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When is voltage generated across a membrane?
I'm very confused so bear with me please.
Electrogenic pumps are carrier proteins that generate voltage through the movement of ions, right ?
When is a voltage generated ? When there's a net movement of ions ?
Doesn't that mean that when any ion passes through a channel protein, voltage is generated ? And energy is released ? Doesn't that make them electrogenic too ?
We need energy to move ions against their concentration gradient but if energy is released when ions move then why do we need energy ?
Is it that a voltage is generated when an ion moves towards the env with the same charge ? So when the movement enhances the overall seperation of charge , a voltage is generated ? And energy is released ?
In other words, the movement of Na+ through the Na+ channel protein down a concentration gradient doesn't release energy because the Na+ is moving towards the -ve environment but it being pumped outside does ? See that doesn't make sense either, because we need energy to pump and ion.
I'm very very confused

The main thing the sodium/potassium pump does is to move sodium and potassium ions, Na+ and K+. It technically generates a bit of charge separation in doing this, but you can ignore it for now.
What is important is that because of the operation of this pump, you now have two sides of membrane with different ion concentrations. One side is high in sodium ions (outside the cell), the other side is high in potassium ions (inside the cell).
So far, that doesn't really do anything electrical, but it does take a lot of energy to get this arrangement: the whole time, the pump is moving sodium ions to where sodium ions are high, and moving potassium ions to where potassium ions are high. Moving things against their concentration gradient costs energy. The sodium/potassium pump gets this energy from ATP.
Now, imagine you open some pores in the membrane (we call them leak channels), that are a particular size that only lets potassium ions through. The sodium ions can't move, but the potassium ions can. A few potassium ions move over to the high sodium side, down the concentration gradient for potassium. This doesn't take any energy, it just happens passively. It also doesn't involve very many ions, just a few, so the concentrations don't change much.
However, potassium ions have charge! These are positive charges, flowing out of the cell: that makes the inside more negative.
Also, because they are positively charged, potassium ions would tend to move towards more negatively charged spaces. So, as the inside of the cell gets more negative, potassium won't leave as quickly. There is an equilibrium, where the forces pulling potassium ions out to where potassium concentration is low equals the forces pulling potassium ions in to where the voltage is negative.
The voltage where this equilibrium occurs is called the resting membrane potential, and for many cells is somewhere between -100 and -40 millivolts: that's the voltage generated across the membrane, indirectly, by the sodium/potassium pump.
Purves' Neuroscience is a good general reference textbook for this sort of thing. The Goldman equation is a mathematical way to figure out what the voltage will be if you know the concentrations and permeability.

I think I understand but 1 more thing, my book says "A solute that exists in different concentrations across a membrane can do work as it moves across that membrane by diffusion down its concentration gradient". Doesn't that mean that whenever passive diffusion occurs, energy is released ?

@Jaca Creating a concentration gradient costs energy. Much of that energy is converted into potential energy, similar to how carrying water up a hill. When water flows down the hill or ions flow down their concentration gradient, that potential energy can be used to do other things.

So, your answer ,in short, is yes ? I get the water example, but I have a question, is this potential energy ( the result of movement against concentration gradients ) electrical when the movement of ions is also down their electrical gradient ?

@Jaca They both apply. In the example I described from potassium above, the potassium ions aren't really available to do any work. They have both a concentration gradient and an electrical gradient, and at equilibrium (for the single ion case) these are equal and in opposite directions. If you want to stretch the water example a bit, you could imagine the electrical gradient as a constant vacuum keeping the water at the top of the hill. The vacuum pulls water up, gravity is pulling down, but when they are in equilibrium the water doesn't go anywhere and can't do work.

@Jaca Also, if you follow the steps in my answer, you could interpret the movement of potassium down its concentration gradient as converting the potential energy of the concentration gradient into electrical potential energy. In biology, either or both can be used to do subsequent work. Sodium would be high outside the cell and also the inside of the cell is negative, so there are both electrical and concentration gradients by which sodium can do work.

So you're saying that when Na+ moves from outside to the inside it is releasing both, potential energy due to conc gradient and electrical potential energy due to electrical gradient ? Then why did you say that the K+ ions weren't available to do work if they're moving down their electrical gradient ? Isn't that supposed to release electrical potential energy ? Sorry for constantly asking but I'm trying to understand

@Jaca High potassium inside the cell, negative voltage inside the cell. Potassium is a positively charged ion. When a potassium ion leaves, it is going down its concentration gradient but against its electrical gradient. Therefore there is no energy left to do work: the concentration energy and the electrical energy sum to zero. Sodium is also a positively charged ion, but it is high outside the cell. For a sodium ion moving into the cell, it is moving down both its concentration gradient and it's electrical gradient, so the potential energy sums to a larger value and can do work.

Oh my god I think I get it, so, to sum up, generally, when an ion moves down both its concentration gradient and its electrical gradient it is available to do work but when it moves down one of these gradients it is most likely not available to do work ?

@Jaca "when an ion moves down both its concentration gradient and its electrical gradient it is available to do work" - Yes, always. "when it moves down one of these gradients it is most likely not available to do work" - Only if it is in equilibrium with the other gradient. You could easily have a concentration gradient that does work without any electrical gradient at all, for example. Really what you should consider is the net electrical+concentration gradient.

Voltage is not generated through the charge movement as such, it the magnetic field that is generated directly through movement of charges, although such movement contributes to voltage generation.
Voltage by definition is a potential to do work (to move charges), it always involves 2 points the difference in electric potential between which is voltage. If you want to measure voltage in a selected area, you always measure it relative to another reference area (like, there always is a "reference electrode"), because you measure the difference in electric potential between these 2 areas.
So, voltage is generated through separation of opposite charges. Like, a negative -80-60 mV resting potential inside a cell is maintained relative to an area of positive charges outside.
"The Na+/K+-ATPase enzyme is active (i.e. it uses energy from ATP). For every ATP molecule that the pump uses, three sodium ions are exported and two potassium ions are imported; there is hence a net export of a single positive charge per pump cycle." (wiki) Thus it can be supposed that energy is consumed by Na+/K+ ion propagation, though the definition of "energy" varies by context, voltage means potential energy.

My book says " A transport protein that generates voltage across a membrane is called an electrogenic pump. The sodium-potassium pump appears to be the major
electrogenic pump of animal cells. ." If that's the case then Na K pumps generate a voltage aka release energy then why do they need energy  ? Also, do Na + protein channels generate a voltage ? Or is that because the motion is from a +ve environment to a -ve environment no seperation of charge is enhanced and no voltage is produced ? Sorry if it's a dumb q I'm only 17 and taking this for the 1st time

"Generate a voltage" is not equal "release energy". If you take a smartphone battery out and measure voltage, it will display a manufacturer's preset voltage, so the voltage would already be generated. But there will not be any "release of energy" unless the battery is (generally) plugged into a conductive circuit, where the potential energy provided by voltage will be transformed into any type of energy used by circuit elements - kinetic, light, mechanical, etc.


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Why doesn't G-actin concentration fall once microfilament polymerization begins?

I don't really understand why the monomer concentration on this graph will stay flat when the monomer concentration is above the Cc.

What do you think might be happening? What starts to happen at the Cc? What is the definition of Cc?

Cc is defined as the critical concentration which is a measure of a solution of G actin to polymerise. What I am thinking is that if the monomer concentration is above the Cc, the polymerisation will occur and forming the actin filament. But if the polymersiation occurs, suppose the monomer will decrease and the graph for monomer should drop. Thats why I don't get why the graph for monomer will be plateau.

Notice the vertical axis is not for monomers, it's for mass.

The critical concentration is better defined as the "equilibrium concentration of the pool of unassembled subunits"1.
An analogy that might be helpful is thinking about a NaCl (table salt) solution — once you add enough salt some will start to precipitate, but the amount in solution will remain the same.
You can think of the solution as having the capacity to support a certain concentration of molecules (or ions) — below that concentration subunits will separate from the polymerized form faster than it can accumulate new subunits, above that concentration the subunits will stick together faster than they "fall off" the polymer.
For more a detailed molecular understanding of why this is so, you probably need to read up on chemical equilibria — for example Chemistry or even Khan Academy might be helpful.
Reference:
1: Lodish, H., Berk, A., Zipursky, S. L., Matsudaira, P., Baltimore, D., & Darnell, J. (2000). Section 18.2 — The dynamics of actin assembly. Molecular Cell Biology.

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How do signalling molecules find their receptors at large distances?
I have been baffled with this question approx. for a dozen of years for now.
There is a default "lock & key" mechanism of action assumed for the interaction between a signalling molecule and its receptor, but while applying a bit of combinatorics and biophysics to it I find the following inconsistencies.
Suppose a long-lasting neuropeptide is circulating in a CSF or blood macrocirculation. Or suppose a norepinephrine or other neurohormones are released by hypothalamic and pituitary cells into the macrocirculation for sympathetic or parasympathetic signalling. Accroding to the logic of "lock & key" mechanism, in order for a "key" signalling molecule to activate its "lock" receptor an active site of this molecule - the molecule partition which directly reacts with the receptor as it is generally not the whole molecule which reacts with the receptor - should come in direct contact with the relevant active site of its in-membrane receptor. So by such combinatorial logic, if there are thousands of receptors on outer membranes of cells in CSF or vessel endotelium along the way of which this "key"-molecule is travelling, this molecule should try to "lock into" every such potential "lock" receptor in order to "check" if this is the right "lock". In other words, while travelling across long distances such "key" signalling molecules should not just float in CSF or blood vessels as is generally depicted, but slide across all outer cell membranes in CSF or across vascular endotelium in blood or lymph circulation in order to "check" every potential "lock" receptor for finding their relevant receptors for eventual activation. It is definitely not the case, but it the result of applying combinatorial "lock&key" logic.
Somehow it seems (for myself, at least) that it is just assumed that a "key" molecule released at distances which are millions> of times larger than the molecule size should just "lock" for granted into its appropiate receptors throughout the organism. But suppose a "key" molecule travels in CSF or interstitial fluid in the vicinity of its appropriate membrane "lock" receptor, but with the molecule's reaction (active) site pointed away from its receptor or at an angle. Should the "key" molecule not then react with its "lock" receptor?? Is there a minimum effective reaction distance established between a "key" molecule and its "lock" receptor in order to effectively activate the receptor?
The latter argument holds true also for small distance 20-40 nm synapses with molecules released in it whose size would be minimum 1000 times smaller than the synapse size. Should a neurotransmitter molecule not react with its receptor in a synapse if the molecule's active site would be pointed 180 degrees away from the receptor's active site?

Yes, any individual ligand may have the wrong orientation to interact effectively with an individual receptor, but so what?  There are typically thousands of each type of receptor on a single cell1 and there will be many molecules of a given ligand present as well.
For your synapse example, I suggest looking up:

How many neurotransmitter molecules will be present in a synapse
How many receptors will present in a synapse
How many of those receptors need to be bound to get a signal

I think that will help you make sense of this phenomenon and I encourage you to post a detailed answer to your own question!
You might also want to look into molecular dynamics simulations ...
1: Milo, R., & Phillips, R. (2015). Cell biology by the numbers. Garland Science.

The ligand orientation is a subquestion and synapse is a short-distanced space. The main question is related to ligands at long distances, flowing in cardio-vascular, lymphatic systems and between cells, as well as ligands for extrasynaptic receptors.

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What slope do I need to prove a hypothesis?
I am conducting an experiment for school in which I am measuring people's heart rates as music plays at different tempos. My hypothesis is that as the tempo of the music increases, so will the subject's heart rate. After recording data from many subjects, I will use linear regression to find the overall function to represent my data.
What slope would I need on my function to prove my hypothesis correct?

As your hypothesis states: relating the tempo of music and the heart rate, the slope must be greater than zero.

I'm voting to close this question as off-topic because it belongs at SE-Cross validated (https://stats.stackexchange.com/)

I would worry less about the slope, and more about the p-value of the correlation.

It seems like you need to calculated a correlation ; It varies from 0 to 1.

Hi, welcome to Biology.SE. It seems like this question isn't quite about Biology, you seem to be asking a much more general statistics question. However, there isn't nearly enough here to motivate a migration to CrossValidated.SE. The general area you are looking for information in is called "power analysis" - I hope reading about power analysis can either help you directly or help you formulate a better question for CrossValidated.

You will get a much more complete answer on a statistics forum, or by simply consulting some basic tutorials on linear regression.
But a little intuition should tell you that setting a cutoff on the value of the slope does not make sense. For instance, suppose you measured heart rate in beats per second instead of beats per minute. All the y-values would be 60x lower, your slope would be 60x lower, but intuitively, nothing should change about your interpretation.
When you calculate your linear regression, you'll be able to obtain a correlation coefficient and a p-value, which tell you how well your data fits the line and the probability of obtaining such a result if there was no relationship between the data. These will be based not on the slope, but rather on how well your data fit the line and the number of points you have (the more data you have, the more confident you can be of the effect).
But you will never prove your hypothesis. The best you'll be able to say is "if my hypothesis were false, the probability of obtaining the result I got is less than X%". The clearer your data, the smaller X will be.
You would also do well to consider sources of systemic bias, not just statistical power. For instance, could the music affect the accuracy of the measurement? Do you always gradually increase the tempo of the music, or do you randomize the order? Just some examples off the top of my head, I'm sure you can think of others more relevant to your setup.

Sorry, the word I meant to use was "accept" I asked this question on stats.stack exchange( https://stats.stackexchange.com/q/435803/265532) and posted some more details on it


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Infectious diseases spread by insects
if blood feeding insects can transmit many diseases(west nile,...,etc.),why cannot all infectious diseases like AIDS,Ebola be vectored by insects?

Regarding AIDS, you can find some answers in this paper : https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3352396/

Possible duplicate of Why doesn't blood remain on a mosquito's proboscis in quantities that could spread blood-borne diseases?

Diseases that are spread by arthropods (I'm including things like ticks here as well as insects) are generally highly adapted for that lifestyle, and there are many specific adaptations that are needed to make this efficient. They're not simply passively carried by the arthropod; they actually replicate in the arthropod as well as in their vertebrate host, and since there is an enormous evolutionary gap between arthropods and vertebrates, the pathogen basically needs to have two, parallel and separate, lifestyles prepared.
If they don't undergo these adaptations, they'll be rapidly destroyed in the arthropod by being digested, or simply because the volume of blood is so small that unless they actively replicate there wouldn't be enough pathogen to transmit.
To give a sense of the double specialization an arthropod/vertebrate pathogen needs to undergo, here's a brief summary for tick-borne viruses:

Arboviruses differ from other viruses in their need to replicate in both vertebrate and invertebrate hosts. ... Arboviruses transmitted by ticks must adapt to the peculiar physiological and behavioral characteristics of ticks, particularly with regard to blood feeding, bloodmeal digestion, and molting. Virus imbibed with the blood meal first infects cells of the midgut wall. ... After infection of midgut cells, tick-borne viruses pass to the salivary glands for transmission during the next blood-feeding episode. To do this, the virus must survive molting by establishing an infection in at least one cell type that does not undergo histolysis. ... The infection can then persist for the life span of the tick with little evidence of any detrimental effects on the tick.

--Adaptations of Arboviruses to Ticks
So to be a tick-borne virus, these pathogens have to survive being eaten by the tick and avoid being digested. They infect at least three distinct types of cells, and have to survive the tick molting period. In the second set of cells they set up a life-long infection. And they need to do this without making the tick unhealthy, so that it can go and bite more vertebrates.
The question specifically asks about West Nile virus, which goes through a similar path of infection in mosquitos, first infecting midgut cells and then spreading to the salivary glands where it replicates to high levels (West Nile Virus: Biology, Transmission, and Human Infection).
And then after the tick bites a deer, they have to go through the whole thing again, in a brand new host that's completely different from the tick in just about every way.

A critical point is that mosquitoes and ticks inject saliva into their host, not the contents of their stomach.

Arboviruses, including dengue and West Nile virus, are injected into vertebrates within mosquito saliva during mosquito feeding. Mosquito saliva contains anti-haemostatic, anti-inflammatory and immunomodulatory molecules that facilitate the acquisition of a blood meal.

http://ncbi.nlm.nih.gov/pubmed/18342898
So for a virus carried by an earlier host of the arthropod to infect a later host of that arthropod, it's not enough to survive in the gut, the salivary glands must be infected. This isn't possible for viruses that aren't adapted to arthropod cells.


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Which bird is this?
Found this today in my neighborhood, my mom says it's a baby vulture and she has seen many during her childhood (in 1970's) while she lived in a small town around 200kms away from our city. However I want to know of it is really vulture cause there are less than 1000 left in whole state and certainly they don't usually fly around here. Even Monkeys (which are, FYI, common in India in small cities and are not afraid by humans) are mad because of this bird's presence but perhaps too frightened to go near him/her. It'd be nice if you guys can tell me what it is :).

I live in Gujarat, India if it helps.

See a very similar ibis species form Australia here: Bird species ID in the Northern Territory, Australia

@theforestecologist Yeah, ty for the info, good to know that.

It looks a lot like a African sacred ibis (Threskiornis aethiopicus) (wikilink). However, given your location in India, the closely related Black-headed ibis (which some consider to be part of the same species) might be more likely.
The African sacred ibis is native to mainly sub-saharan Africa, but is considered Invasive in some parts of the world (inkl. Europe and parts of Asia). The Black-headed ibis is however a native breeding bird to large parts of Asia (inkl. India), which makes this more likely.

(Black-headed ibis from wikipedia)

Yesss! I was just googling using features and found this bird and then at the same time saw yr answer, I'm quite certain now after your answer that this is it! Thanks a lot


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Can a brain be damaged by overstimulation?
I am wondering what, if any, long term health effects there are from high levels of brain activity.
I don't mean cases where a brain is being artificially stimulated, but rather where there is a high (as in the high end of normal, not as in shell-shock) sustained level of sensory input, or simply that the brain in question is "thinking too much".
Assuming a person could sustain high levels of neural activation, is there a chance that the brain could "strain" itself or somehow "wear out" or come to some other kind of harm?

(This is such a difficult question to begin answering in any satisfactory manner, though I think can be addressed for pedagogical purposes in line with the aims of this SE.)
Before we address the question, I think it is prudent to think about the difference between stimulation and activity. A neuron can be self-activating without external stimulation, or it can be highly stimulated by sensory input and yet have low or inhibited activity. You do not specify, so I think the discussion must necessarily be very incomplete on this topic.
Your question is also naturally a little unclear and difficult to answer methodically, especially because 'damage' in this case is a very subjective term. As with all biological systems, there are self-protective mechanisms and reflexes and feedback circuits in place to prevent 'you' or your brain from overdoing anything. A dysregulation in neuron activation, or activity, would probably be a state of illness, such as having a seizure. I don't think it is possible for a typical person to expose themselves to sensory extremes without consequently feeling tired or bored as a result (e.g. looking into a strobe light or listening to loud music for inordinate amounts of time), which may be the result of an internal homeostasis, just like blood pH or blood sugar level, though regulated through physiologically-dependent behavior (sleep, concentration levels, apathy, etc.)
More strictly and scientifically speaking, all activity wears all tissues, including the brain. This would make 'brain activity' a process contributing to aging. However, once again, one can interpret anything as 'damaging'; breathing is damaging (oxidation! the cellular definition of wear-and-tear), but it also sustains you. Calories sustain you, but caloric restriction extends lifespan in virtually all animal models.
A recent publication in Nature (Oct 2019) suggests that the global inhibition or decrease of all neuron firing seems to be related to increased longevity which may suggest the opposite case to your question: lower neural activity may lead to extended lifespan. This suggests, though does not demonstrate, that over-activation may contribute more 'damage' and accelerated aging, compared to lower levels of activation. This conclusion is also based on evidence associated with a global - whole-central nervous system - effect, and does not indicate that one should under-stimulate parts of their nervous system to achieve the same result. Also, keep in mind that stimulation and activity are entirely separate things, so such a conclusion does not answer your question.

Thank you for attempting to answer. I have edited the question to clarify that I am asking about high levels of activation (and assuming that high levels of stimulation could be one cause).


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Why does glomerulus don't allow white blood cells to leave?
The glomerulus in nephrons are just a ball of capillaries, so why can't it allow the white blood cells to squeeze though the epithelial cells into Bowman's capsule just like the formation of tissue fluid in other capillaries by filtration?

Red blood cells, White blood cells, platelets and proteins with large molecular weight cannot pass through the podocyte and fenestrations in glomerular capillary, but small molecules like water, salts and sugars are filtered out as part of urine.
As these cells and proteins are large to cross through this filter, they remain in the capillary and create osmotic pressure within the capillary. Bowman’s space has osmotic pressure approximately zero. So, only hydrostatic pressure works in this state and help in movement of fluid across the capillary wall.
Via:  https://opentextbc.ca/anatomyandphysiology/chapter/25-5-physiology-of-urine-formation/

So it means that the epithelial cells (podocyte) in the glomerulus are more closely packed so they don't allow the filtration of white blood cells like other capillaries in the human body? Thank you very much

Yes, in association with endothelial capillaries and basement membrane they form filtration barrier in glomerulus.


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Identification of an alpine blueberry type
I'm trying to figure out what kind of berry this is. It can be found all over the Swiss, French, and Italian alps, generally right where ordinary blueberries are (the ones one would eat). However, they are distinctly different:

The flower attachment spot (sorry, non-botanist here) at the tip is square shaped (see photo)
Their leaves turn red much later during the season
The berry is more elongated when compared to ordinary blueberries, a bit of an ellipsoid

Possibly Vaccinium gaultherioides (sometimes considered a subspecies of Vaccinium uliginosum), which are present throughout the Alps.
For example, see InfoFlora*:

 Vaccinium gaultherioides Bigelow, © Konrad Lauber – Flora Helvetica – 2012 Haupt Bern
You can see the prevelance of this species throughout the Swiss alps in the below range map (also from InfoFlora):

______________________________________enter preformatted text here
* the national data center for the Swiss flora
I don't know the flora of the Alps personally and I feel you post lacks enough detail for me to confidently pick and choose among many Vaccinium candidates. From those I've examined, this species seems most visually similar to yours.

That's definitely it! Thank you so much. I didn't know about InfoFlora. Now I have a way to figure out questions like that in a structured manner, which will be very helpful.


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Mushroom Identification: Small conical light-brown mushroom
I found a small single mushroom growing on grass and I decided to try to identify it.
Characteristics:

Region: Brazil southeast coast, state of São Paulo, predominantly Atlantic forest
Gilled mushroom
Substract of growth: Grass
Dark coloured spores (I'd say yellow-brown. Picture Below)
Gills either free or adnexed (My mistake this time, the cap was conical and small, so I couldn't have a clear view of the end of the gills. Should have cut it)
Cap 1.6cm in diameter, conical shaped
Height of about 6cm
Very fragile, specially stipe. Dry texture
Cap color: Like a faded orange or very light brown. Stipe color: Light cream

I tried to follow some identification keys (mostly this one, but that one also seemed to go the same direction) and it pointed me towards the Conocybe genus, possibly Conocybe apala (item 45a on the key from the link, you can follow back to the beginning going to the item on the parenthesis).
However, from what I read it's very hard to identify Conocybe mushrooms to the species level, because some are only differentiated by some microscopic features. They are also sometimes confused with mushrooms of Bolbitius or Galerina genus. Most mushrooms pictures I found from Bolbitius and Galerina give the impression they are a little more "fleshy" (not sure that's the word), and mine had this dry-fragile texture, which most pictures of Conocybe apala seem to align with.
Below are some pictures:

Is it likely a Conocybe apala or are there any other possible candidates?


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Can a ladybug be determined just by its number of points?
I saw a ladybug on my balcony one day and I just counted the dots.
There was 18 black dots on a red/orange elytra.
The location is in Europe (Geneva, Switzerland) and usually we have quite different endemic ladybugs and also the invasive asian ladybug Harmonia axyridis.
I did not found any local ladybugs with such dot counting except articles saying the Harmonia axyridis can be found with a lot of variations (elytra  color, points or stripes, etc...).
The question is: Can I be sure that a ladybugs with 18-points (found in Europe area) is of the genus Harmonia axyridis?
Note that I have a picture of the animal but I want to focus my question on the number of dots exclusively.

No, most of the time you cannot. There is a large diversity of ladybug species (several dozens in western Europe), and many of them can have the same number of spots. Moreover, as you already said, there can be intraspecific variation in the number of spots.
I do not know if there are specific numbers of spots that would be associated to only one species - but for most numbers, it is not the case. For instance, yes, it is common for Harmonia axyrids to have 18 spots (source). But Anisosticta novemdecimpunctata, which  can also be found in Europe - and can also be orange ! - may have between 15 and 21 spots (though it more frequently has 19) (source).
Thus, the number of spots cannot be used as a sole criterion to identify ladybugs: other criteria usually include the general shape, colour of elytra, size, shape and colour of the pronotum, length of antennae, etc. (See here for examples.)
First picture: Harmonia axyridis

Second picture: Anisosticta novemdecimpunctata

You're right, you found a potential species that have the same number of spots. Another criterion would also be the distribution (the Anisosticta novemdecimpunctata seems not  present in Central Europe). Accepting the answer then.

Actually it is present in all Europe (although not as common as H axyridis) see here for instance:
https://fauna-eu.org/cdm_dataportal/taxon/e8c617e8-591c-466b-8f0d-6ecf4411c72f
Distribution + number of spots are often a good proxy, but one must be cautious about intra-specific variation in the number of spots.


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Myelination and time constant
In textbooks, it says that myelination doesn't really affect the time constant as tau=RC where R is the membrane resistance and C is the membrane capacitance. Myelin increases membrane resistance while decreasing membrane capacitance so there isn't really an overall effect on the time constant. However, during active regeneration of the action potential, the current only goes the path with least resistance i.e. the nodes of Ranvier, so wouldn't the R be the resistance of the node of Ranvier instead of the resistance of the entire membrane as stated in the textbooks? If this argument is correct then wouldn't myelination increases decreases time constant? Thanks!

For the saltatory propagation of the action potential the constant of interest is not the membrane tau constant, but the spatial lambda constant. The decrease in membrane resistance due to mielination increases lambda, allowing the current to travel farther to the next Ranvier node.
In the Ranvier node there's a high concentration of ion channels that generates the current necessary to depolarize the next node.

No. When a signal is sent through a myelinated axon, the Nodes of Ranvier act as repeaters in electronics. The signal/action potential will disperse down the axon, the Node of Ranvier will pick up the signal, amplify it, and send it to the subsequent Node of Ranvier. I think you're thinking of the Nodes of Ranvier as cracks in the myelin/axon rather than as mini re-amplification sites.

Welcome to Biology.SE! This looks like it might be a good answer, but answers are much more likely to receive a favorable response if you include supporting references (primary literature is best, but textbooks can be OK). Without that support, your answer is indistinguishable from opinion. This is a good example of how to format references. ——— You may also want to take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site. Thank you!


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How fast do we fall asleep?
When looking at the process of sleeping, most research I find point to a group of mutually inhibitory cells which form a sort of biological "flip flop."  There's cells that promote awakenness and cells that promote sleeping.  The process we typically think of as "falling asleep" is getting to the point where this transition can occur, but I'm interested in the transition itself.
How fast is this transition? In engineering, we'll typically measure the speed of such a transition as a 10-90 measurement: the time it takes to go from a 10% signal to a 90% signal.  Is there a similar measurement made in such biological systems?

Good question. Please be aware that in biology, we are concerned with a subject with high variation. In other words, as you very well must know, the time needed to fall asleep varies very considerably between people and also within a single person, from day to day. I think the second paragraph in your question is counterproductive, I would edit it out to prevent answers going off at a tangent.

@SPr I'll have to think about how to best reword that second paragraph.  I put it in there because, when it comes to flip flops like this I know that it's a continuous process with no clear start an end, but the the duration of the middle of the flip is easier to quantify.

Our ability to maintain sleep or wakefulness is because of "mutual inhibition" between the wake-promoting neurons and the sleep-promoting neurons. The areas in brain which regulate wakefulness by activating the cortex also inhibit neurons present in ventrolateral preoptic nucleus (a cluster of neurons situated in the anterior hypothalamus). And when VLPO neurons are activated, they induce sleep, and this also inhibit activity in the arousal centers like neurons in tuberomammillary nucleus (TMN).
Transitions between these states of wakefulness and sleep is very rapid, usually in seconds. Various researchers have reported this neurological mechanism for "flip-flop switch" in form of electrical circuit.
The mechanism  for mutual inhibition is regulated by sleep drive or the circadian signal. When one of this body signal is sufficiently strong, it transits to the opposite state from wakefulness to sleep or vice versa. This mechanism is analogous to mechanism involved in  transition between rapid eye movement (REM) sleep and non-rapid eye movement (NREM) sleep.
Humans require some time to relax and then fall asleep, and deep sleep needs 20 or more minutes after sleep onset. Sleep onset and associated loss of consciousness is related to one another and occurs instantly.
Many intrinsic and extrinsic factors  regulate sleep cycle. Adenosine is one of the chemical which accumulates during wakefulness and later induces sleep by inhibiting wake-promoting neurons. And caffeine inhibits adenosine activity and helps in wakefulness.
The time needed for transitions between sleep and wakefulness  is  maintained by biological clock located in the suprachiasmatic nucleus. This is small structure consisting of about 50,000 brain cell. And it receives light signals from eye  via  optic nerve. Light controls the day-night cycle and which in turn regulates various biological functions including temperature, hormone release,  sleep and wakefulness. The SCN stimulates wakefulness by producing a  alert signal which inhibits sleep. The SCN also helps in inducing sleep by turning off alert signal.
(Via:  http://healthysleep.med.harvard.edu/healthy/science/how/neurophysiology)


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What does the presence of 6 molecules of water in this equation indicates to?
so I was studying biology today and I went over this weird question that says:

The presence of 6 molecules of water in this equation:
C6 H12 O6 + 6O2 --> 6CO2 + 6H20, Indicates that the:
a) Complete Glycolysis of a glucose molecule (Obviously not correct)
b) Occurrence of Krebs cycle Twice
c) Complete occurrence of oxidative phosphorylation process
d) Storage of energy in NADH and FADH2 molecules

Alright so this is the oxidation of one mole of glucose equation (Without the ATPs) but till now I don't exactly know the correct answer for this question, but to not create any confusion this question is related to the Aerobic respiration (Glycolysis, Krebs Cycle and Electron transport chain).
Here's how I approached this question:
(a) is obviously not correct because the products of glycloysis are 2 pyruvate molecules and 2 ATP molecules so I checked off this choice.
(b) However seems correct because the products of 2 Krebs cycle is 4 CO2 and there is already 2CO2 when the pyruvate acid formed the 2 acetyl CoA molecules so in total that's 6CO2, but still what about the 6 Water molecules?
(c) is a very debating choice because when there is a "Complete occurrence of oxidative phosphorylation process" so that means 2 Krebs cycles had already occurred and formed the 6CO2, and during the oxidative phosphorylation process Water molecules are formed. and ATPs too? I don't exactly know about the ATPs, but aren't they supposed to be in the equation's products in order for this choice to be correct?
(d) This choice indicates to Krebs cycle but the water molecules only are formed during oxidative phosphorylation only.
So basically all the choices seems very debating and confusing and if I were to choose then I'll go with (C) because it's the only choice that makes sense for the water molecules (and the question asks for water), but I want someone to please answer this question with a brief explanation to why he chose this answer,
Thanks :)

You have my sympathy. Even for an MCQ this is a really stupid question. Nobody cares about water molecules in biochemical pathways, nor is it generally practical (or at least the practice) to count their production. The purpose is presumably to have you look at the pathways and see where the water is generated. Forget about everything else (i.e. the important stuff). PS You could improve your writing style by not imitating informal speech patterns. "So" is not required to start a sentence, is bad style, and removing superfluous material improves readability.

This reaction only means complete oxidation of glucose to 6 molecules of carbon dioxide and 6 molecules of water.
Reaction presented in question is very generalized, but the presence of six water molecules only means complete cellular respiration. Check out the actual biochemical pathways which take place to oxidize one glucose molecule.
And other options do not represent the complete cellular respiration, so there will not be formation of six water molecules, only option C means complete oxidation of glucose.

Via: https://en.wikipedia.org/wiki/Cellular_respiration
Water molecules shown by solid blue arrows.
During glycolysis, One glucose molecule releases two water molecules. This is the 9th step  of glycolytic pathway controlled by Enolase. Two water molecules are produced because two reactions are taking place.

(Image source:  https://johncarlosbaez.wordpress.com/2016/01/08/glycolysis/)
During Citric acid cycle, 2 water molecules are used in two enzymatic reactions performed by  Fumarase and Citrate Synthase. And Aconitase performs the  isomerisation of citrate to isocitrate so it has no net effect on water molecules. So, 4 water molecules are used here.

(Image Source: http://www.biosciencenotes.com/citric-acid-cycle/)
During Electron transport chain, 12 water molecules are produced due to oxidation of NADH (FADH2).
As electrons in this chain are passed, they move from higher to lower energy state, and release energy. Some of the energy is used to transport hydrogen ions across the membrane. This creates electrochemical gradient. And electrons are transferred to molecular oxygen to form water.
This makes net total of 10 water molecules. But 4 water molecules during cellular respiration are used in substrate level phosphorylation. Check out its explanation here   (Via : https://onlinelibrary.wiley.com/doi/pdf/10.1016/0307-4412%2895%2900140-9)

(Image Source: https://www.khanacademy.org/science/biology/cellular-respiration-and-fermentation/oxidative-phosphorylation/a/oxidative-phosphorylation-etc)

Couldn't agree more, thank you for sharing your knowledge! But don't you know anything about wither they should add the ATPs to the equation or not?

The reaction catalyzed by aconitase doesn’t have any net usage or production of water (it’s an isomerization), which is actually shown in the diagram you used. Ignoring the water produced by ATP synthase, 10 molecules of water are produced by the biological oxidation of glucose, not 6.

yes..you are right, then why don't we show 10 water molecules in this reaction.

@canadianer I tried to improve my answer. Kindly explain me why we only show six water molecules. Thankyou

Good question. Check out this answer, the paper linked to therein, and Roland’s comment underneath.

Thanks a lot for making it clear

Although I tend to agree with David on the validity of the OP example as a good MCQ question, I think that the 'required' answer is (c) Complete occurrence of oxidative phosphorylation process.
However, I think that this answer is potentially flawed (see below) and a more acceptable alternative might be something like

(c) Complete oxidation of glucose via cytochrome oxidase of the respiratory redox chain.

Glucose makes 12 pairs of electrons (all 'held' in C-C and C-H bonds) available to cellular respiration. (See, for example, the letter on TCA cycle confusion by D.E. Atkinson published in TIBS and kindly made available by David).
It takes four electrons to produce 1 water molecule in the cytochrome oxidase reaction.  Therefore, if six water molecules are produced, all of 24 electrons 'supplied' by glucose have been passed to water: glucose has been 'completely' oxidized.
The reduction of oxygen to water is a four-electron transfer.  A two-electron reduction produces H2O2, and a one-electron reduction produces superoxide.  If either of these compounds were produced, or if electrons from glucose were 'diverted' elsewhere (thus never 'arriving' at cytochrome oxidase) the stoichiometry of water production would be less.
However, possibility (c) specifically states "Complete occurrence of oxidative phosphorylation process. This, to me, is confusing and is arguably false. There is no requirement that oxidation and phosphorylation be coupled in order for six water molecules to be produced in the respiratory redox chain. In the presence of (excess) of an uncoupler such as dinitrophenol, no ATP is produced (oxidation and phosphorylation are completely uncoupled) but this in no way precludes all 24 electrons from glucose being passed to oxygen resulting in the formation of 6 water molecules.
For example, if possibility (a) were to state 'complete oxidation of a glucose molecule', then IMO that is by far the best answer (and all others are false or ambiguous).

Yes exactly, this question is very inaccurate, but I guess I'll just go with (C) as it's the most suitable answer for this question, Thanks for your answer.


text:
Why was the precipitation-streamflow correlation greater in the intact catchment at Hubbard BrookI
I gave an assignment and ran a class on this data last year.
https://lifediscoveryed.org/r290/hubbard_brook_streamflow_response_to_deforestation
Its a classic small watershed experiment where streamflows and precipitation are compared for two catchment areas, one with intact tree cover, the other deforested.
Streamflow and precipitation are, unsurprisingly correlated, but this correlation is apparently much greater for intact (0.91) than deforested (0.72) watershed.
I had no explanation to offer students for this, (I'd expect the opposite) which is OK, but if I run it again I'd like to have one up my sleave.


text:
adverse effects of reduced food variety on microbiome
We often see, in science fiction, food being produced from, say, algae or yeast. Any idea what could be the effect of such a limited diet on the gut microbiome? Could there be any side-effect that would have an influence on the brain?
I know that gut microbiome has been tentatively linked to the autism spectrum in some cases, and that heavily processed food may affect it (don't worry, I don't equate "natural" with "good for you"). I'm thinking that food designed only with the needs of human metabolism in mind might ignore the needs of gut bacteria.
I understand this is very speculative, I'm just hoping someone would know of any research in that field.

Hi, and welcome to the site!  Unfortunately, this question is way too broad to be answerable in a specific way... You would have to narrow it down to a very specific diet, and ask about a specific issue that that diet could cause in order for us to be able even to adress the issue.  And even at that, I have a feeling that there will be a lot less solid answers than simple speculation, since science fiction is generally not the realm studied by scientists.  :)  Anyhow, please [edit] to make your question more specific.  Thanks!

In addition to following the guidance from @rotaredom, I encourage you to take the time to take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!

I interpret your question as essentially asking this:
What is the effect of a limited diet on the gut microbiome? Can a limited diet affect the brain via the microbiome?
To simplify the answer, let's make some assumptions --

This "limited" diet is nutritionally complete, meaning that it contains all the macro- and and micro-nutrients needed for human metabolism.  This includes all nutrients that we normally receive via microbiota, such as vitamin K2. Said another way, this diet only affects host health via the microbiome, and there are no effects of malnutrition that would confound our inferences.
There is no flow of genes between organisms in the gut microbiome or introduction of new organisms from outside sources, i.e. only the organisms that are present at the start of the dietary change will be present throughout.  Thus, all observed changes are directly attributable to changes in species abundance.  In reality, there is extensive horizontal gene transfer in the gut microbiome, with new genes obtained from endogenous and exogenous sources.
Following the logic of point 2, there is no mutation.  The microbes present at the end of this diet are clones of the microbes present at the beginning.  Likewise, competitive exclusion does not lead to the disappearance of low-fitness microbes in the microbiome, just a reduction in their relative abundances.
The human host of this microbiome is healthy and not undergoing the physiological changes associated with aging during adherence to this limited diet.

In this simple system, the only things that will change are (1) the total number of microbes and (2) the relative abundances of microbial strains.  Different microbes contain different genes for metabolizing different food sources.  For example, if this simple diet contains carbohydrate A that is metabolized exclusively by the enzyme encoded by gene α, then microbes that both contain and express gene α will grow in abundance.  Some different microbes may then be able to use the products of the metabolism of carbohydrate A, and those microbes may also grow in abundance.  The metabolic interaction network of the human gut microbiome is extremely complex, as it includes both microbe-microbe and host-microbe metabolite cycling.  Eventually, with the same limited dietary input, the microbiome will reach an equilibrium state where the abundance of each microbe is essentially fixed.  The microbes that are best able to utilize the nutrients provided by the food will maintain a high abundance and can be said to be "very fit" in this particular niche.
Keep in mind that this system is extremely simplified, and that microbial fitness in a particular context depends on gene copy number, expression level, enzyme efficiency, microbe-microbe antagonism, and a menagerie of other factors, notwithstanding regulatory signals from human epithelial cells.
Even if we had two people eating the exact same diet with the exact same initial composition of their microbiomes, human genetics plays a role in the carbohydrates available to commensal microbes, as can been seen with salivary amylase copy number.
...
Considering the "brain" part of your question, I suggest you Google "Gut Brain Axis".  Here's a good summary article with references at the end.


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Do new neurons divide propotionally?
Do new neurons divide propotionally?

if i try to improve my reasoning skills,are the new neurons only made for that specific region of the brain that controls reasoning skill?
i have heard that one side of the brain controls the other side of the body, if i try to use my non-dominant hand(left hand in my case),are new neurons only made for right side of the brain,does it improve only some of the brain regions?

There is no evidence of new neurons except in the hippocampus and the olfatory bulb, and the evidence in humans is still controversial.
Skills are not acquired by the addition of new neurons, but by the formation of new pathways between existing neurons. These pathways are highly specific, while your examples are rather vague, like the sort we read in pop magazines: "brush your teeth with your non-dominant hand to become smarter" - it would be great if it were that easy, unfortunately this is just pseudoscience.

Thank you, I always thought that it was real.

So If you take too many IQ tests you won't get smarter in other areas(things) other than the IQ test , you only get smarter at IQ tests, right?

Similarly some brain games, tests claim that they can boost your brain, however they only form new pathways between existing neurons in your brain, therefore you only get better in that specific pattern of the game, test, if this is true most brain games are pseudoscience, am i right?

Yes, most likely the claims of common "brain games" are essentially pseudoscience

It seem's you are assuming that your / the adult human brain produces new neurons over time- this is (largely) incorrect: neurons are non-dividing cells and are all formed throughout embryogenesis and very early childhood / infancy (see also this question).
Only very exceptions to this are known as adult neurogenesis (generation of new neurons), the most likely or active region in humans would be the hippocampus, however the extent or importance of the process in humans is still not really known. Additionally the hippocampus is an area of the brain that mostly holds memories and is not really related to reasoning skills or body / motor control.

If i use my non-dominant hand, does it improve some regions of the brain while having no effect on the other regions of the brain?

"Regions" is to broad: it will have no effect even in the same "region" as a whole.. Anything learned will make new pathways between existing neurons. But these are highly specific, and you wouldn't expect any improvement except in the very skill you have practiced, regardless of the brain regions used in that skill.

@Gabriel are the "new pathways between existing neurons" in the same regions of the brain that was used in that skill?

Not an answer, but a clarification. By "hippothalamus" (a probable typo) above it is probably meant "hippocampus", as is mentioned in wiki link. It is hippocampus which is known "to hold memories", but it is a part of a larger "memory" circuit and is a bit similar to temporary memory responsible for holding only recent memories and integrating recent memories into long-term memory.
This overview of neurogenesis can also be useful.

Yep, that was an error in my answer, thanks for pointing it out - I fixed it now (normally this should probably have been a comment to my answer, but you probably don't have enough reputation for comments yet)


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Is p53 a cyclin dependent kinase?
I've been reading some research papers about p53 and associated tumour suppressor proteins, such as p21. I see them referred to and associated with cyclin-dependent kinases. Is p53,p63 et cetera part of the CDK family?

Welcome to Biology.SE! We encourage you to do some research on your own and then, informed by what you have learned, ask any questions you might still have (ideally with references to reliable sources). To start there is an extensive wikipedia page that contains links to many other resources. ——— Thank you for taking the [tour], but please also take the time to go through the help pages starting with [Ask] questions effectively on this site. Thanks!

p53 is not even a kinase forget cyclin dependent kinase.

No, p53 and other tumor suppressor proteins do not belong to Cyclin dependent kinase(CDK)family. p53 blocks the cell cycle by promoting the synthesis of Cyclin dependent kinase inhibitors (CKI proteins). These CKI proteins bind with the Cyclin and CDK complex and inhibit the cell cycle at G1 checkpoint.

(Image Source:  https://www.khanacademy.org/science/biology/cellular-molecular-biology/stem-cells-and-cancer/a/cell-cycle-regulators)
p53 also plays role in activating DNA repair enzymes and if DNA is not repaired, p53 will promote apoptosis, so that defective DNA is not passed on.
These all proteins are structurally homologous to p53, so together they are known as p53 family.
(Via: https://www.frontiersin.org/articles/10.3389/fonc.2014.00285/full)

This is a nice answer, but please don't answer homework style questions — this is something the OP could (and should) have looked up for themselves!

ok..I’ll keep that in mind for future

Fluffy question, good answer :)


text:
Scorpion in Ohrid, Macedonia, 5cm long

Hi, can u please help to identify what kind of scorpion is this? A friend of mine found it at home, in urban area in Ohrid, Macedonia. It is aroun 5 cm long.
Thank you.

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


text:
What is the word for being inured to loss of biological diversity?
In the title.  The word has been coined relatively recently for the phenomenon of getting used to loss of diversity because of the gradual rate it happens at.  For example, not finding it strange that there are far fewer invertebrates around now than there were 30 years ago - car windscreens in the summer were covered in dead insects, whereas now that rarely happens.  Both time points are noticeably distinct in biological richness, but we quickly get used to the state of things now.  I can't find it on Google!

biocide conditioning/acculturation/habituation. Naturacidal ambivalence.

I'm voting to close this question as off-topic because it is a language question, rather than a question about a problem in biology.

@David It's a question about terminology within ecology. I'd say that fits in Biology

Actually this is a question about the word used to describe a psychological response to a biological phenomenon.  I have to agree that this doesn't seem to belong here — maybe Psychology & Neuroscience? —— Please take the time to take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!


text:
What tool can I use to align multiple protein sequences to one reference sequence?
I have a protein of interest which is ~300 amino acids in length. I also have around 40 short sequences (all 9 amino acids in length); these are all very different from each other. I would like to perform multiple pairwise alignments to see if these sequences match up with (or have high sequence identity similarity) any areas in the protein of interest.
Since the short 9-a.a. sequences are very heterogeneous, they will have similarities in different regions of the protein of interest. I would like to know if it is possible to perform the alignments for all 40 sequences in one step, rather than using COBALT 40 times (and checking each of the short sequences against the reference sequence individually).
Please let me know if the description of my problem is not clear enough, I would appreciate any help in identifying a way to do this.

Hi and welcome to Bio.SE! It sounds like you are reinventing BLAST. I'd be careful about aligning those short regions. I don't see a problem with running 40 pairwise alignments if you can run the pairwise alignment programmatically.

Possible duplicate of Do all multiple sequence alignments employ global alignment algorithms?

This appears to be a bioinformatics question rather than one about biology. —— Please take the time to take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!

What you want to perform is commonly called a multiple sequence alignment.  As @Wayne_Yux said, the first step is to put all of your protein sequences in a single fasta file.  You can then use one of several online tools to apply different alignment algorithms to your protein sequence set.
A popular sequence alignment algorithm is Clustal, which progressively builds a multiple sequence alignment from all of the pairwise alignments.  genome.jp hosts a web-based alignment tool that allows you to choose from Clustal and other alignment types (1).  For alignment of many small sequences to a single larger sequence, you should use the "SLOW/ACCURATE" option (2).  After you upload your fasta (3) and execute multiple alignment (4), an aln file will be generated which you can download (5).

You can then take this aln file and upload it to a different tool that allows you to visualize alignments.  Personally, I like ESPript, which gives color-coded alignments in pdf or image formats.  Because you want to compare many sequences, it will probably be necessary to change the "Alignments output layout" parameters, e.g. change "Gap between blocks" to a smaller number to fit all of your sequences in one frame.

You can store the 40 sequences in a fasta file and then use blastp to align them all at once to your reference sequence.
After that, you can inspect the alignment hits and see wether they fit your quality expectations

In a multiple sequence alignment, the algorithms will attempt to align the sequences along their length (global alignment). What you need is a local alignment approach with a high penalty for base mismatch.
The E-INS-i algorithm in MAFFT might provide the desired functionality. Select the Advanced Settings and there:

Strategy -> E-INS-i algorithm
Align unrelated segments -> Leave gappy regions

Depending on how heterogeneous your sequences are, you might need to fine-tune other settings as well. Without the data, it is impossible to provide a more detailed guide.


text:
How is plasmin formed from plasminogen?
In Ganong's Review of medical physiology it is mentioned that plasminogen is converted to active plasmin when tissue type plaminogen activator hydrolyses the bond between Arg560 and Valine 561. Can anyone show the molecular mechanism ? What happens to the two different parts of the hydrolysed chain.

I'm a bit unclear what you mean by "molecular mechanism" - are you looking for the mechanism of the cleavage itself? The change in conformation that makes plasmin active while plasminogen is inactive? The general principles or those specific to this particular protein?

Tissue plasminogen activator is a serine protease consisting of approximately  530 amino acids and about 13% carbohydrate.
This enzyme is made up of five domains performing different functions. The finger domain and the two kringle domains are involved in the binding of t-PA to fibrin, whereas the epidermal growth factor domain is responsible for activating EGF receptor. Kringle 1 also help in transport of this molecule via liver's endothelial cells. Kringle 2 also helps in binding with inactive plasminogen. The serine protease domain cleaves the plasminogen at  Arg561-Val562  and activates it into plasmin.

(Image Source: https://www.researchgate.net/figure/Structure-and-functions-of-tissue-type-Plasminogen-Activator-tPA-A-Structure-of_fig1_284797342)
Plasminogen is the precursor for synthesis of protease plasmin. Plasminogen is converted to plasmin by cleaving Arg561 and Val562. The  activated plasmin is formed by making disulfide-linkage between these two polypeptide chains.
The heavy chain  is at the N-terminal and light chain is at C-terminal.  The activation takes place by removing the signal peptide and activation peptide  by autolytic cleavage. This activation peptide is released from the N-terminal  to convert Glu-plasmin to  Lys-Plasmin. The active site which plays role in binding with fibrin is situated on the light chain.

(Image Source:  https://www.sigmaaldrich.com/life-science/metabolomics/enzyme-explorer/analytical-enzymes/plasmin.html)
So, this proteolysis only produces one working peptide sequence, as the peptide bond cleaved and then amino acids are again joined by disulfide bond. And this peptide bond between arginine and valine is at 561/562 instead of 560/561 according to various sources.


text:
Why are HeLa tumors purple?
I remember hearing that the tumor where HeLa cells originated from was purple and jelly like, and I've seen pictures from studies with rats and HeLa tumors, and their tumors appear to also be purple. So what makes these tumors purple?

HeLa cells themselves are not pigmented, and usually appear translucent/gray under light microscopy. The growth medium may however be colored, and a common color is magenta.
The tumors themselves will appear purple, as most tumors do, due to the broken vascularization. Tumors commonly secrete growth factors leading to angiogenesis, but the resulting vessel networks are convoluted and not well organized, commonly full of anastomoses. The resulting poor vascularization leads to significant hypoxia, which results in a bluish coloring of the blood.

It would be nice if you could add some references to back up your answer.


text:
Can IPSPs produce an action potential?
This picture was taken from Purves' Neuroscience, chapter 5:

Image (C) shows a inhibitory postsynaptic potential whose reversal potential "goes"  to the action potential. If two or more IPSPs occur, will temporal summation cause an action potential?

What do you think, based on the other information in C?

@BryanKrause I would say yes, but this seems to contradict the "inhibitory". Also, why is this "homework"?

This is exactly how I would write a homework or exam question for a basic neuroscience course. We don't allow answers to those sorts of questions, because the whole point is to work through it yourself. There are 2 other lines besides the IPSP voltage trace drawn in panel C. What do they mean? Also, have you looked at panel D? What is it telling you?

@BryanKrause Well, it isn't homework... It's a question I come up when reading Purves. I see that Panel D say say if the reversal potential is below the threshold the postsynaptic potential, and according to Purves, this is inhibitory because the change in V will be "pushed" toward the reversal potential of the specific synapse (GABA in this case). But if many inhibitory occur by definition, why can't the temporal summation of IPSPs be enough to reach the threshold value to fire the AP? this sum I'm thinking of can occur by different receptors.

What is the meaning of the reversal potential for a given ion or type of channel?

@BryanKrause The reversal potential is the equilibrium point given by Nerst's equation that separates two opposite directions of flux for the ion, this is to say that if a ion has a outward/inward flux, in the reversal potential the flux is zero, and past the reversal potential becomes inward/outward flux. Is this correct?

Yep. So what happens if you open a chloride channel when the cell is resting near the reversal potential for chloride?

@BryanKrause I think the voltage will be pushed towards the chloride reversal potential, because the flux of chloride will itself move towards its equilibrium potential.

So can IPSPs sum past their reversal potential?

@BryanKrause I feel the answer you expect is "no", but I'm not sure if I can give an argument for it. Would an explanation like this be valid? - If two channels X and Y are open, but with reversal potential lower than the threshold voltage, the SP are added as long as they are below the reversal potential (same direction of flux), and are subtracted if they are past the reversal potential (because the ion flux has changed direction). So the general answer is no.

Don't think of IPSPs/EPSPs summing necessarily. Opening conductances pushes the membrane potential towards whatever their reversal potential is (weighted against all the other open conductances). For excitatory conductances, summation is an okay approximation only because the difference between rest and threshold is small compared to the difference between rest and the reversal potential for typical excitatory receptors. I'll reopen and possibly write my own answer because I feel like you've done enough thinking now, but it would be best to edit your further thoughts into the Q.


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From DNA data, is it easier to conclude that chimpanzees are our close relative, than it is to do a paternity testing?
Well, today I was contemplating on how to explain evolution, approaching with the dialectic method. When it came to why chimpanzees and us being so close in the tree of evolution isn't outright absurd, I formulated a witticism, "Well, today a glance at humans' and chimpanzees' DNA would confirm how much close we are. Compared to that, if you were to do a DNA paternity testing, you would have to do a bit more grunt work in that you would have to look for more nitty-gritty details that separate (and make similar) one human from another. So, ours and chimpanzees' closeness would actually be easier to conclude than to tell your parents apart from non-parents."
Well, was I correct? That this would be easier than that?

Hi Tony and welcome to Bio.SE! If I understand your question, you are asking "is a paternity test easier than a chimpanzee-human comparison"? This is true, but not for the reasons you suggest. Paternity testing uses minisatellite comparisons. This involves looking at specific regions of repeating regions where the number of repeats varies between individuals. Those tests are cheap. Comparing species, on the other hand, requires WGS (whole genome sequencing) which requires much more work and gear. These can cost more than 10 times as much as a DNA fingerprint test, depending on the species.

Please re-read the Tour for this site to find out why this question is a bad fit. It is not about a biological problem, but asking for subjective opinions about the comparative difficulty of two procedures. As far as subjective opinions go, I doubt that your students will find your “witticism” either witty or helpful.

@James's comment is an answer.

@David, I don't agree that this is a subjective question.  It's a question whose answer could be complicated, but the answer concerns how genetic data has to be processed and tested statistically for different purposes.  Both paternity testing and genetic comparisons of species have methods that have been discussed in numerous publications.  That is not to say that there is an easy, simple, or single answer--the relevant methods change over time--but that should not be the criterion for questions.  Other SE sites don't require that.

@Mars The question hits on a few topics and biological concepts all at once. My comment only addresses which experiment is easier to do today. A complete answer would have to be a bit more comprehensive.

The answer is complicated. In the early days of molecular phylogenetics, it was extremely difficult to demonstrate whether chimps or gorillas are our closest relatives. This is because the common ancestor of chimps and humans lived between 5 and 8 million years ago, and the common ancestor of gorillas and humans (and chimps) lived around the same time, just a little older. This means that there was a rapid split of three lineages, and it was difficult to disentangle them. As molecular phylogenetics advanced, we could generate larger datasets, and it because clear that chimps and humans were sister taxa. The smoking gun that demonstrated that chimps and gorillas were not one another's closest relatives was found when sequencing across the chromosome region in humans that corresponds to where two of our ape ancestors chromosomes merged. Orangutans, Chimps and Gorillas have 24 pairs of chromosomes, humans have 23. Sequencing across this region shows the exact splice site, which can be associated with the same regions on two chimp or gorilla chromosomes.
To answer your specific question, if you sequence any two genes between chimps and humans, you will find that the sequences are almost identical, with perhaps 1 in 100 nucleotides being different. If you sequenced a human and a gibbon for the same gene, you would find more differences. But finding that the sequences are similar is not the same as finding relationship, which requires sequencing multiple genes from multiple animals. For example, some genes between humans and rabbits would be extremely similar. So inference of relationships takes a lot of data from a lot of different animals. As for paternity testing, these practical tests are based on a different technology, targeting many DNA repeat regions or single nucleotide polymorphisms at specific sites that vary among human populations. But since the test is prescribed, and established, they are cheap, quick, and easy.


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Can a bacterium express a virulence gene and not produce toxins and what may be the cause of this?
I am preparing a seminar on viable but non-culturable (VBNC) state in bacteria, mainly foodborne pathogens and I just saw this line in a journal article by Lothigius et al that "the expression of the virulence gene in VBNC cells does not necessarily indicate the cells will produce toxins". Any explanation on what this statement means?
Lothigius, Å., Sjöling, Å., Svennerholm, A.-M., & Bölin, I. (2010). Survival and gene expression of enterotoxigenicEscherichia coliduring long-term incubation in sea water and freshwater. Journal of Applied Microbiology, 108(4), 1441–1449.

Where in the article do you find the quoted sentence? Or is it an interpretation of yours from the article as a whole?

To expand a bit on @Mohamed's answer, there are several mechanisms by which virulence gene products can be up- or down-regulated without changes to mRNA expression.
Post-translational modifications
Adenylate cyclase-hemolysin (AC-Hly) is a toxin produced by the Bordetella pertussis, the causal agent of whooping cough.  There are very few amino acid differences between the AC-Hly of B. pertussis and closely related Bordetella species.  Palmitoylations of lysine residues on the C-terminus of the B. pertussis AC-Hly are necessary for its specific cytotoxic activity.  [Bouchez 2017]
RNA secondary structures
After transcription, mRNAs can form secondary structures by base pairing, preventing ribosome binding and translation.  For some pathogens, virulence gene mRNAs forms these structures, which melt at human body temperature, allowing for fast production of toxins without the need to increase virulence gene transcription. [Narberhaus 2010]

Gene expression means making mRNA and then translated to protein. Their might be many steps unders regulation in this path where a gene makes mRNA but then that mRNA is not translated (like degraded or inactivated).


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Which birds are capable of flying both forward and backwards?
Very random question - but it's often said that the hummingbird is the only bird that can fly backwards (for example, https://www.worldatlas.com/articles/which-is-the-only-bird-that-can-fly-backward.html).
Is this true? Aren't there any other birds that can fly both forward and backwards? Is it some kind of bird category of its own?

Welcome to Biology.SE! We encourage you to do some research on your own and then, informed by what you have learned, ask any questions you might still have (ideally with references to reliable sources). For this question you should also carefully define what you mean by flying backwards (many birds flying into the wind can move backwards)! ——— Please also take the time to take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!


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How many water molecules will be produced starting from acetyl-CoA in citric acid cycle
I am puzzeled by the answer. Acetyl-CoA when enter citric acid cycle, it produces 3NADH, 1FADH2, total 4 reducing equivalents. If each one makes 1H2O, then 1acetyl-CoA should make 4H2O. Why some textbooks make it 2H2O. In addition, almost like all (or many) do not balance oxygen; they say entering 16O2 and making 16H2O, so how?
Thank you.

Acetyl-CoA has three carbon-hydrogen and one carbon-carbon bond, and it is electrons 'held' in these bonds that are available for biological oxidation.  Thus we say that acetyl-CoA contributes four reducing equivalents. In the TCA cycle, these are transiently passed to NAD+ (to give NADH) and to FAD (to give FADH2): the cofactors may be considered intermediate electron carriers.
It takes 4 electrons (2 reducing equivalents) to make 2 water molecules from 1 O2 (or 4 electrons to reduce 1 oxygen 'atom' to 1 water molecule), but this takes place in the cytochrome oxidase reaction of the respiratory redox chain (with reduced cytochrome C as electron donor), not in the TCA cycle.
It is important to realize that water contributes no reducing equivalents to cellular respiration, and that hydration reactions are neither oxidation or reductions. For water to contribute reducing equivalents, it would have to be 'split', as it is in photosynthesis.
In addition, oxygen is not consumed or produced in the TCA cycle.
The assertion that water can pass electrons to NAD+ in the TCA cycle is an infamous 'textbook error', notably advocated by Efraim Racker in A New Look at Mechanisms of Bioenergetics, and my opinion on this (for what it is worth) is given in this SE answer.
For the role of water in the TCA cycle and the controversies surrounding it, I would recommend the letters by (i) D.E. Atkinson and (ii) Herreros & Garcia-Sancho on TCA cycle confusion published in TIBS and kindly made available by David.  (These references are not indexed by Pubmed and are apparently not available from the TIBS website)

Many thanks user1136. When you say:(or 4 electrons to reduce 1 oxygen 'atom' to 1 water molecule), do you mean 4 electrons or 2 electrons. My main concern is the number of electrons. In Lehninger, the  chapter for oxidative phosphorylation and the figure for path of electrons in complex IV (cytochrome c oxidase), he draw 4 electrons coming from cytochrome c and then to make 1 H2O. I think it is an error. 4 electrons means 2H2O not one (because we breath O2 not single oxygen atom).


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DNA described somewhere?
This is not purely biological question but how do the companies making DNA analysis know what your DNA means? Is there some database describing human DNA?
I watched some documents about DNA, gene editing... and people in the documents were often working with some infographical like documents which described some chromosome or desease (I don't know what exactly that was, I am an amateur trying to make sense of it) but I was not able to find anything as they had on the internet.

They don't know what your "DNA means", but there's data about the function of particular genes and the effect of some mutations in these genes. "Describing human DNA" is hard to interpret, I think; the full sequence of human genome has been sequenced since 2003, but the "meaning", the full implications of the sequences is still a matter of research. The Human Proteome Project is one initiative headed in this direction of study.

It might be useful to look at how 23andme works, to see how this analysis product is generated, in general:

The 23andMe genotyping platform detects single nucleotide polymorphisms (SNPs). A SNP is a DNA location, or "marker," in the genome that has been shown to vary among people in terms of the DNA base or bases. There are four DNA bases: adenine (A), thymine (T), guanine (G), and cytosine (C). So, for example, at the same genomic location, you might have a C and someone else might have a T. These DNA base differences are known as "variants."

These SNPs can differ by population types. Some subsets of a population type might suffer a disease and appear to have SNPs that others do not. So-called GWAS studies (discussed below) work at associating SNP distributions with diseases or other phenotypic traits.
You send some spit to 23andme, they tell you who you are likely related to and what diseases or other physical attributes you may have, based on patterns of these SNPs.
23andme uses Illumina chips for figuring out what genotypic variants you have in the spit sample you send to them. Illumina is a company that manufactures "chips" that react to the presence or absence of markers in the DNA sample you send to 23andme. Each chip in this platform calls different sets of markers.
These markers often have identifiers associated with them, each called an rsID.

The rsID number is a unique label ("rs" followed by a number) used by researchers and databases to identify a specific SNP (Single Nucleotide Polymorphism). It stands for Reference SNP cluster ID and is the naming convention used for most SNPs.

They also map variants that do not use rsIDs, and instead use some other internal identifier.
Whatever the identifier, GWAS — Genome-Wide Association Studies — are research projects that analyze populations of people in different ethnicities or other cohorts, looking for over- or under-presence of various markers, compared with the larger human population.
For instance, here is such a GWAS study that is used by 23andme to indicate risk factors for Parkinson's disease, in sample donors who have these variants. There are other such studies for schizophrenia, for autoimmune diseases, and so on.
The power of these studies to make a positive, correct association depends on various factors, but the product 23andme sells is ultimately a packaged summary of a lot of work by researchers around the world.

Great read and links, thank you. :)

This question is both easy and hard to answer: DNA and its (known) functions have been described in scientific literature, textbooks and databases for the last few decades, but because this is a enormous amount of data there is no single source or collection that could comprehensively catalog all this information.
Information on genomes and genes has been collected into (somewhat) standardised databases hosted by NCBI or ENSEMBL, however those will probably not be helpful to anyone without established background knowledge. Indepth information about specific genes, procedures or diseases is usually just linked in these databases and comes from actual research papers.
If you want to understand more about DNA genetics and so on the best approach is to start with the basics and take a look at a textbook or online course, if you then have specific questions you can still come back here and ask those.

Thanks, I glanced over NCBI before and as you say, I was quite lost. ENSEMBL looks more useful to me. I wish some compilation of all those research data will eventually be created, it would be incredible to have possibility as an ordinary person to see what part of DNA (at least from the known parts) is responsible for which manifestation of human body. Anyway definitely gonna dive deep on this one. :D


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Gaba and Magnesium
I read read that magnesium divalent ion binds to gaba receptors and induces the same effects as if gaba has binded. Does anyone know what happens to the gaba that would have been synthesised and otherwise bind to the gaba receptor if the magnesium divalent ion wasn't there. E.g is the gaba broken down, does it wait till the magnesium unbinds from the gaba receptor and then attaches itself to the gaba receptor?

Please give a reference/link/full citation of what “you read”. That way we can identify possible misunderstanding you may have of what you have read, which is suggested your writing “if the magnesium divalent ion wasn’t there, and renders the question unclear, at least to me.

Welcome to Biology.SE! We encourage you to do some research on your own and then, informed by what you have learned, ask any questions you might still have (ideally with references to reliable sources). ——— Please also take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!


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Biological & Evolutionary Reasons for Palm (Bi)Symmetry

The fingers of the human palm exhibit a (bi)symmetrical pattern with regards to their size, in the sense that the thumb and the pinky are almost the same size, and the same holds for the index and ring finger. I was wondering what the biological imperatives and/or evolutionary advantages behind this physical characteristic are.

The only rationale I personally am able to come up with is that this particular arrangement might be optimal or ideal for grasping, handling, and manipulating objects, but am unsure of its truthfulness, and, even if correct, I would still be interested in exploring other possible avenues.

Possible duplicate of What is the evolutionary cause for various finger lengths?

The thumb is NOT the same size as the pinky.  You are perhaps looking only at the first two bones of the thumb.  Look at all three bones, and you will find that it is longer: probably longer than any of the other digits.  (At least it is on my hands.)

@jamesqf: All fingers, not just the thumb, extend into the palm of the hand.


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Are there animal species where some females have greater amounts of male-associated qualities than average males?
In the human species, some women ( a meaningful, though not large percentage) are taller and stronger than the average man.
Is a similar thing true in the animal kingdom? Are there some meaningful percentage of hens that would make better fighters than the average (game) cock? Cows that would be better at pulling plows than the average bull? Lionesses that could beat the average lion in a stand-up fight?
The point of the question is are there overlapping "bell curves" of size, strength, etc. so that "strong" females, while a clear minority, are nothing freakish. Or is it true in most (mammal) species that male strength is "off the charts" compared to female strength, except for "freaks."

What's a meaningful percentage, and how do you expect us to have these percentages? What makes you think that humans are the only species to have members of a sex that can outperform the other sex? Variation between individuals is often, perhaps usually, larger than the difference between the sex average on quite a lot of measures. Height and weight are two such cases, I think.

@SPr: The point of the question is are there overlapping "bell curves" of size, strengths, etc. so that "strong" females, while a clear minority, are nothing freakish. Or is it true in most (mammal) species that male strength is "off the charts" compared to female strength, except for "freaks."

There exists a very impressive variety of cases for either extreme case. This of course includes species where females are dominant, without exception. So you see, the variation in biodiversity covers both cases considerably. This is why attaching a single number can be misleading. Let's take the case of some hymenopterans, like bees and ants. Compare the queen to the size of a worker ant. Entire colonies of dozens of thousands of ants live and die by a single queen. These are the most abundant animals on earth by biomass and by individual number. What gives?

Outside of mammals larger females is actually fairly common, the most extreme version I can thing of is angler fish, where the females are dozens of times larger than the males.

Spotted hyenas are a matriarchal society and female hyenas are larger than males. Also, female hyenas dominate males.

they also have pseudopenis. so they are really pushing the look more masculine than males thing.


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Mithradates - Developing immunity to poison?

According to legend, Mithridates studiously researched and examined all known toxins and experimented with potential remedies by using prisoners as his guinea pigs. Supposedly, Mithridates’ toils paid off because numerous ancient authors, including Pliny the Elder, claimed that he created and regularly ingested a universal antidote for all identified toxins, and it became known as mithridate (mithridatium).

It was said that he was pretty much ingesting small amounts of poison to develop an immunity to it.
Whether universal poison or ingesting each type one by one, is this possible to build up your body to resist or be immune to poison/venom/toxins in general?

Hi mph85 and welcome to Bio.SE. I hate to be boring, but the answer is that it will depend on the specific compound. Perhaps you could narrow down the question to a specific poison?

May I remember you that Mithridates' body actually got tremendously marred from such treatment, (according to the same sources you have quoted).

Welcome to SE. Edit: The answer is in two parts based on the mechanism of action of the toxin. Courtesy: @David and @jamesqf
Immunity
The white blood cells in the body are responsible for recognizing self or non-self peptides and form the adaptive compartment of the immune system. The B lymphocytes have a receptor that can bind to various peptides. Upon recognition of foreign peptides in the body, they go through a reaction (somatic hypermutation) to become further specific to the foreign peptide. They also differentiate into Plasma cells which can now secret another protein (antibodies) which neutralizes the foreign peptide.
Small amounts, which are non-lethal, but in enough concentration to drive the B cell reaction creates an immunological "memory". This memory allows a faster response to the same peptide compared to the reaction. This in order allows the body to withstand a higher concentration of toxic peptide, which otherwise would have been lethal as its being neutralized.
Vaccines work on a principle very close to this.
Homeostasis
Every toxin interacts which some biological process and drives it out of balance. The body actively tries to restore the balance by some means.
For example, if a ligand is depleted the body can increase the number of receptors to counter the effect and vice versa.
By ingesting small amounts of toxins body can adjust the equilibrium by very small amount at a time adjusting the concentration of relevant ligands or receptors.
Again, the person who has been through this process can withstand a higher dosage of the toxin compared to a person who hasn't.

At least two problems with this answer: size of antigen and mode of presentation. Also, answers are answers to questions, not to people. This question is about immunity to poisons such as cyanide, arsenic, alpha-amanatin. Do you have any evidence that these can provoke an immune response?

@David I agree that it is dependent on the size of the antigen and mode of presentation to a certain extent. The last line in the description asks for a general possibility and I have only included details which I thought are relevant for the answer. OP also doesn't mention Cyanide, Arsenic, alpha-Amanatin specifically or any other particular category or toxins.

@Cheesebread: Or things to which you can become habituated, as for instance opiate addicts who can tolerate doses that would kill a naive user.  I've also read that one can develop a tolerance to arsenic (and perhaps other things) by taking gradually-increasing doses, to such an extent that suddenly stopping the dose will cause death.

@jamesqf — me too. Wasn't Rasputin supposed to have done that in relation to arsenic? But the point, then, is that this is nothing to do with lymphocyte-based immunity, so a good answer needs to consider the different situations.


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How to model species interactions on population size dynamic?
Here are two classical discrete time models of population size dynamic. The exponential growth model
$$N_{t+1} = r\cdot N_t \qquad\qquad(1)$$
and the logistic growth model
$$N_{t+1} = r\cdot N_t \left(1 - \frac{N_t}{K}\right) \qquad\qquad(2)$$
, where $r$ is the growth rate, $N_t$ is the population size at time $t$ and $K$ is the carrying capacity.
I am wondering how are species interaction generally modelled into this framework. Let's consider three interacting species called "a", "b" and "c" with populations sizes at time $t$, $Na_t$, $Nb_t$, $Nc_t$, respecitively. The effect of these three species on the focal species are $\alpha_a$, $\alpha_b$ and $\alpha_c$.
How do we typically compute, for both a logistic and an exponential discrete time model, the recursive equation of the focal species' population size?
For the exponential model, is it
$$N_{t+1} = r\cdot N_t \cdot (Na_t \alpha_a + Nb_t \alpha_b + Nc_t \alpha_c) \qquad\qquad(3)$$
or
$$N_{t+1} = r\cdot N_t + Na_t \alpha_a + Nb_t \alpha_b + Nc_t \alpha_c \qquad\qquad(4)$$
or something else? And for the logistic model, is it
$$N_{t+1} = r\cdot N_t \left(1 - \frac{N_t}{K}\right) \cdot (Na_t \alpha_a + Nb_t \alpha_b + Nc_t \alpha_c) \qquad\qquad(5)$$
or
$$N_{t+1} = r\cdot N_t \left(1 - \frac{N_t \cdot (Na_t \alpha_a + Nb_t \alpha_b + Nc_t \alpha_c)}{K}\right) \qquad\qquad(6)$$
or something else?
It is possible that we typically define more parameters that just the $\alpha$ values I define above to describe a species interaction even in the simplest models. Ideally, I would love an answer that draws from a source (a textbook in theoretical ecology, a peer-reviewed article or whatever).

You can write these equations in the form of ODEs but it is not really essential.
This is my analysis (just the model formulation and not literature):
The effects of interactor species may or may not be dependent on the population of the species that is being analysed (recipient). Now you have to model based on how you would realistically expect the interactions to have an effect on a species. A simple assumption would be that the interaction improves or reduces fitness (growth rate), additively. So you can model the effects as:
$$N_{t+1} = (r_0 + \beta_a + \beta_b + \beta_c) N_t$$
where $\beta_x$ denotes the effect of species $x$ which in turn you can model as dependent ($N_tN_{x_t}\alpha_x$) or independent ($N_{x_t}\alpha_x$) of the recipient population. Now, you can also impose a condition that the growth rate cannot increase beyond a certain value and so you can model it as a saturating function. A logistic or a Michaelis-Menten like function would work. For e.g:
$$\begin{align} r &= \frac{r'}{K+r'}\\[1em]
 r' &= r_0 +  \beta_a + \beta_b + \beta_c\end{align}$$
You can likewise adapt model using the logistic equation.

What you are looking for can easily found in any undergrad text on ecology and it goes by the name (competitive) Lotka-Volterra Equations. This is a system Ordinary Differential Equations and in my opinion, can easily be converted to recursive or difference equations. Your guess with logistic growth is fairly close to these equations. You can remove the term corresponding to intra-specific competition $\alpha_{ii}$ from those equations and you get the exponential model.
Please let me know if you'd like me to elaborate on my answer.
Lotka-Volterra Equations
Competitive Lotka-Volterra Equations
The book I know (Ecology: From Individuals to Ecosystems) has the 2 species interaction model.


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How does coffee cause calcium loss in our body?
Recently on radio a doctor advices to reduce the consumption of coffee as it leads to calcium loss(as my mother described). My initial response was: How could such thing be possible? What kind of experiment have been done to assure that the coffee is the cause and not something else? But then I found this article on internet, though it doesn't go into depth of the topic. So I'm wondering :

How does coffee cause calcium loss?
What is the related chemical reaction?
Does it just happen in intestine or elsewhere in the body?
What amount of coffee consumption would make it severe?

Caffeine and coffee do not seem to have any significant adverse effect on calcium metabolism. The supposed mechanisms are inhibition of calcium absorption in the intestine and stimulation of calcium excretion in the kidneys.
Effects of caffeine on bone and the calcium economy (Food and Chemical Toxicology, Journal, 2002):

Caffeine-containing beverage consumption has been reported to be
  associated with reduced bone mass and increased fracture risk in some,
  but not most, observational studies. Human physiological studies and
  controlled balance studies show a clear but only a very small
  depressant effect of caffeine itself on intestinal calcium absorption,
  and no effect on total 24-h urinary calcium excretion. The
  epidemiologic studies showing a negative effect may be explained in
  part by an inverse relationship between consumption of milk and
  caffeine-containing beverages. Low calcium intake is clearly linked
  to skeletal fragility, and it is likely that a high caffeine intake is
  often a marker for a low calcium intake. The negative effect of
  caffeine on calcium absorption is small enough to be fully offset by
  as little as 1-2 tablespoons of milk. All of the observations
  implicating caffeine-containing beverages as a risk factor for
  osteoporosis have been made in populations consuming substantially
  less than optimal calcium intakes. There is no evidence that
  caffeine has any harmful effect on bone status or on the calcium
  economy in individuals who ingest the currently recommended daily
  allowances of calcium.

The Association between Coffee Consumption and Bone Status in Young Adult Males according to Calcium Intake Level (Clinical Nutrition Research, 2016):

This study analyzed and compared the BMD [bone mineral density] and
  bone metabolism markers according to coffee intake in Korean young
  adult men aged 19-26 years. No significant associations were found
  between current coffee consumption level in Korean young men, and bone
  status and metabolism according to the calcium intake levels.


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Which lipoprotein has the highest protein content?
I know that HDLs have the highest protein/lipid ratio but know that the HDLs are very small molecules too and I couldn’t find the exact answer for this question. I mean, by amounts which of these lipoproteins have the most protein?

Please do not use the title of a question in lieu of the question itself. You need to carefully define numerically your concept of “highest protein content” and explain how it differs from protein/lipid ratio. At the moment it is completely unclear, at least to me.

LDL has the higher protein content than HDL. LDL consists of Apo B48 and Apo B100. These are proteins with higher molecular weights between 250 kDa to 550 kDa as compared to other apoproteins. And these apoproteins are not present in HDL.
And if lipoprotein (a) is included in comparison then it has highest protein content.
(Via:  https://lipidmaps.org/resources/lipidweb/index.php?page=lipids/simple/lipoprot/index.htm)