text:
How do you accurately measure anguiliform (eel) locomotion?
In one of my courses, we were discussing a paper by Muller and van Leeuwen (2006) which made a lot of comparisons the differences between carangiform (mullet) and anguilliform (eel) locomotion. While reading the text, one of the passages stood out to me:

When comparing the estimates of vortex ring height with those of ring width, mullet and mackerel shed approximately round vortex rings, whereas eel vortex ring are almost twice as wide as they are tall. Such distorted rings are less likely to form and once formed, they are more likely to break up, all of which results in a different vortex pattern in the wake.
The time-resolved flow fields of eels indeed support the notion that the vortices in its wake break up: two independent studies, visualizing horizontal cross-sections through the eel’s wake, observed that individual vortex cores elongate and split into two (Muller et al. 2001; Tytell 2004a). We can therefore conclude that the shape of the propeller, and hence implicitly the propulsion mechanism, might affect wake shape. This observation also implies that a propeller shape that promotes the formation of a suboptimal wake is less efficient, and therefore the absence or presence of a wake that is predicted to maximize efficiency is a valuable indicator for the hydrodynamic efficiency of a fish’s swimming design.

So, essentially during carangiform locomotion the body of the fish moves 1/2 wavelength whereas anguiliform swimmers make 1 wavelength. My questions are how can they make such a statement when particle image velocimetry (PIV) does not adequately measure the movements of anguiliform swimmers, let alone their efficiency, when they are essentially swimming through their own vortexes? Are there any studies that address this issue in anguiliforms?

Can you elaborate on why PIV is inadequate for studying anguilliform swimmers?

Just to add to @kmm , what are your qualms with the application of PIV here? ( I work in one of the labs cited, and don't understand your question)


text:
Differentiation of norepinephrine and epinephrine in indications
Norepinephrine is less beta2 adrenomimetic than epinephrine so more selective so less bronchospasm so may be therofore better in treatment of cardiac failure and different shocks.
However, I am not sure.
I have some intuition that some of them is somehow analog of the other one.
PubMed about norepinephrine in Pharmacology

Sympathomimetics
Adrenergic alpha-Agonists
Vasoconstrictor Agents

PubMed about epinephrine in Pharmacology

Bronchodilator Agents (beta2)
Mydriatics (beta2)
Adrenergic alpha-Agonists
Sympathomimetics
Adrenergic beta-Agonists (this causes those two first indications)
Vasoconstrictor Agents

which is logical because epinephrine is nonselective beta2.
However, I am not sure if those properties include all accepted indications.
This proposes me that norepinephrine can be used better in acute situations.
However, I know that epinephrine injections are more given to allergic people to carry for anaphylactic shock.
Why so?
Probably, because of price.
How does the indications of norepinephrine differ from those in epinephrine?

You're proposing several problems: cardiogenic/septic shock, bronchospasm, and anaphyllaxix. Cost isn't the factor. Epinephrine is the drug of choice for anaphyllaxis because it decreases edema through its alpha-1 adrenergic vasoconstrictor effects on the small arterioles and precapillary sphincters in most body organ systems. If blood pressure were the major consideration, another agent would be used. Dobutamine is used for cardiogenic shock because it is also a positive inotrope. You can't pick two drugs and ask how they differ (too broad) without the effect (indication?) you're looking for.

The differences in the action/indication is because of differential affinity of the two molecules to different adrenergic receptors. The wikipedia page on Ardenergic receptor has a table which summarizes this.
Wikipedia doesn't cite references for it. You may have a look at some of the following old articles.

α- and β-Adrenergic Receptor Subtypes

In the periphery, α1-receptors are located postsynaptically, mediating the excitatory effects of catecholamines at α-receptors. α2-Adrenoceptors, on the other hand, are autoreceptors involved in the regulation of noradrenaline (norepinephrine) release. In the central nervous system, both α1- and α2-receptors exist on postsynaptic cells; there are also 2 principal subtypes of β-adrenoceptors. β1-Receptors have a high affinity for both noradrenaline and adrenaline (epinephrine) and are found in the heart, brain, and adipose tissue. β2-Receptors have a low affinity for noradrenaline and are involved in mediation of relaxation of vascular and other smooth muscles and in many of the metabolic effects of catecholamines.

β-Adrenergic Receptor Subtypes: Properties, Distribution, and Regulation

                  NE=Norepinephrine, EPI=Epinephrine, ISO=Isoprenaline

NE properties seem to go little over each other: its alphanergic properties cancel out some of its betanergic properties. This may result in the fact that epinephrine is more potent drug than norepinephrine. At least, it is used more widely and has more indications including PCR and acute anaphylaxis, in contrast to norepinephrine. I wonder if there are any indications of norepinephrine where you cannot use epinephrine. Probably, one such a property is acute hypotension. Probably some stability issue with the epinephrine or something.

@Masi α-receptor mediated responses would be more responsive to NE; I don't think it will cancel out. α-receptor mediated responses are synaptic. Very localized and not endocrine....... I don't think there is a stability issue. NE is specifically administered for acute hypotension. There are other synthetic agonists that target only one type of receptor like salbutamol.

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sort: votes


text:
Low copy numbers of plasmids
I have a plasmid with the P15A origin which apparently has a low copy number (see here). This would explain why my purification yeilds for subsequent digestion are low (gel shows the plasmid after digestion and clean-up with 5µl being loaded). I am currently growing my E. coli containing plasmid up in 5mls overnight before doing a miniprep. My question is should I grow my 5ml cultures up for longer (2 days) or just give it up and do a larger amount for Midiprep.

I am also curious as to what actually controls the plasmid copy number inside cells. An explanation of the regulation of plasmid copy number would be much appreciated.

What is the basic name of the plasmid? How much plasmid did you actually use for the digest? What are your yields from a miniprep?

@Chris It's called pACYCHO so I am guessing it is a derivative of the pACYC plasmid. Oh and thanks WYSIWYG, I didn't know that was how you do links.

I am sure you have done it; just a note to others: do a PCR screen to
ascertain that the plasmid is there.
For minipreps you generally do not need a starter culture.
If you have screened your clones and now just want to amplify and keep the plasmid for cloning purposes then go for a maxiprep with 200-400ml cultures.
Do not overgrow the cells, your extraction becomes difficult and you would get even worse yields. Just set up a huge culture and pool the cells before extraction. Always seed and harvest cells that are in exponential growth phase.
If you need to screen the plasmid for clones or something then do a colony PCR, keep the colony inoculated in a small culture (make a temporary glycerol stock if your screening is taking time). If screen is positive then incoulate the starter culture for maxiprep/gigaprep culture with this stock.

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How is satiety measured?
I am aware of satiety only through experience, rules-of-thumb and possibly myths. For example: white bread is not filling, a pasta meal can be filling but because we "burn" carbs quickly pasta itself is not, and I personally find fruit in the melon family filling. (But that could be because I hate them ;) )
Is there a formal measure of satiety? How does it work?

Can you clarify your question, actually it is not really clear for me what you are asking.

I am aware that the wording is not especially good for biology, but I had to migrate. The feeling of satiety has nothing to do with cooking, and the human physiology of eating food is strictly off topic on cooking.se. It is probably a bit more confusing because the OP imagines something which doesn't (and cannot) exist: some kind of universal scale saying that pasta is X times more filling than bread. But an explanation how the feeling of satiety emerges, as the reason why the scale doesn't exist, can be quite interesting.

Satiety is complex, and there are several kinds of satiety, all of which come into play in different circumstances. Things that decrease or halt our eating are called satiety signals. Different satiety signals are put out by different substances (carbohydrates, fats and proteins) as well as by things like gut stretching and other signals. There is also a psychological component to override satiety signals (company during meals, appearance of food, cost, etc.). The best measure of satiety may well be when a person stops eating a given meal. In lab conditions, the meals are carefully calibrated, but people (and animals) can feed as long as they desire to (ad lib).
Historically, satiety was thought to be the end product of serum glucose, available energy based on body heat, fat utilization by the liver, and the generation of ATP and other energy-rich molecules by the liver and/or brain. For the most part, these hypotheses have not withstood the test of time.
Three major signals influence food intake: satiety signals, adiposity signals, and central effectors. For the sake of simplicity, I'll deal only with satiety signals. Satiety signals (SS) arise from the GI tract and related organs during a meal, and influence eating behavior by activating peripheral nerves passing from the GI tract to the brain, or by recognition by brain receptors.[1]
As food interacts with the lining of the stomach and intestine, gut peptides and other signals that coordinate/optimize the digestive process are secreted. The signals that inform the CNS function as satiety signals. Different signals are secreted in response to carbohydrates, fats, and proteins, and it's the specific mix of signals that informs the brain as to what precisely has been eaten.[2]
Cholecystokinin (CCK) is the most extensively studied gastrointestinal satiety hormone. It is secreted by cells in the duodenum and jejunum in response to ingested fat and protein in chyme (food plus gastric fluid). Giving CCK IV decreases ad lib meal size, while blocking CCK receptor sites will increase ad lib eating per meal.[3][4]
Carbohydrates and fats as the most effective stimulators of Glucagon-Like Peptide (GLP-1) and Peptide YY (PYY). IV GLP-1 decreases meal size by promoting early satiety.[5] Within the CNS, PYY is detectable in the hypothalamus, medulla, pons, and spinal cord.[6]
Enterostatin is a protein which is broken down into a digestive lipase and a five-peptide fragment (Ala-Pro-Gly-Pro-Arg (APGPR) in humans). The appetite regulating effects of APGPR in the brain are specific to high-fat or fat diets but not towards diets rich in protein or carbohydrate.[6][7]
Amylin decreases meal size in rats, probably through the same pathway as CCK. Oxyntomodulin (OXM) and pancreatic polypeptide (PP) are also meal terminators. Pre-prandial subcutaneous administration of OXM to overweight and obese humans over a 4-week period resulted in a significant reduction in body weight of 2.3 kg, compared with 0.5 kg for the placebo arm.[9]
This is a growing field, and there is more suspected, and more to prove. But one can see that there is no one measure of satiety.
[1] That satiety signals come from the stomach and beyond was shown by "fake eating", that is, diverting swallowed food from the stomach by creating a fistula. If food is allowed to enter the stomach, satiety signals are elicited; if not, eating continues for a long time.
[2] Gastrointestinal Satiety Signals I. An overview of gastrointestinal signals that influence food intake
[3] Gastrointestinal hormones and satiety
[4] Rats with spontaneous mutations of the CCK-1 receptor (called
OLETF -Otsuka Long Evans Tokushima Fatty- rats) eventually become obese
during their lifespan.
[5] Glucagon-like peptide-1 promotes satiety and reduces food intake in patients with diabetes mellitus type 2
[6] Introduction to Gut-Brain Interactions
[7] Enterostatin inhibition of dietary fat intake is dependent on CCK-A receptors.
[8] Amylin decreases meal size in rats
[9] Gut-Brain Interrelationships and Control of Feeding Behavior

nice answer.. can  you expand on the role of hypothalamus..

@WYSIWYG - I can, but this answer is long enough. :) If you want to ask a separate question, I can do that.


text:
(how) is it possible to choose the biological sex of a child?
I recently read of a study that investigated the ethics of child's biological sex choice in humans, and now I want to find out how this can/could be done. Does anyone know of scientific papers or journals that describe the methods in some detail? The answers I was finding in my own search were not as specific as I would like.

Do you mean sex selection? Keep in mind that gender and sex are not the same thing. If you mean gender then I think that this question is more suited to the cognitive sciences SE.

Yes you are right, I mean sex selection.

I mean that there is research involving giving couples the ability to choose whether their baby will be male or female.

The article you read had to do with ethics. So are you interested in ethics or in science? Are you interested in the methods that offer couples the opportunity to choose the sex of their baby or are you interest in how some species manage to chose the sex of their baby (which is particularly the case when there is environmental sex determination (ESD)). This wikipedia article might be a good start.

I read an article about ethics, but I wanted to learn more about the science behind giving humans the option to choose. I don't really care about the ethics at this moment, I'm more concerned with how it is done. I did some searches on Google, but I was getting generalized, nonspecific answers. I would prefer to find something from a journal or research paper that actually talks about the methods, success rate, and why it works (or why not).

Ok, so you are looking for a review (in a peer reviewed journal or not I suppose) of the methodologies that can be used for parents to chose the sex of their offspring, is that right?. You maybe want to make clear in your question that you are looking for a list of methodologies. The question is interesting (I am totally ignorant in the subject). I just wonder whether wikipedia is not already a very good source of information given how broad is your interest.

This question is too broad. Can you add some details

I looked at the wikipedia article you suggested; it does provide some detail, but I do still have more questions. I'll check the references there later in case those contain further detail. I did not realize wikipedia would contain that much information. Thank you for your help.

The main technique is sperm separation or sorting, where you separate sperm by gender, and only use the gender that you want. Existing techniques aren't perfect. AFAIK, they are typically less than 90% accurate, but it is still better than 50%. Typically, this involves some type of cell sorting device often with some kind of fluorescent tag marker.
The second technique is embryo screening. Often, with IVF, you screen and can confirm the gender that you want before implanting the embryo in the mother.
Links:
http://www.fertility-docs.com/programs-and-services/gender-selection/select-the-gender-of-your-baby-using-pgd.php
http://www.in-gender.com/Gender-Selection/MicroSort/


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What are limitations on the number of objects the eye determine at a glance?
Take two people Sam (average human) and Jack.
Jack says to Sam "I'm going to show you some skittles (or other object) and I want you to tell me as quick as you can how many I'm holding." He opens his hands and there are three. Sam can instantly tell there are three. Then Jack shows five to Sam, who takes a little longer, as he knows there are around 4/5 but can't tell so has to count.
As the number of skittles increases, Sam takes longer and longer to answer to the point where he needs to count the skittles one at a time to be sure, and sometimes to even recount them.
Why is it that we can instantly if we are looking at three maybe four objects but any more than this we cant? It gets harder and harder to estimate?

The answer to this question is complicated, but assume it's not for the moment. The easy answer is that our eyes can detect patterns we're familiar with and "produce" an answer in the form of a number. Unfamiliar patterns do not produce this 'number'.
Take a die. We are immediately aware of the number of dots in the typical arrangement of one to six. We need expend no counting to do so. If the skittles are arranged in the familiar die pattern, we will have no problem knowing if there are 4 or 6 skittles.
Given a pair of dice, any gambler can tell you what number any two faces adds up to without counting the spots. Do it long enough, and your brain is on auto-recognize. In your example, if Sam is a gambler, and the skittles are arranged like the spots on two dice, again, no problem telling between 2-12 skittles.
If you arrange things in a comfortable pattern, this can go on into the hundreds.

The above was easily recognized by you as nine, I presume.

Someone good with pattern recognition will know that the above left is 25 dots. However, they will not know that there are 25 dots in the above right.
So, the easy answer is that the eye can grasp high numbers of things if they are presented in a familiar pattern. The normal mind, however, is not able to do so with higher numbers arranged in a random pattern. And, random is how most things present themselves. So, we need to count.

While this is interesting, this sounds like pure conjecture. Do you have sources for this information?

@gravityassist - I hope you realize that by eyes, I don't mean the retina.

I didn't make that assumption. I just wanted op to have that information.  Still doesn't change the fact that you have no sources to back up your answer.

Ahh so its not neccesarily amount of objects but the pattern they are arranged?

This question appears to be related and the top answer lists a number of sources:
https://psychology.stackexchange.com/questions/3475/what-is-the-maximum-number-of-objects-an-average-human-being-can-recognize-at-on
Summed up, the average human can apparently recognize the exact number of up to 3-4 items almost instantly, but for anything above that either needs a counting mechanism that somewhat linearly grows with amount of items (which for 4-8ish can still be super fast, so you wouldn't necessarily notice the difference yourself) or there needs to be a familiar pattern which helps you determine the number more quickly.

I have modified your answer, in particular substituting number for amount. Amount should only be used for non-countable objects in English, which in this specific instance is particularly pertinent. As an aide memoire — "amount of  sugar (non-countable), number of lumps (countable)".

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text:
If gene differs between chromosome pair does individual get a mixture of protein shapes?
Do diploids such as humans end up with a mixture of two different shaped proteins where the appropriate gene is expressed differently in the two halves of a chromosome pair or is there some governing factor that dictates that only one of the alleles is ever used to direct protein synthesis?

Yes, that mixture of shapes can happen.  Differences in the nucleotide base sequences between the two alleles of a gene can lead to differences in amino acid sequence, which in some cases large differences in protein shape.  One example would be if one allele changed a cystine codon to any other codon, leading to loss of a disulfide bond needed to stabilize the tertiary structure of a protein.  For an extreme example, consider a mutation causing sickle-cell anemia; in this case, the disease-causing allele leads to altered shape of the entire red blood cell.
If a heterozygote carries a healthy allele and a disease-causing recessive allele, the protein produced by the healthy allele provides enough activity to mask the lack of activity of the "broken" protein provided by the recessive allele.  If, instead of being a true recessive, the disease-causing allele is partially penetrant, then the heterozygote would suffer from the reduced level of the active protein (only one allele is providing the good stuff).


text:
Why do some internal organs regenerate?
I have been reading about the human liver and zebra fish heart muscle having the ability to regenerate. It seems to me that these organs have very little chance to become damaged or worn out. At the very least their chances of being damaged are comparable to other internal organs. So why those particular organs have the regenerative capability?

It makes perfect sense for the liver as this is the organ which carries the biggest load in terms of metabolism. The liver is also very important to metabolize a lot of substances that we take up (think of the Cytochrome P450 system). So it is a good idea for this organ to be able to regenerate.

I am unsure of what exactly you are asking. Is your question "Why does the liver regenerate but not other organs?" or "What important organs have the capacity to regenerate?"

@Chris - it doesn't make perfect sense to me on that basis. That argument can be made for any organ: "it's function is vital, therefore it makes sense that it has regenerative capability."

see @Chris, liver perform many vital tasks but those tasks wont cause it to physically worn out. Or do they? I am not sure.

@anongoodnurse why not what.

@anongoodnurse The liver plays a central role in removing toxins. So it can get exposed to a too high dose and suffer damage. See alcoholism for example. You can treat your liver very bad for years and it will still work somehow.

The liver's position in the circulatory system means that it's the first organ hit by toxins absorbed by the intestines (except maybe the intestines themselves). Detoxification of these compounds can involve generation of reactive oxygen species that damage DNA or protein. It doesn't even need to be chronic damage, excessive acetominophen with a little alcohol can destroy a liver pretty quickly. carbon tetrachloride or galactosamine are used to induce liver failure in lab animals.

Chris and user137 makes sense :) similar things should be true for other animals too I guess. Great guys :) thanks

@Chris and user137: could you make an answer out of your comments? It is all based on obvious knowledge so don't bother with too much cites. Just to prevent deletion - I like the question as it has crossed my mind often!

@PankajPhartiyal I made some edits to the question to try and make the grammar and wording more easily understood. Please check the edits to make sure I haven't accidentally changed the meaning.

I think it is fairly obvious what is being asked here. The main question is, are there other organs - besides those listed - that can repair/regenerate? If there are why do those repair/regenerate while others do not.

Edited the question again. Thanks for the help Chris Stronks. I was not aware of the damage a liver undergoes and I wanted to ask why internal organs have regenerating capacity at all if they don't wear out. Seems Liver do wear out constantly.

It is not really essential that all vital organs should have regenerative potential (for example brain).
The cellular composition of a tissue is a big factor in deciding if the organ/tissue will regenerate or not. Some cells divide while others do not; highly specialized and polarized cells like neurons do not divide perhaps because the act of division itself will compromise their function. That doesn't mean these tissues cannot regenerate; they would need stem cells that can differentiate into the type of cells that died.
So regeneration can happen via:

Division of the tissue cells (skin healing, liver regeneration)
Differentiation of stem cells (erythropoesis, muscle regeneration)

Organs that do not have non-dividing cells can regenerate by simply proliferating whereas others would need to maintain a stem cell niche- which is not possible in all tissues. Maintenance of stem cells also adds up to the cost of metabolism; so there is some tradeoff.

authors: Александра Гридина


text:
What causes feeling of feet falling asleep to be delayed?
This answer explains the sensation of extremities "falling asleep" as a result of sustained pressure on a nerve. The answer links to an external web page that says that the feeling "quickly goes away once the pressure is relieved."
In my experience, however, it doesn't usually go exactly like this.  For me at least, usually what happens is I will start feeling a tingling sensation in my feet after sitting in an awkward position for an extended period of time. If I ignore the sensation for long enough, it continues to get worse until I finally do stand up.  But after I stand up, rather than the sensation quickly disappearing, I find that usually it suddenly gets much worse for a period of time.  What started as an annoying tingling when I was sitting quickly turns into something quite uncomfortable upon standing up, even to the point where I am not able to walk around properly until the sensation passes a few minutes later.
But once I am standing up, the nerve shouldn't be pinched anymore, so why does the sensation of my foot being "asleep" remain for a few minutes after standing up, and why does it actually seem to briefly get worse after I have already stood up and "unpinched" the nerve?

This is a personal medical advice question. I should be aware of many other factors to answer such a question satisfactorily. Has this kind of behaviour occurred in you all your life or started just recently or during your university years?

I believe this sensation can be generalised to everyone. It's the feeling you get when you fall asleep with arms/legs crossed and wake up with the strange tingling feeling.

@wysiwyg why was my answer deleted?

possible duplicate of What actually happens when my leg 'falls asleep'?

@majid This question is different because it is asking about the delayed feeling.

This paper, while mainly dealing with chronic nerve compression, appears to explain the effects of nerve compression on the blocking the transmission of neural impulses (causing the "sleeping limb" syndrome).
This paper describes how the application of pressure on a nerve causes a miniature case of compartment syndrome, where the pressure causes the intraneuron pressure to increase, leading to paresthesia. Edema also occurs within the neuron, causing pain signals to be sent out. In the experimental rats which were unable to relieve this pressure, permanent nerve damage resulted.
When the effects from the nerve compression exceeds a certain level, the pain/tingling will result in you releasing the pressure from the limb in order to prevent nerve damage.
However, the nerves are still blocked from transmitting their impulses due to the  compression blockage described in Paper 1. When the blockage is resolved, the neurons are now capable of transmitting their pain signals, which continue for a period of time until the pressure within the limb falls sufficiently below the pain threshold.

Paresthesia is defined as the abnormal sensation of the skin, such as numbness, tingling, pricking or burning. Paresthesia is a diverse medical condition and the definitions seems too vague. Most of the books define Paresthesia as a symptom of some other disease. Mostly Paresthesia is categorized as transient or permanent. Paresthesia can arise from several causes like artery related, nerve related, migraine, vitamin B deficiency, brain related and may cause from side effects of other drugs.
Classification of transient and chronic Paresthesia is described in detail here.

Nerve impulses require a healthy energy supply, known as the axonal transport system.  This well developed micro-vascular distribution method provides the blood flow needed to maintain the cells in good working order. If pressure is put on the correct spot, though, all the tiny arteries, veins and capillaries that supply the nerves’ nutrients become pinched off and the nerve cells begin to function abnormally.
Compression isn’t the only thing that can cause limbs to fall asleep. Excessive vibration will also lead to paresthesia. Operating hand-held vibrating tools is an extremely common cause of this
Reference

As simulation level increases transient Paresthesia may occur, usually disappearing with in a few second

Localized paresthesia or pain occasionally results from a specific
mechanism. Mechanical irritation of a peripheral nerve can project
such sensations to their periphery.If the pressure on a peripheral
nerve provokes paresthesia, then a neuroma or chronic compression
occurs. If the pain is initiated by the movement of a joint, there may
be a ganglion affected by the process.
Reference : Neurological Differential Diagnosis -- Marco Mumenthaler

The paresthesia mentioned in the question is transient, mostly paresthesia can happen in cold weather conditions or can happen when sitting in a particular position for long time. Several types of paresthesia exist and there are several reasons for the occurrence. But most of them are attributed to the strain in  peripheral nerve. When we stand up, the itching effects get increase and it slowly fades out, this is because when the nerve resulted in the formation of paresthesia is stressed more when we take a stand up poster. As some paresthesia is caused by the lack of blood supply, blood supply itself is not always causes paresthesia but there are cases when blood circulation to the nerve is interrupted and this may result in stress of nerve and which may cause paresthesia. These kinds of paresthesia is common and it only last for minutes. So when we stand up the tension to the nerve increases, also the blood pressure increases and blood is slowly available to the nerve. When we try to stand, the nerves are burdened with more tension and paresthesia increases but after sometime the blood flow become natural and paresthesia  diminishes slowly. Paresthesia   can be reduced by massage or applying pressure on the affected areas, all these are helpful for people having transient paresthesia. Chronic paresthesia and paresthesia due to other medical conditions need more complex treatments.
Causes for paresthesia

References
Clinical Guide
Clinical Neurology of the Older Adult --  Joseph I. Sirven, Barbara L. Malamut
Paresthesia and Dysesthesia

why does standing up cause tension in the nerve to increase? If that were the case, I would expect my feet to fall asleep whenever I was standing and spotting awkwardly would make it better.

According to the post you linked, paresthesia causes the "falling asleep" notion. According to Wikipedia, there are two types of paresthesia, transient and chronic. Transient paresthesia is the type you are describing.

Paresthesias of the hands, feet, legs and arms are common, transient symptoms. The most common, everyday cause is temporary restriction of the blood supply to an area of nerves, commonly caused by leaning or resting on parts of the body such as the legs; other causes include conditions such as hyperventilation syndrome and panic attacks.

Other places like this link mention that parethesia is caused by:

• Obdormition: Obdormition is a numbness caused by prolonged pressure on a nerve,
  such as when a leg falls asleep if the legs are crossed for a prolonged period. It
  disappears gradually as the pressure is relieved (1).
• Whiplash: Paresthesias in the upper extremity may occur after
  whiplash injury (2), a type of cervical soft tissue injury (3). Pujol
  et al showed that 13% of patients with whiplash had associated
  paresthesias (4). Recovery usually arises within 6 months after injury
  (5).
• Hyperventilation syndrome: Paresthesia constitutes 35% of presenting
  complaints in patients with hyperventilation syndrome (6) and may
  begin after as little as threeminute of hyperventilation (7). After
  increasing the depth or frequency of respiration, www.intechopen.com72
  Paresthesia the alkaline shift produced selectively increases Na+
  conductance and ectopic discharges in normal cutaneous afferent nerves
  can be induced (8). Other electrolytes, i.e. magnesium, potassium,
  chloride, phosphate and bicarbonate, also demonstrated significant
  changes in concentration (7).
• Panic attack: Paresthesiae of the mouth, hands and feet are common,
  transient symptoms of the related conditions of hyperventilation
  syndrome and panic attacks. Ietsugu et al demonstrated that
  paresthesia can be used as a reliable indicator of severe panic
  attacks (9).
• Transient ischemic attack (TIA): TIA may be manifested by
  paresthesias. Several reasons may cause TIA such as thrombosis,
  embolus, intravascular debris and blood vessels disruption. Perez et
  al. reported the initial manifestation of cardiac myxoma can be
  paresthesias caused by TIA (10). Post-ischemic paresthesia occurs when
  hyper polarization by the Na+/K+ pump is transiently halted by
  elevated extracellular K+. The electrochemical gradient for K+ is
  reversed and inward transport of K+ triggers regenerative
  depolarization (8).
• Seizures: Paresthesia may happen during and after a partial seizure
  (11). Treatment of seizures with vagus nerve stimulation can also
  trigger paresthesias and is considered an adverse event associated
  with this treatment modality (12).
• Dehydration: At around 5% to 6% cumulative water loss, paresthesia
  may occur.
• Insufficient blood supply: Circulatory disorders could lead to
  transient or chronic paresthesia.

As you can see, there are many causes for paresthesia. The most common is the pressure on the nerves and the loss of loss supply.
Usually, the feeling quickly goes away once the pressure is relieved. But in your case, the paresthesia is delayed because it's caused by restriction of blood flow. Because it is caused by restriction of blood flow, it may take time  for the blood the reach the area and oxygenate the nerves.
Why does it get worse? Well, because the action of standing up causes the blood pressure and heart rate to increase, decreasing blood flow to the nerves (read the abstract of this). Another reason is that when standing up, there is increased pressure on the nerves, causing paresthesia. Together, these effects, may increase paresthesia for a few seconds. But when the blood flow becomes normal and the pressure on the nerve decreases, the paresthesia goes away.
There you have it! Nice and concise hopefully... @Daniel if you have more questions, you can ask them by adding a comment to this post.


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Duration of selection and survival of the fittest
I feel there is a part of the theory of evolution I'm not understanding correctly or maybe I'm missing it, but would like cleared up.
From what I understand, over time random mutations occur which in some cases provide an advantage allowing that animal to survive and reproduce. Its children will have that mutation allowing them to survive and so on over many many years until it evolves into a new species and / or the old ones become extinct.
For example the rock pocket mouse.
The part I'm getting stuck on is that unless these mutations happen instantly and in a large number, given its over such a big time scale how do animals who are not well adapted get enough time to evolve to survive?
Another example is fish that evolve to be able to "walk" out of the sea to escape predators.
If moving out allowed them to survive how did they get enough time to evolve and not be made extint in the time they didn't not have these limbs.
Hopefully I have explained myself clearly :)

Could not fit in a comment..
Welcome to Biology.SE! Here are a bunch of comments.

The sentence until it evolves into a new species and / or the old ones become extinct sounds weird and there seems to be some confusion between evolution and speciation. Also it seems that you have a very static view of what is a species, as if species were predetermined categories into which evolution came to show itself!
I am not sure but I think your question has to do with "valley crossing", that is "how can a population evolve toward some phenotypic trait if intermediate phenotypic traits are not fit?" Is that your question? You may be interested in "shifting balance theory" but it might be a bit too advanced.
It is common to overconsider the valley to cross (the deleterious impact of interemediate traits) and those traits are not necessarily so deleterious
Mutations do not always have small effects on traits. One mutation may have some very important impact and therefore, one mutation alone might be enough to cross a whole valley! You amy be interested in Fisher's geometric model. Fisher's geometric model is just some very arbitrary model and is not much inspired by any biological observation but it helps getting the concept of how mutations impact fitness (=function of survival and reproductive fitness).
When you say how do animals who are not well adapted get enough time to evolve to survive? I may use the word animals to refer to populations or to individuals in a population (extinction of genotype is a population and extinction of populations are two different things). If you referred to individuals then, your interest seems to be into "valley crossing" and "mutational effect"(effect of a mutation on phenotype or fitness). If you referred to populations, then you may be interested in "evolutionary rescue" or more broadly speaking in the so-called "theory of extinction".
There are probably other posts (or part of answers) on this site that will help you. A very good answer would be very very long. But maybe a moderately good answer may be relatively short!

From what I understand, over time random mutations occur which in some cases provide an advantage allowing that animal to survive and reproduce. Its children will have that mutation allowing them to survive and so on over many many years until it evolves into a new species and / or the old ones become extinct.
The part I'm getting stuck on is that unless these mutations happen instantly and in a large number, given its over such a big time scale how do animals who are not well adapted get enough time to evolve to survive?

You are quite confused about what is evolution!
The idea is not at all that all the individuals of a population will acquire the same change and become another species.
One individual gets a beneficial mutation and thus reproduces faster than others. So this mutation spreads little by little in the population because eventually only descendants of the first individual bearing the mutation will remain.
This is what is called a selective sweep. But it has nothing to do with the concept of species, which involves much more complex processes.


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Anesthetics, specifically inhaled anesthetics
I have had a look at previous inhaled anesthetics and many of them appear to be fluorocarbons. What could be the mechanism behind fluorine's anesthetic properties? Is it the specific bonding pattern or the molecules involved?
I realize anesthetics are rather unknown I just wondered what people have as a hypothesis?

Note that Fluorine is not anaesthetic. Inhaling fluorine would give you a permanent anaesthesia. :P

The following is one of the many elegant statements in General Anesthetic Actions on GABAA Receptors:

It is the fervent view of the authors that general anesthesia is no different from any other pharmacological process: exogenously administered drugs interact with key sites on cellular proteins in the body which results directly in the alteration in the function of these proteins, in the present case, neuronal proteins that control how information is conveyed through the nervous system.

Isoflurane, Sevoflurane, and Desflurane, the current inhalation general anesthetics, along with Halothane and the intravenous anesthetics Propofol, Etomidate, Methohexital and Thiopental, enhance the function of GABAA receptors (GABAARs), the most abundant fast inhibitory neurotransmitter receptor in the CNS (ligand-gated chloride ion channels) by increasing the affinity of the receptor for GABA. Since these receptors are abundant in parts of the CNS that process higher-order brain functions, it stands to reason that GABAAR function is central to memory, awareness and consciousness. GABAARs are involved in mediating hypnosis, depression of spinal reflexes, and amnesia, three of the classical components of general anesthesia. Isoflurane, Sevoflurane, and Desflurane enhance the amplitude of responses to low concentrations of GABA and prolong the duration of GABA mediated synaptic inhibition.
A very good starting point for your investigations can be found by clicking on the linked article above.
Agent-selective effects of volatile anesthetics on GABAA receptor-mediated synaptic inhibition in hippocampal interneurons
The sedative component of anesthesia is mediated by GABA(A) receptors in an endogenous sleep pathway

You would find it interesting that Xenon is also an anaesthetic (blocks NMDA receptors) [ref].

@WYSIWYG - Yes, it is very interesting! But, as you pointed out, the receptor is different, and I stuck with GABA(A)Rs (as OP wanted info on the halogenated anesthetics), but it's all very interesting. That was a nice article, thanks! Very informative.


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Why can't people talk while inhaling?
Why do we have to exhale in order to talk? From looking on Wikipedia, it seems like it has something to do with the glottis, but I'm not clear on the mechanism that makes speech sound so different when air is coming in.

As I understand it, speaking requires exhaling because air must pass in a forward motion across the vocal chords.

Via deep scientific analysis (i.e. trying it myself 5 seconds ago), I have determined that you can in fact speak while breathing in, it just sounds funny.
Think of the vocal chords as being like the body of a flute. As air passes by them, they vibrate and make sounds. Through careful modulation of their shape, specific sounds can be reproducibly made (this is equivalent to opening and closing the stops on the metaphorical flute). The way the pressure in your throat changes when you inspire (breathe in) is very different from the way in which the pressure changes when you expire (breathe out). These pressure differences are a large part of the reason why you sound different when you speak during inspiration as opposed to expiration, just like breathing into a flute differently would produce different sounds (although potentially the same notes).
Other physiological, neurological, etc. effects probably also cause differences in the vocal cords during expiration/inspiration and thus also contribute somewhat to the differences in the sound.

I agree. I knew someone who spoke on inhalation most of the time. It was disconcerting.


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If my brain lost all of its activity for a moment, would my memory be gone too?
I can't remember which question it was, but in the past here, it was explained to me that memory is actively stored in the brain, rather than "physically". Meaning, memories are made up of the brain's activity, not its physical cell structure.
I'm not sure I have that right though. I mean, that, for one thing seem inefficient and overly complex. It seems like a vast amount of energy would be required to store so much information in the form of activity patterns. Maybe I misunderstood. So I'm asking. If my brain lost all of its energy (activity) for a moment (for example, one second), would my memory be gone too?

Summary
Working memory on a current task could be distorted, but I cannot find a reason to suggest sudden loss of electrical information would permanently alter short or long term memory.
Hopefully a neuroscientist can answer with a more electro-chemical oriented answer, but fundamentally I think the experts aren't sure what a memory actually is (there are only a handful of theories each that are understudied or flawed). This is also a fairly hypothetically question. Baring these points in mind, treat not only this, but all answers skeptically and take with a pinch of salt!
LTP
A recent review by Baudry et al covers the modern biochemical view on  long-term potentiation (LTP) of the hippocampus that is probably responsible for things like learning and memory. It is a complex protein formation involving BDNF, calpain, and synaptic modifications. If hypothetically you became 'brain dead' for a moment, this way of looking at memory probably wouldn't take a hit.
Engrams
Something I have less of a grasp on is Richard Semon's Engram, but was more heavily studied by Richard Thompson. Even the most modern studies describe this kind of brain mapping as chemical and cellular rather than electrical. So again perhaps nothing other than the unstored would be lost.
Working Memory loss
This rather technical article discusses primate prefrontal cortex neurone firing as a persistent stream needed for a "working memory". I am out of my depth here, but it seems like some "forming" memories may be lost if there was momentary activity loss, but I don't see why the underlying biochemical state that cause this effect would be lost, so very little information would be directly lost.
Memory loss. Diseases that cause memory loss involve tissue and protein changes along with other physiological changes. Memory loss induced by trauma is likely caused by swelling where the neurones are damaged by swelling or the trauma itself on a cellular level. It seems to be the case that the electrical information isn't the important factor to memory loss.
Note: I think memory would be lost indirectly, perhaps removed in a similar way as when you wake up from a dream or in cases of trauma. I am also ignoring that there would be a reasonable probability that this would induce seizure, stroke, or other bad health effects!

Memories are dynamic; that is not equivalent to "memories are evanescent". Cellular structure and composition controls memory, not just a continuous passage of signals. This point is already discussed in the comments.
Loss of energy (in the form of ATP) would cause memory deterioration and in some cases neuronal cell death too— strokes, which happen due to lack of blood supply to brain (and hence unavailability of nutrients and oxygen) can cause amnesia.
But one second will practically not affect anything.

I found the answer to my question here, however not linked to a duplicate question, so I'll quote:

Memories are represented in the brain as patterns of firing neurons.
  Let's say, for simplicity, that each neuron can either be on or off.
  Since there are 86 billion neurons in the brain, we can experience
  2^86bn possible brain states. That's a lot.
Of course there are a lot of simplifications here--most notably, there
  is a lot of structure to the brain, and so i'm not suggesting you can
  store 2^86bn memories--but the logic is the same. Even with only 1,000
  neurons, we can store a ridiculous amount of information (2^1000).
  - Jeff

And from the comments, I understand that this quote is not totally accurate, as a brain state is not a memory, and we just simply dont know enough about memory to do this kind of calculation, but the start of this quote is the key to the question:
Memories are represented in the brain as patterns of firing neurons.
Meaning yes, if the brain lost activity for a moment, its stored information would likely deteriorate tremendously, if not completely. That is, if my cited information (and interpretation of its effect)  is correct.

@Jeff I quoted you.

I cannot find any academic literature about memories being "firing neurones". Could you cite this please? I am quite interested!

@GoodGravy This is only information that I'm citing from another answer. It could be incorrect.

I found an article about persistent firing in the prefrontal cortex (responsible for conscious thought), and as a part of the study they found persistent firing, but this wasn't really to do with short or long term memory as far as I can deduce, but rather "working memory". As described in my answer, this firing is still the result of chemical cellular states, so might not take as big a hit as it would first seem.

There is no basis for this conclusion: "Meaning yes, if the brain lost activity for a moment, its stored information would likely deteriorate tremendously, if not completely. That is, if my cited information is correct." Since the neurons themselves are still extant and unchanged, as soon as they started firing again, the memories would all be there.

@anongoodnurse don't neural connections weaken when not active? Is that not a fast process?

You would have to define a time scale, its probably much much slower than axon firing.

@GoodGravy I edited the question to specify a period of one second.

@CuriousProgrammer - It takes longer than a second to disrupt neuronal pathways.

@anongoodnurse When you talk about disrupting neuronal pathways are you talking about altering synaptic connections, or how long it takes a voltage to be passed along the length of an axon?

@GoodGravy - altering synaptic connections.

@anongoodnurse Yes that would take time. I think what Curious is asking is that what if you removed the voltage from everywhere in the brain for a second. Would this change, or alter synaptic connections after a "reboot"?

@GoodGravy - Even though this is impossible to demonstrate, I'm pretty sure it would not have a significant effect.

@anongoodnurse I totally agree.

Let us continue this discussion in chat.


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A few questions regarding immunology
I know that there is a variable region on antibodies which can recognize a wide variety of antigens, and that germinal centers create more "fit" antibodies to respond to an infection.
So I was just wondering:

Does this process itself evolve? Only vertebrates have this type of immune system if I understand correctly, do we actually get better (faster/more efficient) at responding to disease?
Is there any antigen which antibodies don't recognize?
Can an organism be so efficient at this process of immune response, that it essentially never gets sick or dies of disease?
There are cases where organisms contain viruses which do not harm them. Could an organism have this relationship with all viruses? As in, no virus is actually a disease to them?

Your question(s) is too broad. You should narrow down to a specific point.

This is a pretty broad question, but I will try to give an answer:
This process will undergo further evolution over time, no question. It has evolved into the current state and there is no reason to assume that this ended. When there are mutations which prove advantageous, they will evolve. This may also involve a faster response time for example, but we can of course make not definite claims about it.
There are antigens which are not recognized by the immune system, the process is called molecular mimicry. In it, microorganisms mimic molecules or structures which are found inside the body of the infected person and which are therefore not recognized by the immune system (if the immune system recognized self-antigens, this leads to autoimmune diseases). Have a look at the references 1 and 2 for more details.
This is a rather theoretical question. Our immune system is really efficient in clearing potential threats before you get a real infection. You can see the difference when you compare healthy individuals with persons which are immuno suppressed because of a transplantation. These persons need to be very careful about their environment in avoiding the exposure to potential pathogens. And they easily get infections. Additionally microbes evolve to evade our immune system. So I think the answer here is no.
These are viruses which co-evolved with the organism, an example would be the ebola virus in certain fruit bats. Here it does no harm, while it is a big problem for humans. As there is a really, really big number of viruses available in nature, it is quite unlikely that we learn to tolerate all of them. Additionally viruses mutate and change over time, so we would have to learn again to live with them.
References:

Molecular mimicry
Molecular mimicry and immune-mediated diseases.


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Why do we have two of some organs, but not all?
We have two eyes, but we don't have two hearts.
Why do humans have two of some organs, but not all?

I think the question is answerable, so long as OP doesn't want to know about EVERY organ!

Several processes come into play here, e.g. 1) functional redundancy, 2) evolutionary contingency, 3) energetic costs of redundant organs and 4) developmental constraints (related to evolutionary contingencies).

Also the fact that you can easily use some of the already developed genes .

We don't have that many double organs (https://en.wikipedia.org/wiki/List_of_organs_of_the_human_body): Most of musculoskeletal system. Digestive: salivary glands. Respiratory: bronchi/lungs. Urinary: kidneys&ureters. Reproductive: ovaries/testes + tubes. Endocrine: parathyroids (four even), adrenals. Circulatory: Mostly two for minor vessels, lymph nodes, bone marrow. Nervous system: Mostly two in PNS, two eyes & ears. Plus mammary glands. Everything else usually exists only once (though possibly symmetrical).

The body appears so symmetrical mainly due to the musculoskeletal system and a handful of large organs.

Here is my overly succinct answer.
I doubt we will ever know this for sure. But, it basically comes down to ancestral bilateral symmetry in development; this defaults to two organs and is broadly symmetrical except where the organs are central. See this article for a more thorough answer regarding bilateral symmetry.

Further exceptions to symmetry occur where evolution pressured the body into not bothering to grow the second of an organ due to a waste of resources for the body, or functional advantages emerged from asymmetrical evolution. I always like the ears of an owl for an excellent example of two asymmetrical features that provided a discrete advantage when it comes to locating the source of a sound.

@DavidBlomstrom The function reasoning doesn't explain how or why two organs are generally prevalent. Using function as an explanation for evolution is the wrong way around and arguably is retro-causation. You could say "symmetry resulted in two eyes and natural selection kept them for functional advantage" but not "We got two eyes for functional advantage and hence symmetry emerged."

The heart is centrally located in fish. And when you look at how the heart develops... it is symmetrical until it starts twisting upon itself and growing partitions in its middle. https://www.google.com/search?q=evolution+of+heart+in+vertebrates&biw=1138&bih=515&source=lnms&tbm=isch&sa=X&ved=0ahUKEwikze2Ay77RAhXJ7iYKHWrMB9UQ_AUIBigB#imgdii=1axaY6MFMVEcmM%3A%3B1axaY6MFMVEcmM%3A%3B1ZMer0S_aEDmwM%3A&imgrc=1axaY6MFMVEcmM%3A

How about octopuses? Octopuses have 3 hearts

@Pablo People dedicate their lives to studying the evolution & function of the octopus anatomy! You could ask a new question on some specific piece about that. Let's not forget that the OP is aiming to find out about why human anatomy seems to have one or two of each organ.

I didnt mean to make the question about octopuses. What I meant was, if humans have one heart because they only have duplication when the organs arent centrals, shouldnt octopuses have one heart also? The comment is meant to question if humans have only one heart because the heart is in the middle , considering that rule doesnt seem to work in other species

@Pablo The three hearts of the octopus is a bit more nuanced than you've made it out to be. It has one main heart and two auxiliary organs pumping blood to the gills. Why? I have no idea, but it doesn't seem to go against anything in the answer.

For some organs, the function is really dependent on having two: two eyes offer the possibility to appreciate distances, two ears to appreciate directionality of sound and to balance oneself.
Bilateral symmetry is both a good way to obtain these twinned organs, and may also be physically easier to obtain in the course of evolution (see the work by Vincent Fleury, University Paris Diderot, e.g. http://www.ncbi.nlm.nih.gov/pubmed/21784360). Perhaps this is mechanically quite advantageous to have symmetry for balance reasons. You'll note that the vehicles designed by the human are mostly symmetrical too.
This may explain why there are two lungs, e.g. Two brain hemispheres are justified with a symmetric body plan as many anatomical features are mapped directly in the brain geometry (see Fig 5.6 in http://www.bem.fi/book/05/05.htm, of course sensory and motor are in both hemisphere). But evolution has also been able to depart from this symmetrical plan when having twin organs would be more of a coordination nightmare: e.g., two hearts would make it difficult to have a sensible circulatory system (at least some dyssymetrisation would be needed so that they would direct the flow in the same direction! [no reference on that, you can draw a symmetric circuit with two pumps and see for yourself])

Edited. As the post covers a number of subject, it'd be good to know where the moderator feels more references are needed.

@DavidBlomstrom The function reasoning doesn't explain how or why two organs are generally prevalent. Using function as an explanation for evolution is the wrong way around and arguably is retro-causation. You could say "symmetry resulted in two eyes and natural selection kept them for functional advantage" but not "We got two eyes for functional advantage and hence symmetry emerged."


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Modified Mendelian Ratios Problem
I'm studying modified Mendelian ratios. I've got a theoretical problem that I'm stumped on:
A species of bird may have normal wings, or a mutation that causes frazzled wings.
I do 15 identical breeding pairs, crossing a male bird with frazzled wings to a normal winged female. The progeny obtained are 46 with normal wings (22 male/24 female) and 23 frazzled, all male.
Afterwards, I mate the normal winged females to the normal winged males obtained from the above cross. The progeny obtained all have normal wings.
I figured out a possible solution, and would like to know if it makes sense:
Z(f) = Z sex chromosome with normal wing gene, recessive
Z(F) = Z sex chromosome with frazzled wing gene, dominant
W =  W sex chromosome

Z(F)/W = abnormal wing female bird (does not survive as not enough
gene product produced)
Z(f)/W = normal wing female bird
Z(F)/Z(F) = abnormal wing male bird (does not survive as not enough gene product produced, or possibly survives as just enough is produced by 2 mutant genes, doesn't matter anyway)
Z(F)/Z(f) = abnormal wing male bird (survives as wildtype gene produces enough product)
Z(f)/Z(f) = normal winged male bird

My crosses:
P1: Z(F)/Z(f) × Z(f)/W
Progeny: Z(F)/Z(f), Z(f)/Z(f), Z(F)/W (fails to survive), Z(f)/W
F1: Z(F)/Z(f), Z(f)/Z(f), Z(f)/W in 2:1 normal:frazzled wings
F2: Z(f)/Z(f) × Z(f)/W produces Z(f)/Z(f), Z(f)/W

This would account for the phenotypic ratios seen in the problem, and also uses the ZW sex chromosome system found in birds. The genetic explanation would be that a single Z(F) does not produce enough product to thrive, for whatever reason. The trait is sex-linked dominant on the Z chromosome.

Can you shorten your question. Just keep the latest part that you want to ask with minimum required background.


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What makes DNA sticky-ends sticky?
When restriction enzymes jaggedly cut double stranded DNA it results in so called sticky ends. What is the substance that makes the DNA sticky?

Sticky ends also called cohesive ends, in DNA the ends are sticky means they combine together as glue, because they are complementry.

What are sticky ends.
There is no substance that is attached making the DNA ends "sticky". What has actually happened is an overhang of at least a few nucleotides. Blunt ends are another kind of cut, but have no overhanging residues.

Why are sticky ends sticky?
Restriction enzymes usually cut these ends deliberately so that a four nucleotides are overhanging on the 5' end of the double strand. These are complementary to other overhangs and because they are less stable than a bound double strand region, and are able to hydrogen bond easily with complementary bases, they are easier to attach with a ligase.
Below is an image of the base pairs interacting via H bonds.

The sticky ends are sticky because they have complementary bases. Typically used restriction enzymes cut the two complementary DNA strands at different spots, generating 'overhang', or sticky ends:

These overhangs allow for perfect base pairing (C with G, A with T), which is the result of hydrogen bonding. Just like water molecules show strong affinity to each other or other molecules with -OH and -H groups (e.g., alcohol), hydrogen bonds between nucleotides glues the ends together.
The principles of base-pairing has been nicely answered by @MadScientist in "Why does A pair with T and G with C?"

The "substance" is hydrogen bonds (H-bonds), or rather the potential to form them. Each of the unpaired A/T bases in the sticky ends have the potential to form 2 H-bonds with a complementary T/A, and each of the unpaired G/C bases have the potential to form 3 H-bonds with a complementary C/G.
From the perspective of a biophysicist, H-bonds are often thought of as being the strongest intermolecular interactions. I personally think that it's a little bit lazy and unphysical to see things this way, but the prevailing view in the field is that H-bonds determine specificity in all macromolecular interactions (e.g. the specificity that causes a single DNA strand to bind mostly to complementary DNA strands and poorly to random DNA strands).


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How does the eye know whether to focus further out or nearer in order to bring a blurry object into focus?
If the eye sees an object, but the object is out of focus, the eye could be focusing too near or too far. How does the eye (or the brain) distinguish one situation from the other?
How does it know whether to focus closer or further?
I'm interested in the case when:

only one eye is open (There must be another way besides parallax clues).
The object is an unfamiliar size
The object is an unknown distance from the eye.

Ideas so far
Does the eye try focusing either a little nearer or further and then if that doesn't help to make the object clearer then the eye focuses in the opposite direction?
Or is there some light-sensitive apparatus that is always a focused a little nearer or further than the rest of the eye, and so for instance if the cells which are focused further out are giving a clearer picture than the other cells then the eye knows to focus further out?
Or is the blurriness of a object closer than the focal point a distinguishably different sort of blurriness than an object beyond than the focal point?
Or is there some other mechanism altogether?

This may be a nobody knows kind of question! My pure guess would be that without depth perception your brain tries to make out edges. If the edges are sharp, it is focused, if its not sharp, it tries refocussing until it gets a sharp edge.

Interesting question! Determining the focus of a visual image is carried out in the visual association area of the brain. Ultimately, this process results in focusing of the retinal image by adjustment of the shape of the lens in the eye. Lens shaping to focus the image is called accommodation
The neuronal circuitry involved in accommodation includes the following structures:
The input to the accommodation response is provided by the retina, optic nerve, thalamus, and visual cortex. The visual cortex projects to the association cortex.
The (simplified) output scheme is the following: The association cortex projects to the supraoculomotor nuclei, which in turn generates motor control signals that initiate the accommodation response. The signal is then sent bilaterally to the oculomotor complex, and hence input from one eye is enough to focus both eyes.
The motor output regulates the ciliary muscles that control the shape of the crystalline lens. Negative accommodation  adjusts the eye for long distances by relaxation of the ciliary muscles. Positive accommodation  adjustment of the eye for short distances by contraction of the ciliary muscles Medical Dictionary.
As to the second part of your question: how out-of-focus images are functionally recognized:
There are at least three mechanisms responsible for accommodation:
1) Detection of image blur: if an image is blurred / out of focus the edges are not clearly defined. Retinal blur can be detected (edge detection) and assessed in the brain. Correction is then initiated as described above, and is basically done by trial and error. If adjustment results in a change of blur, the accommodation response (lens deformation) is detected as useful and accommodation is initiated. The accommodation itself is also based on trial-and-error: if blur increases the accommodation is reversed, if it decreases accommodation is increased in the same direction. (Philips & Stark, 1977). Image blur operates monocularly and is sufficient for accommodation to occur and is likely the most important mechanism for accommodation. It can occur without prior knowledge of distance, size etc.
Two more specific cases also result in accommodation, with likely similar neural circuitry involved:
2) Vergence / retinal disparity. This stimulus is generated when the eyes move both in opposite directions, i.e. when focus shifts toward objects closer or farther away. The temporary displacement on binocular retinal images is detected and leads to initiation of accommodation Fincham & Walton, 1977.
3). The near response: While 1) and 2) are retinotopic responses, the near-response is initiated by spatiotopic stimuli, including perceived depth and distance of objects, which are derived from cues such as relative size, overlap, perspective, shading and texture gradients as well as small timevarying dynamic depth cues which include motion
parallax, loom and motion in depth. Dynamic cues provide time-varying references for perception of relative depth whereas static cues allow simultaneous comparison
of separate absolute distances from which relative depth is perceived (Schor et al., 1991).

If this is the case, what will happen if the object i am seeing does not have sharp edges? For example a blurred image on a computer screen

The neurology of vision is an extremely complex subject and is difficult to describe with any brevity, because there is so very much going on in so many parts of the brain. It is estimated that about 50% of the pathways of the brain, and about 30% of the cortex are involved in vision (where only 8% of the cortex is devoted to touch, and 3% to hearing). Some research estimates that eighty to eighty five percent of our perception, learning, cognition and activities are mediated through vision.1
The ability to accurately focus on an object, sustain that focus, and to change focusing when looking at different distances is called accommodation. That happens with the pupil size, the lens shape, etc. but it doesn't tell us how the brain chooses on what to focus. The short answer is that it's much more than focusing like a camera lens. We have retinal areas that simultaneously pay attention to further and closer areas, light/dark, edges, and more, all going on at once. That and much more information carried to the brain is processed, and efferently focus is honed. It's even more complex when two eyes are involved.
There are so many aspects to sight that an enormous number of kinds of optical illusions exist. They are involuntary. That's why they're fun. In fact, if you weren't tricked, it would indicate a problem in part of your brain. Here's one that relies on processing contrast:

As you scan looking at the white dots, your peripheral vision seems to be able to see black dots, but it's clear on scanning them one row at a time that there are no black dots.
In the following illusion, the red vertical lines are parallel.

The following are summaries of the neuroanatomy of vision.
Eye, Brain and Vision
Anatomy and physiology of the afferent visual system
1 Vision Is Our Dominant Sense


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Intro Bio question: dihybrid punnet square
Today we had our exam. There was a punnet square for two genes. and when I multiplied , for example, Ry × rY I wrote the answer as RyrY. When I returned back home I realized that I may have made a mistake because the book used to write them as RrYy. So is my answer write or wrong? why? I also freaked out because there were 16 boxes in the punnet square so does that mean that I'll lose 16 points? I got everything else in the exam correctly. So I'm freaking out because I don't know if I'm getting a 100 or 86 which will throw all my work the entire semester. Please respond as soon as you can. I feel like I'm having a panic attack.

Hah! You can relax. There's no difference between RyrY and RrYy, as there is no fundamental ordering of genes like that. That being said, the standard convention would be to write RrYy (or at least RryY), so if your grader is a pedantic hardass they might take off a couple of points, but probably not the whole 16.

I LOVE YOU! I've been worrying so much. This literally made my day


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General time reversible model of evolution and Felsenstein model
I would like to get suggestions for the books related to General time reversible model of evolution and Felsenstein model etc. Specifically the mathematical treatment of these topics and concepts related to general balance and detailed balance etc. Can someone point out any books, links etc related to these.

I never heard of these terms. To satisfy my curiosity and assuming that you have some reference, can you please provide a link to the definitions of these things (or to the original articles)? Time reversible model of evolution kinda sound like coalescent theory. Are you sure those are not the same thing? There is a very good book by John Wakely called Introduction to Coalescent Theory.

You can find some information, with references to the original papers, on this Wikpedia page: https://en.wikipedia.org/wiki/Models_of_DNA_evolution#GTR:Generalised_time-reversible.28Tavar.C3.A9_1986.29.5B9.5D (I won't try to offer a summary, because it's not by field.)

The classic answer would be Joe Felsenstein's Inferring Phylogenies. It has substantial technical discussion of GTR and Felsenstein models, among others.
However, it does not have any index entries for "general balance" or "detailed balance". I was not familiar with these terms, so I googled them and they do not appear to be common terms in the phylogenetics field.
These terms do pop up in the MCMC literature a bit regarding transition probabilities, so it seems likely that it is somewhat related in terms of underlying math. However, I think that you are more likely to find phylogeneticists talking about "stationary" or "equilibrium" models rather than in terms of "balance". Possibly a difference in terminology between fields.
It might be helpful to know more about what you mean by these terms and why you are interested in them, in the form of links or otherwise.

I was curious to read about these when I was doing course work. Thanks for the response. Now I have moved into a different field. But I will go through it when I find free time.

Of course- I have started answering older unanswered questions because I think it's useful for future users at least. It is understandable you might have moved on, this is from 5 years ago after all!


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How does a multicellular, eukaryotic body treat heat-resistant pathogenic bacteria?
How does the said body treat heat-resistant pathogenic bacteria? If fever is the body's response to foreign microbial invasion, then what happens if the bacteria is heat-resistant but the body's own cells and enzymes start to denature due to the excess heat? Are there other mechanisms that the multicellular, eukaryotic body can use to defeat foreigners?

I am confused. 1. Do you think fever in response to infection actually cooks people (denaturing proteins)? 2. What about heat-resistant bacteria would prevent the body from making antibodies to it?

The usual 'heat resistant' bacteria or thermophiles are free living organisms with specific niche and are not pathogenic. Most pathogens are mesophiles and that is why they are grow in the body temperature. Spores are thermotolerant but spores are dormant and are not actively growing microbes.
Having said that, different mesophiles can have different levels of thermotolerance. Pyrexia (fever) is not necessarily a defensive mechanism and is more of a by-product of a systemic inflammatory response. Moreover bacteria are more tolerant to temperature changes than our body; there are definitely other mechanisms to combat infection. Read about innate and acquired immune response.

Additionally, the niche of thermophiles is the hot pond they live in. They need these temperatures and don't grow at lower temps. Growing them is a real pain.


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Separation of closely-sized isoforms
I have to separate two proteins of 86kDa and 80kDa respectively, however, I just cannot get a decent separation even in 6% polyacrylamide gel. To make matters worse, these two proteins are isoforms and there is no commercially available antibodies to differentiate either one. I am pretty sure raising an antibody against one of the isoform is not an option for me.
I am tying with the idea of reducing the gel to 4% (I am pretty sure I am pushing it already) or a 2D gel (both isoforms seem to have the same IP though).

Why are you reducing the gel % ? Increase the % for resolution.

6kDa are usually enough to separate two proteins in my experience. Try the other way, use a 7 or even 8% gel. They run longer but have a higher separation capacity. If you look at this figure from the LabFaQ, you see that you can use a higher-percentage gel:

The other thing are the antibodies: Where are your isoforms different? 6kDa are 55 to 60 amino acids more for the long form, so there should be enough possibilities to make specific antibodies.


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Is sexual selection evolutionarily advantageous?
Our biology teacher says that peacocks will soon become extinct because of bigger and bigger (and heavier and heavier) tails. Why natural selection did not eliminate sexual selection?

If that's a direct, unqualified quote your biology teacher doesn't know what he's talking about.

Wasn't there a study showing a correlation between attractiveness of peacock tails and some positive attributes (egg size?) of the offspring? I.e. it is just signalling?

What does "evolutionary advantageous" mean?
First note that is sexual selection evolutionarily advantageous? is a question that makes no sense. An allele or a trait can be evolutionarily advantageous if it increases the fitness of its carrier. If an allele, an evolutionary process or an environmental change decreases the risk of extinction for a species, then you cannot talk about evolutionary advantage. Selection (whether natural, sexual, artificial or whatever) does not (necessarily) minimize the risk of extinction of species.
This post is very related to your question and is definitely worth reading.
I hope your teacher didn't really say that! Assuming he did say that, then know that it is really not as easy as he's suggesting.
There are a number of studies that address the question on whether Sexual Selection (SS) and Natural Selection (NS) have opposite or antagonist effects. The subject is not easy and as SS is not my field of expertise my answer will not be complete. I will talk about two possible hypotheses for explaining the existence of SS and what they mean in terms of probability of extinction.
Good Genes
Under the "Good Gene" hypothesis, females' preference (we'll assume that females are choosy but there are many species where males are choosy) of some traits evolve because those traits are correlated with the global health of the male. In consequence, by choosing a male carrying some trait, the female makes sure that her offsrping will receive good genes from their father. This hypothesis assumes that poor males cannot produce fancy phenotype, while good males can. This is called Zahavi's Handicap Principle.
Under this hypothesis, if a trait become too costly for a given male, the male will just die, therefore limiting the evolution of secondary sexual traits. As a result, the population will no get extinct. Furthermore, under this hypothesis, SS may actually increase the effect of NS making sure that only the best male reproduce. In results the mean absolute fitness of the population should increase faster in a population where "Good gene"-SS occurs.
Sexy Son
Females preference for some trait may also evolve because mating with a sexy male means having sexy sons. This is called the "sexy son" hypothesis.
Under this hypothesis, again if a sexy male has a low enough survival, then a female has better to mate with a less sexy male (even though her offspring won't be very sexy) so to increase the survival of her offspring. After a bunch of generations, all females will end up preference mating with non-sexy male, changing the concept of what we call sexy in this population and therefore reversing the effects of SS.
You may also want to read about Fisher's runaway processes.
Just an article among others
Aneil Agrawal has some nice articles on SS that may interest you. This article for example discusses how sexual antagonist genes influence whether SS has an antagonist or parallel effect to NS.
Is SS really different from NS?
Your question Why natural selection did not eliminate sexual selection? assumes that NS and SS are two different things! This is a very old-style point of view. Charles Darwin coined these two terms thinking of two, unrelated processes. Today, most authors see SS as being part of NS (if a chestnut tree is a type of tree, SS is a type of NS). And many of the processes that are termed SS has actually not much to do with "competition to access a mate" but only has to do with NS. For example, many people talk about SS when talking about sexually antagonist genes or sexual conflicts. In short, the concepts are kind a mixed up. You may want to read about the work of Hannah Kokko about the semantics of terms related to SS.


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Can rapid eye blinking induce epileptic seizures?
Photosensitive epilepsies are characterized by visually-induced seizures. Flashing-light stimuli are known to induce seizures in some (but not all) patients. My question is whether people with this type of epilepsy can self-induce seizures by rapid eye blinking?

I'd guess not - a strobe light's pulse can last a few milliseconds, while a blink can last a hundred times as long.

Photosensitive epilepsy is often evoked at flicker frequencies of 3-30 Hz, which should be feasible through eye blinking. However, I couldn't find any info on self-induced seizures, and it is not listed in common causes of flash-induced seizures. E.g.: http://www.epilepsysociety.org.uk/. More common causes are computer games, TV screens etc.

@Bez and others - Why is this question put on hold? There isn't any self-referral present? I find it rather interesting and couldn't find anything on it.

This is an interesting question and NOT a personal medical question!

@ChrisStronks reopened for your pleasure.

“Self-induction” in photosensitive epilepsy is a well-described and fascinating  phenomenon. Photosensitivity itself is rare, occurring in only ~5% of patients with epilepsy.1 Among this group it has been estimated2 that 25% self-induce epileptiform activity. The most common methods appear to be passing a hand with open fingers repeatedly across the visual field and, as you query, blinking.
Quoting from a classical paper on the topic by Andermann et al:3

The method of inducing seizures varies
  both in detail and in principle. Light contrasts are always brought about, but they may either be applied to and alternate for the whole visual field—an effect produced by blinking or batting the eyelids and induced by any flickering light—or else the attack is elicited by the spatial displacement of brightness and darkness  over the retina.

This phenomenon is most common in epileptics with established photic triggers, and the scenario triggering an attack is often in the context of bright sunlight. However, this has also been described in epileptics who are not otherwise photosensitive. See, for example, “Seizures triggered by blinking in a non-photosensitive epileptic.”4
Notably, some authors have questioned whether blinking and other “triggers” are actually themselves ictal phenomena (i.e. representing the initial phase of an epileptic event) rather than a form of voluntary self-induction. For more on that hypothesis, see Ames, 1971.5
Presuming that this is, in fact, self-induction as has been traditionally postulated, the question of why such patients repeatedly self-induce seizures is perhaps the most interesting aspect of this. There has been some research2 considering the psychiatric factors underlying the behavior. Quoting Andermann3 again:

The reward a patient seeks by self-stimulation may lie in escape from unwanted situations, in attracting attention, in punishing those around him, or, indeed, in deriving pleasure from the attack.

References

Kasteleijn-Nolst Trenité DG. Photosensitivity in epilepsy. Electrophysiological and clinical correlates. Acta Neurol Scand Suppl. 1989;125:3-149.
Ng BY. Psychiatric aspects of self-induced epileptic seizures. Aust N Z J Psychiatry. 2002 Aug;36(4):534-43.
Andermann K, et al. Self-induced epilepsy. A collection of self-induced epilepsy cases compared with some other photoconvulsive cases. Arch Neurol. 1962 Jan;6:49-65.
Rafal RD, Laxer KD, Janowsky JS. Seizures triggered by blinking in a non-photosensitive epileptic. J Neurol Neurosurg Psychiatry. 1986 Apr;49(4):445-7.
Ames FR. "Self-induction" in photosensitive epilepsy. Brain. 1971;94(4):781-98.


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Which three functional groups are found in the general structure of amino acids?
Yes, I know, not two, but THREE.
EDIT: Yes, sorry but I did quite a bit of research, searching my notes and textbook for the answer, but all I could find was TWO functional groups as a opposed to the three my guide said there should be. Trust me, I looked quite a bit and there were many conflicting sources with different answers.

Your original statement of the question is a little bit lazy and lacking in background info. Please reword your question a little bit, and explain more of the background context and your own thinking on the matter, and then I'll update my answer, including the version of it that your professor was probably looking for in the first place.

Amine, alkyl, and carboxylate.

I'd guess the part that you're having trouble on is that the alpha carbon in the center of the generic AA structure is part of an alkyl functional group
Edit
The original answer that I gave might have been too clever for its own good. Depending on how one looks at the question, the third functional group could instead be the functional group of the particular side chain, i.e. for Alanine it would be a methyl group, for Tryptophan it would be an indole group, etc.

Please read our homework policy before answering questions such as this. We should not be giving out free answers to students who have not even done the most rudimentary thinking about their problem. This doesn't help them learn at all. Instead, I would recommend that you leave a comment asking for which groups they've already come up with, wait for an answer, and then ask them to think about the central carbon, and see if they can come up with the answer themselves. Spoon-feeding direct answers is not terribly helpful.

Homework question or no, it seemed interesting enough to merit an answer on this site. Also, having had a couple of hours to think about it the answer I gave is probably wrong, but out of deference to your concerns I won't correct it.

as long as the answer is here, you may as well correct it. I also agree that the question is interesting, all I was trying to say is that ideally, you want to get the OP to think about their problem a little bit. Suggest that they edit their question to describe what they've already tried. Some people are genuinly stuck, and it's fine to help them, but it's best to try and get some more info out of them first.


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Do the right-handed people tend to use the right side teeth of their jaw to chew food more often than the left-handed people?
And vice versa, do the left-handed people tend to use the left side teeth of their jaw to chew food more often than the right-handed people?Or the frequency of food chewing distribute fairly to both sides of the jaw?

Related: https://biology.stackexchange.com/questions/57361/do-animals-exhibit-handedness-paw-ness-preference

Individuals have not only hand dominance but also a dominant foot, eye and ear. There has also been a belief that this sidedness applies to chewing as well. However, the short answer is that no one is sure, but that it may be related to handedness. I only looked at studies done after 2000.
One large study[1] found a questionable to weak correlation, not consistently maintained through different dentition (baby teeth, mixed, and permanent). A slightly smaller study showed a correlation; in 78% chewing side preference correlated with other tested lateralities (footedness, handedness, eyedness and earedness).[2] Another similar sized study found none.[3]
A small 2012 study found that there was a preference for right sidedness when chewing hard food (73.68%) and for soft food (57.89%) but failed to correlate this with hand/other-sidedness.[4] Another small study tested for sidedness, finding that 55% of subjects did not have any side preference, 30% preferred to chew on right and 15% preferred the left side, and this was reproducible in 90% of subjects only with almonds (a medium hardness food) as opposed to jerky or asparagus. Unfortunately they did not measure sidedness. Their findings were that chewing-side preference is not a fixed characteristic, and texture seemed to affect sidedness.[5] A review article determined that a person's dental condition to a large extent dictates how they chew.[6]
The studies were mostly designed very differently, making good comparisons difficult. I think it's safe to say it's possible but not known with certainty.
[1] Absence or weak correlation between chewing side preference and lateralities in primary, mixed and permanent dentition
[2] Chewing side preference as a type of hemispheric laterality
[3] Relationship between chewing side preference and handedness and lateral asymmetry of peripheral factors
[4] Chewing side preference in first and all mastication cycles for hard and soft morsels
[5] Chewing-side determination of three food textures
[6] Adaptation of mastication in response to the characteristics of the individual or the food


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Can a rotten egg actually hatches to a real life?
First of all, I'm no expert in biology. I failed a lot in high school. Please bear with it if it's a stupid question.
For the past few days, I got a rotten smell as if an animal died in my kitchen. I cleaned and didn't find anything until I found the culprit today: leakage of rotten eggs.
There were two eggs in a hard plastic container, and one of them leaked a bit. Then I saw around 4-5 insects-kind of thing lurking around. It looks like a worm and if you ask me how those things look like, it's as if the egg yolk itself separated into the shape of worms and started moving. If I remember correctly, I believe I saw a pair of white dots (their eyes) in each.
Did those eggs (which was stored in a warm place) actually hatched and gave to a life? I threw all of them away, but I still feel really sick. Is it because of my carelessness that the egg yolk actually became alive in such shape?
Thanks beforehand.

The eggs only come to life when they get fertilized, which is not the case for hens which lay eggs commercially. Of course insects can live from the broken egg - it's pretty nutriceous.

The only thing that is going to hatch from a chickens egg is a chicken, not a worm. As chris said - commercial eggs are not fertilised so will just go rotten. The worms you saw can from another source.

Even if it were a fertilized egg, it wouldn't give rise to worms. If fertilized eggs are not refrigerated properly, they will also rot, not hatch a chicken. This is a question almost akin to spontaneous generation.

A chick can't develop outside of it's egg, so you won't see an embryonic chick growing and wiggling in a pool of substance leaked from a cracked egg.
Centuries ago, people believed in spontaneous generation: that life can arise from non-living things. A common example of this was the fact that maggots would "arise" from rotting meat if left to rot.
Although this theory was disproved, it is not rare to find someone that still believes it, because they seem to see it happen.
In the 1800's, before DNA was discovered, it became accepted that "like gives rise to like" - that is, chicken eggs will hatch chicks (not peacocks or mice), pea seeds will always give rise to peas, etc.
DNA was 'discovered' in the late 1800's by Johann Friedrich Miescher. He extracted a new king of organic moleculr out of cell nuclei, which he called "nuclein". Although Miescher did develop some hypotheses about how "nuclein" might be involved in heredity, he ascribed to the view at the time that any one type of molecule would be too simple to account for all the variation seen within species.
It would be about 75 years before the magnitude of Miescher's discovery would be fully understood, and that DNA is the basis for heredity.
Chicken eggs, if they give rise to anything (which will depend on if it is fertilized and properly incubated) can only give rise to chickens. Whether they are fertilized or not, they can't give rise to worms. A chick can't develop outside of it's egg, so you won't see an embryonic chick growing and wiggling in a pool of substance leaked from a cracked egg.
If you buy bananas and let them ripen and rot on your kitchen counter, you will suddenly find a lot of fruit flies in the house. The fruit flies did not spontaneously arise from the bananas; they came from eggs laid on the bananas before you bought them.
If you buy bananas and wash them well when you get home, and let them rot, you will not find fruit flies buzzing around them.
That is why your rotten egg didn't give rise to those little worm things.

In response to your first statement - that a chick can't develop outside of an egg - please see my new question. http://biology.stackexchange.com/questions/47924/can-a-chicken-really-be-hatched-outside-of-the-egg


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Does a bird know it's different?
I live in Northern Virginia, USA. As I am sitting here there is a large flock of small (blackish) birds in a tree. They are quite prevalent here. For the sake of brevity I will call these birds "sparrows." I don't believe it matters what they really are.
There are also several medium-sized blackish birds perched on the eaves of the townhouses. Again, I'll call these birds "crows". (We have a committee of large vultures (yes, really) in the neighborhood as well, which is why I call the crows medium-sized.)
The crows (tend to) lay their eggs in the sparrow's nests. Little crow hatchlings are then "raised by" the sparrow parents, along side thier smaller "siblings".
Does the now adult crow think it's just an oversized sparrow? (IOW, do all of the crows I see have identity issues and feelings of inadequacy due to their extreme gigantism? :) )

Any answer that attempts to directly answer this question would be conjecture.

Could this be not opinion-based if OP says instead: What phenomenon or phenomena does this most resemble?

Crows don't lay their eggs in sparrows' nests - they lay them in crows' nests. What you're describing, though, here is brood parasitism. This relieves the parasitic parent of the responsibility of rearing young, building nests, protecting the eggs, etc.
Brood parasitism is seen in a number of duck species, with females laying their eggs in the nests of others. One example is the goldeneye, Bucephala clangula. Interspecific brood-parasites include the most cuckoos and cowbirds, black-headed ducks, and indigobirds, whydahs, and honeyguides. About 1% of all known bird species are obligate brood parasites (never make nests, need a host).
Here is a picture of a reed warbler feeding a cuckoo which was a parasite, its egg having been laid in the warbler's nest.
Parasite nestlings suffer a relatively high mortality, either from rejection by the host (host bird will not feed the parasite) or rejection before fledgling (once nestling graduates to tree branch, the hosts stop feeding it). However, clearly since cowbirds and cuckoos are still alive and well, enough of them do survive.

Do they think they are of the host species? There was no literature I could find on this. While the parasite messes up the host parents and 'siblings' (when there are surviving 'siblings'), there is much less follow-up done on the behavior of the parasite once fledged. Common sense will therefore need to come into play.
If a cowbird thought it was an indigo bunting, it would not be able to reproduce, as it would try to attract a bunting mate and fail. Since the hosts continue to experience parasitism over many generations, and the population of parasites does not necessarily decline in a given area over several generations (in some areas, it is the host population that declines), I would have to say, yes, the bird 'knows' it's different (probably only on an instinctual - not cognitive - level); the parasite bird feels nothing about its bad behavior, and does not learn their own behavior from their host parents. Instinct takes over; they mate with their own kind, and continue to parasitize the host birds' nests.
Brood parasite
Host–parasite coevolution beyond the nestling stage? Mimicry of host fledglings by the specialist screaming cowbird
Brood parasitism by cowbirds: risks and effects on reproductive success and survival in indigo bunting
Brood parasite

When the baby cuckoo comes out of the egg, the first thing s/he does is that s/he pushes the legitimate egg(s) out of the nest! This means that the cuckoo instinctly knows that s/he is different.


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What is phenotyping of blood during transfusion process?
Thallaesemic patients are advised to have only "phenotypically matched blood".I mean the transfusion problems arise mainly due to "grouping problems" like mismatch b/w ABO & Rh+/- so what do this phenotyping mean? Isn't "grouping" of blood enough?
Statutory declaration- the link provided in the q is only to clarify in which context the q is asked & nothing more, like promoting Egyptian Gov. Health Service...(or any other CRAZY INTERPRETATIONS like that)**

This question appears to be off-topic because it is about a special process of the egyptian blood transfusion service, which we will not be able to answer.

excuse me....but I think you need to delve deeper into a q b4 u make such....naive comment.....Indian blood transfusion process also follows this....& if you really want to , then try to get through Wintrobe's Clinical Hematology (which is not possible for me at my stage)....

I do not think this question should be closed since I know a similar advice is dispensed in many middle eastern countries!

In response to the above q. many have commented that the process is only limited to Middle Eastern countries....I think the term 'only' will be better substituted by 'mainly', the reason to which , is explained later ....
Now, the main clarification lies in the fact that,

....there are more than 600 known antigens besides A and B that
  characterize the proteins found on a person's red cells. A combination
  of some of these less familiar but commonly occurring antigens are
  absent from the blood of an extremely small percentage of the
  population. There are also a few antigens that almost all people have
  on their red cells but that some lack. - One In A Million
  American Rare Donor Program

Now patients receiving a 1st time transfusion normally do not show any reactions or cross-matching problems with these blood subgroups but during repeated transfusion process like in case of thallaesemia , the receiver's blood gets sensitized against the donor's blood & the problems ensues...

Dr Therese Callaghan said, “All other antibodies are unexpected and
  are of two distinct types, alloantibodies (which target an antigen
  that is not present on your own red blood cells) and autoantibodies
  (which target an antigen that is present on your own cells).
“Patients receiving a transfusion for the first time do not normally
  have problems with matching blood types and antigens. However it is
  during subsequent transfusions when more care needs to be taken. If,
  during a later transfusion, the blood contains the same antigens as an
  earlier one, the patient’s immune system recognises the transfused
  blood cells as ‘foreign’ and the antibodies (formed after the first
  transfusion) will destroy the blood cells the patient has been given.
  This is called a transfusion reaction and can cause serious illness or
  even death if not treated quickly. That is why matching the blood
  phenotype is so important.”

Now coming to "Why mainly in Middle-East ??"
These rare blood groups are distributed into major 30 discrete system, which mainly  are present in different ethnic groups & communities...mainly living in Middle-Eastern states & Asia...& also in African countries...
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3353626/table/T3/
Intersted people may also check the following articles (or simply search Google)
To Provide Phenotype-Matched Red Blood Cells or Not – That is the Question!
13.3: Pre-transfusion testing- Joint United Kingdom (UK) Blood Transfusion and Tissue Transplantation Services Professional Advisory Committee
& for a complete picture plz browse through- Immunohaematology