text:
Is Chargaff's rule really applicable?

Chargaff's rules states that DNA from any cell of all organisms should have a 1:1 ratio (base Pair Rule) of pyrimidine and purine bases and, more specifically, that the amount of guanine is equal to cytosine and the amount of adenine is equal to thymine.

As in the table $A \ne T$ and $C \ne G$.
So I was wondering if Chargaff's rule is really applicable?

BTW did you try reading Chargaff's papers? This was way before the discovery of DNA structure. Even their method (at that time) of DNA extraction and analysis was not as refined as the ones that we have now. You may not find Chargaff's paper that easily but have a look at one of my answers in Chemistry.SE.

In addition to Remi.b's answer, it should be noted that the phage Phi X 174 is the only organism in your list which significantly deviates from Chargaff's Rule (by more than 1-2 percentage points for the A-T pair). While sampling errors are indeed more likely in organisms with small genomes, there is in fact another factor in play here.
This is because Chargaff's Rule only applies to double-stranded DNA, due to the complementary base pairing that occurs between A-T and C-G. Since Phi X 174 is in fact a single-stranded + sense bacteriophage, Chargaff's Rule is inapplicable to it, since it does not obey the standard Watson-Crick base pairing that is the molecular basis of Chargaff's Rule. In fact, the Wikipedia article from which you obtained the chart states this as well:

The following table is a representative sample of Erwin Chargaff's 1952 data, listing the base composition of DNA from various organisms and support both of Chargaff's rules. An organism such as φX174 with significant variation from A/T and G/C equal to one, is indicative of single stranded DNA.

Oh... how did I miss that?! Very good point! +1

@Remi.b because OP should have read about dsDNA

Does Chargaff's rule hold true on these data?
From the table:

Ratios A/T and G/C are close to 1 with an extreme at 0.77 and 1.05.
Ratios A/G and T/C are quite far away from 1, with several extremes around 2 or 0.5.

So, yes Chargaff's rule seems to apply quite nicely.
Why isn't the ratio A/T exactly 1?
The question of why the ratios A/T and G/C are not closer to 1 is interesting though. To fully answer this question I would need to go back into the primary literature who produced those numbers.
It appears that the three species of the list that have the smallest genome size ($\phi X174$, E. coli and yeast) are also the three species that show the greatest deviation from unity. The two species that have the largest genome size (maize and wheat) have the smallest deviation from unity. Overall, this suggests that this deviation is only a consequence of sampling error.
Did you say Sampling error?
This is just a small stat reminder
From Wikipedia

In statistics, sampling error is incurred when the statistical characteristics of a population are estimated from a subset, or sample, of that population. Since the sample does not include all members of the population, statistics on the sample, such as means and quantiles, generally differ from statistics on the entire population

Sampling error is not an error that a researcher does but an intrinsic property of the sampling process. Expected deviation from the true value is decreasing as the sample size increases, i.e. small sample size will show greater deviations (on average) from the true value than the larger sample size.

I would put it down to straightforward experimental error rather than sampling error. The methods used to obtain the numbers are relatively crude chemical methods.

Not sure if you mean "measurement error" or "bias" when talking about "experimental error". In any case, I am personally not be able to give my opinion on this matter as I haven't read these papers.

Preamble
My original answer to this question has recently fallen into the third circle of hell because of a contrast I made between physics and biology which seems to have offended some biologists. I shall let that rest, but provide a new answer to make one point that I feel some biology students need to absorb.
Answer
The use of the word ‘rule’ should be regarded with great caution in biology. There may be some rules or laws in biology that justify the name (e.g. those that apply to classical genetics), but in many cases, the term is misused.
I maintain that the word ‘rule’ was misapplied by Chargaff to what was actually an observation. In science what is important about observations is how their interpretation can lead to an understanding of fundamental processes — in this case, the base-pairing in the double-helical model for the structure of DNA in many chromosomes.
This is what the modern student should focus on — the understanding of the fundamentals — so that when faced with observations about a particular chromosome that are inconsistent with the double-helical model he considers whether the fundamental model of the chromosome might be different in this case, rather than frets about some incomprehensible ‘rule’.
In the case of 174 this leads to the answer provided by @MarchHo, that the chromosome is single-stranded. Another possibility one might have considered would be that there were other bases than ATG and C that had not been detected (we now are aware of chemically modified bases in genomes). The fact that this would have been incorrect in this case is irrelevant — it would be the way one would want a student to approach observations.
Footnote: History and Science Education
I am not against making students aware of the experimental basis of our current views of molecular biology, and (given my age) have been in a position to do that for a number of posts. In general, it is a difficult task because so much is known. However, I feel that the teaching of ‘Chargaff’s rules’ (and Crick’s wobble ‘rules’) is often done without due reflection because they have a certain scientific celebrity. As a teacher one needs to have the courage of one’s own convictions. I feel it helps students if one always refers to ‘Chargaff’s observations (his so-called rule)’ and ‘Crick’s wobble predictions (his so-called rules)’.
And it seems that I’m not the only one. In the 5th edition of Biochemistry by Berg et al. we have no mention of Chargaff’s ‘rules’. Instead we have:

“In 1950, Erwin Chargaff reported that the ratios of adenine to
  thymine and of guanine to cytosine were nearly the same in all species
  studied. Note in Table 5.1 that all the adenine:thymine and
  guanine:cytosine ratios are close to 1, whereas the adenine-to-guanine
  ratio varies considerably. The meaning of these equivalences was not
  evident until the Watson-Crick model was proposed, when it became
  clear that they represent an essential facet of DNA structure.”

Seems that there are some people who still need the security blanket of rules (and rulers?).

March Ho's answer is correct. However the important thing to learn from this is that biology is not physics, and there are no rules — only observations and explanations. What Chargaff made was an observation for which he had no explanation. It was only when Crick and Watson postulated AT,GC base-pairing in double-stranded DNA that the observation was rationalized. More important, those DNAs that were exceptions to the 'rule' could be rationalized as differing from the Crick/Watson model. In the case of phiX 174 it was because it had a single-stranded genomic DNA, but one can envisage other (incorrect as it turns out) explanations in terms of modified bases that were not detected in the assay. Biology is a science of exceptions rather than rules.

While the answer is otherwise good, I don't understand what you mean by "biology is not physics and there are no rules". As far as I know, rules are violated rather often (relativity vs Newtonian mechanics for example) in physics as well.

Rules (indeed Laws) in physics tend to involve equations based on a conceptual framework. Deviations of observations from equations (one can stick to Newtonian mechanics and look at deviations from Boyle's Law, I seem to remember) lead to modified equations based on additional assumptions rather than fudge factors. I don't see any equations or theory in biology, except at the very basic chemical level. It seems to me more that Nature finds one solution to a problem, we observe it, but it isn't a rule as somewhere else she solves the problem with a black swan.

Did you just say I don't see any equations or theory in biology?? You should read some primary literature then. I am a theoretician working in the field of population genetics (subfield of evolutionary biology) btw.

Well I'm molecular biologist turned bioinformatician with a first degree in chemistry. Sure there's a role for maths and theory in your sort of biology, but it doesn't underpin the subject like it does physics. And my answer was intended to help the questioner in a wider sense. Namely that she should not be looking to learn or lean on apparent rules, but to look for the pattern behind observations and prepare herself for Nature's variety of patterns. Shine and Dalgarno, won't prepare her for Kozak, and Kozak won't prepare her for internal initiation. Nor Mendel's 'laws' for McClintock.

@David biology has not been classically employing mathematics which the field of physics has been since ages ago. This is changing as more and more mathematicians (and even physicists) are applying mathematical models to explain biological systems. The issue is that biological systems are way more complex than a bouncing ball (or even space rockets). People like Remi and me and many others are working in this interfacial area where mathematical principles are combined with biological observations.

Fair enough. But there is a difference between mathematical modelling of complex systems and blindly learning 'rules', which the questioner seems in danger of doing. In this respect she is not unlike many very non-mathematical biology students of my experience, and my reply was an attempt to get such students to think about principles rather than parrot stuff from Wikipedia. The negative votes my answer has attracted seem to reflect the antagonism this guidance usually receives (unless it comes from people who think biology is physics). There's none so blind...

@david 1.I don't find anything in this question that a math-minded student would avoid. If a math-minded student avoid this; that means they missed or failed to detect an anomaly in a mathematical model. 2.if person/society deals with rules by blind memorization; that is the fault in learning & teaching, not the subject or area. 3.There are no difference in various subjects when we enter deeper understanding. Different 'subjects' are just to sort informations. in nature everything exists together. So, 'mechanics is the physics part and phenotype is the biology part' is a wrong way of thinking.

(…contd) As well there are yet-unexplored area living objects; such as consciousness. What you are telling; are some past and present ‘strategies’ to study life.  but that is not everything about life.  4.You’re trying to mean a ‘biological-rule’ is basically a description of a pattern or behavior. But isn’t’ even simplest rules of mathematics and physics are just description to universe’s behavior? Isn’t an anomaly in a genetic-language quite  same with  ‘another possible answer’ in a math.expression such as sq.rt.( 4) could be= -2 also, which is often not ‘passible’ in daily-life examples?

The asker is very appropriately wondered because they probably  appropriately understood how chargaff's rule (or pattern, whatever you say) could be derived from watson-crick's base-paired double helix model.

@David One good thing you observed... Mendel  to McClintock is not Copernicus to Newton. But Mendel to McClintock must be equals to Dalton  to Avogadro. and Wohler to Mullis is much like Copernicus to Newton or Galvani to Volta. Isn't? As well it is true that OP gives an example where we're discovering something from an exception, not from a uniformity. But  this as one and only possible strategy to living system, is quite oversimplification.


text:
What biological functions does crying serve?
Tears suddenly start flowing out of our eyes when we find our long lost friend or when someone unexpectedly decides to break up with us. Do tears really save us from harm? Or are they just the reflex shown?
What biological purpose do tears serve for the body?
As I understand it, crying causes endorphin release, specifically leucine-enkephalin. This serves as a painkiller for us. Are tears the only way to accomplish this? It seems I am missing something because oozing out of our eyes is an inferior pain distribution system to say; the circulatory system.

Homeostasis is the property of a system in which variables are regulated so that internal conditions remain stable and relatively constant. Your concluding sentence makes sense (what is the function of tears), but linking it to homeostasis per se draws the question specifically to the realm of fluid balance and ion balance. You should clarify this question I think.

I've edited it. If they don't account for homeostasis then why we consider them as reflex?

I would read the wiki page on Tears first

@علیآفاق I've made some big edits to the question to move it away from homeostasis. Feel free to roll back.

Emotional-tears (tears of cry) are different in biochemical composition than other-sorts of tears. Emotional tears contain higher concentration of neurohormones and it is believed that unwanted (toxic) level of neurohormones drained out in this way. view https://en.wikipedia.org/wiki/Tears#Chemicals_in_tears and https://en.wikipedia.org/wiki/Crying#Function.

Lets break this question into parts and answer them one by one.

Do tears really save us from harm?

Well, yes. Tears, mucus and saliva contain an enzyme lysozyme that breaks down the cell wall of many bacteria. Those that are not killed immediately are trapped in mucus and swallowed.1
You can, obviously, search on google for another reference if you do not believe this one.

Or are they just the reflex shown?

It depends on what type of tears you are talking about. Tears are divided into 3 categories:

Basal tears
Reflex tears
Psychic tears

In "reflex action" part, the cause is reflex tears. Reflex tears result from irritation of the eye by foreign particles, or from the presence of irritant substances in the eye's environment, which trigger TRP (Transient Receptor Potential) channels in the ophthalmic nerve. It can also occur with bright light and hot or peppery stimuli to the tongue and mouth... These reflex tears attempt to wash out irritants that may have come into contact with the eye.
These are, of course, different from those tears which "suddenly start flowing out of our eyes when we find our long lost friend or when someone unexpectedly decides to break up with us". These are psychic tears i.e. increased tearing due to strong emotional stress, pleasure, anger, suffering, mourning, or physical pain. This practice is not restricted to negative emotions; many people cry when extremely happy such as during times of intense humour and laughter.2
But the actual relation of tears with emotions can be summarized as:

There is an area of your brain specifically to deal with your emotions, called the limbic system (specifically the part of it called the hypothalamus), which is hard-wired into your autonomic nervous system (that’s the part you don’t have any control over).
This system, via a neurotransmitter called acetylcholine, has a degree of control over the lacrimal ‘tear’ system; and it is this tiny molecule which then stimulates tear production.
So in short, your emotional reaction to the break-up triggers your nervous system, which in turn, orders your tear-producing system to activate.3

Moving on to next part:

crying causes endorphin release...Are tears the only way to accomplish this?

Certainly not. Even when you exercise, your body releases endorphins. These endorphins interact with the receptors in your brain that reduce your perception of pain. So, tears are not the only way to accomplish this.4
At last, I would answer this part

What biological purpose do tears serve for the body?

as tears are necessary for the continued health of the ocular surface. Normal constituents include water, mucin, and lipids, electrolytes, non-electrolytes, and proteins. Retinoids are also important for ocular health and prealbumin may be a carrier for vitamin A in the tears to supply corneal epithelium with its requirements. Changes in tear constituents may cause certain ocular disorders.5
It is important to know here that by the above part, I meant basal tears and not psychic ones. Basal tears lubricate the eye, and help to keep it clear of dust. Tear fluid contains water, mucin, lipids, lysozyme, lactoferrin, lipocalin, lacritin, immunoglobulins, glucose, urea, sodium, and potassium. Some of the substances in lacrimal fluid (such as lysozyme) fight against bacterial infection as a part of the immune system. Lysozyme does this by dissolving a layer in the outer coating, called peptidoglycan, of certain bacteria. It is a typical body fluid with a salt content similar to blood plasma.
EDIT 1: Now, as you asked in the comments

what if we don't maintain our ocular surface?

I can tell you a very common example of dry eye syndrome. Dry eye syndrome is a common tears and ocular surface multifactorial disease, described by changes in the ocular surface epithelia related to reduced tears quantity and ocular surface sensitivity, leading to inflammatory reaction. It is believed that decrease in the tear volume on the corneal and conjunctival surface caused by either a decreased tear secretion or accelerated evaporation plays the main role. The clinical features of dry eyes include ocular discomfort, feeling of dryness, feeling of eye fatigue, hyperemia, kerato-conjunctival epithelial disorders and abnormalities of vision.6
EDIT 2: When it comes to function of psychic tears, then how could one leave talking about why we feel better after crying (except headache). It is now proven that psychic tears contain a higher amount of hormones than basal or reflex tears. See this article7:

Emotional tears are composed of more protein-based hormones, such as prolactin, adrenocorticotropic, and leucine enkephalin (a natural pain killer), which is suggested to be the mechanism behind the experience of crying from emotion making an individual feel better.

Though these hormones do not have any direct relation with emotions (excluding prolactin which counteracts the effects of dopamine), they can be related to emotions as long as another biological reason for their secretion through tears is discovered.
Bonus: From the same article 7, here is a very unusual function of tears i.e. controlling arousal! See this paragraph:

On a study conducted by the Weizmann Institute of Science in Rehovot, Israel, emotional tears from women have been found to reduce sexual arousal in men. Also, emotional tears are made up of a different chemical component than those evoked by eye irritants and can relay chemical messages to others. The change in sex drive could be attributed to a drop in testosterone provoked by the tear chemicals, reducing aggression. In the animal world, it has been found that some blind mole rats rub tears all over their bodies as a strategy to keep aggressive mole rats away.

This way, we can soon have a long list of functions. I hope these many functions are enough to answer your question.
References:
1: The body’s first line of defence
2: Tears - Wikipedia
3: Why do we cry? The science of tears
4: Exercise and Depression
5: Eyelid secretions and the prevention and production of disease
6: Recent developments on dry eye disease treatment compounds
7: Chemicals in tears - Wikipedia

In the last part you've talked about"Tears are necessary for the continued health of the ocular surface" but we do cry hardly a year ( males) what if we don't maintain our ocular surface?
can you elaborate it little more ( last part) ?

This does not seem to actually answer the question: you didn't explain what is the biological reason of what you called "psychic tears". It is not obvious why emotional stress should trigger a response which basically serves to "wash" the eyes.

@علی آفاق as I have told in the answer, crying is actually psychic tears, which is only one type of tear. Ocular health is maintained by basal tears. I will describe them too in the answer.

@gIS I have added that part too in the answer, hope this helps :)

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Metabolic activity postmortem
I read some papers about studies on metabolism in post-mortem tissues in human, but I do not exactly the reason about why our brain continues to have activity after death.

Welcome to Bio. Could you link those papers? I also think the definition of post mortem is important. Do you have one at hand?

Many definitions of death include brain death which is often defined as cessation of electrical activity in the brain (i.e. no metabolic activity).

Your question is a little vague and as Christiaan mentioned, linking to the papers would be useful. If I understand, though, you want to know why cellular metabolic activity that takes places after someone dies?
If that's the case, the answer is essentially that whatever kills a complex organism in the sense of causing the heart to cease beating, doesn't immediately cause every cell in the body to stop functioning at the same moment.
Now for a slightly longer answer...Consider someone who suffers a heart attack and dies. Blood stops flowing through their veins and cessation of breathing means gas exchange stops. For cells with extremely sensitive oxygen and nutrient demands like cardiac cells, cell death begins to occur rapidly. Other cells farther down the blood and oxygen supply chain have a greater tolerance to disruptions in nutrient supply and would have at least some store of nutrients to work with after blood flow stops. Those cells will keep doing whatever they were doing for a little while; metabolizing nutrients, transporting metabolites, transcribing genes, etc.
After a while, though, even they will feel the lack of oxygen. At that point, most cells will switch over to anaerobic respiration. The eukaryotic fraction of cells in our body isn't particularly good at this, but can struggle on for a little bit until they simply run out of fuel and begin to die, largely through apoptosis.
Apoptosis of some cells will actually help prolong the lives of some of the cells neighboring the apoptotic ones, an effect that probably encouraged the evolution of apoptosis. After a while, though, too much apoptosis will have occurred and an uncontrolled sort death called necrosis will begin, leading to cascades of cell death and cessation of cellular metabolic activity. This process can take days to occur, depending on many variables surrounding the death of the organism.
So far, this has all been about eukaryotic cells; cardiocytes, adipocytes, myocytes, etc. These are the smallest fraction of cells in our body, by cell count. The rest of our bodies are composed of prokaryotic, or bacterial cells. This is our microbiome and this is where (for me) things get really interesting.
Although our microbiome exists in a symbiotic relationship with our eukaryotic cell fraction, many members of the microbiome are less dependent on the nutrients found in our blood system than those eukaryotic cells. The cells of our microbiome are also frequently much more capable of surviving in low-oxygen or even anaerobic environments. These parts of us will continue to thrive for some time after we "die".
Some of our microbial cells, if left to their own devices, could even find new environmental niches outside our bodies and continue to live long after "we" have died. The quotes around 'die' and 'we' become necessary at this point because from here, questions of identity and life branch into the philosophical.
This became a lengthy answer, but I find it a really interesting topic. Here's a nice article from the Guardian, that discusses post-mortem cellular metabolism and our microbiomes in particular: https://www.theguardian.com/science/neurophilosophy/2015/may/05/life-after-death

It all comes down to what death is I guess.

True that. Definitely not a cut-and-dry definition... =P

I edited the tag wiki in an attempt to clear things up a bit. +1 for your efforts

Nice description @Forest (+1), especially how you took the topic from biology to philosophy ;-)

To elaborate on the comments - I think the question hinges on the definition of 'death'.
A brain-dead person is considered clinically dead. However, vital functions such as respiration and blood flow can be maintained artificially and pretty much indefinitely. So under active ventilation, a person in a brain-dead state feels warm to the touch and seems to be breathing normally. Yet, the person is dead (source: WebMD).
So as to your question I dare say that after death, there is no neural activity.
Conversely, when there is still brain activity I do not think the person is declared clinically dead. For example, cardiac and respiratory arrest can be acted upon by resuscitating the person. If the brain of such a person ceases to show activity, then little chance such a person will survive.
Reference
- Goilar & Pawar, Indian J Crit Care Med; 13(1)
PS: I edited the tag wiki to define human death more strictly

I would like to know what happen in the brain exactly

@user22053 - you really have to be more specific than that -

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Can bacteria, viruses, and cancer cells be destroyed by resonance?
Radiotherapy has been used to treat cancer.
Can the resonances by coordinated electromagnetic waves (and/or other forms of waves), of various frequencies, amplitudes and pulse rates, directed from various directions, be used to destroy harmful viruses, bacteria or cancer cells in a human body, without damaging the other parts of the human body?
(* NOTE * This question was posted here in Physics Stack Exchange too, but is possibly going to be closed in that forum as some claimed it is not so much about Physics.)

Welcome to Bio. This is definitely Bio and not a Physics question in this form. What do you mean with resonances?

By resonance I mean the molecules/structure of a, say, virus is made to vibrate with increasing amplitudes until the structure gets destroyed.

You cannot take things like that. Viruses/bacteria are made up of billions of atoms/molecules, all of which have their own resonance frequencies, and most of which may not coincide. To destroy a bacterium/virus, you will have to attack it with all of those billions of frequencies, millions of which will affect/destroy the neighboring cells too. It would be just like you make a man explode just by putting him on a speaker which produces that man's resonance frequencies. ;-)

Well, we don't have to explode something entirely to kill it.

...and we don't have to kill something to make it dysfunctional.

Your question included "other forms of waves" so I'm going to assume that the use of ultrasound to destroy cancer cells qualifies.
A paper published in the British Journal of Cancer in 2009: "[High-intensity-focused-ultrasound in the treatment of primary prostate cancer: the first UK series]"1 describes the use of a "Sonablate 500" device used to treat 172 men with prostate cancers at two hospitals in the UK, and its use is described as resulting in "acceptable short-term levels of cancer control."
However, the paper does lament the deficiencies of research in this area, the number of other treatments available, and the lack of longer-term follow-up to this research.
The answer to your question appears to be yes, with the qualification that this is an example using sound waves, rather than electromagnetic waves - isn't radiotherapy, mentioned in the first sentence of the question, electromagnetic waves?

Interesting. Yes, I am referring to all forms of waves, including perhaps magnetic fields, which have been used in MRI. I hope more research can be carried out in these fields.


text:
Definition of general anesthesia
To quote Goodman & Gilman :

An alternative way of defining the anesthetic state is to consider it
  as a collection of “component” changes in behavior or perception. The
  components of the anesthetic state include:
  • amnesia
  • immobility in
  response to noxious stimulation
  • attenuation of autonomic responses
  to noxious stimulation
  • analgesia
  • unconsciousness

My question is, does not the state of Unconsciousness already imply other components of analgesia and amnesia? Analgesia is the absence of the perception of pain, which is granted if there is unconsciousness which would be the absence of all perceptions.
I am not certain if unconsciousness also entails amnesia, but it seems that remembering what happened when unconscious seems considerably unlikely.
Apart from a reductionist argument for minimizing the constraints required for classification as a general anesthetic, I am more interested in cases where unconsciousness would be achieved without analgesia or amnesia, which could be a likely rationale behind including the additional caveats in the definition.

Well, I looked up the definition from Merriam Webster. But I guess what you state could be classified under the reflex autonomic loops, which I don't think are included under unconsciousness. And I think, probably, that the sensation of pain would begin only when he becomes conscious.

I guess the issue is what we mean by perception. If it strictly means stimuli perception, I guess it's not lost when unconscious. But I meant it more in the sensation way, the feeling of pain way. Sorry for the vague seemingly unscientific usage.

A state of unconsciousness does not guarantee analgesia nor amnesia. Besides, a muscle relaxant is often paramount to prevent movements. The perfect general anesthetic would do all of this and have hypnotic, analgesic, amnesic and muscle relaxant properties. Such compounds do not exist, because each effect works on a different part of the brain or elsewhere.
In practice, therefore, multiple compounds are administered to obtain the desired effect. A cocktail anesthetic not only ensures all the desired physiological changes, it also reduces the chance of toxic side effects relative to giving one constituent in a large enough dose to encompass all the effects. And there lies an important point, namely anesthetic depth.
If anesthesia is deep enough, all effects may, perhaps, be reached to some degree with a single compound, but the dose likely becomes so high that the side effects become too large. An example in this realm is alcohol, which when consumed in copious amounts, may come close in reaching all desired effects at least to some degree. A related compound is ether. But even with ether, which has been used in early days of surgery, surgical stress caused patients to die intra-operatively due to cardiac hyperactivity. Surgical stress needs to be minimized and that's why an analgesic is needed in the cocktail.
Commonly applied anelgesics in the OR are opiates, such as fentanyl. Anelgesics are critical for invasice surgery, because the body reacts to trauma even when the brain cannot process the information to the degree necessary to turn it into a conscious experience.
For instance, a widely used cocktail is propofol-based anesthesia: A propofol injection might be used to start anesthesia, fentanyl (injectable) is used to blunt the stress response, midazolam (injectable) given to ensure amnesia, and sevoflurane (inhalant) during the procedure to maintain the effects.

Great answer! +1. I was hoping, though, that the answer would give a passing nod to the need for an amnestic. Not a very comforting prospect.

Thanks a lot for a great answer. But my primary concern was the discrepancy in the definition. If there is a loss of consciousness, can there be a memory of what transpires therein? Are there cases wherein a person can be rendered unconscious but still not amnesic about that state? And second, if I understand correctly, analgesia in the definition mean a loss of afferent nociceptor input and not just a loss of the perception of those inputs?

A person may be unconscious but still can retain a feeling of something traumatic having happened during the surgery. This is called recall. You might want to read https://en.m.wikipedia.org/wiki/Anesthesia_awareness


text:
What are in common between transcription factors?
In terms of their structures (primary to tertiary) and locations?
Why do they have these commonalities? Or are any of these commonalities critical to their functions?

Transcription factors are a very heterogeneous group of proteins. Their two main objectives are to bind DNA & to recruit polymerase to that site. There are a of ways for them to accomplish these tasks.
To bind DNA, all they need is a pocket of positive charge, which are found in several structural motifs across many proteins. The wikipedia page actually provides a good sample of this diversity: https://en.wikipedia.org/wiki/Transcription_factor#Structural
The other co-factors that transcription factors recruit to get polymerase to the DNA strand also vary pretty widely. They link together through structurally complementary pockets of opposite charge, but beyond that, the details get pretty messy and there are a lot of details. Even reviews of transcription factors tend to focus on a specific class. If you want more than that very simplified explanation, I would actually recommend reading some reviews on the subject. Here are a couple:
http://www.ncbi.nlm.nih.gov/pubmed/25755661
http://www.ncbi.nlm.nih.gov/pubmed/25640595

Thank you very much for the answers. That is very clear.


text:
Protein-protein interactions search
I used STRING db in order to find all the interactions of the precursor protein APP. What I specifically need is a confirmation (supported by some article and experiments in it). But significant amount of interactors have only "Database" confirmation (mostly relaying on Reactome and KEGG data). Searching in these db's gives me neither article nor even the presence of these proteins in one pathway (what's weird). How can I obtain the data?
Thanks in advance!

Could you add the specific KEGG identifier?

@James As an example for some protein?

There are several reasons why you might not be able to find the references. You might not know what you're looking for or perhaps the specific protein is unreferenced. It would be useful to start with your example and work from there.

You can try to use IntAct Molecular Interaction Database. The data in this database is based on:

data from the literature or from direct data depositions by expert
curators
<300k binary interactions in 2011  developed by the EBI's
Proteomics Services Team
recent reference: Aranda et al. '10

This is also mentioned in the summary of the Aranda et al.'10 article:

IntAct is an open-source, open data molecular interaction database and
  toolkit. Data is abstracted from the literature or from direct data
  depositions by expert curators following a deep annotation model
  providing a high level of detail. As of September 2009, IntAct
  contains over 200.000 curated binary interaction evidences. In
  response to the growing data volume and user requests, IntAct now
  provides a two-tiered view of the interaction data. The search
  interface allows the user to iteratively develop complex queries,
  exploiting the detailed annotation with hierarchical controlled
  vocabularies. Results are provided at any stage in a simplified,
  tabular view. Specialized views then allows 'zooming in' on the full
  annotation of interactions, interactors and their properties. IntAct
  source code and data are freely available

Further you can use the Evidence tab in String(I assume you have already tried this but in the case you did not):

You can then click on Experiments, then something like this will show up:

You can see how (e.g. Reconstituted Complex assay) and you can see from which article this interaction is coming from if you click on an item in the table:

STRING database shows the protein-protein interaction network and scores according to the presence and absence of experimental verification which can be protease assay, bait coimmunoprecipitation, western assay etc.
if you need further confirmation you should read as much as related articles as possible related to APP.


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Population dynamics ODE with Allee Effects
From reading about Allee effects, it appears that there is a modification of the one-dimensional logistic equation to account for an allee effect given by:
$$\frac{dN(t)}{dt} = rN\left(1-\frac{N}{K} \right)\left(\frac{N}{A}-1\right)$$
Here, $r$ is the species growth rate, $K$ is the carrying capacity, and $A$ is the threshold for the population to not go extinct $(0<A<K)$.
A few questions about this model:
1) What is it in this equation that determines whether or not the allee effect is strong or weak? It seems like the parameter $A$ would determine where the threshold is but not whether or not the effect is strong/weak.
2) I'm interested in an extension to a system of $n$ interacting species. Suppose I have $n$ competing species where each one is subjected to its own allee effect. Is this a suitable modification of the above ODE for $n$ species?
$$\frac{dN_i(t)}{dt} = r_iN_i\left(1-\frac{\sum_{j=1}^n\alpha_{ij}N_j}{K_i} \right)\left(\frac{N_i}{A_i}-1\right)$$
where $1 \leq i \leq n$. In that regard, the first two terms are the usual Competitive Lotka-Volterra model, and the last term accounts for the Allee effect.

First, Allee effects (also positive density dependence) can be modelled in several different ways, and the equation you give is one example. The terms weak and strong Allee effects are in my experience used in a couple of different ways. Most often, strong density dependence is used to denote Allee effects where the per capita population growth rate can become negative, which means that there is a critical point in population size, below which the population will tend towards extinction. Weak Allee effects are then used to describe cases where the population growth rate is negatively affected by low population sizes, but where the per capita population growth rate cannot go below zero (so populations will grow at low population sizes). Remember that in the classic logistic model, per capita population growth rate is maximized when population size is low (limit towards N=0), while it is maximized between N=0 and N=K in models with an Allee effects (in the model includes a concept of carrying capacity).
Using this definition of weak vs strong,  your model has a strong Allee effect, since per capita population growth rate will go below zero at the threshold A (see below). However, sometimes strong/weak is used to denote some sense of relative influence of the Allee effect on population dynamics, for instance if per capita population growth rate at low population sizes is decreased a lot or a little compared to the logistic model, even if both cases would correspond to a weak Allee effect in the first sense.
For comparison, here are two examples of how an Allee effect can be modelled, that shows how the per capita growth rate is affected with an weak Allee effect (see e.g. Boukal & Berec 2002 and Ferreira et al 2012) or a strong Allee effect (your model):
$$\frac{dN(t)}{dt} = \frac{r}{K}N^2\left(1-\frac{N}{K} \right) \tag{weak}\label{}$$
$$\frac{dN(t)}{dt} = rN\left(1-\frac{N}{K} \right)\left(\frac{N}{A}-1\right) \tag{strong}\label{}$$
If per capita population growth rate (dN/dtN) is plotted against population size for these two models, as well as for the standard logistic model, this is what you get:

In these examples, r=0.7, K=100 and A=20. As you can see, there is a big difference between the weak and strong case. The population growth rate (dN/dt) at different N is shown below:

As you can see, if populations using the strong Allee effect are started below A (in this case 20) the populations will decline towards extinction (since dN/dt is negative below A).
The multi-species extension including species interactions that you propose looks ok to me, for that particular formulation of the Allee effect.
Also, for a flexible way to study the Allee effect, you might be interested in this formulation (see Boukal & Berec 2002), which can produce both a strong and a weak behaviour:
$$\frac{dN(t)}{dt} = rN\left(1-\frac{N}{K} \right)\left(\frac{N}{K}-\frac{A}{K} \right)\tag{flex}\label{}$$
This function will produce a weak Allee effect if $A \leq 0$ (very weak if A is far below 0) and a strong effect is $A>0$. The weak model I give above is a special case of this formulation with $A = 0$. Per capita growth of this model is given below, for two values of A (with r = 0.5 for the logistic model and r = 0.38 for the flex models)

As a sidenote, I've also seen cases where negative density dependence at low population sizes is described as an Allee effect (so that Allee effect can be used to denote both positive and negative density dependence at low population sizes), but this is not very common. For a particular species, negative density dependence at low population sizes (in excess of what is found in the standard logistic model) could e.g. be found in situation where predators have a switching behaviour, so that they stop eating the prey when it becomes rare.

This was an absolutely wonderful answer and very well-explained for someone like me who is a math guy with little biology experience. Thank you VERY much!

@Brenton I'm glad you found it useful!


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What are the evolutionary benefits for herbs having beneficial health effects on humans?
There are many types of plants which produce chemicals which can be beneficial in treating human illnesses, or at least alleviate painful symptoms.
Why would they do that?
Is it just random chance, like some plants being poisonous, some having no effect, and some having beneficial effects? However, for poison there are evolutionary benefits, as it might reduce the chance of animals eating the plant.
Many plant species produce tasty fruits for the purpose of having animals eat them and disperse the seeds. However, for most plants used for medicinal purposes, the leaves, roots or flowers are used, the cultivation of which doesn't seem to be useful for the plant itself.

Fruits serve a purpose, they contain seeds which are dispersed by the consumer. There is generally no benefit to having leaves and roots eaten, any effects on consumers are likely to be coincidental... I think that's the general principle - that may be wrong and there will probably be exceptions so I'm not posting it as an answer

Also note that not everything evolves for a reason, there are four mechanisms of evolution - only selection leads to adaptation (ie gives things a reason to have evolved) see illustrations here http://biology.stackexchange.com/questions/5007/how-is-evolution-possible-in-contemporary-humans/5058#5058


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Statistically, why is the number of mutated genes in eggs treated with chemical mutagenesis one?
Excerpted from the Guide to Research Techniques in Neuroscience [1]:

In chemical mutagenesis, a scientist applies a mutagenizing chemical, such as ethyl methane sulfonate (EMS) or N-ethyl-N-nitrosourea (ENU), to thousands of eggs/larvae, which statistically creates lines of ani- mals with mutations in a single gene in the genome.

My hypothesis is that the discrete probability distribution of the number of mutated genes can be approximated by a normal distribution with mean=1, thus it is said statistically the number of mutated genes is one. But how can the scientists know which organism or cells contains only one mutated gene, or for that matter one mutated gene that is caused only by chemical mutagenesis?

[1] Carter, Matt, and Jennifer C. Shieh. Guide to Research Techniques in Neuroscience. Academic Press, 2015. ISBN: 978-0-12-374849-2

The expected number of mutation would not follow normal distribution (ND) as you speculated because a ND would have negative values too as it ranges from $(-\infty,\infty)$, as Remi has also pointed out. In many cases a ND can be approximated because the variance would be so less that you can practically find no negative values. However, it is a wrong assumption to consider all biological statistics as ND by default. Please see this post. Basically, ND approximations can be made on multiple measurements that follow the central limit theorem. Now, in your case of a ND centered at 1, I'll tell you how that is impossible. You can have 2 and more than 2 mutations but you cannot have less than 0 mutations. The distribution is not symmetric and is skewed towards right. You also cannot have fractional mutations and therefore the distribution has to be discrete and not continuous.
Mutagenesis itself can be modelled as a Poisson process. For more information on this please see this post. So the probability of $k$ mutations in a time window, $t$, can be represented by the following equation:
$$P(n=k)=\frac{(\lambda t)^ke^{-\lambda t}}{k!}$$
Where $\lambda$ is the rate of mutagenesis.
The mean number of mutations (and also the variance for a Poisson distribution) would be $\lambda t$.
Now, the rate of mutagenesis would be proportional to the concentration of the mutagen. I speculate that the relationship between them would follow a saturation kinetics (like Michaelis-Menten) but at lower concentrations it would be essentially linear.
Moreover, the rate of mutagenesis would also depend on the cell type.
Therefore, standardization is required and labs working in this area for a long time develop standardized protocols (with specific mutagen concentrations and treatment times) which would let them avoid multiple mutations. Even then, they have to screen a lot of individuals to filter out the non-mutants.
Basically, there is no magic number.

What I think the text is saying
The text you quote is a little unclear (note that it is not a peer-reviewed article given the language used). I would think based on the quotation that the treatment is chosen so that the expected number of mutations is 1.

But how can the scientists know which organism or cells contains only one mutated gene?

You assume they are screening through the lines to find out those who contain a single mutation. This is not what the quoted text is claiming. The quoted text only states that the treatment create mutations at a rate of 1 per genome.
If they would have to screen through the lines to select those that have had one single mutation somewhere, then sequencing would be the only solution.
Note on Stats
The number of mutated genes after treatment is probably Poisson distributed, not normally distributed. A normal distribution is a continuous probability distribution anyway and is bounded between $-\infty$ and $+\infty$, while a negative number of mutations makes no sense.
Note on the design of the post
You should link to you source directly. It will be easier for those willing to answer

Not just because of the continuous nature, there cannot be a normal distribution with mean at 1 because there cannot be negative values for this whatsoever whereas there can be more than 2 mutations (which will skew the shape). You are right about Poisson distribution as we have discussed in your other post.

With the forward genetic screen approach you would treat the organism with your mutagen, and cross them to produce mutants. With forward genetics, you're using a phenotype to map out a gene. You isolate the mutants based on phenotype, and perform a complementation test to determine if the mutation was on the same gene or different genes. This was classically done with Drosophila.

By the classical genetics approach, a researcher would then locate (map) the gene on its chromosome by crossbreeding with individuals that carry other unusual traits and collecting statistics on how frequently the two traits are inherited together. Classical geneticists would have used phenotypic traits to map the new mutant alleles. Eventually the hope is that such screens would reach a large enough scale that most or all newly generated mutations would represent a second hit of a locus, essentially saturating the genome with mutations. This type of saturation mutagenesis within classical experiments was used to define sets of genes that were a bare minimum for the appearance of specific phenotypes. However, such initial screens were either incomplete as they were missing redundant loci and epigenetic effects, and such screens were difficult to undertake for certain phenotypes that lack directly measurable phenotypes. Additionally a classical genetics approach takes significantly longer.

Source: Wikipedia
The reason that I posted this answer is due to the context of chemical mutagenesis, provided on 335 of your source:

Chemical mutagenesis The use of chemical agents, such as EMS or ENU, to mutagenize
  hundreds or thousands of eggs/larvae for the purpose of performing a forward
  genetic screen.


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Relation b/w venation and transpiration
What purpose does reticulate venation in dorsiventral leaf or parallel venation in isobilateral leaf serve?
Does it have any relation with unequal transpiration in dorsiventral leaf or equal transpiration in isobilateral leaf?


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Why is mRNA used as a biomarker for cancer over tRNA or rRNA?
I cannot find a clear explanation for why mRNA is used as cancer biomarker and not tRNA or rRNA. Is there something peculiar about mRNA which cannot be fulfilled by tRNA or rRNA?

@ParthReghav what source are you seeing that mRNA is used as a cancer biomarker? mRNA is the protein coding RNA and it is proteins that are tumor suppressors or oncogenes - the answer to you question likely has its roots in that explanation

mRNAs encode specific genes and perform specific functions whereas the other two perform housekeeping functions in all cells. Changes in their expression are related to global changes in the cell.
The expression of rRNA and tRNA is affected in certain conditions such as stress and also possibly cancer (may be due to high replication rates). However, even if they are affected in cancer you cannot use them as markers for specific cancers as they are present and highly expressed in all cells.
Therefore specific tumour suppressor genes and oncogenes are studied.


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Color of DNA, available absorption energy levels of DNA molecule, mutations
I have done a couple of DNA separations and observe that the clumped strands of DNA are white.
Is that an artifact of the chemicals used in standard separations? Or is it indeed the case that the DNA molecule in standard conditions does not absorb many or any photons in the visual range?
If that is right, can we use this as evidence for why visible spectrum light doesn't cause mutations, unlike say higher energy photons in the UV range?
Looking forward to your thoughts.

The reason why visible light doesn't cause mutations are simply because it has not enough energy. For this reason it doesn't penetrate far enough into the skin and has not enough energy to do the damage. DNA itself is not white, this is only because it is clumped together and reflects the light.

Thanks @Chris. Even in theory, can a visible spectrum photon cause a mutation?

@SimonS Some chemicals can be photo-excited to form reactive intermediates and these in-turn can damage the DNA. Visible light per se cannot do any damage.


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I get regularly get déjà vu - but I know it's not a memory recall - I always think it's from a dream
My apologies if this is not the right forum for a neuroscientific/psychological question, especially not one coming from personal experience. Please close/move as appropriate :)
Doubtless we're all familar with déjà vu - people invariably describe it as the feeling of recalling their current situation from memory, as though they're repeating something they've experienced in real-life before.
I've regularly had this experience - it happens about once every month or two, the experience never lasts more than 5-10 seconds, and it can be unnerving. However my experience is different from what others always describe: when I'm having an episode I know I'm not re-experiencing something I've done in real-life before, instead I have this feeling that I'm experiencing something I've had in a dream before - a dream premonition, not a memory of real-life. After the experience fades I return to normal and recognize that I have no dream-memories of whatever it is I just experienced - a false feeling of post-hoc premonition.
My father reports the same as well, that he has times where he swears he's "seen this before in a dream" instead of a momentary false memory - he named the experience "breaking a dream" - no-one else seems to using the same terminology as my dad so searching for that online comes up blank. I do see very rare reports online of similar experiences but we "false-dream" deja-vu subjects are definitely in the minority.
I'm curious where my (apparently inherited) ability to slightly discern deja-vu experiences from false memories might come from, and how this "false dream-memory" vs "false real-life memory" difference has a basis in neurology.

Is this probably more suitable for cognitive science (cogsci.stackexchange.com)?

@Chris - nope, it's a personal question - I voted to close because of it here, and will do the same at cogSci.

@Christiaan I suspected that.


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Choice of Molecular markers to carry out molecular phylogenetics
For evolutionary analysis of different individuals within a population, the preferable molecular markers are non-coding regions of mitochondrial DNA. My question is that why they are used what is the logic behind that and why specifically mitochondrial non-coding region is taken for evolutionary analysis between them?

The molecular markers need have an appropriate amount of divergence to resolve the phylogeny at the desired scale. If the markers are too conserved, there will not be enough characters differing between taxa. On the contrary, if the markers are too divergent, the sequences may be somewhat randomized, there may be misleading convergences between distant taxa...
Non-coding regions are usually less constrained than coding regions, so they can accumulate more mutations. This makes them more suitable for studies at small evolutionary scale.


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Mitochondrial Genetic code
We know that the genetic code is universal. My query is why the mitochondrial genetic code is different from universal genetic code?

Your premise is incorrect, the genetic code is NOT universal. There is a 'standard' genetic code, which is found among higher animals and plants and most bacteria, but there is a variety of other genetic codes found in the main genome of more obscure organisms. These are listed at: http://www.ncbi.nlm.nih.gov/Taxonomy/Utils/wprintgc.cgi .
There is also no mitochondrial genetic code but a variety of mitochondrial (and plastid) genetic codes. One feature of genomes with non-standard genetic codes is small size, so that the number of proteins influenced by a change from a common precursor genetic code would have been small.
In the case of mammalian mitochondria there are fewer tRNAs and these have non-standard anticodon-codon interactions. Thus rationalization of these genetic codes may have been due to pressure to reduce the size of the genome.


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Is it possible that by mutation a human could see infrared or other 'colours'?

Incoming light reacts with the several types of cone cells in the eye. In humans, there are three types of cones sensitive to three different spectra, resulting in trichromatic color vision. Each individual cone contains pigments composed of opsin apoprotein, which is covalently linked to either 11-cis-hydroretinal or more rarely 11-cis-dehydroretina.
The opsins (photopigments) present in the L and M cones are encoded on the X chromosome.  A very small percentage of women may have an extra type of color receptor because they have different alleles for the gene for the L opsin on each X chromosome. X chromosome inactivation means that only one opsin is expressed in each cone cell, and some women may therefore show a degree of tetrachromatic color vision. Tetrachromacy is also demonstrated among several species of birds, fish, amphibians, reptiles and insects.
Humans cannot see ultraviolet light directly because the lens of the eye blocks most light in the wavelength range of 300–400 nm.
So, besides above mentioned exceptions, is it possible due to mutations or genetic engineering to see UV or infrared. What kind of mutations should be made or are the changes to be made in the opsines to big to create 'alien' eyes?

It might be easier to embed a microchip and a camera, though.

I seem to remember that kids can generallybsee farther into the UV range than adults typically do, perhaps because their lenses are smaller... but don't take my word for it.

UV sensing is possible and some animals do have UV-sensitive opsins. IR cannot cause electronic transitions. They can only affect vibrational states. Therefore the mechanism of IR perception would be totally different from that of the UV-visible spectrum.

@keshlam: afaik this is because the lens filters UV and the older you are the more it filters. People without a lens (or artifical lense) are indeed able to see UV, just not as a further colour, more like an overall white glow.

You might be interested in tetrachromates (https://en.wikipedia.org/wiki/Tetrachromacy) there seem to be some humans that are able to it.

Yes.
Far-red vision (>700nm)
The ability for retinal-binding proteins to absorb far-red (between 700nm-850nm) light has been experimentally confirmed in this paper. While the authors did not attempt this in vivo in an animal model, they managed to use directed mutagenesis to induce a significant shift in the absorption peak of the chromophore of the retinal binding protein.
The authors show the shifts induced by these mutant proteins in the figure below. The mutants have significantly different absorption peaks, and assuming that the proteins do not lose their ability to transduce signals via optic nerves, they would allow vision in different wavelengths.

Ultraviolet vision (300-400nm)
It is known that humans lacking a lens (aphakia) are able to see ultraviolet light. As noted in the question, the lens blocks out long-wave UV, and its removal or absence results in ultraviolet vision (although with low sharpness due to the lack of a lens).

However, aphakic patients report that the process has an unusual side effect: they can see ultraviolet light. It is not normally visible because the lens blocks it. Some artificial lenses are also transparent to UV with the same effect. The receptors in the eye for blue light can actually see ultraviolet better than blue. Military intelligence is said to have used this talent in the second world war, recruiting aphakic observers to watch the coastline for German U-boats signalling to agents on the shore with UV lamps.

I am not too sure about IR absorption. IR does not have enough energy to cause electronic transitions. Moreover I could not find a mention of "IR" or "infrared" in the linked paper. The wavelengths mentioned there correspond to far red.

Many animals that "sense" IR use thermoreceptors for it. The mechanism is totally different from that of opsins.

@WYSIWYG I don't get what you mean by "doesn't have enough energy". There is an entire field dedicated to absorbances caused by electronic transitions in the infrared region. Furthermore, thermoreceptor-based IR sensing works for far longer wavelengths from 5-30µm. I edited the answer to say "near-infrared" instead, since the M11 mutant has significant absorbance over 700nm (the rightmost boundary of the graph).

IR spectroscopy measures vibrational transitions as clearly mentioned in the first line. I meant that IR does not cause electrons to be promoted to an excited state (that is what I mean by electronic transitions). They cause stretching and bending of bonds (which are vibrational transitions). What you are referring to is called far-red.

YES Once I COULD saw , in a very dark place, a very very faint red or orange glow of light in a CCTV's IR-illuminator which was quite big in size (may be 10-12 cm  diameter), and containing many IR-LEDS; when we were transporting musical instruments from a programme in a school-building. Initially I suddenly thought, would I look something strange?  or illusion? for a while later  I could see (as if we feel at night stars come to notice with time) yes there the shade of darkness is quite different more reddish, dot-dot. With mobile-torch I found it was a CCTV  camera.

Far red (such as 780 nm) is indeed not the same thing as true infrared (beyond c. 800 nm) which can’t activate the normal human red-sensitive opsin. Ī̲ have some mild sensitivity to far red—that is, see a dim red light where some other people see nothing—but it’s IMHO not really “infrared sensitivity” even if LEDs which emit some amount of far red light are labelled as “infrared” for some reason.

March Ho's answer is quite good.  A few extra tidbits:

The population of humans contains DNA encoding for two substantially different M receptors.  (differing by more than normal variation) See tetrachromacy in humans.  (This doesn't produce IR vision except ...)
The population of humans contains DNA encoding for several different L receptors.  Two well studied variants have very similar peak absorbances at $555\,\text{nm}$ and $559\,\text{nm}$.  Although one variant has a slightly fatter "tail" out into the IR, this doesn't normally result in significant IR vision, except ...
People who work with intense near-IR lasers do report seeing a variety of "weird pink" from sufficiently intense lasers.  This happens with scotopic adjusted eyes and seems to be a "hard to interpret" mixture of rod+L excitation.  Also, some people report seeing the Wood Effect (intense IR scatter of sunlight from grass and leaves) when visible wavelengths are filtered out after scoptopic adjustment.  One theory for IR vision in humans is that detection is via a two-photon process in the rods.  Given that only intense sources are perceived, this isn't too far fetched.  (... and is quite cool -- nonlinear optics in your own eye ...)


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Is heat released during work due to ATP breakdown or a increased blood flow?
Is heating up of a body during work or exercise an effect of increased speed of blood or is it because of the extra energy released while harvesting energy from the ATP

ATP breakdown is the major cause of it. The body can use 45-55% energy liberated by ATP hydrolysis, and the rest part dissipates as heat.

Additionally, increased blood flow occurs as a result of increased ATP hydrolysis.

@Forest umm I doubt it. Any reference for that?

@another'Homosapien' I'm not sure why the first suggested edit you made was automatically rejected, probably because I was editing my own post at the time. Could you please suggest that original edit again and I'll approve? Thanks!

@another'Homosapien' - I figure that increased blood flow is due to increased heart rate, which means burning more energy, which must involve ATP hydrolysis. I suppose I could have included those steps in my first comment...Does this make sense to you, though?

@Forest as you say "increased heart rate, which means burning more energy" the only thing I can conclude from this is that increased heart rate leads to more ATP hydrolysis. So ATP hydrolysis seems more like a result than a reason for increased heart rate.

Is heating of a body the result of increased blood flow or extra energy from ATP?
It is mainly because of the breakdown of ATP (Adenosine Triphosphate, a type of nucleic acid with an Adenosine base, a Ribose sugar, and 3 Phosphate groups), alternatively and more formally known as ATP Hydrolysis. During hydrolysis by water, ATP splits into Adenosine Diphosphate (ADP) and an inorganic Phosphate (Pi), releasing some energy. I'll explain more below how exactly this works.
How or why does ATP Hydrolysis release energy?
If you take a look at a diagram of an ATP molecule, you'll notice that it has 3 phosphate groups, each with a Hydroxyl group (-OH) that has a net negative charge due to Oxygen being highly electronegative and hogging electrons from the Hydrogen bonded to it. Consequently, you have 3 molecules with slightly negative charges attached to each other. If you've ever played with magnets, you'll know that like charges repel. So overall, the ATP is highly unstable because of these repulsive forces that are situated so close to each other. When the bond between the 2 inorganic phosphates is broken, a large amount of energy is released. Here's a diagram from Campbell's Biology 9th ed (note that the Hydrogens in the phosphates are not shown for simplicity):

When the last phosphate is broken off, you are left with one molecule of Adenosine Diphosphate (ADP) and an inorganic phosphate group (Pi). Energy has been released. However, this is not the entire story. Generally speaking, ATP Hydrolysis does not occur without another component: an endergonic process. An endergonic metabolic process is any which requires energy input in order to proceed. Think of it with the following analogy: imagine a ball trying to roll uphill by itself. At the bottom of the ramp, the ball is very stable and has low potential for performing work. But uphill, the ball would have a higher potential energy. It is impossible for the ball to roll uphill from a state of low energy to a state of high energy. Thus, we first need an input of energy--say the mechanical energy of our hand pushing the ball--in order for it to move up.
Our endergonic process (such as in protein synthesis by a ribosome or the phosphorylation of glucose in glycolysis, the first step of cellular respiration) requires some energy input from ATP in order to proceed in an exergonic manner--that is, in order to release energy without any help. With our analogy, this is like pushing the ball to the top of the ramp and then letting go, allowing the ball to roll back down from a state of very high potential energy (and therefore instability) to a state of low energy. The energy that we had to input from ATP is known as "activation energy", because it's literally energy that we need in order to unlock or "activate" an endergonic pathway.
Example of ATP Hydrolysis releasing heat:
When you have an infection in your body, your hypothalamus will raise the body's set temperature point to induce shivering. Shivering consists of many muscle contractions, all of which require hydrolysis of ATP. The result is a release of a large amount of heat that increases body temperature to a point at which pathogens cannot survive.
What about blood flow?
Blood flow does not actually produce heat by itself, but it can direct heat to the surface of the skin, such as when the body needs to cool down. The main source of heat in the body remains the ATP.
EDIT: much of the information here can be reviewed in this wonderful YouTube video by Andrew Douch

I'm afraid this is not very accurate. ATP is only one form of energy in metabolism, and ATP hydrolysis is thought to be only about 1/3 of heat loss in typical oxidative metabolism; respiration itself, ion gradient dissipation, and ATP synthesis make up the larger part. Note that this concerns heat, for free energy, ATP utilization is indeed the major portion. The details of ATP structure and activation energy are not really relevant here, this is a question of thermodynamics.

My apology if the post is not helpful to the OP. I was just trying to be thorough so that I wouldn't have to explain various things in multiple posts. I felt like ATP structure was relevant, since structure is related to function and the OP's question was related to ATP function in heat production. Also, I'm about 99% sure that ATP's role in metabolism and activation energy are fairly relevant to thermodynamics. I was just trying to explain "how" exactly the heat is produced, since I've had far too many teachers who just tell me "well, it just does".

Is heat released during work due to ATP breakdown or a increased blood flow?
Short answer: neither. Most of the heat generated is due to poor efficiency of metabolism.
It is a common misconception that ATP is the same thing as energy when it comes to metabolism. ATP is certainly a very important energy carrier, but human metabolism is far from efficient at capturing the energy in nutrients in the form of ATP. A large fraction of the energy stored in sugar, fat, or other substrates is lost as heat already in the process of making ATP, much in the same way a car engine runs warm because most of the energy in gasoline cannot be captured in a useful form.
It is thought that most of the heat produced during oxidative metabolism (as in muscle contraction) occurs during respiration and ATP synthesis in mitochondria. This is probably because the mitochondrial respiratory chain involves physical pumping of protons across membranes (chemiosmosis) which causes a lot of "friction" (rougly speaking). This review estimates that only about 1/3 of the heat generated comes from ATP utilization and downstream processes, like actin-myosin contractions. It is difficult to quantify heat loss in metabolism, so I think all estimates should be taken with a grain of salt, but I think this general picture is correct.


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Soft Agar Substitute
I've got petri dishes with a base agar layer ready for E. coli culturing. However, I do not have soft agar in which to dilute the E. coli before pouring it on to the plate.
Any suggestions on what substance I can use to substitute for soft agar, or how I might be able to make it? I have the following at my disposal from the lab at school:

Tryptone base agar
Nutrient broth
MacConkey agar

The original soft agar medium had the following composition:

10 g Bacto™ tryptone
9 g Bacto™ agar
5 g KCl
1000 mL water

You want to take up the cells in a medium containing agar and then plate them?

@Chris Yes! I was originally using a soft agar solution composed of 10 g Bacto™ tryptone, 9 g Bacto™ agar, 5 g KCl, 1000 mL water.

And I guess that your standard plates are made with your media + agar?

@Chris Correct, the E. coli in the medium is poured over the base agar so the standard plates have the media and the agar.

Ah, I prepare the plates with medium + agar.

The good news is: You don't need any agar in your plating media, since the bacteria grow on the surface anyway and the plate can take up some additional moisture from your plating media.
What I usually do is to dry the plates for a while (and also let them warm up, since they are stored in the fridge) with the plate upside down and opened a bit. Contamination is usually not a problem here.
Then I dilute the cells in an appropriate volume of media, then plate about 50 to 100µl on the agar and spread it with a Drygalski spatula. Put the plate in the incubator and everything is fine.


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What are sources for learning bioinformatics for self-learning?
What are the sources for learning bioinformatics(books, websites/MOOCs)? Does it require prior knowledge of programming language because I am a complete noob when it comes to programming language.

If you want a simple place to start, try Rosalind http://rosalind.info/problems/locations/

Coursera has good introductory R and Python courses. They also have good intro courses for genomic data science. Edx also offers some interesting stuff for biological data science. You can find more but those are the courses I personally looked at and had a little fun with.

I agree with @CMosychuk - coursera is a great place to start learning for this field.

If you're looking for a book, Vince Buffalo's book "Bioinformatics Data Skills" gives a nice overview.  The first chapter is titled: 'How to Learn Bioinformatics'.  There are several chapters on familiarizing yourself with unix and one rapid introduction to R.  When I read the book I thought to myself, I wish I had this when I first started!

I recommend starting with a programming language that you are likely to use soon. And nothing in biology is more crucial than statistical analysis for which R is the golden standard. Datacamp.com has wonderful and coherent online site for learning R and applying it to statistics. I'd suggest to start with the free "Introduction to R" & "Intro to Statistics with R: Introduction" courses. They only take several hours and get you going. Then it is 9$/month (for students) for the other courses, but it's well worth and you can complete most of the courses in just  a few months anyways!

Learning a language such as python or perl is almost necessary.
You might have a look at coursera.
There are quite some bioinformatics-oriented courses:
https://www.coursera.org/courses?query=bioinformatics&languages=en
University of California San Diego has a series of bioinformatics courses, with one that seems made for beginners in programming:
https://www.coursera.org/course/algobioprogramming
I haven't had a detailed look at this one, but I liked their more advanced courses.
In coursera, the courses are often organized in so-called "specializations" which give you a certificate, but are not free. However, you can normally enroll to individual courses without paying.
I would also advise learning how to use a UNIX-like command-line environment, and tools such as sed, awk, grep.
The following sites might be good for this:
http://www.grymoire.com/Unix/
http://software-carpentry.org/lessons/
The scope of the latter is broader, and the things they teach could be valuable if you want to do scientific programming in general.

From what you say I would definitely not start by learning a programming or scripting language which may only be applicable to certain types of problems.
I would start by reading an introductory book on bioinformatics with a wide general scope. Then you can see what area or areas interest you and find out what tools (programming or otherwise) you need to become familiar with to solve problems in that area. (Because to really learn bioinformatics you have to solve problems.)
There are no doubt several suitable books. The one I am familiar with as it was used in my University is "Introduction to Bioinformatics" by Arthur Lesk (Oxford) 4th ed (2013). However it doesn't cover RNAseq, so unless there is a new edition in the pipeline you may be better with something more recent.


text:
Derivation of Michaelis' Equation from Michaelis' Constants
The enzyme reaction condition, $E + S \leftrightarrow ES \rightarrow E + P$ uses $\kappa_{1}$ (forward reaction), $\kappa_{-1}$ and $\kappa_{2}$ as the rate constants.
E: Enzyme
S: Substrate
P: Product
What is the relationship between $\kappa_{1}$, $\kappa_{-1}$ and $\kappa_{2}$ to yield Michaelis's constant:
$\kappa_{m}$ = ($\kappa_{-1}$ + $\kappa_{2}$) / $\kappa_{2}$ ?
I understand that $\kappa_{m}$ = $S$ at $1/2 \times V_{max}$, however I do not understand the relationship of the rate constants based on the enzyme reaction condition.
This question has been marked as a repeat of the question "How does pH affect Michaelis' constant". I am not asking for any affect with pH, just a proof for the mathematical relationship of the factors shown above.

I edited this question to ask for a proof, rather than a relationship with pH.

If you're asking for a derivation of the Michaelis-Menten law, I think that is actually a good question, because many biochemistry books are not very clear on this, even though the law itself is common knowledge. The best derivation I have found is the one given in Atkins' Physical Chemistry, http://www.amazon.com/Physical-Chemistry-Edition-Peter-Atkins/dp/1429218126

I've made some formulaic layout edits, if they are incorrect could you change them @rocc also could you say what all the letters mean (e.g. ´´where $E$ is for Elephants´´)

They are correct, thank you. I will put in the variable names.

@Roland, yes I am asking for a derivation of the law, but preferably in standard proof format. I will look at the link you posted.

I realized the Wikipedia page https://en.wikipedia.org/wiki/Michaelis%E2%80%93Menten_kinetics  does a pretty good job with the derivation actually. Also, please note that the Michaelis-Menten reaction rate formula is often used phenomenologically without really considering the model, just to have some rough description of saturation w.r.t. the substrate.


text:
How to transform snail shells into a fertilizer?
I heard that the chemical structure of the snail shell has elements that help in waste water treatment and in some cases as a fertilizer?
What is the process used to render snail shells into fertilizer and how effective is the derived fertilizer compared his regular peers on the market ?

Snail shells are composed largely of calcium, which is often used as fertilizer. As for wastewater treatment, I've heard about shells in general being used, mostly for their absorbent properties. I found this paper, which isn't long & might provide a bit more detail.
Hope that helps!

May I ask about the quality of the fertilizer derived from the shells and their effectiveness compared to other fertilizers on the market ?


text:
Effects of antibiotics on bacterial growth
I will do an experiment on effects of antibiotics on antibacterial growth and I will use three antibiotics: ampicilin, chloramphenicol and streptomycin. To make a hypothesis I must have a guess on which antibiotic will have the most severe effect on bacteria. So, do you know any source to find this information out or I would appreciate if you explain the reasoning behind a comparison of how severe these antibiotics.
Edit: Bacteria that will be used is E.coli.

This is impossible to answer without specifying what bacteria, and even so most antibiotics will not be effective against all bacteria of the same species (due to resistance). All these antibiotics are broad-spectrum and will have a "severe effect" on some types of bacteria.

Sorry, I edited the question.

I mean, theoritically which one is the most harmful?

The dose makes the poison.

@MarchHo - Not necessarily.

There is no previous research i guess

@BobSacamano there is research on this. Look for minimum inhibitory concentration (MIC) and LD50 values for these antibiotics. I hope your E.coli strain is not naturally resistant to either of these. Is it a lab strain such as K-12 or DH5a?

What would you recommend


text:
Molecular/cellular biology textbook to consolidate what I know about molecular/cell biology
I'm a medical student (who is halfway through med school) looking for a textbook that will consolidate some of the biology I already know. While I've read a lot of books that go into great detail about genetics, immunology and cell signaling, I've not found many books that focus on clear insights.
After recently having perused a very well-written nanotechnology book geared towards bionanotechnology ("Bionanotechnology: lessons from nature," by Goodsell), I found many cell biology topics very well explained. For example, it states simply that "lipids are used for infrastructure [in the body]", and that "polysaccharides are used in specialized structural roles". Such sentences I've personally never really come across in any of the "standard" molecular biology texts (Alberts, Cooper, etc); I found that they focus far too much on detailing exactly the components of the DNA polymerase, or the ribosome (which are very important, but also something I'd like to go "beyond".)
Clarification on what type of book I seek:

A book within cell or molecular biology
Scope of book; a book that covers any of the following: biochemistry, genetics (replication, translation, transcription, gene expression and its regulation, epigenetics, heredity, genetic engineering), developmental biology, cell biology (cell structure, organelles, cellular processes, cell signaling) and molecular biology (techniques such as high-throughput biology; concepts such as enhancers, repressors) and molecular evolution.
Level of the book doesn't matter, although I have completed all the subjects above at an undergraduate (bachelor) level - the book could thus be directed towards graduate/masters students.

Any books/texts that will hone one's knowledge on the subjects mentioned will be warmly received!

my opinion... but, if you're half finished with medical school I'd work on understanding clinical medicine - there is plenty to work on there and you can always come back to intensive molecular biology/etc after you've mastered clinical medicine

While I find this has little relevance to my original question, I'm currently looking to do systems biology research alongside medical school. I feel that a stronger intuition for cellular processes will probably do some good for an aspiring clinician-scientist.

Please have a look the tag-wiki for [tag:book-recommendation]. If you do not address all the points mentioned there then your question may be put on hold. These kinds of questions often lead to opinon-based answers.

Campbell's Biology is, I quote my biology teacher, "the Bible of AP Biology". I know you're a medical student and therefore far past that introductory college level, but Campbell's does quite a good and thorough job of explaining a plethora of biology topics. It's a fairly reliable textbook, I think you might like it. It also gives a good deal of examples for the various concepts and avoids such abstract statements as those you quoted from your textbook. I would suggest skimming through the book at a local bookstore if you can and seeing if it fits your criteria.


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Why is HIV associated with weight loss/being underweight?
It seems that people with HIV are often underweight, is there something (or multiple things) which cause HIV sufferers to lose weight? What is happening within the body as a  direct effect of HIV that will lead to increased weight loss?

"without all these headaches".. why? Do you plan to reduce weight by acquiring HIV??!! It sounds like that from your question. It is a disease which takes toll on the body. There are several AIDS related complications and the medicines can also have some side effects. Please improve your question.

This is the future, folks. People looking to acquire HIV so they can lose weight quickly. All the doctors hate it.

I've edited to make more about the mechanisms underlying weight loss in HIV patients.

Whatever you do, don't get HIV to lose weight. Dealing with HIV is going to be a much, much greater annoyance than losing weight is. I don't have it myself, but I know someone who does, and it isn't pleasant.

Here is a brief dissection of the causes of weight loss associated with HIV which are listed by AidsMap.com. Most were quite obvious (disease and side-effects of medicine often cause appetite loss, diarrhea, vomiting etc. - kind of trivial components of the answer) but the first two were more interesting (and new to me).

HIV can increase the rate at which the body uses nutrients (increased
  metabolism)

It seems that, at least in the early phases of HIV, the metabolic rate is higher. In one study, the resting energy expenditure of HIV patients was ~8% higher, and fat oxidation was increased. This will result in more calories being burned on a daily basis, and, to put it in perspective, ~8% of a males recommended daily allowance of calories is 200 calories, or about one 40g bar of chocolate. Patients will have to consume more calories just to meet their basic daily needs.

HIV can alter the lining of the gut, making it harder to
  absorb nutrients (malabsorption)

It seems the HIV virus is associated with inflammation in the gut, causing damage to the intestinal lining. The intestine is a major area of where we absorb nutrients from our food, if efficiency is reduced by damage and inflammation, then fewer calories will be absorb. Patients will have to eat more food to get the same amount of calories in to their system.

other gut infections can cause
  malabsorption and/or diarrhoea

Many illnesses that a HIV patient will contract will causes these problems.

you may eat less than you used to (and
  need to) because of loss of appetite during ill health

Simple one, less energy in = less energy to absorb, weight loss is all about calorie intake vs. calorie usage.

specific
  conditions may make it harder to eat, such as mouth and throat
  infections

Obviously some infections, such as herpes and canker sores, will make it unpleasant to eat. HIV leaves patients more prone to such problems so they will more frequently avoid eating because of the discomfort and pain.

some drugs may suppress your appetite or cause side-effects
  that put you off food, such as nausea, vomiting, indigestion or
  altered taste.

A lot of drugs, not just those that fight HIV, cause side-effects on appetite, vomiting, etc. Here is a list of various HIV/AIDS drugs and their common side effects. A quick eyeballing of that table suggests around 20 of 28 (~71%) are associated with some kind of vomiting or diarrhea.

why you mention "you" in answer? i am not facing HIV.

those are quotes from http://www.aidsmap.com/Unintentional-weight-loss/page/1044802/


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Can Bacteria Repair Dephosphorylated Plasmids?
I have been trying to insert a short sequence of DNA into a plasmid. I wanted to make two different versions, with the insert at different locations. I chose HinDIII and SalI sites approximately opposite each other on the plasmid and designed oligos with HinDIII or SalI sites, and of course extra bases on the ends to allow proper cutting.
I cut the plasmids and oligos and dephosphorylated the vector to help prevent empty vector ligations. I mixed the plasmid and oligos and ligated, then transformed into bacteria, all standard stuff.
The HinDIII version worked the first time, with few colonies on the empty vector control plate, and more colonies on the plates that received oligos during the ligation. I confirmed insertion by using the BpmI cut site the oligos just happened to carry.
However, the SalI version has failed every time I tried it. The empty vector control and all other plates are a just a carpet of cells. There are very few individual colonies, and the ones that exist don't look right, too small. I haven't even tried a miniprep, too likely to get an empty vector back. I did do a nontransformed control, where the cells were not given any DNA and were just directly plated. Those cells died, indicating it's not an issue with my ampicillin.
My hypothesis is that unligated empty vector outnumbers the correctly ligated plasmids, and that cells that pick up a copy of the unligated DNA somehow repair the cut, even though it's dephosphorylated. This is made more likely because I only used a single digest, so the plasmid has matching sticky ends, however the HinDIII version used the same strategy. I have been including a 1 hour 37 C SOC media incubation, which could allow the bacteria more time to carry out this repair. If I skip the incubation, maybe that would prevent unwanted repair.
I am testing this hypothesis with some additional controls, including transforming bacteria with empty vector that hasn't been treated with ligase to make sure the ligation reaction isn't the problem, as well as using the previously ligated DNA without the SOC incubation. I will report that data as it becomes available. I am short on competent cells, so I can't do much else right now.
Also, what do you think about treating the ligated DNA with klenow to blunt any remaining sticky ends before transformation?
EDIT: I have the data for the transformations that skipped the ligation and SOC media incubation. Skipping the incubation did not change anything, neither did skipping the ligation. All plates continue to show a carpet of cells.

So your insert has same sites on both ends— a non-directional cloning? Plus, do you see the linearized plasmid on the gel? Do you use gel purification? Also, how much plasmid did you use for digestion and ligation?

It is indeed nondirectional. I'm just inserting a zinc finger binding site, I don't care about direction, just need to make a zinc finger protein we already have bind to this plasmid. I have confirmed that SalI cuts the plasmid, but have not used gel purification. Since it's a single cut site there would not be extra DNA to remove. I have not run a confirmation gel every time I have tried the experiment either, so hypothetically the enzyme could have stopped working. The oligos I am adding are short, 56 bases, but I suppose a high density polyacrylamide gel might work to see cuts there.

But you can see the linearized plasmid when you do a gel purification. No need to look for the drop-out. How do you clean up your digestion reaction? Just simple column-purification? There is a likelihood that your enzyme did not cut properly. Bacteria can repair nicks but I am not sure if they preferentially phosphorylate one enzyme site. You can try blunting and see if the problem persists.

I do phenol chloroform purification and isopropanol precipitation after digestion and dephosphorylation for both vector and oligos. (I don't dephosphorylate the oligos obviously) And when I say I have confirmed the digestion, I mean I did the SalI digest and ran a gel, and it was cut. There was a section of the plasmid where we weren't sure of the sequence and I needed to make sure it didn't contain any SalI sites. I do not run the gel every time I attempt the cloning.

@WYSIWYG I think you were right. I finally got around to trying this again, using gel purification as recommended. The gel revealed that the SalI enzyme was not cutting the plasmid very well, with most of the DNA still in the supercoiled form, and a lot as nicked circles. I carefully cut out the linear DNA in the middle and the control plate had only 1 colony. The problem is that the experimental plates have 2 - 5 colonies each, I'll have to see what I get on miniprep. Also, my gel extractions have been poor. When starting with 4 ug of DNA, I get less than 100 ng of DNA after extraction.

You can summarise all of these, post it as an answer and accept it.

As per WYSIWYG's suggestion, I tried the digest and dephosphorylation again with SalI and ran a gel. The gel showed that SalI was less than ideal at cutting this plasmid.

As you can see, the most intense band is the bottom band, which is most likely supercoiled DNA, with the linear DNA I want appearing in the middle, and open circle DNA coming in third. I very carefully cut the middle band out and did a gel extraction. When I ligated this the control plate had 1 colony. Unfortunately, the experimental plates had between 2 and 6 colonies each. I am running minipreps on those now, will just have to see what I get.
This explains why the previous attempts produced so many colonies on the control plates, most of the DNA was uncut, so no amount of dephosphorylation would help it.
One thing that does bother me, is that my gel extractions seem like they have had really poor yields. I typically start a digest with 4 ug of plasmid. After phenol:chloroform extraction and isopropanol precipitation, I'll usually recover 2 - 3 or more ug of DNA. After gel extraction, I'm lucky to get 300 ng of DNA. To make things weirder, the liquid that comes off the spin column in the final elution step will gel up, like a low density agarose gel. The only explanation I can come up with is that residual agarose in the spin column is somehow forcing its way through the membrane and into the elution buffer. The goo clogs pipette tips and makes life difficult.

SalI is a fussy  cutter; I avoid it for routine cloning where possible.  Since it's cutting poorly you'll need to gel purify, as you found.  Be sure you're getting anything cut at all, I'm not convinced by your gel that you are. Use an alternate enzyme if possible.  If you're doubting your gel purification, use a commercial product e.g. one of Qiagen's columns (or competitors, I have no particular attachment to Qiagen); they are more expensive but are pretty reliable.  Don't waste your time with transformations until you know you have clean linear DNA. Good luck.

This is why I often recommend running a negative control of uncut plasmid in parallel to verify that your identification of the supercoiled band is accurate.

@iayork I just got my sequencing results back last week, and my "Successful" plasmids have absolutely no difference from the original plasmid. Now that I can order oligos again, I think I'll try a PCR based cloning without using any restriction sites. If it works, I can avoid the SalI issues and I'll have a method to insert the binding site sequence anywhere I want. I couldn't do it earlier due to weird rules with the budget, we couldn't spend any money during the last month of the fiscal year. Now it's a new fiscal year and I can order as many oligos as I want.

Budget issues are exasperating. Can't spend $50 on a primer, but it's OK to waste a week of your time ...


text:
Is there an evolutionary basis for why women mature faster than men?
Females develop both physically and mentally earlier than males do. For example; females start puberty at an earlier age than males, and females brains mature more quickly than male brains.

Girls have always developed earlier than boys - on average the onset
  of puberty happens between the age of 8 and 12 years in girls and
  between 9 and 14 years in boys.

Is there an evolutionary basis for this? Are there theories for why females mature earlier in life?

Hi @WYSIWYG, I am not able to understand your comment. Perhaps it would be helpful if you could advise how I should clarify on the meaning of "evolutionary basis". Thank you.

You should clarify what you expect to know when you ask for evolutionary basis? Do you mean to ask "whether it has/had any evolutionary advantage wrt fitness" or something else? Moreover, the linked article does not really say that the female brain matures faster than the male brain- if I am not wrong it is about brain network reorganization. I am not also sure what you mean by brain maturation. Can you please clarify this too?

I think it's a legitimate question, there is sexual dimorphism in maturation & onset of puberty, why is a genuine and interesting question

To higher the survival rate of the species

You mix males/females and men/women. I know comparison with other species is useful, but is your question about us humans, or is it about a larger branch of the Tree of Life?

Reproduction is kind of the definition of biological success. Logically, it works because it works because it works. Provided that the mother is responsible and healthy, there's a good chance the offspring will survive and reproduce. And since health and age are like opposing forces, the sooner a female develops and develops responsibility, the more likely they will be to reproduce and supply viable offspring to the population.
Similarly, males remain verile for many years past their prime. Since it doesn't matter (as much) whether the father survives child birth, his health is less important. More important (genetically) is the spread of his DNA. The more time a male has to do that the more his DNA will spread. So why not start earlier? Reproducing for an extra ten or twenty years will cause the spread of a much greater amount of DNA than 1 or 2 years early on, and (plausibly) since the male often has a dangerous occupation, males that develop(ed) later (when their size/strength was greater), probably help(ed) ensure the males' survival.
And there is something to say about sexual preference. It is likely that the males' disposition toward healthy females and a females' dispositon toward successful males is genetic... much like a bird who sings the best song. Why? Because it is/was a successful cascade of events.

You may think about the reproductive success of a family, which depends on the reproductive success of sons and daughters.
The reproductive success of the sons is theoretically unlimited, provided they are big enough to win many competitions. To get bigger, it's good to have a larger growth period. Thus, latter maturation.
The (direct) reproductive success of daughters is limited by the duration of their fertile years. Thus, the more years of fertility, the bigger the reproductive success. Thus, early maturation.
EDIT
Somebody asked for references, so study evolutionary theory:
Darwin, The Origin of Species.
Dawkins, The Selfish Gene.
Futuyma, Evolutionary Biology.
Wilson, Sociobiology.
Wright, The Moral Animal.
I truly hope that's enough. If it isn't, just don't pretend to understand evolution, and quit trying to understand biology.

Wow, you totally stole my answer.

@BenWelborn I didn't even read your answer.

I think you are on the right track. It would be great to (1) further the answer by including references about this hypothesis and typically (1bis) report and explain a published analytical model to explain this concept and (2) eventually cite a paper (if any exists) that apply this concept to humans

@Remi.b I hope you're satisfied now.