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What are the advantages of forgetting?
How  forgetting things is helpful for the brain or the human body  biologically? This web page

After some moment of being rude, selfish, or weak, either we are able to put it behind us, or the person who suffered at the result of our imperfection moves on. The reason for this is our ability to forget about it. We forget not because we have an imperfect hippocampus (our brain’s memory organ); it's actually an evolved solution. The ability to lose information allows new information to come in that is more relevant, more pertinent to an ongoing reality. Forgetting allows us to update.

and this Huffington post article

According to a study in Nature, our awareness is limited to only three or four objects at any given time. To be able to think at your highest level, you therefore must be very efficient at filtering out all of the background noise: Your racing thoughts, the ringing phone, your neighbor’s barking dog, and the list goes on.
The Nature study found that when participants were asked to “hold in mind” certain objects while ignoring others, there are significant variations in how well each of us can keep irrelevant objects out of our awareness.
The researchers concluded that our memory capacity is therefore not simply about storage space, but rather “how efficiently irrelevant information is excluded from using up vital storage capacity.”

provide some backgrounds.

That link is to a psychology article titled "Why Forgetting the Past Can Be a Good Thing, in other words, remembering the time you were drunk and did something incredibly embarrassing to you is better fot your self esteem to forget. This is not a biology question. Maybe Cognitive Science.SE

I'm voting to close this question as off-topic because cogsci.se is a better place for it.

But I don't want to know the psychological answer . Psychological answers are plenty available on the net

I think that link was the culprit :-)

This is more of an idea I have than actual research and the other answers are better, but it occurs to me that we think of as "memory" as being a record of past events for its own sake, but there is zero reason for us to evolve a record of past events for its own sake. Memory certainly evolved as part of our general cognition because it allows to better model, predict and function in the world, but it would evolve only insofar as it does help with those things. So maybe the assumption that remembering is the default and forgetting needs to be explained is wrong.

Because not every association the brain makes is correct. Imagine never being able to learn to spell cat (cat) if the first time you tried you spelled it (kat).

Darn, the answer is on the tip of my tongue!

What if your body never "forgot" that it was injured?

I used to know the answer to this one...

@John: But I can readily remember getting things wrong the first time around (or indeed, the first few dozen times), yet still know the right way once I've learned it.

you remember more recent error or particularly egregious ones but you don not remember the vast number of corrections your brain has made. you don't remember all the times you flailed around trying to learn your limbs or the first time you wrote letters.

Because the human skull has a finite volume and new memories consume some of that volume e.g. memories require matter. So if we remembered every single thing we ever experienced, we'd all be far less attractive. Think 1950s alien movies. Big blue heads. This is just one of the many purposes of sleep btw - optimising how useful info from the day is sorted and stored and then throwing away the rest, one by product of that process of knitting in the new pages of memory is of course "dreams".

I voted to re-open as I do not see any benefit in closing a well upvoted question that received an accepted, well received answer 5 days ago. See the corresponding meta question

"I'm voting to close this question as off-topic because cogsci.se is a better place for it.".. This is no valid reason. This question is on-topic. If it is a better fit elsewhere then a mod attention flag could have been raised for a suitable migration. @Mesentery It would be great if you can summarize the linked pages so that the question is somewhat complete by itself.

Short answer
It has been shown that loss of long-term memories may enhance the retrieval of others. Short-term working memory is explicitly designed to be volatile and non-lasting. However, there are many other types of memories where memory loss may not be explicitly beneficial, or even outright debilitating such as in the case of Alzheimer's or stroke.
Background
First off all, there are many types of memories, including sensory memory, motor memory, short-term (working) memory, long-term memory, explicit & implicit memory, declarative & procedural memory and so on. Hence, because the question is quite broad, I will focus on long-term memory, short term-memory and sensory memory to discuss that memory loss can be beneficial, neutral, or detrimental.

Beneficial effects of loosing memories
Long-term memory is probably what you are after and there are studies in that field that have linked the loss of memories to enhanced processing of other memories. More specifically, there are adaptive benefits of forgetting, namely a reduced demand on cognitive controls during future acts of remembering of other stored information. Even more specific: retrieval of memories after forgetting others are thought to reduce the necessary engagement of functionally coupled cognitive control mechanisms that detect (anterior cingulate cortex) and resolve (dorsolateral and ventrolateral prefrontal cortex) mnemonic competition (Kuhl et al., 2007). The improvement of particular memory processes by forgetting others may be linked to them being closely related. Indeed, motor tasks more remote do not benefit much from forgetting unrelated ones (Shea & Right, 1991).
Inherently volatile memory
Short-term working memory is explicitly designed to aid in on-demand task performance. Short term memory is for example used to remember a set of components (e.g., colors) and use that information to deal with a certain task at hand (which objects depicted here match the colors you just saw?). If all these memories would be retained, tasks dependent on working memory would not be possible. Sensory memory an ultra-short term memory that is kept only for very short amounts of time, allowing people to, e.g., track a light and make a symbol or letter out of it before the information is funneled to the short term-memory.
Neutral effects of loss of neural function: a side track off memory lane
However, forgetting may be simply another example of the use it or lose it principle that applies to pretty much everything in the human body; when you don't walk, the bones in the legs will weaken along with the musculature used for locomotion. Similarly, when the inner ear or the retina becomes dysfunctional and degenerate, the deafferented auditory nerve and optic nerve start to degenerate, respectively. The associated deafferented sensory cortices will slowly be taken over by other adjacent cortical areas due to the plasticity of the cortex. In blind folks, for example, the tactile and auditory cortices have been shown to take over the primary visual cortex. Given that the visual cortex is huge compared to the tactile and auditory cortex, one would expect substantial increase in performance on tactile and acoustic tasks in blind folks. Yet, this is debated (Stronks et al, 2015). In fact, normally sighted folks can learn braille as well as their blind peers, suffice they get an equal amount of practice. In other words, practice is the key, not enhanced areas of cortex being available per se. Hence, 'forgetting' to see or 'forgetting' to hear is, as far as my knowledge goes, not associated with any benefits whatsoever, barred a minority of studies that showed a slight benefit of being blind in auditory tasks (Stronks et al., 2015).
Pathological memory loss - not so good:
However, forgetting of memories may also be pathological; think of the impaired short-term memory of Alzheimer's patients, or amnesia due to stroke. Forgetting is not always beneficial.

References
- Kuhl et al., Nature Neurosci (2007); 10: 908-14
- Shea & Right, Res Quarterly Exercise Sport (1991); 62(3)
- Stronks et al., Brain Res (2015); 1624: 140–52

Wow, so much research :D

@ABcDexter - Thanks mate! No half-baked answers here ;-)

! second @ABcDexter's comment. And I learned an exciting new word, too: *deafferented". Clearly I haven't been reading enough neuroscience. :)

@anongoodnurse - thanks for the compliments and I'm glad I was able to add a word to your dictionary ^__^

Re: "Short-term working memory is explicitly designed to be volatile and non-lasting": Can you maybe find a more scientific way to express this idea? (By the way, you mean "lose" rather than "loose", though in context it's clear. :-) )

Interesting answer !!! I didn't expect this question to be answered by the previous comments.Extremely thankful for answering the question.+3 @AliceD

Interesting recent paper on exactly the subject of benefits of forgetting (creatively rebranded as "transience" of memory): http://www.cell.com/neuron/fulltext/S0896-6273(17)30365-3

Memory is formed by building connections between nerve cells (i.e. neurons). These connections are called synapses. The synapses form a network between several (or tens or hundreds) of neurons, therefore giving us the ability to retrieve something we had memorized before.
Learning something new requires building new connections, but the older connections might interfere with the new ones and thereby interrupt our memory or what we have learnt. So sometimes older connections must be broken in favor to new connections and new abilities. For instance, you might remember crawling on both hands and knees as a child, but slowly you practiced walking and at one point you stood up and never crawled again. Children crawl like it's no big deal, but grown-ups have to think and struggle and in the end it's not gonna be very good. That's because older connections regarding crawling have been broken in favor to new connections for walking.
Check out: Izquierdo, Ivan. "The art of forgetting." Springer International Publishing, 2015.

I really think you need to cite some sources. You're very short on evidence here. For example, "older connections must be broken." What does that actually mean? Is it loss of facilitation, loss of synapse, or something else? It sounds good, but it sounds like a lot of opinion as well.

@anongoodnurse I agree, especially with regard to adults having difficulty crawling. I can think of many reasons why an adult might struggle to crawl, none of which is at all related to missing memories.

I agree with the above, and @Dan's comment in particular: Conversely it does not seem clear to me that "children crawl like it's no big deal". (Also fwiw I don't find crawling difficult at all.)

@anongoodnurse (and everyone else) Thank you very much. That's a fair comment. I wrote this on the go and couldn't look up my sources, but my main source is the book I introduced. (thumps up)

I think this is the article about babies forgetting things: http://dx.doi.org/10.1126/science.1248903.  I had read it when it came out. @hossein Please check and incorporate if necessary.

One famous person, Solomon Shereshevsky, had an unusual ability to remember everything he encountered: sights, numbers, words in foreign languages, events from infancy, and more.

Unfortunately, S’s gift was a serious handicap. He was unable to block unwanted memories. Also, he had a terrible memory for faces because he memorized them so exactly. People’s faces change with time, lighting, mood, and expression. S had difficulty recognizing faces because they looked so different to him from the ones he had completely memorized in the past.

Extrapolating from that, one could conclude that the inability to block unwanted memories could easily lead to the development of PTSD — especially if, as in Shereshevsky's case, the total recall is combined with synaesthesia.

Who says it has to be good?
We cannot assume that every trait that evolves is beneficial to the species. A lot of people assume that the species of an ecosystem will evolve optimally; that is, they assume each species evolves to have the best possible genes for its environment. My understanding is this is not the case. Species have to adapt or face extinction, but they only have to adapt to be good enough. Perhaps it's not that forgetting is good, but rather it just doesn't impede survival or reproduction. (Well, except when you forget your spouse's anniversary!) Which leads us to the next point...
It's a side effect of how human memory works.
First off, storing a memory in the brain is not like running a tape recorder or camera. The brain actually stores very little of the information coming into it, just enough so that it can later fill in the blanks and make a decent reproduction. In computer terms, the data is filtered through a very lossy compression algorithm before being stored. It's just good enough that we usually don't notice, but sometimes things go wrong and we get phenomena like confabulation.
Now about how that data is stored. As you know, the data is stored by the synapses in the neurons. But here's the thing: those synapses aren't dedicated to that specific memory! Storing a new memory affects synapses that are part of other memories. One synapse might be storing a piece of information for any number of memories, because those memories all have some tiny thing in common. I wish I could explain this better and in more detail, but this became pretty obvious to me when I read up on artificial neural networks, which are crude models of brains.
Sometimes, neurons just die. Obviously this is going to affect the brain's ability to recall the information the dead synapses contained. There's enough redundancy built into the brain that this is rarely a problem, except in cases like Alzheimer's, where the brain just suffers too much damage.
To me, the question isn't why we forget. The question is how we can remember stuff at all!

You're right that forgetting doesn't have to be "good" but I think @AliceD's answer has some well-cited research for why indeed forgetting is beneficial in some cases because of the evolved environment and how memory works.

True. But the OP seemed to be making assumptions before verifying that they actually hold; a big part of my aim was to make counterpoints to those assumptions. A bit of a gentle Zen slap, if you will. I figured the existing answers were sufficient to address the idea that forgetting is indeed beneficial, so I wanted to take a different approach.

What are the advantages of forgetting?

Perhaps the question asked should be what is the disadvantage of remembering every little detail?
The answer is cost. It cost energy/neuron to remember everything. Neural tissue are expensive to maintain and feed. At rest, the human brain consume 20% of all calories. And that is alot of energy when the human brain is only 1% of all tissue in the body.(http://www.nature.com/neuro/journal/v1/n1/full/nn0598_36.html)
It is also inefficient. If you remember everything, it will take time to reach the appropriate memory. When time is life, it is inefficient to have a large store of unimportant memories to search through for the one important memory.
Also, this being biology... is there a selective drive for perfect memory? Without a section pressure for perfect memory, it won't evolve. Memory that is good enough to survive is what we will get. We do not get cheetahs which are as fast as biologically possible. We get the cheetah that can catch the slowest gazelle.

Please provide sources supporting the claims you suggest in your final two paragraphs. Also, please avoid simply copying links, but instead provide them some context (e.g., what part of your answer they actually support, etc.). This can be done through tagging links with some statement using "" or through endnotes, parenthetic citations, etc.


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Why should the pharyngeal cavity be essential for articulated speech?
In a lecture, I've been told that one of the signs that homo habilis and homo erectus couldn't speak was that they probably lacked the distinction between oral and pharyngeal cavity. But do we really use it, apart from the nasal consonants?

This bit of the book Developmental Neuropsychiatry: Fundamentals describes the difference between the oral cavity in humans and other animals. It doesn't refer to Homo habilis in this context, but it says:

As a result of this anatomical pattern, the range of sounds that an animal can make is limited because of the pharyngeal cavity, which is necessary of sound amplification, is small.

and:

Still, this lower position of the larynx produces a larger pharyngeal space above the vocal chords, which makes possible a greater range of sound modification and becomes the key to the production of articulare speech.

Which suggests that the pharyngeal cavity has a more general use in speech than just making nasal consonants.
This article goes into some detail about Human speech anatomy and its evolution; what it says about the pharyngeal cavity is less about the cavity itself than about the position of the tongue, which allows the separation of that cavity into different sections, leading to different wavelengths being produced. They further say that apes have their tongue entirely in their oral cavity, and are as a result unable to make vowels other than schwas (the basic vowel you make when you're making no effort whatsoever) (they do mention one exception but that species apparently doesn't use its pharynx to make vowels like we do).
The article makes another very interesting point that is relevant to your question, I quote:

Speech communication would be possible without quantal vowels [note from me: the sounds it was talking about that we can make but monkeys can't]. Indeed, there would have been no selective advantage for retaining whatever mutations led to the evolution of the human supralaryngeal vocal tract unless some form of speech had already been part of hominid culture.

That is an excellent point, which is that we need to separate the concept of "speech" from "fully modern speech". Things evolve gradually, and there will have been a continuum from simple communication and vocalizations that our latest common ancestor with other apes likely did, to modern speech with its sounds, grammar, and anatomical and cognitive abilities it implies. And since we no longer have examples of anything on that continuum, we don't know which parts of it we'd be more or less likely to think of as "speech".

Wait...why isn't it possible to articulate without having an extra cavity where the tongue can operat?

If I understand the article correctly it's not about having an extra cavity, it's about the tongue and cavities being in a position where you have two cavities at right angles, and the tongue at the angle between the two able to affect their geometries relative to each other. And the other article refers to a role in sound amplification. It's all about resonant frequencies I figure; in a closed space waves bounce back and forth, and strengthen or weaken themselves depending on their wavelength with respect to the size of the space. Control the size, you control which wavelengths are amplified.

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What is the smallest touch sensation that a human can feel?
What is smallest touch (pressure) sensation that a normal, healthy person (not hypersensitive nor insensitive) can feel on the palm of the hand?

@fileunderwater - of course it's all about population averages. However I do agree with daniel; there are still many variables left; static pressure thresholds differ from hose obtained by vibrotactile stimuli. Furthermore, sensitivity goes down from fingertips > palm > back of the hand

What happened to all the previous comments? They are hardly irrelevant to the current question. @AliceD, do you have any idea?

@AliceD My point was not that it is about population averages, but that the smallest sensation/stimuli that a person can feel is likely to differ alot between persons, so the question is ill-posed. And removing hypersensitive persons feels like an arbitrary cut-off, when sensitivity is likely to differ dramatically between "healthy" persons.

@fileunderwater - the other comments were dealt with and I'm afraid I might have flagged your commentfor deletion - too quick perhaps. But let me put it this way - in psychophysics there is always a huge variation between people. Detection thresholds are subjective - people draw their own threshold. I, for example, generate relatively a lot of false positives, because I tend to feel stuff that is simply not phsysically present (it may be present in my mind for sure). Other folks pick a more stringent threshold and only say 'Yes' when they are absolutely sure they are feeling it

Short answer
The detection threshold of static indentation stimuli on the palm of the hand is approximately 10 to 40 micrometers, dependent on the exact location under investigation.
Background
The sensitivity of a sensory system can be expressed as the detection threshold. This threshold is in psychophysics generally defined as that stimulus level where, on average, 50% of the stimuli are felt.
There are several types of touch receptors that can be investigated, each with specific types of stimuli that are associated with them (Fig. 1)
 Fig. 1. Skin receptors and their response properties (Delmas et al. (2011)
The question specifically targets detection thresholds of indentation stimuli. These stimuli are typically expressed as distance units (meters) or pressure units (Newtons). The skin indentation under constant force is dependent on the area of contact, skin type and other parameters of lesser importance. Hence, indentation units using distance metrics may be the most appropriate way of expressing static detection thresholds. Johansson & Valbo (1970) investigated static detection thresholds on the palm of the hand (Fig. 1) and found average thresholds of 10 to 40 micrometers indentation. This variation was due to geographical differences; towards the fingers sensitivity is higher and thresholds are hence lower (Fig. 2).

Fig. 2. Detection thresholds of static stimuli on the palm of the hand. source:  Johansson & Valbo (1970)
References
- Delmas et al. Nature Rev Neurosci (2011); 12: 139-53

Definitely seems like research that would've been done in the 70s :p. Anyways, nice answer! And interesting too!

I wonder if the number of false positives (or possibly the sensitivity) would change if the subject were first exposed to a video of fleas or other light-touch parasites. Or better, if they were exposed to live fleas jumping on them for a while...
I know that I definitely feel hypersensitive to microtouches if I feel I might be crawled on, and I understand that this is not uncommon.

@DewiMorgan personally, I check for false positives by including catch trials where  subjects are provided  with the regular visual cue for "stimulation is up", but no tactile stimulus is presented. A "Yes" answer is per definition a false positive. If the false positive rate surpasses the 25%, the subject is instructed to raise their internal subjective  threshold and the run is restarted.

@AliceD: Oh, I know it can be compensated for. I was just interested in whether the sensitivity or error rate changed with the same subject, according to mental stimuli like that.

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How do I read an RNA expression pattern?
When reading about diseases one can find links to proteins and their associated genes, an example of which is here.
I'm wondering how to decode/read the following graph as a non-specialist in this area:

What does it all mean?

This is not a particularly specialist graph, so like any other graph you (and we)  need to know what the axes are, what the colour-coding means, and what203411_s_at (i.e. the title info) means. Is there a figure legend? If so, please provide it in your question. I could explain what I think it is about, but you need to put some effort in yourself first.

This image shows the expression of a gene (in your case Lamin A/C) in various tissues. A picture with a higher resultion for mouse looks like this (from here):

You can see the median expression (calculated from all samples) and can also see, in which tissues this gene is highly expressed and in which there is less or no expression.
This is important if you want to analyze the function of a gene. The tissue specific expression pattern can vary strongly between different tissues (as you can see in the figure) which can give information about the function of the gene. The same is true if you look on the time distribution of gene expression, you can identify genes which are important for different steps of differentiation.

That makes a lot of sense. To make sure I understand, does the above graph indicate that lung tissue expresses that specific gene more (on average) than all other tissues? What do the numbers mean?

@UltimateHawk Yes, exactly. I am not sure about the number at the moment, but I guess they are relative to some normalisation.


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Do all organs of our body secrete hormones?
My teacher says that all organs of our body secrete some kind of hormone so they are all glands.
Is the statement entirely correct without any exceptions?
Till date I am unable to find any exception for that statement.
Could anybody provide an exception if any present?

Oesophagus is one such e.g that comes to mind

Oesophagus contain adipose tissue which secretes hormones like leptin, adiponectin and resisting.

How do you define an organ? Paracrine signalling factors are not considered hormones. If you consider interferons and chemokines as hormones, then cells that secrete these are found almost everywhere.

Good question! The major and most common endocrine glands in the human body include pituitary, thyroid, parathyroid, thymus, adrenal, pancreas, gonads and pineal gland, along with neuroendocrinol glands like hypothalamus. Some other, not-so-common, examples include heart (Anti-Natriuretic Factor), GI tract organs (gastrin, secretin, etc.), placenta (estrogen, progesterone, etc.), kidneys (erythropoietin, renin), skin (cholecalciferol) and adipose tissue (leptin)1. Even the lungs are known to secrete calcitonin2.
In spite of this, I can think of quite a few examples of organs which do not act as endocrine glands. That is because there is a difference between the organs secreting hormones and endocrine glands. The definition of endocrine glands is as follows1, 5, 6, 7, 8:

Endocrine glands are glands of the endocrine system that secrete their products, hormones, directly into the blood rather than through a duct.

So, if these organs don't directly secrete the hormones into the bloodstream, then they are not endocrine glands. Leading this way, emotional tears are known to consist of hormones such as prolactin, ACTH and leucine-enkephalin3, 4. Thus, though eyes do secrete hormones, they are not endocrine glands. Also, not sure about this, but lungs still do not seem to fit in the category of endocrine glands.
In short, all the organs of the body might secreted hormones, but they all cannot be considered as endocrine glands.
References:

Endocrine gland - Wikipedia
[Hormone expression and opioid receptors in fetal and adult lung]
Gómez-Román JJ, Cifrián Martínez JM, Fernández Rozas S, Fernando Val-Bernal J.
Frey W. H., DeSota-Johnson D., Hoffman C., McCall J. T. (1981). Effect of stimulus on the chemical composition of human tears. Am. J. Ophthalmol. 92 559–567. 10.1016/0002-9394(81)90651-6
What biological functions does crying serve? - Biology Stack Exchange

Mesentery too contains adipocytes implying that these adipocytes too secrete leptin and other hormones, thanks for efforts.

It would be much better to add definition from a authority holding site, Wikipedia page there does not cite any source either.


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Can rigor mortis change the anatomical position in which a person died?
I've been told as an undergrad in anthropology that the flexed position of the body in which some Neanderthal skeletons were found indicates that they were deliberately buried. Apart from the good preservation of the remains, one of the arguments for deliberate burial was that if the individual had died in this very flexed position during sleep, rigor mortis or post-mortem bloating would have caused the body, if not already buried, to extend (see e.g. Villa's [1989:325] comments to Gargett 1989). Barring sudden death by rockfall and ceiling collapse, this suggests that the body was completely buried before rigor mortis set in, or was deliberately placed in this sleeping position after rigor mortis faded by those that buried it.
But I thought I had heard in a biology course that rigor mortis stiffens the muscles, but does not contract them (see e.g. Faux et al. 2006). If someone died during sleep, could rigor mortis really straighten a highly flexed death position?

rigor mortis doesn't cause any movement so the body remains in that position stiffly.

Rigor mortis does not cause movement. It causes rigor (Latin for stiffness.)
This is only a comparison, but think of it this way. Superglue doesn't shrink or change the shape of the connection of the two things glued together; it just holds them there with powerful 'stiffness'. So imagine that at death, part of our muscle cells exuded superglue. You would get stiff (the muscle to bone/fascia connections would not change) but you would not move. Immediately after death, some muscles relax; most obviously the eyelids open partially, the mouth, hands, and sphincters relax (you won't have to pry a gold coin from someone's dead hands like in the movies.) But aside from general relaxation, you very closely stay in the position you were in when you die.
Physiologically, this is roughly how muscles work: muscle cells are filled with filaments, actin and myosin (I'm leaving out tropomyosin and  troponin for brevity.) Contraction occurs when the myosin can bind to the actin, break the bond and reform it on the next spot on actin, and repeat, like crawling along the actin. ATP and Calcium ions are necessary for this crawling movement. In death, ATP is quickly depleted (aerobically then anaerobically), whereas Calcium floods the cell, and the bonds within each muscle cell which were formed when death occurred become stable. The muscle does not contract any more; it just stiffens. But since stiffening requires contraction in life, it's called contraction in death.
As a parallel, touch your fist to your shoulder. Without resistance, there is some contraction there. Now keep it there while someone tries to move it; that requires much more forceful contraction, but the position of your arm doesn't change (remember, you're keeping your fist to your shoulder.) All this is thanks to the number and stability of those tiny bonds between actin and myosin. Those tiny bonds develop and stabilize in death. But they don't last forever, hence rigor reverses.
Rigor mortis has been studied extensively for an astonishing number of reasons including forensic studies and how it affects the meat we eat.
I have seen a lot of death; one of my duties was to "pronounce" people dead. Sometimes when someone died during the night in a nursing home, a nurse would wait until morning to call - what difference did it make, anyway? - and I saw bodies in rigor. They were not all drawn up as in a fetal position. The nurses would usually straighten the patients out before rigor set in to make it more dignified and easier to transport the patient. If rigor caused movement, they wouldn't be straightened yet stiff  (rigor is something one needs to document, as is lividity.)
Rigor Mortis

Excellent answer! I realise that you're writing from experience and know what you're talking about, but might you have a source for this? I had indeed seen the word "contraction" been used in a rigor mortis context but it was not clear the word had another meaning. I'm really curious, could bloating change the position if it were originally flexed? This bloated pig does not look in a normal position: https://bugwitch.files.wordpress.com/2013/05/img_4276.jpg

@TheThunderChimp - The Link explains it better than I did. Once rigor passes, many things can change the position the body is in, such as gas, etc.; for example, drowning victims are usually face down bottom up in the water, whereas scuba divers are found face up, bottom down.

But if someone died in foetal position in a locked, clean room at normal temperature, would the remains still be in foetal position 1 month (or 100 years) later?

@TheThunderChimp - Yep. Absolutely.

Thanks @anongoodnurse. If you had a source to the effect that bloating does not change position I'd be delighted

@TheThunderChimp - I'm sorry, I don't have such a source. Bloating isn't something I see very often in humans, thank goodness.

This timelapse video here suggests the limbs move outwards during bloating if the individual is on its back (warning graphic stuff): https://www.liveleak.com/view?i=5bd_1306689849


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Question on Viruses

A recent study has provided evidence that two types of equine (horse) herpes viruses have an unusually broad host range. This fact supports which of the following statements?
a. The lytic cylce occurs in horses while the lysogenic cycle occurs only in other species.
b. The virus is transmitted from one host to another by mosquitoes.
c. In a population of horses, many of the individuals will become infected
d. Horses, rhinoceroses, and polar bear can become infected
e. In an individual horse, many different type of cells will be infected

According to the answer key, the answer is D. My question is why isn't E also a correct answer? I thought host range means "the range of cells that can act as a host to a virus".

A host is an organism, not a cell of an organism.

Welcome to Biology.SE. Please do not just upload images but make the effort to rewrite the text. Images are not searchable and is a trouble for people with visual impair. Also, your title is not helpful. Of course the post will contain a question, so it is useless to use the word question in the title. Try to be more specific.

You must provide text for questions otherwise they will be removed as they cannot be indexed properly. A scan is not acceptable.

I think this is a good question because it highlights a critical pitfall in any field of science: making broad assumptions with too little or poor data. It also in part highlights poor test questions/mentoring that lead people into these pitfalls. See in my comments on Yordan's answer.

"host" refers to the organism as a whole. So two types of equine herpes viruses have an unusually broad host range means here that these two viruses have the particular ability to infect various animals, and not only horses.

And yet that statement still doesn't support any of the possible answers. Is that a fussy assumption?

@CMosychuk My guess is that the question is badely put. It should have been more like 'Based on this fact, which of the following statements can be considered as true?'. Then d. is the correct answer because the fact that these viruses have a broad host range is enough to explain why polar bear and rhinos can also be infected. However, it is kind of a circular reasoning.

The correct answer is D and there is nothing wrong with the question. @user34748, the very definition of host range is the range of species a virus can infect, not cell types. See the Wikipedia definition of host as used in biology: In biology, a host is an organism that harbors a parasitic, a mutual, or a commensal symbiont, typically providing nourishment and shelter.  This is why the answer is D, not E. If the question specified host cell types, then E would have been the correct answer.
The problem is that you are supposed to know the definition before you go to exam and host has very clear definition in parasitology in general as the organism the infectious  organism infects, not its cell types! In fact if the answer was to be E the very structure of the question had to be changed to include a special close specifying it is host cell types, not the hosts themselves the question is about. And this is clearly not the case here. This is why the answer is D, not E. Even from a testological point of view there is nothing wrong with the question. The methodology used to compose it is within the limits of what you are expected to know and the reasoning you are expected to be able to use. It's legitimate virology question.

As I understand it, the correct answer is that multiple species (polar bear, rhino, horse) can get infected because these viruses have a broad host range. But I guess that the very definition of having a broad host range is being able to infect various hosts. So, in the end the reason why d. is correct is that d. is correct...

No, the reason why D is correct is because you definition you should have known before entering this exam is " In biology, a host is an organism that harbors a parasitic, a mutual, or a commensal symbiont, typically providing nourishment and shelter." If you knew this definition, you should not have had any problems choosing D as answer. See definitions are important in biology, if you don't pay enough attention to them you can easily make mistakes later on in both interpreting and even noticing important tendencies in your data. You should have paid attention to the definition of host!

Basically the entire question revolves around knowing or not what the definition of host is in virology. If you have considered that host is always an organism and not just a single cell you would never had failed the question and ask it here. I advise you the next time you go take a test-learn your definitions better. Hope you make good lesson out of this experience.

Well, I did not fail the question, because I did not take the exam. I'm not the OP, I'm just confused by the way the question is asked. And for that matter, I am well aware that definitions are important in biology, as in every other field of science.

On Northwestern University's website in states that the definition of a host range is, "The range of cells that can act as a host to a virus or bacteriophage." So according to what you are saying, this definition is wrong? http://groups.molbiosci.northwestern.edu/holmgren/Glossary/Definitions/Def-H/host_range.html

I'm very sorry @Flo for taking you for the OP instead of the editor, I just didn't see it. Sorry again. Now I looked at the link you provided and this is what is says: 1. The spectrum of strains of bacterial species that a given strain of phage can infect.
2. The range of cells that can act as a host to a virus or bacteriophage.

It isn't "wrong" per se, but just more specific. It is designed specially for bacteriophages, not for host range in general. In the case of bacteriophages the cell is the organism, so one doesn't need to add anything more specific to understand any difference between a cell and an organism. In this case there is no need to specify any cell types. However, the OP's question has a possible answer specifying cell types, therefore, the lecturer should haven't ever used such definition for his/hers course or otherwise this questions would indeed have been wrong to ask.

Then my arguments is: Did the lecturer in the OP's course used the definition you provided or did s/he used the broad definition of a host in parasitology? If s/he indeed used the definition you provided the question was indeed wrong to ask. However, if s/he didn't used this definition, but one similar to the broad parasitological definition, then it's the OP's fault to have failed the question. Do you know what definition the lecturer of the class used or even what was the class about?

Without explicitly demonstrating the virus in a polar bear or rhinoceros, how would the statement "a virus has more than one host species" lead you to assume a polar bear or a rhinoceros can be infected? Why not bobcats or barn owls? That requires more data than this question provides, and here's the actual paper being referenced (1, 2). You can see how they can make that assumption, QED.

@CMosychuk , still the OP should have known the definition of a virus in parasitology and should have thought out the question carefully. If s/he drew on the information provided in the question and what s/he was supposed to know is a host range, s/he wouldn't have made the mistake. There is enough information provided in the question to come to the right answer.


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Reproduction number of a SIR model with mortality
We know that reproduction number $\mathcal{R}_0$ is $\frac{\alpha}{\beta}$ for the following system, such that if $\mathcal{R}_0>1$, there is an epidemic in the population.

Now, assume the system below with mortality rate of $\delta$:

I'm wondering which one of options below represents ${R}_0$?

${R}_0 = \frac{\alpha}{\beta + \delta}$
${R}_0 = \frac{\alpha}{\beta \delta}$
${R}_0 = \frac{\alpha}{\beta}+\frac{\alpha}{\delta}$

Could you mark the right option with its justification?
Thanks

The only answer that makes numerical sense is 1. The product of two rates beta and delta (recovery * death) doesn't mean anything in SIR. And in answer three you're doubling the rate of infection (alpha). Looking at the other way, for R_0 it doesn't matter how people leave the Infected class, once you're either dead or recovered you no longer are transmitting the disease. Therefore you can say that some value Zeta is the exit from Infected class and Zeta would be the sum of all rates which remove a person from being Infectious

Granted, I haven't worked with SIR-models, but to me the answer is definitely nr. 1.
Fundamentally, $R_0$ is defined as the number of secondary infections from a single individual in an uninfected population. It is sometimes described as:
$ R_0 = \gamma *c * d $,
where $\gamma$ is the probability of transmitting the disease, $c$ is the average contact rate (encounter rate with other individuals), and $d$ the average length being infectious (which is $1/\beta$, there $\beta$ is the recovery rate). In your expression above $\alpha = \gamma*c$.
In this simple model of $R_0$ adding a mortality rate basically equates to adding another way of being removed from being infectious (you can either recover or die). Therefore, the expected time being infectious (previously $1/\beta$) is now the sum of two rates, $1/(\beta + \delta)$, where $\delta$ is the death rate (multiplying the two rates would be similar to estimating the probability that someone both recovers and dies from the infection). This means that $R_0$ with a death rate is:
$$ R_0 = \frac {\gamma c}{\beta+\delta} = \frac {\alpha}{\beta+\delta}$$
However, there are also more complicated (and realistic) ways of modelling situations with a death rate.
(I began my answer before @Artems nice answer, which is why I'm posting this as a complementary answer.)


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Why do I still see a bright light after looking directly at it?
When you look directly at a bright light, maybe accidentally when looking at the sun, the shape of the image may persistently be perceived even after you look away.
Does this image persistence have something to do with the light hitting the back of the eye and leaving an imprint, or is something else going on?

What do you know about the retina and sight? If you know, share. If you can, try to find an answer and share that, too. That way, we don't have to explain from the ground up, which would take a very long answer.

@anongoodnurse oh ok

@anongoodnurse - you're totally right but I couldn't help myself answering O.o

@AliceD - I know; this is one of your areas of expertise. ;) And an optical example, too!

@anongoodnurse - biased to the bone

Short answer
The effect you describe is called a negative after image. It can be explained by adaptation effects of the photoreceptors in the eye.
Background

source: Dresden University
Steadily fixate on the black lightbulb for thirty seconds or more and then immediately turn your gaze to the white region on the right. The illusionary glowing white bulb you perceive after fixating on the black picture is called an afterimage.
When the eyes and hence the photosensitive layer therein, the retina, is focused on an image, light-sensitive photoreceptors in the retina respond to the incoming light. In turn, secondary neurons carry the information to the brain via the optic nerve. When photoreceptors are continuously activated, they become desensitized (or fatigued); it is said they adapt to the stimulus (Kalloniatis & Luu, 2012).
Adaptation occurs at multiple stages in the visual system. One of the important processes behind visual adaptation in this example is photopigment "bleaching" due to constant stimulation. The desensitization is strongest  for cells viewing bright stimuli and is caused by the photopigments in the photoreceptors being all used up after continuous activation.
Back to the light bulb illusion above: photobleaching is strongest for cells that were activated by the bright parts of the image, but weaker for cells viewing the darkest part of the figure. Then, when you avert the focus onto the white screen, the least depleted cells (the ones not adapted) will respond strongly, while the adapted cells will be unresponsive. hence, the retina focused on the black light bulb will respond vigurously, while the more peripheral parts of the retina that received the white part of the image surrounding the bulb will be silent. Hence, a glowing light bulb will be perceived in the after image.
This particular phenomenon is called a negative afterimage, in which bright areas of the figure turn dark and vice versa. This will happen when looking for prolonged periods of time to a certain image (this answer), or when looking directly in very bright sources like the sun (as in the question). Positive afterimages also exist, but do not apply to this specific question.
Reference
- Kalloniatis & Luu, Light and Dark Adaptation. In: Webvision (2012). Utah University

It's also worth knowing that photoreceptors are technically activated by darkness, from a physiological point of view. Light hyperpolarises the photoreceptor, which reduces neurotransmitter release.
Fatigue and photobleaching still occur, but it's the time taken to restore neurotransmitter release that leads to the afterimage.

Interesting notes, but could you add sources?

The original article's a bit old: 1979, here's a more up to date review.


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Oxygen supply in a trickling filter
I'm using a 300l/h trickling filter consisting of 4 round chambers in vertical alignment with 11cm diameter, 5cm height and 5cm distance for the trickling (100 to 500 holes per level) in a 15cm pipe. The top is open in order to allow air exchange. 2 chambers are filled with 2 to 4mm gravel, one with filter cotton and one with clay pipes. It is used for nitrification of aquarium water.
The filter is loud and I want to muffle it. I already figured out that laying 2 levels of microfiber towel on top of it helps. I also have the option to build a wooden enclosure.
What measures should I take in order to reduce the available oxygen for the nitrifying bacteria as few as possible? Could the exchange through the towels be sufficient? Should I use a special membrane in the enclosure? Does it make sense to connect an aquarium air pump to the inside of the filter?


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How do genes code for differences in arms and legs?
So to me it seems like arms and legs are pretty similar that they almost have the same blueprint. And if you change part of it like the number of digits, you will have 12 fingers and 12 toes.
But at the same time there are differences.
So my question is, are arms and legs encoded with the same piece of DNA? Or two very similar pieces. But in that case why would a change in the arm blueprint to give you 12 fingers also give you 12 toes?
On the other hand if arms and legs are encoded by the same piece of DNA. How do legs develop heals and arms develop wrists?
Are arms and legs only different by their shape (morphology?).
Equally if a thumb is encoded by the same DNA as encodes fingers, (i.e. all are similar and have fingernails), why are thumbs different?

Welcome to Biology.SE. You might want to have a look at wikipedia HOX genes for a start.

I think that you might be interested in searching this: "Epigenetic mechanisms in fetal development"

it also helps if you don't think of DNA as a blueprint it is more like a recipe. there is no code for number of fingers there is a process that produces 5 fingers. you might want to do some background research on the wiki for limb development to get started. Then you should look up something called HOX genes. https://en.wikipedia.org/wiki/Limb_development

I think those other resources might be a bit too advanced. The simple way to consider genes is that they each have a thing that they do but that's only a tiny fraction (~2%) of our genome. Large amounts of the rest of the DNA controls /how/ those genes are expressed. So as our cells develop they go through a kind of dance. The DNA tells each cell how to prepare for the next move of the dance and depending on the cells environment (and other cells) the next moves of the dance can change. So many of the same genes used in making Arms are used for Legs, but it's a different way the cells dance.

So is the DNA a bit like this: [both][both][both][only-arm][both][both][only-arm][both][both][only-leg]. And the a protein(s) in the limb (arm) or (leg) tells which bit of DNA to activate? I guess that would make sense. I guess an [only-hand] bit of DNA could create a new protein (hand) and so on. Although maybe thats too complicated as hands and feet are very similar.


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Structure of an Ecosystem

Changes in WHICH of the following factors will result in a change of an ecosystem's structure and composition?

A: nutrient availability
B: temperature
C: number of trees
D: light intensity

I got this question from an online "fun" quiz.
I understand that nutrient availability would affect the carrying capacity of an ecosystem. Temperature, if there was a big shift, could cause a change because some organisms would thrive and others would not. Light intensity affects the autotroph population.
But why would the number of trees not change it? I would think that if the number of trees changes, then the structure of the ecosystem would also have changed.

Yeah, I thought about it some more. The number of trees is not a factor, it IS part of the structure that might change if one or more factors is changed.

Well IMO, that's a bad question coming from your online quizz! As you said, C is not so much a causal agent than a change in itself. All the other agents are likely to affect the ecosystem by its structure and composition (whatever the definitions of structure and composition in this context).

Structure of an ecosystem deals mainly with species decomposition (Ref: On the Origin of Ecological Structure: https://web.stanford.edu/~fukamit/stokstad-2009.pdf). But I remember from one of old lectures, that species structure includes vertical stratification also (have no reference for it).

Maybe the assumption is that if you remove some trees they will just grow back to whatever they were before due to factors like nutrient availability and temperature that dictate the ecosystem's composition, but that is ignoring that trees do have causal influence on ecosystem structure in addition to being part of it. Depending on the environment the trees may be part of a positive feedback loop that maintains certain conditions, and once you get rid of them those conditions will change.

I'd vote for E: all of the above.


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Cows milk protein transferability through breast milk
I understand that cow's milk protein(casein) transfers through breast milk via the mother's diet.
I'm looking for the process as in what hormone does it bind to to allow this process in some women and not others?

Can you please show some of the research you have put into this question?


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Why is thrombin time (TT) normal range longer than prothrombin time (PT)?
Reference range for the TT is longer than that of the PT.

This is a great question.
I'm going to hypothesize here because I haven't had a chance to test my theory and I'm afraid that by the time I get around to it, I may forget about this question.
The real question is, what is the variable that makes the thrombin time act differently than what you would assume? I’d wager the answer is temperature.
Protimes are performed at 37 degrees in order to simulate the in vivo environment, but also because most coagulation factors aren't active at room temp, or at least they are very slow-acting at room temp. Heating the environment speeds this process up so the test doesn't take all day.
Now, we know if you take a tube of warm normal plasma and add calcium and thrombin to it, it clots right away, right? But this is a problem because the thrombin time is a quantitative assay and we need it to be sensitive, especially for those super old-school clinicians who use it to monitor heparin instead of a more modern test like the APTT or Xa inhibition. We need to be able to tell the difference between a patient that’s gotten a bolus of heparin and a direct thrombin inhibitor. So, if you remove the heat, you slow down the conversion of fibrinogen to fibrin, and in the process you stretch the calibration curve, effectively increasing the sensitivity of the test. But this also has the effect of slowing down the conversion to where it takes 14–18 seconds rather than one or two.
If you change your test setup to have the thrombin reagent heated, my hunch is that your analyzer will give an error because the sample will have clotted by the time the analyzer reaches minimum threshold time. Or better yet, try this experiment on a fibrometer. I don’t have access to one so I can’t try it out as I’d like to.
I’d be interested in discussing this with any other experts out there, especially those that have played around in the coag lab. I may have occasion to test this out in the coming weeks; I’ll try to do it and update my answer with my results.


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About the formation of protein
There is a question in my textbook which asks: "What does the glucose produced from photosynthesis form?" However one of the answers said that glucose forms protein.  But I'm quite sure that amino acids form protein, don't they?  I would be grateful if anyone out there could help me out.

What research have you done before asking it here? Hint: glucose is an energy source.

I only know that excess protein can be converted into glucose in our body for energy, but i dont know how glucose can be converted into protein :(

Who asked converting glucose into protein? Also, it is possible to convert gluocse to amino acids.

Can you be more specific about "one of the answer" ? Was this a multiple-choice thing ? What was the exact sentence involved ?

Photosynthesis results into formation of a carbon skeleton (a 3C or 6C skeleton). These newly formed carbon skeleton can be used to form a large number of bio-molecules which are required by a cell. For example the glucose can enter into aerobic respiration and the intermediates thus formed are used for synthesis of several molecules.

As you can specifically see from the above figure, alpha ketoglutarate is converted into glutamate which is then used for synthesis of proteins.
Alpha ketoglutarate is a keto acid can easily be aminated to give rise to amino acid.

Good answer. The often taught idea that photosynthesis produces glucose is an oversimplification. It would be better to think of it as a process of carbon fixation. The resulting organic molecules can be used to synthesize the precursors of macromolecules (nucleic acids, fatty acids, amino acids and carbohydrates).

In addition, it is not necessary that glucose will be synthesized and then it will be used for respiration. The triose (3C carbohydrate) can directly enter into glycolytic pathway.


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Is Fluoride really that good for tooth enamel?
Recently, I started to pay more attention to my teeth because of the high number of tooth decays, and I'm trying to understand different concepts and biological functions of the teeth and bone. By searching around, I have found that enamel is the strongest bio-material in our body and that it is the main player in tooth decay. So I started searching for methods to restore the enamel, and I can see that most of the dentists recommend using Fluoride-based toothpaste. At the same time, the literature tells us that Fluoride is quite toxic. So I looked for healthy options available for end-users, and the organic toothpaste that I found are all without Flouride.
Now my questions are:

Should I go for an organic Toothpaste without Flouride or a non-organic with Flouride for restoring the enamel?
Is Flouride really the only enamel restorer?
Can it be replaced with something else for the restoration?

I'm a mechanical engineer and I can understand technical language, therefore any type of technical explanation would be great (even with chemical reactions)

"At the same time, the literature tells us that Fluoride is quite toxic." Does it tell you the doses it's toxic at ? How much toothpaste are you planning on eating ?

Here is a reference where you might find some information. And here another one dealing with an in vitro comparison of the effect of organic and inorganic fluoride on enamel.

this paper answers your second and third question :http://www.jisppd.com/article.asp?issn=0970-4388;year=2012;volume=30;issue=1;spage=2;epage=6;aulast=Goswami

Getting fluoride in drinking water is more effective, since its concentration in water depends on the temperature , it may lead to overdose and may cause mottled teeth.

Thank you guys for the links! I will start reading it. Not sure how to interpret your last comment JM97. Edit: I'm not trying to kill myself :-) At least not yet.

This question appears to be framed in more of a "personal health question" vs asking strictly about the biology/biochemistry involved in the fluoride-enamel "strengthening"  process. As a result, I think this question will be voted to be closed as being off topic. However, even with additional edits, I'd say you'd find your answer through a quick google search.


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How can we define complexity in the context of biology?
Can somebody provide a definition of complexity in the context of biology?
Is it something of a personal opinion on the side of the user to decide precisely what s/he means by using the word complexity or is there something all biologists can agree upon? Is there any "standard" for the use of the term complexity or is such standard simply unattainable in our current level of knowledge and/or understanding of the living world?
To the moderator-I want to know What is complexity in biology?  in GENERAL, not only in the specific example of measuring it for an individual. One can argue complexity can be used to compare and even to "cast a vote" about the superiority or inferiority of many objects of study in biology, not just individual organisms. What about the complexity of an ecosystem, of a particular organ, of the interactions of macromolecules and so on. Are they not legitimate instances when the term complexity can be used without inferring to its meaning? This is the purpose of my question, not to merely measure the complexity of an individual. This is why I don't think it's duplicate of the question you mentioned. How is my reply?

Totally subjective. Just like saying in a paper that X was very Y (Y being big, small, long, complex etc)

So, there isn't anything like some biological "standard" for complexity. Is it what you're saying?

Biology is a broad subject. You probably need to be more specific for useful answers. What subjects of biology are you interested in? In loose terms, relative complexity is often used (something is more complex than something else), but clear definitions (where there are any) are likely to be sub-field dependent.

Biology is a rabbit hole that only gets deeper. Real complexity is falling further than anyone else ever has and trying to see an end in sight. You can also construe this as insanity, but to each their own.

@RozennKeribin To me, this question seems broader, so I don't think it is a duplicate (it might be too broad though).

As I mentioned above, I think you need to narrow down the answer set. Otherwise the question is too broad/vague. Complexity is just a word, and it is used differently in different areas of biology. Therefore, there doesn't exist a single definition, and a question such as "What is complexity in biology?" is too broad to be covered in the SE-format.

I think complexity is not always subjective; rather it is quite similar to quantitative variables. Say a plastic-comb is more complicated than a plastic rod. Or an asymmetric irregular shape is more complicated than an ellipse and an ellipse  is more complicated than a circle. Or the arithmetic procedure (or steps) procedure to find square root of a number, is much more complicated than the arithmetic procedure (or steps) to find sum of 2 numbers. Though it is not so easy to define and formulate; different  possible values of complexity exists.

IMO this question should be moved to mathematics.se with an edit suggestion "could we define and measure complexity of a system?" (instead of only biological system). Probably there would have the expertise to measure things like "probability", "importance", "advantage" etc. that could not be measured directly with a scale or an weight box etc.

This is known as complexity in biology.

I don't think this question is a duplicate, but the answer seems trivial: there isn't a single definition of complexity.

I think marking this as a duplicate is the best solution - although the question here is more broad than the question there, I think the accepted answer to that question is 100% applicable to this one, and I don't think it is possible to come up with a better answer. That answer makes clear why having a definition for complexity is important, explains how the answers you get will completely depend on that definition, and gives some examples for the OP to consider when possibly reformulating the question.

I had to once again edit the question to satisfy you. Are you going to accept it now?

Oh, come on, what would it take you to accept a good question about complexity in biology?


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Problem with an analogy (Cell Membrane)
I'm studying biology for the first time seriously. I've been reading OpenStax College's material.
In the section of "The Cell Membrane", I have the following problem:
Choose the answer that best completes the following analogy: Diffusion is to ________ as endocytosis is to ________.

filtration; phagocytosis
osmosis; pinocytosis
solutes; fluid
gradient; chemical energy

I chose number 1, but the site says the correct answer is number 2. Could someone please explain why?

[EDIT]
I chose number 1, because diffusion and filtration were passive ways to transport, while endocytosis and phagocytosis are active. I didn't not take in to account that 2. fitted better, because the osmosis part was confusing me.

I'm not sure why this question has 5 upvotes. This is a homework question with no attempt at working out an answer.

@James, sorry I thought of writing something else, but since this was an analogy I didn't know what else to put. Is it necessary to delete this?

Why was the answer to this question moved to the comments?

@AnaGalois It sounds like your question is actually about osmosis rather than anything else. If you are confused about osmosis, then ask a question specifically about whatever is confusing you about osmosis. This sort of MCQ format isn't a good for SE. See this meta discussion.

Osmosis is the diffusion of water.  Pinocytosis is the endocytosis of liquid/water.

While your answer is undoubtedly the one the question is looking for, osmosis is not the simple diffusion of water.


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Oxygen Uptake Rates in Microbial Cultures
Normally if air is sparged into a fermenter, the oxygen uptake rate is roughly equivalent to the oxygen transfer rate:
KLa(C* - CL) = Xμ/YX/O2.
How would this equation change if the oxygen became limiting (DO < 0.3 mg-O2/L)?

If you share with us your background research, it would be useful to the community, and also help us understand your question

I know under steady state conditions (ie when oxygen transfer is limiting) the OUR = OTR - this i know from background research. But if the dissolved oxygen drops below the critical dissolved oxygen concentration wouldn't that change the above expression?

Also, please explain the equation; explain what the symbols denote (what are the constants/variables).


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Cells of umbilical cord - mom's or son's?
Let's say we have a mother giving a birth to a son. In a very clear manner the cells of these two individuals are very different, of course. Yet there is an umbilical cord connecting them. Then there should be a clearly defined "border" somewhere on its way where the mother's cells meet the cells of her son, is that so? How is it even possible?! ;)

Cells of umbilical cord - mom's or son's?

Answer: Son's.
The interface you are looking for is in the placenta. https://en.wikipedia.org/wiki/Placenta
Formally the fetal side of the placenta is called the Chorion frondosum, which develops from the outer cells of blastocyst (trophoblast), and the maternal side of the placenta, Decidua basalis, which develops from the maternal uterine tissue.

How is it even possible?

Immune tolerance in pregnancy or gestational/maternal immune tolerance
The placenta functions as an immunological barrier between the mother and the fetus, creating an immunologically privileged site. For this purpose, it uses several mechanisms

It secretes Neurokinin B containing phosphocholine molecules. This
is the same mechanism used by parasitic nematodes to avoid detection
by the immune system of their host.
Also, there is the presence of small lymphocytic suppressor cells in the
fetus that inhibit maternal cytotoxic T cells by inhibiting the
response to interleukin 2.
The placental trophoblast cells do not express the classical MHC
class I isotypes HLA-A and HLA-B, unlike most other cells in the
body, and this absence is assumed to prevent destruction by maternal
cytotoxic T cells, which otherwise would recognize the fetal HLA-A
and HLA-B molecules as foreign. On the other hand, they do express
the atypical MHC class I isotypes HLA-E and HLA-G, which is assumed
to prevent destruction by maternal NK cells, which otherwise destroy
cells that do not express any MHC class I. However, trophoblast
cells do express the rather typical HLA-C.
It forms a syncytium without any extracellular spaces between cells
in order to limit the exchange of migratory immune cells between the
developing embryo and the body of the mother (something an
epithelium will not do sufficiently, as certain blood cells are
specialized to be able to insert themselves between adjacent
epithelial cells). The fusion of the cells is apparently caused by
viral fusion proteins from endosymbiotic endogenous retrovirus
(ERV). An immunoevasive action was the initial normal behavior of
the viral protein, in order to avail for the virus to spread to
other cells by simply merging them with the infected one. It is
believed that the ancestors of modern viviparous mammals evolved
after an infection by this virus, enabling the fetus to better
resist the immune system of the mother.

Other mechanisms include exposure to immune modulating factors present in seminal fluid from vaginal and oral sex. https://en.wikipedia.org/wiki/Pre-eclampsia#paternal_tolerance

just to add the placenta evolved from the yolk of the ancestral eggs, It makes it a bit easier to see how the structure could evolve.


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Can an octopus survive if one of its three hearts stops working?
While reading the book "The Soul of an Octopus" by Sy Montgomery, I learnt that Octopuses have three hearts. This is very fascinating. According to a Wikipedia article,  two of the three are used to  pump blood through each of the two gills while the third pumps blood through the body.
So, my question is can an Octopus survive if one of these hearts stops functioning?

This is not he definitive answer, but a comparison. Your own heart has two sides, one to pump blood to the lungs (for oxygen exchange, much like the function of gills), one to pump blood to the rest of the body. If one side of your heart stopped working, do you think you would survive? The question is whether an octopus can survive on one gill alone. In either case, it's survival would be severely compromised if at all possible.

I thought many people live with partially functioning hearts. Is that not true?

Not in the way I described. A poorly functioning heart still sends blood to both the lungs and the body but does each less well. There is right and left sided heart failure, but it's a relative failure, not full failure. Full failure of either side = death.

The Wikipedia entry you linked and the other answer both state that...

... the systemic heart is inactive while the animal is swimming and thus it tires quickly and prefers to crawl.

I tried to find an accurate source corroborating this (by accurate I mean a paper in a peer-reviewed journal or a zoology book), but I couldn't. The best source (scientifically speaking) I found was this page from the Smithsonian Institute, which says:

Octopuses have three hearts. Two of the hearts work exclusively to move blood beyond the animal’s gills, while the third keeps circulation flowing for the organs. The organ heart actually stops beating when the octopus swims, explaining the species’ penchant for crawling rather than swimming, which exhausts them.

A much more reputable source is Octopus: Physiology and Behaviour of an Advanced Invertebrate. It says:

If an octopus is surprised by a sudden movement on the part of an observer, or a thump on the side of its tank, the systemic hear may miss one or more beats.

Which is, evidently, way less dramatic than having one of the three hearts stopping.
The same author says, talking about Octopus vulgaris:

Together with changes due to exercise and arrests attributable to sudden tensing of the body musculature, any prolonged recording reveals apparently spontaneous changes in amplitude that are not obviously correlated with anything that the animal can be seen to be doing. From time to time the heart stops for several seconds (as it does, for longer periods, in O. dofleini).

Thus, apparently, the maximum we have here is periods longer than several seconds (which the book, unfortunately, doesn't determine more precisely).
In conclusion, despite their circulatory system being very complex and the systemic heart being able to stop beating for several seconds (or during the whole time of swimming, as the Smithsonian says), it doesn't seem possible that octopuses can survive if one of their hearts stops (forever). Have in mind that the hearts are not redundant, that is, one heart cannot perform the function of the other (if that other one stops).
Source: Wells, M. (2013). Octopus. 1st ed. [Place of publication not identified]: Springer.

I heard that when some octopuses swim, their third heart (which pumps blood through the body) stops, which is why they tend to crawl.
I only heard it, though, and I haven't verified.

Welcome to Biology SE. Your answer is correct. However, it's a good practice here to quote reputable sources. This is a book called "Octopus: Physiology and Behaviour of an Advanced Invertebrate". Please, have a look at the chapter I'm linking, copy some quotes to your answer and cite the book as reference: https://books.google.com.au/books?id=AM_tCAAAQBAJ&pg=PA37&lpg=PA37&dq=octopus+systemic+heart+inactive&source=bl&ots=jKYBJeDjWD&sig=Zzdf8khH1AJRgNI9yTStGX8eqWw&hl=en&sa=X&ved=0ahUKEwiGmeGh3pbUAhUGmZQKHT6IDTwQ6AEIMDAC#v=onepage&q=octopus%20systemic%20heart%20inactive&f=false

Well, since you didn't edit your answer, I provided mine.


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What is Genome Folding?
Why does genome folding have such great interest?
For protein folding I could say that's important because protein's functionality closely depends on its folded state, since it affects its mechanical properties etc.
But genome? What does it even mean to be folded? Where does it happen? Any reference to papers would be appreciated.

probably supercoiling see: https://www.ncbi.nlm.nih.gov/books/NBK6243/. supercoiling is important to regulate transcription. Offcourse protein folding is important but to produce protein we need RNA and to produce RNA we need transcription. By tightly wouding DNA around proteins "we" can prevent RNA polymerase from transcribing the DNA and thereby silencing genes

They are not talking about supercoiling, at least solely. You said that protein function depends on its 3D structure. Well, the function of DNA  often depends on its spatial organization as well. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4792841/

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What happens to the enzymes produced by the digestive system?
Our digestive system produces a lot of enzymes and they help to catabolize the food, and after completing their work are they excreted out or as they are also made up of proteins are they catabolized and assimilated back?

Yes,Enzymes too get degraded and catabolised, if not then we would be wasting a lot of proteins.

@JM97 ,Which enzymes help in degrading the other enzymes?

Proteases, being themselves proteins, are cleaved by other protease molecules, sometimes of the same variety.

The answer is autodigestion fascilitated by denaturation of the digestive enzymes.
EVIDENCES OF AUTODIGESTION OF THE DIGESTIVE ENZYMES
1.The concentration of digestive enzymes is found to decrease from the small intestinal ileum to the large intestine.

There is a general trend to a decrease in the enzyme concentration the furthur down in the intestine the samples have been collected inspite of a concentration of the intestinal content in the same direction (see Figure1).This fact must indicate that the enzymes are partly inactivated or autodigested in the lumen of the small intestine.[pg 1529].

2.Essential amino acids have been found in the small intestinal lumen even if the food ingested didnot contain them which suggests that their source was the hydrolysed digestive enzymes which would eventually be re-absorbed in the small intestine to prevent their loss from the body.

Amino acids from dietary digestion are not alone, because the ingestion of food-even non-nitrogenous food-stimulates the digestive tract to secrete endogenous protein, derived from the sloughing of intestinal cells and used up digestive enzymes. These recycled proteins are a rich source of essential amino acids.Studies by Nasset show that regardless of the amino acid mix of the meal, the intestinal tract maintains a remarkably similar ratio of essential amino acids.[source]


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Does self replicating RNA occur in nature?
Do self replicating, independent RNA strands occur in nature? They are often used in laboratory experiments but I have not heard of any wild populations. I mean independent of other organisms and able to reproduce on their own in the environment. I.e., not just viruses or transcription RNA.

I believe what you are looking for is Autotrophic self-replication, and no one has not been discovered, but that makes a lot of sense since the source molecules such a replicator would use are valuable biological molecules quickly gobbled up by bacteria. Prior to the evolution of these bacteria however that would not have been an issue. And as Rodrgo mention the replicator itself would be helpless food for any bacteria. This is why laboratory studies are so important since the can be done in the absence of bacteria.

They probably existed in the beginning of life (on Earth or somewhere else). But any free RNA now would be almost immediately devoured by bacteria or other organisms.
Bacteria are ubiquitous. That's one of the first things you learn in a microbiology course. We do this experiment a few times: open up a Petri dish far from a Bunsen burner, and in a few days you can see how many bacteria and/or fungus colonies have grown in the Agar. Any good microbiology book will show you this. I have none right now with me, but have just found a few links by  searching for "bacteria are ubiquitous" on Google: Understanding Bacteria, The Purple Phototrophic Bacteria, Bacteria in Agrobiology: Plant Probiotics and Public Health and Infectious Diseases.
As for the science studying the origin of life, I recommend The Fifth Miracle: The Search for the Origin and Meaning of Life, by Paul Davies.

While the answer might well be correct, it would be important to have a reference to backup your claim. Also, you should probably address the question of viroids as it is, IMO, unclear from the OP's question whether viroids would be an accepted answer.

@Remi.b References added. IMO, "independent RNA" excludes parasites.

Kind of; they're called viroids. If you mean RNA that also catalyzes it's own replication independent of environment then I'm not aware of any that exist in nature But one could make the argument that all 'life' is simply self-replicating ribosomal RNA which exploits proteins to do other functions and DNA to store it's information more stably.
It's a bit arbitrary to exclude other cells as an environment though.

Including the term "able to reproduce on their own in the environment" rules out viroids and all other parasites.

Their environment is by definition in and around cells, it's an artificial distinction.

"independent RNA" excludes parasites.

I also thought of viroids at first. The question of the OP is a little vague in the sense that it does not really allow us to know whether viroid would fit the category. I would rather disagree that "independent" means "not parasitic" and I would disagree to not consider another cell as not being ones "own environment". +1


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Why does the scalp hair become grey first?
I understand that when the hair follicles produce less melanin or stop producing melanin altogether, hair becomes grey. But it seems like it is the scalp hair that becomes grey first. If follicles are producing less and less melanin, shouldn't the hair everywhere become gradually grey? Why is it that the scalp hair greys first?

Did you do any searching for an answer? What did you find? Please share, as per our guidelines on showing your research. Thanks.

I didn't do much research for an answer. Prior to posting the question, all I read was an article (https://medlineplus.gov/ency/article/004005.htm) that didn't explain it other than saying that it is usually the scalp hair that becomes grey first. Will research more. Should have researched more.  Thanks.

The answer is right in the article: "Graying is largely determined by your genes." Scalp hair is genetically programmed to go grey first if a person's hair will go grey.

What do you mean "scalp hair"? The hair on top of the head? As far as I know, it's the temple hair (above the ears) that usually go gray first. But in different people the exact place may differ, I've seen right above the forehead, as I've seen the beard too.

From my own observation, it's usually the chin & jaw that goes gray first, not the scalp.

@anongoodnurse "Determined by your genes" doesn't come anywhere close to providing an answer about a mechanism. Presumably the "genes" are the same in all parts of the skin.

@BryanKrause - why would you think that regulation of hair on the scalp and hair on the mons pubis are exactly alike? Skin cells have the same genes; some skin is thick, some is thin (and it's not solely due to use.)

@anongoodnurse I don't think all hairs are identical, just that all of the cells have the same genes - that isn't the same as expression. Saying "it is because of different expression of gene XYZ" is a good mechanism answer. Saying something "is determined by your genes" suggests you are talking about differences between individuals, which is not what the question is about.

@BryanKrause - A kinda fine line which I accept. Thanks.


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Have evolutionary biologists ever done anything like this?

Pick a protein that you claim evolved.
List the mutations that you claim happened during the evolution of the protein.
Pick one of these mutations.
Prove that it could happen in nature and produce a viable organism.

This seems like a way to test evolution.

Try looking at the long term E coli experiment, they have even show predictable and more importantly experimentally repeatable evolution. http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0014184

incorrect they showed evolution quite clearly. I also reccomend the research on evolution in response to changes in the  the thermal environment http://myxo.css.msu.edu/PublicationSearchResults.php?group=ve or the ones on antibiotic resistance http://myxo.css.msu.edu/PublicationSearchResults.php?group=ar

No they showed a change in protein expression quite clearly, if you are looking for a change in the protein structure I suggest the work on nylonase. https://www.ncbi.nlm.nih.gov/pubmed/17512009 including it induced occurrence in a different bacterium, https://www.ncbi.nlm.nih.gov/pubmed/7646041

If you think the sudden emergence of a new protein from nothing is predicted by evolution you don't understand evolution, nylonase is a different protein sequence with different structure and function, produced through a known mutation in the DNA sequence of a different protein. I honestly don't know what you are asking for at this point.

@John this "lad" obviously doesn't know anything about biology, but also doesn't want to learn (at least he doesn't show the humility typical of a real apprentice).

I have accused you of nothing. I am trying to ascertain what you are asking for. Now however that you have deleted your responses that prompted the statements shows you are only interested in an argument and not information. you have been given an example that fits your exact criteria as stated. so either change your criteria to reflect what you are actually asking for or indicate why you think it does not fulfill your criteria or we can only conclude you don't actually want an answer.

How exactly do you believe new proteins evolve? ALL proteins are changes in existing sequences.

I'm voting to close this question as off-topic because it is not a question about biology but a statement of a debating position. As usual with such trolls the final argument is completely vague.

@David AliceD and Chris, I disagree with the off-topic conclusions (and the down votes btw).  I believe this person framed a good question (although showing research would have helped) and deserves a chance for people to answer.  Saying it's "Off-topic" when clearly it's not is not a good response.

@RunzWitScissors — I think the way you can distinguish an on-topic and an off-topic troll question is to ask whether or not the poster really is asking for an answer to a biological question. In this case the answer is no. What the poster is doing is really saying "I think such and such is the key test of evolution and nobody has done it therefore …" If this were a discussion group he could/would have come straight out and said this. Because this is a Question/Answer group he is resorting to this subterfuge. He is abusing this group and we should not tolerate his behaviour.

@RunzWitScissors I have to agree with David. You should have seen all the comments he wrote and later removed. Some are still here, so you can have an idea of the situation.

Yes, actually LOTS of proteins have already been sequenced in many different organisms, and the more related phylogenetically those organisms are, the more similar the corresponding proteins. You may go to the National Center for Biotechnology Information and see for yourself. Or you can work in a lab and sequence some proteins yourself, or just ask to see how people in such labs work.
Even more, we already know some proteins evolve fast, other slowly. Even more, some parts of proteins evolve faster than other parts, and that's related with the function that each part does.
But really, do you think biological evolution still needs to be "tested"? What about Newtonian physics? What about Einsteinian physics? What about the Periodic Table of Elements? Is it because of religion that you accept most physics and chemistry of the last 150 years, but not the main biology from the same period?
So you want an example?
Here is the insulin from Pan troglodytes (common chimpanzee):
malwmrllpl lvllalwgpd pasafvnqhl cgshlvealy lvcgergffy tpktrreaed lqvgqvelgg gpgagslqpl alegslqkrg iveqcctsic slyqlenycn

Here is the insulin from Homo sapiens (humans):
malwmrllpl lallalwgpd paaafvnqhl cgshlvealy lvcgergffy tpktrreaed lqvgqvelgg gpgagslqpl alegslqkrg iveqcctsic slyqlenycn

As you can see, they're very similar, except for a few letters (each letter represents a single aminoacid).
Now let's take a more distant animal, let's say, a pig (Sus scrofa):
malwtrllpl lallalwapa paqafvnqhl cgshlvealy lvcgergffy tpkarreaen pqagavelgg glgglqalal egppqkrgiv eqcctsicsl yqlenycn

Can you see there are more differences now?
The National Center for Biotechnology Information is free for you to research any protein you like, from any organism you like. As I said, there are probably millions, maybe billions, of proteins already sequenced. You can find out which aminoacids became different in the course of evolution, but you cannot come back in time to sequence the animals that lived millions of years ago. But one thing you can do is to search Google for "evidences of evolution" or buy books about basic Evolutionary Biology. I can suggest some if you want.

What's pathetic is your desire to prove evolution wrong, certainly because of religious bias. I may assume you are following the Abrahamic god, because only their followers are so eager to disbelieve biological evolution.

Evolution could be a mythology, like any science, like any religion. The difference is that the evidences are so overwhelming, that you need to close your eyes to them, so you won't lose your faith in a single old book.

Why don't you go to study the subject you pretend to be willing to understand?

Yeah, maybe evolution is wrong. Maybe a god and a goddess together created everything in a way that we believe evolution took place. OK, I can live with that.

Evolution is obviously wrong because it doesn't work even in basic tests like this question.

You should first study biology, learn the difference between apomorphies and plesiomorphies, understand how cladistics works, see how hierarchical are the phylogenetic groupings, among other things, before coming here with all your "certainty". Funny how you religious people never worry about physics and chemistry...

nylonase.
nylonase is a different protein sequence with different structure and function from its parent protein. It does something the parent protein could not do. It is produced through a known mutation in the DNA sequence of the parent protein.
ncbi.nlm.nih.gov/pubmed/17512009
this capability shift through mutation has even been induced in other bacterium with similar starting proteins. ncbi.nlm.nih.gov/pubmed/7646041
A review of all three sequence studies can be found here. ncbi.nlm.nih.gov/pubmed/11092619

What do you mean by new mutation? It binds and digests a molecules that did not exist until 1935. To answer your first question yes. https://www.ncbi.nlm.nih.gov/pubmed/11092619

my previous statement does, in addition I have added a reference in my answer.

no they actually can't, the parent protein cannot digest 6-aminohexanoate-oligomer, the substrate in question. Simply increasing the amount of present will do nothing. the Ell' sequence is different than the parent sequence. .

you believe an inactive protein sequence existed to digest a molecule that was invented in 1935? And if you want more information you could look at the papers' references, which identify the separate parent enzymes in detail. Or you could just read more than the abstracts since the parent proteins are identified.

Then you are not reading the papers, at least not past the abstracts, and since you seem unwilling to even bother reading the sources given you I suspect you are not actually interested in an answer. Since comments are not for discussion and you can't articulate a reason the sources given are insufficient, I will leave you here.

"Plus its not even on a gene. Its a plasmid. So its like saying tossing your breakfast around in your stomach is evolution" ________           now have evidence you don't even know what you are asking for. I suggest you take a few biology classes so you know something about genetics and proteins before you ask the question. I also suggest you look up what a plasmid is.

Its an independent set of DNA in the host. So whatever evolution happens on the plasmid is only those changes which the host has already adapted to. In other words not evolution at all.

t makes no sense, a mutation in a gene on a plasmid is the same is a mutation in any other DNA loop. It shows you don't understand bacteria genetics. If you wish to continue this, Isuggest you create a discussion thread.


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How to convert skin temperature to core temperature?
As opposed to regular invasive thermometers, there are non-invasive IR thermometers to measure the temperature. For example Thermofocus.
I read in many sources that these IR thermometers only measure the temperature of the object's surface. However, Thermofocus seems to measure the patient's core temperature*.
My question is how to convert someone's skin temperature to their core temperature (Thermofocus does it so I understand that it's possible). I need to use an IR thermometer to measure a patient's skin temperature (say forehead) and predict their core temperature.
*core temperature: I hope this is the correct phrase... I mean the inner temperature as measured with a regular invasive thermometer.

The measurement of core temperature (it is the right term*) is easy using an invasive method. It is also reliable since:

Core temperature is easy to measure and temperatures are relatively
  homogeneous throughout the trunk and head[PMCID: PMC1752199];

However, the measurement of skin temperature is highly dependent on the location of measurement and also ambient temperature, as explained here[DOI: 10.1039/C6EE00456C]:

Also, Xu et. al. concluded in "Relationship between core temperature, skin temperature, and heat flux during exercise in heat" that:

Algorithms for T_c measurement are location-specific and their
  accuracy is dependent, to a large degree, on sensor placement.

They also proposed two relationships for calculation of T_c based on T_s (Core temp. based on surface temp.) which is included in the paper (regarding copyright laws, I'm not allowed to put it here. you have the DOI and can look it up).
*Here is the list of few publications which are using "core temperature" to address the temperature inside the body:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1752199/
.../pubmed/23775374
.../pubmed/10655798
Gender Role:
In a study in University of North Texas Source it is concluded that men has different skin temperature, due to different methods of temperature regulation compared to women:

We found gender differences at four different skin temperature locations. These changes might suggest that men retain more metabolic heat in various locations on the back when exercising in a hot, humid environment compared to women.

Also This Work shows that, although the temperature distribution pattern among genders are similar, women have lower skin temperature.
This Masters Thesis from University of South Florida indicates findings in regards to clothing and metabolic conditions role on core temperature, i.e. no statistical difference between T_c of genders. Look at Figure 3 in page 23 for heart rate vs. metabolic rates. In page 24 there is a table for measurements for T_c.

Thank you that's a good finding!
In DOI: 10.1039/C6EE00456C, are the formulas based only on surface temperature?

Yes. They used the surface temperature measurements according to the manuscript.

@AlaaM. I also found more work based on the conversion of surface temperature to core temperature. Updates include citations for those works.

Looks good. I'll check them out. DOI: 10.1039/C6EE00456C is available only by purchase though, am I correct?

It is correct. I'm student I have access through university.

I have the document (DOI: 10.1039/C6EE00456C). At what page is the formula that converts skin to core temperature? Thanks!

Their equation is based on the article by Xu et. al. "Relationship between core temperature, skin temperature, and heat flux during exercise in heat." Here is the summary:
They suggest this: Tc =Ts+HF (d/Lambda) as the steady state condition equation where HF is heat flux (calculated and represented in Table 1 - page 2385) and d and lambda are thickness and conductivity of the tissue.
Lambda value ranges are 0.20–0.70 W/mC (Werner and Buse 1988; Shitzer et al. 1996).
For transient condition, meaning that there is a T variation with time, there are two other equations (Page 2384).

This is not a public document and you shared it as such


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Difference in ATP synthesis in mitochondria and chloroplast
The mechanism of ATP synthesis in mitochondria and chloroplasts are almost the same, but there is a big difference: the f1 particle in mitochondria uses 2 H+ ions to synthesize one ATP, whereas in chloroplasts the f1 particle uses 3 H+ ions for the same. What make the difference?

Any reference for f1 particle uses 2 protons?

It was mentioned in my text book, local  publication.

see this http://biology.stackexchange.com/questions/3186/given-atp-synthases-structure-how-can-3-33-protons-ultimately-synthesize-one-a

Does this mean that the ATP synthase works same in both mitochondria and chloroplast. But what I have read is that 1 NADPH in mitochondria is capable of sending 6 H+ ions in to the space between the two membranes of mitochondrial. And it obviously produces 3ATP , so 2H+ for one ATP.

1 NADPH does not produce exactly 3 ATP

Also NADH is used for atp synthesis not NADPH, and 1NADH pumps 10 protons , not 6 protons, provide any reference please.

This may help:http://www.madsci.org/posts/archives/1999-01/915551393.Bc.r.html

Reference: one of our coaching institute's book (akash).

So the book mentioned it wrong I will intimate them the same, and thanks for the link.

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Why does lactate build up prevent a further increase in the speed of an athlete?
This question was triggered by an exam question that I was doing on the following paper (Q2 part (b)(i)):
http://qualifications.pearson.com/content/dam/pdf/A%20Level/Biology/2013/Exam%20materials/6BI05_01_que_20120307.pdf
Here is the markscheme:
http://qualifications.pearson.com/content/dam/pdf/A%20Level/Biology/2013/Exam%20materials/6BI05_01_msc_20120215.pdf
I do not understand why the decrease in pH results in the lack of of increase in speed, despite hours of research. Here are my best attempts:
The build up of lactate will have to keep the power output of the muscles, as a whole, constant, rather than allowing it to continue increasing. Therefore, there must be a link between the increased acidity of the muscle cells and the limiting of the power output. Now, if the markscheme is correct and the increase in acidity causes a decrease in the ATP production, this means that the ATP concentration within the cell decreases. However, the decrease in ATP concentration should decrease the power output rather than limit it, because less myosin heads will be able to contribute to the pulling of the actin filaments during the contraction of a sarcomere. Am I correct, or is there more to this? If so, why is there a limiting of the power output of the muscles rather than a decrease in it?

There is not complete shift to anaerobic respiration.

@JM97 may you please elaborate? How does that ansswer my questions? Moreover, what are your comments on my deductions? What am I missing?

During sprinting the runner maintains constant output not only just because of anaerobic respiration but also aerobic respiration, limited supply of oxygen limits the output.