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Why Goldman Equation cannot be used to calculate dynamic changes of membrane potential
I'm reading about Goldman Equation and I've seen in some resources that it calculates the resting potential (not membrane potential in general) and that this equation cannot be used when membrane potential is changing. One example is in Kandel textbook:

This equation applies only when Vm is not changing. Principles of Neural Science. Eric Kandel, Fifth edition. p. 135.

I don't really understand why this equation cannot apply when Vm is changing. Precisely, I understand that this equation defines how membrane potential changes taking into account permeability and concentration of ions. If you "give" to it the concentration-permeability changes for each moment, it'll show the Vm for each of these moments.
Could someone explain that to me?
Thank you very much!

What's the purpose of the Goldman equation?
I think that statement you posted from Kandel is a bit misleading, though not incorrect - I think he's just warning against a pitfall he's seen students make.
The Goldman Equation is an equation for steady-state voltage or in other words the reversal potential, not for Vm. It will only give you Vm in a (mostly) steady-state condition, like in the context of a resting membrane potential. However, that doesn't mean it isn't useful to calculate the Goldman equation voltage when Vm is changing or that it doesn't apply, but rather that it is not sufficient to use. It will still accurately tell you what the reversal potential is at any moment in time, but it can't tell you what Vm is at that moment.
How the Goldman equation can be helpful in understanding dynamic voltage changes:
Importantly, the rate of change of the voltage of the cell is going to be proportional to the difference between the reversal potential (from the Goldman equation) and the current voltage Vm, and after a long time the voltage will eventually asymptote to the Goldman voltage.
Therefore, if you know the current Vm, and you calculate the reversal potential with the Goldman equation, you can make some inference about what will happen to the voltage at the next moment in time: it will change in the direction of the reversal potential by a magnitude proportional to
Vm - Ereversal
Why the Goldman equation is not sufficient while Vm is changing:
I suspect what Kandel and others are warning about is that this isn't quite enough information to know what happens in the next moment of time:
It takes time to reach a steady voltage, and you need to know the membrane capacitance, which isn't represented in the Goldman equation, to know what the actual change in voltage is after $\delta$t, or how long it will take to reach a particular voltage.
Also, because of voltage-dependent conductances in a neuron, the permeabilities to different ions are also changing as a function of Vm, so the reversal potential is also changing constantly.
Furthermore, simulations of Vm sometimes need to consider the changing concentrations of individual ions, because the reversal potential will change as ion concentrations change. Therefore, it typically makes more sense to think about the driving force of individual ions given by the Nernst equation rather than the Goldman equation which gives you the net reversal potential across all ions.
Summary
In summary, authors that warn against using the Goldman equation when Vm is changing are reminding you that voltage changes take time and depend on membrane capacitance as well as changes in conductance from voltage-gated channels. However, the Goldman equation is still a correct way to calculate the instantaneous reversal potential at any moment in time (but not Vm), even if Vm is dynamic.
You could edit Kandel to say:

The Goldman equation only outputs the present Vm when Vm is not changing; also, when Vm is changing, the output of the Goldman equation is also changing due to changing conductances and ion concentrations.

..but you can see this is a bit verbose.

Thank you Bryan for your very complete response.
Do we have an equation that permits us calculate Vm when the cell is not at resting levels?

@Alexei You need to use differential equations, because the Vm will always be a function of itself as well as other parameters. There are lots of different ways to express these equations, you can find some of them here: http://www.cns.nyu.edu/~david/handouts/membrane.pdf In practice, though, changing voltage-dependent conductances mean that a lot of the quantities that seem to be constants in these equations are also functions of time and the other parameters, so in that context you need a model like the https://en.wikipedia.org/wiki/Hodgkin%E2%80%93Huxley_model

I've found this resource http://www.physiologyweb.com/lecture_notes/resting_membrane_potential/resting_membrane_potential_in_real_cells_multiple_ions_contribute_to_the_membrane_potential.html
Focusing in the text that refers to Figure 1, would you say that this part is wrong or, at least, not totally correct?
Reading this resource I thought I've understood the lesson, but your responses have made me see that it's no so easy :(

@Alexei Without going into it line by line, that figure seems fine, but what is important to realize is that this is a toy example showing you how relative permeabilities influence the membrane potential if one sets them magically in a model. It's really important to understand how this works, because it's an important building block to understanding the rest. Then, when you move on to real cells, it's important to recognize that the permeabilities are all changing dynamically because they are driven by physical channels rather than experimenter-set variables.

Then I understand that de GHK equation can serve as an introduction to the "picture" but isn't the whole picture at all. Thank you Bryan for your kind responses :) You've been very helpful.

@Alexei Glad to help. If this answer was useful it's appropriate to vote it up; if you think this answer fit everything you needed then it's appropriate to accept it, otherwise the community bot will keep bumping the question occasionally, assuming it doesn't have an answer yet.

Nicely answered


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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 does the olive tree produce a bitter tasting fruit?
What is the survival value for the olive tree to produce a bitter tasting fruit, even when it is ripened?
I realize some fruits and berries are species specific, i.e., meant for specific animals to eat and disperse the seed widely. Is this the case of the olive?

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How many genders are there?
These days it is often contested how many genders is there. So my question is how many genders is there and is it unnatural for evolution to generate multiple genders.

this is a much better fit for the social sciences.

this is a bad question as shows complete lack of googling beforehand. I suggest you do some research and come back, asking "hey here is what i know, here is what i don't understand"

Sex vs Gender
Sex is defined by the anatomy of an individual. The majority of people can safely be categorized as either male or female. There are exceptions and limit-cases of course such as intersex people for example.
Gender is a social construct. It is therefore not the role of a biologist but the role of a sociologist to address the details of the concept of gender. I am therefore not trained to discuss these points but I will just say a few introductory words.
The gender can either refer to a social role based on the sex of the person (gender role) or personal identification of one's own gender based on personal appreciation (gender identity). The two most common genders are male and female which are named after their sexual equivalent. However, there are other types of genders. Btw, you might want to make sure to avoid confusion between gender and sexual orientation. It is also important to distinguish between "gender role and "gender identity"
Have a look at wikipedia > Sex and gender distinction for more information.
Note that, in biology, as we are not dealing with the social construct of the gender, we tend sometimes to use the term 'gender' as a synonym of 'sex'. Using the term gender instead of sex also has the advantage in biology to avoid the confusion between 'sex', 'sexual reproduction' and 'sexual organ'. I will below use the term 'sex' and 'gender' as defined by sociologists.
Answering in the text

These days it is often contested how many genders is there. So my question is how many genders is there[?]

There is no true answer to this question. There are as many genders as we want to as it is a social construct. There are only two sexes (and limit cases).

is it unnatural for evolution to generate multiple genders.

For reasons explained above, the question makes no sense. But let's replace 'gender' by 'sex' and rephrase your question as

is it unnatural for evolution to generate multiple sex?

There are species with a number of genders different from two. There are of course also species where single individuals have carry organs of both sexes. There are species where reproduction is asexual. There are species with sex but very little sexual dimorpisms (thanks @TimonG.), there are species with sexual reproduction but not sexes (sometimes mating types), etc... So, no it exists.
In humans however, there are only two sexes (plus limit cases).
Sex and sexual orientation
Of course, sex and sexual orientation are not the same thing. While there are only 2 sexes in humans (and as many genders as we want), there may be a lot of different sexual preferences. In fact, if we go into the details there are probably as many sexual preferences as there are people! Typically, we categorize those sexual preferences into a few sexual orientation. Note that there is nothing "unnatural" (whatever this term mean) to having a sexual orientation that differ from what the majority of the people with the same sex have.
You might want to read the post How can homosexuality evolve despite natural selection?

I think a noteworthy addition to this is that there are also species which do have different sexes but don't exhibit sexual dimorphism (outside of perhaps their genitals) or exhibit it to a much larger or much lesser degree than humans do. Physical and behavioral sexual dimorphism is present in humans but isn't a "biological necessitiy" in species which have sexes.

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What do you mean by non cellular matrix
What do you mean by the non cellular matrix in which connective tissues are embedded?

You're looking for the extracellular matrix:

In biology, the extracellular matrix (ECM) is a collection of extracellular molecules secreted by cells that provides structural and biochemical support to the surrounding cells.

Its main component are fibers, that can be strongly interlaced as in the case of the dense connective tissue or more loosely distributed as in the loose one.


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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


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Do Marsupials have a standard classification system for their blood groups?
I've seen a limited amount of animal blood groups listed...like dogs, cats, horses, etc. But what blood types do marsupials have?
To clarify, what I want to know is if the species has a classification system similar to the ABO blood group? For example: Blood Type A, Blood Type B, etc.
Or in the case of Dogs, the classification system is labeled as: Dea 1.1, Dea 1.2, etc.

I'm interested in this myself, as we are developing a school program on genetics and would like to include this info if it is available. A quick Google search comes up with the Wikipedia page that includes dogs, cats, horses etc. that you mentioned, plus a couple of research papers on the grey opossum and a 1960 article on koalas. I suspect that this won't change unless a large number of people start to keep marsupials as domestic pets, and the inevitable large number of injuries or operations requiring blood transfusions by the local vet.


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Microbroth dilution
I have performed MIC test for fungi candida albicans, Cryptococcus neoformans and Aspergillus fumigatus in a 96 well plate by broth microdilution method by drugs Amphotericin B and fluconazole..followed was picking up colonies just after the result i.e. after MIC test.. the next well with growth to be plated onto SDA plates then after incubation and further growth..now I have been asked to transfer them to SDB (500ml) in flasks..I would like to know why is this done..thankyou.


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Firing rate of retinal ganglion cells
I have few questions about the firing rate of retinal ganglion cells.
1) How to explain the baseline firing rate if either the entire receptive field is stimulated or there is no light stimulus at all? That behaviour means that the intensity of light does not have any effect if the entire receptive field receives the same stimulus. I don’t understand how horizontal cells let that possible.
2) When the on-center is stimulated, the firing rate is maximized at the beginning and it diminishes with time to reach the baseline rate. Why does the firing rate decrease? What is responsible for that?

3) Is it possible to have a simple mathematical model of the process with an artificial neural network?

It's best to limit one question per question, especially when they are not closely related (Q3 here, e.g.).

1) This is a bit simplified; in reality, flashes of light or dark that cover the whole receptive field do influence the firing rate somewhat, just not nearly as much as an on-center stimulus for an on-center RGC. Your textbook is using a bit of an idealized interpretation to convey the concept of center-surround organization. I'm not sure what your confusion related to the horizontal cells is, however.
2) This is usually called "adaptation" and is a general principle in nervous systems (particularly on the sensory side). Multiple systems influence adaptation, including depletion of neurotransmitter-containing vesicles, metabotropic receptors activated by high concentrations of neurotransmitter that have opposite-sign effects to ligand-gated receptors, feedback systems that suppress the potency of second-messenger systems, accumulation of extracellular inhibitory neurotransmitters, etc. For the eye, there are additional sources of adaptation that come into play, depending on the experimental paradigm.
Without knowing the exact paradigm your textbook is meaning to indicate, it's probably more important at this point to just recognize adaptation as a normal aspect of sensory processing. The specific mechanisms can be understood later.
3) Yes - but you don't need to go to anything as complex as an artificial neural network. Basic image filters like the Laplacian of Gaussian (LOG) filter are basic approximations of center-surround organization in the retina.

Thank you very much for your answer! Retina horizontal cell article on Wikipedia says that horizontal cells allow eyes to see under different light conditions. So I deduced that they are responsible of the "adaptation" you are talking about. That's right?

@ardayigit That's an incomplete explanation from Wikipedia then about the role of horizontal cells. They can have some role in adaptation, but there are many other mechanisms for adaptation and horizontal cells also have a role in making center-surround organization more robust.

so many cells are involved in adaptation. I can not say if it is done by photoreceptors, bipolar cells, etc.


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A Brain Implant improves memory--but how?
https://www.nytimes.com/2018/02/06/health/brain-implant-memory.html
A new therapy could improve memory by "sending electrical pulses to aid the brain when it is struggling to store new information." I'm trying to figure out how this works physically, in terms of how it actually helps the brain. I would imagine that it has something to do with the neurons getting past the threshold for firing a signal with more ease, but is this because the threshold is suddenly lower because of the presence of the current, or what?
Could anyone provide me with an explanation of the science behind this in lay terms?
Many many thanks

From what I understand, when we learn we go over things quite a few times, this is so that our brain goes over the memory cells where we store that information with electrical impulses. Thus when an electrical impulse travels over some branches they strengthen the branches, (I don't know the science behind this). This is what helps us memorise data. So if we ran lots of Impulses over the branches it could help strengthen them or fry your brain, just saying try this in a safe environment such as a lab and not in a homemade electric chair. Also like you said it helps them run easier over the brain which makes it a lot easier to remember things.
Hope this helps,
IbnJalal

Answers here need to be referenced and based on scientific information, not just ad hoc hypotheses


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What is this flat dry stick-like leaf that rattles?
I googled those terms but came up empty, here are three photos with a ruler for scale:

The hole and scratches are my dog's teeth, so as you can tell, it is strong yet not brittle. When you shake it, it rattles, like maybe there are seeds in there.
It's from a public irrigated park in a Northern Hemisphere hot desert climate (BWh) region, and I picked it up today, so spring time if that will help.
My dog is usually the one to find it, and we play fetch with it.

I believe this a seed-pod from an Inga or Delonix plant.
Inga are native to South America, while Delonix are native to Madagascar. But they've been introduced to other places and I've seen similar plants in the northern hemisphere. Inda and Delonix are both members of the subfamily Caesalpinioideae. I found the name by searching for "seed pod shaker". Sometimes you just need to know what terms to google.
Shown in the image below is pacay, or Inga feuillei.

But your pod could also be from the flame tree, Delonix regia.

It is a large seed pod of a leguminous tree (Fabaceae family).  This is one of the largest plant families that there is, so it is impossible to identify the species exactly without more information.  Many trees of this family are drought (desert) tolerant as you mention BWh region of northern hemisphere. The seed pod in your photo looks very much like Delonix regia. A couple of links are below.
https://garden.org/plants/photo/125733/
https://en.wikipedia.org/wiki/Delonix_regia


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Why does GLUT2 (With a high Km), bind less glucose at a lower glucose concentration (below Km)?
A text I am reading says
"GLUT2 is a low-affinity transporter in hepatocytes and pancreatic cells.
After a meal, blood travels through the hepatic portal vein and GLUT 2 captures excess glucose for storage.
When concentration drops below Km, much of the remainder bypasses the liver and enters circulation. The Km of GLUT2 is quite high so  the liver will pick up glucose in proportion to its concentration in the blood".
I know Km is a measure indirectly of binding affinity.
Rate also is based on concentration so at a higher concentration the rate is higher.
But the passage seems to be saying that at low Km, most of the glucose will not be transported, while at high glucose concentrations, more will be transported.
But i thought Km was a constant so I am confused.

Km is a constant which follows the unit of substrate concentration.It has a constant value. "Km of GLUT 2 is quite high" which implies that it's substrate affinity is low (inversely related). When the substrate concentration drops below that required for binding with GLUT 2 (Km value) obviously there would be bypass and no uptake by liver.

It would help if you would either copy the text acurately or provide a link. You are obviously a non-native English speaker as you have left out the articles, and probably other things besides. I assume that the sentence actually reads or means "When the concentration of glucose drops below the Km of GLUT2…" Km has units of concentration, so there is no question of the Km changing, it is the concentration of glucose that is changing, and its relationship to the Km of GLUT2 that determines whether this transporter acts on it, in the way described in any text.

I'm voting to close this question as off-topic because it is based on a misreading of a text.

Agree with @David - you're misreading... Km is the concentration that the transporter works at one-half the maximal rate (velocity) of transport. There's nothing in what you type that says anything about changing the Km (Km is a property of the GLUT2 transporter).

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Why don't cells of aquatic animals burst?
We know that if we keep plant cells in water, they don't burst because of a cell wall. But the cells of aquatic animals lack cell walls but they still survive. Why?

Comparative physiology of body fluid regulation in vertebrates
Cells are not passive components that always return to osmotic equilibrium. Through hormonal, cell signaling, and the number of pores for ion and water exchange marine animals can maintain osmoregulation in various aquatic environments. In land mammals osmoregulation is more passive since it is controlled by the endocrine system.


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Is their goli in plant cell?
We know that plant cells have dictyosomes instead of golgi but in my book it was written that plant cells have golgi apparatus?

Please try doing these before posting a question:

Consider the fact that this is not really a chatroom and posts should be written using proper and clear sentences (we can help if your English is not great but please put in some effort).

There should be some research effort from the side of the asker (did you try looking up reliable sources?).

There should be some context and explanation (for e.g. "We know that..." and "my book says"; I am not sure which "we" are you referring to and which book you are reading)

I am reading my course book

From wikipedia > Golgi apparatus

The Golgi apparatus, also known as the Golgi complex, Golgi body, or simply the Golgi, is an organelle found in most eukaryotic cells.

and further

In plants, Golgi stacks are not concentrated at the centrosomal region and do not form Golgi ribbons. Organization of the plant Golgi depends on actin cables and not microtubules. The common feature among Golgi is that they are adjacent to endoplasmic reticulum (ER) exit sites.

and also

The [trans Golgi network] may act as an early endosome in yeast and plants.

The dictyosome is a part of the Golgi apparatus. There is no english wikipedia for dictyosome but here is the french one


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Hybrid, Japanese or European larch please?

pictured in NE Scotland 29th April

To tell these larches apart from each other the shape of the scales on the cones is a good place to start.
European larch have cones with scales that are straight, rather than curving outwards.
Japanese larch have cones with scales that curve markedly outwards as in this photo below.

From Wikipedia - Larix kaempferi
Hybrid larches, being a cross between the European and the Japanese, have cones that are in between. But as this Forestry Commissions publication,
 "Know your conifers", mentions there is some variation so it is useful to look at cones from more than one tree across a stand.
Summary: Your photo shows a cone with slightly curved scales or bracts, so I don't think that it is European larch. But it could be, it is slightly misleading as the seeds (the thinner bits are protruding).
Japanese larch cones are really curved, which when I was being taught tree ID were described as 'like roses'. So a definite, not Japanese.
So in my opinion it is most likely to be a Hybrid larch, but as the cone is not fully mature and open, and there is only one to look at it could be a European larch.
When looking at cones, I find it best to find old cones on the woodland floor that way you can see them at there most fully developed, and the differences between the species are more marked.
There is another ID feature between European and Japanese, and that is the colour of the stems. The former are straw-coloured and the latter are darker, brown/purplish colour. This becomes more obvious as the season progresses.
There are quite a lot of photos of cones on the web that have been given the wrong names, which makes it quite confusing. Best stick to Forestry Commission literature, or educational institutions.
When looking for photos I came across this YouTube video by Harper Adams University which is good and actually features the Japanese Larch photo that I found on Wikipedia.

Many thanks for your comprehensive and hugely helpful reply.  I will certainly look out for other clues as this is a single specimen growing in a small amenity stand of mature beech so it should be easy enough to monitor


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What are these tiny, almost transparent, dots in my vision?
Sometimes when I stare at a very bright thing such as the sky I see little dots. It's actually more of a circle with a little dot inside it. They are half-transparent and they move around a lot. When I first see them they tend to appear in a group out of nowhere. I have seen one that is gray and almost black. What is this?

You are probably seeing floaters.

Floaters are deposits of various size, shape, consistency, refractive index, and motility within the eye's vitreous humour, which is normally transparent. At a young age, the vitreous is transparent, but as one ages, imperfections gradually develop

You might as well be seeing Scheerer's phenomenon

The blue field entoptic phenomenon or Scheerer's phenomenon [..] is the appearance of tiny bright dots (nicknamed blue-sky sprites) moving quickly along squiggly lines in the visual field, especially when looking into bright blue light such as the sky.

Please have a look at the wikipedia article for more information.
I only now realize that your question is a duplicate of Seeing strange things in light


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What is the role of a chemotroph in an ecosystem?
Chemotrophs are bacteria that synthesize ATP based on favorable REDOX reactions. This solves the problem as to how they can survive. But what exactly is their function in an ecosystem? For example, can they provide nutrients for algae?
I want to know if we can cultivate chemotrophic bacteria to provide nutrients for plants. This way, we could grow them in a place like Mars where the soil is made of a lot of inorganic material. I was especially interested in algae because some species can provide a lot of nutrients humans need.

The problem is that just any old inorganic material won't work.  You need materials such that the chemotrophs can cause them to undergo an exothermic reaction and harvest the energy from the reaction to support their life processes.  In a sense, they're not that much different from animals: it's just that the food they eat doesn't come from plants via photosynthesis.

Chemotrophs are usually found in extreme environments where they can be the source of all energy for the ecosystem also called the primary producers. Deep-sea hydrothermal vents are a great example of a chemotroph primary producer and support the growth of large eukaryotes like the tubeworms (Below). The chemotrophs supporting life at the vents can oxidize Sulfur to create ATP.

But chemotrophs don't just have an impact on these small ecosystems, they are actually responsible for earth-scale geochemistry affecting all life. (Cool paper on that here). The reason why chemotrophic bacteria are usually not found in "normal" environments with algae is simply competition. A heterotroph using hydrocarbons will occupy a niche faster and more efficiently than any chemotrophic bacteria.
You are definitely right on the Mars soil question, where chemotrophic bacteria could be used to fix carbon or nitrogen and solubilize nutrients for future plants on mars. But maybe some cool chemotrophs are already living there!

Just to shore up this vocab a bit, all organisms that rely on chemical energy (as opposed to photonic energy) are chemotrophs. This includes essentially all non-photosynthetic organisms, not just extremophiles. Chemoautotrophs can use carbon dioxide as their only carbon source and are rightly considered primary producers, but they aren't really limited to extreme environments either. Most are oxidizers of reduced inorganic compounds like ammonia, dihydrogen, and various compounds of iron and/or sulfur (also making them lithotrophs, as opposed to organotrophs).


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Why do nerve impulses utilize potassium and sodium instead of other Group 1 metals?
Rubidium and potassium are very similar, yet the body utilizes sodium and potassium for nerve impulses. Why is this the case? Why not any other element? Likewise, why not Lithium? I've read a research (https://www.ahajournals.org/doi/pdf/10.1161/01.RES.24.2.157) that says that rubidium has similar results as potassium in nerve impulse transmissions, the only difference being slight differences in intensity of muscle contraction (K leading to slightly stronger contractions). Additionally, it seems Rubidium, Lithium, Potassium, and Sodium have very similar Standard Electrode Potentials in Aqueous Solution at 25°C. Furthermore, why wouldn't calcium be used for nerve impulses? Does that extra electron make a difference?
Background: I am currently preparing a presentation for a chemistry class at my university. The presentation deals with periodicity. Basically, I am required to select three elements and explain how their chemical and physical properties differ according to their place in the periodic table. Thus, since there are differences between Group 1 elements, I believe there should be a reason as to why we use potassium and sodium for nerve impulses instead of other elements. In other words, I want to be able to explain why the body uses potassium and sodium instead of other elements by basing myself off the periodic table (i.e. atomic radii, electron configuration, etc).

Look to the stars to see your fate.  No, seriously!  Rubidium costs about 1/3 as much as gold because it is a heavy, rare element.  Lithium is cheaper, but it is still a comparatively rare element.  What the two have in common?  The CNO cycle doesn't make them.  (I'll leave you to guess three elements of life it does make)  You could go into nucleosynthesis much more deeply than I understand it, but rubidium is apparently r process or s process, while lithium is apparently produced in small amounts by proton bombardment.
The problem for living things is that they can't make elements.  A biochemistry that depends on an ion will be restricted according to its occurrence.  Related taxa that lack this limitation should thrive and evolve over a wider area, eventually supplanting their competitors.

It does make sense if we look at abundance. However, why not use Calcium. That element is quite abundant. I think what I am trying to ask is if there is some sort of chemical or physical property that both K and Na have that makes them ideal for nerve impulses.

@BrianBlumberg Calcium is quite important for neurons as well.


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Spectogram of mimicry vs original
Suppose the mimicry of a voice is very accurate. Will it  have similar spectogram as the original voice?


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DRD4 genes and their connections to Dopamine 2 subtype
I am trying to find out how the DRD4 gene correlates with the dopamine 2 family subtype receptor in the brain. Does a certain amount of methylation of DRD4 affect how much Dopamine is present in the brain?


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Measure Water-Use Efficiency without using carbon isotope fractionation?
I read "Measurements of delta (C-13) in C3 species may usefully contribute to the selection for transpiration efficiency." I think the device to measure carbon isotope fractionation is very expensive. Are there some easier ways to measure the water-use efficiency of plants, please? Thank you.


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Caterpillar identification - found on a coffee plant inside a house
Today, I've found a twig-like caterpillar hanging down from my homegrown coffee plant (which explained why some of the plant's leaves appear to be eaten away). What specie is this insect? It was about 2 cm long, I live in Central Europe.
Image of the caterpillar is attached below, and here is the movie of me annoying it.


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What specie of flying insect is this?
The insect pictured below just flown into my room. I live in Central Europe (Poland), it is about evening now. The thing is about 1,5 cm in length (not sure about this, I was too focused on driving it out). Its white stripe on abdomen seemed to be translucent. What is this insect?

It's a pellucid fly, a species of hover fly. scientific name: Volucella pellucens
https://www.naturespot.org.uk/species/pellucid-fly

Thanks. But isn't Gemeine waldschwebfliege a German name? I am not a biologist, but I thought those scientific names are always Latin-based.

my bad, I don't know why but my webpage translated the species scientific name into german which has never happened before so I didn't notice. I just changed it to its latin scientific name. .


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What is the Darwinian explanation for hallucinogenic plants?
What advantage is there to being hallucinogenic when eaten by some or most species for survival? I can only think that perhaps it stops the organism from eating the rest of you as they are confused? Perhaps some animals seek out hallucinations thereby increasing the amount you are eaten so you can spread seeds?
I am not a biologist by any means but can understand basic biology any information would be gladly appreciated

Related: Why are there so many medicinal plants?

Is the hallucinogen properties of plants something that's useful to the plant, or did the particular chemicals evolve to do something else, and it's only an accident that they have that effect on human nervous systems?  It seems unlikely that they would have evolved as a deterrent, since a reasonably large critter could eat a whole bunch of plants before the onset of hallucinations.

In hallucinagenic mushrooms there is psilocybin, which I can't find a reason for being created for the mushroom on an evolutionary or a reason to do with growth for the mushroom, and it has been created in mushrooms several times (in multiple different evolution chains I believe). Are all hallucinogens not understood yet like this one?


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What exactly does 'reverse use-dependence' mean?
I understand 'use-dependence' related to a drug, for instance, more angiotensin2 effects in a hypertensive more prominent is the action of angiotensin2 receptor blockers. But I do not get the term, 'Reverse use-dependence'.
https://en.m.wikipedia.org/wiki/Potassium_channel_blocker
In this site, in Medical Uses, the term is mentioned.

Reverse use dependence is the reduction of a drug's efficacy with the repeated use of the target. This contrasts with ordinary use dependence, for instance with $\mathrm{Na}^+$ blocking local anaesthetics, where they exert more block after tissue use. Reverse use dependence is particularly (but not exclusively) seen with channel blockers such as quinidine.
Quinidine is a $\mathrm{Na}^+/\mathrm{K}^+$ blocker that can slow heart rates, and does so more effectively when the heart rate is already slow. Increased use of the tissue, with a raised heart rate, reduces the effectiveness of the drug. So, strangely, quinidine exerts less block when the target is in use. This is shown in figure 4 from (Breithardt et al., 1995). As the tissue is used less (cardiac cycle length increases), the effect of the drug becomes stronger (action potential duration prolongation increases).

The reverse use dependence of quinidine can be demonstrated on a molecular level with application of quinidine to a voltage-clamped channel with an $\mathrm{i}_\mathrm{Ks}$ current. We see better block when short electrical pulses are given than when longer ones are. The mechanism behind use- and reverse use dependence is by state-dependent affinities, e.g. the drug can bind more easily to the channel in open/closed state. For example, a channel blocker whose binding site becomes occluded when the channel is opened could exhibit use dependent block.
But be warned: reverse use dependent drugs may also exhibit normal use dependence. Quinidine is not just reverse use dependent, but also use dependent
as a $\mathrm{Na}^+$ blocker. The type of tissue and its state change the effect of the drug and must be taken into account.
See (Breithardt et al., 1995) for a review of the topic:

In 1990 Hondeghem and Snyders introduced the concept of reverse use dependence as being a drug effect which is less marked with increased use. Specifically
  quinidine, N-acetyl-procainamide and sotalol lengthened action potential
  duration markedly at slow heart rates but much less or not at all at fast heart rates
  (Fig. 4 [27)). Frequently, reverse use dependence has become equated with reverse
  use-dependent block of ion channels. Although reverse use-dependent block of ion
  channels can lead to a reverse use-dependent drug effect, this does not need to be
  the case. Worse, reverse use-dependent drug effect does not require reverse use dependent block of channels.

References:

Breithardt, G., Borggrefe, M., Camm, A., Shenasa, M., Haverkamp, W. and Hindricks, G. (1995). Antiarrhythmic Drugs. pp.97-98.


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How does 2,3 biphosphoglycerate works to release oxygen bound to the hemoglobin?
I read on Wikipedia that 2,3 BPG binds with the deoxygenated state of hemoglobin and helps in stabilizing it. It was also written that it helps release remaining oxygen from the hemoglobin. How?
https://en.m.wikipedia.org/wiki/2,3-Bisphosphoglyceric_acid

Possible duplicate of Effect of 2,3-bisphophoglycerate (2,3-BPG) on haemoglobin

You've answered your own question. The association/dissociation of oxygen is an equilibrium reaction. If you stabilize one state, you move the equilibrium to that state. 2,3-BPG helps release oxygen from Hb exactly by binding and stabilizing deoxy-Hb.

If I understand your question, you want to know, HOW the 2,3-biphosphoglycerate helps release the oxygen from the heme. In addition to other factors like the blood temperature, the pH, and the ambient pCO2, it modifies the heme oxygen affinity. It binds, using salt bridges to lysine and histidine of deoxygenated heme subunits and, by this, changes the deoxygenated heme's conformation. The so modified heme conformation renders the (oxygenated) heme-oxygen bond instable. The altered heme subunit conformation cannot hold the oxygen atom anymore, which dissociates from the heme subunit and diffuses to the mitochondria, thus allowing for ATP production. This process is called "the hemoglobin oxygen affinity is being reduced" and one of the promoting factors of this process is 2,3-DPG.

This looks like an informative answer, but it would be made more helpful for others if it cited sources or linked materials.

Comment to M.P.'s note from Aug 25, at 22h14

Comment to M.P.'s note from Aug 25, at 22h14. From my point of view, the 2,3-DPG does not stabilize the hemoglobin but the oxygen's affinity to hemoglobin, as is stated in the original Q and also in the first A to the original Q, This is far from being the same thing. My intention was to draw attention to this fact, which was incorrectly stated in the original Q and also in De Novo's upvoted answer. The source of my A (answer) is : https://en.m.wikipedia.org/wiki/2,3-Bisphosphoglyceric_acid

It's helpful to have these sources in the answer. I don't take a position on the subtleties of deoxy Hb stabilization mechanism, but if these subtleties exist, it's handy to have very clear visuals or explanatory references, e.g. slides 15-20 or so of this presentation. Wiki is also generally fine, your page looks reasonable, though I don't see any notable distinction between the answers. The important thing is to have all this stuff in the answer itself.

From more mechanistic point of view, 2,3-biphosphoglycerate contains 2 negatively charged phosphate groups, which interacts with positively charged groups of each beta-chain within deoxyhaemoglobin decreasing the oxygen affinity (see good old Stryer Biochemistry)


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Wild bee hive indoors - can I move it?
Wild bees decided to build their hive in my shed, right above the table where I work on occasion.
The image is rotated 90 degrees left.
It started out as a single bee from what I could see two weeks ago. I thought fine, we won't bother each other and I like the company. But now two weeks later the bees are busily constructing and it is quickly growing larger. It started with a smallish dome, and new layers are being added from the outside. Every now and then a drop of some fluid falls out of the hive, and also small black grains, perhaps bee poop? Any ideas what these are?
Anyway, I have no idea how big this hive will become, so it is is probably a good idea to move it (it is around 15 inches from my head ;-)). Any suggestions?

I think there are professionals you can hire to do this. Are you sure those are bees? That looks like a hive made of paper.

Those aren't bees; looks like a paper wasp of some type. Though it varies by species they are sometimes more aggressive than honeybees. They can be beneficial as pollinators (though not as much as bees) and insect control, but many treat them as pests.

While honeybee relocation specialists exist, they won't do this job; this is an aboveground hornet or yellowjacket (Hymenoptera: Vespidae: Vespinae; the photo isn't clear enough to tell us which of three possible genera is involved) colony, which in this case will have to be (unfortunately, as these insects can be beneficial to a degree) exterminated; it's much too close for comfort.

Those aren't bees, they're a kind of paper wasp. As you observed, they start small and seem innocuous at first, but be warned, as the nests grow in size, the inhabitants become more protective of their nest and are more likely to see you as a threat to attack than as a peaceful cohabitant (at least this has been my experience.)

Nest construction starts in late spring and continues throughout the summer. The last brood raised includes males and next year’s queens. Due to the importance of these reproductives, the worker wasps become very protective and aggressive toward those who venture too close to the nest this time of year.

Somehow we seemed to have a number of attractive habitats for paper wasps (and mud wasps) and had to deal with them when too large or in a dangerous place (e.g. in a door frame.). A honeybee relocation service will do you no good in this situation.
You have a few options to consider, I recommend sooner than later. First, at night and while wearing protective clothing and gloves, you can simply whack the nest off at the base and run away as quickly as possible); Plan/clear your escape route in advance! Stay away for a couple of days as it often takes this long for them to completely abandon the young inside. If these are bald-faced hornets, their sting is quite painful, much more so than a bee or a yellow-jacket.
Or, if this doesn't bother you (it does bother me), you can light the nest with a burning roll of paper (it is, after all, paper, and will burn quite rapidly. The 'good' part of this is that the flame usually destroys the wasps' wings as well, and they're less likely to be able to attack you. This is best done on a cool night after all or most activity around the nest has ceased. The fire flares brightly and burns the nest very quickly without setting fire to adjacent structures, but a fire extinguisher should be kept nearby just in case.
Third, you can buy a spray, but I found them to be ineffective against the kind of paper nest shown in your picture, because the envelope protects the wasps inside. I used up two large cans of foaming spray (in spite of hating insecticides, as it wasn't a spot I could safely whack) without any obvious result. I ended up doing multiple whack-and-runs.
Finally, you can hire a professional, something I never did in my 28-odd years of dealing with them, but which is often recommended.
Yes, it's probably poop.


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Immunofluoresence and vaccines
Can you use indirect immounofluoresence to verify if a vaccine will work against a virus?
Using the vaccine antibodies against the virus, plus a second antibody with fluorophore that will join the first.

I don't think that experiment would prove that the immune system will be sufficiently stimulated by your vaccine to elict the desired response.

A vaccine isn't antibodies.  It's bits of virus or microbe that elicits a response from the immune system, the most important component being the creation of specific memory cells which are ready to react if the real invader is introduced.

You can use an immunoassay like a homogeneous sandwich FRET assay: You can use donor-dye-labelled fluorophore antibodies that are able to recognise specific antigens on the virus to bind the virus antigen, then introduce a second set of antibodies labelled with acceptor-dye fluorophore. If the vaccine works and produces an immune response in the in-vivo model that destroys the virus, the antigen that joins the donor-labelled and acceptor-labelled antibodies is also destroyed and can no longer “sandwich” the two antibodies close together within the Förster distance to exhibit FRET.


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Why is the relative expression in qPCR so low?
When analyzing different mutations through qPCR I found the $2^{-\Delta\Delta ct}$ value for each mutation. All the mutation have similar values compared to the wild type gene, however one of the mutation has an extremely $2^{-\Delta\Delta ct}$ value. Having $1$ for the wilde type, and an average of $0.9$ for some mutant genes, the exceptional case has a $0.05$ value.
I think one could argue that this mutation deletes a sequence from the wild type gene, but I believe other things can be suggested from this.

It may be a particular mutation that affects expression altogether. Through qPCR you're able to tell the relative difference in mRNA levels of a particular gene between, say, a WT and a mutant. It may be that this particular mutation damages some regulatory sequence within the body of a gene (e.g. a downstream promoter element) or some regulatory sequence upstream. To me, this suggests that you're dealing with such a case here. Anyways, you'd need more data to tell for sure. You should have the mutation mapped, if you haven't already and check if the primers you used were  okay. This mutation clearly hampers expression, as long as everything was okay with the procedure.


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Immediate cause of death due to dehydration
When we don't drink we get dehydrated and after some time we die. What is the cause of death on the lowest level?
I would assume the dielectric properties around/in the heart tissue get imbalanced and the heart stops beating.
Then lack of oxygen in the brain. Then...?

The simple answer is dehydration kills you by causing the blood flow to become completely ineffective.
Dehydration limits the amount of water in the bloodstream causing an increase in blood viscosity, and thereby an increase in blood pressure.  As this process gets more extreme the body has a difficult time getting the blood to the places it needs to be, and will limit blood flow to non-essential organs (kind of similar to what happens when it's cold outside and your fingers go numb).  At the same time waste is beginning to build up as the kidneys cannot filter the blood effectively, and the internal temperature rises because of the lack of sweating.  This process gets more extreme until one of your essential organs cannot take it anymore and shuts down, likely the liver first.
Most everything I got for this answer was from a PopSci Article. Although there is also a nice 1935 study with many measurements from real people.

Thank you for your answer. Could you please explain the reason one dies after the liver stops working? How long would one die after liver failure?

There are over 500 functions of the liver, many of them vital, including producing hormones, detoxifying blood and generating digestive fluids.  A failure of one function won't kill you, but an odd combination of several can combine to cause additional effects, such as electrolyte dis balance or blood clotting that in total overwhelm the body.


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How much energy we get from oxygen?
During a whole day breathing, how many kcal or watts do we get from the oxygen we breathe?

Why would you want to know something like that? What possible scientific interest does it have for you?

I'd say the only way this question would be answerable (see the comments and existing answers) is if we tried to transform it into "How much energy is produced via aerobic versus non-aerobic metabolism (in a human)?" - it's not really the same question, though, and might not really be what you were after, especially considering the content of the answer you hastily accepted. I think if you made this change it would be better to close this one and start a new question, rather than edit, given the existing answers here.

No scientific interest. It was an informal conversation and I am curious.

I know that you already picked an answer, but I found an alternative answer for you. On average a person consumes 550 litres of oxygen in a day. Now, our body could burn carbohydrates or fats or proteins to produce energy. Each litre of oxygen can produce 5.04 kcals if it burns carbohydrates, produce 4.68 kcals if it burns fats or produce 4.48 kcals if it burns proteins (reference). That being said, if I consider that all 550 litres were used to burn carbohydrates, a total of 550 x 5.04 kcals will be produced which is 2780 kcals.

It really does not matter very which answer the poster accepts as he generally is in the poorest position to judge. Not like Stack Overflow where you can test somebody's code. So do answer this question if it amuses you, but think how many significant figures it is useful or appropriate to cite. Six is absurd, especially as one of your figures has only four.

@David Where did I cite 6 figures? I just felt like answering it. Doesn't really matter who he picks or not

27.7585 kcal! Four decimal places, but six significant figures.

@David ah.. u can edit it as u seem fit.

OK. Have done that. Reduced to 3 significant figures as determined by values of 4.68 and 5.04. Anyone who doesn't understand this may be interested in my self-teaching web application on this topic at https://www.mvls.gla.ac.uk/Teaching/SLS-FTB/sigfigs.html.

I am not a biology expert (not even familiar with biology). I was just curious so I assumed all the answers are OK. But I like now this one more :) Thanks!
And come on, discussing for some decimals?

Just looking at the numbers, I get the impression that that 550L/day a number for males, because the resulting 2.7KCal number is pretty close to the average calorie consumption for males.

This question is not actually answerable.
Consider this.  Take a nice campfire.  It's warm and toasty.  How much energy comes from the wood you piled at the bottom.  It's a lot right?
Now how much energy comes from the oxygen the fire consumed?
We know that a fire needs three things to burn: fuel, oxygen, and heat.  How much energy comes from the heat?
Who creates a baby, the mother or the father?  Obviously the mother caries it to term, but the creation itself takes two, interacting.
These questions don't have clear answers because there's no natural division to be made.  We can't state how much energy came from the fuel or how much energy comes from the oxygen, because it is not the fuel nor the oxygen which provides the energy, but the reaction between the two.
In general, we find oxygen is more accessible than fuel.  We can always get oxygen from the air by breathing, but one has to find oxidizable fuel (food).  As such, we find it convenient to associate all of the energy of the reaction to the fuel, for bookkeeping purposes.  But that's just bookkeeping.  We do this because, if we're short on oxygen, we just have to breathe a little more.  If we're short on fuel, we have to go find fuel (food).

But in a combustion there is a clear amount of energy taking place, I do not care where it exactly comes from. What I wanted to know is how much energy does breathing give to our body in average.

@JaviV The human body burns roughly 2000 Calories a day (roughly 8.3MJ/day).  Thus, in exactly the same sense that "in a combustion there is a clear amount of energy taking place," breathing gives an average of 8.3MJ/day.

Of course, it's not the breathing that releases the energy.  The energy is released in the cells themselves, through the Citric Acid Cycle.  All breathing does is simply make sure there is oxygen available in the cells.  The cells do the releasing of the energy.

Also, note that that average does vary significantly based on food consumption, because the body regulates itself to avoid running out of stored fuel.  If you go on a diet, consuming fewer calories, your body will adjust the amount of oxygen it brings (by breathing less and/or using less oxygen from each breath)

@CortAmmon Roughly 8.4 MJ/day if you round the numbers correctly.

Oxygen does not provide any calories (energy) or watts (power), just the same as a water bottle states it contains zero calories.  Energy is held within glucose, or other macromolecules than can be broken down to supply electrons that generate ATP, or other similar molecules.

Well yes and no. The reaction of oxygen with the terminal electron acceptor of the electron transport chain provides the necessary Gibbs free energy change to allow the chain to continue, producing a chemiosmotic gradient from the oxidation of NADH and FADH2. Energy is not held within molecules. It is produced by their chemical reaction.

I would argue energy is held between the bonds of atoms, unless you are talking about quantum effects.  Thank you for correcting my knowledge ETC, but I nevertheless believe that ATP is not going to be produced with oxygen alone and in a biological sense and therefore does not biologically contain energy.  However I also think this question was poorly asked.

I didn't say that energy could be produced by oxygen alone — obviously it cannot. And yes, sugars etc are a potential source of energy because they have the potential to participate in reactions that are endo-ergonic. But to participate in the types of reaction we are considering — oxidation — they need a co-reactant that is also going to be changed. This is important. You can get round this to some extent by looking at the electrode potentials for the half reactions here, but it turns out that they are both +ve, so both are contributing to the –ve free energy change.


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What could an increase in systolic blood pressure and decrease in diastolic mean?
Sorry if this is a really simple question but my academic background is in completely different sciences. I recently made a computer game for an experiment that was related to anxiety and relaxation. One of the ways that I measured for success was to record participants blood pressure before and after they played the game.
There was a slight increase in systolic BP after playing the game, but not by a statistically significant amount. However the data shows a decrease in diastolic BP that is statistically significant. I've been trying to figure out why this might have happened but can't seem to find any answers. My brief overview of search engines and journals only seem to relate these changes to certain types of exercise. Which doesn't help as the participants of the experiment were asked to remain seated for 20 minutes by the time the second BP recording was made. Just wondering if anyone has any information in relation to relaxation techniques that might result in this pattern?
If it helps heart rate has mostly uniform throughout the experiment.

This is a question better suited to Health.SE.

First, a couple of considerations

Heart rate (HR) is lower when seating, and even lower when lying. I assume that participants were seated when the first measure was taken.
Cardiac output is not constant during the day. Depending on the moment, some factors such as digestion have an impact in Cardiac output, so take that into account when carrying out the experiments.

Normal walking may cause that blood pressure pattern. I think that you should not consider the increase in systolic pressure if it is not significant, as something as simple as crossing your legs when seated can increase your systolic pressure and normally diastolic pressure provides more information for physicians. Relaxation techniques usually decrease heart rate, which can affect the blood pressure. However, the point in this case seems to be that HR remains constant. I suppose that Mean Arterial Pressure $(MAP)$ has decreased.
If we part from:
$\textit{MAP} = (CO \cdot SVR) + CVP$
where $CO$ is cardiac output, $SVR$  is systemic vascular resistance and $CVP$ central venous pressure.
$CVP$ is usually depreciable. $CO$ is defined by $SV \cdot HR$, where $SV$ is the stroke volume. Then, if the HR is constant, only $SV$ or $SVR$ could have changed. Maybe the heart is pulsating more vigorously, or a vasodilation is decreasing $SVR$. I find the latter more likely. However, I don´t know why the smooth muscle could be relaxing. Make sure that heart rate is not changing and consider your sample size.
I hope it helps, at least to focus you search on cardiac regulation. It is difficult to conclude anything without seeing the data but I tried to answer from my limited knowledge since I am not specialized in cardiac physiology.


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Is there a specific terms to describe variant of existing genes in bacteria?
I have a question regarding a specific term that describes the variant of existing genes. I am analyzing whole-genome sequencing of a bacterial isolate. I found there are a large number of genes that have partial sequence identity or subject/query coverage to the known reference genes.
Now I know that by looking at sequence identity and coverage may not be enough to analyze the genes. I know some gene can have 30% sequence identity and still folded the same way as the original genes. However, let's say these genes are truly variant of the existing genes based off sequence identity. What is the term to call them?
My PI told me they are rapidly evolving genes. I searched some paper and found rapidly evolving genes are genes that are subjected to positive selection. While I agree for some of these are rapidly evolving genes as they probably subject to positive selection, I cannot see that all of the genes actually undergoes selection at same time. I am wondering if there is another term to call these gene variants. If there is any paper to define them that will be great.
Thanks

Allele
From wikipedia > allele

An allele is a variant form of a given gene

I somewhat disagree with this definition in the sense that it is not general enough. An allele is a variant at any locus (locus = position in the genome). You can talk about allele at non-coding sequences. Also, if you are talking about a coding sequence, you can define different sequences as belonging to different alleles whether or not their protein products differ in function or not. The proteins might even be the exact same one for two different alleles if the only difference between these alleles concerns a synonymous mutation (or a mutation in an intron).
You can feel free to define that different sequences as being different alleles by any kind of arbitrary threshold measure. You will just need to define it. For example, you can define that different sequences are different alleles only if they have at least 5% pairwise differences or if you found out by some biophysics computation that they ought to fold differently or for whatever another arbitrary measure.
The term allele is used very often in evolutionary biology and you'll find its usage in any intro course to evolutionary biology.
Rapidly evolving genes
As far as I know, there are no commonly agreed upon definition for what a rapidly evolving gene is. To me, a rapidly evolving gene is simply a coding sequence which evolved more rapidly than other reference sequences. Per se, although it would very likely involve positive selection, I don't think it is a requisite by the definition of rapidly evolving genes. It could, for example, be caused by a very high mutation rate at this particular sequence or by balancing selection causing any new rare alleles to be beneficial.

Thank you for your answer. Yes, I am mainly talking about coding sequences. I will try to find a better definition of rapidly evolving genes.
The reason I don't want to use positive selection as definition for rapidly evolving genes because it make it sounds like there are over half of my coding sequence are under positive selection which doesn't make sense to me. If they are under selection and are mutating fast enough that should be better.


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Distinction between primary and secondary tumor
How can a primary tumor be distinguished from a secondary tumor? I tried finding it on the internet but it only said that they are found by means of immunohistology but I couldn't understand how.Please elaborate

Different tissues express different proteins, and cancers are often allocated to their primary tissue by virtue of expressing proteins specific to the type of tissue they arose in. Of course, with primary tumours there is also the advantage of imaging ; lung cancer, for example, can be localised to the lung based on a PET scan.
Sometimes though there are cancers of unknown primary , where a metastasis is picked up, but allocation to the primary tumour is not possible because it wasn't detected. In this case, it is possible to use epigenetic profiles to predict the tissue of origin for the tumours in question. See https://www.thelancet.com/journals/lanonc/article/PIIS1470-2045(16)30297-2/fulltext

The difference is pretty easy to understand. The secondary tumors is metastiesed tumor sped to enother parts of body. On the other hand the primary tumor is the source of the metastiesed.

I give you one example of this. On of the most common tumor of testicles is seminoma metastiesed to the peritonium, lungs, brain.

The secondary tumor is usually hard to distinguised with primary. But usually if there is specific antigen which can be recognised by antibody. The antibody is usually cultivated in mice. But this antibody have to be recognised by enother antibody. The second antibody to mice antibody is cultivated usually in rats. After that the secondary antibody is usually modified by fluorescent chemical. This is indirect immunohistochemistry. Direct is usually only the first antibody modifided by some fluorescent.

So first of all you have to do biopsy of that potential tumor. After that the sample is usually fixated by freazing and sliced by cryomicrotom. Than samples is usually put in to petry dish and poor with izotonic solution. Then the primary antibody is add. It take some time to react (find the antigen), thereafter is add the secondary antibody. To view the antibody you have to activated fluorescent by laser in fluorescent microscope. So if the fluorescent is in the sample, the tumor should be secondary.

Nevertheless is still hard to distinguish secondary tumor from the primery. Usually is up to experiencies with the tumors and how they are behave in body of patient. This is one of the reasons why is hard to treat the cancer.

By the way you can see the antigene as adress to cell and antibody as post man.


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Program (on Mac) to show 3D protein structures?
I have an assignment for 6th grade biology. I have to look at a 3D structure of a protein and manipulate it so it only shows the AA I’m interested in currently.
what I already did
I already looked up the programs most used for this and they point me to JMol and Yasara but the download files are .bin files and the like and I don’t I don’t understand which file is the one I should download and how to install it.
Can someone help me please ?

Jmol: how to install
Here are instructions for getting Jmol to run on a Mac (or with a slight variation in the runtime file you need to download and the security warnings, on a PC).

Download Jmol from
https://sourceforge.net/projects/jmol/files/latest/download?source=files
The name of the file will be something like Jmol-14.29.16-binary.zip. Double-click to unzip.
The unzipped folder has a confusing variety of files. This is because most are used for setting up web pages with Jmol embedded. However there is a double-clickable desktop application without any icon and the unpromising name of: Jmol.jar. When you double-click to launch it you will most likely get a message as shown below (1):

To get round this you must either control-click or right-click and select `Open With > Jar Launcher as shown above (2).
Click ‘Open’. (Next time it will just launch without right-clicking.)

Now, in my case the program launches because I have the Java runtime installed on my machines, but you will probably have to download and install this.
Go to the Oracle Java website at http://www.oracle.com/technetwork/java/javase/downloads/jre8-downloads-2133155.html
Download and install the appropriate Java SE Runtime Environment, e.g jre-8u172-macosx-x64.dmg
Try launching jmol.jar again. It should work this time.

Jmol: how to use
Because of their emphasis on Jmol in relation to the web, the developers of Jmol do not provide an easy entry to the desktop program. However you can find a clearly illustrated series of web tutorials at the MSOI Centre for Biomoleclar Modelling. I’d highly recommend this as a starting guide.
Although I am not going to describe how you can visualize particular amino acids as that is part of the poster’s project and can be found in the instructions. there are a couple of pointers I would make about things that are not entirely obvious.

After you have loaded a protein from the file menu, you will probably want to change its representation, not least because it may be surrounded by red balls (oxygens from water). To do this you need to right click (or click on the Jmol text on the bottom right) and go through two levels of submenus to select an appropriate representation, as shown.

In order to make the selections you require you will need to issue commands in the ‘Console’. This can be selected from the File menu:

I've just updated my post with a link to a site with a well illustrated introductory tutorial. I use Jmol/JSmol myself, so I am happy to try to answer questions that member may have.

I've expanded my instructions for getting started because this is not intuitive.

You could use an online molecular viewer for this. A fairly complete list is available in Wikipedia as well as in JMol wiki.
In particular, JMol that you tried to install has also a JavaScript version called JSMol that you can use on any website that embeds JSMol:
RCSB, Proteopedia, a JSMol tutorial, and many more. To load own structure in JSMol: right click and select File > Load > Open Local File.
If you'd prefer a desktop program, there is also plenty of them: JMol, PyMOL, Chimera, VMD, CCP4mg, etc. All of these are free for non-commercial use (some are even free for commercial use) and work on Mac.
The most popular file format for storing 3D structures of protein is the PDB format. If you would not be able to make your viewer of choice to show only the amino-acids you want, you can always open the PDB file in a text editor and remove lines (atoms) that you don't need.

Avogadro has a mac version you can use. https://avogadro.cc/
I found it simple.
edit:
You can view the protein you listed here, maybe?  ( I am on windows so I do not know if this web app works perfect on mac OS)
https://www.ncbi.nlm.nih.gov/Structure/pdb/1C9O
then in the bottom left corner of the structure image box, there will be a small box icon with arrow.
.
Then you can click on View Sequences and Annotations, under the window tab.

You can then click on the details tab and then left click and drag on the Amino acid sequence to highlight them on the sequence and where they are on the corresponding structure.

Crashed when I tried to load 1c9o.pdb on Mavericks.


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How does one identify a seed's species & variety?
How does one identify a seed's species & variety, could it be done by some means of DNA or by use of a microscope?
Say for example, I had a pumpkin seed, I knew that it was a "small sugar pumpkin" variety, but how would one scientifically identify it to know that it was infact a small sugar pumpkin as well as a pumpkin without going through the process of planting it. Is there some kind of indicator on a DNA level that shows "This is what I am?"
My knowledge regarding biology is extremely basic, but I am very interested in knowing the full process of how this would work.

You sure, could identify plants by genotyping them. For many species, you can probably identify morphologically. For example, I am sure you are able to tell sunflower seed apart from flax seeds. Now, it will depend a bit about how accurate you want the identification to be. Sequencing would ultimately be most accurate (and most expensive) method.

@Remi.b: I disagree.  The most accurate method would be to plant it and see what grows :-)  I'm not sure sequencing would be that accurate, unless you have a pre-existing reference sequence for comparison.  Even then, I doubt that all small sugar pumpkins are genetically identical.  Could the gene(s) that differentiate a small sugar pumpkin from say an ordinary Halloween jack-o'-lantern one be reliably distinguished?

@jamesqf Ha ha that's right. Of course you;re right, identifying by genotyping will depends upon reference sequences. It will for sure be helpful to grouping related individuals in one's sample though.

Yes, their name are "molecular marker". Every gene carrying a phenotype, quantitative or qualitative, is identified as an allele of every gene encoding for proteins.
In order to identify a phenotype using just infos gained from DNA, you'll need a previous library made by these gene regions, were every polymorphism between them is associated with a phenotype. For example, a kind of marker used for this kind of work is SSR , or "Simple sequence repeats" : it is made by a simple sequence of DNA interspaced between two other region. The number of repeats of the internal sequence could be associated with a phenotype.
So, by a simple PCR you could amplify this regions:

And by a electrophoresis you could see how much repetitions are in your band, using just the molecular weight.
Here is an example of SSR used for phenotype/genotype screening


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Phylogeny: Hybridization between different species sharing same genus?
I am doing a cross-breeding project with Capsicum chinense x Capsicum baccatum. I'm planning to breed them until 6-8 gen.
My question: What will the completed breed be classified as? Would it be a new species or will it be considered as a strain of chinense or baccatum? Thanks.

Hybrids are not considered named species of either of their progenitors, but classified as hybrids of both. So they would be called Capsicum chinense x baccatum.

Well.... all eukaryotes are hybrids.


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Can anyone identify this seed or nut?
I found many of these nuts in a botanical garden in Sweden (outside, not in a greenhouse) but was unable to find the plant it belonged to. The garden has species from all over the world. I don't recognize it as a native plant, but I could be wrong on that.
I've tried to use various identification webpages to find it, but failed. I would love to know the species, so that I can get more info on the plant and its seeds! The Bic lighter is there for scale.
The nuts (or seeds, or whatever they are) are very hard, like a peach stone or other drupe stones.
This is a crosspost from Reddit where no-one has answered the post(yet).


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Can trial participants get tests?
I saw a news story about someone who had participated in a COVID vaccine trial, and he said that he had taken an antibody test that came back positive, and he had concluded that he had not gotten the placebo, but the vaccine, and it had made him immune.
Isn't that problematic behavior? The trial is supposed to be double-blind. Are there ethical guidelines about trial participants getting tested?

Just because an Ab test came back positive doesn't mean the participant got the vaccine - they may very well have gotten the placebo and later acquired a non-symptomatic infection.

Welcome to Biology.SE! Please take the [tour] and then go through the [help] pages starting with [Ask] questions effectively on this site. In particular, this question seems to be off-topic since it is about ethics rather than biology and "answers" will thus be opinions rather than facts. Thanks!


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Effects of X-ray exposure on upcoming pregnancies
Recently we had a little fight with my girlfriend about the risks of genetic diseases for our potential baby. The thing is that she had her medical check recently and it included an X-ray examination of her chest. The doctor performing the scan warned her that she should not get pregnant for 3-6 months after the examination.
A note on the wall also read similar to this (in Chinese):

医生建议与X光射线接触的备孕期的女性朋友，最好在3个月后再进行怀孕，以降低胎儿畸形的风险。

Which translates roughly as:

To reduce the risk of fetal malformations, doctors suggest that women who have had X-ray expose are better to avoid getting pregnant withing three months.

(I guess, this advice might come from the fact that an egg develops for about 150 days before being released to the ovary?)
However, since the average radiation dose of the X-ray chest exam is reported to be around 0.1 mSv (which is about the dose of radiation you get by a couple of round-trip flights: from the US to Paris and back), I have doubts that this piece of advice has any solid scientific foundation to it. (Otherwise, I guess, airline companies should be legally bind to warn any female clients of dangers of transoceanic travel.)
Are there any studies that show effects of X-ray exams on future pregnancies? Can the risk of "fetal malformations" for any pregnancy starting shortly after an X-ray exam really be assessed?

Hmm. Why downvote?


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Is an X ml dose of a drug at 50% bioavailability roughly equivalent to a 2X ml dose at 25% bioavailability?
For the sake of simplicity, assume:

The two doses are the same drug metabolized in the exact same way, and the only difference is the amount that reaches the bloodstream (and thereafter the brain).
This drug is only meant to influence the brain, so differing concentrations in various organs don't matter.
This drug is short-term and nothing lingers in the body after it has been excreted or broken down.

My understanding is that bioavailability means the proportion of drug that reaches the bloodstream. So, all things being equal, does that mean an administration of a drug will be twice as potent if the bioavailability is doubled?

All things being equal, does that mean an administration of a drug will be twice as potent if the bioavailability is doubled?

Bioavailability is initially taught, and sometimes reported as a proportion, $F$, the concentration in drug in plasma under a test condition (typically oral administration) over the concentration of of the same dose of the drug under a reference condition (typically IV administration).
In the simplest case, under zero order kinetics (the rates of all reactions that cause a change in concentration of the drug are independent of that drug's concentration), you can substitue $F\cdot D$, for a dose, where $F$ is the bioavailability and $D$ is the dose (see equation 2-16 in Goodman and Gilman's The Pharmacological Basis of Therapeutics, Chapter 2).
So, for your question, you can write down the state with equal plasma concentrations, $0.5\cdot D_1 = 0.25 \cdot D_2$, which reduces to $2D_1 = D_2$
Potency is a hairy term, defined in many different ways (some with more hand waving than others), but lets say for the purposes of this question that potency is the oral dose $D$ required to produce a measurable effect, $E$, and relative potency is the oral dose of formulation 1, $D_1$ required for a set effect, $E$, over the oral dose of formulation 2, $D_2$ for the same effect (modified from Goodman and Gilman Chapter 3). So, if the effect of your drug is directly proportional to its concentration in plasma ($E = kC$), then yes, the formulation with twice the bioavailability will be twice as potent.
I was going to write a long treatise on why this is not necessarily going to be the case, but since you were so specific about all things being equal, I'll just say this: bioavailability is often not reducible to a single $F$, which is why the FDA requires a lot of information on Bioavailability. This is for good reason, because kinetics are often not zero order, and even once we get to plasma concentration, the concentration term that drives efficacy can be $AUC$, $C_{max}$, time above a threshold, and sometimes even hard to correlate directly to plasma concentration at all. But, in the simplest case, all things being equal, your answer is yes.


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What is the purpose of the “No DNA control”?
What is the purpose of the “No DNA control”?
Recently I have done a forensic DNA lab experiment and I still cannot understand the use of “No DNA control”

No DNA controls (or water control, also "no sample control") are important to rule out false positives results due to contamination.
If your reagents/pipettes/equipment you use is clean, this reaction (I suppose in PCR) gives you no band. If you have a contamination, this will show up where no band should be and shows that you have a problem. In this case you cannot trust the other results as well.

Isn't it to know the protein level backgrounds in the given sample?

This is an instance of the general concept of a negative control -- a very important part of every experiment


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What values to be taken for x-axis and y-axis?
I did a lab on form and function in photosynthesis and I recorded the values of absorption spectrum in spinach chlorophyll extract. I have the following data and I need to draw a graph. I didn't understand what I should take for x-axis and for y-axis. Can anyone please explain this.

@NabeehaChowdhury I need to draw a graph which describes, how many peaks does the absorption spectrum contain? and at what wavelength is the photosynthesis greatest? How does the color of an angiosperm leaf relate to the absorption spectrum you have generated?

It doesn't matter really, but for aesthetics sake, you'd plot the wavelength on x and the absorbance on y. We tend to visualize such data as spectral or absorbance as "peaks" on the range of interest. There's a fairly good example here. It has something to do with convention: traditionally
 the independent variable on x and the dependent variable on y. There's a good answer on cross-validated on the matter, too.


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How do you check how many cones you have in your eye?
Following my previous question: What color does the other cone in Tetrachromacy correspond to?
People with normal color vision posses 3 cones in their eye. But there are some rare cases when people can have 4 cones (Tetrachromacy). These people, some of them will notice the shades difference in the scene through their eye. And the rest won't notice it, because simply their 4th cone is activated in the close peak value with the the L-cone. Therefore eye will not find any difference and will encode only one color even if it's coming from 2 cones stimuli.
How do you check, to know how many cones you have in your eye ? If the case is, even people who posses 4 cones can't even notice the shades difference ?

Regarding your last question: article.

One of the two confirmed cases of tetrachromacy was confirmed genetically:
From this Popular Science article:

Based on Antico's genes, Jameson has determined that Antico's fourth
  cone absorbs wavelengths that are "reddish-orangey-yellow, but what it
  appears to Concetta is uncertain at the moment," she added. Since the
  tests aren't calibrated for this wavelength, empirically demonstrating
  tetrachromacy is still really difficult.

Color vision is connected to the X chromosome and mutations in the X chromosome cause less or more color vision.  In the above case, the theory that people with 2 mutated X chromosomes could have four cones instead of three was tested.
This image from Scitable by Nature Education articles simulates regular vision on the left and tetrachromatic vision on the right:

As far as how to test to see how many cones you have, there are some online test that may or may not be very reliable.  This Metro news article has a test produced by Professor Diana Derval, author of "DesigningLuxuryBrands: The Science of Pleasing Customers’ Senses.  However, due to the limitations of computer screens it would not be reliable to test for tetrachromacy.

Thanks a lot! Very informative. And the reference, the reference also very interesting.

Well, this article says one can't check if [s]he is tetrachromat using LED displays. In the original image I could see 37 colors but I hardly have some kind of outstanding vision. This means it is not just not reliable test, but that any trichromat can finish as tetrachromat. And the article says that many of those who have 4 cone types may be trichromats.


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What is an "Alternative Sensation"?
As far as I know, alternative sensation it's a sensation to distract people from the original stimuli, for example when you have to get an injection, the nurse will pinch you in the other arms so your brain is distracted and will not focus on the original pain in the arms that's got the injection.
But I also read here, alternative sensation refers to the brains that can process stimuli from multiple senses, for example when the eyesight is bad, the ears will take up and boost the visual system to help and stimulate the visual system (Visual + Auditory) .
Which one is exactly an 'alternative sensation'? Also, what is Time-Frequency in alternative sensation ? I would appreciate any references too.

My goodness, neither one of you gave an upvote to the other! Question was taken seriously, nice answer written, and then accepted, and yet both currently sit at zero upvotes, zero downvotes! I'm tempted to down vote you both ;-) (just kidding on the last part)

"Alternative sensation" is not specific terminology in neuroscience - it is just the noun "sensation" with a descriptive adjective "alternative." It just means that it is referring to a different sensation than whatever the "primary" one is.
Knowing what this term means in a given context depends entirely on that context, and may not have any relationship to other contexts.
Time-frequency refers to how something varies in time and frequency. In the context of stimuli, for example, an auditory stimulus can have different "tones" or "notes": those are different sound frequencies, and those frequencies can happen in sequence. To describe a sound visually, one will often present a 'heat map' showing when (time) and at what frequency that sound has energy. Touch stimuli can also have a time-frequency representation, where the frequency indicates the vibration speed of the touch.

My goodness, neither one of you gave an upvote to the other! Question was taken seriously, nice answer written, and then accepted, and yet both currently sit at zero upvotes, zero downvotes! I'm tempted to down vote you both ;-) (just kidding on the last part)


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Reusing pipette tip
I'm new to research and one of the things I'm learning is pipetting. I've got the basics down but say I'm reusing a pipette tip because the solution I'm using is the same. So first I depress to the first stop, aspirate liquid, then release the liquid to the second stop. However after this, do I take the pipette out and release to the very top then back down to the first stop to gather more liquid or do I take the pipette out and raise it to the first stop and gather more liquid?

Once you've depressed to the second stop, you need to remove it from the liquid, else you're re-aspirate OVER the defined amount. You also won't then be able to eject it all fully. If your pipette is set to 1000 uL, for instance, the tip volume will be 1000 uL from first stop to first stop. The second stop depression is purely there to ensure all the liquid is expelled from the tip.

Once you dispense the liquid after the first shot, you raise the plunger back all the way to the top, and start the whole process over, as if you had a fresh tip. (the first of your two options)

One thing you should do if you are new to pipetting is to pipette water into a weigh boat on a precise scale. Pipette 100 microliters, 10 times in a row, tare, and repeat. Make sure each shot weighs 100 milligrams, just to test yourself.


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In what does Genetic clustering and Cline sharpness differ?
They are  both ways to measure divergence in species but I'm not understanding in what exactly the differ if both use hybrid zones and gene frequencies in the study.

The concept of cline sharpness is not a common one to my knowledge. I suspect you encountered this concept in a hybrid zone literature. Can you please link to the paper where you found those two concepts.

I am voting to close as unclear because we would need the original text on which you've encountered those terms.

It's in the first chapter of "Ecological Speciation" from Patrik Nosil pp 5. He gives examples on measures of divergence in the first table. The examples are from Jiggins and Mallet 2000; and Barton and Hewit, 1985.

Clustering and Clines are two fundamentally different approaches to target the population structure problems. Because many results in classical population genetics are derived from a panmictic population, it is natural to extend them to multiple panmictic populations with some degree of gene flow in between, such as Wright's Island model and Kimura's Stepping stone model. In these discrete models, we view each subpopulation as a breeding group and hence the clustering algorithm can be used to a large number of individuals to classify them based on which subpopulation they belong to. It is 100% valid if the real population is actually discrete (such as in Galapagos), but not so if the real population is distributed continuously in space. In the latter scenario, cline may be more appropriate to describe the spatial variations of the population.
You can check Montgomery Slatkin and Nick Barton's papers on cline theory back in 1970s and 1980s to get the details, but the general property of a cline is that if divergent selection is the primary cause of the cline, then the cline steepness is proportional to the selection differences, but there is a characteristic spatial scale of variation $\sigma/\sqrt{s}$, below which any spatial structure will likely to be swamped by dispersal ($\sigma$ is the mean dispersal distance of an individual, and $s$ is the selection intensity).So Even if the cline is a step function, which is not realistic at all, the cline will still be of finite steepness. As long as $\sigma$ is not zero, you will not get a clear-cut boundary between the two sides of the population, thus invalidating the assumption of clustering algorithm. However, although clustering is not very rigorous in a continuous population, we can still use it to make qualitative explorations of our genetic data and population structure, in fact many people prefer to use that because they are conceptually clear and easy to manipulate in a computer.


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How long does it take for DNA to degrade
Can i still use 3-4 years old bacterial DNA template for my PCR? They were kept in -20 all this while. Will the DNA degrade?

Degradation of DNA is gradual, but continuous, even in the freezer. However, they can sequence DNA from ancient animals in permafrost, or Neanderthal teeth. Fresh is always best, but there is no reason not to try PCR on your samples.

Yes, 3-4 years at -20ºC should be fine. I have never had any problem with plasmids stored this long (or even longer). Shorter and linear DNA fragments might be a bit less stable.

Not only can one sequence DNA from permafrost, but it can remain sufficiently intact to produce a living plant after 30,000 years.


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How to determine which is the nucleotide sequence of a gene?
I have came across a few  genes that show different nucleotide sequence in different databases. I then found out that the sequences are actually reverse complement of each other. How do i determine which is the actual nucleotide sequence of a gene,and not the reverse complement version of it?

Usually the reported sequence for a mRNA in NCBI is the sense strand. Can you give an example of a gene whose sequence you are unsure of?

Possible duplicate of What direction is a sequence in databases written?

Hi @WYSIWYG below are the nucleotide sequences of the rplC gene. The first one is from NCBI, while the second I received from a sequencing company for my strain:

ATCC 19977 R rplC ncbi
CTACTTCTCACCTCGCTTGACAGCGGTGCGGACCACAACCAAGCCACCCTTACGTCCGGGGATGGCACCC
TTGATCAGCAGTACGCCGTTCTCGGCATCGACCTTGTGCACCACCAGGTTCTGAGTGGTGACGCGATCGC
TACCCATACGTCCGGACATCCGGGTGC
M61 S
ATGGCAAGAAAAGGAATTCTGGGCACCAAGCTGGGTATGACGCAGGTGTTCGACGACAAC
AACCGGGTTGTCCCGGTAACCGTCGTCAAGGCCGGCCCCAATGTGGTGACCCGCATCCGG
ACCACCGAGCAGGACGGCTACAGCGCCGTGCAGCTCGCGTATGGCGAGATCAGCCCCCGC
AAGGTGACCAAGCCGGTCACCGGTCAGTTCGCCGCCGCGGGC

It's really important for me to know the exact sequence, as i am looking for a nucleotide change at a specific location

You run a blast of your sequence. Then explore the results and you'll see somewhere that says "strand"  and is indication whether is plus/minus.
https://blast.ncbi.nlm.nih.gov/Blast.cgi
Also blast has a graphical interface in which you'll clearly see the matching and non-matching bases. Therefore it should help you to identify the differences between the 2 sequences.

In general, if you look up a transcript sequence it will be in the correct orientation.  If you look up a gene based on genomic coordinates, it may not be.
We can't tell you why your first sequence is in the wrong orientation from what you pasted.


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Using cell concentration
I am doing an experiment in which I plate for example 3x10^5 cells, and every day I have to count the cells growing. I find the number and a convert it in x10^5. In my graphs I have to use the cell concentration. I am not sure which units are used for cell concentration. Is it ml, μl or anything else?

This site is for questions about biology. Your question is a basic question about units which you could find by an internet search. The units you cite are units of volume. You have my sympathy if you don't know what concentration means but you'll have to find out elsewhere.

Use cells/mL, I find it easier to discuss that way. Also look at it like this: Cells grow exponentially, so you can express your concentration axis on a log scale.

@David Thank you but you could answer more politely:)

What is a concentration
A concentration of cells is the number of cells per unit of volume.
You are free to choose the units you like
It is very much up to you to chose the units you want as long as they express a concentration. There is no right or wrong.
You can express your graph in cells per liter or in 100,000 cells per $\mu$l or in billions of cells per ml, all would be correct. Of course, some are more intuitive than others. I would advice you to avoid expressing in cell per square meter or in billions of cells be nanoliter because the numbers will be very small and very large respectively and will not convey much intuition.
A good intuitive unit
I don't know what kind of concentration you have in you data but a priori, I would recommend expressing your concentration in cells/ml is quite intuitive.

Really! If you respond to this sort of question the site's quality standards may not be met any longer

Yes, I agree with @David. Not every question deserves an answer.

Every question deserves an answer please think out of the box!:)

@Claudia In fact, not every question deserves a question. Some questions that are too broad, unclear, not about biology, do not show any effort and others are typically considered as off-topic and should be closed here. I personally considered your question very introductory and by its nature only remotely related to biology but I'd have a hard time to imagine where you'd ask your question otherwise, so I decided to answer it. But it was a little bit of a limit case in my opinion. Anyway, if you think I've answered your question, you can click on the check mark.

@Claudia btw, it is usual to get its question closed when you arrive on stackExchange. It takes a bit of time to learn the rules here. Welcome to Biology.SE.


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Do different people have the same number of mitochondria in comparable cell types?
e.g. will a lymphocyte in one person have roughly the same number of mitochondria as a lymphocyte in another person.

I can't provide a reference but I believe mitochondria are sparce in lymphocytes, perhaps 6-10 per cell but their numbers vary depending on the cells activity so I don't understand why you want to compare numbers between different people.

Careful in asking for the number of mitochondria. In a non-dividing cell, mitochondria are normally organized in a net-like structure (more here: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4672710/). Maybe it'd make more sense to ask about the number of mtDNA nucleoids.

".... The number and shape of mitochondria vary dramatically in different cell
types and can change in the same cell type under different physiological conditions, ranging from multiple spherical or cylindrically shaped organelles to a single organelle with a branched structure (a reticulum). The arrangement is controlled by the relative rates of mitochondrial division and fusion, which are regulated by dedicated GTPases that reside on mitochondrial membranes' In addition, the total organelle mass per cell can be regulated according to need.
For example, a large increase in mitochondria (as much as 5-10-fold) occurs
when a resting skeletal muscle is repeatedly stimulated to contract for a prolonged period."
Alberts, Bruce; Alexander Johnson; Julian Lewis; Martin Raff; Keith Roberts; Peter Walter, Molecular Biology of the Cell, 5th Edition.
As the Paragraph above explains, it can be assumed that due to different metabolism in different people, a specific number of mitochondria in the same cell types for different people may not be assumed.

No, because there are 3 different types of muscle fiber, each containing different numbers of mitochondria, each correlating with a different requirement for oxygen and glycogen.
You also have different muscle types throughout your body - cardiac muscle, smooth muscle, skeletal muscle.
Different people of the same group (e.g. region) will have minor genetic differences which will result in different proportions of muscles and muscle type distribution in their bodies.
Different people across groups (e.g. different countries) will also have different environments to deal with, and different strains on their muscles, which result in muscles developing differently over time. People in Kenya run for miles to get water, and require high-endurance, while people in California spend a lot of time in the gym doing weights, which require less endurance and more power.
This goes into a lot of detail.
I would expect that this is true for other cell types as well, as different environments and differences in genetics will result in different requirements for cellular metabolism, all of which will dictate the number of mitochondria needed.