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Regulation of the TCA cycle and glycolysis by adenine nucleotides
Why is the tricarboxylic acid cycle regulated by the ADP/ATP ratio as stated in the following quote :

Isocitrate dehydrogenase is allosterically stimulated by ADP, which enhances the enzyme's affinity for substrates.1

while glycolysis is regulated by AMP/ATP ratio as in the following quote from the same book :

Why is AMP and not ADP the positive regulator of phosphofructokinase? When ATP is being utilized rapidly, the enzyme adenylate kinase (Section 9.4) can form ATP from ADP by the following reaction: 2

I want to check my hypothesis that it is because the TCA cycle needs acetyl-CoA ( which can come from glycolysis and other sources such as beta-oxidation of fatty acids) in order to operate, so it gets acetyl-CoA from many sources and isn't dependent on glycolysis alone, and that's why it is affected by ADP (which increases upon initial exercise) while AMP stimulates glycolysis (increases after more exercise) to give more acetyl-CoA and that's rate of the TCA cycle is faster than glycolysis?
References
1,2 J.M. Berg et al. (2002). Biochemistry, 5th ed. New York: A H Freeman.

I finally found time to provide an answer. It's not short, although I have provided a two-sentence summary. However the situation is extremely complex. I didn't explicitly say that your hypothesis was wrong — it is. The regulation of glycolysis and the TCA cycle energy charge has nothing to do with the particular demands of the muscle as it exists in bacteria and yeast. Regulation of tissue metabolism involves hormonal control of phosphorylation of the enzymes, and as another story in itself.

Summary
Glycolysis and the tricarboxylic acid cycle (TCA cycle) are distinct processes which are not necessarily linked sequentially. It is therefore not surprising that their modes of regulation are not identical and, in fact, involve far more complex regulation than mentioned in the question. The use of AMP rather than ADP as sensor of energy deficit depends on the action of adenylate kinase, which may differ between cytoplasm and mitochondria.
Relationship Between glycolysis and the TCA cycle
The expectation evident in the question that glycolysis and the TCA cycle should be controlled in exactly the same way assumes that either the two processes are inextricably linked or at least that the functioning of the TCA cycle is dependent on that of glycolysis. This is not the case, although the student can be excused this misimpression from the (perhaps unavoidable) way the topics are generally treated sequentially in text books of biochemistry.
The primary function of glycolysis is to produce ATP directly from ADP. The end-product of the pathway, pyruvate, is in some circumstances converted to acetyl CoA for the TCA cycle, and the NADH generated used for production of ATP generation via the electron transport chain (etc) and oxidative phosphorylation. However pyruvate has a variety of other possible fates depending on the type of organism or — in higher organisms — the tissue, and their overall metabolic requirements. For example in anaerobic metabolism — including exercising muscle tissue mentioned by the poster — the pyruvate may be reduced by reactions that regenerate NAD+ from NADH, e.g. conversion to lactate. It can serve as a precursor of the amino acids, alanine, valine and leucine. It can also be converted in the reaction catalysed by pyruvic carboxylase to oxaloacetate, the key intermediate that allows acetyl CoA to enter the TCA cycle. The importance of direct synthesis of oxaloacetate in this way is that it allows continuation of the cycle when intermediates are used for synthetic purposes (discussed below), in which circumstances oxaloacetate becomes depleted.
As regards the TCA cycle, there are sources of acetyl CoA other than pyruvate produced by glycolysis, and it has functions other than energy generation. Acetyl CoA can arise from the breakdown of fatty acids and of certain amino acids. In multicellular organisms, pyruvate can also be produced from lactate taken up from the blood, although in liver cells it is likely to be used for gluconeogenesis. And certain bacteria — acetic acid bacteria such as Acetobacter — can utilize the ethanol produced by fermentation in the TCA cycle. In addition to its function in energy generation some of its intermediates (α-ketoglutarate, succinyl CoA and oxaloacetate) are precursors of biosynthetic pathways, and the production of citrate from acetyl CoA is a means of transferring the latter out of the mitochondrion, where it is reconverted to acetyl CoA by the citrate cleavage enzyme (ATP citrate lyase).
It is therefore not surprising that there will be differences in the regulation of glycolysis and the TCA cycle, and, indeed, that there will be differences between different organisms — something generally not mentioned in elementary texts.
Regulation of Glycolysis
The prime function of glycolysis is the direct generation of ATP (“at the substrate level”), and flux of glucose through it is controlled by the regulatory effects of both ATP (–ve) and AMP (+ve) on phosphofructokinase, which was established and rationalized by D. E. Atkinson (Biochemistry 1968, 7, 11, 4030-4034) in terms of a response to the overall energy charge of the system.

This arises from the ability of adenylate kinase to reconvert ADP to ATP:
               2ADP → ATP + AMP

[from Atkinson and Walton (1967) J. Biol. Chem. 242 3239–3241]
It can be seen that AMP is a much better indicator of low energy charge than ADP in the circumstances represented by the graph above.
Citrate is also a negative effector of the enzyme, providing co-ordination between glycolysis and the TCA cycle. (Hormonal regulation via protein phosphorylation occurs in the tissues of higher eukaryotes.)
Regulation of the conversion of pyruvate to acetyl CoA
In order to enter the TCA cycle, pyruvate needs to be converted to acetyl CoA by the pyruvate dehydrogenase complex. The regulation of this enzyme determines the extent to which this occurs, and, hence, the extent to which pyruvate is metabolized by other processes. Negative regulators here are high concentrations of the reaction products, acetyl CoA and NADH, although in higher eukaryotes hormonally induced protein phosphorylation is important.
Regulation of the TCA cycle
Then first regulatory enzyme of the TCA cycle, isocitrate dehydrogenase, responds to the concentration of the key molecules involved oxidative phosphorylation: it is stimulated by ADP and +, and inhibited by ATP and NADH. It is worth reflecting on the consequences of inhibition. If a build-up of citrate occurs, this can feed back and inhibit phosphofructokinase in glycolysis. However the citrate can move to the cytoplasm of eukaryotes and be converted to acetyl CoA (for fatty acid synthesis) by the citrate cleavage enzyme, which is stimulated by ATP and inhibited by ADP.
A later regulatory stage is α-ketoglutarate dehydrogenase, which is inhibited by ATP, NADH and its product, succinyl CoA. Inhibition of this enzyme would allow a build-up of α-ketoglutarate, which is a precursor of several amino acids.
This the existence of several regulatory steps in pyruvate oxidation and the TCA cycle allows the use of the cycle for both energy generation and as a source of synthetic precursors. Hence it should be evident why its control is similar to that of glycolysis in some respects, but exhibits key differences.

[Berg et al. Biochemistry 5th ed, Figure 17.18]
But why isn’t AMP a regulatory molecule in the TCA cycle?
Glycolysis and the TCA cycle do not need to march in step, although when they are both responding to the need for ATP their key enzymes are regulated by adenine nucleotides, among other molecules. The original question (or a modification of it) remains as to why is AMP a positive effector of phosphofructokinase, but not of isocitrate dehydrogenase, which responds to ADP. It is interesting that in the section of Berg et al. discussing the concept of energy charge, a rather lame rider is added without further explanation to the effect that the ATP/ADP ratio can also act as an index of energy status.
I don’t know for certain, but suspect that the conditions under which Atkinson’s equation for energy charge is valid do not hold in the mitochondrion. This is supported by Sobol et al. (1978) Eur J. Biochem. 87 377–390 who found concentrations of AMP in rat liver mitochondria to be much lower than would be expected from equilibration with ATP and ADP through the adenylate kinase reaction. They suggested additional reaction of AMP with GTP in the mitochondrion might be responsible and also cited reports that adenylate kinase was absent from the matrix of rat liver mitochondria.
At least in rat liver, this would explain AMP would not be a useful regulatory molecule, whereas the ATP/ADP ratio would be indicative of the requirement for oxidative phosphorylation.

I have slightly amended my answer as regards AMP controlling glycolysis but not the TCA cycle. My initial hunch was correct, but the details not. Anyway I think the answer now better addresses this aspect of the question.


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Is there a way to relate the OD to cells/mL without doing a standard growth curve?
I am helping out with an experiment with multiple bacterial cultures (>20 species). I need to a very specific concentration (cells/mL or CFUs*/mL) for this purpose. Unfortunately it appears that standard growth curves (OD** vs. CFU/mL) are not available for these cultures. I am not in a position to generate them afresh either given the sheer number of cultures I have to work with and how laborious the growth curve experiments are.
Given these constraints, are there other reliable (and needless to say fast and accurate) ways through which I can find out how many cells/mL (or CFUs/mL) I have in a given bacterial culture at a given OD? All the more better if the method is parallelizable.
I came across this study (Robust estimation of bacterial cell count from optical density.) where they suggest using silicon microspheres with dimensions similar to E. coli to reliably estimate ODs, but I don't know what the cell sizes for the bacteria I am working with are. In this case, what are some easy and accurate ways in which I can estimate the average size of these bacterial species?
* - CFU - colony forming unit
** - OD - optical density

Do you have access to a flow cytometer? That would be one way of making direct counts of a culture. And, of course, there's always the good ol' hemocytometer.

You really need something tangible to tie back to the OD, whether it's CFU, MPN, or direct cell counts. Without some kind of standard curve, you're basically just guessing. If you have a plate reader, you could do your OD dilution series on that, and follow up with a quick drop plate assay (basically a spot titer for CFU) to get you in the ball park (probably within half a log or so). Should be easy to blow through 20 bugs in a day or so (three or four days if you want a few replicate measurements). Just realize your plate reader OD will not be identical to your cuvette OD.

I would argue that performing a full growth curve isn't strictly necessary to obtain a standard curve to convert between OD and CFU. As long as you're collecting cells in a standardized way, a standard curve generated from a simple dilution series of cultured cells can prove quite reliable.
For example, you can harvest cells from your culture in early stationary phase and generate a 2-fold dilution series, collecting OD measurements for each dilution until you get below the threshold for which your OD reader can generate accurate OD measurements. Then switch to 10-fold dilutions and plate those for CFU counts. You can then back-calculate the CFU/mL present at each of the OD measurements for your standard curve.
The same concept can be applied to overnight colonies suspended in normal saline or PBS. Pick colonies from an overnight streak plate and suspend them in saline until it's turbid, with an OD reading >1.0. Do the 2-fold dilutions to get multiple OD readings until you bottom out, and plate for CFU. This is generally how innocula are standardized for determining MIC values in broth dilution methods, and the range of acceptable CFU concentrations for those methods is often quite narrow.
Whatever method you use, replicate it several times to make sure you're getting consistent conversions, stick with that method for your experiment, and always verify your experimental CFU.

You can estimate cell size through a microscope. However cell size can vary significantly in different stages of growth, or growth under different conditions.

@markur I actually did ask about this also.

ah I see, I deleted my comment

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If plants benefit from carbon dioxide, why is car traffic something bad?
This is going to sound really stupid or as a joke, but... Ever since I was a little kid, I have been confused about the following:

Humans need air/oxygen to breathe in order to live.
Plants/trees/bushes/flowers produce this oxygen, and are thus crucial for humans to survive.
Plants/trees/bushes/flowers need "carbon dioxide" to survive, just like humans need oxygen.
Plants/trees/bushes/flowers MAY also need some oxygen/air? (I assume so.)
Cars (traditional ones) output "carbon dioxide"... yet they are... not good for nature?

I don't understand how this fits together. It seems as if nature should absolutely thrive in the middle of highways and nearby, if they get so much nice carbon dioxide from the cars! Yet cars are instinctively seen (also by me) as "evil nature-polluting machines of death". Car exhaust seems to be the opposite of what a plant or tree wants, yet it's full of carbon dioxide, so... why?
Can somebody explain this once and for all?

There are at least two separate answers to your question.  First, with respect to plants needing CO2, they have evolved to deal with the limited amounts of CO2 normally in the atmosphere.  That's really all they need, or "want": adding more doesn't really benefit them.  Think of it this way: you need water to live, right?  And drink a certain amount of it every day.  But drinking large amounts of water can kill you https://en.wikipedia.org/wiki/Water_intoxication and holding you under water for a few minutes certainly will.  (As in the comment above, and even better example would be oxygen: we need it to live, but too much can cause all sorts of problems: https://en.wikipedia.org/wiki/Oxygen_toxicity )   Likewise, plants need nitrates, but applying too much can kill them.  So extra CO2 in the air is of little or no benefit to plants.
The second answer has nothing to do with plants.  It's that atmospheric CO2 traps solar heat, causing the Earth to be warmer than it otherwise would.  Without the extra CO2 from fossil fuels, Earth maintained a comfortable temperature, one that we'd all (and I mean not just humans, but all life) had gotten used to.  Add more CO2, and more solar heat is trapped, making the Earth uncomfortably warm, to the point that many plants & animals can't live where they are, and generally can't migrate.  So you wind up with a lot of dead plants and animals.
Of course there's more going on than this, things that are feedbacks from and side effects of the increased CO2, such as ocean acidification.  If you really want to know more, here's a good starting place: https://history.aip.org/climate/index.htm

Where is your source for extra CO2 being of no benefit? Here's NASA saying the opposite: https://climate.nasa.gov/news/2436/co2-is-making-earth-greenerfor-now/

@Wayne Conrad: Because there is abundant practical evidence - artificial (or organic) fertilizers, irrigation, &c - that plant growth in natural conditions is seldom limited by CO2.  Even when those other factors aren't limiting growth, predicting long-term response isn't a simple matter, e.g. https://science.sciencemag.org/content/360/6386/317 or https://www.newscientist.com/article/dn11655-climate-myths-higher-co2-levels-will-boost-plant-growth-and-food-production/

@jamesqf It would be helpful if you included that supplementing information into your answer, and maybe add some appropriate caveats as theforestecologist suggests.

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@Wayne Conrad What about some  "extending", not limiting factor:  and does that mean more plants, not just larger ones?

Exhaust gasses from combustion contain many compounds in addition to CO2.
Some of them under the right circumstances‡ can be of limited benefit to some plants, but others such as ozone are damaging to all forms of life.
Other compounds in vehicle exhaust that are known to cause damage to plants are oxides of sulfur and nitrogen — these react with water to form acids and contribute to "acid rain" that lowers soil pH thereby interfering with nutrient uptake and may also directly damage plants1.
Finally, as noted in other answers increasing levels of atmospheric CO2 due in part to vehicle exhaust contributes to climate change that has a global consequences for plants — this however seems beyond the scope of the original question which appears to be about local effects on trees growing "in the middle of highways and nearby".
‡Note: For example, increased CO2 can be growth promoting at least in the short term.
Reference:
1: Oswalt, C. M., & Clatterbuck, W. K. (2005). Impacts of Air Pollution on the Urban Forest. University of Tennessee, Agricultural Extension Service.

Firstly, I don't think it's entirely clear whether the entire premise of the question is correct. I couldn't find any evidence to suggest that plants don't thrive on highways and areas with lots of cars. If anyone has any data on this, I'd be interested in reading it.
Some of the answers here seem to be a bit light on evidence. Let's look at some data on this.
This report shows that there can be around 1.5-2x increase (from the baseline level of around 410ppm to between 600-800ppm) of CO2 levels in areas surrounding highways. This value varies somewhat depending on whether it is peak time or not, but it seems like the median amount is around 600ppm. I'm aware this is only a single study, so it's perhaps not best to generalise too much, but it should give us a broad idea of how much CO2 increase to expect in areas surrounding highways.
In contrast to what jamesqf said, CO2 enrichment does increase the growth rate of plants, under certain conditions. This has been known for quite a while. Mauney et al (1987) state:

Comprehensive reviews of the plant science literature indicate that a
  300 part per million (ppm) increase in atmospheric carbon dioxide
  (CO2) concentration generally increases plant growth by approximately
  30%.

Importantly, the range of increase that you see in areas surrounding highways certainly increases the growth rate of plants. Ainsworth & Rogers (2007) state:

Across a range of FACE experiments, with a variety of plant species,
  growth of plants at elevated CO2 concentrations of 475–600 ppm
  increases leaf photosynthetic rates by an average of 40%

Furthermore, a recent study showed that the human-caused increase in CO2 levels has actually caused a relative greening of the worlds global vegetated area. So this isn't just an effect of ideal conditions in FACE experiments, it also occurs 'in the wild'.
However, it's not quite as simple as increased CO2 -> increased growth. As we can see from the figure above, the levels of CO2 in the highway vary temporally between peak and non-peak times. Fluctuations in CO2 levels actually reduce the growth rate of plants, for various reasons. White et al (2020) state:

..we calculated that yields increased 65% as much in fluctuating
  elevated CO2 of FACE as in constant elevated CO2

So it certainly seems like this might have an effect of reducing plant growth on highway areas.
As other people have alluded to, the other thing to remember is that cars produce a high level of other particulate from the exhaust fumes, which certainly have a large negative impact on the growth of plants. Power et al (2011) state:

A wide range of effects were detected, including growth stimulation
  and inhibition, changes in gas exchange and premature leaf senescence.
  This was complemented by controlled fumigations with NO, NO(2) and
  their mixture, as well as a transect study away from a busy inner
  London road. All evidence suggested that NO(x) was the key phytotoxic
  component of exhaust emissions, and highlights the potential for
  detrimental effects of vehicle emissions on urban ecosystems.

Overall, it seems likely that a combination of fluctuating CO2 levels (rather than constantly high levels) and particulate pollution might cause a reduction in plant growth around highways.

Back in the early days of climate science, there were some scientists who considered the possibility that increased CO2 production would lead to increased plant growth, and that this in turn would result in keeping the oxygen-carbon dioxide balance more or less stable. This was referred to as the "Gaia hypothesis" and basically revolved around viewing the entire ecosphere as a "living organism" that would maintain itself.
To an extent, this does happen.  Increased CO2, by itself, may result in increased plant growth.  So may increased temperature resulting from the increased CO2 trapping the sun's heat (the greenhouse effect).
The problem is that we're producing way too much of it, way too fast.  Even if the atmosphere and climate are becoming more favorable for plant growth, plants can only grow so fast - and it's not fast enough to stop carbon buildup from increasing the planet's temperature to levels that may make things difficult for existing forms of life (including humans).
Also, we're destroying plants, both through direct deforestation and indirect desertification, faster than they can grow even with the more favorable conditions, which doesn't help matters.
So you're not wrong - carbon dioxide production may increase plant growth.  But it also causes problems, and plants can only mitigate those problems - and they can't mitigate them fast enough.

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Ignoring for a moment the other pollutants emitted from car exhaust, increased CO2 levels are warming the planet, through what is called the "greenhouse effect".
Photosynthesis is a set of reactions where CO2, water and sunlight are turned into chemical energy used for plant life.
However, these reactions only work well in a narrow temperature range.
As plants heat up past a certain point, they can't run some photosynthetic reactions as well, or at all.
As the atmosphere heats past a safe range, plants must divert resources to making so-called "heat shock proteins" or HSPs to protect photosynthetic machinery.
If the atmosphere gets too hot, plants suffer irreversible damage, can no longer generate energy to live, and therefore die.
https://bmcplantbiol.biomedcentral.com/articles/10.1186/1471-2229-14-111

You really have a good point, maybe you want to check this paper https://bsapubs.onlinelibrary.wiley.com/doi/full/10.3732/ajb.95.2.165  It looks like C3 plants could thrive in the near future, although C4 species could have an advantage during years with water stress.But temperature wise, in a high CO2 environment C3 plants perform better

It seems as if nature should absolutely thrive in the middle of highways and nearby, if they get so much nice carbon dioxide from the cars!

In fact, some species of plants are likely to thrive from the excess pollution coming from cars, provided they can tolerate the hotter summers and grow quickly enough to take advantage of the higher CO2 levels.  Unfortunately, many of the plants people care about are not going to be the ones that benefit most.

Yet cars are instinctively seen (also by me) as "evil nature-polluting machines of death".

"Nature" colloquially refers to "plants and animals as they are currently".  Pollution doesn't destroy nature, but it does change it, which people tend to perceive as bad because we are prepared for the world around us being a certain way.  For example, more Co2 is likely to be very good for cockroaches and mosquitoes (which thrive in warmer weather), so some of the plants and animals that currently do well will be exchanged for more bugs.  People who have to deal with more roaches and mosquitoes will probably perceive this as bad, even if those insects are still part of nature.

Excellent point about "change" -- the long time scale perspective suggest "change" and not "destruction" its occurring. However, you need to provide citations or other forms of support for the basics points made in your response. Thanks

'Destruction' is only the name we give to rapid changes

Anthropogenic Climate Change is why carbon dioxide, from fossil fuel powered transport in combination with other fossil fuel uses is considered problematic  - i.e. "bad".
With respect to plant health insufficient carbon dioxide is not a problem; even with some plants getting some benefit from raised carbon dioxide concentrations those benefits are outweighed by the harms and costs expected to accrue from climate consequences of profligate fossil fuel burning.
About the climate consequences the US National Academy of Sciences says -

Climate change is increasingly affecting people’s lives. It is having
  significant effects on infrastructure, agriculture, fisheries, public
  health, and the ecosystems that support society. It is also changing
  the environment in ways that affect the distribution, diversity, and
  long-term survival of species of plants, animals, and other forms of
  life on Earth.

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How efficiently does the human body convert the energy stored in fat into kinetic energy?
I read that one gram fat contains 9 kcal energy. There are many tables around claiming that x type of exercise for t duration burns roughly E kcal energy. I'd like to estimate how much weight one will lose by following a certain training plan based on these two values. I don't know whether I need to calculate with the heat loss too, or not. Most of these tables don't tell anything about the method they used to estimate the E values. I could workaround this problem by ignoring efficiency, but I can do that only if it is relative close to 100%. As far as I know fat goes through beta-oxidation and the citric acid cycle. After that ATP is used to move the muscles. It is hard to find anything about how efficient this process is.

this depends on largely how you define it, what we normally measure is efficiency including how much energy is used on metabolic upkeep and heating the body in addition to muscle output. we use oxygen consumption to know exactly how many calories we have "burned" when doing this.  In this study we get between 18-26% efficiency, thats calories ingested to work done. Most of the loss is in converting to ATP (~60% loss) and how much ATP we "waste" heating the body. Note efficiency drops quite a lot when you switch to anaerobic exercise.
keep in mind however the body will not start out burning fat, it has glycogen reserves it will start using first.

"keep in mind however the body will not start out burning fat, it has glycogen reserves it will start using first. " - Actually that is not true. It starts with glycogen and intramuscular fat...

@inf3rno do you have a source for that, its not that I don't believe you but it is the first I have heard of that but it does make sense physiologically.

You can use google to find some. For example this is a good starting point: https://journals.lww.com/acsm-essr/Fulltext/2005/10000/Intramuscular_Triacylglycerol_in_Energy_Metabolism.6.aspx

There was this fat burning myth, that you start "burning fat" only after 20-30 mins of aerobic exercise. That is partially true. You start with IMTG until the triglicerides arrive from the fat cells through the circulation. Without that people on ketogenic diet would not be able to do exercise...

the paper you linked states thew fat in question does not start getting utilized until 60min of exercise.

Yes, there was debate about whether it is 20-30-60 mins to mobilize fatty acids from adipose tissue. I read different values in different articles. It does not really matter though, because the muscles use IMTG until that is done. And they fill the IMTG storages with the fat from adipose tissue after the exercise is done.


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tissue-specific expression of homolog genes
Two or more genes are homolog if thay have similar sequences. homolog sequences between species are called orthologs (caused by speciation events) and homolog sequences in an species are called paralogs (caused by duplication events).
I would like to know what is expression pattern of paralogs or orthologs in an specific tissue. Are paralog (or ortholog) genes have same expression in a tissue or they express different?
I hope my question is clear, but if it has mistakes I appreciate your corrections.

The evolution of new genes is frequently associated with gene duplication. The paralogous genes are then free to evolve on their own into new functions over time. Sometimes (usually) the paralog will end up with a frame shift, or stop codon that inactivates it. But your question is lacking the element of time. At the instant of gene duplication, each copy is identical. However, one copy may lack the control elements (usually upstream), and not be transcribed. Or one copy may eventually evolve a new, tissue specific function. But whether the copy is inactivated, or evolves a new function, or remains active is not the same for every instance. It depends on how each copy changes under the influences of mutation and selection.

Nice answer. can you please introduce me some articles talking about this topic?

I just Googled:    "gene duplication" paralog function.     and got a lot of informative hits.

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How to search for a protein sequence of an specific taxa in NCBI?
My example: Sequence of HBB (Hemoglobin Beta) in Fishes.
How can I do a good search to obtain above sequences in NCBI? (I know hot to download them into a FASTA file)

Try going to http://www.ncbi.nlm.nih.gov/protein and searching for ' (hemoglobin beta[Protein Name] OR (hemoglobin[All Fields] AND beta[All Fields])) AND "Fish"[ORGN] '.
Search filters can be changed with the panel to the left of the search results.

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Connect the inner and outer space of cell with a wire, will there be electricity?
There is a potential difference, but ions can not go through wires, right? Though there is a electric field, but there is no electron source, I am thinking the answer is no, or will there be some chemical reaction?

Let's start with the basics.  The inside of the cell contains predominantly positive potassium ions, and negative phosphate ions, and other negative ions (e.g. from amino acids).  The outside of the cell contains predominantly positive sodium ions, and negative chloride ions.
The cell however sets up a resting membrane potential, due to the cell's semi-permeable membrane, allowing predominantly only potassium to pass through the membrane.  This causes potassium to flow along its concentration gradient towards the outside of the cell, until it is balanced by the electric potential that is consequently set up.
So we now have POSITIVE potassium ions on the outside of the cell and NEGATIVE phosphate ions (or other negative ions) on the inside of the cell, which aren't balanced.  Now as the wire is placed between the inside and the outside of the cell, electrons from the negative phosphate ions will travel through the wire, towards the positive potassium ions on the outside of the cell.
Once this occurs, the potassium from the cell's interior can now continue to flow against its concentration gradient, because the previous potassium ions in the exterior no longer contribute to an opposing electric potential.
Additional note:  As the K+ ion in the extra-cellular fluid gains electrons from the wire to form K, it will react almost immediately with water to form KOH and H2 (hydrogen gas).  The K and OH will be soluble in the extra-cellular fluid, forming K+ and OH- ions.  Over time the K+ ions will be "pumped" back into the cell's cytoplasm.  (The left over OH- ions will temporarily increase the flow of K+ down its concentration gradient, etc.)

Mmmm... I like a good, thorough answer.

I am very skeptical of this answer. Electrons do not simply flow away from phosphate ions because they are negative, nor do they attach to K ions freely (I don't think potassium and phosphate ions react in solution). Patch clamp systems actually do conduct current between the inter and exterior of neurons, but they generally achieve this by exchanging Cl- ions with an AgCl wire, not by exchanging electrons with K/PO4.

Just to clarify your ion/electron question - a neutral atom or molecule becomes ionized when it either loses one or more electrons, becoming positively charged, or gains electron(s), becoming negatively charged. Since the negatively charged phosphate (PO42-) ions have a surplus of electrons, they (the electrons) are free to flow "up" the wire and to the outside of the cell.

For electrons to flow trough the wire you'll need that the wire can have a redox reaction with the required solution, a simple voltage difference is not enough. Given that you may use a silver chloride wire or a platinum wire which can have these kind of reactions with the ions inside of the cell. If there`s no redox reaction, you can still see a transient capacitive current going trough the wire.


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Can in the case of multiple sclerosis (MS), a too high osmotic pressure in the nerve, lead to a high intracellular concentration of potassium?
Can in the case of multiple sclerosis (MS),
a too high osmotic pressure in the nerve,
lead to a high intracellular concentration of potassium,
and also lead to 'pumping up' of nerve cells,
which then due to the strongly increased internal pressure,
the insulating myelin sheath can be pressed broken,
resulting in a lesion,
or a strong reduced transmission of stimuli ?
If that were to happen,
one can expect in cerebrospinal fluid,
cytokines, which are normally also a component of the nerve cell contents,
and that it wrongly can be interpreted,
as inflammatory reaction to a potential autoimmune disease.
Is there research of this ?

Firstly, demyelination has got nothing to do with membrane integrity of the neuron. Demyelination causes the current to "leak" through the ion-channels and thus causing loss of signal.
There is an old article which reports a study on membrane integrity of RBCs of MS patients but there seems to be no connection.
It has been proven that neurons do secrete some cytokines such as IFNgamma but the signaling is mostly para/auto-crine and I dont think the cytokines will accumulate in CSF.
MS is identified by the presence of anti-myelin antibodies, which might be the exact biomarker for the disease. A general neuroinflammation is not concluded as MS.
So to answer your final question

Is there research of this ?

There is none that exactly talks about neuron membrane dynamics in MS. The most parsimonious assumption is that there is no effect, but any hypothesis has to be proven. It might be experimentally difficult to address this question and how to design the experiment for this study would be an interesting question.


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Trigger allergic reaction in non-allergic people?
Is there a proven way to trigger an allergic or allergic-like reaction in non-allergic people? I have wondered if this is possible, since allergies are basically just a form hypersensitivity - so could this be triggered somehow?

Is there a proven way to trigger an allergic or allergic-like reaction in non-allergic people?

No.
At least, not that I've ever heard of. Allergic reactions, as you point out, are an overactive immune system response to an allergen (anything that causes the reaction). What determines who is allergic to what is a mix of genetic and environmental factors, and because an allergic reaction is categorized as an error on the immune system's behalf, inducing an allergic reaction is essentially finding a way to force the immune system to make a very, very specific error.
What can (and does) happen is the development of new allergies. Almost all allergies are acquired after birth, and repeated exposure to substances can lead to the appearance of new allergies - one case that stuck out in my head was a woman developing an allergy to a copper IUD that she tolerated well when it was first put in place.
I am not aware of any ability to predict what substances will cause the development of a new allergy. Both the unpredictability and inability to induce allergies comes down to how the immune system reacts to antigens (foreign substances). The machinations of the immune system's response to an allergen or antigen is fairly complicated, and at any point in the chain of events the potential for an overreaction is there. That's probably another question, though, and a much longer answer.


text:
Loss of allelic variation per generation of full-sib mating
If we take a male and female, cross them, and collect one son and one daughter to produce the next generation (and continually do this for many generations) - (full-sib mating design) how much genetic variance is lost per generation/how do we calculate this?
Assume all sites initially have allelic variation, and we imagine a diploid sexual species.

A classical result from the Wright-Fisher model of genetic drift is that at each generation the heterozygosity ($2x(1-x)$) is expected to decrease by $\frac{1}{2N}$ due to genetic drift. ($x$ is the frequency of one of the two alleles). In your example the expected loss of heterozygosity is $¼$. This same result has been derived from coalescent theory and a similar result is derived from the birth-death Moran model. The issue is that this model assume bi-allelic loci only.
Let's think of 1 tetra-alellic (4 alleles) locus and let's assume that the 4 alleles in our two original parents are all different. We can draw the 16 possible pairs of offsprings and see the probability to lose 0, 1 or 2 alleles in the next generation
lose 0 allele: ¼
lose 1 allele: ½
lose 2 alleles: ¼
lose more than 2 alleles: 0
Therefore, the expected number of lost alleles is $1$!

We can then do the same (calculate the probability mass function) for two parents with 3 alleles and then 2 alleles (with various frequencies). It is not very complicated. But it would be much better to have a general model to describe the loss of heterozygosity through time for more than 2 alleles. This paper probably gives this solution but I haven't read it yet. I will probably read it once and I will improve my answer then!


text:
Is this a soldier beetle? Bug identification
I'm curious to find out what kind of bug this is. Reverse Google image search suggested a type of soldier beetle, but I am not convinced.
The photo is taken in summer, in England
Thanks!

No, it is a longhorn beetle. Cerambicidae.

Welcome to Biology Stack Exchange! Generally, for species identification questions, you'll want to include the geographic area and time of day.

And also the date of photography and the season.

@KarlKjer You can probably make an answer out of your comment

It looks very much like Arhopalus rusticus, a species of long-horned beetle (Cerambycidae) that is found in England. https://en.wikipedia.org/wiki/Arhopalus_rusticus


text:
How are homing pigeons' "homes" changed?
Last night I was watching the David Attenborough minidocumentary on animal navigation, and it talked about the homing pigeons used in the two World Wars.
Apparently they were donated by UK pigeon fanciers for the war effort.
However, when used as war messengers, obviously they had to "home" back to HQ, not their original UK roost.
How do you "reprogram" the pigeons to use a new home? I assume that pigeon fanciers have to do this all the time if they move house?
(I couldn't find a pigeon SE site so hope this is on-topic here!)

My brother captured a bunch of ordinary pigeons at one building where they had been nesting, then kept them in a second building a couple of miles away for about a month, where they nested and were well fed.  He gave them freedom after that month, and most of them kept coming back to the second building.  I suspect that knowing it was a good home and knowing their flock mates might be found there were factors in their "reprogramming".


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What kind of beetle is this? (Black and yellow)

Found this in my house in Colorado. I took this picture before releasing it. I didn't measure it, but the diameter of the cup it is trapped under is about 5.5 cm, so that makes it about 1.1 cm long. It easily climbed up the side of the glass cup.


text:
How long does a mosquito take to land on a host, bite, and fly off?
How long does a mosquito take to land on a host, start its bite, end its bite and then fly off?
And what about different species?
I am most interested in human hosts.
References to web sites or books would be appreciated.
I cannot find this even after extensive trawling of Google.

That's an interesting question and not easy to answer. I haven't found data for humans but from experiments with mice. They analysed how the mosquito actually bites, probes for the blood vessels (not all bites are successful) and finally sucks bloods. In their research  they observed feeding times between 150 and 329 seconds, depending on the size of the blood vessel. The mean feeding time was 240 seconds. It also depends on the age of the mosquito, older mosquitos suck longer. To this comes the time for probing (mean time 142 seconds) and the time before the mosquito starts probing after it landed (mean time 6.5 seconds). This totals to about 389 seconds (or roughly 6.5 minutes) total time after landing. This data can be found in table 1 of reference 2.
This is pretty interesting, they also show videos of the mosquito probing the skin for a blood vessel. You can find a pretty nice summary in the first reference and the original paper in the second:

Here’s What Happens Inside You When a Mosquito Bites
Visualizing Non Infectious and Infectious Anopheles gambiae Blood
Feedings in Naive and Saliva-Immunized Mice.

Table 1 from reference 2 above has additional data on the time to start of probing (mean time to start 6.5 seconds), probing duration (mean time 142 seconds) which I presume are before the feeding time (mean time about 240 seconds). The mosquitoes involved were Anopheles gambiae. It must be noted that this was in a controlled laboratory environment on mice, not humans, but the data is still a very good start.

You are right. So this adds to the 240 seconds, coming in total to about 389 seconds. I know that this is in a laboratory environment but I haven't found any other serious data on this topic.

Nice finds Chris +1

Nice answer +1. Having worked with mosquitoes during my undergrad, I can tell that it very much depend on the activity on the host though. A mosquito coming to bite you the night while you're partying with your friends outside might often just land and go away too afraid that we sensed its presence. But if you're sleeping (and if you're not moving during your sleep), then the mosquito may take longer. I haven't read the paper but those estimates seem to correspond to static hosts.

Btw, I've been told that bites when they have to hurry up hurt more than bites when they had time to suck, make sure to be completely fed and leave when they finished. But that might be a urban legend, I don't know.

Gillett studied the feeding behavior of Aedes africanus and Aedes aegypti, the abstract says that

They showed that while the period between salivary injection and the
  onset of irritation was the same in both species (ca. 3 min)

It seems to me that the abstract does not say whether the hosts were humans or not. Unfortunately I am not able to get the full paper.
GILLETT, J. D. Natural selection and feeding speed in a blood-sucking insect. Proceedings of the Royal Society of London B: Biological Sciences, 1967, 167.1008: 316-329.

This does not address the question


text:
Why do spiders have a leaf at the bottom of a piece of web?
I've lately seen a lot of instances where a leaf is dangling from a piece of web coming down off a tree. What purpose/s does this serve for the spider? Is it some sort of mechanism for the spider to determine the wind / disturbances in that region?
I've seen a suggestion that it's to help act as a plumb during web construction to keep part of it tight, but do we actually know for sure?
Here's a national geographic image showing what I mean:

http://ngm.nationalgeographic.com/ngm/photo-contest/2012/entries/177963/view/

I would think that these leave simply got caught by the net.

It's attached to a single piece of thread, dangling about 5ft from the ground.

Could the spider have used the leaf as support for the web while it was still attached the tree, then the leaf fell off the tree and still hung on the web?

@user137 interesting idea, and would explain why I only see it in autumn. It wouldn't have to necessarily be part of the web for this to be viable.

I've also come to reason that spiders use web to move from leaf to leaf, so it may just be a leaf that's had web shot onto it by the spider and was attached to a more permanent part of the tree.

As far as I know, it has a practical effect. Spiders hunt for small insect and don't like when bigger animals damage their webs. So that they make the web visible for mammals, but in the way which doesn't prevent the prey from being caught.
I don't have reference for this, my colleague (entomologist) told me so.

I like this thought.  It's like the owl decals we put on windows to keep the birds from banging their heads on the glass.  I, for one, won't walk into a web I know is there.

It would be good to have a reference for this claim or to clarify that this is just a guess.


text:
Resources of all known biochemical pathways?
I am looking for a encyclopedia or biochemical pathway atlas of all known or reported pathways. I am very much interested in network and systems biology. Also the references can be open databases, books or whatever. I came to know about a site called wikipathways , but it is not opening for me.

You can find biochemical pathways on KEGG pathway for example.

KEGG PATHWAY is a collection of manually drawn pathway maps representing our knowledge on the molecular interaction and reaction networks for:
  1. Metabolism
      Global/overview   Carbohydrate   Energy   Lipid   Nucleotide   Amino acid   Other amino   Glycan
      Cofactor/vitamin   Terpenoid/PK   Other secondary metabolite   Xenobiotics   Chemical structure
  2. Genetic Information Processing
  3. Environmental Information Processing
  4. Cellular Processes
  5. Organismal Systems
  6. Human Diseases
  and also on the structure relationships (KEGG drug structure maps) in:
  7. Drug Development

To illustrate the information you can find there, here is a screenshot:
If you click on kegg atlas, you get an atlas with all metabolic pathways. You can zoom in to great detail en click for further links.

If you click on glycolysis or oxidative phosphorylation for example, you will get linked to the following page (see picture). In these detailed schemes of the metabolic pathway, each intermediate can be clicked on, leading to a more detailed page.

Nice answer, but I am waiting for some more responses before accepting this.

I don't know if you will get any more :P


text:
Can the axial length of the human eye decrease?
I understand that the axial length of the eyeball grows until you are around 20 years of age, which is why hypermetropia decreases with age but myopia doesn't. My question is: can the axial length of the eyeball decrease, and does it do so naturally?
I know that certain conditions can cause the axial length to decrease, such as very low pressure or disease, but my question is regarding a normal healthy eye.

Weihua Meng, Jacqueline Butterworth, François Malecaze, Patrick Calvas; Axial Length of Myopia: A Review of Current Research. Ophthalmologica 1 March 2011; 225 (3): 127–134. https://doi.org/10.1159/000317072

This study by Meng et. al. (2011) says that with current research we KNOW that the axial length decreases with age this same point was also in a different study based on the idea of a an emmetropizing mechanism for the adult eye but many people have criticised this study and due to this apparently the studies findings should be taken with a grain of salt but if this is the case why is it that many articles do say that the axial length reduces with age is there another study that shows this?

Scott A. Read, Michael J. Collins, Beata P. Sander; Human Optical Axial Length and Defocus. Invest. Ophthalmol. Vis. Sci. 2010;51(12):6262-6269. doi: https://doi.org/10.1167/iovs.10-5457.

This study by Read et. al. (2010) basically used lenses to create hyperopic and myopic defocus in participants and they measured the axial length of the eyeball after exposure to the blur. They found that the axial length did decrease in the case of myopic defocus and increased in the case of hyperopic defocus in order to create a clearer image by focusing the image on the retina. But if this article provides definitive proof that the eye does in fact change its axial length then why is that people still say it doesn't happen?
Also do we know which mechanisms allow the eye to determine whether it is myopic defocus or hyperopic defocus that is presented to the retina?
Lastly, if the eye's axial length is able to reduce wouldn't myopia have a cure or at least a method to reduce it based on the reduction of the axial length of the eyeball?
https://www.quora.com/How-can-the-axial-length-of-an-eye-decrease-as-they-say-that-it-does-with-ageing

Generally the axial length doesn't decrease:
graph
Although there is discussion of various conditions where it has been observed to decrease, i.e. nanophthalmos, microphthalmos, and retinoblastoma... A review of current research is here: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5501611/ quote:
It is considered that the axial length reaches adult length by the age of 13 years, showing no further increase in length. Recent cross-sectional studies found that the axial length in older adults tended to be shorter, suggesting that it may decrease with aging. However, in a recent longitudinal study by He et al., slight increase of the axial length in adults (mean refractive error, −0.44 ± 2.21 diopters) was reported. Conversely, an increase in the axial length in adults with highly myopic eyes is common and has been previously shown in longitudinal studies [5–7]. However, to the best of our knowledge, there have been no studies directly comparing the increase in the axial length in adults with non-highly myopic eyes or highly myopic eyes. In addition, because previous studies on the axial length in highly myopic eyes have not compared between eyes with and without macular complications, their influence on the axial length remains unknown.
Can myopia be treated with a reduction in axial length? Presumably, yes it could, if opticians had figured a way to do it... Do you suggest that a drug or a medical intervention can flatten the entire eyeball a bit? perhaps a drug could but it would reduce the entire eyeball, you'd have to find a way to administer it. Apparently doctors haven't researched that option, but perhaps they will in future. Laser currently seems like a better way.
https://www.google.com/search?hl=en&biw=1706&bih=951&sxsrf=ALeKk01GuiHpl6-_fRp-Bg_UdsYOdqVzbg%3A1596509065944&ei=icsoX9aRObLMgweX6KboCQ&q=%22decrease+in+axial+length%22+of+optical
https://www.google.com/search?hl=en&biw=1706&bih=951&sxsrf=ALeKk03b75zOsA6CN_Ypqdv5v7hqfVWLbA%3A1596509091797&ei=o8soX8ySMIyqUP2dtvgI&q=%22reduction+in+axial+length%22+of+optical&oq=%22reduction+in+axial+length%22+of+optical

Hello, thank you for your answer. I understand that generally the AL doesn't reduce unless a disease is present but I'm slightly confused with the research that I linked above. In the research it says hyperopic and myopic defocus can cause the axial length to increase or decrease respectively, so why is it that we say the AL is unable to decrease am I missing something?

The statement in that paper is contradicted by the paper from 2017 which is a summary of current research, so perhaps they are thinking of eariler on. Teenagers and adults have constant AL.

Although traditionally the axial length of the human eye has been considered to not be able to decrease naturally in healthy eyes, a survey of the most recent peer-review, scientific literature, as of 2024, reveals that it can actually decrease over time  in a long-lasting manner. Human eyeball axial elongation is not irreversible.
The axial length reductions reported in the peer-review scientific literature can be achieved by different means, such as orthokeratology, Repeated Low-Level Red-Light Therapy, as well as defocus, as described in the references below.

Orthokeratology has been shown to cause long-Term axial length
shortening, which can alter the focus of light entering the eye.
However, Further studies are needed to elucidate detailed ocular
biometric changes and potential mechanisms underlying this
phenomenon.
https://iovs.arvojournals.org/article.aspx?articleid=2793222

Repeated low-level red-light therapy has demonstrated capabilities in
reducing axial length by stimulating biochemical pathways that
influence eye growth. In a study, which used Repeated Low-Level
Red-Light Therapy, it was able to achieve > 0.05 mm AL shortening in
39.8% of the participants at 1 month and in 21.6% of the participants at 12 months. https://www.sciencedirect.com/science/article/pii/S0161642021009167

Optical defocus, achieved through specially designed lenses, can
create a defocused image on the retina, which has been found to slow
or reverse axial elongation, as described in Nature Scientific
Reports by Kubota et al. (2022). It has been found that sustained,
long‑term reductions in axial length and refractive endpoints can be
produced with cumulative short‑term exposure to specific myopic
defocus stimuli using a novel optical design that incorporates an
augmented reality optical system.
https://www.nature.com/articles/s41598-022-15456-4#citeas

These findings suggest that the axial length of the eye is more dynamic than previously understood, opening new avenues for managing and potentially reducing myopia progression.
Axial length refers to the distance from the cornea (the clear front surface of the eye) to the back of the eye (the retina). It plays a crucial role in vision, especially when it comes to conditions like nearsightedness (myopia).In a normal, healthy eye, the axial length is typically around 24 mm in adults.
The most common form of nearsightedness is called axial myopia. It occurs when the axial length of the eye is too long relative to the focusing power of the cornea and lens. In axial myopia, light focuses in front of the retina rather than directly on it, leading to blurred vision at a distance.
Factors Influencing Axial Length:
Outdoor Exposure: Spending more time outdoors seems to have a protective effect against excessive elongation of the eyeball. Lack of daylight exposure is associated with myopia development.
Near Work: Prolonged near work (such as reading or using digital devices) at very close distances may contribute to myopia development.
Genetics and Environment: Both heredity and environmental factors play a role in becoming nearsighted
Myopia Control:
Researchers are exploring ways to control myopia progression by managing axial length.
Techniques like myopic defocus (focusing on distant objects) and conscious accommodation of the ciliary muscle during active focus may lead to axial shortening.
Good practices for both close-up and distance vision can help maintain a healthy balance.
References
Tan, Q., et al. (2022). Axial length reduction in orthokeratology: A meta-analysis. BMC Ophthalmology, 22, 2461.
https://link.springer.com/article/10.1186/s12886-022-02461-4
Vincent, S. J., & Collins, M. J. (2022). Orthokeratology and axial length: Understanding the mechanisms. Ophthalmology and Therapy, 10, 644-662. https://link.springer.com/article/10.1007/s40123-022-00644-2
Smith, E. L. (2021). Impact of repeated low-level red-light therapy on myopia progression. American Journal of Ophthalmology, 226, 142-150. https://www.sciencedirect.com/science/article/pii/S0161642021009167
Jiang, Z., et al. (2022). Repeated low-level red-light therapy and its effects on axial length. Investigative Ophthalmology & Visual Science, 63, 3222. https://iovs.arvojournals.org/article.aspx?articleid=2793222
Wang, M., et al. (2022). Optical defocus and axial length control: A new approach to myopia management. Scientific Reports, 12, 15456. https://www.nature.com/articles/s41598-022-15456-4


text:
The advantages of using a strand specific cDNA in RNA-Seq?
May I ask what are the advantages of using a strand specific cDNA library in an RNA-seq experiment? as far as I know it can make us able to read the code region but what about other advantages?

Welcome to SE Biology. Please take the guided tour and then read about how to ask a good question. You will see that you are expected to "Search and Research" before posting. I quickly found a paper on this topic by Googling. If the papers you have found don't answer your question, reference them, say what they do say and why that is insufficient or not what you are after. Otherwise I am afraid your question is likely to be removed.

Hi, I have already google it before posting this question but it is still not clear to me what are the other advantages. Even when you think my question could be basic and silly I still need someone to answer this question in a simple way please.

It is not a question of whether the question is basic or silly, and I did not say that. What I did was review your first post — as is standard practice here — and explained how the site worked giving links, using standard language. I know you haven't completed the introductory tour as you do not have the badge for doing so. If you want to use this site you must follow its rules. Please read them.


text:
Where to begin studying Biology in earnest, with preferably free sources?
I am a biology enthusiast and would like to study Biology in earnest. I have basic knowledge of biology (high school level) and some extended knowledge of small animals, mainly about mammals as I am naturally interested in them.
So I would like to start studying veterinary and Mammalogy first.
I would prefer free sources for studying since I have little money available.

Welcome to Biology S.E. I would recommend to have a quick look at the  tour (https://biology.stackexchange.com/tour), learn about Biology S.E and earn your first badge.

Okey Johhny will do now. EDIT: Got it :)

I think if you can narrow down your areas of interest a lot more, answering the question will be easier, other wise this question is too broad. (I have found that non-specialised, general  biology sites meant for open learning are not great, lack precision.) Narrowing down your areas of interest to something like Evolution, Genetics (if you are into mammals, may be Zoology, or if their behaviour, ethology) will get you good answers(recommendations).

Thank you for response what I am interest in Veterinary itself but for now I will start with Mammalogy I guess :)

Coursera may have some stuff you can use. https://www.coursera.org/learn/becoming-a-veterinarian/lecture/rS68J/teaching-learning-veterinary-medicine You can buy old mammology and vetinary  textbooks, you will likely find some free pdfs of them if you look in the right places. You may need to study up on college level biology first however. .

[Khan Academy > Biology][https://www.khanacademy.org/science/biology] is very good. It offers a good broad introduction to the main fields of biology. It does not talk about mammalogy or veterinary though.

@Remi.b I have found some factual errors at places on Khanacedemy videos especially ones made by Sal Khan (talking about biology videos). So I think grabbing a book is better than learning from these videos.

I have modified your question. You want free stuff. Open source means (more or less) that the code or original material is not protected by copyright and can be modified and redistributed.  You are not interested in this.

Considering books, I guess the Campbell is the best place to start in biology, but it's really a general biology book and it's not focused on mammalogy, even if there are some chapters dedicated to animal physiology and animal diversity... you can probably find it in a library if you don't want to buy it, and there exists a pdf version as well. I hope it helps somehow. :)

Before getting into veterinary and mammalogy, you might want to start with the basics. As many people have mentioned, Campbell and Reece is one of the best textbooks to start a foundation in biology. If you live near a public library you might find a 6th or 7th edition to borrow. Amazon has a few 7th editions for cheap as well. Although it is an introductory biology book, it will give you a wonderful tour of cellular and molecular biology that will make it much easier when studying animal physiology (which they also covered in the later chapters to a limited extent).
Free Biology Text Books:
Boundless Biology: Boundless is a company that has many free textbooks for high school level biology to help teachers in have a free online textbook.
I have also found a list of free biology text books here that might be of use.
Free Mammology Textbook:
As part of a National Science Foundation Grant, the Northwest Center for Sustainable Resources created *Introduction to Mammology*. It is a free textbook that was developed for a two-year Wildlife Technology program. It also contains information related to the lab portion of the program, but you can skip those and focus on the material.
Free Online Coursework:
Coursera: A few people have already mentioned Coursera, which is a Massive Open Online Content (MOOC). Here, you can find many courses across a wide range of biology topics (and others!). You can enroll in a course (for free) and many times they come with accompanying free textbooks as well (at least that is what I have experienced).
edX: Another MOOC that was started by Harvard.
Khan Academy: Another great website for explanations of certain aspects of biology. As Tyto alba stated, there are some errors in the videos.


text:
Why are C4 plants mainly tropical plants?
Why is it that most C4 plants are tropical plants?
As far as I am aware the C4 cycle does not prevent water loss; so having it exist in tropical areas does not serve these plants any good other than preventing photo-respiration. Hence I do not understand why it is solely found in tropical plants and not plants from other areas as photo-respiration is a problem not limited to tropical areas
Reference:
http://lifeofplant.blogspot.sg/2011/10/c4-and-cam-photosynthesis.html?m=1

See c4 cycle occurs in bundle sheath cells which are impermeable to gases. And rubisco affinity for O2 is increased with temp. Tropical regions have high temperatures
So therefore co2 is given to rubisco in these gas impermeable cells in the form of maleic acid in order to reduce photorespiration

This is not my field, so the following is based solely on a brief reading of Internet sources.
The Wikipedia entry on C4 carbon fixation states:

When grown in the same environment, at 30°C, C3 grasses lose approximately 833 molecules of water per CO2 molecule that is fixed, whereas C4 grasses lose only 277.

However it does not explain why this is so.
In contrast, the section in Berg et al. focuses on the energy losses caused by photorespiration and makes the following initial point:

…the oxygenase activity of rubisco increases more rapidly with temperature than does its carboxylase activity. How then do plants, such as sugar cane, that grow in hot climates prevent very high rates of wasteful photorespiration?

The answer to this (didactic) question is the C4 pathway (as described in full in that text), but the answer to the question posted here  is that “tropical plants employ the C4 pathway because of this increased wastage of energy through photorespiration at the higher temperatures in which they live.”

Thank you. This response pretty much sums up my question

Now I think of it,  maybe the increased rate of carbon dioxide uptake due to increased light intensity in tropical areas also play a part


text:
Can plants yield two more molecules of ATP from glycolysis?
Since 2 ATP are used to convert glucose to glyceraldehyde 3-phosphate in glycolysis, can plants bypass this step of ATP investment since they produce glyceraldehyde 3-phosphate directly from the Calvin cycle?
If yes,  what would be the final yield of ATP.
If not,  why not?

Plants produce ATP in the ‘light reaction’ of photosynthesis.
The purpose of the Calvin cycle (the ‘dark reactions’) is to produce glucose, for which it uses some of this ATP to provide the energy to make carbon–carbon bonds.
Glycolyis in plants functions to produce ATP from reserve carbohydrate etc. when ATP is not available from photosynthesis, or in tissues, that do not have sufficient ATP from photosynthesis.

So this question makes no physiological sense†, as it is based on a misunderstanding of the purposes of the differ metabolic reactions in plants. The answer is not that it cannot happen, but that it would not happen — the regulatory mechanisms that prevent futile cycling of pathways would come into operation.
† It is analogous to saying that the liver can perform gluconeogenesis, and so can produce glyceraldehyde 3-phosphate. So can the liver bypass this step...

Isn't the dark reaction of photosynthesis the Calvin cycle?  From my understanding, the Calvin cycle uses most if not all the atp produced from the light dependent reaction to fix phosphate and reduction of PGA to G3P,  which is the final product of the Calvin cycle

@user35897 — whoops! Too busy thinking about the structure to get the detail right. Thanks for pointing this out.


text:
Is APB an antagonist of the mGluR6 receptor?
APB is a glutamate analogue specific to the mGluR6 receptor of ON retinal bipolar cells. It is used in research into receptive field processing by blocking the ON channel. Why is it not called an antagonist?

I have changed the title of this question to reflect its more restricted scope, corrected the spelling of glutamate — the poster should take the trouble to ensure the spelling of key molecules is correct — and changed "function" to "use in research". It is now in a suitable form for SE Biology, so that it is appropriate to vote the answer of @BryanKrause as correct.

Of interest
https://link.springer.com: "Are partial agonists antagonists? A key property of partial agonists is that they display both agonistic and antagonistic effects." With BryanKrause: "it's still an agonist". By definition,  any antagonist's intrinsic activity is zero". Agonists may be - partly - antagonistic. No other way round. Slightest effect will make it an agonist.

APB (2-Amino-4-phosphonobutyric acid) is a metabotropic glutamate receptor agonist, not an antagonist, and in many publications it is indeed referred to as an agonist, so I think your question is somewhat ill-posed. For example:
Yamashita, M., & Wassle, H. (1991). Responses of rod bipolar cells isolated from the rat retina to the glutamate agonist 2-amino-4-phosphonobutyric acid (APB). Journal of Neuroscience, 11(8), 2372-2382.
You can find many many more by searching "2-Amino-4-phosphonobutyric acid glutamate" on Google Scholar.
The reason that APB suppresses ON bipolar cells is because metabotropic glutamate receptors are often inhibitory rather than excitatory. Glutamate is typically thought of as excitatory because ionotropic glutamate receptors such as AMPA and NMDA receptors are non-specific cation channels that depolarize and therefore excite cells. Metabotropic glutamate receptors operate through g-protein second messenger cascades. In ON bipolar cells in particular, there are cation channels that are closed by mGluR6 activation, which therefore inhibits them.
Here's a review article that describes this as well as other basic information about bipolar cell function:
Euler, T., Haverkamp, S., Schubert, T., & Baden, T. (2014). Retinal bipolar cells: elementary building blocks of vision. Nature Reviews Neuroscience, 15(8), 507-519.

Thank you Bryan. As you can tell from my question I am an interested amateur! My source describes the molecule as an analog for glutamate but its function is to block the G protein coupled receptor and prevent any neurotransmitter action that would otherwise result in the closing of the sodium channels. So, in a sense, the analog is performing the role of an antagonist. This was my confused thinking anyway!

@adlibber No worries, interested amateurs are good targets for StackExchange sites. :) "My source describes the molecule as an analog for glutamate but its function is to block the G protein coupled receptor" -
Then your source is either wrong or they aren't actually using 2-Amino-4-phosphonobutyric acid but a different molecule. APB might prevent glutamate from binding the receptor if it is higher affinity than glutamate (not sure if it is but could be), but it's still activating the receptor like glutamate and is therefore an agonist, and it would cause the sodium channels to close.

OK so its an agonist. Thanks for taking me through it :-)


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Why are sugars like mannose expressed on the outside of eukaryotic cell membranes?
Bacteria are able to adhere to sugars (e.g. mannose) on the exterior of eukaryotic cells, leading to infection and disease. Why have eukaryotes not evolved so as to dispense with sugars on their cell surfaces? I assume there must be a positive aspect to having these sugars. What is it?

I have modified your question, in particular making it clear that you are referring to eukaryotic cells (as implied by ‘infection’) and removing all references to cell walls, which animal cells do not possess. Although this is late in the day, I would point out that you are expected to show evidence of your own research before posting here. My own answer is partially based on internet searches for the function of cell-surface sugars.

The “positive aspect” or reasons why the surfaces of eukaryotic cells contain sugars are various. Major ones appear to be cell adhesion and cell–cell interaction.
In fact, the variation of the sugars in certain cell-surface antigens (blood group antigens and histocompatibility antigens may represent the kind of evolutionary response to infectious agents mentioned in the question. The situation with the major histocompatibility antigen is complex, but variation in blood group antigens is thought to be a response to the malaria parasite — reviewed by Cooling.

This is a simple referenced answer to the question by someone who is not an expert on cell-surface sugars, posted to help resolve it. If you have more recent or comprehensive information or references please either edit the answer or post a comment.

I'd look on it from the other side. Thoose structures have certain purposes, such as stability or signaling purposes. Due to their short doubling time compared to most cells of more complex organisms, bacteria is able to adjust to changed condition rapidly and therefore adapts to it's environment. (Just think of mechanisms of resitance to antibiotics: plasmids for example with the information for β-lactamase ere exchanged even between differnet kinds of bacteria) It would therefore not make a lot sense for the slower cells to adjust their usefull structures in order to avoid bacteria, which change way faster.


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What directs macromolecules to their cellular locations
For example I know that after transcription a mature mRNA is sent outside of the nucleus through the nuclear pore and then it goes to ribosome. But as for the free floating ribosomes that are out somewhere in the cytoplasm, how does the mRNA get to those organelles? Is there something else that attaches to the mRNA to help it? Even then I don't understand what force is helping a large molecule (mRNA) find and even larger macromolecular assembly (the ribosome).

I have changed your title to remove the anthropomorphic implications.

Once a eukaryotic mRNA enters the cytoplasm, in most cases it is probably the cytoplasmic concentration of the eukaryotic translation initiation factors that determines whether or not a specific mRNA is translated on the ribosomes.  The concentration of ribosomes in the cytoplasm tends to be quite high, and I think the same is true for the eIF subunits.  The short answer to the first part of your question is therefore: diffusion and the law of mass action.  The last sentence of your question is unclear (to me) and should probably form the basis for two separate questions.

This is fairly often question for molecular biology

how does the mRNA know exactly how to get to those organelles

The secret to understand it, is that nothing knows where to go. Different molecules have different affinity to each other. Molecule A likes molecule B, but not molecule Y. Inside the cell, thermal fluctuations causes disorder that drives molecule A to bump into all kinds of molecules, including Bs, Zs, Ys, and others. However, when stumble upon molecule B, molecule A will very likely form some sort of stable complex with it. One example, is ribosome and mRNA.
When mRNA and ribosome join into complex, their inner parts can be considered in the same fashion: they will jiggle a lot around, but most likely jiggle will produce polypeptide, not, let's say DNA, or not cause mRNA to fall away from the ribosome.
So, you can say that mRNA tries to go everywhere it can, without any clear direction, apart from the fact that it will most likely form something stable (i.e. useful) with ribosome. Or maybe it will be mRNA degradation protein, such as ribonuclease.
PS: "will very likely form some sort of stable complex" means that in some reasonable time mRNA will find and bind to ribosome. However, it might take billions of years for ribosome to bind DNA and produce some sort of polypeptide.


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Consensus symbols in multiple sequence alignment
I was using multAlin for multiple aligning a set of sequences. The output I and came across included the following documentation (English corrected):

Consensus symbols:  ! is any of IV  $ is any of LM
  % is any of FY  # is any of NDQEBZ

I understand what it says but I don't know how to interpret it further. What impact does this have on the sequence alignment?

I find your post incomprehensible and am voting to close. However if you are having a problem with a software program I suggest you consult the documentation, the website or the support community.

Hi, this is the description:
! is anyone of IV
$ is anyone of LM
% is anyone of FY
is anyone of NDQEBZ
I have emailed them for help, and even follow up on that email, but i did not get a reply at all. I really hope some bioinformatics expert can help me here. Thank you

I have edited your question in a readable manner, which I would recommend if you post here again — the clearer you explain your problem, the more likely you are to get an answer. I have also answered your question, including sample output, that you would have done well to include in your question.

The use of these symbols in output of the type shown below is purely presentational, to help you inspect the alignment and identify regions of partial conservation.

                  51                                                 100
          CCPC50  SEEGFK.YGE GILEVAEKNP DLTWTEADLI EYVTDPKPWL VKMTDDKGAK
          CCRF2C  TYPEFK.YKD SIVALGASG. .FAWTEEDIA TYVKDPGAFL KEKLDDKKAK
          CCRF2S  TQADFKGYGE GMKEAGAKG. .LAWDEEHFV QYVQDPTKFL KEYTGDAKAK
          CCQF2R  HKDNYA.YSE SYTEMKAKG. .LTWTEANLA AYVKNPKAFV LEKSGDPKAK
          CCQF2P  TFAGYS.YSP GYTVMGQKG. .HTWDDNALK AYLLDPKGYV QAKSGDPKAN
       Consensus  t...%k.Y.e g..e.gakg. .ltWt#..l. .Yv.#Pk.fl .ek.gD.kAk

This is quite independent of the logic (algorithm) of the program, which is indicated by the documentational comments:

Symbol comparison table: blosum62
  Gap weight: 12
  Gap length weight: 2

This also gives a reference to the original paper you should read to find more information about the program.
You would also be advised to read the Wikipedia entry on Multiple Sequence Alignment and on Sequence Alignment in general. I would mention that this is an old method (as the appearance of the site also indicates). If it gives useful results, fine. Otherwise you might try the more popular and more frequently updated Clustal, which is available online or as a standalone program.


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Sucrose inhibits onion root mitosis? Why?
I am doing an experiment about the growth of onion roots.
I put onion plants in different solutions of sucrose in water — 0.1M, 0.2M, 0.3M, 0.4M, 0.5M — with the root touching the water.
Measurements of root growth tells me that the presence of sucrose in the solution inhibits root growth.
Why does this happen? Does sucrose affect the root's mitosis? If so, how?

Have you used the same onion for all the experiments? If not, it could be due to the onions themselves rather than the enviroments they are in.

A formula does not identify a compound as many compounds have the same formula. This is an old question but I have edited it to replace the formula with the name of the compound I assume is being referred to.

tl;dr you are using a lot of sucrose. You would need to show us the data, but I'm not surprised if the plant gets confused / dies/ doesn't know what to do when you add so much.
An important aspect of experiments in biology is calibrating the treatment you're applying to the biological system. If you give a plant way more of an important signalling molecule than it would usually expect in nature, it may respond in a way that doesn't make any sense.
1M sucrose would be a 34% solution of sucrose (molar mass of sucrose is 342.3 g / M, in 1 L of solution).
If you look at papers or even at hobbyist forums where people add sucrose to stimulate root growth, they seem to usually be adding a 5% solution or less (50g / 1L ~ 0.16M), which is described as "high". So at the highest level you are adding more than 3X as much sucrose as people usually do.
I'd look at your data and try to understand whether the inhibition happens in a dose responsive fashion, and further whether the dose response is linear or whether it just gets weird at the higher concentrations.
As for the expected response, you will see in published work that sucrose or other sugars tend to encourage, rather than inhibit, root growth in most plants. Here for example is Figure 4 from a paper:

The left panel has no sucrose added and the right panel has 30mM sucrose added. You can clearly see longer roots in the presence of sucrose, at least in these young Arabidopsis seedlings.

tl;dr is not standard English but internet slang. Please replace it.

@David it's common parlance everywhere in SE, which is in turn, in (or on) the internet. https://biology.stackexchange.com/search?tab=votes&q=%22tl%3bdr%22&searchOn=3

@uhoh — Correction it is a text/SMS abbreviation. The fact that computing and IT types on Stack Overflow may be inclined to use it has no relevance to SE Biology, which as a scientific site aims for clear, unambiguous and inclusive communication.

@David part of inclusiveness is tolerance - not insisting things be just the way you personally think they should be. We're all just individual users here. The community has embraced tl;dr, it's here to stay. Also, cf. OED and Merriam-Webster

@uhoh — Could we please refrain from personalizing this, either in suggesting that I am being intolerant and that I am trying to force my views on the site. “Biology Stack Exchange is a question and answer site for biology researchers, academics, and students”, with the aspiration of building a library that will be a valuable resource to its users. One of the ways SE attempts to achieve high standards is by allowing edits of both questions and answers, and it allows comments expressly to suggest improvements in answers. The latter is what I did. I also took the trouble to improve the question.

@uhoh (cont)The common language of the users of this SE is standard English, and using slang etc. that is only understood by a subsection of users is a barrier to those who do not understand it, deters serious scientists who might contribute, and results in the adoption of such undesirable terms by neophytes, to their future professional detriment. This holds whether such terms are textese, non-standard abbreviations or foreign phrases (of which I admit to having been guilty on occasions). The inclusiveness of language is part of SE policy. The embrace of niche slang is not.

@David "tl;dr" is perfectly fine in ALL Stack Exchange sites. There's no basis to go around suggesting here and there that people shouldn't use it. If you'd like to start a new site policy, go to meta and ask "Shall we ban tl;drs in Biology SE?" and see what the rest of the community thinks.

To get back to the topic - surely the problem with the higher concentrations is osmotic effects rather than an inhibition of growth as such.

@uhoh wrote “tl;dr is perfectly fine”… …except that it is unnecessarily incomprehensible to a section of native English-speaking qualified biologists. I have not sought to ban anything, nor would it be within the remit of this site to do so. If I migrated this topic to Meta it would not be to micromanage people’s vocabulary, but to explain my view of the practical implications of the principles already adopted by SE to help them implement them theirselves. I have already made myself clear in this particular case, and SE Biology will not disintegrate if the poster chooses to persist.

@bob1 that's a good point. I'll add something.


text:
Do sharks possess a more hydrodynamical shape than dolphins?
I do not study biology at all. Is it known if sharks who evolved over milion of years have more hydrodynamical shape than say e.g. dolphins who evolved for much shorter time. It probably depends on many factors e.g. how fast on average a predator swims, strategy of hunting etc. I think marlin have quite hydrodynamical shape. Generality of this question (which I do not want answer) is how fast evolution produce certain quality. It probably is not a gradual process, I think.
To sum it up: my question is about hydrodynamical shape of body of two species (sharks, dolphins). And second part is: if time of evolution of given species plays a role in hydrodynamical shape?

You really need to do some physics to determine whether sharks are in fact more hydrodynamically efficient than dolphins.  Then you need to consider that hydrodynamic efficiency is not the only factor at work.  Sharks have evolved many variations over the ages, e.g. https://www.fieldmuseum.org/blog/four-fossil-sharks-are-cooler-megalodon  And is the modern hammerhead shark all that hydrodynamically efficient?

Try SE Engineering for questions on hydrodynamics. A separate straight question on evolutionary timescales in relation to trait development would be appropriate here. And if you want to post on scientific sites you need to remember the English you were taught at school. Interrogatives by inversion in the present tense went out several centuries ago except in poetry and didactics. It’s “Do…” (See my correction of the title.)

@David: OP may have English as a second language, or may have other language problems (and not be lazy/forgetful). Editing to correct grammar seems fine; giving questioners a hard time about grammar seems inappropriate.

@BenBolker I have lived or worked in France, Germany, Italy and The Netherlands. The worst possible thing is when people do not help you improve your language by not correcting you. You do not learn, and the implication is that they do not think you are worth the effort of teaching. Have you ever been in that position? Of course the questioner is not a native speaker. I have pointed out to him the specific grammatical details (present tense — "have you seen" works) and literature ("See ye not?"). I have supervised non-native speakers' theses.  I am helping him. (And some people need kicking.)

The question has 3-4 related questions which are all different and very broad, and some mistakes like calling sharks and dolphins species. The fastest sharks are faster than the fastest dolphins, while using less energy, 70kph vs 56kph, while a slow shark is the Greenland shark, top speed at 2.6kmh in cold water, it can live 500 years in deep seas. I can give a good answer to this but not on this forum, consider asking on reddit askbiology/askscience for the leisurely questions.

@David I wasn't suggesting not making the corrections, or even not pointing them out. I was suggesting a slight moderation of tone (which is admittedly tricky).


text:
What is contiguous premise culling and dangerous contact culling?
I am reading this paper related to FMD (foot and mouth disease) epidemics which occurred in UK. It mentioned about terms like IP (infected premise culling), CP (contiguous premise) and DC (dangerous contact cull). IP is the mandatory slaughter of all livestock on an infected premise. But what is CP and DC?

Dangerous Contacts were defined as premises where animals have been in direct contact with infected animals or have, in any way, become exposed to infection
Contigous Premises are defined as a category of dangerous contacts where animals may have been exposed to infection on neighbouring infected premises

Tildesley, Michael J., et al. "The role of pre-emptive culling in the control of foot-and-mouth disease." Proceedings of the Royal Society B: Biological Sciences (2009): rspb20090427.

Oh great. This helped me a lot.


text:
Can someone suggest me good opencourseware links for learning computational biology basics?
My internet is slow and I have only 1GB data usage allowed for this month. And I want to make maximum out of it for learning some basics of computational biology.
Which are the best online course (freely available lectures) suggestions for me?

coursera has some good courses!

MIT-OCW also has decent video lectures.. Bulk download the videos and watch them on your player..

ok let me see. But internet is expensive for me still. :(

http://ocw.mit.edu/courses/health-sciences-and-technology/hst-508-genomics-and-computational-biology-fall-2002/audio-lectures/
Download all the slides if you want good resources.

OK let me see those.


text:
A Genetic linkage problem
I have recently switched from electronics to computational biology. So having some hard time with my homeworks. Can someone guide me on this problem?

Consider 6 genes A,  B, C, D, E, F, G. Some recombination rates are
  given between these genes AB = 0.2, BC = 0.1, AC = 0.25, AD = 0.5, BD
  = 0.5, DE = .1, AE = 0.5 ,EF = 0.1 ,DF = 0.15.
a) Find the number of linkage groups? b) Construct possible genetic
  map showing relative positions of these genes?

http://hos.ufl.edu/sites/default/files/courses/pmb5056/2012_16_Linkage%20paper%20to%20post.pdf

Please show the efforts that you put into solving the question.

@TheLastWord : OK I did it alone. (ABC and DEF in different chromosomes, certainly distance matters)


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How to measure the total number of cells in an average human body?
I have got one assignment to calculate the approximate sum total of all cells in the human body. How to tackle this problem? I know that the current statistics is $10^{13}$ cells. I wanted some hints.

@kmm Actually I don't know where to start.

yes I calculated it by dividing the volumes. Volume of average human body / avg. volume of a mammalian cell. Around 10^14 cells.

So that's larger by only one order of magnitude. Not that bad for a rough approximation.

This is a classic Fermi estimation problem. The usual approach is to estimate the volume of a body, estimate the volume of a cell, and divide one by the other, remembering of course to have both volumes in the same units.
My quick attempt gave 1013 to the nearest order of magnitude.


text:
How can I interface cAMP signal or membrane potential from slime mold to an electrode?
I am very much interested in measuring cAMP (cyclic adenosine mono phosphate) signal and membrane potential from amoeba. Since I want to try this as a hobby, what are the basic steps I must do to view these signals on a CRO (cathode ray oscilloscope). Cyclic-AMP being a biochemical, how can I view it as a corresponding electric signal?

For cAMP there is only one electrophysiological technique I've found.  You can use cyclic nucleotide-gated channels in the cell as a secondary indicator of cAMP activity.  When cAMP increases in the cell, these channel will fast gate which you should be able to pick up.
The issue is standard CNGC's are not overly sensitive to cAMP and are typically more sensitive to cGMP.  But there have been mutants created that have a high affinity for cAMP.  You can transplant these in and have an easier time with the detection.
This paper goes into a a lot more detail on it.

What do "fast gate" mean here ? Also how can I convert this biochemical signal to electrical so that I can see in a CRO?


text:
Reference request: Lipid composition in bacterial, yeast and human membranes
I would like to know about the lipid composition of different kinds of cellular membranes. I remember going through such a table once in a paper, but I am unable to find it anymore. What I am looking for is a kind of tabular data which shows the percentage of phosphocholines, cholesterol, sphingolipids and other kinds of lipids organism-wise (and if possible tissue/organ/organelle wise wherever applicable).
So please share the papers/links/books etc where I may find this information. Thank you.


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Indicators of Ras binding domain (RBD) activity in Ras effector proteins?
Ras family based small GTPase proteins usually have a Ras binding domain (RBD) in their effector downstream proteins like Raf. Roughly Ras proteins cycle between active(GTP-bound situation) and inactive(GDP-bound) states. So what information is passed onto RBD when Ras protein is active in a Ras:Raf complex. It is well known that Switch-I , Switch-II root mean square fluctuations(RMSF) of inactive Ras protein is very high. In the active Ras case the Switch-I RMSF falls by making that loop rigid.
So my question is that is there any observables like RMSF of RBD region indicate the "activity" of effector molecule(like that of Raf). In other words how do I understand that the RBD region is active/inactive (say from simulation perspective or experimental perspective) ?
Please suggest me any related references or links.


text:
Why does throat 'burn' when you've got a common cold?
Apart from pain when swallowing, there's also a persistent feeling of throat 'burning' in the same area.
What causes it and why does it feel that way?

@Brian well yes, pretty much the same.

I guess it is because the throat is sore, thus probably inflammated. Inflammations are hot. Though, I am not a doctor.


text:
The least complex animals with ability to dream
People can dream, dogs can dream, cats probably too when they are sleeping.
What about other creatures?
Can a bird dream?
Do rats have dreams?
Are there any studies about that kind of thing? What is the most simple organism that have brain structures that allow them dreaming during the sleep?

Why has this question been downvoted ?

Yes why has it been downvoted? at least comment feedback to suggest improvement...

Since mammals all share the same neural structures it is quite likely that most non human species dream, but as yet, the simplest animal I could find that has been scientifically demonstrated to dream is the rat, as proven by Massachusetts Institute of Technology (MIT).
MIT not only established that rat were capable of dreaming about the events they had experienced while awake, but that the content of the dreams could be manipulated with audio cues the rats had been trained to respond with in a specific way.
Sources:
http://en.wikipedia.org/wiki/Brain#Mammals
http://web.mit.edu/newsoffice/2012/neuroscientists-achieve-dream-engineering-0902.html

At least one study from University of Chicago showed that birds dream...about singing.