text:
How many sensory neurons are in the human body?
While I understand that there is a wide disparity of precision when it comes to specifying what constitutes "sensory neurons/receptors", I'm trying to find an authoritative source to provide at least a rough order of magnitude estimate on the number of receptors in the human peripheral nervous system (including skin, tongue, eyes, ears; but also mechanoreceptors and proprioceptors as well). The only sources I have found so far (here and here) only provide hints at the answer. I have found estimates as high as 15 billion, and as low as 3,000,000, but none of these guesses cite authoritative sources.
As I'm sure you can tell, I am not a student of anatomy (my interests lie in cognitive science and artificial neural networks), so forgive me if my question is too imprecise.  But to put it simplistically: what I want to know is, roughly how many externally-produced sensory signals (channels) does the human brain have the capacity to process? Again, I am not looking for a precise answer, but I'm hoping to at least reduce the uncertainty to less than four orders of magnitude.

CONTEXT: My purpose in this investigation is to try to quantify the magnitude of the computational capability of the brain with regard to processing external signals. If one were to imagine an "artificial nervous system" (as distinct from an artificial neural network), how many input sensors would it be able to simultaneously process if it were on par with a human brain?

UPDATE: I recognize from the comments the inherent ambiguity of my question, so let me attempt to clarify. Assuming that the number of incoming signals to the brain at any one time is limited by the number of neural connections between the brain stem and the spinal column*, can someone provide an indication of what that number might be.
* (if that assumption is overly simplistic, feel free to enlighten me)

nerve endings are often used to denote free nerve endings that convey pain sensations. Are you after how many receptors there are, as in photoreceptors, mechanoreceptors, olfactory receptors etc etc? Do you want internal sensations too (balance, proprioceptors etc etc)? You might want to define specifically what you are after (which senses, which cells etc.)

@Christiaan - From your description, "Receptors" is what I am really after. I will edit my post accordingly. Thank you.

The problem here is that,  eg, the number of photoreceptors in the retina exceeds by far the number of retinal ganglion cells that make up the optic nerve. Your concluding sentence, therefore, is unfortunate,  as it combines sensors and the brain. It's just quite complicated. If you are after sensors and sensors only, or otherwise,  please specify.

I'm afraid,  actually, that the order of variance you found may be quite acceptable, given the hazy definitions set.

And the 3M is an underestimate I guess. It's likely higher than that, given there are as much as 1M ganglion cells in each retina alone.

@Christiaan - thank you for pushing me to clarify my question. I have attempted to do so yet again in my post. I understand that the physiological complexity of this system might prevent any clear-cut answers. But for the purpose of this question, I'm not interested in how many cells there may be at the extremities of the nervous system, but specifically how many signals can be delivered to the brain at any one moment. If "receptors" is a reasonable proxy to that question, great. But, as I suggest in my UPDATE, perhaps "number of neurons in the spinal column" might be more appropriate.

Not all senses go through the spinal cord - most notably the auditory, visual and gustatory senses all head straight to the brain stem or even the brain. Again, it's not all that simple :) +1 for your continuing effort in improving this challenging yet relevant question.

@Christiaan - again, I really appreciate your help. I think the problem is my ignorance regarding the appropriate terminology. Would it be possible to continue this discussion in chat?

Let us continue this discussion in chat.

I'm voting to close this question because the original question is poorly scoped, but the edits that the original poster made to save the question changed entirely the meaning of the question.

(note: I would strongly recommend OP repost with the new question, if OP is still around)

This is a really interesting question.  However, I'm going to try to address the context and update sections of your post rather then attempt to quantify all afferent signals in the nervous system.  This is because quantifying those signals would be an exceedingly difficult task.  It's not only logistically difficult to measure on an individual level, but to say anything definitive regarding the entire species would be superfluous.  The number of signals at any one time is constantly in flux, as not every sensory receptor generates an action potential at the same time.  Even in instances where similar or "competing" receptor types are simultaneously stimulated, those transmissions will be modulated and/or pathways suppressed.  A good example can be found in this editorial article[1] on pain, where inducing painful stimuli can alleviate an itch sensation.  I reference this to illustrate that sensory signals are not entering the brain unchecked. In the most simple of terms, they are heavily regulated.
Based on the context on your question, it seems what you really want to know is what is the maximum threshold.  In an artificial nervous system, how many signals could we pump into it before it becomes inefficient or overwhelmed?  However, what makes the nervous system unique is that it's a living system that adapts to stimuli.  When there's more signals then it can handle or process, it regulates them.  You can read more about the process and its importance in this article on sensory gating[2].  For this reason, a healthy brain that isn't being artificially stimulated shouldn't become overwhelmed.  In fact, this process makes it far more efficient then any super computer.  A fun example of this was the six chess games between Kasporov and Deep Blue in 1996.  Think of the sheer number of moves Deep Blue could calculate compared to Kasporov: hundreds of millions of moves per second.  It lost that match.  Computational capability isn't conditional on the number of inputs the system can receive, it's how that information is processed, utilized, and applied once it's in the system.
I know I didn't answer your question in regards to a hard number, but hopefully it helped give a different perspective.  Please let me know if you'd like anything further clarified.
[1]: Focus on pain.  Nature Neuroscience 17, 145 (2014). doi.org/10.1038/nn.3644
[2]: Sensory gating, inhibition control and gamma oscillations in the human somatosensory cortex.  Scientific Reports 6, Article number: 20437 (2016). doi.org/10.1038/srep20437

Estimates of the number of sensory cells range from a low in the first decade of millions to as many as double digit billions. The number of neurons going to the brain is not an indicator of how many signals are in the body. Think of it like one would the internet. Billions of people are connected, but they all go to nodes from individual devices to local data centers, to a relatively few major cables to which everyone is connected.
The way this happens on the web is that every individual user has an IP address, and even though the signals pass through cables that carry millions of messages only those directed to that IP address will be received on that device.
This all happens on a digital basis, but the human neural system is analog, which gives a much broader range of possible addresses and data combined than can pass in a digital signal. So what you are asking is far more complex than your question. You need a thorough understanding of analog information transfer as well as the digital domain from which I believe you are operating.

I like how your answer is set up; however, please do add some references.

The difference in your analogy is that digital trunks can handle millions of simultaneous messages, because each message contains its own "mailing address", so to speak (in the packet header). That analogy breaks down in the neural system because there, every message must have a dedicated point-to-point channel to travel on. (I.e., the nervous system contains no routers.)

I disagree on some level with both Richard and @kmote and agree on some level... On one hand, axonal communication isn't truly analog, it's more of a hybrid between digital and analog, with binary signals. There are of course some analog sensory responses, but these are eventually converted to a (mostly) binary signal. And while there are no "routers" there can be information in spike patterns, both spatial and temporal, such that the number of unique messages to be conveyed is not equal to the number of fibers, just like a network cable.

I agree with @BryanKrause. Also, this analogy with computer network can be very misleading.


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Being able to write/type different texts using each hand respectively, at the same time?
Has there been any documentation of being able to either write down (jot down) or type in (key in) different texts using the left hand and the right hand respectively, simultaneously?
So, I'm interested in whether or not it has been documented that certain individuals can do this, and I would be greatly interested in any literature on the subject. For example, have there been any pedagogics who have argued this exercise would be beneficial for the development of individuals?
Note: Of course, many people could do this, if they would do it extremely slowly; so obviously I am interested in the maximum velocity.
See also: Being able to read one text in braille using sense of touch and, at the same time, read another text visually?

If so I'd also be curious to know if said texts were arbitrary, since some, or perhaps even many, people could probably learn to type a very specific sequence quickly with a lot of practice. Also curious to know about keystroke timings, I imagine the ability to type two texts completely independently is very different than, say, alternating keystrokes. Former is much more multitasking, latter is coordination. For instance, one who can type on a regular keyboard effectively with either hand could imagine both hands were on the same keyboard and type arbitrary msgs, but that's not impressive.

US President James Garfield is the first person who pops into my mind. I believe Leonardo da Vinci also could, but I might be wrong...

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Do animals get "unhealthily" fat in the wild?
Looking at a picture of a seriously fat cat, apparently directly nurtured by humans, popping up in a language learning app, I started wondering:
do animals "in the wild" (this might be ambiguous, but you can discuss it in your answer) get obese? If so: which animals and how fat? Under what conditions do they get fat?
To be more specific (following the advice of user theforestecologist):
Do they become unhealthily obese (i.e. so fat that it negatively impacts their survival)?

Yes. Hibernating mammals store fat for the winter so that they don't have to feed all winter long. Other animals eat more fatty foods to build up their own insulating fat in order to survive colder weather.

Perhaps, though, you mean to ask "do animals become unhealthily obese?" (i.e., so fat that it negatively impacts their survival). ??

@theforestecologist I have followed your advice in the OP now, thanks.

http://sciencenordic.com/can-wild-animals-become-overweight

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Why don't my ears pop in the morning going through a tunnel?
I drive through a tunnel (morning and evening) on my normal work commute. In the evenings, my ears will pop going through this tunnel, but they do not pop in the mornings. There are actually 2 separate tunnels for the northbound and southbound traffic, but they are right next to each other, with the same elevation changes.
What is the difference as to why the ears only pop in 1 direction?
Here's a short video of tunnel

Presumably the elevation change is in opposite directions.


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What do we mean when we say that a muscle fiber contracts strongly?
Sounds dumb but anyway, i heard that superfast fibers contract more strongly than fast twitch fibers. And i never thought of muscle contraction as something that has a magnitude (i thought of it as "1 or 0" meaning either contracted or not). So lets say we have two fibers, the same length and thickness, if one contracts more than the other does that simply mean that it becomes shorter ?

i'm no expert but try looking up animations on youtube of muscle contraction that may help, here is one https://www.youtube.com/watch?v=GneonFlcZG8


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What is the difference between an active and inactive T helper cell?
1- Are all inactive T helper cells "T memory cells" ?
2- Is there anything such as active T memory cells ?
3- I have noticed that there is also a third type of T helper cells but i dont know what it is called. They are used in the beginning of the humoral response process (they bind to initial APC cells and then divide producing active t helper cells and inactive t memory cells). How are these different from the active and inactive T helper cells ?


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Why does an increased heart rate mean increased blood pressure?
Say a person starts exercising. If their cardiac volume remains the same but their heart rate increases so that the overall result is an increase in cardiac output, will their blood pressure increase during the exercise ? If it does, why ?

I take my blood pressure frequently during the day and find little or no correlation between BP and pulse rate.

I wonder if the heart is effectively what an engineer would call a "positive displacement pump."

In good approximation, the arterial blood pressure PA depends with
PA = PV + R x dv/dt,
on central venous pressure PV, total peripheral resistance R (also referred to as TPR or PVR) and cardiac output dv/dt (aka CO) – the usually cited equation MAP = CO * PVR is an over-simplification. Since cardiac output is defined with
dv/dt = RH * VS
as a result of heart rate (RH) and stroke volume (VS) the blood pressure should increase if heart rate increases.
However, in reality, the conditions are more complex. In exercise body temperature increases, which leads (via the thermoregulatory system) to vasodilation, so that the total peripheral resistance R decreases, which is able to reduce the blood pressure again.
Decreasing PV in exercise should occur on a very slow time-scale and only be relevant in long-time endurance training.
Concentrations of some hormones change in exercise. Levels of some stress hormones (catecholamines) rise and therefore increase cardiac output, but their action on peripheral resistance is heterogeneous. It goes up, if alpha receptors are stimulated, but decreases after stimulation of beta receptors. Similar to (and partly mediated by) beta adrenergic action classic thyroid hormones (e.g. T4, T3 and 3,5-T2) increase heart rate but decrease total peripheral resistance. It depends on the type of exercise if thyroid hormones rise or drop. They are increased in short-term or endurance exercise (representing type 2 allostasis) but decrease in exhausting exercise (leading to type 1 allostasis).
In summary, it depends on many factors, if blood pressure increases during exercise. In ergometry the blood pressure usually slightly rises.
References
1: GREENE BA. Cardiac output and total peripheral resistance in anesthesiology;
clinical applications. J Am Med Assoc. 1958 Mar 1;166(9):1003-10. PMID
13502096. https://www.ncbi.nlm.nih.gov/pubmed/13502096 https://doi.org/10.1001/jama.1958.02990090011003
2: Mayet J, Hughes A. Cardiac and vascular pathophysiology in hypertension.
Heart. 2003 Sep;89(9):1104-9. PMID 12923045. https://www.ncbi.nlm.nih.gov/pubmed/12923045/ https://doi.org/10.1136/heart.89.9.1104
3: Silva AS, Zanesco A. Physical exercise, β-adrenergic receptors, and vascular response. Jornal Vascular Brasileiro. 2010 9(2). https://doi.org/10.1590/S1677-54492010000200007
4: Chatzitomaris A, Hoermann R, Midgley JE, Hering S, Urban A, Dietrich B, Abood
A, Klein HH, Dietrich JW. Thyroid Allostasis-Adaptive Responses of Thyrotropic
Feedback Control to Conditions of Strain, Stress, and Developmental Programming.
Front Endocrinol (Lausanne). 2017 Jul 20;8:163. doi: 10.3389/fendo.2017.00163.. PMID 28775711. https://www.ncbi.nlm.nih.gov/pubmed/28775711 https://doi.org/10.3389/fendo.2017.00163

Let me give a answer that is more intuitive, without considering other factors. Blood is pumped by your heart to arteries then to capillaries then to veins then back to heart. It is easy to transfer fluids through big tubes like arteries, but is is hard to "squeeze" fluid through capillaries since there is a lot of resistance.
So when the heart pump once, the heart move some blood from vein to artery then stop. The pumped blood are all stored in the arteries because they can't get through the capillaries immediately which make your arteries enlarge and the pressure in arteries get higher and you get the systolic blood pressure. At the same time, the pressure in vein become lower since some blood is pumped away. As the blood stored in the arteries getting drained through capillaries to veins, the pressure in the arteries get lower and lower----until your heart pump again. This is why your blood pressure will be higher if your heart pump more frequently---if the heart rate is slower, the blood pressure in the arteries will drop to a lower value before the heart pump for the next time.
The heart need to pump blood again and again to keep the blood pressure in arteries higher than veins, it is this blood pressure difference that squeeze blood from arteries through capillaries to veins. The higher the difference, the faster blood get transferred from arteries to veins which bring oxygen etc faster to everywhere in your body to satisfy the need during exercise.

Welcome to Biology.SE! Can you cite some references to support your answer? It is always good to provide references so that one can check them for a more thorough information. Good references include peer-reviewed research/review articles, books and some reputed scientific/education websites. Wikipedia is also fine as long as it in turn cites original references.

@WYSIWYG Sorry, indeed this is my theory, only based on observation of my self and basic physics. Even so, I'm confident that it is right in principle. I think intuitive answer may help more people in a higher efficiency way.

By cardiac volume I assume your talking about Stroke Volume, that is, the volume of blood pumped from the left ventricle per beat.

Blood pressure will probably increase.
Stroke Volume depends on contractility, duration of contraction, preload (end-diastolic volume) and afterload.
Exercise usually increases the preload (due to an increased venous return caused by muscle contractions) and contractility (due to sympathetic effects).
So, to maintain a constant Stroke Volume, and cancel out the preload and contractility increments, you need to either:

reduce the duration of contraction (by raising the heart rate beyond 120bpm/ 140bpm, for instance) or
increase the Afterload (by increasing the Total Peripheral Resistance, for instance).

Since blood pressure is positively affected by both cardiac output and Total Peripheral Resistance, unless the Heart Rate gets really high, blood pressure should increase.

The question is about relationship between heart rate and blood pressure. The answer should be talking more about effect of heart rate, instead of stroke volume

@Anonymous did you actually read my answer?

Yes, I read your full answer and that's why I commented on it.

This portion of the text in Robbins Pathology will answer the question;

Blood pressure is a function of cardiac output and peripheral vascular resistance, both of which are influenced by multiple genetic and environmental factors.
Cardiac output is a function of stroke volume and heartrate. The most important determinant of stroke volumeis the filling pressure, which is regulated throughsodium homeostasis and its effect on blood volume.Heart rate and myocardial contractility (a second factoraffecting stroke volume) are both regulated by the α-and β-adrenergic systems (in addition to their effects onvascular tone).

Therefore, increasing the heart rate will lead to an increase in the mean arterial blood pressure.

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Does a generator potential pass along a nerve the same way an action potential does?
I have read that a generator potential is a localized depolarization of a membrane. Does that mean that it does not pass along a neuron the same way an action potential does ? If not, then how do generator potentials from multiple rods in our eyes add up (converge) and trigger an action potential in a sensory neurone ?

Generator potentials (GP) are meant to generate action potentials (AP). An action potential results, whenever the level of depolarisation at a particular place crosses a threshold. This "place" is usually the beginning of an axon of a typical receptor, since it is equipped with all the channels required to begin and propagate an action potential. The purpose of the receptor architecture, then, is to make the threshold go off in a naturally meaningful situation.
There are two possible ways this is done. Say the neuron is transmitting information about the location of a stimulus. Then the "naturally meaningful threshold" would be some spatial cutoff, a minimum area that needs to be stimulated for the action potential to go off. Then, the receptor would have several GP-producing dendrites spread out, each generator potential being summed at the meeting place of the dendrites, which happens to be the cell body and the beginning place of the axon. So the individual generator potential in each dendrite will contribute to the sum, which will be summated and the cellular decision-making process (or a crude example of it) be affected as this summation.
Another way is temporal summation, something which has, for example only one GP-producing dendrite and the axon. Then, for the summated potential at the cell body to cross the threshold, the stimulus must stay, or be summated across, for some time-cutoff. GPs have some decay time, before which if another GP reaches there, it adds up. This would be meaningful in things like the presence or absence of a touch, the cutoff preventing against minor fluctuations.
This said, the situation in the eye in much much more complex. There are several layers of neurons and each neuron performs a lot of different functions and has a specialised architecture for it. The Rods and Cones actually produce hyperpolarizations and not depolarisations (theoretically, both are propagated in the same way, but hyperpolarisations themselves do not initiate AP).
To complicate further, most receptor systems alter the frequency of AP and thus have some basal frequency, this modulation also being important for encoding the message.
An image of GP:

Some of this answer is good but it has major problems. Photoreceptors do not fire action potentials, for example. It is also misleading to talk about "10 layers" of the retina in terms of how many "layers of neurons" there are. There are only 3 in the chain: photoreceptors, bipolar cells, and retinal ganglion cells. Amacrine and horizontal cells also modulate the activity in other cells, but they are not part of the serial transmission chain to the brain.

@BryanKrause I never said that they do. I did mention the modulation of frequency at the end of the paragraph as a general complication in several receptor systems. I did mention the 10 layers to only show the complexity, hence the caveat 10 layers of 'retina' and not neurons. Edited in the answer.

It seemed difficult to explain the retinal neural mechanism in a simple way. Hence, the preceding part is a general way in which GP work. Do let me know if anything needs correction.

I would suggest adding that action potentials are transmitted actively (trough activation of sodium and potassium channels), but localized potentials are transmitted passively with a time and space constant (cable theory).


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Is it hydrogen atoms or electrons that are passed along an electron transport chain?
I am so confused because my book says it is electrons which are passed along the electron transport chain but all we are considering is hydrogen ions (H+) and hydride ions (H-). Can someone clear that up for me ?

ELECTRON transport chain. Hard to answer the other parts without more context from the book/class...

@Zhe  never mind it is electrons in the form of hydride ions. I found out from chem.libretexts.org

As explained on the Wikipedia page of the electron transport chain:

An electron transport chain (ETC) is a series of complexes that transfer electrons from electron donors to electron acceptors via redox (both reduction and oxidation occurring simultaneously) reactions, and couples this electron transfer with the transfer of protons (H+ ions) across a membrane.

Electron are thus transfered from the electron donor (NADH, H$^+$ produced by the TCA) to the electron acceptor (O$_2$) through the successive enzymatic complexes of the electron transport chain.
Complexes I, III and IV are proton (H$^+$) pumps: they use the energy gained thank to the electron transport in order to translocate protons across the membrane.


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References concerning the relative population sizes of predator and prey
In an ecosystem, say there are two species in a predator-prey relationship. What is the most typical ratio of these species' population densities? For instance, it could be that for every fox, there are ten rabbits. Actually, the precise ratios are somewhat irrelevant; mostly I would like to know if we can say that the number of prey is generally larger than the number of predators.
I would like references to articles, textbooks, etc. that contain information about such ratios.
Note that this is aimed at the number of species within a single ecosystem. However, if this information is hard to quantify (perhaps because it is hard to define where an ecosystem ends), global populations could be used as an estimate.
Forgive me if this is ill-defined or trivial, I'm a physicist by training.
Thanks.

A way to reword your question is Typically, how many individuals are there at each trophic level?. Keywords, you should be looking for are "food chain", "trophic level", "trophic dynamic", "cascade effect" and "trophic pyramid".

@Remi.b Ah, that makes sense, thanks! Do I even need a reference to say that there are more individuals at lower levels? Isn't it necessarily so, considering that not all the energy (some is lost) from one level can be transferred to the level above it?

@Remi.b Hmm, but then what if the ecosystem is not very clearly trophically stacked/separated (so it is more appropriately called a food web)?

No ecosystems are. But I would have thought your question as necessarily implying this simplified categorization. The model you present is an even more extreme simplification of the reality of food webs after all. Don't get me wrong, I think the question is of interest (I up voted it). You don't need reference or anything for your post to be valid. I was just trying to offer you some vocabulary that may help you (or other users) to look for such estimates.

@Remi.b Sorry, I should have been more clear: I didn't mean that I needed the reference in order to ask my question, here on the site, but rather for the thesis I'm writing (I'm working with population dynamics), where I claim that prey are usually more abundant in number than the species preying on them. After your comment it seemed self-evident that this was the case, so I was wondering whether a reference was even needed in my thesis.

It is kinda obvious that higher trophic levels have fewer individuals than lower trophic levels but the actual ratio is not obvious of course. It is always good to cite though, esp. for a thesis where there is likely no upper bound on the number of citations.

@Remi.b Right, I agree. If you have any suggestions for useful articles, please do let me know. I will try searching a bit using the key words you suggested. Thanks again!

For your curiosity, the post What prevents predator overpopulation? is loosely related.

You are indeed correct that the prey of predators are usually more common than their predators, especially if you focus on "true" predation (i.e. remove parasitism and parasitoidism). As a rule of thumb, the energy conversion between trophic stages is 10% (first proposed in Lindeman, 1942), which sets one sort of bound on the density relationship between predators and prey. The relationship is extremely variable though, which is easily understood if you consider the density relationships of hares and foxes vs. whales and krill.
For a general reference, Hatton et al (2015, "The predator-prey power law: Biomass scaling across terrestrial and aquatic biomes") might work, even though it is mainly framed in terms of biomass. However, the paper clearly states that biomass and density usually go hand in hand. The main result of the paper is that the biomass relationships between predators and prey collapse to very regular power laws (exponent 3/4) across ecosystems.
As mentioned above, and depending on who you ask, parasitism and parasitoidism are sometimes seen as types of predation. There, the density relationships between "predator" (parasitoid) and "prey" can be very different, especially at certain points in time or at certain lifestages. For instance, in insects it is not uncommon for one "prey" (host) to give rise to a large number of newly hatched "predators". This means that the number of parasitoids can probably outnumber the number of hosts, at least at smaller spatial scales, at some time periods (e.g. late summer, before the parasitoid is hit by high winter mortality).

Thank you for the answer! Another example of predator outnumbering the prey would be phages vs. bacteria.

@Lovsovs Definitely! If you go small and use a liberal definition of predator this is indeed common.

mostly I would like to know if we can say that the number of prey is
  generally larger than the number of predators.

If this is actually your real question, the answer is straightforward: the most widely-used classification of trophic strategies that I'm aware of (Lafferty & Kuris 2002; full reference below) includes the requirement that a predator attacks (first dichotomy) and kills (second dichotomy) multiple victims in its lifetime. So your statement is necessarily true; if each predator kills more than one prey, prey must (generally) outnumber predators.
Be aware that this ignores micropredators, parasitoids, parasites etc, though.
Reference: Lafferty, K.D., and A.M. Kuris. 2002. Trophic strategies, animal diversity and body size.  TREE 17(11): 507-513.


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Maximum parsimony tree - Am I right, or is the correction model right?
Alright. Monday we have a test, and now I was making a practise test.
We have to make a maximum parsimony tree. We must do that monday again, so I want to know if I am thinking wrong, or if the answer model is incorrect.
The sequences are:
Seq     1    2    3    4    5    6    7
1       A    T    A    A    G    C    C
2       T    C    A    C    C    T    G
3       A    T    C    C    G    A    C
4       T    G    C    A    C    T    G

This results in:
          1    2    3    4
----------------------------
   1  |
   2  |   6
   3  |   3    6
   4  |   6    3    6

And eventually, this results in:
          1,3     2,4
-----------------------------
1,3  |
2,4  |    6

This is the tree in the correction model:

My tree has two 1,5's instead of the two 3's at the root of the tree. Because 6 is the last distance. 6/2 = 3, so both branches should get a distance of 3. But, according to some examples I saw on the internet, it's a distance of 3 to the end of tree then, and not 3 to the next node. And there is already a distance of 1,5 in further benches at both sides, so only 1,5 remains (because 3 - 1.5 = 1.5).
So, am I wrong, or is the correction model wrong? Then I know how I must do it at the real test.
Sorry if my English is bad, and it's a little hard to explain because English is not my native language, but if I am right, you should know what I mean.

From your description, this is a distance-based clustering tree (UPGMA), not a parsimony tree. And in this case I believe you are correct, since if you sum up all branches from 1 to 2 or 3 to 4 (1.5 x 4) you will have the original pairwise distances. (The same for 1-3, and 2-4, which are easier.)


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Ion-exchange vs Gel Permeation Chromatography for proteins
For extracting Lysozyme from egg white which method would you recommend and please help me understand why.
Lysozyme has a higher isoelectric
point (pH 10.5) and a lower molecular mass (14 307 Da) than most proteins so both these methods make quite a bit sense. Use Sephahdax G100 for gel permeation chromatography and CM-Sephadex G25 ion exchanger for ion exchange.
From what I can understand, Gel Permeation will separate the egg white based on Mr of the various proteins and compounds. There is quite a bit of variation in the Mr of egg white proteins but lysozyme, in fact, doesn't have the lowest Mr as Cystatin and Ovomucoid have lower Mr. Furthermore, GPC requires around at least a 10% difference in molecular weight for a reasonable resolution of peaks to occur. The range of Mr is also quite broad in this method. Will this be disadvantageous perhaps? So GPC does have the plus side of it having a well-defined separation time due to the fact that there is a final elution volume for all unretained analytes.
Now Ion exchange chromatography is very specific in the nature of how the exchanger interacts with the mixture being separated. Lysozyme has a PI of 10.7 which is much higher than the rest of the proteins in the egg white. As with GPC we use 0.05M Tris-EDTA, pH 8.2, containing 0.05M NaCl as the standard. Can this setup result in Gibbs Donan effect or chromato- focusing ?
I'm currently leaning towards GPC as the option to yield the purist product especially seeing as it can be desalted afterwards with G25.
Please help guide me in the right direction. I'm quite new to this but am ready and very willing and keen to learn and expand my abilites.

Note that GPC does not just separate proteins by Mr but by a combination of shape and Mr (though shape will be less important for you since most small proteins are quite globular)

Thank you very much for this interesting piece of information. I will keep this in mind for a sample containing perhaps a mixture of globular and membrane proteins.

I know this is an old question, but I would question why you don't just purify the lysozyme by crystallization from crude extract followed by polishing with IEC and SEC...

Here is source on how to crystallize directly from egg white. http://www.jbc.org/content/164/1/1.full.pdf&ved=2ahUKEwjehu-86aHjAhWrM-wKHc-5ChIQFjACegQIBBAB&usg=AOvVaw3ZNa3B5FmbhPGFiTZMpTdj

Since lysozyme is so well studied, your best bet is to search the literature and see what methods other people use. See this paper, for example. They report that lysozyme can be affinity purified on Sephadex, but they also reference other methods in the introduction that you could take a look at.
Both of the methods you described sound reasonable. The only way to know which is best is to try them and see. In fact, the best approach, depending on your application, would likely be to use both methods for optimal purity. Even when I affinity purity a protein, I will still often perform ion-exchange as a polishing step.

Here is what I have come up with. Thank you for all your help.
Ion Exchange Chromatography(IEC) will yield the purist product from a single application. The main reason is due to the fact that Gel Permeation Chromatography is compromised by the close proximity of Lysozyme (14.3 KDa) and Cystatin (12.0 KDA) in their molecular mass. Sephadax G100 separates a large range of molecular mass but the downside of large range is low sensitivity at such close proximity. It won’t be able to discriminate between these two proteins during the elution. Due to Cystatin only compromising 0.05% of the sample it will be even more difficult to pick up this contamination even though it is not large. Furthermore, Sephadax G100 will retain Lysozyme for very long as it is one of the smallest in the sample. Hence, a large amount will be retained and a diluted sample will be produced. It should also be taken into account that GPC has a low resolution, low capacity and does not permit high flow rates. GPC is the fastest and most simple method to produce a cruder sample in comparison to IEC. IEC in this case uses CM-Sephadex G25 which means no Lysozyme will be lost due to particle size properties and Mr allowing it to get caught in the matrix as opposed to GPC. This results in a more concentrated sample. If we compare the pI of all the proteins, Lysozyme (10.7) and Avidin (10.0) both are the only cations at initial pH 8.2 . This means lysozyme can easily be removed as pH is continuously decreased through the use of the cationic exchanger without denaturing it or any sample being lost. GPC is only useful as an additional step to IEC using G25 to further purify the sample through desalting and dialysis.

Your answer is much better than mine.


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How to selectively filter BLAST results for an endogenous retroviral LTR to retrieve members of the same ERV family?
I'm running a local BLAST search on a HERV-K(HML2) LTR sequence in the human genome. I get thousands of hits.
I want to retrieve the hits that correspond to other HERV-K(HML2) LTR sequences only.
What alignment length/identity filters should I use on the hits to select LTRs of the same family? Insertions and deletions could easily alter the alignment lengths meaning the cutoff length for the filter I want isn't clear. I can work out what alignment length cutoffs remove what percentage of the results to identify big drops at specific cutoffs, but it hasn't been very helpful.

I don't know what your application is, but RepBase has a curated set of ERV loci in a BED file that you can use to retrieve sequence/define regions of interest et cetera.
Of course, generally speaking repetitive regions may be harder to map in terms of genomic location, and in my lab, where we regularly study ERVs in cancer, we usually map RNAseq data to Repbase sequences in a fasta file to derive total expression estimates on a per-family basis.

I don't think there is a definite answer to this problem, but here are a few things that might help you, apart from a simple length filter for the hits:

Filter for regions: since LTRs are repeats you might get multiple BLAST results from the same repeat region/locus (especially if your input sequence is smaller than said region). You probably want to keep only one hit per region
Check for a conserved (sub)sequence: hopefully your specific LTR sequence has a 'core' that needs to be present, so that it can be considered part of your familiy. You only want to keep BLAST hits that have an absolute match for this 'core'.


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RNA-Seq library construction challenges: the biases of RNA fragmentation vs cDNA fragmentation
I recently watched a presentation on RNA-seq that covered some of the choices one can make along the way, and I didn't fully understand one of the choices in particular.  Near the beginning of the process, you can choose a fragmentation method (e.g. RNA: nebulization, hydrolysis; cDNA: sonication, Dnase I treatment). Each fragmentation method is biased in its own way, and the goals of the study may influence the choice of method.
I didn't fully understand the reasons for the characteristic biases (how do they happen?), and when to choose one method versus the other (which methods work best for which goals?).  Put another way, what are the mechanistic explanations for the characteristic biases that result from each method, and what is the significance as far as downstream processing and associated challenges?
Edit:
The heart of this question is about fully understanding the particular choice of when and how to fragment.  The reason I have not accepted an answer, yet, is that the answers provided so far address the mechanism part of the question, but not the ultimate reasons for choosing one versus the other.

The biases depend on fragmentation methods. DNA is usually fragmented physical shearing. (nebulization/sonication). The overrepresentation is because of the ends being more stable (easy to break a stick from the middle). There are other kinds of fragmentation methods (thermal-catalytic) and there the biases are different (modern kits claim that they have very less bias)

Bias can happen at other levels too- reverse transcription, priming, amplification etc

Good question, a lot of this is still being figured out. Here's what's known so far:
Fragmentation methods based on restriction enzymes aren't random.
Reverse-transcription performed with poly dT-oligomers, which bind to the 3' poly-A tails, is strongly biased towards 3’ end of transcripts.
Reverse-transcription with random hexamers results in an under-representation of 3’ ends. This is from the reduced number of priming positions at which the reverse transcriptase enzyme can start cDNA synthesis.

messenger RNA has a poli A tail at its 5´ end. thus when the poly-dT hybridize the mRNA in the reverse transcription the cDNA will carry this poly-dT at its 3`end. Thus, as reverse transcription will always start at the 3´ and of the mRNA its is more likely that this region is better rev. transcribed. Bigger the mRNA is bigger will be this concern.
About the bias related to RNA fragmentation I don't know, I can make the guess that both ends are more lost due to the fragmentation itself
watch this video from life technologies
http://www.youtube.com/watch?v=0MJIbrS4fbQ


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Can animals absorb atmospheric sulfur?
This is a follow up to this previous question:
In biosynthesis of cysteine and methionine, where does the sulfur come from?
Can animals use gaesous H2S in the atmosphere, say for instance from a sulfur rich hot springs, to aquire sulfur?

No, they can not do this. We don't have the enzymes to metabolize H2S, besides that, it is highly toxic. H2S can be used by some bacteria and archea (so called lithotrophic bacteria), but they are relatively rare.
Sulfur is reduced by plants, which take it up in the form of sulfates and subsequently reduce it to form different sulphur compounds. Animals are dependent on the uptake of sulphur from plant sources, as the sulphur containing amino acids are essential (meaning the cannot be synthesized by themself). The pathway is relatively complex. The image below is from the Wikipedia article on Sulphur assimilation, which I can also recommend, if you want to know all the details.

Geat reference, thanks so much. But one comment, I read somwhere that gaseous H2S in the atmosphere was highly correlated with reduced blood pressure.


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How does tearing work?
I found the question about tear gas very interesting. Shigeta says there that crying helps the cells of the eye to wash themselves clear of the toxic components in the tear gas.

Does non-emotional tearing always work this way? Is tearing not caused by cells in the tear duct working as receptors? If not, why we have tear duct (the first in-eye part of it)?
What is the cause of tear-production associated with crying during strong emotions? Is it due to hormones or nerve activation?

I slightly reworded your question for clarity. Please feel free to roll back.

Tear cleaning can be experienced when dust blows in your eyes.
Your eyes water at that time.

The regulation of tear production (lacrimation) involves reflexes initiated by sensory neurons in the cornea. Corneal pain receptors (nociceptors) and mechanoreceptors detect damaging stimuli and induce tearing to cleanse the ocular surface (and, hence, Shigeta is right as tear gas stimulates pain receptors). Corneal neurons sensitive to drying of the ocular surface also appear to increase tearing. These neurons also respond to cooling and hyperosmotic stimuli (Kurose & Meng, 2013). The tear duct is necessary to drain the tears away from the eye into the nasal cavity (Fig. 1).

Fig. 1. Tear glands and tear ducts. Source: Mayo Foundation for Medical Education and Research.
Strong emotional responses like crying can result in an overflow of tears (epiphora). Epiphora is mediated by the limbic system (the emotional center of the brain), especially the hypothalamus. Such strong parasympathetic stimulation is accompanied by other symptoms, like reddening of the face and convulsive breathing (University of Minnesota, Duluth).
Reference
- Kurose & Meng, J Neurophysiol (2013); 109(10): 2517-22


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Why do most fish move fins orthogonally with their axis of symmetry?
So recently I read the question why are most fishes vertical (in the sense of distribution of their body mass) and it got me thinking what is the reason behind the direction they move their fins. My explanation is that they need to catch the image they several times to truly percieve it, so the eyes have to be orthogonal on the direction they move their fins. Am I correct, therefore they swim like this  rather than this
 because there is more to see on the horizontal dimension in shallow waters?

Can't see a difference in the two pics?

@AliceD The waves illustrate the direction of gravity

The upper fish looks normal, the fish bellow swims breaststroke

I think it's much more a consequence of the way their muscles are arranged.  Dolphins & whales work perfectly well by moving their flukes vertically.

@jamesqf Dolphins...haven't thought about them :) Anyway - is there some kind of evolutionary pattern in the way their muscles are arranged?

@Probably: I really don't know enough about the evolution to do more than guess, but if I had to, I'd guess that somewhere along the line the ancestors of mammals somehow evolved in such a way that it was easier to bend up and down rather than side to side - think of walking movement, then swimming with fins.  Thus when dolphin ancestors started back to the sea, their natural movement was up & down, and that evolved in the direction of improved up & down...

@jamesqf Oh, you might have got it! Dolphins and whales have to breath and this might be the fastest way to get up / there could be predators

@Probably: Not quite what I meant.  Think of Tiktaalik http://tiktaalik.uchicago.edu/meetTik2.html crawling out of the water and scrabbling around on its fins.  Carry on through amphibians & reptiles, and you see legs awkwardly splayed out to the sides, with a lot of side-to-side movement (carried to the extreme in snakes).  But somewhere along the line to becoming mammals, creatures got their legs directly underneath them, which allowed more efficient locomotion - think of a horse or dog running.  Now mammals have this new body plan...

...and those which go back to the sea have to start evolving better swimming from what they now have, and wound up waving their tails up & down rather than back & forth.  But as I said, this is just me guessing...

@jamesqf Oh, that's even more cool than I thought, thanks


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Are there any studies detailing the overall "-omics" effects of using bleach to synchronise a C. elegans population?
I wasn’t able to find papers detailing the changes in the transcriptome/proteome of C. elegans when synchronised by bleaching vs not-bleaching. Hopefully someone can point me in the right direction!


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Why do sea mammals die on land, and drown on sea?
It's quite confusing to me, why do sea mammals die on land, but also die from drowning if they couldn't reach the sea surface to breath?
Excuse my ignorance but I am really confused!

Did you try finding an answer? (Hint: Respiratory organ of terrestrial vs aquatic mammals?) Questions about elementary biological concepts are considered off-topic if those do not show prior research on Bio Stack Exchange. See this policy to learn more.

@Tytoalba I did search before asking, but google keeps showing results of mass sea mammals deaths.. try yourself and see :)

About why they die on land, this question has an answer here.

Mammals use lungs as their respiratory system. These animals in the process of evolution left land and started to live in the water, they developed organs that are used to swim. The shape of body also changed to reduce the resistance of water. In spite of all this they didn't developed gills.
Lungs can help in respiration only in air. So the mammals have to come above water in order to take air. You correctly have noticed that these animals die if they can't reach air, i.e. they die of drowning.
But one thing I want to mention is that they don't need to reach land in order to take breath. They just need to swim up to the surface of water for this purpose.
Anyway, I think you got the point. Feel free to ask if you have further confusion on this topic. I shall explain more if needed.

Welcome to Biology.SE! Please add some references to your answer.

Thank you so much for guiding me. I shall surely add some references.


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Plant identification in UK
I need some help identifying this plant please. It is summer flowering in the UK. Its height is approximately 30cm, flowers approximately 2cm across.

I'm drawing a blank. Any chance of showing us the leaves? Is it a wild flower? Could it be a garden escape?

Unfortunately I have no better images which show the leaves Alan, however I think I may have managed to identify it after much searching. I do believe it is a variety of Viscaria oculata. I sincerely appreciate you going to the trouble of responding and trying to help though, thanks very much!

This plant has been identified as Viscaria oculata.


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I really need some help with a plant identification
I am trying to identify this flower. It was spotted in an Australian Botanic Gardens. I have been advised that the plant was approx 1.8m high and the flowers approx 2cm wide. Any help greatly appreciated.


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Tropical Plant Identification
After searching extensively I have been unable to find a name for this plant. It was found growing in the Eden Project Tropical biome in the UK. The flowers were approximately 7-8 cm across.
Any help greatly appreciated!

Beautiful photo. I'm looking forward to an answer.

Leaf shape often helps identifying plants. Do you remember how the leaves looked like, or do you have photos where they appear?

They seem to closely resemble the shape of the "Golden Chalice Vine" (Solandara Maxima). Although they are a more yellow color and their leaves fold outward rather than inward, it is entirely possible that the flowers you found were still in the process of fully blooming.
I also found a it growing in the Eden Project Biome you mentioned, here is the link to the plant page on their website: http://www.edenproject.com/learn/for-everyone/plant-profiles/golden-chalice-vine
And for some more pictures and information: https://toptropicals.com/catalog/uid/SOLANDRA_GRANDIFLORA.htm
Hope this is the plant!

The Solandra you show doesn't seem to have the thick part on the "leaves" (wich are technically petals and / or sepals) we see on the photo taken by the OP.

Hi Bli, unfortunately I do not have a photo of the leaves. It was a spur of the moment shot due to its location (being on the side of some busy stairs). On future trips I must remember to photograph leaves as well as the flowers of those plant I am not familiar with. Although I can see a similarity with the Solandra maxima that Johnny linked me to, I do agree with you in that the thick bands of green on the petals to seem to be absent in any photos I can find of it online. Thanks very much for taking the time to help me identify this, much appreciated.

Hi Johnny, thanks so much for going to the trouble that you have in helping me identify this plant. I certainly think we are on the right track with Solandra though as I remember the flowers were somewhat smaller than those described in any online site and the thick green bands I witnessed on the photo I posted also seem to be absent. Can I ask whereabouts in the dome you saw it growing? I found this one on the right side of the stairs going down from the viewing platform. If I was still in that part of the country I would go back to get more detail - leaves, growth habit etc. Thanks again!

Sorry, what I meant to say was that I found on the Eden Project Website :P. Apologies. I agree that the flowers are larger than what you described seeing, which is why I thought it might not have been fully formed yet, but I'm no botanist so I can't say much about it, but glad I could help!

After continuing to search I have located the name of this plant. It is Ipomoea alba or 'Tropical white morning glory'.
On locating the area of the Biome on a map where I had found it, I could conclude it grew in tropical and sub-tropical areas of South America and north of there. This narrowed down the search somewhat.
Thanks again to all involved for helping to identify!

Apparently similar to "moon vine" an ipomoea of the US that opens in the evening.


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Bumble bees and wasps
Location:India
My father was telling me yesterday that wasps were building a nest over an abandoned store room in our backyard...But he noticed that the wasps were attacked by a bunch of bumblebees...And the two were locked up in a duel.Several wasps were also found dead on the land...
Today he told me that the nest had almost diminished and several bumblebees were surrounding it...which seemed like they were destroying it
My question is:
Why would bumblebees destroy the wasp nest?
I guessed that they would build their own nest instead (after a few days perhaps) but there were plenty of other places in the yard too like there is big mango tree... it's only a guess and I am too curious to know any biological cause.


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Why doesn't oligodendrocyte produce neurilemma
I was searching literature related to neurilemma and oligodendrocyte and came across these lines from WP (Neurilemma)

Oligodendrocytes do not have neurilemma because excess cytoplasm is directed centrally toward the oligodendrocyte cell body.

I tried tracing more scholarly articles in this  context but I wasn't satisfied.
So my question is: Why doesn't oligodendrocyte produce neurilemma. Any  reference articles would also help.

This statement is made in contrasting oligodendrocytes with Schwann cells. Both of these cell types are glial cells involved in myelination of neurons, but their morphology (shape) is different.
Oligodendrocytes in the CNS "reach out" with extended processes that then envelope axons as a myelin sheath. You could imagine an octopus reaching out arms that then loop around a stick. Like an octopus, they have multiple arms, and each arm can cover a different axon. The nucleus and other cellular machinery is located in the 'head' of the octopus.
Schwann cells in the PNS instead wrap around a single axon. You can think of them more like a fried egg, wrapped around a stick. The egg white is the myelination, the yolk is the nucleus. The outermost wrap is where all the other machinery of the cell is, and this area is called the neurilemma.
The actual presence/absence of the neurilemma isn't that important for the function of myelination, it's just a different shape of the cells.

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


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Why does this tree have a round hole?
One of my soccer students was hiding behind a tree when he discovered this hole. I've tried Googling it but I couldn't find out why this tree has a hole.

It looks like somebody just pulled out the outer layer of bark. I don't think there's anything special about it.

I agree. There was some sort of cut or other injury to the outer layers of the tree (bark and some of the living tissue just underneath it), and when the bark grew back it was not in concert with the rest of the bark, and formed a different pattern.


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What fish is this?
I was out snorkeling at Biscayne Bay in Miami, Florida in the shallow waters near the shore when I saw this fish.

What fish is this?
I see it has black spots at the bottom and five white lines along its posterior fin.

I think this is probably a checkered puffer Sphoeroides testudineus based on your location and picture, with the wave-reflection patterning on the dorsal surface and ventral speckling the most obvious features.

(image from https://biogeodb.stri.si.edu/caribbean/en/thefishes/species/4403 )
Could be a different Sphoeroides, but I looked through other species found off Florida and none had similar patterning.

Would you please let the community know how did you find that?

@JossieCalderon I recognized it as a puffer fish from being familiar with puffer fishes more generally, but had no idea of the genus or species. At that point I went to geography, and got a list of puffer fish found off Florida. I started with this one since it seemed most common (showed up first and often in search), then looked at others found in Florida and tried to rule them out. Some of those are found on this page, too: https://biogeodb.stri.si.edu/caribbean/en/gallery/gspecie/4403

Wonderful. It does resemble a pufferfish. Thank you!


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What kind of object is this?
I'm unsure whether to call it a fruit or a vegetable. I found it on the road in a neighborhood and decided to pick it up before a car squashed it. (Thus, my initial guess was a squash.)

Should be a Papaya, thus a fruit, an outline of your geographical location would be helpful to determine it.


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What bacteria results in a Gram +ve cocci and catalase +ve? What test comes next?
Results so far.
We are trying to determine unknown microorganisms in intro to microbiology course. I first did gram stain and they were all cocci morphology, purple color and clumped together  (actually I'm not so sure if clumped is right word, but they definitely were not in chains and I didn't see any isolated coccus, so if that's qualifies as clumped then they were clumped.
So I have a gram+ here.
Next I did catalase test and got bubbles on slide; I put thick chunk of the unknown on slide and dropped 2-3 drops of ${H}_{2}{O}_2$; instant bubbling.
Next test.
So now I will test for coagulase but I'm uncertain what a positive or negative result will tell me about he organism and whether this is the terminal test (for ID-ing organism I mean)
My notes say that positive for coagulase indicates S. aureus.
But does that mean that it is unnecessary to do the Mannitol test at that point then? Or is Mannitol used as a confirmation test?
Further, if unknown tests negative for coagulase, my notes say that if its also novobiocin sensitive (pos) then it is S. epidermidis.
But my same question then is, is it necessary to still do the mannitol test?

Hi there and welcome to Bio.SE! I've made some edits to make the question fit the site format better (a specific title, a more attractive format etc). Feel free to roll back, or make a further edit. I like the spirit of the question and hope to see more like this on the site generally!

At this point you have staph, you can use this flow chart (from here) to figure out what staph exactly.
If the test comes back as coagulase positive be very careful as Staph aureus is pathogenic.


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What is the theoretical maximum height of a herbaceous plant stem?
Foreword: I'm posting this here instead of, say, Worldbuilding, because while it is based in a speculative concept, this is a question purely of biology as we know it instead of speculative biology under non-real conditions. I would address that later and elsewhere. And sorry if this is actually more physics than biology, I have trouble pinning these things down.
I'm trying to determine what the maximum height of a non-woody plant stem can be (i.e. I don't want the tallest flowers). I think the primary issue at hand is load-bearing and resistance to bending. So I found this 1997 paper by Schulgasser and Witzum that sort of discusses what I'm looking for. It suggests that the plant's ability to resist shear forces is a matter of how bundles of fiber are arranged inside the stem and of the plant's internal pressure, which affects how much weight it can stably bear. But I'm no biologist, so the paper is difficult to penetrate. I'm sure there are other issues limiting the height of non-woody plants, like the maximum height above the ground that capillary pressure can raise water. Considering all factors, what is the theoretical maximum height of a herbaceous plant?
I've found this question, which concerns the tallest real herbaceous plant, while my question concerns the theoretical. But I would like to extend that question - are there any examples of fossil herbaceous plants that are larger than the modern banana plant, and do they run up against the theoretical maximum?

Unfortunately I think, despite your forward, unless you are interested in existing plants this feels a bit to speculative. Maybe you could reformulate and break up your question, e.g., ask what maximum observed root pressures are.

@BryanKrause Well, there is a difference between speculation and calculation based on established knowledge. The 1997 paper has several useful equations - I simply don't know how to use them.

I don't disagree about the relevance of calculations; I think the issue is that your question is putting together a lot of separate calculations and putting them all into a "maximum." For capillary transport of liquids, for example, a factor that is really important is the diameter of the tube. Well, one might be able to make a very small tube and go a long distance, but this introduces other issues, maybe not enough nutrient delivery to support a large enough stem for that height. Can you try to break your question down into the problems you are having with the equations in the paper?

I believe I see your point - that all the potential limits one could calculate based on various factors would be difficult to unify. Well, the larger issue is that I don't know enough about plant physiology to know what things I don't know. The paper is only one side of things. I'll try posing this question on Worldbuilding if it proves unworkable here, but I felt the chance of encountering a plant physiologist who could answer the question was a lot higher on Biology.

I'll let others decide definitively whether your question is indeed off-topic, but I think you could also reformulate a question to try to capture the things you don't know, without requiring speculation. Perhaps a question about "besides capillary limits and shear forces on stem fibers, what key factors limit plant height?" Not being a botanist myself, maybe that question is still too broad, but I think it's more in the right direction for this site. Hope that's helpful.

I think it is a legitimate question, how tall can a herbaceous (non woody) plant grow.  I am not sure what is the theoretical limit is,  but the tallest species of banana tree (Musa Ingens) is 15m tall. And the tallest bamboo species  Dendrocalamus giganteus is 25-35m tall.

A bit related: How do-trees lift water higher than 10 meters

Do you consider palms and bamboo as herbaceous, non-woody plants? They are normally not seen as woody plants since they don't produce wood in the strict sense. This makes a big difference to answers to your question.

Looks like some Cyatheaceae (Pteridophyta) can reach up to 20 meters high.

Update: I have edited the answer for a better structure and for providing reliable references.
Some of the factors that influence growth, while keeping in mind that every species has particular needs:
•   light, temperature
•   insufficient light leads to etiolation
•   water
•   amount of water and dry substances, page 185
•   water influences diameter
•   soil
•   wind
•   macronutrients
•   citokinin
•   genotype
•   heterosis
•   inbreeding
•   pinching the stem stops its growth and promotes lateral stems (I understand that you don't want to, but I list it here so that you can watch out accidents - involuntary pinching has the same effect)
•   root type
•   shelter near a fence or a wall
You might find some info as to what to consider in your calculations in this paper, although it's about trees.
Just for the purpose of knowledge, herbaceous vines like Ipomoea are also stems and they can grow longer than vertical ones. There may be more to add, but I'm only a Horticulture student, not a plant physiologist.
I strongly recommend to ask plant related questions on Gardening and Landscaping SE, a small community, but a very enthusiastic one. Also, hardly can someone become a good gardener without knowing at least the basics of plant biology and psysiology, so you have a major chance there of receiving answers in a few hours, not days.
Good luck with your project and I hope you'll return to tell us your conclusions. We will be happy to see you interdisciplinary approach.

Please add some references to your answer.

Ok, but it's going to take some time searching for them in English, as I have aquired this knowledge from various subjects and courses in almost four years in university and the references were in another language.

Its all right if it takes time. The point is that you must have a citation for your claim in an answer.


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How long will a typical bacterial strain keep in a -80°C freezer?
I know that a -80°C freezer is the recommended means of long-term cell-line storage, and that cells will typically not last long in a -20°C freezer.  But how long will a typical bacterial strain (e.g., E. coli DH5-alpha) actually stay good in a -80?
Searching around via Google, I'm finding a wide range of answers, anywhere from only 3 months to indefinitely, so I'd like to try to get a better grounded way of estimating longevity.

For what is worth, our 6 year old agrobacterial strains in -70 freezer seem to grow just fine. However, I am not sure I would notice if some percentage of cells died, since we don't take precise amount of the mixture when taking a bit for growing.

Exactly: I'm finding lots of anecdotal data points, like this, which makes me very uneasy about predictability of lab operations.

How predictable do you need your storage to be? There are many things that can happen in several years time. Freezer can fail without people noticing until morning. Someone can forget bacteria outside after using them. If my strains die I can make new ones with the same plasmid. For important stuff, there are backups.

Right now, I'm just trying to find out what the baseline is with a standard -80 and typical operations in order to understand the level of worry that I should be starting from.

To be frank, there probably isn't one answer. It will likely depend on the organism and possibly the specific strain you're preserving, how they were cultured, the concentration and type of cryoprotectants used, and the starting concentration of viable cells, among other possible factors. In any case, the decline in viability is likely to progress slowly enough at -80C that you'll notice before total loss of viability, as long as you're using a sound practices.

If you're truly worried about it, in terms of continuity of operations, I'd suggest a regular schedule for replenishing or replacing freezer stocks, either by sub-culturing and generating new ones, or simply ordering new stocks (assuming you're working with commercially available strains).

There are viral strains preserved from 50+ years ago. RNA is generally more sensitive to temperature.

I'm a bit too busy to write a detailed answer, which for bacteria actually seems necessary as they seem to have more variability than viruses in terms of cryopreservation, but see https://academic.oup.com/femsre/article/29/5/897/547905 (in particular section 7) for quite a few details. (Alas that was written 15 years ago.) Strangely enough, for some algae, freezing turns out to select some sub-populations in the process. I have no idea if anything like that was observed for bacteria.

I suspect that it might vary depending on factors such as the species of bacteria, whether they can regrow from spores, and whether or not ice crystals formed inside the cells of the bacteria and killed them.

The actual practical limit may depend on the long term stability of the cooler. For example, firefighter need to be informed, and have access pipes from outside to flood the room and probably the cooler with liquid nitrogen. I am not sure, but I think something like this is done in some maximum security virology labs.

@BagiM In practice the important labs have a combination of 1) really good insulation (this is important for keeping costs reasonable, anyway), 2) battery backups, 3) off-site monitoring with automatic notifications, 4) on site overnight security that can handle the unexpected (by calling the appropriate person for whatever area has alarms going off).

The reason you haven't found a definitive answer is that it depends on several factors.
The first factor that comes into play if we consider only ultra-low freezers (- 80 °C) is the organism you're freezing. Thermofisher gives an approximate time of bacterial cultures viability between 1 to 10 years :
$$\begin{array}{|l|c|c|} \text{Condition} & \text{Temp (°C)} & \text{Time (approx.)} \\ \hline
\text{Super-cooled freezer} & \text{-80} & \text{1 - 10 years} \\
\end{array}$$
For ATCC, the shelf life is even shorter :

-80°C is sufficient for most bacteria and fungi for short-term storage (5 years or less)

However, in Table 1 from She and Petti (2015), we can see that the shelf life - for an ultralow-temp freezing storage (-70 to -196) - varies greatly both between the organism groups and inside each group : up to 1 year for the Streptococci group and up to 3 decades for the gram-negative bacteria for example.
$$\begin{array}{|l|l|c|} \text{Organism group} & \text{Cryopreservative} & \text{Storage duration (yr)} \\ \hline
\text{Streptococci} & \text{Skim milk} & \text{0.2 - 1} \\
\text{Mycobacteria} & \text{Skim milk} & \text{3 - 5} \\
\text{Spore-forming bacteria} & \text{Skim milk, glycerol} & \text{2 - 30} \\
\text{Other Gram-positive bacteria} & \text{Skim milk, sucrose, glycerol} & \text{1 - 30} \\
\text{Gram-negative bacteria} & \text{Sucrose, lactose, glycerol} & \text{2 - 30} \\
\text{Filamentous fungi} & \text{Glycerol, DMSO} & \text{2 - 30} \\
\text{Yeasts} & \text{Glycerol, DMSO, skim milk} & \text{2 - 30}\\
\text{Protozoa} & \text{Blood, nutrient medium with DMSO or glycerol} & \text{} \\
\text{Viruses} & \text{SPGA} & \text{1 - 30}
\end{array}$$
How the stocks are made and used are also important factors :

Among other things, ATCC recommends a gradual freeze and a quick thaw :

In addition to using a cryoprotectant, the rate of cellular dehydration during the freezing process can be managed by using a -1°C/minute cooling rate

Thawing should be rapid at 37°C

ThermoFisher recommends a high cell density as cell death will occur no matter what :

Also, the greater the cell density, the better the recovery is after thawing the cells. For most bacteria, a density of 107 cells/mL will result in adequate recovery if all conditions are properly maintained.

Cell death during storage is inevitable but should be minimized as much as possible

The number of freeze/thaw cycles is critical and thawing even partial should be avoided :

Try not to freeze/thaw your glycerol stock too many times. Placing the glycerol stock on dry ice while streaking onto LB agar will prevent it from thawing completely and will improve the shelf life. from addgene.org

Coming back to the initial question, based on the information above and some of the feedback in this discussion stocks of the typical E. coli DH5-&\alpha& stored at - 80 °C would probably last up to 2 or 3 decades maybe more but depending how you make them and use them it can be much less. To go further, depending on your workflow you may want to consider having working and stock vials to limit the number or freeze thaw cycles or using freeze-dried stocks for longer term storage.
Edit : One thing to keep in mind too is that frozen stocks shelf life is not all about cell viability upon thawing but also about "cell integrity". As mentioned by She and Petti (2015), van Griethuysen et al. have observed the loss of the mecA genes in 2 years old Staphylococcus aureus isolates frozen stocks.

The mecA gene was lost in 36 (14.4%) of 250 methicillin-resistant Staphylococcus aureus isolates after 2 years of storage at −80°C with the Microbank system (Pro-lab Diagnostics, Austin, Tex.). Further analysis of 35 of these isolates confirmed loss of the mecA gene in 32 isolates. This finding has important implications for the management of strain collections.
I personally experience a similar issue with a routinely used strain that lost its adhesive phenotype so we had to use the backup stock.

References :

She, Rosemary C., and Cathy A. Petti. "Procedures for the Storage of Microorganisms." Manual of clinical microbiology (2015): 161-168.
Van Griethuysen, Arjanne, et al. "Loss of the mecA gene during storage of methicillin-resistant Staphylococcus aureus strains." Journal of clinical microbiology 43.3 (2005): 1361-1365.

Richard Lenski's lab at Michigan State university has been doing long-term evolutionary research on E. coli and maintaining a "frozen fossil record" of their experimental populations every 500 generations since 1988. They still periodically release research papers comparing the physiology of evolved and ancestral populations. For example, this recent paper looks at populations collected at 2000, 10000, and 50000 generations. According to this timeline, they used populations frozen over 3 decades ago.
This doesn't guarantee that your specific organism will last that long, but it does show that freezer stocks can remain viable for longer than some research labs will even exist. Most of their protocols are on the website. I've had lunch with Dr. Lenski, and he's a pretty approachable guy. I'm sure if you emailed him with specific questions that aren't covered on the website, he'd try to find an answer for you.
References:
Changes in Cell Size and Shape During 50,000 Generations of Experimental Evolution with Escherichia coli. Nkrumah A. Grant, Ali Abdel Magid, Joshua Franklin, Yann Dufour, Richard E. Lenski, Journal of Bacteriology Mar 2021, JB.00469-20; DOI: 10.1128/JB.00469-20
Lenski Lab homepage: http://myxo.css.msu.edu


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Is it safe to feed the squirrels?
I hope this question fits here, I haven't found another community where it would fit.
Two years ago I was in a hotel in Sri Lanka (south-western coast) and in the hotel gardens there were a lot of squirrels. From what I could find out, they probably were Indian Palm Squirrels, but I don't know for sure. They were striped.
They were very tame and come to the hotel guests, hoping they would get something to eat. You could even touch some of them, so they are probably used to that.
We fed them some roasted peanuts (unsalted) and they were pretty happy about it, sometimes they also just took them by themselves =)
My question is, as I am about to visit the same hotel again this year, is it safe to do so? I know that they mainly eat nuts, fruits and insects, but our nuts were purchased in Germany (though propably imported from elsewhere anyway). Is there any danger for the squirrels or is it a terrible idea to feed those wild animals anyway or is it fine to do so, as long we don't cram them?

@AlwaysConfused: There is no force involved whatsoever =) They eat by themselves, come to humans by themselves. Some eat from the hand and when they have enough they leave. By "as long as we don't cram them" I wanted to indicate that I think it would be a bad idea to just give them too much.


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Why are hydathodes called hydathodes and not hydrothodes?
I can't seem to find any etymological root for the hyda- in hydathode.  I expected the water-relater structure to be called a hydrothode, but it just isn't!

I'm voting to close this question as off-topic because it is about etymology and Greek language.

This may possibly be okay for [hsm.se] or [latin.se] but please verify in their meta/chat first. You may be asked to provide more background.

@WYSIWYG You are correct. However, those studying biology (with a similarly limited knowledge of Greek and Latin) might have a similar question when first learning about hydathodes.  Additionally, the answer given by LinuxBlanket describes the hydathode etymology as being directly related to hydathode physiology, which I think justifies its place in Biology.

The etymology of hydathode, according to the Collins dictionary, is "way (hodos) of water (hydat-)". So the correct way of dividing the word is not hyda-thode, but hydat-hode.
Also, "hydat-" is the genitive of the Greek word for water, "hydor" (literally "of water"), whereas "hodos" is in its nominative form ("the way"). If you want to say "water way" in ancient Greek, you have to use nominative+genitive, not nominative+nominative, but there might be also euphonic reasons to why is not *hydrohode.

Dictionaries are your friend.  American heritage says "Greek hudōr, hudat-, water; see wed-1 in the Appendix of Indo-European roots + hodos, way, road."  Merriam-Webster says "International Scientific Vocabulary, from Greek hydat-, hydōr water + hodos road"


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Are there completely self-sufficient autotrophs?
Are there completely self-sufficient autotrophs which can survive and reproduce indefinitely by consuming exclusively non-organic matter (plus energy from sunlight or thermal vents etc.)? I'm asking specifically.

This is essentially the same question you already asked, but expressed in a more scientifc manner. Please delete the previous question.

It really depends on what you mean by "organic matter".  No cell is going to be able to grow and reproduce without an appropriate source of CHON atoms (plus lesser amounts of the other necessary elements).
So, if by organic matter you mean CHON+, then no, everything needs organic matter to grow and reproduce.
If by organic matter, however, you mean natural organic materials like soil or groundwater, then yes, there are lots of things that can live on chemical mixtures that can be produced by purely synthetic means.  A simple example is M9 media, which is a commonly used bacterial culture medium.

@user1136 You should not answer in the comments: if you have an answer prepared, please post it as an answer and not as a comment.

@user1136 — Re your last sentence. This is not a discussion site so don’t embark on one. Just write an answer of your own to the question as an answer. (I have already flagged for deletion the answer you posted as a comment, which ignored the explicit injunction not to answer questions in comments. I’d advice you to copy it into an answer before it disappears.)

Why would groundwater be considered an organic material?

@jamesqf Natural water sources are typically full of dissolved or suspended organic materials https://en.wikipedia.org/wiki/Organic_matter#Aquatic

@jakebeal: Natural water sources, yes, if you include lakes & streams.  But at least in my experience, most groundwater has little or no organic material.


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Mushroom identification, Hungary
I've found these growing on regular lawn, near some pine trees. In Europe, Hungary, Szada, near the end of October. Could you please help identify it?

Particularly for fungi, treat any ID with caution - don't eat until confirmed by a local expert.


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semantic similarity measurement for cell line ontologies
I have a set of cell line pairs and I want to know to what extent the pairs are similar based on their ontologies.
The problem I have is that I have found a Python library called Fastsemsim, but it has many similarity measurements. Or to be exact, there are actually many ontology similarity measurements. And I want to know which similarity measurement is best suited for my case (cell line ontologies similarities). There might be a couple of good ones that are good for cells ontologies.
These are a set of similarity measurements that are available in Fastsemsim.
Semantic Similarity

SemSim.TermSemSim
SemSim.ObjSemSim
SemSim.ObjSetSemSim
SemSim.SetSemSim
Specific Semantic Similarity measures
SemSim.MixSemSim
SemSim.avgSemSim
SemSim.maxSemSim
SemSim.BMASemSim
SemSim.SemSimUtils

Source:
https://fastsemsim.readthedocs.io/en/latest/library.html

If your question is about python libraries, it would probably fit better (and get more answers) on SE Bioinformatics.

Yes, as it's about algorithm selection SE Bioinformatics is likely better. Also, I think you are using "ontologies" to refer to the terms/classes, when the ontology is in fact the collection of such terms. E.g. CLO and Cellosaurus are ontologies, and they have terms representing particular cell lines.


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Why is coffee a stimulant?
The effects of coffee as a stimulant are quite well-known. What are the mechanisms by which coffee helps prevent sleepiness? I have heard of the presence of caffeine, but what does it actually do inside our body?

This is much more of a biology- (more specifically neurobiology) related question. I would highly suggest seeking more info from the usual wiki(s) and checking out various google results for further explanation of caffeine's effects. Maybe a search for "caffeine adenosine antagonist" will get you further than you might want the chemists here to take you. Cheers

https://www.quora.com/What-happens-when-you-water-plants-with-coffee-or-tea

Adenosine is a naturally produced hormone. It inhibits neurons and makes you tired. The longer you stay awake, more adenosine is produced.
Caffeine is a competitive inhibitor. It will bind to the adenosine receptors and prevent adenosine from binding. The adenosine is unable to bind and thus you don't get tired.
For (much) more detail take a took at the pharmacology of caffeine.


text:
Why are Chloride Anions necessary for gastric acid functioning?
Why do parietal cells of the gastric mucosa release Chloride anions along the H+-ions, which are pumped into the lumen by the proton-pump. Wouldn't the presence of protons alone be enough to denature proteins?

Mebrane divide basicly enviroment to two disimular sections. This sections differ in lots of chemical/ phycical properties. One of those is electrochemical potential which it can be in the very simple way describe as whole charge of disimular section divided by biomembrane.

So if cell  pariental cells pumped into stomach that section will have too much positive value of electrochemical potencial which can repulse pumping more hydrogen ions back to the pariental cell. This lead to freeze hydrogen pumping to  the stomach area. Than chloride aniont came to the scene basicly to reduse positive charge and enable to pump tremendous amount of hydrogen to the stomach.

I tried to make it simple as possible. I hope this still can help you.


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Why haven't humans been able to make blood producing vats?
There are people in hospitals in life threatening circumstances that need blood packages, and they fully depend on blood donors' blood.
With our current technology, we have been able to "persuade" stem cells to differentiate into many kinds of cells or to replicate themselves, and even modified bacterial DNA to produce insulin. Why haven't we still made something that produces blood?

It's more difficult and expensive than expected. There are some prototype artificial blood, but they don't work as well as real blood. https://en.wikipedia.org/wiki/Blood_substitute One umbilical cord can provide 20 units of blood... but the research has hit a technical hitch. Search NEWS for artificial blood and blood pharming to find what has happened lately in the field.

Here is a history of artificial blood from 2019: https://www.popsci.com/artificial-blood-history-science/

Welcome to SE Biology. Please take the Tour to find out what the site is about and what questions are relevant. You will see that this is a question and answer site about specific biological problems, not a discussion site about why medical science has not advanced further.


text:
Are blue feathers better insulators?
I recently found an article talking about the colors of bird feathers. https://www.smithsonianmag.com/science-nature/why-are-some-feathers-blue-100492890/
Apparently, unlike other colors, where pigmentation is at fault, blue feathers are actually blue thanks to their unique structure. According to the article, when the feathers grow, they form air pockets, which then form a pattern that just so happens to cancel out the red and yellow wavelenghts, leaving us with blue.
Now, of course, all feathers have the ability to trap air. It's what makes them such excellent insulators, as air conducts heat very poorly. Bonus points if the air is contained in very small cells, as that increases a materials insulation qualities. It's for the very same reason we also use foam for this. Now my question is: As the blue feathers contain miniature air pockets to give them their color, would that make them, in essence, better heat insulators than the ones of other colors, or do all feathers have such pockets, and the blue birds just so happen to be arranged differently, without actually changing any insulation capabilities?

This article https://www.nature.com/articles/s41467-018-05898-8 is likely relevant to an answer, though it deals with the impacts of reflectance on thermal loads, rather than insulation. In short, other attributes of feathers have large effects on their thermal properties, and can be evolved independently of visible colour. Any direct impact of colouration on insulation might be lost in the noise from these other factors.

As an aside (and from memory), a colleague of mine looking at the costs of sexual ornamentation in blue wrens (Malurus cyaneus) was convinced that blue feathers are worse insulators, based on behavioural observations of males that had molted into blue feathers and others that had not. There was an experimental intervention using testosterone implants, which would cause a male to molt into blue if it wasn't in blue already. I can't find a paper detailing the findings though, so she might not have published them.


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How much can a blue whale lift?
A simple question really. Given that the buoyancy in water kind of helps them under water, I'd specifically like to know, if there was, for Example, a boat, how heavy could it be that the blue whale could still push it out of the water.

This is less of a biology question and more of a textbook physics question.  Wikipedia suggests the max speed of a blue whale is 48 km/h, and the largest whale weighed 173 metric tons.  If you assume collision with a boat is inelastic with force applied perpendicular to the surface of the water, you can calculate a max boat weight for an arbitrary vertical distance for the boat to be pushed (say, 0.5 m?).  Assume also that the whale stops swimming once contact is made.

I’m voting to close this question because as pointed out by @Dirigible this isn't really a biology question as defined for this site. Please take the [tour] and then go through the [help] pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. Thanks!

I don’t think this is completely off-topic though, due to the fact that blue whales can use their muscles to swim and are maybe able to adjust their overall density by holding breath. So I guess this can be decomposed into more questions like: how much force or momentum can a blue whale generate while swimming? How much air can a blue whale hold in their respiratory system?

As I know about that and do research on this and find out some facts and figures I'll talk about both whale and krill. Due to the relative sizes of both the blue whale and krill, they can consume as many as 40 million krill, or 8,000 pounds (3,600 kg) of it daily.
These figures may change according to the age, weight, and other things of whale and krill

Welcome to Biology.SE! Please take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site and then [edit] or delete your answer accordingly. ——— It is best to avoid answering poor and off-topic questions. It also isn't clear that this answers the question asked. In addition, answers are much more likely to receive a favorable response if you include supporting references (primary literature is best). Without that support, your answer is indistinguishable from opinion. Please see the [help] for details about this site's goals. Thanks!


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How long to regrow hair?
This is one of the questions I wasn't exactly sure where to post. Basically, I want to make an X-Men parody, and for the part of Professor X I need to shave off my hair. Now I have a simple french crop, not really long or anything, but I was wondering if there's an estimate for how long it would take me to regrow my hair. Again, sorry if this is the wrong site, but I just thought "human body", so I guess it fits.

According to https://en.wikipedia.org/wiki/Human_hair_growth:

Scalp hair is known to grow between 0.6cm and 3.36cm per month. The growth rate of scalp hair somewhat depends on age (hair tends to grow more slowly with age), sex, and ethnicity. It was previously thought that Caucasian hair grew more quickly than Asian hair and that the growth rate of women's hair was faster than that of men.
However, more recent research has shown that the growth rate of hair in men and women does not significantly differ and that the hair of Chinese people grew more quickly than the hair of French Caucasians and West and Central Africans.

Depending on your age, follicle-condition, nutrition or possible inhibiting factors it can vary how long it will take until your hair has grown back to the previous length.

With that in mind, I should be back to full lenght in 1-2 months. That's doable, thank you.

@MatNX Pleasure (gern geschehen), if you take the average (1.98 cm/month) and estimate a french crop with about 4 cm, it should take about two month ;)


text:
Per Capita Population Growth Rate and Exponential Growth. Rate constants
As many of us might know, the set up of a differential equation relating instantaneous population growth with respect to time to the per capita population growth rate and current population size at an arbitrary time is as follows:
dN/dt = rN
Now, we are told that the constant, r, is the per capita population growth rate. N is the current size of the population at some time. "r" is the "organisms added per reproductive period" divided by the total population at that time. For instance, if 10 rabbits are born per month and the current population is 100 rabbits, then r = 0.1.
Let's consider a case where a population is doubling every reproductive period, modeled by 2^t. we can choose to model 2^t in base e and equivalently we have e^ln(2)t. So  2^t = e^ln(2)t = e^kt where e^kt is a general formula for exponential growth or decay. For doubling, k = ln(2).  In differential equation form we have dN/dt = kN , k = ln(2)
You can't get natural log of 2 by taking the number of organisms added to the population and dividing by the current total population. r does not equal k no matter how you set up your growth rate, but the structure of the relationship is the very same differential equation for exponential growth: dN/dt = kN, which we can integrate to a general form such as A*e^kt.  Why do we use this "r" contrivance at all? I am not sure I understand this choice. How is r different from the standard exponential growth factor k? What does it help us to understand in modeling the population growth rate?

I'm confused.  Your first two paragraphs basically make sense (except that I don't understand why you switched notation from r to k, these seem to be exactly equivalent). I don't understand your last paragraph at all; can you try to clarify?  Are you confused about the switch between discrete- and continuous-time models?

Integrating $\frac{\mathrm{d}N(t)}{\mathrm{d}t}=rN(t)$ gives you $N(t)=N(0)\exp (rt)$. Doubling would mean the ratio of the population at time $t$ to time $0$ is 2; i.e., $2 = \frac{N(t)}{N(0)} = \exp (rt)$. You can see how $r \neq \log (2)$. As pointed out by @BenBolker above, I think you may be cofounding instantaneous, continuous-time growth (differential equation) with incremental, discrete-time growth (difference equation).


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Can the dietary fibres as chemical compounds be regarded as polymers?
At the level of molecular structure, can the dietary fibres be regarded as polymers?

About which dietary fibers are you thinking?

Dietary fibers are the indigestible portion of food derived from plants.
Most of these are indeed polymers of sugars (that is, a chain of repeated basic unit of carbohydrate), for example cellulose, alginate or pectin. They have glycosidic bonds that cannot be broken down by enzymes found in humans, and are thus indigestible.
But there are exceptions, for example raffinose, a trisaccharide found in beans & cabbage, is also categorised as a dietary fiber, as it is not breakable by human enzymes.


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Questions about scientific method in neuroscience
In what ways does intuition from subjective experience guide topic choice in neuroscience? How important is it to frame research questions quantitatively? Can our own beliefs about how we think bias what topics are studied in neuroscience?

Beliefs can always bias a study. Questions and Studies should have some numerical base to be considered scientific, in that sense they use measurements and statistics, using standards statistics methods and a numerical deviation in the certainty of the results, i.e. to within 5 percent. The first question is vague. Topic choice is vague, for students, researchers, reading materials. For students it's course based and for researchers it's interest/finance/other based.

Can you please specify why your question is specific to neuroscience? I think this is a question of philosophy of knowledge and the nature of human bias in the scientific methodology. Such question (especially if refined) would be on topic on Philosophy.SE but not here. I am voting to close.

Belief will always bias topic choice in science. Because, if we would know everything about it already we don't need to study it. If we don't know everything, there is just the belief that there is more interesting stuff to be known. It's not like I ask a computer to randomly generate letters until it spells out a possible research topic.

Of course.  Our beliefs govern what topics we study, we look for the proof of existing hypothesis and tend to blindly blunder toward what we "know to be true" ignoring all indications to the contrary.  We set out to prove what we believe, it's all very artificial.  However, ironically this could be correct because there is a psychological argument to suggest that what we believe governs what becomes anyway.


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What motivation is there to create general, cross-species neural models which account for the variation between species in different environments?
The main components of human neuroanatomy have been mapped out. What attempt has there been to map a broad (many-species) spectrum of functional parts of the nervous system? Such a mapping could be useful in behavioral ecology, which associates functional behaviors with driving environmental forces.


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Can any systems biology model be complete?
In systems biology, models identify the primary actors in the body system, but can any model which does not include all secondary actors be said to be complete?
The current sysbio paradigm is to identify and study biological subsystems. However systems and interactions are subtle and numerous, and no scientist will be able to identify and describe, by hand, how the system works in its entirety. What attempts have there been to model a complete ecological system of internal chemical dynamics?

"All models are wrong but some are useful". This goes for both mathematical and experimental models.

That's right, but some models are less wrong than others.

@Jamie Your comment reminds me of George Orwell's quote from Animal Farm - "All animals are equal, but some animals are more equal than others"

Your question is quite broad. People are constantly making efforts to make better models. With increased computational power, simulation of complex models is no longer difficult. However, you should also keep in mind that if the question that you are asking can be explained by a simple model then no need to complicate things. Choose the model with the least number of parameters.

True, what I am looking for is a discussion of "completeness" of a chemical-biological model. If you consider the human body as a complex system, what reduction can be made to computer data? Clearly there is no representation which recovers the entire system, but if you model a human as a cellular automaton, what data and rules of evolution could capture a smaller system that works on the same principles?

Here's another way to phrase: A biological systems model is a reduction of the entire biological system, which is exactly the positions and velocities of all atoms. How is it that we can make such reductions, and how can we define the notion of a biological model? Are some models more complete than others?


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Muscle contraction/extension percentage during normal ranges of motion
What is the typical percentage range/limits of extension/contraction during normal ranges of motions for muscles?  Assuming a rest length in a typical relaxed state.
I'm mostly interested in humans but I am also curious if it is typically the same range across other animals too?

can you be a little more clear - do you mean what percentage of muscle shortening occurs (i.e. with 100% defined as resting/non-stretched muscle)?

Yes so for example given a rest length at 100%, saying typically muscles extend to 110% and contract to 80%.  Specifically it's to determine a sensible default starting range for a motion simulation I am working on.