4-FADH2 will be formed (22[2 in glucose{fadh2}]and [maltose=glucose+glucose])and such 10 molecules of maltose so40 FADH2(410).And each FADH2 produces 2ATP during oxidative phosphorylation so TOTAL ATP formed-80(40*2)

i know it's not a homework question (if u take the meaning literally). What I'm saying is try to make your question look much more presentable (like add your methods,thinking,reasoning,sources you use,etc.). If you don't show your efforts in finding out the answer, people will be less interested in answering it. And it'll also get downvoted since it'll seem like you didn't even take the effort to do it. You just posted it to get the answer. You're new to this site, so it'll take sometime to get used to it. So, don't worry if you're getting downvoted. just better luck next time!  =)

As far as i can see, you have done nothing wrong. Maybe the answer given is wrong?

@Bhavya-No problem =)


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Hardy-Weinberg sex linked formula
The "big five" assumptions are the ones listed in the main text. However, the basic formulation of Hardy-Weinberg equilibrium also relies on a few other assumptions;
Allele and genotype frequencies don't differ between males and females. That is, the basic form of Hardy-Weinberg does not cover sex-linked genes.
so, is there a modified formula?

What "main text" are you referring to?

Also, exactly what is your question (modified formula of what?)? Is it on how to calculate genotypic frequencies in the presence of sex-linkage, or on how sex-linkage affects the HW-equilibrium?

Solving Hardy-Weinberg problems
First of all, you might want to have a look at the post

Solving Hardy-Weinberg problems

and eventually at

Assumptions of Hardy-Weinberg rule

After reading the first post, you should be able to answer your question yourself. I encourage you to try it before reading what follows.
Hardy-Weinberg for sex-linked loci
I will make an example. Let's consider a case where males are XY and females XX (like in mammals for example). Let A and B be two alleles of a bi-allelic present on the X chromosome. The frequency of these two alleles in the entire population are $p$ and $q$. Let's assume the locus is present on the X chromosome. We will assume that the allele frequency do not differ between males and females.
In males, there are two possible genotypes. A and B. Their frequency among males are noted $f_{m,A}$ and $f_{m,B}$ are
$$f_{m,A} = p$$
$$f_{m,B} = q$$
In females, there are three possible genotypes. AA, AB (or BA) and BB. Their frequency among females are noted $f_{f,AA}$, $f_{f,AB}$ and $f_{f,BB}$ and are
$$f_{f,AA} = p^2$$
$$f_{f,AB} = 2pq$$
$$f_{f,BB} = q^2$$
If the sex ratio (the ratio of the number of males over the number of females) is $r$, then the genotypes frequencies in the overall population are the ones from above multiplied by $r$ and $1-r$ for males and females, respectively.

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


text:
What are some good examples of open-source articles in which the synergy of two medicines is demonstrated?
I am doing research on Stochastic Cooperative Game Theory (a subfield in mathematics), which I will henceforth call SCGT for convenience. In this theory, entities can work together to receive a bigger combined payoff than they would otherwise receive if they had not worked together.
In the stochastic version of cooperative game theory, the payoffs are not deterministic, but follow a probability distribution.
It seemed to me I could apply this theory to drug synergy. If there is drug synergy, there is a (high) chance that two medicines combined are better at healing a patient than just multiplying the dosage of either medicine by $2$. With SCGT, I could determine how much each medicine contributes to the healing of the patient, if some information is known about the drug-response curves. This in turn could tell us something about how much the manufacturers of each drug receive to be paid (in theory).
However, I am not quite well-acquainted with the literature on drug synergy. Furthermore, I can't access many articles on the topic without paying a lot (as I'm with the mathematics department at the university, I can't view articles on biology for free).
So my questions are:

Do you know any open-source articles in which it is shown that two drugs work in synergy according to the Bliss Independence model?

and:

Do you know any open-source articles in which it is shown that three or more drugs work in synergy according to the Bliss Independence model?

The same questions apply to the Loewe additivity framework.

This list is about biology, not about literature. It is valid to ask for examples of studies on the topic that interests you, but not, in my opinion, about articles in a particular type of journal. An good answer describing and referencing such studies would be of general interest here. An answer with a mere reference would not be suitable. The type of the journal (open access, written in English etc.) is no concern of biology.


text:
Can VMD change its cartoon representation for secondary structure according to trajectories?
I am using VMD to visualise the secondary structure of protein.
The trajectories are from my Gromacs simulation. Firstly I use File - New Molecule... to load the protein.gro file. Secondly I use File - Load Data into Molecule... to load my protein.xtc trajectories.
Then I use Cartoon to visulise the structure. As I drag the time frames, all the secondary structures (e.g. alpha-helix, beta-sheet) keep the same. But I am pretty sure some of them are changing, as I look into the Timeline analysis for secondary structure.
So how to use VMD to see the secondary structures at different time frames?
Thanks a lot for @Stefan's help! It finally works! So follow Stefan's guide, and replace the molid with the number under the ID in the VMD Main.

I see this was asked first on bioinformatics.SE: https://bioinformatics.stackexchange.com/questions/3432

yes, because no one answer it.

And could you please tell me, where is rule that I cannot ask a repeated question in two sites? @marcin

@lanselibai it is all over the place, check this answer by the cofounder of SE for instance.  And it's not a rule per se, but its generally preferred that you tailor your questions to the audience of the site you're posting on.

I understand the necessity to ask only in one place. But because there is not a clear boundary line regarding my VMD software issue, I feel it can fit both sites. So, it would be better if there is an explicit definition of where my question should be posted.

@lanselibai: "Animating the secondary structure" http://www.ks.uiuc.edu/Research/vmd/vmd-1.3/ug/node256.html

As Martin pointed out, VMD doesn't update secondary structure content over the course of an MD trajectory. You can easily do this in VMD by using the SSCache script:
http://www.ks.uiuc.edu/Research/vmd/script_library/scripts/sscache/sscache.tcl
I believe it ships with the newest versions of VMD, actually, but I'm not exactly sure; even if not, you can easily source it:
Extensions > Tk console (in the console, type source Downloads/sscache.tcl (or where ever you've saved the script)). Once you've sourced the script, the easiest thing to do would be to load your topology and trajectory and (in the Tk console) issue the command start_sscache molid, although I advise having a look at the examples and options in the script.

thank you very much. Both source Downloads/sscache.tcl and start_sscache molid could use. However, as I move along the time frame, I could not see any secondary structure (SS) change. I was using Extensions - Analysis - Timeline- Calculate - Calc. Sec. Struct. to visualise the SS, so I know the SS is definitely changing. So I wonder if the sscache is adopting the same algorithm as Timeline (which is STRIDE) for SS?

'molid' in this example is just a substitute for your system's ID; you can see it under ID next to the number of atoms in the VMD main window. If your system is called 'myMolecules,' you issue start_sscache myMolecules in the Tk console (you have to issue source Downloads/sscache.tcl, of course)

Animating the secondary structure in VMD

The secondary structure definitions for the molecules in VMD don't
  change during an animation but they can be made to do so with a trace
  on the vmd_frame($molecule) Tcl variable. The simplest way is to call
  vmd_calculate_structure(molecule) every time the frame changes . . .


text:
Where is DNA during the process of RNA extraction using Trisure?
Where is DNA during the process of RNA extraction using Trisure described here? Given that DNA is also a nucleic acid, should I expect the isolated RNA to also contain DNA? However, Bioline claims RNA 'with
virtually no genomic DNA contamination'.

Expectedly, they don’t really want to tell you what TRIsure is. What they do say is that DNA is found in the organic or interphase after extraction whereas RNA partitions to the aqueous phase. This is almost certainly some variant of acid phenol extraction. As confirmation, the MSDS lists phenol, ammonium thiocyanate, guanidinium thiocyanate, glycerol and citric acid as its components.

But why does the DNA end up in the organic phase? Isn't it as hydrophilic as RNA?

I found this in the link you provided: 'The nucleic acids (RNA and/or DNA) partition into the aqueous phase, while protein partitions into the organic phase. The pH of the mixture determines which nucleic acids get purified.[3] Under acidic conditions (pH 4-6), DNA partitions into the organic phase while RNA remains in the aqueous phase. Under neutral conditions (pH 7-8), both DNA and RNA partition into the aqueous phase.'

@charlesdarwin That’s a good question to which I don’t know the answer.


text:
Why don't chromosomes double in S-phase?
DNA doubles in S-phase, but chromosomes don't double in S-phase, in spite of the fact that chromosomes are formed by the condensation of DNA. Why is this so?

My answer won't be precise, so I post it as a comment. It's a question of terminology, and it's normal to be confused: a chromosome can have one or two chromatides, but we can talk about a single chromosome in both states. For less confusion, we could talk about a replicated chromosome when one chromosome is composed of two chromatides. But I'm looking forward for a better answer than mine, since I'm still a student myself and don't exactly know why we call them like that.

First, chromosomes are composed of an original and a replicated chromatid, called sister chromatids. Chromatids are composed of tightly packed DNA.
DNA is replicated after the end of the S-phase, or in other words, the material composing the two sister chromatids is there. The catch is that chromosomes and chromatids aren't actually condensed yet, the DNA is still completely unpacked at this stage. So in fact, while you do not see actual chromosomes, the material composing them has been duplicated during the S-phase.
DNA condensation occurs two steps later during the prophase, where distinct sister chromatids/chromosomes are then formed from the packing of DNA that was duplicated during the S-phase.


text:
How did humans know the process of domesticating animals?
If people in ancient times had no scientific knowledge  about natural selection and Darwinism, how were they knowledgeable about animal domestication and artificial selection?
What tools and techniques did they use to intercept animal reproduction and obstetrics? Did they use any artificial insemination tools?

Humans do not need to understand it to do it, nor is any technology needed. Just keeping the wolves we liked and driving off/eating the ones we did not for hundreds of generations got us dogs. there is no forthough necessary just favoritism.

It's common sense for 3-4 generation families living in tribes and cities to see heredity around them and learn from spoken tradition. tempers and physical traits are inherited. Conceptually they would also understand from mixing food ingredients, from mixing inks, that when you add two things together, you get a combination of the two. It's easy for them to consider using the largest animal of every generation to make the largest stock. Prehistoric people would not use freezers and condoms:) they would not complicate the act of putting two animals in the same room.

Prehistoric people had a similar intelligence as today, they just didn't have books. They knew absolutely millions of things about nature and conception. If you go to a yanomami village you realize that there is a lot of method and the magic explains only things that are not logical, linear, additive, related, visible, heredity is fairly straightforwards, it's very additive and visible.

That might be more a history or archeology question than a science question.
Early domestication
While there was no concept of long term evolution, many people could witness that offspring of individuals (whether plants or animals, incl. humans) looked like their parents. From there, it is not much of a stretch to understand that by breeding individuals with desired traits, you would get offspring with desired traits. This is artificial selection at play.
Artificial insemination
Early animal domestication did not use much artificial insemination. According to Britannica.com, the first successful artificial insemination in animal was in 1780s only.
Intended vs unintended selection pressures
Note however that I do not want to claim that most of the domestication traits evolve by the human intention to make them more frequent in the population. It might be just that individuals poorly adapted to domestication would flee or get harmed or something and would therefore have lower survival. For example, aggressive individuals could get hurt by their farmer.
Note btw, that wether the selection pressure by the farmers were intended or not, we still typically use the term artificial selection.

It would be good to leave a comment when down voting so that I can improve upon the answer.

I think this is a very interesting question but not necessarily directly related to genetics. This is more a question related to fields such as cognitive archaeology/anthropology and technological lithic analysis of how tools were made.
I'm not too familiar with Homo sapiens myself as it's unrelated to my field, but a close friend of mine is an evolutionary anthropologist who specializes in Homo neanderthalensis but knows a whole lot more about this than I do. I asked him for some suggested reading about this and here are his suggested introductions to the subject.
General interest but very comprehensive and in depth: Stringer, C. & Andrews, P. (2011). The complete world of human evolution. London New York: Thames & Hudson, Inc.
College textbook: Boyd, R. & Silk, J. (2009). How humans evolved. New York: W.W. Norton
The 2nd source actually delves into the topic of evolution of human intelligence, behaviour, culture, genetics and mating. If you want to learn more about the technological evolution, development, production and sophistication of stone tool making I suggest reading about things such as the Levallois technique. I hope this provided an answer to at least some of your questions! :)

That sort of makes sense, but I was interested in the techniques and practices of agriculture, animal domestication, and possibly plant domestication. How humans were able to control the mating of species to get them to do what they wanted to do, and even though the knowledge of how animal reproduction wasn't there, they still had instinctually messed with nature--whether it was for good or for bad you decide.


text:
Why can't we move our toes and some fingers separately?
In our feet, other than the large toe, the other toes cannot be moved separately. If we try to move them, then all the four toes move together. We cannot move each toe by itself.
Same thing occurs in the hands of some of us, where we cannot move the little finger by itself. While folding the little finger, the ring finger before that also has to be folded to some extent, and vice-versa.
An explanation to the problem with the ring finger and the little finger can be found here.
The phalanges make the toes. Are the phalanges of the small toes connected, such that we cannot move them separately?

While I agree there are limitations to the phalanges you mention, I can easily move only my ring finger inwards towards my palm. I think there may be a more definitive way to describe the limitations on motion?

The answer here: https://biology.stackexchange.com/q/60075/107, effectively answers this as well.

Perhaps you should ask this question on the Music site, with special reference to pianists, harpists, and the like.  Or someone like me, who's typing this comment with all 10 fingers. With fingers, it's basically a matter of training.  I expect much the same would be true of toes.  Searching for "toe dexterity" gets over 600K hits, including this: https://themovementfix.com/how-to-improve-your-toe-dexterity/

A relatively new area of the brain's cerebral cortex evolved to enable humans and other primates the necessary small motor skills to pick up small objects and deftly use tools, scientists now say. https://www.youtube.com/watch?v=zyl6eoU-3Rg
Primates can move their ears too, here's a theory of it. Other motor skills that are not often developed are individual eyebrow movement, pectoral flexing, ability to sneeze with your eyes open.
Hand movement is new and developing compared to chimps.
Toe movement is latent and receding.
The human hand is built up onto a squirrel/clawed paw, If you take a while to rotate your forearm and the flexors of the fingers, you will see that it's a mutated simple flexing mitt thing with with a new fine motor dexterity that you use all day, added on top of the vestigial clawing and grasping hand.
https://www.youtube.com/watch?v=vlwAoKpSI7s
This page says:
Signals generated in the primary motor cortex travel down the corticospinal tract  through the spinal white matter to synapse on interneurons and motor neurons in the spinal cords ventral horn. Ventral horn neurons in turn send their axons  out through the ventral roots to innervate individual muscle fibers.
The motor cortex is subject to plasticity and remapping. To know this question is beyond my field of knowledge, someone else can go on from here :) you'd have to learn about the motor cortex, plasticity, vestigial nerves, nerve mappings, it's a fantastically complex topic.
What's interesting is the variety and quantity of different muscular abilities that are inherited by a population, it reflects an optimized level of evolutionary plasticity and specific types of variety of useful traits like muscle and joint proportions to ensure fast and flexible species development.

plenty of humans can move their ears.

Other motor skills that are not often developed are individual eyebrow movement Interestingly, I can do this.


text:
Does TA-65 cause cancer?
I heard about this supplement that lengthens telameres, slowing down aging. Does it cause cancer? I can't seem to find any definitive proof either way... https://www.tasciences.com


text:
Purpose of the conversion of 3-PGA to G3P in the calvin cycle?
3-PGA ($\ce{C_6H_7O_7P}$) is converted to G3P ($\ce{C_6H_7O_6P}$) before it is able to be made into glucose, with an expansion of 6 ATP and 6 NADPH. My question is why this process is needed and why the loss of 1 oxygen atom decides whether a sugar molecule can be synthesized into glucose. My take on this matter is that if they incorporate 3-PGA directly into glucose, they can save time and also energy in the form of ATP and NADPH.

Obviously not a complete answer, but I wonder if it's partially because NADP+ is needed to absorb the electrons and protons at the end of the ETC at PS-I to avoid a surplus of NADPH and H+, resulting in a dangerously acidic environment.  Good question, btw.

@rotaredom — Please observe the text that appears in the comment box: "Use comments to ask for more information or suggest improvements Avoid answering questions in comments." Comments are not for answers, complete or incomplete.

Please refer to chemical compounds by their names as well as their abbreviations for clarity and indexing. 2. This is a question of chemistry which is covered in any biochemistry text. Your naive remark about "saving time and energy" and your emphasis on irrelevant chemical compositions suggests that you should consult such a text before posting. I suggest Berg et al. online Chapter 20. This wouldn't be a homework question by any chance?

Although I liked answering this question, it did not take me more than 5 minutes to gather all the required stuff for this answer. From next time, @user35897, please show some research effort before asking a question. As of now, I am voting to close this question.

Nice question! To see what trouble that extra oxygen can cause, lets get to the core of the reaction i.e. Calvin-Benson cycle; one step at a time. To start with, have a look at the detailed Calvin-Benson cycle (following image taken from here):

As becomes quite clear from this image, the actual use of Glyceraldehyde-3-phosphate is at the step of formation of Fructose-1,6-bisphosphate. Yet, we don't know why we cannot use 3-Phosphoglycerate instead at this step. For that, lets go a step further and see how the concerned enzyme, fructose-1,6-bisphosphate aldolase/phosphatase (aka aldolase), works.
Since the full article is behind a paywall, lets get a sneak peak into it. See this image1:

Pay attention to the steps where G3P enters i.e. steps between b and c. Even without entering into details of the mechanism, we get two factors which can prevent 3PGA from being utilized in this reaction:

Steric Hindrance: replace the terminal -H with -OH of G3P in the first image in your mind. You can clearly see that this would cause some steric hindrance and prevent formation of covalent bond between DHAP and G3P.
Formation of Geminal Diol: again, replace the terminal -H with -OH, but this time in the second image, in your mind. You get geminal diol in the resultant molecule, which is famous for its reactivity and instability. Thus, by adding 3-PGA instead of G3P in the reaction, we might end up with unstable molecules that cleave themselves up. I hope this is what you were looking for.

Reference: Juan Du, Rafael F. Say, Wei Lü, Georg Fuchs, Oliver Einsle Active-site remodelling in the bifunctional fructose-1,6-bisphosphate aldolase/phosphatase Nature 478, pages 534–537 (27 October 2011)
doi:10.1038/nature10458

Hi sorry I missed your answer. So just to clarify, the reasons are 1)NADP+ is needed to absorb the electrons and protons at the end of the photosystem 1 electron transport chain,  or else it would result in an acidic environment in the chloroplast.
2)It will prevent covalent bonding between the DHAP and G3P, causing steric hindrance.
3)An unstable molecule (Geminal Diol) would be formed, which will cleave itself much like the intermediate 6-carbon molecule which was formed after carbon fixation.

are there any more reasons or holes in the above summary?

The first point seems to come from @xusr's answer, so I cant be so sure about it. The other two points seem just fine though (sorry for being late, I really cant get time to access this site)

Thanks for the help! Much appreciated. I tried researching on this myself actually but I couldn't find anything useful

Anytime, mate! Thats what we're here for ;)


text:
Which filament slides past which?
Somehow I haven't found anyone on the internet can answer this: during muscle contraction, does the thin myofilament slide past the stationary thick myofilament, or does the thick myofilament slide past the stationary thin myofilament?

think of it this way : the thin filaments are attached to the Z-line(with the help of Z -disc) and thick filaments with the help of a spring like protein(titin). Now, when contraction occurs, myosin head pulls the actin filament towards it (power stroke) : i.e. Z-line is pulled towards the centre and the length of sarcomere shortens. So, actin is pulled towards the centre : Thin filament slide over the thick ones. PS: I'll try to add a detailed ans later on. =)

This is an article on muscle contraction. It'll help to solve your problems. Especially read the part where the information about mechanism of power stroke is given (above figure 11.24).
Ask if you have furthur questions after reading this article!
https://www.ncbi.nlm.nih.gov/books/NBK9961/

thick filaments slide over thin as cross bridges are formed by thin filament which slides thick filament and sandwich like structure is formed and Z-line disappears

Thank you for answering. Do you have any credible references however?

actually i read abou that in my state board textbook of biology

can you reference the textbook then?

i already reffered it and wrote answer

That's not a reference, what is the title of the book? Who is the author or publisher? What year was it published?


text:
Octopus behaviour

When visiting a museum in Malmo my friends and I came across this little guy. While we observed him wandering around his tank he suddenly opened a channel on the side of his head and shot some red string out of it. The string seemed kind of sticky, nothing like ink. We are still wondering what it was and why he was doing it. Maybe some kind of defensive behaviour or just usual octopus stuff?

Just a guess, but could the octopus have been pooping?
This is a gif of an octopus pooping. It matches your description except for the colour, so I'm not quite sure. Did it look like this? Also, could the substance look red because of the tank lights? After all, your photo looks weirdly violet overall.
Fun fact: octopuses have their anus channeled in the siphon (the "channel on the side of his head" you observed) and this has been object of a question here in Bio.SE.

Was also one of our guesses. The link doesn’t show a pooping octopus though. Really just that foto, we had plain sight on it.

@PeterS whoops, sorry, now the link should redirect you to the correct page...


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How can epigenetic changes be erased if they are inherited?
I’m a little bit confused about DNA methlyation reprogramming and about the nature of an epigenetic phenomenon. According to Wikipedia:

After fertilization the paternal and maternal genomes are once again demethylated and remethylated (except for differentially methylated regions associated with imprinted genes). This reprogramming is likely required for totipotency of the newly formed embryo and erasure of acquired epigenetic changes.

I don't understand how something can be thought to be both heritable and erasable. Any help would be greatly appreciated.

I'm voting to close this question as off-topic because the poster has already answered the biological question by his own research, for which he is to be commended. He can find the origin of the term in a similar way, but that is not biology.

@David Are you kidding? There is a terminology tag on this website. Maybe I should have use it, but I don't think my question deserves to be closed for that.

The tags that people use do not define the purpose of this site or the acceptability of questions. This is explained in the Help on Asking questions. Questions on why something has such and such a name are generally of little interest to biology, except for its history, and, in any case you show no evidence of trying to find definitions yourself. A Google search for "Epigenetics Definition" includes a definition by Robin Holliday that might remove the unstated and erroneous assumption of your own on the meaning of the word.

@David - there is definitely important misunderstanding still present in the question that was not addressed by the OP, and it seems this is a misunderstanding you have as well. I see absolutely no reason to close this question, because even if its title seems to be about semantics an appropriate answer would not need to be.

@David All the websites and sources I used before posting this question mentioned that "Epigenetics is the study of heritable changes in gene function that do not involve changes in the DNA sequence." (This comes from the wikipedia article about epigenetics, but this isn't the only source that mentions the heritable character of epigenetics phenomena). I know that we are supposed to make some efforts before asking anything here, and that's what I did. Unfortunately, I didn't find your Robin Holliday definition before, so sorry about that. In all cases, I still think my question matters.

@BryanKrause — It is not just the title that is about semantics, it is the concluding sentence in the question, clearly meant as the key question because it is in bold. There may be interesting answers on epigenetics, but they need a clear biological question first. This is not.

@David The answer is because some portion of epigenetic changes are indeed heritable. How would you propose the questioner reframe their question to fit your narrow view of what makes a good question here? Their curiosity is clearly based on the biology of the situation. SE English language and usage is not for scientific terminology.

(1942) "Biology. of or relating to epigenesis, or the successive differentiation of undifferentiated cells in an embryo." This just illustrates that words are coined, used in different contexts, get contorted in the public mind by political and religious misuse (Lysenko, anyone?), but that most English-speaking professional scientists manage to live with their scientific usage, understanding what they mean. The structure of a compound word coined in German, for example, is clear to German speakers. English speakers often neither know or care about the structure of words from Greek or Latin.

@David I don't understand the point of your last comment, but I'm not a professional scientist (still a student), and my mother tongue isn't English either, so sorry again about all that mess. Anyway, I don't really see how to improve my question. What I don't understand is that epigenetics phenomena are supposed to be heritable, while apparently those changes are erased after fertilization... which doesn't make sense to me. I don't really care about the origin of the word "epigenetics", I just would like to understand how changes can be inherited and erased at the same time.

@BryanKrause — Not nice, saying that I have a narrow view on the suitability of questions. I not only exercised my right/duty to maintain the standards of the site, but explained to the poster my reasons for doing so, something I am not obliged to do. I refered the poster to the SE Help, as the source of information on posting good questions, and told him how to find the origin of the word himself, together with naming a SE site that is more appropriate — SE EL&U does take questions on technical English.

OK. If that's your question, I'll edit it in that direction. Perhaps @BryanKrause will add further, and then I'll withdraw my close vote.

@David Thanks for editing it. I just made it "sound" a little bit more like I would have written it. Hope you don't mind. :)

I have done a presentation in epigenetics and the main topic was imprinting.
This paper will answer all your questions https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3941233/
I am adding some glimpses from this  paper here
Mammals are diploid organisms whose cells possess two
matched sets of chromosomes, one inherited from the mother
and one from the father. Thus, mammals have two copies of
every gene. Normally both the maternal and paternal copy of
each gene has the same potential to be active in any cell.
Genomic imprinting is an epigenetic mechanism that changes
this potential because it restricts the expression of a gene to
one of the two parental chromosomes. It is a phenomenon
displayed by only a few hundred of the approximately 25,000
genes in our genome, the majority being expressed equally
when inherited from either parent. Genomic imprinting affects
both male and female offspring and is, therefore, a consequence
of parental inheritance, not of sex. As an example of
what is meant by this, an imprinted gene that is active on a
maternally inherited chromosome will be active on the maternal
chromosome and silent on the paternal chromosome in
all males and females.
Hope this help and please ask if you do not understand the paper.Thank you


text:
Are new blood vessels able to deliver oxygen to hypoxic tissue before the establishment of blood circulation?
Sprouting angiogenesis - the growth of new blood vessels from a preexisting vasculature - can be triggered by cells in hypoxia in order to re-stablish the oxygen and nutrients supply to the tissue.
The formation of a new vessel is a multistep process starting by the activation of the Endothelial Tip Cell (ETC) phenotype that migrates through the tissue guided by chemotactic cues, such as the Vascular Endothelial Growth Factor (VEGF) concentration. The cells near to the ETC gain the Endothelial Stalk Cell (ESC) phenotype and start to follow the ETC and proliferate in order to form the new branch.
The Endothelial Cells (ECs) re-arrange in the new branch, forming the lumen. Thus Smooth Muscle Cells (SMC) and pericytes are recruited to maturate the new vessel. Consequently the vessel is filled with blood from the main branch.
My question is: when does the new vessel starts to deliver oxygen to the surrounding tissue? Can it occurs before the anastomosis formation where the circulation is stablished, even for a short period of time due to the plasma that filled the new branch? (See the following picture where they represent the cells near to the new branch with a high concentration of oxygen even without anastomosis/blood circulation)

Image Source: Peter Fraisl et al. Regulation of Angiogenesis by Oxygen and Metabolism. DOI 10.1016/j.devcel.2009.01.003

It is true that for long-term oxygen delivery the new vasculature must establish circulation. However, when the new vessels are starting to maturate they are filled with blood coming from the main vessel, which carries oxygen.
Since the endothelial cells of the new vessel derive most of their energy anaerobically through glycolysis (Quintero et al, 2006; Dagher et al, 2001; Krutzfeldt et al, 1990; Peter Fraisl et al, 2009), a metabolic mechanism  activated in critical microenvironments like hypoxic tissue (DeBerardinis et al, 2008), the oxygen in the lumen is free to be immediately delivered to the tissue.
Thus it is fair to assume that  at least for a short period of time the cells near to the new vessel are being oxygenated.

References:
Quintero, M., Colombo, S.L., Godfrey, A., and Moncada, S. (2006). Mitochondria as signaling organelles in the vascular endothelium. Proc. Natl. Acad. Sci. USA 103, 5379–5384.
Dagher, Z., Ruderman, N., Tornheim, K., and Ido, Y. (2001). Acute regulation of fatty acid oxidation and amp-activated protein kinase in human umbilical vein endothelial cells. Circ. Res. 88, 1276–1282.
Krutzfeldt, A., Spahr, R., Mertens, S., Siegmund, B., and Piper, H.M. (1990). Metabolism of exogenous substrates by coronary endothelial cells in culture. J. Mol. Cell. Cardiol. 22, 1393–1404.
DeBerardinis, R.J., Lum, J.J., Hatzivassiliou, G., and Thompson, C.B. (2008). The biology of cancer: metabolic reprogramming fuels cell growth and prolif- eration. Cell Metab. 7, 11–20.

But if that blood doesn't circulate, why would it not be in oxygen equilibirium with the tissues around it? If anything, the citations that new endothelial cells use anaerobic energy sources seems to support an idea that the new vessel does not supply oxygen, contrary to the answer given.

@Bryan 90% of the energy is coming from anaerobic glycolisis, but 10% is still obtained from the oxygen carried by the blood that fills the new branch. The lumen is formed due to hydrodynamic pressure imposed by the blood coming from the main vessel and that blood is known to bring oxygen. The endothelial cells use almost none oxygen because they activate a different phenotype in order to survive in the hypoxic tissue and they continue like that until the tissue is completely irrigated with blood circulation.


text:
Why doesn't surgical steel cause inflammation?
It seems some very specific alloys like implant surgical steel and titanium don't cause inflammation in the human body, but when I asked my doctor about it, they simply said "it just has some chemical property that doesn't cause it."
So...what exactly is special about these metals compositions as to not cause inflammation like most other things would?

Surgical steel can cause some inflammation (basically everything can) -
it's just far less inflammatory than other metals and many other materials. You may want to edit your question to avoid an attack from the pedants. I'd also suggest removing the x-files references, they're mostly just distracting and not important for your actual question if you want it to be about biology and not science fiction.

Usually people irrationally complain if there's no context or apparent reason for a question.

Some can
First the terms you are looking for is biocompatibility and bioactivity. The study of them is called biomaterial science. Both fields are relatively new so complete answers do not exist, there has been a certain amount of trial and error in find suitable materials.
There are a dozen factors that go into these things, toxicity, whether they corrode in the body, whether they are soluble, chemical reactivity, whether they trigger an immune response, whether they can bond with bone or other tissues, mechanical resilience, steric and electrical properties, wetting, even how smooth it can be made can have an effect. The other important thing is many materials have very different biocompatibility depending how and where they are used, different parts of the body can have very different conditions, for instance material used in a bone screw might be useless in a dental implant (different PH and chemical exposure) or a heart valve (different mechanical and electrical requirements).
Titanium has remarkable biocompatibility with internal bone implant, its already low reactivity actually gets better as its surface oxidizes as it becomes slightly polarized and will incorporate many cellular surface molecules(passivation). Many of the factors that make titanium useful in this way are still being studied.
Surgical steel is a broad term that covers several types of steel used for  multiple medicalpurposes, it includes steel implant and steel only used for instruments. Some forms of surgical steel work great for instruments but are rarely for internal implants, often because the same nickel content that makes them corrosion resistant is also bioreactive, triggering an immune response, but its superior mechanical properties means it still is sometimes used as implants, especially temporary implants were corrosion is less of an issue.  (paper, sorry it is only available in German). Nickel free surgical steels used in cutting implements is stronger and harder (what you want in a medical blade) but  without nickel it will quickly corrode in the body.
Part of the reason your doctor did not know was some aspects are still unknown in general and the study of these properties is rather specialized so a general practitioner may have never studied the parts that are known. Consider an  pilot still know very little detailed metallurgy of their engine components, and still be an excellent pilot becasue they don't really need to know.  Heck most of reason I know anything about it is I used to hang out with a guy who made titanium implant screws for a living and it just sounded kinda interesting so I read up on it.

Coincidence ? Vitallium has been used in gas turbines since the 30's ( the first engines, and it still has a place in these engines.)

As far as I know "surgical steel" for cutting tools is never used for implants . And, reactions to metals are mostly allergys. Surgical steels are martensitic ( hard) chrome stainless , eg 440 A, B, C, and 420. Some surgical tools are 316 stainless which is also used for implants. Better implants are made of titanium usually with a titanium oxide surface ; bone will attach to the oxide surface but generally not to 316 SS. There is Ni in 316 stainless and some people are allergic to Ni. Anything with Cu would be a terrible choice as it has strong toxic properties; eg , it is used to clad ships to prevent barnacles . There are some other minor use of ,eg. Vitallium ( alloy of chrome and cobalt) and others.

After looking at Johns' reference above, I see Vitallium ( aka. Stellite 21, aka cobalt/chrome) is becoming more common again .It is likely replacing some 316 SS because of nickel allergies. And is cheaper than Ti after you put on the plasma spray oxide . Ti is still the better choice , good bone bonding, lower density , lower stiffness - more like bone.

Surgical steel doesn't cause inflammation because (i) it has very little solubility, and (ii) what little iron ions do get dissolved into bodily fluids are chemically too simple to be recognized by the immune system and trigger an immune response. Moreover, the human body naturally contains small amounts of iron, e.g. bound to myoglobin in cardiac and muscle tissue.

I would think a practicing graduate physician for 20+ years would know an answer like that off the top of their head, are you sure it's that simple? Copper metal itself is insoluble, and copper is also found in the human body, and copper metal has an extremely simple chemical formula Cu, and yet something tells me a copper implant is still going to cause inflammation if insert it into someone. Could it possibly be more related to the ligands it forms?

Copper and iron have slightly different physical and chemical properties, but basically that's it. Steel is used because additives like silicon or carbon permit fine tuning of different physical properties like tensile strength and expansion coefficient + it's cheap and abundant. Most things you can achieve with steel you can achieve with titanium as well, but titanium is a lot more expensive, so you use it only when you really need to.

But see what are those "slight differences" that define whether something causes inflammation or not?

Inflammation may be caused by complex macromolecules such as proteins and nucleic acids, which are recognized by the immune system or (a lot more rarely) simple molecules, which become bound to larger molecules, like proteins. In the latter case, the immune system is able to recognize the small molecule-protein complex, which initiates inflammation; such a potentially inflammatory molecule is called a hapten. Copper may be slightly more prone to binding/adsorbing to proteins because of factors such as electronic structure, the solubility of the specific material/alloy, and others.


text:
How does use an action potential from innervation selectively modify tropomyosin over time?
Within a myofibril, the myofilaments move past one another to product muscle contraction if and only if the actin binding sites are exposed to the myosin by locally removing the tropomyosin by binding it with calcium ions
What isn't quite clear to me however is: what does a pulse from a motor neuron do to the tropomyosin in order to to excite this initial change to move the tropomyosin away and expose the actin?
Then, how does the muscle cell and/or motor neuron sustain this state of contraction, and then finally decide to end this state of contraction and return the muscle cell to its relaxed state?
Also, where exactly is the tropomyosin going after it binds with calcium ions?

At the neuromuscular junction, motor neurons release acetylcholine which binds to nicotinic acetylcholine receptors on the muscle. These receptors are ligand-gated ion channels that are permeable to small cations.
Opening these channels depolarizes the muscle cell membrane, which causes the opening of calcium channels, primarily on the sarcoplasmic reticulum (SR) for skeletal muscle. The key channel is called the ryanodine receptor and is either mechanically coupled to a voltage-gated calcium channel (skeletal muscle) or activated by calcium released from voltage-gated calcium channels (smooth & cardiac muscle), but in both cases the change in voltage is the initial signal.
Calcium concentrations are very low in the muscle cell at rest, but high within the sarcoplasmic reticulum so calcium rushes through and some of it binds with troponin (not tropomyosin itself, but they are associated/attached with one another), which releases the hold of tropomyosin on the actin filament.
The calcium-bound tropomyosin doesn't go anywhere, but as calcium is quickly pumped into the SR or buffered up by calcium-binding proteins, troponin is no longer bound to calcium, allowing tropomyosin to block the myosin binding sites.
The increase in calcium concentration is transient, and travels in a wave down the muscle. If there are no further action potentials, the muscle will relax. Constant contraction requires a constant train of action potentials, and the overall strength of the contraction can be regulated by the firing rate of the motor neuron.
The Wikipedia pages for muscle contraction, tropomyosin, voltage-gated calcium channel, and ryanodine receptor can all be helpful. I'd also recommend a basic textbook on neuroscience, which typically covers neuron effects on muscles and some of the mechanics of muscle contraction. I typically recommend Purves, see https://neuroscience5e.sinauer.com/ or a library or anyplace you get books from (any edition is fine).


text:
How do I name a binding antibody? “Binding antibody to”, “binding antibody against”, or “anti-[antigen] binding antibody”?
I'm translating a text that describes how an immunogenicity of a drug is measured by assaying the levels of binding antibodies to the drug. Or is it "against the drug"? I'm wondering how to name these antibodies. Let's say the drug is cetuximab, and I'm writing the title of a document section:

Assay of binding antibodies against cetuximab in serum.
Assay of binding antibodies to cetuximab in serum.
Assay of anti-cetuximab binding antibodies in serum.

I googled for "binding antibodies to" and "binding antibodies against" and got only several dozen results for each of the two options. Therefore I came up with "anti-[name of the antigen] binding antibodies", but don't know how to google for it, hence my question here. Would option 3 look nice to a native speaker?
P.S. Alas, it is exactly "binding antibodies to" in my Russian text. I cannot omit the adjective "binding" before "antibodies"..

Связывающие антитела к цетуксимабу.

I quote from the Wikipedia page on neutralizing antibodies:

Most antibodies work by binding to an antigen, signaling to a white blood cell that this antigen has been targeted, after which the antigen is processed and consequently destroyed. The difference between neutralizing antibodies and binding antibodies is that neutralizing antibodies neutralize the biological effects of the antigen, while binding antibodies flag antigens.

My authors use the adjective "binding" to distinguish binding antibodies from neutralizing antibodies, just like in this paper, for instance: BAbs and NAbs. Another section in my document gives the results of an assay of NAbs against the same antigen.
Explanation of the difference between binding and neutralizing antibodies from the FDA:

(ADA: anti-drug antibodies)

Not worth an answer, just a comment: antibodies can be abbreviated to Ig, too, so in-text you could also call them "anti-cetuximab Igs" if you find the full expression to be too verbose.

@xusr - I'm afraid "assay for" would imply only the description of the procedure, but in my case the section describes both the procedure of antibody concentration measurement and the results of the procedure. Would of look really odd there?

The adjective “binding” is not used to qualify “antibody” in English scientific usage because linguistically it is thought to belong with the antigen the antibody binds.
Generally it is omitted if the prefix “anti” is used, e.g.

anti-cetuximab antibody

(e.g. “two or more anti-hapten antibodies” here)
However if you wish to refer to the particular small portion of the antigen that is recognized (the epitope), you might write, e.g.

tyrosine-binding antibody

(e.g. “Hapten‐binding antibodies…” here)
As far as the use of prepositions is concerned, “to” is used with binding, although it is optional. However generally with the antigen, e g.

cetuximab binds to the antibody

(e.g. “Antigen binds to the antibody on the B-cell membrane.” here)
But

the antibody binds cetuximab

(e.g. “An additional VNAR, Help6, which binds Hepatitis B precore protein” here.)
Completely illogical, I know, and this distinction is not universal.
However, “against” is used in relation to preparing or raising antibodies, e.g.

We raised an antibody against cetuximab…

(See the legend to Fig 1. in this paper.)
So in general one would write:

Assay of anti-cetuximab antibodies in serum

Addendum: Binding antibodies v. Neutralizing antibodies
The revised question makes it clear that the authors are referring to “binding antibodies” as a specific contrast to “neutralizing antibodies”. This expression was not known to me (I am not an immunologist), and, although the poster documents it, its use would appear to be limited, perhaps because the topic is or was controversial.
The question remains, how to express this idea in a clear and unambiguous manner, with the specific problem that the poster is a translator, not an editor. I would still try to avoid the use of the word “binding” in the expression. I have two suggestions:

I believe that an alternative expression would be “non-neutralizing antibody” (the paper just quoted does not hyphenate this term, but others do, and I would). If this belief is correct, one could write:

Assay of non-neutralizing anti-cetuximab antibodies in serum

Alternatively one could use the abbreviation, “BAb”, from the paper cited by the poster, although this would have to be defined somewhere.

Assay of anti-cetuximab BAbs in serum

Indeed, you are correct, good sir. You know what they say - there's more than one way to refer to an antibody!

I was preparing this answer on SE EL&U when some idiot commented that he should post elsewhere — not necessary — and I couldn't post my answer as the question had been deleted. Hence the somewhat linguistic tone.

Ah, but the linguistic tone is not at all out of place in SE Biology; quite the contrary, it is most welcome.

@Stefan — Not what I was saying earlier today, but I could hardly send him back to EL&U.

I know. I mean I enjoy the linguistic tone no matter where I come across it.

I figured it out. My authors use the adjective "binding" to distinguish binding antibodies from neutralizing antibodies, just like in this paper: BAbs and NAbs. Another section in my document is dedicated to the results of an assay of NAbs against the same antigen.

I have included an addendum in response to your clarification. As both Stefan and I were confused by the use of the word “binding” I would still advise against using it.

@David - thank you for the addendum, David! My customer won't ever let me edit out the adjective "binding".. Because there are many translators working on many documents for this customer, and the majority of them will use the word "binding" as an adjective there without blinking an eye, and it would be sheer hell to make them all adhere to "non-neutralizing" or to just "BAbs". But thank you for your effort!

@CopperKettle — Sure, I understand your situation. I'd go for 3, then, perhaps hyphenating binding and antibody to emphasize their association.

In English, you say that antibodies bind to something (X), not against something. You can use the phrases "X-binding antibodies," "X-specific antibodies," "X binders" (when referring to the antibodies that you've previously introduced in the text), to name a few. You can use "antibodies binding to X," but not "binding antibodies to X," people will misinterpret the latter, because it means something else is binding to the antibodies or you are trying to bind something to the antibodies.


text:
Does dreaming have any physiological impact on our body?
Personally speaking, when I wake up after a really good dream, I feel really happy, similar to how I would feel if something good has happened in reality. This makes me wonder if we are actually going through stress when we are having a nightmare. Is there an increase of epinephrine in our body when we dream about being in trouble or running away from a scary situation? Similarly, are endorphins released when we are experience a happy moment in our dreams?