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How precisely can we sense temperature differences?
We have thermoreceptors, thus we can sense temperature (both warm and cold).  I'm interested in the sensitivity of our thermoreceptors - What is the smallest temperature difference that we can sense? I assume that different parts / organs may have different sensitivity (eg. lips vs fingers), thus I'd like to narrow my focus on the palms / fingers. But if someone has comparative data, that is welcomed too.

This varies enormously across the body, and also with age. One good starting place would be Stevens, J. C., & Choo, K. K. (1997). Temperature sensitivity of the body surface over the life span. Somatosensory & motor research, 15(1), 13-28.

Short answer
Temperature differences of 0.02 degrees Celcius can be distinguished, dependent on various factors including experimental conditions and bodily location.
Background
The ability to discriminate temperature differences depends on whether it is a cooling or heating pulse, the skin temperature, the duration of the temperature stimulus, age, bodily location among other factors. Unfortunately I cannot access the primary literature other than a few isolated smaller studies. However, Scholarpedia has a very nice entry and associated references, and I quote:

The thermal sensory system is extremely sensitive to very small changes in temperature and on the hairless skin at the base of the thumb, people can perceive a difference of 0.02-0.07 °C in the amplitudes of two cooling pulses or 0.03-0.09 °C of two warming pulses delivered to the hand. The threshold for detecting a change in skin temperature is larger than the threshold for discriminating between two cooling or warming pulses delivered to the skin. When the skin at the base of the thumb is at 33 °C, the threshold for detecting an increase in temperature is 0.20 °C and is 0.11 °C for detecting a decrease in temperature.
The rate that skin temperature changes influences how readily people can detect the change in temperature. If the temperature changes very slowly, for example at a rate of less than 0.5 °C per minute, then a person can be unaware of a 4-5 °C change in temperature, provided that the temperature of the skin remains within the neutral thermal region of 30-36 °C. If the temperature changes more rapidly, such as at 0.1 °C/s, then small decreases and increases in skin temperature are detected. [...]

You also were interested in the palmar skin: here average difference limens are 0.02 - 0.06 °C, dependent on the temperature step used. These values were obtained using cooling pulses. In other words, differences in two cooling pulses of 0.02 - 0.06 °C were discernible, with higher limens needed for higher pulses. Baseline temperatures (29 - 39 °C) had little effect (Darian-Smith et al., 1977).
Reference
Darian-Smith et al., J Invest Dermat 1977;69:146-53
Note
The Stevens, J. C., & Choo, K. K. (1998). Temperature sensitivity of the body surface over the life span. Somatosensory & motor research, 15(1), 13-28 article as commented on by Corvus is indeed a must-read, but my uni library does not have access to it unfortunately.

This is an important point for our previous argument. As you now point out the perception of temperature is not only dependent on the relative temperature difference but also on the absolute temperature.

@WYSIWYG - Yes.. and no. Surprisingly Darian-Smith et al., 1977 found no effect of base temperature (at least across 10 degrees C). However, according to Weber's law, the difference limen increases when the reference temperature is higher. This does apply to the temperature step, but base temperature may be another story?

Here's another question. Is the human body capable of sensing a continuous change in temperature or does it just sense when change occurs in bulk? I mean to say, is the "sense" continuous or discrete?

@PriyanshuDas good question - please ask new questions as a question - Make sure to add a little of your own research, for instance by linking to this question or answer and explaining it doesn't answer your current question.


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Is hands-only CPR as effective as traditional CPR?
Is hands-only CPR as effective as traditional CPR ? Wouldn't 30 chest compressions + 2 rescue breaths be more effective if the person doesn't have a pulse AND not breathing?
From my understanding (correct me if I'm wrong) by doing chest compression you manually make the blood continue to circulate the body in order to deliver oxygen to the organs (and most importantly, to the brain), but after some time (several minutes?) all the oxygen from the blood will be used up, and if the person is not breathing, that means that no new oxygen is entering the bloodstream, so that would mean that chest compressions alone won't provide oxygen to the brain anymore, so they would be useless... am I wrong?

@MuditKapil I don't think that is what is being asked here. What's being asked is, if you are doing hands only CPR as opposed to CPR + rescue breathing aren't you just circulating the same O2 depleted blood?

I taught CPR for 4 years for the Canadian Red Cross. In a very practical sense good quality hand-only CPR is what every lay person should be doing. Call 9-1-1 as fast as possible. Push hard, push fast and don't stop for interruptions. Either you caught the person in the 10 minute window where they are still oxygenated and medics/physicians can save them in which case breathes are not useful (blood ox is still high) or they're blood ox has dropped and likely noone can save them. Keep in mind a barely alive person has very little oxygen demands.

The wikipedia page for CPR actually goes into some detail on this, going to block quote the section here for ease of access,

Compression-only (hands-only or cardiocerebral resuscitation) CPR is a technique that involves chest compressions without artificial respiration. It is recommended as the method of choice for the untrained rescuer or those who are not proficient because it is easier to perform and instructions are easier to give over a phone. In adults with out-of-hospital cardiac arrest, compression-only CPR by the lay public has a higher success rate than standard CPR. The exceptions are cases of drownings, drug overdose and arrest in children. Children who receive compression-only CPR have the same outcomes as those having received no CPR. The method of delivering chest compressions remains the same, as does the rate (at least 100 per minute). It is hoped that the use of compression-only delivery will increase the chances of the lay public delivering CPR. As per the American Heart Association, the beat of the Bee Gees song "Stayin' Alive" provides an ideal rhythm in terms of beats per minute to use for hands-only CPR. One can also hum Queen's "Another One Bites The Dust", which is exactly 100 beats-per-minute and contains a memorable repeating drum pattern. For those with non cardiac arrest and people less than 20 years of age, standard CPR is superior to compression-only CPR.

The American Heart Association has assembled some efficacy testing studies in the following review article, Hands-Only (Compression-Only) Cardiopulmonary Resuscitation: A Call to Action for Bystander Response to Adults Who Experience Out-of-Hospital Sudden Cardiac Arrest. Importantly, the human clinical studies reported no significant difference between those who received conventional cpr and those who received compression-only CPR. Some animal efficacy studies are noted, and with respect conventional CPR, the animals that didn't receive "rescue breaths" experienced a lower survival rate. In the end they note some limitations to hands-only CPR:

"...raised concerns about the possibility that recommending hands-only CPR for witnessed sudden cardiac arrest will, in fact, increase the complexity of decision-making for bystanders or that unresponsive victims of noncardiac medical emergencies (eg, drowning, drug overdose) will not receive rescue breathing."
"There may be situations in which ventilation alone could be life-saving but is not provided. There may be an interval after cardiac arrest when ventilations become absolutely critical for survival."

And as to the content in the second paragraph of the original post,

"It is important to acknowledge that during cardiac arrest without lung inflation and ventilation, there is a continuous decrement of blood oxygen saturation. At some point in time, the possible hemodynamic advantage conferred by continuous chest compressions (without ventilations) will be offset by this reduction in oxygen saturation, and the ultimate result will be a compromise in oxygen delivery. One porcine cardiac arrest study (3 minutes of untreated ventricular fibrillation, then 12 minutes of CPR) suggests that after 4 minutes of continuous chest compressions without rescue breathing, the delivery of 2 rescue breaths every 100 compressions provides a survival advantage over chest compressions alone."

The paradigm, again, is that hand-only CPR provides opportunity to get some help, other than no help at all, but the review also notes that more clinical data is needed on all fronts.

I might add that not doing un-protected rescue breathing is being recommended as a way to prevent infection (same reason we wear disposable gloves when handling bodily fluids).

Thanks for your response, but it doesn't answer the 2nd paragraph of my question, which is what I'm interested in knowing.

I can get how "Stayin' Alive" will keep you in rhythm, but I am not sure if humming "Another One Bites The Dust" won't scare the daylights out of any bystander/helper who is not familiar with this exact recommendation.

Sorry, i wasn't available to edit in more information due to some time constraints, but I've begun updating the answer to something acceptable.

I will address your second paragraph. When you compress the chest, you are also compressing the lungs and some of the air in the lungs leaves. This air is them replaced when you come off the chest. And the lungs naturally reinflate. The mechanism alone in higher quality cpr helps circulate the blood and it is oxygenated with the air that is moving through the lungs from the compressions.
When I was working in the ER in Arizona, Tucson was one of the city's that did a pilot program using hands only cpr in it's ambulances. This was prior to making the changes in 2010 and the survival rates were much higher. Of course they did obtain an advanced airway when there were respiratory issues and once they arrived at the hospital. This allowed the second rescuer to start a line, place the patient on the monitor and AED etc.
Hope this helps!

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Are unilaterally deaf people able to determine where sound comes from?
My question is on people deafened in one ear, but normal hearing in the other.
Time and level differences between the two ears are only part of how the human body can localize the source of the sound. So what other factors are there and are they enough to help accurately determine the location of the sound for unilaterally deaf people ?

The ear (including the external flap) can do quite a lot of directional determination via phase-angle measurements. It's not like the  eyeball, which measures only intensity.

A good friend of mine is deaf in one ear. He can usually tell where sound comes from based on volume and how muffled it is. But also, if the sound is on his bad side, he often doesn't hear it at all. So I think he may just be assuming that whatever he hears is on the good side. He swears that he can tell, though. He does get it wrong from time to time too

From what I could gather, there is a decent amount of variability in the ability to detect which direction sound is coming from in unilateral hearing impaired people. It would appear that some people have severely impaired localization skills, akin to someone with an earplug in one ear, but others can use their monaural hearing cues to better locate sound.
Monaural cues seem to be based on the structure of the outer ear as well as how the sound bounces off of the head and shoulders.
http://www.sciencedirect.com/science/article/pii/0378595594900531
http://en.wikipedia.org/wiki/Sound_localization#Monaural_cues

Short answer
Sound localization in the vertical plane should not be affected too much, while localization in the horizontal plane is impaired in unilateral deafness.
Background
The two most important mechanisms used to localize sounds can be grossly divided into localizing sounds in the horizontal (azimuth) and vertical plane (elevation).
In the horizontal plane it is the exquisite capability of the auditory system to distinguish between slight intensity, latency and phase differences between the two ears that allow the brain to deduce where a sound is coming from. For low frequencies it is mainly the inter-aural time and phase differences that play a role. For high frequencies, the difference in sound level between the ears becomes more important (head-shadow effect). For example, if a sound is coming from the left, the left ear will receive the highest sound level. The sound stimulus will also have a shorter latency because of the intervening head tissue, and a phase difference due to the time lag (Van Wanrooij & Opstal, 2007).

Head shadow effect at high, but not at low frequencies. Source: University of Edinborough
In the vertical plane and front-back discrimination it is the analysis of spectral shape cues that lie at the basis of directional hearing. The spectral cues arise from direction-dependent reflections within the pinna (described by so-called head-related transfer functions, see below figure graphs). The pinna provide a monaural localization cue for sound frequencies exceeding about 3–4 kHz (Van Wanrooij & Opstal, 2007).

Head-related transfer function due to the pinna. Source: University of California
However, this hard distinction between elevation and azimuth directional analysis is somewhat simplified, as it appears that elevation is also analyzed in terms of binaural cues, and azimuth is also identified using monaural cues. Hence, all available cues seem to be integrated for both vertical and horizontal localization. Nonetheless, the two distinct pathways are the primary and preferred ways of the auditory system to determine elevation and azimuth. However, when one ear is plugged, or in unilateral deaf people, the textbook binaural hearing in the horizontal plane may be substituted by monaural cues, and I quote from (Van Wanrooij & Opstal, 2007):

[L]isteners rely on monaural spectral cues for sound-source azimuth localization as soon as the binaural difference cues break down.

Therefore, to wrap up, unilateral deafness degrades directional hearing and in particular in the horizontal plane. However, the use of monaural cues may still allow localization of sounds in the horizontal plane in unilaterally deaf subjects, albeit less effectively than normal-hearing subjects using binaural hearing (Van Wanrooij & Opstal, 2007).
Reference
- Van Wanrooij & Opstal, J Neurophysiol 2007;97:715-26

While this is a very good answer, it ignores our ability to move our heads. While for very short sounds we cannot move our heads fast enough, for longer sounds, head movements should introduce a host of monaural cues.

@StrongBad - yes certainly, this answer pertains only to the situation where the head is fixed. Of course, when folks are allowed to move their heads or move toward a  source they will definitely find it through intensity cues based on trial and error. This answer deals with short tone bursts and fixed head position.

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Cause of hexadactylisim in Amish people
Is it caused by inbreeding of many generations within an isolated population?

Short answer
Yes, you pretty much nailed it. Inbreeding of (and from) an isolated population.
Long answer
According to wikipedia > polydactyly, there are 39 known polmorphic sites underlying variance in polydactyly. It is therefore not a trait with a simple mode of inheritance.
There are two important (somehow related) concepts to understand to explain the relatively high frequency of polydactyly (and other genetic disease such as maple syrup urine disease) in Amish.

High inbreeding
Important population bottleneck

If you have no absolutely no background in biology, the following might be a little bit complicated. You might want to make sure you know some concepts (such as deleterious, recessive, dominant, homozygous, Hardy-Weinberg equilibrium, locus, allele and of course inbreeding and population bottleneck) by googling them.
Inbreeding
I will, here talk only about one mechanism by which inbreeding causes those diseases.
There is a positive correlation between how deleterious is a mutation and how recessive it is (the more deleterious, the less dominant, the more recessive). The post "Evolution of dominance of alleles" will probably help you to understand why this is true.
Inbreeding increases the frequency of homozygote loci and therefore, increase the probability of a locus which polymorphism explain variance for the disease to be homozygote deleterious. Using Hardy-Weinberg formula with Sewall Wright work, if at a given locus the allele A is deleterious and is present at frequency $p$, then the frequency of the homozygotes AA is $p^2$ without inbreeding (under Hardy-Weinberg assumptions). Taking inbreeding into account, this frequency becomes $p^2 + Fp(1-p)$ (where $F$ is the coefficient of inbreeding). In words, the higher is the inbreeding coefficient, the higher is the frequency of homozygotes (including homozygotes for the deleterious alleles).
In short, inbreeding matters because of dominance. There are other reasons why inbreeding matters though but that would be the subject of another post.
Bottleneck
In population biology, a bottleneck is is a sharp reduction in the size of a population. Imagine you have a population of size $N$ and you selection a fraction $\frac{N}{1000}$ of this population, you are going to lose a lot of alleles due to random sampling. Most of the times you are going to lose deleterious alleles (as they were already present at low frequency in the original population) but sometimes you are going to pick up a deleterious allele. The frequency of this deleterious allele was maybe 0.00001 in the original population and then suddenly its frequency jumps to 0.1. This is a big deal.
The Amish went though an important bottleneck, there was a time when the descendent of the modern-day Amish reproduced with everybody and at some point, they stopped doing so as they decided to create the amish community (I actually know little about the Amish history but I assume something similar happened). This community was formed by about 200 families only (according to this not-necessarily-trustable source, so very little genetic variance) in 1693 in Switzerland (according to wiki). They probably "won" by not having the alleles coding for clubfoot, sickle-cell and cystic fibrosis alleles (just to cite a few example) but they "lost" by drastically increasing the frequency of alleles coding for polydactyly (and some other diseases).

Great answer. +1. One question: I thought that genetic drift was a slow random process http://www.nature.com/scitable/definition/random-genetic-drift-genetic-drift-201 and that it has not a diect link to a sudden reduction in #individuals in a populaton?

From wiki: Genetic drift (or allelic drift) is the change in the frequency of a gene variant (allele) in a population due to random sampling of organisms. A bottleneck is a sampling process where the number of individuals sampled is much lower than the number of individuals in the previous generation. I felt like it would lead to confusions though. I might as well just take my parenthesis away. Thnks

Short answer
Yes, the high frequency of polydactyly in the Amish is caused by inbreeding.
Background
The polydactyly in the Amish is just one of the symptoms of Ellis-van Creveld (EvC) syndrome. EvC syndrome is an autosomal recessive disorder, involving polydactyly of the hands (see figure), short stature with shortening especially of the forearms and lower legs and, in at least half of all cases, congenital heart malformation. In the Amish of Lancaster County (Pennsylvania), EvC syndrome occurs at high frequency and is caused by mutations in the EVC gene.

Source:  McKusick (2000).
The Amish have two characteristics that resulted in the high occurrence of EvC syndrome. First, they are descended from a limited number of founders who immigrated during the eighteenth century to the United States from Switserland,  via Germany in the 1690s. Second, the Amish are endogamous, i.e., they marry only within their community. Hence, gene flow is exclusively centrifugal, i.e., members may leave the community but ‘outsiders’ do not join it and thereby introduce exogenous genes.
All EvC cases in the community are traceable to a single couple, Samuel King and his wife, who immigrated to Eastern Pennsylvania in 1744, thus demonstrating
founder effect and a recessive pattern of inheritance.
Reference
- McKusick, Nature genetics (2000); 24: 203-4

Good answer, simple and without explanations of why inbreeding and founder effect can cause higher prevalence of a disease (but making a complete explanation would ask for writing a book). +1. Your first sentence says Yes, the mutation [..] is caused by inbreeding which is of course wrong.

@Remi.b - Thanks for the appreciation! And also thanks for pointing out that mistake :) I fixed it!


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Why is the pituitary gland located in the brain?
Why is the pituitary gland located in the brain in humans, instead of elsewhere in the body? Why would this be an evolutionary beneficial adaptation?

The evolutionary pressure on the location of the pituitary is likely not the reason why it resides at the basis of the brain. Instead, its (partly) neural origin makes it anatomically (and functionally) part of the brain. Why would it migrate out of the brain when it doesn't have to? What would the evolutionary pressure be on increasing the length of the axons connecting it to the other parts of the brain? It is part of the brain, hence it is located there. It clashes with the principle of parsimony to have the pituitary evolve to a structure located farther from the brain.
The neuroanatomy of the pituitary is schematically as follows (Fig. 1):

Fig. 1. Pituitary gland. Source: Imagekb.
The posterior lobe of the pituitary gland consists largely of extensions of processes (axons) from the hypothalamus and are part of the neurohypophyseal system. There are neural connections to the brain and other centres of the hypothalamus. Hence, the posterior lobe is neural tissue.
The cells constituting the anterior lobe of the pituitary gland are embryologically derived from an outpouching of the roof of the pharynx, known as Rathke’s pouch.


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What is the purpose of the incus?
The three bones in the middle ear -- the malleus, the incus, and the stapes-- play a role in transmitting sound waves to the inner ear (the cochlea). I understand that the malleus is the bone closest to the tympanic membrane (and therefore the primary receiver of information) and I understand that the stapes is responsible for transmitting the information to the cochlea... so why even have an incus bone?

The incus is there in humans because it is there in our mammalian ancestors, and it is there in our ancestors because the mammalian three-bone ossicle system was inherited from early amniotes.
The synapsid ancestors of mammals had the ancestral jaw articulation between the articular (later called malleus) and quadrate (later called incus). This is the bottom image below. There are fossil species with a transitional form in which there are two jaw joints (e.g., Pachygenelus). In extant mammals, the jaw joint lies between the dentary and squamosal (part of the temporal bone), while the old articular and quadrate are part of the ossicle system (top image below).
There is a lot of material on the web about this:

http://crompton.oeb.harvard.edu/publications/transformation-quadrate-incus-through-transition-nonmammalian-cynodonts
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3552421/
http://www.zoology.ubc.ca/~millen/vertebrate/bio204_labs/Lab_3__Skull.html

So in short, the incus is there because there was no other way for the mammalian ear to evolve from the ancestral system. It doesn't have a purpose per se, except that it's always (at least going back to jawed fishes) been attached to the stapes and articular (malleus).

Great answer thank you, so would there be a serious problem if a human was born without the incus, or if they had an ear infection that caused the incus to malfunction?

Nice answer +1. Interesting yet complicated material. I've added an answer from a functional perspective. Thanks for this excellent overview of the evolutionary perspective. I refrained from answering initially, given the dreaded duality in the "why is there X" anatomical questions. Kudos

Short answer
The incus forms a lever with the malleus, thereby amplifying incoming sound and aiding in the impedance-matching function of the middle ear.
Background
In addition to kmm's excellent evolutionary perspective, I'd like to add my two-cents worth in terms of the functional advantage of the incus.
The tiny bones in the middle ear (ossicles) constitute an important mechanism to increase auditory sensitivity. The auditory receptors of the inner ear (the hair cells) operate in a fluid environment, but acoustic stimuli enter the ear via air. When sound in air strikes a fluid boundary (i.e., a boundary between media with different acoustic impendances) 99.9% of the energy in the incoming sound may be lost due to reflection. This loss equals 30 dB, which is a substantial reduction in stimulus intensity and quite noticeable to a listener.
For what it's worth, as a personal anecdote - I have around a 30 dB loss in the 125 to 500 Hz frequency range due to genetic reasons and that substantially reduces my speech understanding, especially in noisy environments.
In order to overcome the mismatch in the impedance of air and fluid, the middle ear, which is interposed between the tympanic membrane and the oval window, is designed to amplify the incoming sound. This process is referred to as impedance matching.
There are two major middle-ear structures in place that passively amplify sounds:

The tympanic membrane;
The malleus-incus lever.

The effective area of the eardrum is about 21 times that of the stapes footplate. Thus, the force caused by a given sound pressure in the air acting on the area of the eardrum is concentrated through the ossicles onto the small area of the footplate, resulting in a pressure increase proportional to the ratio of the areas of the two structures which, in humans, is about 21:1.
It also happens that the lever arm formed by the malleus in rotating about its pivot is somewhat longer than that of the incus, giving another factor of about 1.3 in pressure increase.
The 21x of the drum/footplate area ratio, multiplied by the 1.3x lever arm factor, yields about a 27.3x increase in pressure, which is 29 dB, thus just about overcoming the theoretical 30 dB loss due to the air/liquid interface. Hence, the middle ear matches the acoustic impedance between the air and the fluid, thus maximizing the flow of energy from the air to the fluid of the inner ear (Fig. 1).

Fig. 1. impedance matching properties of the middle ear. source: Wisconsin University
Impairment in the transmission of sound through the middle ear creates a conductive hearing loss.
Source
- Wisconsin University


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Online Database for PPG (Photoplethysmography) signals (both Infrared and Red light readings)
I am looking for an online Database for PPG (Photoplethysmography) signals for SPO2 (oximetry) analysis. I have tried several sources but they only have single datasets labelled "PLETH" and not individual IR (Infrared) and Red Signals. Please help me find such database or let me know any workaround for this.

It may be me, but I don't understand all these acronyms.

I edited to question

Thanks! I'll not pretend knowing the answer, but at least I know it's about measuring oxygen :) I retracted my close vote.


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Are there animal species that sense infrared light with their eyes?
I asked a question earlier today about birds with infrared vision but this time I am asking about animals in general. I know that many snakes have receptors between their eyes and their snout that allows them to sense infrared radiation but I am looking for an animal that actually uses its eyes.
Googling and searching around found me this statement:

It's worth noting that, though there are numerous animals that sense
  infrared light, relatively few of them sense it with their eyes

The article didn't list any specific animal that used its eyes to sense infrared light, it just says 'very few'. However, I haven't been able to find any species that can sense infrared light with their eyes.

It is possible that the "relatively few" refers to invertebrates.

@BryanKrause Ah yes, that escaped me. I'll edit my thread accordingly.

It may be worth noting that, if an eye is defined as an organ that detects light, then the definition answers the question: if an organ detects IR light, it is a type of eye, therefore all animals that detect IR light do so with their eyes. This definition of 'eye' is currently used in, e.g., the wikipedia for 'eye':
"Pit vipers have developed pits that function as eyes by sensing thermal infra-red radiation, in addition to their optical wavelength eyes like those of other vertebrates".
https://en.wikipedia.org/wiki/Eye

@bshane then eyeballs (?)

@bshane If you look up scientific literature on pit vipers, however, their sense is (mostly?) never referred to as vision: sometimes 'vision' in quotes like that. I think, although a broad definition of eyes can be used for certain organisms, for vertebrates, arthropods, and mollusks, each of their eyes share a genetic and developmental origin, so when you talk about "eyes" those are the organs you refer to.

@BryanKrause In that case, a very good answer would say why IR pit eyes aren't 'true' eyes, whereas similar non-IR organs are called eyes.
AliceD's answer distinguishes between 'organs that detect IR' and 'organs that detect IR and other wavelengths', using 'and other wavelengths' as a stand-in for 'eye'. This answers the question the OP meant to ask (I think - and so have +1'd), but sidesteps the problematic definition of 'eye'.

Short answer
As far as I can see, there are no animalia with high-sensitivity infrared photoreceptors in their retinae. Instead, infrared is detected at low thresholds with a dedicated sensory system in some species - the pit organ. This organ is separate from the retinae and its output does not merge with the retinal image. However, red cones, and even green cones for that matter, have low sensitivity to infrared light and when intense enough, infrared stimuli may be detected by the eye, as was shown in a small study in ferrets.
Background
Infrared (IR) light is classified as light at wavelengths of 700 nm and up. In Fig.1 is depicted the light sensitivity of man under scotopic (dark-adapted) and photopic (light-adapted) conditions. It is readily apparent why we cannot perceive IR.
Species that can detect IR use it in general to detect heat. Notable examples are the blood sucking species, including mosquitoes, bed bugs and vampire bats as well as nocturnal predators including species of snake (source: National Geographic). Although this heat detection can be classified as IR vision, IR is not detected by their eyes. Instead, all of these species use specialized IR-sensing organs called pit organs to detect IR. Basically, these are heat detectors (source: NSF). While snakes are able to construct heat-maps, the IR image and visual images as detected by the retinae are not combined into a single image. As far as I understand, the visual image and IR images co-exist in snakes and are not fused (or 'overlaid') (Campbell, 2002).
So the most notable of IR detecting species have IR vision, but these heat maps are sensed by dedicated pit organs separate from the retinae and as far as I can see the images are not combined.
However, last but not least - IR cameras are often used to study nocturnal critters as it is assumed they cannot detect the IR. Interestingly, a study on a small population of 5 ferrets showed that 3 of them responded at above-chance level to light stimuli well into the IR (870 nm) (Newbold, 2007). It should be noted that sensing of stimuli is all about thresholds. The Fig. 1 shows a nearly zero-response in humans at 700 nm, but when we would make the stimuli strong enough, we may elicit a small response nonetheless. Fig. 2 shows the absorption spectra of red and green cones. As becomes apparent here, red cones and even green cones have spectral sensitivity in the IR domain. Then it might become a question not whether we can sense IR, but at what level we can detect it. Under normal everyday lighting conditions, we obviously can't, but that does not exclude the possibility we may perceive it at extreme light intensities.

Fig. 1. Human spectral sensitivity. source: Webvision

Fig. 2. Spectral sensitivities of red and green cones. source: Dowling, 1987)
References
- Newbold, Master's thesis. University of Waikato, NZ
- Kalloniates & Luu. In: Kolb et al (eds). Webvision. The Organization of the Retina and Visual System
- Schnapf et al, Nature (1987); 325: 439-41

Yes, Mantis shrimp have 12 photo-receptors and can detect the low-end of IR.
In H. trispinosa one of the photoreceptors, R3P, detects right at the edge of 'deep red' light and would detect infrared (700+ nm). Although this study didn't explicitly measure infrared detection, by the shape of the curve it's not a huge leap that they detect infrared at significant levels. Below is the link and a link to human photo-sensitivity curves for contrast.
Keep in mind 'infrared' is not a universal biological property, it's simply defined by the fact that our species doesn't see it.

Mantis Shrimp photoreceptor sensitivities
Link without paywall. Figure 1A
Human photoreceptor sensitivities for contrast
Electromagnetic emission from the sun

Enright, et. al. (2015) found that several vertebrate species -- including zebrafish and bullfrogs -- under certain environmental conditions red-shift the rods and/or cones in their photoreceptors by something on the order of 30 or 60 nm ("beyond the range of human vision", per article summary). The mechanism for this is production of Cyp27c1, which serves to convert vitamin A1 to A2 in the photoreceptor. Bullfrogs are found to have the A2 vitamin solely in the dorsal (top) retina, Likely enabling them to look downwards into murky water while at the surface (Figure 1, note G).
Enright, Jennifer M., et al. "Cyp27c1 red-shifts the spectral sensitivity of photoreceptors by converting vitamin A1 into A2." Current Biology 25.23 (2015): 3048-3057. Link.

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Homework : Sodium Potassium pump
Why does sodium-potassium pump consume about 2/3 energy of a cell ?
A.maintains appropriate membrane potential
B.helps in co-transport
I think it should be A.

I don't know the answer, but my feeling is that it will be (b). If the cell isn't a neuron then there will be no processes directly collapsing the resting potential. There will however be lots of symporters and antiporters carrying out secondary active transport by tapping into the gradients of sodium and potassium ions.

@AlanBoyd Aren't the "leaky" channels and other free ion channels (on top of secondary transporters) tending towards obliteration of the membrane potential in most cells, so that the pump is required to maintain steady concentrations and hence a steady potential? In the absence of the pump, the channels would allow a steady ion flux completely neutralizing the membrane potential from the active GHK potential to the donnan-equilibrium state This would mean (a) is the answer. But I am not sure on this.

Neither of the options explain the 2/3rd energy consumption. So the question should either be: why is Na/K pump important or How much energy does a single Na/K pump consume in an event of transport. Rest everything is situational. As @AlanBoyd points, Na/K pump performs additional functions in electrically excitable cells.

UNIMPORTANT COMMENT..... I wonder who gives you these homeworks :P

I can't yet comment, so here's a (sort of) answer:
I've only ever heard the "2/3 of cellular expenditure" rule applied to neurons, and frankly, it wouldn't make much sense in any cell other than a neuron.  The Guyton and Hall Textbook of Medical Physiology says, "For some cells, such as electrically active nerve cells, 60 to 70 percent of the cells' energy requirement may be devoted to pumping Na+ out of the cell and K+ into the cell."  A cardiac muscle cell, for example, would probably use more of its energy for contraction than pumping ions.
In a neuron, the bulk of energy expenditures are for electrical signalling done via allowing sodium and potassium ions to temporarily run DOWN their respective gradients.  As such, the "purpose" of a neuron is to pump ions across a membrane and then let them run back when needed.  Since a neuron doesn't really DO much else, it makes sense that the bulk of the energy produced will go towards pumping ions.  A practical example is the use of barbiturate comas to reduce metabolic activity in the brain.  Flat-lining the EEG drops metabolic requirements by ~50% (Source: Medscape).
Please keep in mind that this answer is specific to neurons...other cells perform other functions, and those other functions will take up significant fractions of energy produced.  Further, other cells probably aren't devoting large fractions of their energy towards signalling, and so the fraction of energy devoted to pumping ions will be markedly less.  They'll still be pumping ions to maintain a gradient to perform tasks like membrane transport and osmotic control, but those tasks are ancillary to the "purpose" of those cells.  I can't find any solid numbers for Na/K ATPase energy expenditures in non-neuronal tissue at the moment, but if I do, I'll update appropriately.
UPDATE:
With regards to the question itself, which I apparently forgot to answer:
Can a cell function without an appropriate membrane potential? Can co-transport run without a membrane potential?

Why does sodium-potassium pump consume about 2/3 energy of a cell ?

It's A, assuming we're talking about a cell-type that heavily utilizes the potential.
On to some of the comments...

If the cell isn't a neuron then there will be no processes directly collapsing the resting potential. - Alan Boyd

Incorrect, Pacemaker cells collapse the membrane potential frequently and don't have any resting membrane potential, only hyperpolarization-repolarization cycles.
Neurons are merely the most prominent users and best examples as they're entire existence is dedicated to the membrane potential.

In the absence of the pump, the channels would allow a steady ion flux completely neutralizing the membrane potential from the active GHK potential to the donnan-equilibrium state This would mean (a) is the answer. But I am not sure on this. - Satwik Pasani

Correct to some extent. The leaky ion channels (which are usually K+ channels) would allow the equilibrium to be reached for a handful of ions. This still prevents utilization of the potential, however, and is an easy way to kill something.


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Why do brain cells use shuttles that pass electrons from NADH to FAD?
Brain cells are cells require one of the highest amount of energy of any cell of body. So why do they use a shuttle which will transfer electrons from NADH produced in glycolysis to FAD(and there by reduce the no of ATP that can be made ) ?

No that doesn't happen. are you sure ?

@WYSIWYG she is correct. Her question refers to the glycerol phosphate shuttle which is more prominent than the malate asparate shuttle in brain and muscle cells.

@SatwikPasani.. Sorry, I didnt know about it so thanks for letting me know. I did a quick check and I could only find this article on G3P shuttle and brain; I couldnt access it right now but the abstract says that G3P shuttle is minimal in neurons and almost zero in astrocytes.

@WYSIWYG Actually, as is already mentioned in the reference abstract you cited, it is not very clear what the distribution of these shuttles is. But the extract refers to pharmaceutical determination studies only. Earlier biochemical studies showed high G3P shuttle prominence in muscles and neuronal tissues but has always been under active controversy. My information was older but Your reference is quite recent and may have solved the issue, but for me it's behind a paywall.

I looked at that WYSIWYG's abstract and it doesn't explain the poster's main concern, namely that moving a hydride via NAD has a different energy yield than moving one via FAD. Won't it be irrelevant if the reducing equivalent enters the mitochondrion via glycerol phosphate shuttle vs malate aspartate shuttle?

In the absence of unanimous consensus and sources regarding the actual distribution of these shuttles,(wikipedia favours G3P shuttle abundance) let me try to explain the cause if the glycerol-phosphate shuttle is assumed to be prominent in brain cells. Several possible reasons might lead to this:-
1) The existing metabolic pathways are all intertwined to form a complex metabolic net. This means that invariably, the intermediates of any pathway are the products or intermediates of several other pathways. Therefore, the G3P shuttles require Glycerol-phosphate and Glycerol-phosphate dehydrogenase (I and II) which might be naturally abundant in brain owing to its use in strict lipid metabolic control in nervous tissue. This means that tapping the already high G3P for use as a shuttle compared to synthesising and operating a distinct metabolic shuttle is more profitable. Furthermore, operating Malate aspartate shuttle migh require intermediates whose high concentrations (required to maintain the shuttle) might negatively interfere with existing metabolic pathways like protein synthesis and regulation.
2) This shuttle has much faster operation time than Malate-Aspartate shuttle and hence is very useful in shuttling reducing equivalents fast in muscles and brain. Compared to the malate aspartate shuttle, it is shorter and hence faster and less prone to cessation due to unavailable intermediates or enzymatic disruption. Due to several enzymes working in Malate-aspartate shuttle, it has a narrower pH and temperature optima than the G3P shuttle which is shorter and depends on lesser intermediates, and hence is less prone to disruption.
3)The last and the most far-fetched (but relevant)reason is that the loss of one ATP may not cause much of a problem because of already high respiratory rate, high Oxygen delivery to brain and ability of the body to quickly transfer available energy sources to brain at the cost of other parts, at times of energy stress. This means that replacing the shuttle with a more energetically conserving one may not have a strong driving force for evolution to operate on, and therefore the presence of G3P may be because of something like phylogenetic inertia, that is, the prevalence of an ancestral character just because it is neutral and does not influence the fitness in a considerable manner. Therefore, the ancestral G3P shuttle would just not have been replaced here but this is very unlikely as G3P shuttle is prominent in 2 very high energy-demanding organs, muscles and brain.
Except the last outrageously far-fetched reason, all other reasons should be enough to explain its prominent presence (if it is true) in brain tissues.

Looking at this question, which has resurfaced after five years, I was not really convinced by any of the possibilities suggested in the answer from @stochastic13, commendable attempt though it is. It happens that I have just been consulting the section on these shuttles in Berg, Tymozcko and Stryer where the following is written:

When cytosolic NADH transported by the glycerol 3-phosphate shuttle is oxidized by the respiratory chain, 1.5 rather than 2.5 ATP are formed. The yield is lower because FAD rather than NAD+ is the electron acceptor in mitochondrial glycerol 3-phosphate dehydrogenase. The use of FAD enables electrons from cytosolic NADH to be transported into mitochondria against an NADH concentration gradient. The price of this transport is one molecule of ATP per two electrons. This glycerol 3-phosphate shuttle is especially prominent in muscle and enables it to sustain a very high rate of oxidative phosphorylation.

I know little about brain metabolism, but if the demand for energy in brain is higher than in other tissues (as stated in the question) then the above would seem to provide the explanation: the greater production of ATP by oxidative phosphorylation possible when NADH entry into the mitochondria is independent of its internal concentration more than offsets the price in ATP of that entry.


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Rate of Evolution of population of long lived individuals
Is it necessary that rate of evolution of longer lived trees will be lesser than that of annuals ? I understand that new individuals will come up faster in annuals  and it may adapt to varying conditions faster but does it necessarily imply that long lived trees will evolve slower ?

That is true to a certain extent in normal environments, where there is not an excess prevalence of mutagenic elements. The "Generation Time Hypothesis" explains why a smaller generation time and hence a higher reproductive rate ( as in annuals) corresponds to a higher rate of mutation (substitutions in DNA) and therefore have a faster evolutionary rate as compared to slow reproducing and longer generation time individuals(for example, long-lived trees).
Since "fitness"-increasing adaptations produced by somatic variations are very less, the formation of new offsprings giving rise to individuals carrying a DNA which has been subjected to processes (Repeated divisions, replications and translations, amphimixis, and different environment) making it more vulnerable to mutation, becomes mandatory, to propel evolution. This process is much faster in annuals than in long lived trees like Sequoia. Moreover Sexual selection (especially in animals) operates at a much slower rate in longer-generation time individuals. Next, smaller individuals, having higher metabolic rates usually have shorter generation time (more pronounced in case of animals). Higher metabolic activity is linked to greater mutation rate (Due to metabolic intermediates acting as mutagens) and hence faster evolutionary rate. Higher metabolic rate also is linked to higher temperature (faster mutation) and these individuals have a geographic distribution favouring the tropics.(Again increases evolutionary rate)
All these, imply faster evolution for short lived individuals(which usually have higher reproductive rate) as compared to long lived trees. But under "normal" environmental conditions (not drastic and fast changes), the evolutionary rate of large individuals is fast enough to preserve their existence (as the Sequoia prevalence indicates). However, in fast changing environment, larger and long-lived individuals are more likely to be wiped out (probably, this applied to Dinosaurs!).


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How are T cells transported?
T cells are formed in bone marrow and mature in Thymus. How are they transported from bone marrow to thymus ? Through the lymph vessels ?

The progenitor cells of T-cells (they do not develop into T-cells and show their characteristics before reaching the thymus) are mobilized into the bloodstream and enter the thymus from it by crossing the endothelial barrier. The figure shows schematically the development of the precursor cells from hematopoietic stem cells (HSC) and the migration of the precursor cells (it is from the paper linked below):

See this review for the details (if you have problems accessing the article, let me know):

The long road to the thymus: the generation, mobilization, and
circulation of T-cell progenitors in mouse and man.

prothymocytes are attracted to the thymus from the Bone Marrow by a chemotaxis , thymotaxin, a factor from thymic epithelial cells.
then it enters into the thymic cortex where Thy-1  and terminal deoxynucleotidyl transferase (TdT) is expressed. During TCR gene rearrangement, TdT increases TCR diversity by inserting nucleotides at the D and J junction sites. IL-2 and IL-2R are expressed leading to autocrine proliferation of T cells.
now the  pre-T cell  rearranges TCR genes (gamma/delta, alpha/beta). At this stage the pre-T cells are CD3+CD4-CD8- or "double-negative" cells. Double-negative cells that productively rearrange gamma and delta chain gene segments develop into CD3+CD4-CD8- gamma/delta T cells that are exported to the periphery in small numbers. Successful rearrangement of a set of TCR genes suppresses further rearrangement of TCR genes on the sister chromatid , thus each cell only expresses TCR with a single specificity.
The majority of double-negative cells will go on to rearrange alpha and beta chain gene segments. The beta chain genes are rearranged and expressed first with a pre-T alpha chain to form the pre-TCR . Once the pre-TCR recognizes some intrathymic ligand , a signal is transmitted through CD3 which:
halts further beta chain gene rearrangement (allelic exclusion)enhances alpha chain gene rearrangement causes CD4 and CD8 to be expressed
The alpha beta T cells now become CD4+CD8+ or "double-positive" cells. T cells which fail to productively rearrange TCR genes die by apoptosis.
At this point the T cells are in the deep cortex which contains epithelial cells expressing both class I and class II MHC molecules. T cells with alpha beta TCR which are capable of binding self-MHC on epithelial cells continue to proliferate and differentiate into CD4+CD8- or CD4-CD8+ T cells. Nonreactive (not self-MHC restricted) T cells die by apoptosis. Thus, T cells are positively selected for self-MHC restriction in the thymus.
T cells that survive positive selection traverse the junction between the cortex and medulla. Some of these T cells have low affinity TCR for self-MHC alone or combined with self-peptide while others have high affinity TCR. The medulla is rich in BM-derived dendritic cells and macrophages which express high levels of class I and class II MHC. T cells with high affinity TCR for self-MHC alone or combined with self-peptide interact with these dendritic cells and macrophages, and are eliminated by apoptosis. Thus, negative selection eliminates self-reactive T cells  in the thymus.

Hi Krushna, I'm not sure this answers the question of how T Cells move from bone marrow to the thymus beyond your very first sentence.


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Evolutionary conservativeness

List the following proteins in the order of decreasing evolutionary
  conservativeness of their primary structure:

Somatotropin.
Catalytic subunit of a DNA – polymerase.
Histone H1.
Prolamines (storage proteins of cereals).

What I think : I am sure that 4th one should be last. I believe that H1 sequence is not that important as I had read somewhere that a cell can survive even without H1 histone. I also think that catalytic subunit is most important. So, according to me the order should be : 2,1,3,4.
Am I right ?

I believe it should be 2,3,1,4, since the histones are involved in several epigenetic regulations, lyonisation and transcriptional regulations, and since these regulations greatly change the phenotype under consideration, I think conserving the histones' primary structure should be more favourable as compared to Somatotropin, since slight modifications in hormones might not affect much due to absence of perfect specificity, presence of hormones with supplementary action, and so on.

@chris Thanks! yes, it was in yeast. I remember reading it in Bruce Alberts.

One of you should attempt an answer !

Do you think so? It would still be something like a comment.

@Chris I guess Unless there are any publications to provide data on the conservativeness of these proteins' primary structure, your comment is the best answer that can be given, as far as logical reasoning is considered.

Ok, if you say so...I can have a look if there is some data available later.

This is such a crappy question (not yours @biogirl, your teacher's). You cannot answer this question without actually checking the sequences. For example, the cell can survive without H1, OK, but H1 cannot function without it's structure since it's function is very dependent upon the structure. Therefore, it would not surprise me if it were exceedingly conserved. The question is an example of a lazy teacher, all you can offer is conjecture.

Even when you can live without Histone H1, its a widely distributed protein which you find in basically all living cells (except for some yeasts if I remember correct). This points to the fact that it must be available for quite a while. The same is true for the catalytic subunit of the DNA polymerase. Somatropin is still pretty important (and can be found in a lot of organisms), prolamines are quite specific to certain cereals. I would group it 2-3-1-4.

bacterial requirements for histones is not as great as euks I would say - what cell can reproduce without DNA polymerase?

@chris Does conservnativeness mean that it is present in most organisms or does it mean that the sequence/structure is not changed?

@shigeta hats why I think that the DNA polymerase is higher conserved. But the histone comes next.

@biogirllajja It can mean both :-) And its connected - proteins which are old in an evolutionary sense (like a DNA polymerase or something like cytochrome P450) are also highly conserved (for structural and functional motifs) on the sequence level.


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Constitutive mutation in operator gene
If a constitutive mutation happens in the operator of an inducible operon, does that mean that repressors won't be able to bind them ? Or does it mean that even if repressors are bound, they will not have any effect on the gene ?
I am specifically talking about lac operon.

For the lac operon there are two possibilities for constitutive expression mutations:

The operator is never closed.

Reason: Mutation of the repressor, so its not present, doesn't bind or binds only with very low affinity for the operon.

The repressor can not bind.

Reason: The binding site for the repressor is mutated.
See this Website or this Website for more information.

What is the meaning of "the operator is never closed" ?

I have expanded my answer.


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Identify this insect - unknown location
Please help identify this insect - genus, species and anything interesting about it.
(Part of this old thread.)

The link is broken...

yes, the link isn't working. so i don't know if the link would have explained that this and your other question is about computer modeled insects. https://www.cgtrader.com/3d-models/animals/insect/insect-collection-vol-2 i'd think that's kind of important to know!

It is a beetle of the genus Eudicella.
There are several species and some look quite similar, they are from tropical Africa.

which would you pick for species identification?

Eudicella gralli would be my guess but I do not know enough the group to be 100% sure.


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Myopia as a microscopic superpower?
A few years back my Physics professor made a joke that his myopia (i.e., nearsightedness) gave him a "superpower" that allowed him to see close objects much more clearly than someone with typical eyesight. For example, reading small fine print or tiny details on a surface. The physics made sense, as a person with myopia should have a closer near focus point.
Recently, this belief was challenged by a normal-sighted friend. I did some Google-ing and couldn't find any evidence or articles confirming or refuting this belief. All I found was a lot of anecdotal evidence.
My question is: Is this belief correct? Are there any scholarly articles or similarly trustworthy sources confirming this?

I have never seen such an article, but I agree with your professor. I used to have 7 degrees of myopia, and it allowed me to see insects very close, in great detail. Now I have operated, and don't have this "superpower" anymore.

I would love to find more details about this, only found this old thread from 2015. I have myopia and can say that this is true, I called a superpower myself a couple times too, hahaha. It’s actually helpful for some ordinary tasks during your day. It would be nice to find some tests about this subject.

With all respect to the answers given above, they are incorrect. I cannot detail why but they simply are.
I know of two people with very high degree of myopia that appear to have a near 20x microscopic sight, tested on many occasions.
A true superpower.
Both of these people do not advertise this at all, perhaps not surprisingly. The interesting thing is that both could see security details on banknotes when I couldn’t see the details using a 7x lens. I wish someone could try to explain this without assuming it’s urban myth. It isn’t

Short answer
Myopes may have some benefit in terms of identifying small objects due to their ability to focus objects nearer to their retina than emmetropes, but only marginally so.
Background
The more myopic you are, the more blurred your distance vision, but the closer up you can see clearly. Hence, myopes have a range of clear vision that is closer to their eyes than emmetropes (normally sighted people) (Triad Publishing).
A young emmetropic adult can focus at an object some 10 cm away, which is defined as an amplitude of accommodation (lens adjustment) of 10 diopters.
A severely myopic eye can be up to minus 6 diopters, bringing the tally from 10 to 16 diopters, meaning you can view something up to 6 cm instead of 10 cm.
Bringing objects closer increases retinal image size and hence increases spatial detail. Going from 10 to 6 cm increases the retinal angle by 10/6 = ~1.7 x, so not even a doubling of the angle.
A random search for a magnifying glass for the visually impaired that aids in reading small print (newspapers etc.) yielded one that magnified 4x (16 diopters):

Clip on reading aid. Source: Eschenbach
Microscopes typically have lenses with magnification factors from 4x to 100x.
So in all, myopes do not have microscopic superpowers. A standard magnifying glass for the visually impaired magnifies several times more than a severely myopic eye.

The changes in image size in myopic eyes are not as large as one would imagine. In fact, they are pretty close and the myops are probably not aware of them until the proper correction is placed which affect the image size in a much greater degree.
You can see on the image that the sizes of retinal images are very similar - the uncorrected image size is shown in Y' row:
(Y'' is an image size with a proper corrective lense)

It is true the near point of accommodation of myopic eye is closer that of emmetropic eye, but it is war away from "superpower" mentioned by the professor.
In addition, the discrimination ability in myopic subjects are greater than of emmetropes, because they able to see smaller points, but at the same time the image quality is affected as well, thus overall image quality is more compromised compared to emmetropic eye.


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Survival with only water but no food
How long can the average, healthy adult human survive with only water?

this seems to be an opinion-based question. Also, it would be better to post your research as well as question. What sites are you talking about? Any papers? what is particular side of such survival are you interested in?

@aandreev this question is not opinion based. You cannot survive forever without food, at least as far as I know.

Definitely not opinion-based, actually a great question - but a dupe

On average, it has been stated to be about five weeks however it differs from person to person based primarily on physical stats.
The process that would occur :

First food that remains in your stomach is digested
Readily available energy is then absorbed (This includes glucose, carbohydrates, anything that generally doesn't mean fat)
Your body then begins to convert fat into a source of energy. Your body would then begin to lose the resources to make protein and you would experience various effects such as night time blindness due to vitamin deficiencies
As you lose salt and other minerals the water you consume begins to build up in your cells via diffusion
You can either die of not enough energy or lack of protein or too many cells disintegrate from too much water

Source(s) : Biology book, Internet, Knowledge.


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meaning of the "reads" keyword in terms of RNA-seq or next generation sequencing
I'm an undergraduate student at computer science and currently, I'm interested in bioinformatics. Today, I've started to read a paper about clustering and classification of non-coding RNAs can be found here and I've seen a word RNA-seq read. Altough I searched a lot to learn about, I can not find the definition of it, the thingsI found was about performance issues of techniques rather than explanation of the word. So, is there anyone who can simply explain me what is the meaning of this word as well as RNA-seq technique?

In RNA sequencing, the RNA is fragmented, DNA is synthesized complementary to the RNA fragments, which is  followed by a complementary strand synthesis. Fragmentation can be done after the cDNA synthesis too.
This DNA is then amplified to form a cluster that is sequenced. Most Next-Gen sequencing approaches sequence a short segment of the DNA (it has improved with experimental and technical optimization).
A read refers to the sequence of a cluster that is obtained after the end of the sequencing process which is ultimately the sequence of a section of a unique fragment. If an RNA is expressed in high copies then there will be more reads coming from it; reads can be redundant as well.

Courtesy


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Mitochondria variability per tissue in humans?
I would like to know the distribution of mitochondrial content per tissue type in humans. I understand the simple metric that energetically active or energy requiring tissues will have more mitochondrial content, however is there any study/link for a more quantitative estimate ?

Welcome to Bio.SE. You ask for mitochondrial content per tissue type? Are you asking for help in searching for a proper database or are you expecting folks to sum up every tissue type in man along with its mitochondrial content? I would suggest to specify your question.

check this out. Not able to access it as of now.

@WYSIWYG I think we convergently cited the same paper :P

@MarchHo perhaps. This is another one. Can't access this one too as of now.

BioNumbers is a great site to answer this kind of question.
This search produced a link to this paper , which has measurements for mitochondria per cell for multiple species and cell type.


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What is pQTL and why do we need eQTL?
eQTLs are genomic loci that contribute to variation in expression levels of mRNAs (wikipedia).
There is data out there that shows that ~60% of the time, the amount of mRNA in a cell is directly proportional to the level of protein coded by that mRNA.[1]
It means that even if the abundance of mRNA is high, we cannot be sure that the abundance of protein is high as well. Why do we still need eQTL if we cannot derive abundance of protein from mRNA transcripts? In the end, the abundance of protein influences the disease rather than the abundance of a transcript.
Does a pQTL implement the idea of a relationship between a genetic variance and the abundance of a protein? I do not understand how a genetic variance can influence the protein level. I assume it is related with a post-transcriptional modification but how?

There is regulation at the protein level ie post-translational modification, autophagy, protein stability etc. Simply knowing total amount of protein does not tell you everything. Knowing eQTL helps to sort out how much of variation in protein amount may be due to the transcription pathway

Genetic variation can affect the levels of protein; consider a variant that reduces the amount of mRNA transcribed, this could have a profound effect on the amount of mRNA available to translate into a protein.
Consider another variant that does not affect the abundance of the mRNA transcribed, but alters one of the many important sequences that are required for translation (co-factor binding sites, ribosomal binding sites, start site, etc.).
These are just a couple of examples that first came to mind, but there are many more. For instance, a variant may increase expression of a particular microRNA that in turn inhibits the translation of another mRNA molecule. I have not included any references as this is more a logical exercise - doubtless there are many more ways a genetic variant can affect protein abundance.

Considering your first two examples and the citation from researchgate about that 60% of the time,  the amount of mRNA is directly proportional to the level of protein coded by that mRNA, I still do not understand why eQTLs are so important in those two cases as we cannot derive the amount of the protein from the amount of the transcript.

The amounts of protein and mRNA are correlated, if not directly proportional. I understand what you are saying, that changes in the amount of mRNA do not necessarily equate to a change in protein abundance, but it seems quite logical to me that if a SNP either changes the mRNA sequence, or changes the abundance of the mRNA, the SNP could affect the amount of protein - this will differ in every case of course, and pQTLs that have been documented presumably do alter the final protein (either in form or abundance), otherwise they would not be reported as pQTLs.


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SNPs in DNase hypersensitive and histone marks sites
I am investigating a role of SNPs in DNase hypersensitive sites and in the DNA regions of histone marks and have some questions about it.
SNPs in DNase hypersensitive sites might mean that those SNPs are in enhancer regions and might influence TF binding affinity what can influence a transcriptional output. Is it correct?
SNPs in histone marks sites
I have the number of SNPs that fall in the peaks (chip-seq) for the following histone modifications of healthy patients:
H3K27ac,H3K4me1,H3K4me3 (represent the active chromosome)
H3K27me3, H3K9me3 (represent the repressed chromosome)
Histone modifications represent if the chromosome is active or repressed. A SNP might change the binding affinity of a histone. It means that if I have a SNP in data for active chromosome (H3K27ac,H3K4me1,H3K4me3), it might change the status of a chromosome, namely turn it into a repressed one or it might induce a histone not to bind at all(it means that this region is still active,no?) Is it right? I am not sure I understand the possible influences of a SNP histone marks sites.

Enhancer regions or other protein binding regions of DNA will not be DNAse hypersensitive.

@WYSIWYG Why? I though it chromatin is not repressed, then it is nucleosome free.

Protein bound regions will be protected- same principle as in case of nucleosomes.

Why will it be protected? In case the TF did not bind to it, it will not be protected. I have seen lots pf plots where DNA hypersensitivity coincides with TF binding sites (chip-seq peaks). What is then hypersensitivity sites and why do we want to explore it? Wiki suggests: "These accessible chromatin zones are functionally related to transcriptional activity, since this remodeled state is necessary for the binding of proteins such as transcription factors."

First off let's define some concepts.

DNAse hypersensitive regions are DNA regions which are in an open chromatin conformation (i.e. euchromatin). This means that those regions are more active at the genomic level (i.e. higher gene expression, gene regulation and higher TF binding) and are less prone to form nucleosomes.
Histone mark sites are DNA regions known to bind certain type of histones and therefore also influences the chromatin conformation leading to the same effects described previously. The critical point is that the histones you are listing do not primarily bind a specific DNA sequence (as described by @mdperry) but rather DNA sequence marked by epigenetic modifications such as methylation and acetylation.

Now for your first questions, SNPs in DNAse hypersensitive regions might influence the chromatin state and therefore yes might influence gene expression and gene regulation. Will those SNPs also influence TF binding? Well they might indirectly via chromatin modifications. They will not directly act on TF binding if not located in a sequence known to bind TFs (TFBS). DNAse hypersensitivity is not a synonym for transcription factor binding regions/sequences.
For your second question, SNPs in histone mark sites are a little bit more difficult to interpret. They might, or might not, provoke chromatin changes by influencing the binding of histones but not in a direct way. CpG islands are, for example, DNA regions known to be greatly under the influence of epigenetic marks and therefore mutations in those specific regions (e.g. a C -> T mutation) might influence the relative methylation/acetylation state and therefore the binding of histones. SNPs might therefore influence gene expression via chromatin changes which leads to higher/lower TF binding but again not in a direct way. Here again a SNP would influence TF binding directly only if the mutation is located in a TFBS.
As you can see my answer is full of "might" and the reason is that it is very difficult, at the current state-of-the-art, to determine the exact impact of a SNP on the 3D conformation of the chromatin and therefore predict the effect on specific gene expressions.
An advice would be to try to co-localize your SNPs with known TFBS either predicted In-silico or measured via CHiP-SEQ experiments and merge that with the information about DNAse hyperactivity and histone marks you already gathered. For example a SNP in a TFBS in a DNAse hyperactive region is very likely to have a greater impact than a SNP in a TFBS in a non active region.
I am sorry I cannot be more specific but this is a very active research area in genetics and there is still a lot to understand, especially for the interactions between all the players influencing the chromatin conformation.

(at)Tonja, you could search far and wide on the Internet and you would not find a more cogent or on point discussion of these concepts than the one @cagliari2005 very patiently elucidated for you.

Keep in mind that it is not individual histones that are binding, there are 8 histone proteins forming a compact nucleoside particle, and the particle has 146 bp of DNA tightly wrapped around it.  Since the interaction between the histones and the DNA are not sequence-specific, it is unlikely that a single nucleotide polymorphism would have a measurable affect on the occupancy of the nucleosome at that site.

"interaction between the histones and the DNA are not sequence-specific". So, in fact the more SNPs are situated in 146 bp region, the more effect they have? I have lots of papers which refer to SNP in histone sites but non of them tells about the consequences.

No, you are approaching it like a classical lac Repressor <-> lac operator interaction where you can measure the moles of free protein, free DNA, and bound protein-DNA complex, and use those values to calculate the Kd, and a binding affinity. That model is for sequence-specific DNA binding proteins, and yes, the more nucleotide sequence mismatches you introduce into the recognition site, the weaker the affinity. The histone octamer core will bind to any DNA, and is by definition not sequence-specific. So introducing SNPs is unlikely to affect occupancy


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Are four-leaf clovers mutations, developmental errors, or something more complicated?
What causes about 1 in 10,000 clovers to have four instead of three leaves? Will progeny(?) grown from its flower's seeds have a higher probability than that of also having four leaves?
From the Wired article The Mysterious Genetics of the Four-Leaf Clover

A clover’s lucky fourth leaf is presumably specified in its DNA. But the clover genome is surprisingly complicated, and finding the genes responsible—and under what conditions—for the four-leaf mutation is a still-unsolved biological puzzle.

From the Wikipedia's Four-leaf clover: Cause  (emphasis mine):

It is debated whether the fourth leaf is caused genetically or environmentally. Its relative rarity (1 in 10,000 clovers[ref]) suggests a possible recessive gene appearing at a low frequency. Alternatively, four-leaf clovers could be caused by somatic mutation or a developmental error of environmental causes. They could also be caused by the interaction of several genes that happen to segregate in the individual plant. It is possible all four explanations could apply to individual cases. This means that multiple four-leaf clovers could be found in the same clover plant.[citation needed] (emphasis added)

A recessive gene for four leaves has been identified (Tashiro et al., 2010). The clover is a tetraploid species and together with the fact that environmental conditions may also suppress the development of the fourth leaf, it indeed takes a lot of luck to find one. If it will bring you any is another question though.
In fact they are aiming at making a four-leaved cultivar (source: New Scientist).
Reference
- Tashiro et al., Crop Sci (2010); 50: 1260–8

That was quick! OK I'll give it a read.

Some of the links in the New Scientist paper aren't working, but I did find this one :)  Also this is interesting.


text:
Novel bacterial strains of bacteria first isolated on the International Space Station, did the space environment lead to these genetic changes?
Question
Methylobacterium ajmalii sp. nov., Isolated From the International Space Station (Bijlani et al. Frontiers in Microbiology, 12, p. 534, 2021) is a thorough analysis of "novel strains" of bacteria isolated from the International Space Station (Characterization of the total and viable bacterial and fungal communities associated with the International Space Station surfaces)
Question: Bijlani et al. 2021 is written at a very dense and technical level that is challenging for me to understand. I'd like to know:

Does the article suggests these may be newly discovered species or only that they are novel strains of known species of Earth bacteria?
Does the article suggest that the environment on the ISS selected for these species or strains, and they resulted from some genetic changes due to the ISS environment, or if we looked hard enough we'd expect to find the same ones on Earth and they just happened to be identified first on the ISS because of the rigorous studies of those samples?

Background
I was lead to the paper after seeing the ink the BBC's Could humans have contaminated Mars with life? which is primarily about a different topic.
The paper is one of 10 papers the 2021 topic Extremophiles: Microbial Genomics and Taxogenomics.
The ISS is a unique closed environment with plenty of surfaces with sometimes problematic mold growth, and a population of usually 3-6 humans with regular rotations every 5 to 6 months who maintain an array of biological experiments including a sustained effort to try to grow vegetables and flower hydroponically and in soil.
The atmosphere is maintained similar to Earth's surface (oxygen/nitrogen ~1 bar) with 60% relative humidity and often has a CO2 concentration slightly higher than the astronauts would prefer.

The authors propose that this is a distinct species based on a number of physiological and genetic tests. To quote the summary of your linked paper

In summary, the phylogenetic and genetic distinctiveness and differential phenotypic properties were sufficient to categorize these three ISS strains as members of a species distinct from other recognized Methylobacterium species. Therefore, on the basis of the data presented, strains IF7SW-B2T, IIF1SW-B5, and IIF4SW-B5 represent a novel species of the genus Methylobacterium, for which the name Methylobacterium ajmalii sp. nov. is proposed.

This indicates (emphasis mine) that they think that these isolates are distinct enough from species that we have found on Earth to make the isolates a species. This is a species that we haven't found on Earth, but unsurprisingly it is closely related to species from the same genus that have been found on Earth and on the ISS

The authors make no statements about how the species came to be there that I could see, only that it is a novel species from the ISS, which has not been found on Earth. No mechanisms for arisal are postulated, and the authors wisely did not speculate on this at all (speculation on results is frowned upon in science). One of the reasons they did not speculate on this will be that testing mechanisms whereby speciation has occurred is very difficult, especially as they would need to mimic in the lab the conditions in the ISS and show which conditions were important for the speciation. These experiments would be technically challenging and very time consuming.

It is worth noting that we don't really know the rate of species differentiation on Earth, let alone in space, partly because Earth is so covered in bacteria that proving that one evolved in the environment is difficult as it is hard to prove that you didn't just miss it last time you looked. To quote the paper I linked above:

For example, a single gram of soil can harbour up to 1010 bacterial cells and an estimated species diversity of between 4·103 to 5·104 species .

However, the ISS is one environment where it might be easier to see these sorts of events because it is relatively micro-organism free, and we have prior samples to go back and compare to. For some comparison of the numbers, I turn to the second paper you linked, which found:

Of the total bacterial and fungal isolates that grew, 133 bacterial isolates and 81 fungal isolates were identified by Sanger sequencing...   ...When the ASVs were summarized to the genus level, 121 taxa were detected, 77 of which could be assigned to known genera

and

Overall, the number of bacteria (combination of R2A and BA growth) isolated from the ISS from all 24 samples ranged from 6.7 × 103 to 7.8 × 1010 CFU/m2

So quite high numbers of cultivatable bacteria (CFU = colony forming units, a measure of how many bacteria will grow per sampling), indeed as high as those found in a gram of soil, but very low species diversity compared to the soil.
It is still difficult to prove that this is a new species evolved strictly on the ISS, but it does seem logically likely that evolution will happen on the ISS, as it does anywhere that life is present (as far as we know).

+n! Thanks you for writing such a thorough post at a level that I can readily understand and appreciate, and outlining several important concepts that apply here. I will think about follow-up questions like "Can a new bacterial species arise in as short as 10 or 20 years given unusual human habitat conditions?" and "Simple way to understand how scientists decide when two strains of bacteria are actually sufficiently different that they are two different species?" But first will reread this a few more times, then re-read this paper, then look through previous Q&A here before posting.

@uhoh - no problem. The answer to your first one is yes. Model bacterial replication takes ~20 min under ideal conditions, so about 3x an hour. Multiply that by a year and you get something like 26,000 rounds of replication. This is plenty to speciate on - think where our ancestors were 26,000 generations (~780,000 years) ago.

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


text:
What does the energy in an energy pyramid represent?
Suppose the energy at the second trophic level as given in an energy pyramid is 100 kcal per square metre. It could mean either of the two following things:

100 kcal is the energy this primary consumer has stored in its flesh - that is, the energy left over from the amount consumed, after assimilation and respiration. This would be the net productivity of that consumer, or the energy available to the secondary consumer which feeds on this.
100 kcal is the energy this primary consumer consumes. It will utilise a part of this in respiration, lose some amount in assimilation, so that a small amount is left over which is then stored in it as mass, or flesh - which would be its net productivity.

Similarly, the first trophic level, the autotrophs' energy could represent either the total amount of food they make (the GPP), that is, the energy akin to the second case above, or the energy stored in them and available to the next trophic level (the NPP), like in the case 1 above. So which of these is correct - what do we represent as the energy of a trophic level in an energy pyramid? I think it should be the first case, the stored energies, since after all these are what you will measure as the energy of any trophic level - the stored energy at that level.

Each layer in the energy pyramid represents the stored energy in biomass in that layer. This energy is obtained from the previous layer. Because every layer uses a certain amount of energy needed for survival (combustion of sugars and fats through respiratory processes) obtained from the previous layer, each subsequent level is smaller than the previous one. Also, the autotrophs in the photosynthetic layer use up (solar) energy for living. The higher up you get, the more energy is cumulatively taken away to sustain life and growth of the previous layers. Therefore, it's a pyramid shape.

Energy pyramid. Source: Biocab


text:
Why did humans evolved the scratch reflex?
I've been wondering about this for some time, and I can't come to an answer...
Everybody keeps telling me that scratching one's own skin is bad. It damages the epidermis, creates the hazard of malicious bacteria getting past the skin barrier, and creates the vicious circle of scratching increasing the itching, and itching increasing the scratching (I think I recall reading that this vicious circle also happens even without any special skin diseases, like atopic dermatitis - I might be mistaken here, however)
So, it seems there are hardly any benefits for the body from the scratch reflex. However, if this was true, then "grandma Evolution" wouldn't have given this to us!
What are the benefits of scratching? Are there any benefits of it from the evolutionary point of view? I can come up with just one such benefit, namely fending off insects such as ticks, mosquitoes, fleas or lice. Would this be the evolutionary benefit of scratching?

Not enough time for a real answer, but I see the scratch reflex as vital. It rids the body of irritants, such as burrs/thorns, insects walking around, poison ivy/oak/sumac/etc. oils, and more. In the cases where the irritant has already affected us (we got bit by the mosquito, a rash from poison has already developed), scratching focuses our attention on the site, and the ensuing irritation works as a strong warning to not keep performing whatever behavior resulted in the irritation in the first place.

Bacteria aren't malicious. 2) Not everything that no longer serves a purpose "devolves". Evolution is not a controlled, intelligent mechanism ("grandma evolution"). 3) Not every itch which is scratched results in an itch-scratch cycle. 4) Scratching an itch is not necessarily bad. There are at least 4 faulty presuppositions in your question.

Humans didn't evolve the scratch reflex. We inherited it from 350 million years of mammal ancestors.

With about 20 square feet of skin constantly exposed to potential irritation, itching must serve an important protective/defensive function.
The "scratch reflex" (I'm not sure I would call it that) is necessary to life and limb. Itch is a major somatic sensation, along with (and different from) pain, temperature, and touch. Itch can be an acute sensation, e.g. a mosquito bite, or a chronic condition (peripheral or internal disease).
Research on itch signaling is still at its infancy, and basic mechanisms by which the itch sensation is transmitted and regulated have yet to be fully understood. It is meant to give us information about how we are interacting with our environment. Loss of such fine sensation, such as occurs with Hansen's Disease - aka leprosy, where patches of skin become painless and do not itch, so are ignored by the patient - leads to festering wounds and resultant problems.
As @MattDMo stated in a comment, sensation allows us to respond appropriately to irritants which, if ignored, might lead to festering wounds: thorns and other foreign bodies, sucking or biting insects (parasites or other, which can act as disease vectors as well), etc. It allows us to learn how to avoid and treat such irritants.
Various types of itch can be classified by the origin of the itch, which could be skin-related, neuropathic, systemic, or psychogenic. The most common cause of itching is dry skin; tiny cracks in the skin cause an inflammatory response, which (within reason) is not a problem in and of itself. The response to the itch, though, can be beneficial or damaging. One can treat dry skin, wash off irritants, treat infections, avoid causes, etc.
Scratching can be benign if done sensibly, or it can injure the skin, allowing infection, etc. However, the benefit of having such sensation under normal circumstances certainly outweighs the inconvenience.
That is not to say that pathological conditions that cause itching are not problematic. They are, and one might reasonably curse the sensation under those circumstances.
Edited to add: Itching, or pruritus, is defined as an unpleasant cutaneous sensation that serves as a physiological self-protective mechanism to prevent the body from being hurt by harmful external agents. (Nature, 2007)
Scratching is simply a reasonable response to itching from any source and is not necessarily harmful. It's not a reflex per se. You can avoid scratching. Some animals must actively seek out a way to scratch. This takes it well outside of the terminology of reflex as neurologically understood.
Itch Signaling in the Nervous System
Pruritus
When you have an itch, what is happening under your skin?

Great. But, itching causes scratching. Scratching is not a good way to deal with dry skin (it only worsens the problem), and not a good way to deal with thorns or insects (thorns should be pulled off, insects smashed). You say: "Scratching can be benign if done sensibly". But I can't see how?

@gaazkam - People scratch itches all the time without drawing blood or causing infections; even in situations where it's advised strongly not to scratch, such as with chicken pox, it's very uncommon to see bacterial superinfection caused by doing so. Scratching sensibly means gently and with clean fingers, short nails. Gouging yourself is not sensible; it is done, however  by people with intractable itching. When that's the case, they need medications to control the itching. Scratching does not always increase the itching, but tends to in certain situations.

OK, so scratching doesn't need to be malicious. But what are the benefits?

@gaazkam - Beyond chasing mosquitoes and other bloodsuckers away in the initial act of attack, it relieves the itch. That in itself feels good. Because severe itching can't be relieved by scratching, it teaches us about avoidance of skin toxins, e.g. poison ivy.

So, to sum up, scratching is good just because it relieves itching. Great. But why did such mechanism evolve, since scratching can do nothing about the cause of the itch? ... all right. One possibility is this mechanism is a leftover from earlier mammals... perhaps scratching is the best way for a cat or a dog to fend of insects or remove thorns from their fur, but definitely not for humans! Yet this now useless mechanism (of scratching, not itching) has not yet devolved.

@gaazkam - you make assumptions: 1) that scratching is a useless mechanism (what would you do if you had an itch but no fingers? Rub yourself up against a tree? That's what bears do. Obviously, scratching an itch feels good!, and 2) that every "useless mechanism" should devolve. That's a fallacy. Humans don't have tails, yet we still have tail bones. They break and cause pain. Why don't we just devolve them? You have been so resistant to this answer that I doubt I'll ever answer one of your questions again. That's not said in a huff. Your attitude is simply unpleasant.

I'm not arguing with your answers. At least, that's not what I'm trying to do. I see nothing wrong with what you claim here, and I find all of this very interesting. I'm sorry if you find my behavior inappropriate; it's just that if I'm curious about something, I tend to belabour just until I can finally fully understand it. I know, however, that my interpersonal skills leave very much to be desired, and I should definitely work on this.

Perhaps I was failing to ask my question accurately. Thank you for pointing me out that scratching doesn't have to be bad, that itching itself is beneficial, etc. What I couldn't understand, however, was something like this: why did the scratching (and not any other behavior, or no behavior at all) evolve to relieve itching, since scratching didn't seem to me to resolve the cause of the itch? Note that pain, for example, doesn't have such relieving mechanism.

I finally came to the conclusion that the said mechanism is just a leftover of previous evolution stages. It did serve a purpose previously; but it no longer serves one, but it didn't just "go away". Perhaps this is exactly what you answerers were trying to tell me all the time; if so, sorry for not getting it in time.

But I wrote it in one of my comments. This implies that I understood that evolution is not an intelligent mechanism (note the ""'s enclosing my "grandma Evolution" statement). As to the other "faulty assumptions": 1) I understand that not all bacteria are malicious; that's why I wrote "malicious bacteria" to denote the harmful ones (regarding to human organism); 3 and 4) Thanks for pointing this out for me, I accept this.

Happy Easter to you BTW.

@gaazkam - Happy Easter to you, too. :) If that's what you want to know, then that is what you should ask. In fact, we do have a similar reaction to pain: we cradle, message, grab, lay a hand on an area that hurts. If we have a backache, we rub our backs to try to make it go away. A cramp in out hands? We message and stretch the hand with the other. Smash your thumb? We'll grab the hand - even though it doesn't help the pain, and cradle it. We do try to make pain go away with our hands. Just like scratching an itch. But it doesn't work nearly as effectively. (cont)

When people have bad cardiac chest pain, they so frequently try to grab their chest that we call it the positive fist sign. People who have stomach aches will often try to alleviate or soothe themselves by gently rubbing their bellies. Note also that we respond to a cold feeling by briskly rubbing, If someone applied an ice cube to your forearm, I'm pretty sure you would rub the spot for a moment. So, do you see that scratching is not a unique response?  We just happen to be able to actually do more about an itch than about a pain. But a response is a response.

"because it feels good" is not a reason why something harmful would evolve

@endolith - what a silly comment! How do you explain racing, skydiving, shooting heroin, and the other hundreds of potentially lethal activities humans engage in because they feel good? Write a better answer with sources.

@anongoodnurse Humans have an instinctive biological motivation to skydive?  I would have guessed the opposite.

Short answer
People scratch to alleviate the itchiness.
Background
Itch (pruritis) is caused by a moderate stimulation of pain receptors. There is not such a thing as an itch receptor. Due to the neural circuitry involved, rubbing a painful bruise actually dulls the pain due to stimulation of the tactile sense (Kakigi & Shibasaki, 1992). This may explain the familiar first action one does when injured - grabbing the injured spot and rub it (cats lick their wounds, likely dulling the pain and cleaning it up at the same time). Given the similarity with the neural processing of pain, it is not surprising that a very similar mechanism applies to scratching - scratching relieves the itchy sensation (Nillson et al., 2003).
So while evolutionary explanations may be valid, they can never be proven. And in fact, too much scratching can be harmful, and I quote from Dermnet:

Itch [...] provokes the desire to rub or scratch the area to obtain relief. [...] Constant scratching to obtain relief can damage the skin (excoriation, lichenification) and reduce its effectiveness as a major protective barrier.

Hence, from a behavioral and neurophysiological point of view, we simply want to get rid of itchiness and we scratch. Whether this is evolutionary advantageous other than to provide a means to temporarily reduce debilitating itchiness, is questionable.
References
 - Kakigi & Shibasaki J Neurol Neurosurg Psychiatry 1992;55:282-6
 - Nillson et al. J Eur Acad Dermatol Venereol 2004;18:37–43

OK, so now I know how scratching relieves itching. But what are the benefits of scratching to the whole system? Or, more precisely - what are the benefits of the mechanism of scratching relieving itching?

@gaazkam - my point is, as I conclude in the last sentence, we cannot tell what then benefits are of scratching. My guess is that it feels good, as it relieves the itch. The evolutionary advantage regarding ticks and flees etc. is the fact that we feel itching. That warns us and lets us undertake action. If this action is scratching, it is important to realize that settled ticks don't care about scratching, flees are notoriously hardened critters and mosquito bites only start to itch when the deed is done; scratching in itself has no obvious advantage, other than to relieve itching.

So, to sum up, scratching is good just because it relieves itching. Great. But why did such mechanism evolve, since scratching can do nothing about the cause of the itch? ... all right. One possibility is this mechanism is a leftover from earlier mammals... perhaps scratching is the best way for a cat or a dog to fend of insects or remove thorns from their fur, but definitely not for humans! Yet this now useless mechanism (of scratching, not itching) has not yet devolved.

Are pain and itch the same mechanism? I have read otherwise.

@anongoodnurse: you may both be right to some extent: "In general, pruritus involves activation of the pruriceptors of specialized nerve cells called C-fibers. These C-fibers are identical to those associated with the sensation of pain, but they are functionally distinct and only convey the itch sensation—they comprise about 5 percent of the total C-fibers in human skin. "

And yes, this has been stated by more serious sources: https://doi.org/10.1016/S0140-6736(03)12570-6