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How does aminoacyl-tRNA synthetase recognize different tRNAs?
There are about 20 aminoacyl-tRNA synthetases, one for each amino acid. Each aminoacyl-tRNA synthetase has a binding site that recognizes a specific amino acid, and other binding areas that recognize a particular tRNA through unique identity sites at the acceptor stem and/or anticodon loop of the tRNA.
When there are different tRNAs for the same amino acid, the aminoacyl-tRNA synthetase that recognizes a specific amino acid must also recognize the set of tRNAs that can be charged with that amino acid. Given that all tRNAs have different anticodons, how does the enzyme achieve the aforementioned task?

https://www.ncbi.nlm.nih.gov/books/NBK22356/#A4154

like you already said: each aminoacly-tRNA synthetase has 'binding areas that recognize a particular tRNA through unique identity sites at the acceptor stem and/or anticodon loop of the tRNA' - the anticodons only thing that are needed/used for the recognition

You give the answer in your question:

binding areas that recognize a particular tRNA through unique identity sites at the acceptor stem and/or anticodon loop of the tRNA.

The point is that aminoacyl-tRNA synthetases that recognize tRNAs with different anticodons have to supplement any partial codon recognition with recognition of common features elsewhere, in particular the anticodon loop. Unfortunately this has evolved on a case-by-case basis and there is no simple ‘code’ one can refer to.
Thus, Berg et al. (Chapter 29), in discussing  threonyl-tRNA synthetase, write (my emphasis):

As expected, the CCA arm extends into the zinc-containing activation
  site, where it is well positioned to accept threonine from threonyl
  adenylate. The enzyme interacts extensively not only with the acceptor
  stem of the tRNA, but also with the anticodon loop. The interactions
  with the anticodon loop are particularly revealing. The bases within
  the sequence CGU of the anticodon each participate in hydrogen bonds
  with the enzyme; those in which G and U take part appear to be more
  important because the C can be replaced by G or U with no loss of
  acylation efficiency.

The four codons for Thr are ACN, so in this case recognition of two bases of the anticodon will identify all tRNAs.
A diagram from Berg et al. showing the multiple interactions in threonine tRNA-synthatase is shown below.

Hi David, thank you for your answer.     I was wondering, when different codons code for the same amino acid, it is because these codons differ in the 3rd base, not the first. So wouldn't the interactions between the first 2 bases of the tRNA anticodon be more important than the 3rd base? I am operating under the assumption that each enzyme recognizes a specific amino acid, and the set of tRNAs which the amino acid is supposed to be attached to, but the anticodons of this set of tRNAs differ in the 3rd base.

@JonathanSmith — The confusion here is caused by using first and third, rather than 5' and 3'. Thus the codons for threonine are 5'-ACN-3' (with N, the ‘wobble’ base), whereas the tRNA anticodon that Berg et al. refer to is, in my opinion, best written 3'-UGC-5', so that the complementarity to the codon bases is evident. (Strictly they are correct to write CGU, as the direction is assumed to be 5' to 3', but in a text book every effort to make things clearer is appreciated by the reader.)


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Does male or female DNA contain more information?
I wonder if the male or the female DNA contains more or less information than the other?

Related: https://biology.stackexchange.com/questions/57479/do-men-and-women-have-the-same-number-of-genes

Define "information" — females have more base pairs and more individual genes because X's are larger than Y's, but males have a large number of unique loci and thus unique genes, because they have an X and Y chromosome.

source: Stack Exchange

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Can controlled dose of Codeine improve brain's functionality?
What I know so far about drugs (codeine, heroin, etc) is, the first time you take them you will feel better, think sharper, and act better, just like a supercharged engine. But as this goes on a regular basis, it will stop being efficient and causes addiction.
So what I can understand of this, is that our brain can function better but for some unknown reason (to me) it doesn't. However its functionality increases for a period of time after you take a dose of these drugs.
Now I have a few questions about this:

If our brain can function faster than normal, then why it demands additional drugs to do so?
Can we inject a controlled dose to brain (not by needle to the brain obviously, I mean pills, tablets, etc) of these drugs to keep the brains functionality at a higher rate?
When a drug actually charges our brain, is it taking any damage? The same way you overclock a CPU and it might cause damage to it over the time.

PS: I'm asking this on Biology instead of Health since I'm talking about brain's behavior about addiction, not just to confirm whether or not i can use drugs on a regular basis.

What on earth makes you think heroin will supercharge you? Ever looked at a person under influence of heroin? I have. And the last thing that comes to mind is charged. Burnt out gets a lot closer.

@BryanKrause, really, your comments are as good as any answer will ever get on this question :)

@AliceD I suppose I could move them to an answer, though I don't really feel like tracking down citations etc for all of this. I guess I'll do it and let people decide if they want to upvote or not.

@AliceD Take a look at someone who is on a dose of heroin for the first time. And see what happens to them in the first half an hour. Also I like how some people zoom in 6 letters of a 4 paragraphed question, to find something to criticize in the comments.

the first time you take them you will feel better, think sharper, and
  act better

You are probably thinking of amphetamines, not opiates. Militaries have used amphetamines for just that purpose for decades, particularly for situations where long periods of attention are necessary. The problems are addiction, adaptation (lessening effects over time), withdrawal, side effects, etc.
Caffeine has very different cellular effects, but is also a stimulant, albeit a much weaker one. People around the globe use caffeine to achieve much of what you are suggesting on a daily basis. I actually think caffeine is a great example of what you are proposing, because (at least for people who tolerate it well and don't have any other conditions) it is safe, effective, and has less serious withdrawal symptoms and is somewhat less addictive than many other drugs. That said, among people who use caffeine regularly, some of the benefits begin to wane, and people start needing caffeine to maintain their normal level of alertness.
People with ADHD (and some others without, particularly students) also take amphetamines to help with attention (Adderall is an amphetamine; Ritalin/methylphenidate is closely related). There is a bit of controversy over whether that's a good idea or not. All of these things have side effects, including potential for changes in personality, anxiety, and various peripheral side effects, as well as the risks of dependency and symptoms of withdrawal.
Codeine and other opiates, on the other hand, are primarily useful for blocking pain. They are often associated with euphoria, but their other psychological effects are mostly depressant: drowsiness, respiratory depression, suppression of gut motility leading to constipation, etc. I'm not aware of any cognitive enhancement from codeine, unless the cognitive task you are trying to perform is sleep.

Thank you for the answer. I get migraine attacks once in a while (a week or so) , and i use a low dose of codeine to fade it away. I feel the drastic effect of it on my mood every time. It just makes me do anything faster, better, and more accurate, however i don't stick to it since I don't want to be dependent. Does the effect wane after a while because the blood contains more of that substance by using it over and over?

In general, though there are always exceptions, tolerance occurs because of down regulation of receptors for a drug, or compensatory up-regulation of other proteins. If you suffer from migraine headaches and codeine helps your cognition, that's probably mostly from the relief from the migraine. Tolerance is usually best avoided by keeping doses low and infrequent. Sometimes infrequent dosing can encourage addiction, but if doses are low and only used therapeutically, that is less likely.

I actually tried a codeine tablet once, when I didn't have an attack. It warms the head and you know... felt way better than a smoke or 2 cups of black coffee. I don't take the pill unless the pain is unbearable, since being addicted is the last thing I would ever want ;)

That's called "euphoria" and that's basically why people get addicted to things like heroin. Especially when injected, so you get it into the bloodstream quickly, it gives a really fast immediate euphoria, much better than a codeine tablet would do. Doesn't make you better at anything, just feels really good. It basically hijacks the brain's reward system and goes right to that high. The problem is, people end up chasing after that high the rest of their lives sometimes, and they can never get it back because it won't beat the first time, unless they use more and more.

Exactly that is the point of addiction. More and more. But for example when I can't concentrate, it really helps me focus quickly and resolve a problem (math for instance) that I'm stuck in at for a while. I'll mark it as accepted a while later to encourage other answers. Gratz!

From your comment I took a brief look through recent literature on codeine and cognitive abilities in case there was something I was unfamiliar with...all studies I found showed either a mild impairment or no effect of codeine (on measures of things like attention, memory, alertness, vigilance, at therapeutic doses for pain/cough). There aren't any studies that show enhancement. Just be cautious in case the euphoric effects are tricking you into thinking you do better on the codeine.

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Why are proteins in the insoluble form when they are in frozen water?
Why would lowering the temperature of water change the intermolecular forces so much that proteins once soluble in water, become insoluble? I know freezing can create a crystal lattice, but I don't see how temperature would connect to the inter-molecular forces of water? If it even does?
EDIT:  So why would a temperature decrease change how a protein interacts with a POLAR solvent

This answer is about cold denaturation of proteins rather than the effect of freezing.
The folded structure of a protein is thermodynamically stable as a result of a small favourable difference between the free energies of the folded and unfolded states. For a small single-domain protein this difference is usually only equivalent to the strength of a small number of hydrogen bonds - folded states are not very stable.
Electrostatic interactions, hydrogen bonds, and van der Waals interactions within the protein, interactions within the solvent, and interactions between the protein and the solvent all have to be considered, together with any entropic effects.
One factor that plays a part is the effect that an exposed non-polar group from the protein can have upon the solvent. Because the water molecules next to such a non-polar group cannot form hydrogen bonds with it they become more ordered or ice-like as they can only hydrogen bond with each other. This is the basis of the hydrophobic effect - as a protein folds and sequesters its non-polar groups in the protein interior then the unfavourable entropy change in the protein (i.e. it has become more ordered) is offset by the increased disorder in the water.
As the temperature falls the water becomes more structured anyway, so an increase in entropy of the water is no longer available to offset the decreased entropy of the folded polypeptide. The thermodynamic balance sheet is altered and the unfolded state is favoured.

If proteins change from being water soluble to water insoluble it means that their three-dimensional structure changed, because this determines how the protein interacts with the water. Most proteins have hydrophilic residues on the outside in their normal structure configuration, which makes the soluble. If this changes and some of the hydrophobic residues come to the protein surface the protein may not be soluble anymore.
The process of the structure changing (sometimes also called 'denaturing') can be caused by a lot of different factors - basically everything that is different from the inside of a cell (for humans: ~37°, salt concentrations, ...). If water freezes then the ice-crystal lattice can force the proteins out of their normal conformation/structure, after thawing the ice they may not get their structure back on their own (this depends on the protein).
To give an answer to your edit: the temperature does not affect the solubility directly, the effect is indirect through a change in structure

I am asking what physical and or chemical properties of the water and or the protein. make a protein go from being soluble to insoluble in a POLAR solvent such as water. Regardless of the temperature of the solution, the solvent remains polar. So why would a temperature decrease change how a protein interacts with a POLAR solvent

@Confusedbyeverything I already explained that: the change in temperature/crystal formation changes the structure of the protein, this in turn changes which residues of the proteins interact with the water/solvent, which changes its solubility

Here is my confusion: how do the changes in the temperature/crystal formation change the structure of the protein and why would this favor the formation of an insoluble form ?       I understand how PH, salts, inter-molecular forces, can effect protein folding. I can even understand how temperature can denature a protein by offering it more energy to undergo different chemical reactions, but what is the underlying concept that explains the change from soluble to insoluble when we decrease the temperature?          PS I am not a chemistry major so thanks in advance


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

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

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

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

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

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

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

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

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

@Anonymous did you actually read my answer?

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

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

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

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

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

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

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

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Why does high EDTA concentration cause swelling of platelets?
According to this textbook, high ( >2mg/ml of blood) EDTA concentration causes swelling of platelets which lead to their fragmentation.
I know that high concentration of EDTA increases plasma osmolarity which leads to cell shrinkage , as is the case in all other blood cells, but why does it have opposite effect on platelets? Why osmotic effects aren't seen in platelets?

what does 'high' mean in this context?

Edited the heading.

I followed the link- apparently >2 mg/ml EDTA has this effect.

Oh, you mean the context in that way. Ok I will add it.

That's ~5 mM. Is that really enough to have an effect on osmolarity?

But the same concentration is having osmotic effects on other cell, for instance RBCs.

Is it having an osmotic effect, or some other effect?

I think it's osmotic effect, because if were some other effect then why would it not affect when it's concentration is less?

I should warn you that I have no idea what the answer is, these are just some thoughts I had. Could it be related to the chelation?

As it's reported in an old 1968-article by J. G. White:

Chelation of membrane calcium by EDTA appears to cause marked
  irregularities in the platelet wall and massive swelling of the
  canalicular system. Swelling of internal channals is the dominant
  alteration in EDTA platelets, and this change appears ultimately to be
  related to the breakdown of platelet granules.

Many articles followed the one reported above, but it seems that the main cause of platelets swelling in presence of EDTA is the reduction of calcium levels that causes a sort of platelet activation.
This acivation could also be linked to direct EDTA action as reported in this article by Golański et al.:

The influence of EDTA on platelet membrane dynamics closely mimicked
  the alterations induced upon the interaction of fibrinogen with
  platelet GPIIb-IIIa. Thus, the EDTAK2-induced platelet activation
might result from an interference with platelet membrane protein
structure and conformation and possibly relate to an “unspecific”
  trigerring of a signal transduction pathway.

Anyway in normal conditions the laboratory platelet volume quantification using EDTA tubes seems not to be affected if executed in 1 hour since the collection (as reported in this article by Dastjerdi et al.).

I like the answer but I'm a bit hesitant on the idea that this is a sort of platelet activation (I may be wrong)...my recollection is that calcium increase is necessary for activation. Maybe a morphological change similar to activation is occurring through a separate pathway? I don't know for sure but maybe you can clarify a bit?

@Bryan Yes. You are right , platelet activation requires increase in intracellular calcium levels, which is initiated by entry of ecf Ca2+.

Why doesn't it show osmotic effects while other cells show?

@JM97 maybe EDTA has osmotic effects but there is are greater effects that hide it

@BryanKrause added a quote to better explain this "sort of platelet activation"

I think your question is relying on two completely different definitions of "high" EDTA. Really, both concentrations are "high" but one of them is "really really high."
The only references (for example, here or here) I can see that say anything about osmotic effects of EDTA is in the context of blood sample collection, and specifically when too small a volume is drawn into a larger tube, for example 0.5mL blood in a 5mL tube. In this circumstance, a ~liquid (blood) is added to solid EDTA powder sitting in the tube. This is already a high concentration of EDTA, it's enough to mop up all of the calcium around to prevent coagulation.
However, if you only fill the tube 10% full, there is 10X more EDTA powder pre volume than necessary to prevent clotting. This isn't just high, it's incredibly high. EDTA is usually as a potassium salt in this context, so that could be as much as ~100mOsm which would definitely cause osmotic effects, but that's on the order of a 10-fold higher concentration than your reference for platelets (which I can't access unfortunately). When you state in your question:

I know that high concentration of EDTA increases plasma osmolarity which leads to cell shrinkage

...this seems to be the best explanation, unless you can show another reference that demonstrates substantial cell shrinkage at lower (~2mg/ml) concentrations. I'm not saying there can't be some osmotic effect at that level, just that it would only be a couple percent of cell volume and would not be noticeable on anything but the finest assays.
Then on the other side of the equation, the effects on platelets are not to do with osmotic effects but rather due to a somewhat paradoxical activation of platelets, as in @DavideN's answer. Think of platelets as cells that are "primed" to expand when needed to stop a bleed; in some circumstances, it seems like EDTA can be a trigger for this process to occur, though not in others (again, see @DavideN's conflicting references).

References:
Goossens, W., DUPPEN, V., & Verwilghen, R. L. (1991). K2‐or K3‐EDTA: the anticoagulant of choice in routine haematology?. International Journal of Laboratory Hematology, 13(3), 291-295.

So when EDTA is >2mg/dl( not 10x the required amount but slightly higher) it's causing swelling of platelets due to chelation of membrane calcium, but is causing shrinkage of other cells. If  this shrinkage is not due to osmotic effects then what's the reason for their shrinkage?

I think in this answer you're talking only about osmotic effects, and you are not giving a different answer to the question.

Anyway looking at guidelines (e.g. CLSI), in case of incomplete filling using standard K-EDTA tubes (as many other types of tubes) is cause of sample rejection and no tests should be done on that.

@JM97 Do you have a source for EDTA~=2mg/ml (not dl) causing obvious osmotic effects in non-platelets? I think there are two answers to your question: DavideN's, which answers "why do platelets swell" - they don't really swell, they go through an unspecific triggering of platelet activation, and mine, which answers "why don't platelets show osmotic effects."

@DavideN Yes I think your answer is good for telling why platelets activate, but the original question also asks: "Why osmotic effects aren't seen in platelets?" I'll edit my answer to be a little more clear, but I think the problem is the OP's question is erroneously conflating two definitions of "high" EDTA.

@DavideN And thanks for catching the university link...I really wish publishers had more standard URLs, that's the first time that's happened that the library account got carried through to the final URL.

"Anyway looking at guidelines (e.g. CLSI), in case of incomplete filling using standard K-EDTA tubes (as many other types of tubes) is cause of sample rejection and no tests should be done on that." Yes definitely. But I can't see any support for the OP's assertion that EDTA causes (clear) osmotic shrinkage of cells in any other situation but this.

@BryanKrause No, I don't have any source for that, my textbook just states that other cells just shrink( and the reason for that shrinkage is osmotic effects, was my speculation). After reading your answer I see that some other mechanism is also involved in obvious shrinkage of those cells.


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Is it possible to make bones ossify much slower in adults?
According to Can we artificially increase human growth using HGH,

But during normal human development bones ossify in the process, and in human adults the bones are completely ossified and can't grow in length anymore.

Is it possible to make the ossification process much longer?

Your question title and body don't match. I think you might be misunderstanding the statement. It isn't saying that bone can't ossify in adults and therefore it can't grow, it is saying that because they have already ossified they can't grow. Ossification is basically hardening; completely ossified bone is completely hard and has nowhere to grow from. Ossification can still happen in healing bones in adults after a break, however.

I do understand, but just missed the "not" in the question. Thank you!

Ah yes, that changes the meaning entirely, much better now!

I think what you are asking about is delaying the closure of cartilage growth plates, so that bones continue to grow longitudinally for longer.


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Cat's tail movement as an indicative of tension
It appears to me that tail's twitching in the cats indicates how much tension the individual is under. During a hunt, when a cat tries to stay invisible, while approaching a target it is almost immovable, yet the tip of the tail keeps on moving restlessly.
Is there an explanation for such a behavior? How does it help?

No idea of the biological explanation but as someone who 'knows' / grew up with cats yes, it seems exactly like that
Tail lashing is a sign of stress, mild beating is mild irritation and so on
Often a growl will be followed by beating the tail
Anyone can guess at the reasoning but I' say it's not unlike a person tapping or drumming their fingers or hands - depending on the strength it can mean different levels of annoyance and different 'messages' but I assume they're satisfying the same urge that makes people pace or drum their fingers while waiting / annoyed

According to Desmond Morris in Catwatching: The Essential Guide to Cat Behaviour, a cat wags its tail when...

The cat is in a state of conflict. It wants to do two things at once, but each impulse blocks the other. (emphasis mine)

Then, some pages after that, Morris talks about what he called the dilemma of the suburban cat hunting a bird on a lawn:

To start with, the open, manicured lawn robs the cat of all its natural cover, exposing its whole body to view. This is doubly damaging to its chances. It makes it almost impossible for the cat to creep near enough for its typical, close-quarters pounce without being seen. This puts it into an acute conflict between wanting to stay immobile and crouched, on the one hand, and wanting to rush forward and attack, on the other. The conflict starts its tail wagging furiously, and the same lack of cover that created the conflict then cruelly exposes the vigorous tail movements to the frightened gaze of the intended prey. (emphases mine)

That being said, your observations are probably of urban cats in this kind of conflict, in a situation where a successful attack is almost impossible. It's the conflict that makes the cat wag its tail and, as you can see, this behaviour doesn't help the cat at all.
A feral cat in the wild, in a effective attack, will not wag its tail.

Agreement with Geraldo's that a cat experienced in hunting doesn't do the conflicted tail wagging. On a number of occasions, I've watched cats who weren't feral but were experienced hunters and they simply get down to business when hunting. No tail wagging.


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Isoelectric point of aspartate

On the 3rd diagram (from left), the one with net charge = -1 ,
Why did it lose the H to OH- from the CH2CO2H from the neutral form ?
I was told that while moving to the right , the OH- will take H+ electrons meaning it should take H+ from NH3 .. ?
Is there any reason why they took the H from CH2CO2H ?
Any help would be appreciated!

The -CO₂H groups are carboxylic acid groups, better represented as -COOH. These, being acidic, have a lower pKₐ than the -NH₃⁺ group and so as the pH increases these -COOH groups lose their protons first.
The pKₐ values for the three are shown below the arrows: as you can see the α carboxylic acid is more acidic than that in the side chain, but they are both much more acidic than the protonated amino group.


text:
Can enzymes catalyze thermodynamically unfavorable reactions?
Can biological enzymes catalyze thermodynamically unfavorable reactions? I read that an enzyme lowers the activation energy of a reaction by offering an alternative reaction pathway with a lower activation energy, however the ΔG of the reaction is unchanged. If enzymes can do this, then how exactly does this work?

I've deleted the comments as the question has an accepted answer and flags started to pour in. Please go to chat to resolve outstanding matters, if any. They served their purpose as a few good quality answers are in place now. Q and A's also seem to be on the same page now in terms of the can and how issue.

"I read that [...]" - for completeness, could you add where you read this?

I read this in my school homework question, hence the tag. But there's a link here that mentions something to that effect: http://www.rsc.org/Education/Teachers/Resources/cfb/enzymes.htm

Enzymes can catalyze a thermodynamically unfavorable reaction by coupling it with a thermodynamically favorable reaction. Most often, enzymes use ATP hydrolysis reaction (energetically favorable) as a source of energy (in simple terms) to drive the unfavorable reaction forward. One important point to keep in mind here is that enzymes don't drive a reaction equilibrium forward or backward; they just help in achieving the reaction equilibrium faster. Also pay attention that enzyme itself does not change the thermodynamics of a reaction (as you say, ∆G of the concerned reaction remains the same, except at equilibrium), coupling of a favorable reaction with an unfavorable one only helps in making the overall reaction favorable. This phenomenon, of one reaction changing the rate of another reaction, is called induced catalysis and has nothing to do with the enzyme itself.
I will talk about how enzymes do this using examples, while the other answer talks about the semantics. An example which will help you understand this concept is ATP synthase. It is an enzyme found in the inner mitochondrial membrane which allows the movement of H+ from the inter-membrane space towards the mitochondrial matrix, using the energy of movement (since this is favorable and exergonic) to generate ATP. The reaction would look like this:
$$\ce{ADP + P_i + 3 H^+_{IMS} \rightarrow ATP + 3 H^+_{matrix}}$$ (remember that exactly 3 H+ are not required, this is a simplified version)
But, ATP synthase does not drive the reaction forward; it just helps in reaching the following equilibrium faster:
$$\ce{H^+_{IMS} \leftrightharpoons H^+_{matrix}}$$ i.e. keeping the amount of H+ in inter-membrane space and matrix the same. This is why a constant gradient is required to keep them in working condition. For this, the electron transport chain continuously throws H+ into the inter-membrane space to maintain an electrochemical gradient. Along with this, enzymes ATP-ADP translocase and phosphate carrier continuously take out ATP from the matrix and throw in ADP and Pi. However, this lowers the electrochemical gradient (exchanging ADP3- for ATP4- in inter-membrane space, while phosphate carrier catalyzes electroneutral reaction), making the final reaction: $$\ce{ADP + P_i + 4 H^+_{IMS} \leftrightharpoons ATP + 4 H^+_{matrix}}$$
However, since the enzyme just helps in maintaining equilibrium, it can also work backwards i.e. it can also transport H+ against electrochemical gradient (unfavorable), coupling it with ATP hydrolysis (favorable) to reach equilibrium. The enzyme is now called ATPase and the reaction becomes: $$\ce{ATP + 4 H^+_{matrix} \rightarrow ADP + P_i + 4 H^+_{IMS}}$$
There are many more such enzymes which couple ATP hydrolysis (or other favorable reactions) to catalyze reactions which are either unfavorable or very slow (i.e. require a source of activation energy) under normal cellular conditions. Another factor, as the other answer explains, which helps in this is changing the concentration of products. As seen above, ATP-ADP translocase and phosphate carrier continuously decrease the concentration of products (ATP) and increase concentration of reactants (ADP and Pi) so that the overall equilibrium shifts forward and the enzyme keeps on driving the reaction forward (this, again, has nothing to do with with the enzyme itself, it is called Le Chatelier's Principle). Again, the other answer focuses on this issue.
References:

Enzyme - Wikipedia
Cellular Respiration

This is at the best a misreading of the question and at the worst casuistry. If an energetically unfavourable reaction is coupled to a more energetically favourable reaction you have an overall reaction that is energetically favourable. The enzyme has nothing to do with the thermodynamics. The fact that the poster has accepted the answer implies that this answer has mislead him or, more likely, bamboozled him by giving such an unnecessarily esoteric and long example of the concept of coupled reactions which could be written as three simple A+B=C type equations.

@david Well, I reread my answer and don't find any line which says that enzyme has something to do with thermodynamics. In fact, it is this point itself, to disregard which I say again and again that enzymes only help in attaining equilibrium faster. I don't know how you concluded that point from my answer, but I don't think anybody with even basic knowledge of enzymes would get misled by my answer. Also, I don't like giving one-line answers & try to add as many details as possible. Yet, you can post an answer if mine 'bamboozles' you.

Excellent, clear answer. I don't know what David is on about, I can't see any way this answer would be misleading to the OP.

What does "Yes they can" mean in relation to an question that asks "how"? It would be good if people were encouraged to pose clearly researched and defined questions so they could be answered (or not) properly at the appropriate level.

Ah, I wrote that before editing the question, thanks for pointing out :) as for the lack of research effort, I too have voted to close this question. I just answered this because I find the question itself rather interesting and worthy to be answered. And I don't think I can do much after voting to close, downvoting, and warning about lack of research (as a matter of fact, I'll retract all these once proper research effort is shown by OP).

@David Is that really the basis of your complaint about this answer? The original question was "can" - the rest of this answer addresses "how".

Perhaps coupled reactions is what the OP was looking for, but it so that's not clear from the question. Coupling two reactions is an entirely different concept than catalysis, which simply means lowering the activation energy, so I think the wording of this answer is confusing. The correct answer is that catalysis has nothing to do with whether the reaction is favorable or not, as @David points out. (Also, ATP synthase is a rather poor example of a coupled reaction I think, as it is not fully stoichiometric; something like hexokinase would be better.)

@BryanKrause — I made clear the basis of my objection in my original comment. Roland, at least, seems able to understand it.

@Roland I don't think OP was looking for anything in particular in a correct answer. I suspect, though I don't know for sure, that the OP is trying to come to terms with two obvious facts: 1) Not all reactions in biology are, by themselves, energetically favorable, and 2) Enzymes can't change ΔG, effectively they only alter reaction rates. So how does this work? This answer clearly answers that question.

@BryanKrause  Yes, I think you're right.  I don't mean it's a bad answer.  It's just that this is a difficult topic where there is a lot of confusion in the biological sciences, and therefore I think it's particularly important to be crystal clear about the definitions.  It's not just arguing about terminology.  If one believes that catalysis and coupling are the same thing, then one might conclude that, for example, coupling ATP hydrolysis to a reaction makes it go faster ...

@tomd (and others too) why can't we...say, assume, that when OP talks about ∆G, they know the difference between ∆G and ∆G°? Also, I still don't find any line in my answer which says that enzymes do change either the equilibrium constant or ∆G°. I still don't find the answer misleading buddy, these are just the points which I did not mention.

@tomd better now? I don't get "A coupled reaction is a biochemical abstraction, without any thermodynamic 'slight of hand'"

Can enzymes catalyze thermodynamically unfavourable reactions?
Enzymes don't change the equilibrium of a reaction, but the fact that an equilibrium exists means that the reaction proceeds in both the forward and reverse directions. Before equilibrium is attained, ΔG for the reaction is not 0. Thus, by definition, one direction is thermodynamically favourable (ΔG<0) while the other is thermodynamically unfavourable (ΔG>0). Since an enzyme lowers the activation energy of a reaction, it is catalysing both the forward and reverse reactions. This is a semantic argument since the reaction will still proceed in the direction which is thermodynamically favourable.

How can enzymes catalyze thermodynamically unfavourable reactions?
Other than in the sense I described above, enzymes do not catalyze thermodynamically unfavourable reactions. However, biological systems can make unfavourable reactions favourable. In addition to the reaction coupling discussed in the other answer (sometimes referred to as pushing) thermodynamically unfavourable reactions can be made favourable by pulling. In this case, for reactions where ΔG°>0 (ie the reaction under standard conditions is unfavourable), the reaction can be made favourable by decreasing the concentration of products relative to reactants, such as by immediately using them in a subsequent, thermodynamically favourable reaction. Mathematically, the relationship between the free energy change of the reaction under standard conditions and the actual reaction is given by:
$$\Delta G=\Delta G^{\circ} +R T\ln\left(\frac{[P]}{[R]}\right)$$
As the ratio of product to reactant concentrations decreases, the actual free energy change of the reaction decreases and can be made thermodynamically favourable.
To be clear, it is not the enzyme that makes an unfavourable reaction favourable (again, it only lowers activation energy). Rather, the enzyme is catalyzing a reaction that is now thermodynamically favourable.

Sorry for cluttering your answer again, but I just love the dualistic approach. +1 it also points out a fundamental problem on the why versus how questions though. Often they seem to go hand in hand and obscuring the question core. Your approach solves matters nicely :)

Nice answer, +1! At least now I understand what I was missing in my answer ;) I've edited my answer to make clear the difference between what mine and your answers discuss :)

Annoying pedantic guy here :)  Two points: (1) I think it's a bit dangerous to argue using equilibrium, as this often leads people to think that enzymes are at equilibrium in living organisms. A lot of biochemistry textbooks do this, and it causes no end of confusion. The key point is not that enzymes "don't change the equilibrium";  it's that enzymes don't change the Delta G.  (2) Strictly speaking, the second part is not an answer to the new question, because it's not about the enzyme at all. It says "maybe other enzymes can help drive the reaction", which just shifts the problem.

@Roland (1) I'm not sure I appreciate this point, yet. (2) The answer is that enzymes don't make unfavourable reactions favourable. Then I go on to explain what can make unfavourable reactions favourable.

@Roland (this applies to your comment here and on the other answer as well) - I think the discrepancy here is between biochemistry of enzymes as functionally interesting in and of themselves, and the OP and the answers are in a different mode of thinking, where enzymes are a means to an end, part of the rest of biology. Neither approach is wrong, but for the second approach, it is still within the scope of the problem to include other helper mechanisms, because the goal is to understand the whole process, not the action of one enzyme or one specific reaction.

If we were talking about cars, in answering "how does pressing the accelerator make a car go faster?" someone could answer that "well it lets fuel and air enter the engine faster which increases RPMs and translates to torque that makes the car go fast." Then someone else says no no the accelerator pedal doesn't do any of that, that's the job of the butterfly valve and the transmission and the wheels. The pedal just signals the car, mechanically or electrically, to open the butterfly valve. Both answers are right, but at OP's level of understanding the first answer makes more sense.

@tomd,  I disagree. Reactions in living cells are not at equilibrium, because at equilibrium there can be no net flux.  The precise magnitude of Delta-G is less important, but I would say that modern studies disagree with Newsholme's 1973 textbook; see for example  http://www.nature.com/nchembio/journal/v12/n7/abs/nchembio.2077.html
Delta-G-0 is just one particular choice of units, it's not very important here. The key is that, whatever the Delta-G is for a reaction system (at steady state), adding an enzyme does not change it.

@tomd,  I did not quote you at all ...  I'm saying the conceptually important point is that enzymes are not at equilibrium in living cells, and therefore it is usually not helpful to to explain enzyme thermodynamics using equilibrium arguments. Precisely how far (or close) to equilibrium various enzymes are in cells is less important, and experimental data like Rabinowitz' paper often disagree with textbooks on Delta-Gs anyway.
But I think this discussion should be moved to chat.  When I have time I will write up an answer of my own to highlighting these issues.


text:
Is it possible to Breed an Animal to have more Females than Males?
Minute Earth talked about environmental factors that cause animals and humans to have more male or female children: https://www.youtube.com/watch?v=3IaYhG11ckA
Presuming that is accurate, I was wondering if you could artificially select for people or animals who have more children of a certain gender?
As far as I know, there are no animals that do produce notably more males than females, or vice versa, except maybe some insects.

Presuming that is accurate, I was wondering if you could artificially select for people or animals who have more children of a certain gender? As far as I know, there are no animals that do produce notably more males than females, or vice versa, except maybe some insects. natural-selection pregnancy gender

I guess this answer is accidental?

Do you have some limiting criteria for "animal". Various animals have different influences in sex determination, and some have factors that are easier to adjust than others (e.g. some amphibians and reptiles will have an entire nest of eggs result in one gender based on temperature, which isn't an influence for mammals).

@HarrisWeinstein The question is related to a fictional race of reptiles (snake based), so that's pretty relevant. It's a story about the Naga, said to be spirits of rivers and snakes (like a centaur or mermaid, upper body human, lower body snake). I also wanted to learn about the subject in general, as I was taught that all creatures have a 50/50 split in gender.

Yes.
 What you are looking for is a meiotic drive, it's a genetic factor that favors its own transmission. Sex linkage is very common in these due to sex chromosomes not undergoing recombination. Once such driver, R2D2 (I shit you not) is a Y linked gene that drastically increases the number of male offspring in a mouse that carries it, to the point it can cause a population collapse from lack of females.
Several such drives are known, none quite as drastic as R2D2.

That is awesome! Thank you, I never heard of this. If I may ask, is there any comparable gene known of in the human genome?

I don't know of any sex linked ones in humans, but there are a few other kind. https://www.nature.com/ng/journal/v31/n3/abs/ng910.html


text:
Why did evolution make people's skin dark?
Why do people living in the equator have dark skin?
I know that Melanin acts as a protective biological shield against ultraviolet radiation.
But doesn't black absorb all light in a way making the body more heated than the surroundings ?

It didn't, the basal condition for humans is dark skin, all other pigmentation patterns evolved from it. Additionally Dark skin is not monophyletic/homologous in humans,
 that is some darks skinned humans evolved from light skinned humans who in turn evolved from ancestral dark skinned humans, (Evolution made skin lighter then made it darker again in other regions). Skin dark/lightness is also well correlated with latitude (which is correlated with UV levels).

First it helps if you remember skin is translucent so even very light skin absorbs a great deal of light. Additionally black also radiated heat better than white its is a double edged sword so to speak, it absorbs heat better but also sheds it better.
But the current hypothesis about why light skin evolved is due to vitamin D. The skin absorbs some UV radiation to manufacture vitamin D. Dark skin blocks more of this radiation reducing vitamin D levels. As humans migrated into higher latitudes with less UV radiation they needed lighter skin to harvest more of it. If your skin is too light you have issues with sunburn, skin cancer, and folic acid destruction darker skin protects from these. Now in modern humans clothing and diet completely swamps these effects, so studying it is difficult. the use of clothing in humans moving into colder climates may have exacerbated this effect. The later evolution of lactase persistence could further confuse the effect.
Note that this hypothesis is controversial and only weakly supported because it is extremely difficult to test and the the multiple confounding factors.
http://evolution.berkeley.edu/evolibrary/news/140305_skincolor
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3024016/
https://www.ncbi.nlm.nih.gov/pubmed/16766240
https://dl.dropboxusercontent.com/u/38568440/admixture/shriver01.pdf
https://en.wikipedia.org/wiki/Human_skin_color

Thanks for shedding light on how skin types evolved. But  the question asks why black ? Why did people from hot parts of the earth have black skin when we know that black absorbs heat making it uncomfortable. Why did evolution occur this way? http://scienceline.ucsb.edu/getkey.php?key=3873

@nishanthmenon maybe you are forgetting that its (comparatively) easier for our body to deal with heat than to deal with skin cancer. So which one is on high priority in our preventions list?

@another'Homosapien' maybe you should read the question properly. I know that it saves and protects us from UV rays, but the question is why Melanin causes the skin to become darker and not lighter thereby solving both the issues at once.

@NishanthMenon Melanin is a brown-black pigment. How would it make the skin become lighter?

@nishanthmenon in a way, that'd be asking why chlorophyll is green, hemoglobin is red or why water is colorless. Thats nothing about biology, but about the optical properties of the compound. Melanin makes the skin darker becuase melanin itself is dark. BTW your question's first line says, "Why do people living in the equator have dark skin?" No offence but...

@NishanthMenon dark skin does absorb heat better, but it also sheds heat better, so it warms up faster but also cools down faster, but really since skin is translucent and not opaque it really doesn't matter much the color has a much weaker effect on temperature in a translucent media .

Good answer, @John, but this is technically wrong: "dark skin is not monophyletic..." Monophyletic refers to a group, not to a feature. You probably meant "dark skin is not a homology...".

@GerardoFurtado It can also refer to a group defined by a feature, but your right homologous would be better.


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What is the genetic explanation for gall forming in erythrina by gall wasp?

http://www.cabi.org/isc/datasheet/46220
Gall wasp  layed egg in the stem of the erythrina variegata,  the larva make gall, I like to know how the gall formation occurs in erythrina variegata


text:
Human's capacity to withstand extreme heat in dry air
What is the maximum temperature a human can withstand for short periods of time in an environment with dry air (e.g. oven @+300F, other confined spaces) and what would be the immediate risk of being in such environment be (lung damage, core temperature, etc.).


text:
Neanderthal/Human Genetics
"According to preliminary sequences, 99.7% of the nucleotide sequences of the modern human and Neanderthal genomes are identical, compared to humans sharing around 98.8% of sequences with the chimpanzee."
https://en.wikipedia.org/wiki/Neanderthal_genome_project
What precisely is the issue with the supposed 2-4% of Neanderthal genetic material, how does that connect with the general near-total-identity of genetic material?
Does the 2-4% refer largely to analysis of haplotypes, which I take to mean clusters of alleles/ groups of specific traits, which reveal direct contact between the populations?

Related: Why are the genomes of Humans 99.5% the same?

The 2-4% of Neanderthal genes refer to alleles, as you guess.  If, for a super simplified example, a human genome has
ALLELE_1__ALLELE_2__ALLELE_3__ALLELE_4__ALLELE_5__ALLELE_6__ALLELE_7
and the Neanderthal equivalent had
ALLeLE_1__ALLELE_2__ALLELe_3__ALLELE_4__ALLELE_5__ALLELE_6__ALLELE_7
(note the two lower-case 'e's), then they are 97.1% identical (67/69 characters), but if we sequenced a human and found
ALLELE_1__ALLELE_2__ALLELe_3__ALLELE_4__ALLELE_5__ALLELE_6__ALLELE_7
then we might infer that "ALLELe_3" came from Neanderthals and that that genomic region was 14.2% Neanderthal (1 of 7 alleles).
(Obviously with only 7 alleles there would be other interpretations, but I don't feel like typing out 10,000 alleles right now.  You can see how you'd get enough information in a longer stretch of DNA.)
This is exactly the same as when you say "Half of my DNA is from my father and half if from my mother."  Obviously (one hopes) your parents were both human, and their genomes were virtually identical, but it's still possible to identify -- through allelic variation -- which segments came from which side.


text:
Why females don't have much sexual desire when compare to males?
I read this Wikipedia article about Playgirl, It is made especially for females. but Its Spokesman Daniel Nardico revealed subscriptions are generated more from males.

In a February 2010 interview with the Associated Press, Playgirl
  spokesman Daniel Nardico stated that he considers the magazine
  appealing to both men and women, although the audience is
  predominantly male

I found another source here to claim,

They did not find a single study that showed that women had a higher    sex drive than men.
But Majority found that men had higher drive than women.

Why females don't have much sexual desire when compare to males?

Welcome to Biology.SE. In order to ask Why, one must first show that the claim is true or instead start by asking whether the claim is true, otherwise the question must be closed as opinion-based. I am afraid that a wikipedia article about Playgirl reporting an interview with a nightlife impressario is most definitely not an evidence that females have less sexual desire than males. I am voting to close as off-topic because it is opinion-based

In fact, if you just google Do females have more sexual desires than males? you'll get plenty of hits like this one, which although they don't cite a peer review paper rather suggest that your claim is wrong.

Where did you get the hypothesis from that more male subscribers for a magazine equals less sexual desire for females?

@Remi.b I added another source link to claim it, still is it closed?

Males often have more desire from a distance, but up close they turn cold. The opposite applies to females.

@The two added quotation seem to come in opposition.... I am definitely not convince yet that it would be true that females have less sexual desires than males.


text:
How are hereditary neural circuits created in the brain during early development?
Whilst our experiences shape the specifics of our brains throughout life, we know that there are a lot of shared properties between us. We all share the same basic layout as, for example, the V1 cortex is always in the same place. Thus it is evident that whilst some of the neural development is experience-dependent, some of it is hereditary/genetic or "hard wired".
It would seem to me that the extent to which the brain is "hard wired" depends on the species. Humans seem to have a lot more room for specialisation in life, whereas some animals don't exhibit much individuality, tending to follow very regular behavioural patterns that have no doubt evolved over time, subject to natural selection.
I have read up to some degree on how experience-dependent development works, but have been largely unable to find any detailed research into how experience-independent development works. That is, how does DNA encode these "hard wired" neural circuits?
Furthermore, the human brain contains some 100 billion neurons. If I assume that maybe 1% of them are "hard wired" into circuits from birth, that's still a billion neurons, each with several connections to other neurons that need to be somehow coded into a DNA sequence which only amounts to a couple of gigabytes worth of data. So how is the complex structure of these "hard wired" (experience-independent) neural circuits encoded in such a limited amount of DNA? How much of the brain is actually hard wired in this way and how much is open to experience-based development? Am I right in associating this process with the phenomenon of "instinct", that is, "hard coded" behavioural patterns in animals which appear to be hereditary?
Is there a name for this field of study? Specifically the study of how neural circuits are generated in the earliest stages, to lay down the high level structure of the brain before experience-based development can take over?

To be as clear as possible. If the brain developed completely independently through experience, then we would all have a different neurological "layout". The fact that the large scale structure of the brain is consistent across humans, and the fact that we are born with certain neurological innate abilities tells me that neural development is subject to the same kinds of morphogenesis processes as the rest of the body, shaping the brain and creating useful circuits before we are even born. My question is, how? How is this information encoded into DNA and how are the circuits created from DNA?

Developmental neurobiology is probably the closest field of study, there's a journal: http://onlinelibrary.wiley.com/journal/10.1002/(ISSN)1932-846X I don't know enough about the genetics really help though.

This is one of the most important question in neurosciences and we are far from understanding it. This is also the topic of the entire subfield of neurodevelopment (to answer your last question).
First, you are right that the exquisite degree and physiological correspondence between individuals of a species, and even between species, indicate a strong genetic component. But you are also right that we have good evidence for a developmental component to brains physiology. Here are a few random examples (at the top of my head, so maybe not the most important/influential papers):

Cells selectivity in the primary visual cortex depends on visual experience. Animals housed in an environment with only horizontal or vertical stripes will have cells selective only to horizontal or vertical orientations (Blakemore & Cooper, 1970).
At birth the primary visual cortex doesn't have cortical maps. They develop over time (e.g. Chapman, Stryker & Bonhoeffer, 1993).
Due to synaptic pruning, newborn have actually more connections than later in life. These connections will be progressively eliminated during youth.
Inserting a third eye in the forehead region of frogs makes connections to their optic tectum and creates columns of ocular dominance just as their normal 2 eyes (Constantine-Paton & Law, 1978). Even though having a 3rd eye is clearly not genetically encoded.
Similarly, rewiring the retinal projections of ferrets to their auditory cortex will form orientation columns just as in the primary visual cortex (Sharma, Angelucci & Sur, 2000), even though this area usually processes a completely different modality.
Putting amblyopic (a developmental visual disorder) rodents in complete darkness for some time seems to "reboot" their visual system and cure them from amblyopia (He, Ray, Dennis & Quinlan, 2007).
Efficient encoding of natural statistics mimics the response properties of cells in the nervous system (e.g. Olshausen & Field, 1996).

What these different experiments suggest is that the overall structure of the brain is genetically determined, but development is truly what shapes the function and selectivity of cells.
Blakemore, C., & Cooper, G. F. (1970). Development of the brain depends on the visual environment. Nature, 228(5270), 477-478.
Chapman, B., Stryker, M. P., & Bonhoeffer, T. (1996). Development of orientation preference maps in ferret primary visual cortex. Journal of Neuroscience, 16(20), 6443-6453.
He, H. Y., Ray, B., Dennis, K., & Quinlan, E. M. (2007). Experience-dependent recovery of vision following chronic deprivation amblyopia. Nature neuroscience, 10(9), 1134-1137.
Constantine-Paton, M., & Law, M. I. (1978). Eye-specific termination bands in tecta of three-eyed frogs. Science, 202(4368), 639-641.
Sharma, J., Angelucci, A., & Sur, M. (2000). Induction of visual orientation modules in auditory cortex. Nature, 404(6780), 841-847.
He, H. Y., Ray, B., Dennis, K., & Quinlan, E. M. (2007). Experience-dependent recovery of vision following chronic deprivation amblyopia. Nature neuroscience, 10(9), 1134-1137.
Olshausen, B. A. (1996). Emergence of simple-cell receptive field properties by learning a sparse code for natural images. Nature, 381(6583), 607-609.

+1, especially for the Constantine-Paton & Law, 1978 reference which I was not aware of. By the way, they saw connections in the optic tectum (i.e. superior colliculus), and not in the visual cortex. You may want to correct that in your answer.

If I remember correctly, amphibians don't really have a visual cortex and have weird brains with a different number of layers. I simplified for clarity, which is not really a good excuse.

I will not offer you a description of 'experience-independent' development, as this is not my area, but here is a view on what its limits are. Effectively I am answering:

How much of the brain is actually hard wired in this way and how much is open to experience-based development?

Where a brain area will form is determined by the genotype and the micro-environment that any particular cell faces during development. Or, put in other words, I am not aware of any study showing that experience during development can drastically alter the topography of the brain. The same goes for axons and dendrites of particular cells, although they exhibit higher flexibility after drastic manipulation of experience such as sensory deprivation within the early stages of postnatal development.
This means that inter-areal connections are hard-wired by development in the sense that the target areas of a brain area or particular cell are fixed. As an example, some thalamic neurons are predetermined to target the cortex and vice-versa. A way that experience can influence that fact is by destroying the connectivity between the two areas (e.g. monocular deprivation). But I would be extremely surprised if a study claimed that by some manipulation of experience during development the same portion of the thalamus that normally projects to the cortex now projected to a totally unrelated, distant area such as, say, the brain-stem.

It would seem to me that the extent to which the brain is "hard wired" depends on the species. Humans seem to have a lot more room for specialisation in life, whereas some animals don't exhibit much individuality, tending to follow very regular behavioural patterns that have no doubt evolved over time, subject to natural selection. [...]
  Am I right in associating this process with the phenomenon of "instinct", that is, "hard coded" behavioural patterns in animals which appear to be hereditary[?]

I would challenge you to support this claim by research, as it does not echo anything I know about the nervous system. If anything, primates just have relatively more room for connections in the cortex and the cerebellum even after taking into account their relatively larger brains. Thus, it's not that they are less "hard-wired", in the sense described above, but rather that they have an enormous potential for synaptic plasticity in two key areas of the brain associated with more complex behaviour. When you compare reasonably closely related vertebrates, you find that the phylogenetically ancestral areas are mostly shared and thus their "hard-wired" areas are very similarly connected. Hence, primates only put an extra layer of complexity on top of this ancestral pattern of connectivity by having more space for change.
In conclusion, only the "highways" of the brain are pre-determined during development. The actual connectivity is sculpted by experience. Since the overall layout does not change by experience, animals adapt to their environment mostly through small-scale, synaptic changes.

This is a cool question and while I'm not a neuro(bio)logist, I've tried to quickly look into this.
Basically what you are asking for is the part of the (human) connectome (this is what researchers call the map/data/... of neural connections), that is hard wired. You may want to take a closer look at the human connectome project, if anyone is going to have/find the answer to your questions, it's going to be them. This paper seems to describe the latest state of the project and this one focuses more on the connection between the connectome and genomics. Sadly both papers are pay-walled and I don't have any access to the Elsevier journals right now, so I can't give you more info than that.

Is there a name for this field of study? Specifically the study of how neural circuits are generated in the earliest stages, to lay down the high level structure of the brain before experience-based development can take over?

The short answer is the field is called "Axon guidance" as a subfield of developmental neuroscience.  It essentially studies how early neurons send their projections (axons) to their broad target areas where they will make their connections (synapses).  This process is programmed genetically and occurs by itself using "guidance cues" that literally direct their growth through the brain (attracting to some areas, repelling from incorrect areas). see [Ref .1]
After the broad axon pathways are set up, early experience/learning will shape the connections further so that useful ones are kept and non-useful ones degenerate.
It's amazing stuff, check out movies of live axons growing through the early developing brain [Ref. 2]. I was lucky enough to do my Ph.D. studying this phenomenon :)
[Ref .1]: Seminal review of the Molecular biology of axon guidance
[Ref. 2]: Growth of axons figure


text:
What does probe number and segmentation mean in copy number variation (CNV) data
In TCGA Copy number variation (CNV) data there is a column with title Num_Probes. What is the meaning of probe number with respect to the sample data below?
Chromosome  Start   End Num_Probes  Segment_Mean
1   61735   62152   4   1.1973
1   62920   12777697    6514    2.2882

According to wikipedia, probes are usually 100-1000 bases long. Then does it mean in the first row above that, it took 4 probes to identify the region(61735 - 62152). In that case what would be the meaning of Segment_Mean?

The data you posted looks like it was produced by GISTIC, a program commonly used by TCGA to detect copy number changes. Assuming the data really is GISTIC-produced, my understanding is that "Segment_Mean" refers to the average Log2 Ratio of the probes in that particular segment. Looks like the copy-number of your 4-probe segment in your example is slightly less than half the copy-number of the longer segment.
You can also try using the GISTIC Google-Group to learn more.

If a a sample has a CNV gain at 12792599 - 13278863 with probe no 100 and segmentation mean 0.4 and if another sample also has a CNV gain at the same position 12792599 - 13278863 with probe no 200 and segmentation mean 0.5, does this mean 2nd CNV region is more important than 1st CNV region? I don't understand the importance of segmentation here.

Simplistic Answer: higher segment mean == higher copy number. The number for probes for each region probably doesn't matter. Also, a difference of 0.1 between each regions' segment mean probably doesn't matter much either.


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Genetics and blue eyes
Blue eyes are a recessive trait in humans. I read an article recently which stated:

People with blue eyes have a single, common ancestor, according to new research.
A team of scientists has tracked down a genetic mutation that leads to blue eyes. The mutation occurred between 6,000 and 10,000 years ago. Before then, there were no blue eyes.
"Originally, we all had brown eyes," said Hans Eiberg from the Department of Cellular and Molecular Medicine at the University of Copenhagen.

Which appears to be a mainstream hypothesis today. My question is, if there is a genetic mutation that occurred in one individual which made their eyes blue, and the rest of the population is brown eyed, how does this make so many individuals blue eyed? If the blue eyes are recessive, the individual's children would mix with the other brown-eyed individuals and their offspring will be brown-eyed. How does anyone treat this theory seriously?

I think you just stopped at the F1 generation, just take it a step further and you have your answer (I know I am using the terminology miserably)...

"The blue eyes are recessive in humans" - This is not fully true; there is one recessive blue eyes allele for one gene but eye color is actually polygenic. That said, the answer below covers clearly why recessive alleles don't just disappear which is the more important part of your question.

This single-mutation theory seems over-simplified.  What about people with other eye colors, like gray or green?  Or two eyes of different colors, or even two colors in the same eye?  (Hetereochromia)

@another 'Homo sapien' is basically correct, and what they were getting at, is that in just the F1 generation, you're right, any recessive traits are masked. However, if you continue this onward, in subsequent breeding, recessive traits are unmasked. (This is basically why inbreeding is a bad thing).
If we use the traditional Punnet square method for determining genotype:
if A is a Brown-eye dominant allele, but a is a blue-eye recessive allele:
F1:

You can see that a single recessive allele is now present in 50% of the offspring of a given pair of parents.
Now, if in F2, we assume that 2 of those recessive offspring were to mate, the recessive gene would be unmasked in 1 quarter of the offspring (statistically speaking), and 50% would be carriers.
F2:

Now it gets a little more complicated. Our double recessive F2 member has blue eyes phenotypically, they aren't just a recessive allele carrier.
F3:
So, if in F3, our aa mates with another aa, (ignoring spontaneous mutation for simplicity) it should be obvious that all of their offspring in F3 would have blue eyes (and I can't quickly find a Punnett square in Google showing this).
However, if our aa now mates with an AA (homozygous dominant brown), we will get 100% offspring with a heterozygous Aa genotype - in other words, all blue eye carriers, but with brown eyes phenotypically.
If aa mates with a heterozygous individual though (Aa), we have the following:

And thus, 50% blue eye individuals, with 50% brown heterozygous dominant. And so on and so forth, ad infinitum.
Hopefully that explains how a recessive allele can go to fixation despite only occurring once.


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What kind of red and black insect is in the photo?
I was wondering what kind of insect this was that I found on a flower on my deck this morning?

The insect was in my flower pot on my deck. I took the picture from my cell phone and zoomed in for a clearer shot. The body of the insect (not counting the antennae) was about an inch.

Please provide your location, approx size of the insect, and any better photos if you have them. Thanks.

This is a nymph of some species of Hemiptera, or true bug.
Specifically, this appears to be the nymph stage of a wheel bug (Arilus cristatus) or some other species in the family Reduviidae.

 Source: David Larson

 Source: Debbie Roos 2005
Here is a picture of an adult (with name-sake dorsal wheel):

 Source: Donald W. Hall
You'll notice that the nymph is quite different looking:

Nymphs have been described in detail by Readio (1927). Smaller nymphs are bright red with black marks. The last instar nymphs are darker. Nymphs lack the "wheel" or crest. For a diagnostic key to identify nymphs of the family Reduviidae to genus (including Arilus), see Fracker and Usinger (1949). [Source].

If you're truly interested in accurately  IDing to genus/species, you might check out Fracker & Usinger 1949$^1$, Herring & Ashlock 1971$^2$, or papers that cite their work.

You can find more information about A. cristatus here.

Citations:

Fracker S.B. & Usinger, R.L. 1949. The generic identification of Nearctic reduviid nymphs (Hemiptera). Annals of the Entomological Society of America 42: 273-278.
Herring, J.L. & Ashlock, P.D. 1971. A Key to the Nymphs of the Families of Hemiptera (Heteroptera) of America North of Mexico. Florida Entomologist 54: 207-212.

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


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Why do bumble bees run repeatedly into walls?
I have noticed on dozens of occasions that bumble bees will run repeatedly into a wall. Usually between 1 - 5 times before clearing the obstacle or flying away.

 Credit: Spine Films
This source suggests that this might be due to "unpredictable, unsteady airflow ... [that results in them being] buffeted back and forth by wind."
However, I've seen this occur in very clear, calm weather.
Further, I do not see other genera of bees colliding into things with anywhere near the frequency of bumble bees.
So what's going on here?
(FYI: their eyes, though primitive, are not likely the reason. Nor is their intelligence).

Stubbornness? If they have so many positive traits (like advanced navigation or emotions) like your links say, why shouldn't they have developed some of the more... mixed traits that exist?

Crall et al., 2015, studied bumblebee collision avoidance (note the senior authors are the same from your link). It seems that, contrary to popular belief and experience, bumblebees are actually quite good at avoiding collisions, but they are also in an environment that has a lot of obstacles, so collisions still happen frequently.
There is a lot of interesting content in that paper, but one of the interesting discussions was about types of collision avoidance by body size. The authors note that for larger animals, collision avoidance strategies tend toward reversal/slowing down to reduce impact, whereas in smaller animals, strategies tend toward direction-change. This might be because collisions at high speeds are more dangerous for larger animals, so slowing down is the priority. Accelerating in a lateral or vertical direction, instead, would result in a full-force collision if the acceleration was insufficient to avoid the object (I have to admit, though, your gif doesn't seem to show any deceleration).
Larger individuals in their study performed more slowly on their obstacle course than smaller ones, but it seemed like all the bees were pretty good at avoiding obstacles.
Based on this study, I don't know that we can conclude definitively why bumblebees repeatedly run into walls, but given how well they navigate an obstacle course like this I am guessing it isn't simply because they are incapable, but rather has to do with a few things:

Walls are somewhat unexpected obstacles; bumble bees are probably best evolved for navigating around foliage that has a limited horizontal size, and once headed home they are expecting a direct route to be most efficient. A good transit strategy in that case would be to fly slightly laterally in the event of a collision to find a new opening, but not deviate too much from the original path of travel.
Speed/collision tradeoff. Getting home fast can have some obvious advantages because it increases the effective foraging potential. If collisions can be mitigated or aren't damaging, it might make sense to fly at high speed and just deal with the collisions as they come.
Bumblebees are big. Therefore, it's harder for them to stop, and they might use a strategy for collision avoidance that reduces impacts rather than avoids impacts altogether.
Cognitive biases in humans. Bumblebees make quite the racket when they run into things. You're going to hear it each and every time if you are nearby. The same isn't necessarily true for other bees or other insects.

References
Crall, J. D., Ravi, S., Mountcastle, A. M., & Combes, S. A. (2015). Bumblebee flight performance in cluttered environments: effects of obstacle orientation, body size and acceleration. Journal of Experimental Biology, 218(17), 2728-2737.


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Is it mostly true that predators or parasites traverse wider spatial areas than their prey or hosts?
Does it tend to be true that as you go up the food chain, the species tend to cover wider areas?  I am basically asking whether a population's prey varies spatially more than a population's predators and parasites, which would vary more temporally: the predators and parasites to which a population is exposed tends to be the same across the population but the prey vary more spatially because the prey tend to traverse smaller areas.  I would think this were true, since predators have larger body sizes and my thinking is that species with larger body sizes tend to travel farther and parasites may locate on multiple hosts, which collectively carry them farther than any single host.  This is my inference, but I do not even know what to type into Google Scholar in order to check this.

Please show your own attempt at answering the question to avoid having your question downvoted. Thanks.

I edited the question.

Related (but different!): https://biology.stackexchange.com/questions/60627/references-concerning-the-relative-population-sizes-of-predator-and-prey

many prey species have exceeding large migratory routes saying they travel less then predators is unfounded. predators do not always have larger body sizes either.

The ability of prey to find refuge in predator-free habitats is a fundamental hypothesis for predator-prey stability. The availablility of predator-free patches allows the prey metapopulation to maintain positive population growth in some patches, despite being decimated by predators in other patches. If the predators are far superior dispersers, they would eat all the prey, possibly driving the prey—and themselves—extinct.
That being said, it's difficult to make generalizations about spatial food webs. In nature, prey, predator, and parasite populations persist due to a multitude of factors, including the spatial configuration of suitable habitats, their dispersal rates, interactions with competitors and mutualists, etc. For example, in a system where carnivores hunt herbivores, sure, the predator may disperse across the landscape, hunting across more than one herbivore metapopulation; in other systems, such as those that may be more spatiotemporally variable (e.g., prone to disturbance and local extinctions), the ability of the prey to disperse faster than the predator could be a crucial aspect of predator-prey stability.
Some theoretical resources include: Comins et al. 1992, Holt 2002,
Amarasekare 2008.
A foundational experiment is that of Huffaker, who dispersed mites on oranges: Huffaker 1958. Also, take a look at work on host-phage interactions: Schrag and Mittler 1996.
For Google Scholar searches, try various combinations of the following words: spatial, host, parasite, predator, prey, stability, coexistence, food web.

Yes there is a bit of correlation for animal weight, it's a very vague graph. No, food chains don't correlate predictably well because of the different locomotion energies of birds, mammals, insects, wind transport, river and tide transport, and ecosystem differences.
Every time there is a different locomotion type and energy, it makes exceptions. flying animals like geese, sparrows and locusts can travel thousands of miles compared to their all of the predators, eagles, foxes and spiders.
It's too general. It's 50 questions in one, you encompass millions of species. There isn't a clear study to consider for it. Parasites places in the food chain is not very clear, it's another topic too. Parasites are the contrary, they are small, so the host can travel more than the parasite, even if it's attached like a tick.
Elephant home range varies from 50 to 3000km,
here are home ranges, which can vary 10,000 times for the same wieght animals:


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What would bees be doing inside my furniture in the beginning of summer
I have an old chest of drawers in my garden shed. I've been noticing individual bees entering a closed drawer through the keyhole. Recently they've sealed that keyhole with a gray goo that's solidified and seems very hard to the touch at this point. I don't have anything terribly important in there but I'd have to break the goo if I wanted to pry the drawer open. What am I likely to find in there? If I don't disturb them should I be worried about a swarm of angry bees exiting at some point? It's currently the beginning of summer here in Europe.
EDIT:
I photographed 2 bee types that fly around in my garden (though another species might have been around a couple of months ago):

Sounds like they would be building a home or laying eggs. Are they still entering and leaving, or were those solitary bees?

Doesn't sound like honey bees (or other social bees). I'm guessing some sort of mason bee (Osmia) that has layed egg(s) and then covered the entry (that's the "masonry"). If it's not an emergency I'd say you should wait and let them grow up in there, they won't do any harm to you or your stuff.

I only saw solitary bees entering or leaving. It's not an emergency and I'm happy to leave them to grow up in there, the only thing I'd be worried about is if they are easily aggrevated when they mature since kids might disturb them by accident.

don't worry, they are absent parents. they leave food for the larvae and then leave. it's mostly social wasps that need to defend their colony that are aggressive.

As @picapica says, it could well be mason bees (Osmia spp.). Another possibility (but less likely) is carpenter bees, which will actually burrow into the wood. I'm reluctant to give a confident identification from your description without better ID of the actual species, though - if you can get a photo of a dead bee that would be better, or if you can simply describe them it would be a start.

I can't remember exactly what they look like because some time has passed between me noticing bees and then noticing the barricade they've built, but I remember them not seeming very different to the other bees (we have plenty of flowering plants in our garden so bees are very common) and the usual bee here looks like what a beekeeper might keep (I used to know a few).Sorry for the lack of detail but I'm a programmer, not a biologist.. There are also no dead or alive bees around the drawer right now, they are currently in total stealth mode.

@arboviral yes, my guess wasn't meant to be definitive. this question could possibly be considered answered (they are making nests for their young) but getting it down to species will be impossible without more information. keep an eye out for the new generation when they appear!

@picapica Oh yes, I understood. I would agree that mason bees are the most likely culprit, though!

@picapica will keep an eye out for them - I'll take a photo if possible, or of their nest if they escape before I can snap the photos. Any best guesses as to when I can expect them out?

I took photos of the 2 types of bees I can find in the garden now; one of them is very similar to bumblebees which is supposed to be typical of carpenter bees, but mine don't look like the carpenter bee pictures on Wikipedia (mine have hairier butts :P )

Since you have more than one species of bee this might help you.http://bugguide.net/node/view/475348 as should this site which has a dichotomous key for identification. http://www.discoverlife.org/ed/tg/How_to_use_the_discoverlife_guides.html

Thank you, that guide is explicitly made for North America though and I'm from Europe, would that information still apply to Europe in general?

you should add your location to the question. your pictures look like a honey bee and a bumble bee to me, but keep looking!


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What is this large beetle from Shirpur, Maharastra (central India)?
I found this beetle in my college in Shirpur, Maharastra (central India). What is it? It is very large, and I have never seen it before. I believe it may be Titanus giganteus but I'm not sure.

Welcome to Stack Exchange! Please take the tour. Could you add more information about the beetle - size (as accurately as possible), anything you noticed about the markings, etc? It doesn't look much like T. giganteus to me - the elytra (wing cases) are the wrong shape and the mandibles are much bigger and shaped differently. Also, as far as I know T. giganteus is found only in south America.

As arboviral said, please add more information.

Clearly not the best picture, but from the poor quality image it does appear you have a longhorn beetle (family Cerambycidae) in the subfamily Prioninae.

They are typically large (25–70 mm) and usually brown or black. The males of a few genera sport large mandibles that are used in fights with other males, similar to stag beetles. These beetles are commonly nocturnal and are attracted to light. The majority of the Prioninae whose biology is known are borers whose larvae feed on rotting wood or roots.

For example, your specimen looks a lot like Toxeutes macleayi from Australia.

 Source: England London - Natural History Museum
I'm not sure whether other closely related species live in India (none of the related Indian species that this site mentions look like your specimen), but I would guess if you look into it you might find a local bug guide that might help you find some other related species.
Based on your location in India, I'd say one place you could start looking is through species in the genus Prionus.

they're also large, generally brown or black, are nocturnal. Additionally,

All members of the genus Prionus have twelve or more strongly toothed or even flabellate antennomeres on their large antennae.

You'll obviously need to provide a better picture for us to examine that detail of your specimen.

I also recommend you examine the list of Indian Prioninae species listed here, including relatives of similarly sized/colored species with large mandibles such as Dorysthenes huegelii and Rhaphipodus fontanieri.
Again, your picture is too low of quality for an accurate ID, but these links should likely help you parse through similar species and hopefully find your answer.


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Is DEET (as in the mosquito repellent), a substituted phenethylamine?
Am I correct to say that N,N-diethyl-meta-toluamide (DEET) is a part of the phenethylamine class? It's structure meets the requirements to be a phenythylamine, however, I was not able to find anywhere on the internet that it is part of the phenethylamine class.

Do you mean phenethylamine? That's the only thing google turn's up. If so, they don't seem to be related (1 less carbon between ring and N, carboxylic-bound N versus amine N)

@Nicolai Sorry I usually type in Word which autocorrects me, but you are correct on the first part. But I'm confused on your second point. How come it passes the requirements to be a substituted phenethylamine (https://en.wikipedia.org/wiki/Substituted_phenethylamine)?

Selegiline is a good example of what I mean, it has a carbon bound N but is part of the PEA class. Why is this then...

Also, technically DEET has a NH group because groups share atoms with the linked group, so writing N-CH3 is the same as writing NH-CH2. There is no difference, unless it crosses over 1 link.

I'm voting to close this question as off-topic because it is not about biology, but is a question about the chemical structure of a proprietary product.

While I feel like this might be a better question for the chemistry SE, lets take a look at the molecular structures:
The basic structure of a phenethylamine (left, modified from here) versus DEET (right, modified from here):

The important chemical differences are:

DEET only has a C-alpha between the nitrogen and the ring, whereas phenethylamines have a C-alpha and a C-beta (see red annotation)
DEET has a carboxylic functional group (an amide bond), whereas phenethylamines have an amino group (see green boxes)

Taken together these differences mean that DEET is not a phenethylamine.

So are you saying that 1-phenethylamine is not part of the phenethylamine class?

https://en.wikipedia.org/wiki/1-Phenylethylamine

Note, I am not talking about b-phenethylamine which is the one you pointed out

@kirill2485 At least based on the different carbon chains of these molecules I wouldn't group them together. I'm not a chemist however, so if you want to now how they categorise this, ask the question at chemistry.SE

I agree with @Nicolai I can't see any reason it would make sense to consider DEET a phenethylamine; it doesn't have an "ethylamine" on it anywhere: that would be 2 carbons followed by a nitrogen. It's an N-substituted amide group (one carbon) on a toluene.