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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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What are some good biological tests you can do to yourself?
I would like to do things like study my own blood and DNA. What kind of things can one do at the present time that are fairly simple. Or require minimal equipment like a microscope?
Are there some genetic diseases or predispositions that one can do self tests?
I mean there are a few tests I know of that are very simple, like measure your own heartbeat or eyesight. But these are a bit too easy.

what is your final goal? if you want to self-diagnose, i doubt this website is a good place. If you have concerns about your health, you should consult medical doctor or other health professional. Maybe check https://health.stackexchange.com/

no my health is fine. Just have intellectual curiosity to study one of the most advanced systems in existence. (me!)

One category of tests that are relatively safe to perform on yourself - are reflex tests. Some of them are actually very fun to test, say Babinski reflex.
No body fluids are used; however, I would still qualify those as "biological" enough.

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Why have we evolved to snore yet find snoring so annoying?
Human's snore. I doubt this is a new occurence over the last millenia. I find it hard to believe that for the past million years, no human ancestor has been a snorrer.
And yet, the sound of snoring is incredibly irritating to humans.
Could there be any evolutionary basis for these two facts?
One thing I could think of is perhaps snoring serves a purpose of making adult males seek out their own homes and families.
A male child may be inclined to be so annoyed by his father's snoring that he goes off into the world to seek his fortune.
If it didn't serve a useful purpose, surely it would have died out, simply because other humans would be so annoyed by snoring that they would murder snorrers in their sleep and hence reduce the genes for snorring.

Possibly relevant: https://biology.stackexchange.com/questions/35532/why-do-some-bad-traits-evolve-and-good-ones-dont

We didn't evolve to snore, snoring is a byproduct of other traits, mostly the ones that allow for speech.

Who is "we"?  Not all humans snore.  Snoring is basically a symptom of illness.  We cough and sneeze as well, and sniffle when we have colds, all of which many people find annoying.

Human are not the only animals that snore.

So humans are not the only animals that snore and also snoreing is a symptom of illness? So does that mean only ill animals snore? So are you saying there is a trade-off between speaking and snoring. If so, why haven't we evolved to not find snoring so annoying?

A very common misconception about evolution is that traits are directed toward a function. It a trait exists, it must be adaptive. This is false. As for snoring, people generally do not snore until they are past the age humans evolved to survive (about 35). To be selected against, those who snore would have to be less fit (fitness defined as the number of offspring produced). Traits that develop after an organism has reproduced have absolutely no bearing on selection. Similarly, we don't evolve resistance to heart disease, or cancer, because these diseases occur after we reproduce.

But we do have some degree of resistance to heart disease & cancer, enough that our odds of getting those things are a good deal higher if we adopt lifestyles that we would have been unlikely to encounter during evolutionary history.

Yes.And this is another example of an anachronism when it comes our best options today vs. 10,000 years ago. Our genes lag far behind the present conditions.

Where do you get that we evolved to survive to 35? That sounds doesn't sound true.  Just thinking about the Native American tribes, there are lots of photos of them with very old people. Many people believe we evolved to live long lives and be grandparents to pass on our wisdom. If you're thinking of average life expectancy don't forget to remove all the humans that died in childhood. Those that survived childhood tended to live long lives.

Perhaps snorring is annoying to make females mate with males under 35! If you think about it, what young human female wants to mate with a middle aged snorring man. Snoring could indicate bad health or age like you say.

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How was it discovered that flouride helps stop tooth decay?
Apparently flourinated water helps stop tooth decay. So I have some quesions about this.
Firstly how does it stop tooth deacy?
and
Secondly, how was it found that out of all the chemicals, it is flouride that stops tooth decay and nothing else?

What research of your own have  you done on this topic? If you look at the related questions on the sidebar you will see that there is one entitled "How does fluoride prevent tooth decay?" which is your first question. Please check out previous questions before posting.

Possible duplicate of How does fluoride prevent tooth decay?

@David that's a totally different question.

Please don't post answers in comments. @zooby it seems like you have 2 questions here, one of which is answered already elsewhere. If your question is totally different, then that part you wrote in your body must not be part of your question, so you should edit it out. Otherwise, people might think it looks like the same question and it will be closed as a duplicate and you won't get an answer to your actual question.

There is an interesting historical story of fluoride use in prevention of dental caries.
Interestingly the journey started with a "mysterious disorder-fluorosis."

In 1909 Dr. McKay (r) persuaded the Colorado State Dental Association to invite Dr. Green Vardiman Black (l), one of the nation's most eminent dental researchers, to attend 1909 convention where McKay's findings were to be presented. The two men began joint research and discovered other areas of the country where brown staining of teeth occurred.

Fluoride research had its beginnings in 1901, when a young dental school graduate named Frederick McKay left the East Coast to open a dental practice in Colorado Springs, Colorado

McKay collected the samples. And, within months, he had the answer and denouement to his 30-year quest: high levels of water-borne fluoride indeed caused the discoloration of tooth enamel.

Dr Dean recalled from reading McKay's and Black's studies on fluorosis that mottled tooth enamel is unusually resistant to decay. Dean wondered whether adding fluoride to drinking water at physically and cosmetically safe levels would help fight tooth decay.

This finding, considering the thousands of participants in the study, amounted to a giant scientific breakthrough that promised to revolutionize dental care, making tooth decay for the first time in history a preventable disease for most people.

These are excerpts from the article
Another reference
In 1802, Sir James Chrichton Browne suggested the probable cause of dental caries as a change in bread, which did not have bran or husky part of wheat containing fluorine.
Now your next question on fluoride stopping the tooth decay.
So yes apart from preventing tooth decay, research has found that fluorides like silver diamine fluoride can be treatment of choice for dental caries.

The silver component provides an anti-bacterial effect while the fluoride promotes remineralization of tooth structure.

I hope I have answered your question :)

@zooby you may accept the answer if you are satisfied so that in future this will motivate others to answer your questions


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Is there evidence that children should play in dirt to get healthy?
I've heard it said many times, that we should let children play in the dirt as it builds up their immunity and prevents things like allergies in later life.
I have another suggestion which, to me, is equally plausible. In older times when families had lots of children, and they used to play in the dirt, those weaker children used to get ill and die. Leaving the `stronger' children who were less suceptible to allergies and diseases to grow to adulthood.
So in our cleaner lifestyles where we prevent our children from playing in the dirt, actually we are just letting children who would normally have died off early grow to adults. (Which is a good thing from a moral standpoint - although overall it means the human population as a whole grows weaker in the short term).
Therefor telling people to let their children play in the dirt is bad advice if this is true.
Which of these two options do you think is the truth?
(Mathematically, let us assume that by random chance 50% of babies have bad immunity, but that parents have an average of 4 children. This means if half the childen die in childhood, the adult population would be full of people with good immunity. This is my terrible conclusion which has no moral solution.)

This answer focuses primarily on allergies, for which there is more reliable research, but touches on general immunity towards the end.
It is certainly true that the prevalence of allergies is increasing worldwide, and seems to be related to a rise in the so-called 'modern lifestyle' which avoids exposure to potentially harmful environmental factors.

The prevalence of allergic diseases and asthma are increasing worldwide, particularly in low and middle income countries. Moreover, the complexity and severity of allergic diseases, including asthma, continue to increase especially in children and young adults, who are bearing the greatest burden of these trends. - World Allergy Organisation Journal

The idea that playing in the dirt builds an individual's immune system and reduces the chances of allergies etc. is known as the "hygiene hypothesis" (or, more accurately, the hygiene hypothesis states that

due to reduced exposure to microbial components, the proposed allergy-preventing potential of these factors is no more present in sufficient qualities and/or quantities, which leads to an imbalance of the immune system with a predisposition to the development of allergic disorders." - Epidemiological and immunological evidence for the hygiene hypothesis.

)
Aside from potential mechanisms, there is certainly evidence for the hygeine hypothesis

The researchers studied the immune system of mice lacking bacteria or any other microbes ("germ-free mice") and compared them to mice living in a normal environment with microbes.
  They found that germ-free mice had exaggerated inflammation of the lungs and colon resembling asthma and colitis, respectively. This was caused by the hyperactivity of a unique class of T cells (immune cells) that had been previously linked to these disorders in both mice and humans.
  most importantly, the researchers discovered that exposing the germ-free mice to microbes during their first weeks of life, but not when exposed later in adult life, led to a normalized immune system and prevention of diseases.
  Moreover, the protection provided by early-life exposure to microbes was long-lasting, as predicted by the hygiene hypothesis. - Microbial Exposure During Early Life Has Persistent Effects on Natural Killer T Cell Function

As far as I know there is no consensus on this issue, however a number of scientific studies have proposed potential mechanisms to explain the rise in allergies and other such conditions; one of the most widely accepted ideas is that an avoidance of germs and microbes early on in life leads to

changes in the fine balancing of T helper cell 1 (Th1), Th2 and regulatory T cell (Treg) responses which are triggered by altered or missing innate immune cell activation. In fact, proper activation of cells of the innate immune system via their so-called pattern recognition receptors has been demonstrated to play a crucial role in early shaping of the immune system and suppression of the development of Th2-driven allergic immune responses. - Epidemiological and immunological evidence for the hygiene hypothesis.

this would seem to explain the observed phenomena.
It is definitely true though that there has been and will continue to be an element of natural selection involved here, as you have pointed out, because it is a force that is found pretty reliably in these sorts of situations. It is certainly logical that exposure to microbes during infancy will help weed out those with a weaker immune system (assuming they died because of infection/disease etc.), which over time would create a population and species that was more resilient. However, I can't find any studies to back up this idea. It is also a somewhat separate issue to the idea of the hygeine hypothesis, which describes changes to a specific individual within their lifetime rather than necessarily across a population due to natural selection and evolution, which is the explanation you have provided (unless I misunderstand your point?).
I only have a general understanding of immunity, however it is generally accepted that exposure to a pathogen (if this episode is survived) will result in an immune system which is better able to counter that pathogen in the future - this is the whole concept of vaccinations. therefore it makes sense that, again, low levels of contact with 'germs' will build a child's immunity.
Overall I think that it is a complex issue without a generally accepted answer as yet, however it seems to me based on this research that "playing in dirt" (in other words, being exposed to low levels of pathogens, microbes and toxins) does in fact build immunity and reduce the likelihood of developing allergies in later life, even if we don't know the exact mechanism for this yet.
aside from any potential immunity benefits, most children find playing in dirt fun (I know i did), so for the most part i'd say let them do it anyway!
My sources:

https://www.sciencedaily.com/releases/2012/03/120322142157.htm
https://www.ncbi.nlm.nih.gov/pubmed/17544829
https://waojournal.biomedcentral.com/articles/10.1186/1939-4551-7-12

Thanks for your answer. I didn't mean exactly natural selection in the terms of evolution over a long time. I meant really in terms of it may be "natural" for a human to have 4+ children and for only the strongest to survive each generation. And that all through human history perhaps women have always had half their children with bad immunity. So my suggestion is that this is nothing new. Even those with bad immunity, their children may have half-good and half-bad immunity. So I'm not saying immnuty is passed on by any means, more that is is just random at birth.


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Why some tissues like small intestine epithelium are able to be replaced so often, yet they are not one of the most common cancers?
My small intestine epithelium cells are replaced thousands times more than my prostate. Yet I'm much more likely of getting a prostate cancer than cancer on my intestine epithelium. Is there a known cause for this?
Does our body have better DNA-repairing mechanisms or something like that for those tissues ?

Just a quick thought: These cells have a relative short livespan and thus less chances to develop into cancer cells. This would be different for the prostate for example.

Interesting question!  @Chris has a good point. I think the relevant factor is how often a long-lived stem cell (or similar) would divide in these two tissues. Is prostate less proliferative than small intestine in this regard? Also, some cell types maintain a more differentiated state while proliferating (hepatocytes in regenerating liver, for example) and this could be a factor I think. Just some suggestions.

@Roland There are stem cells present in the small intestine, which clearly play a role in regenerating the tissue. I can look up some references for this later.

The human prostate has two main epithelial cell types, basal and luminal, as well as a minor population of neuroendocrine cells. Primary prostate cancer nearly always has a luminal phenotype characterized by atypical glands, strong androgen receptor (AR) signaling, and an absence of basal cells .                  Intestinal epithelium. The intestinal epithelium is the single cell layer that form the luminal surface (lining) of both the small and large intestine (colon) of the gastrointestinal tract.

Hi malay and welcome to Biology.SE. Your answer has unfortunately two flaws, while it highlights the difference between the 2 tissue it does not address why one would be more likely to develop cancer (the original question). Moreover it lacks of references. References are really important to verify the source reliability.

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Can a same gene stretch from one chromosome to another separate chromosome?
Can a gene continue on from one chromosome to another separate chromosome? For example, can part of an eye colour gene be on one chromosome and the rest of it be on the next chromosome?

Usually not (as described in the other answer, non-contiguous pieces of DNA are not considered as a part of a single gene). However there are some cases of trans-splicing in which the spliceosome can splice together RNAs arising from different genomic locations. But these are rare and do not have a direct effect on distinct phenotypes such as eye colour, to be classified as genes. Not much progress has happened in this aspect of transcriptomics, actually.

In the small free-living soil nematode, C. elegans, and in many other members of this phylum as well, ~ 85% of nuclear transcripts are trans-spliced to a 22 nt splice-leader sequence (usually just upstream of the AUG translational initiation codon). The splice leader 1 (SL1) is next to the 5S RNA gene: both of themes are repeated about 100 times on the right of the gene cluster on chromosome V.

@mdperry thanks for that information. In fact it has been most well studied in nematodes. There are some trans-splicing databases afaik.

Gene is usually defined as piece of DNA that produces certain product, be it RNA or polypeptide molecule. In both cases RNA is produced as intermediate or final product. Nature of RNA production from DNA (aka transcription) is such that it requires double-stranded DNA as substrate, that is a continuous polymer of nucleotides.
So, only parts of chromosomes (which are really long linear polymers) can be used as substrate or template for RNA production.
However, regulatory elements, which are extremely important, can be anywhere, as long as they are able to function. Since those elements are just special sequences of DNA that interact with transcription factors and other elements of DNA->RNA machinery, they can be on different chromosome than gene of interest.

No, a gene is confined to a single chromosome. A gene is characterized by a start sequence in the DNA (among many other things), which indicates that the nucleotides are to be read and transcribed to RNA. This stretch of DNA in the gene is contiguous, although some parts may be skipped in transcription. Because different chromosomes are physically distinct, the cellular machinery would require two start sequences, which really means there are just two separate genes. Instead of finding one eye color gene on multiple chromosomes, you instead find multiple eye color genes on multiple chromosomes.

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Which step in endocytosis requires ATP?
Everybody seems to agree that endocytosis is an energy-using process, and as such requires ATP hydrolysis. However, which particular step requires it? More precisely, which 'molecular machine' involved in endocytosis requires ATP? I cannot seem to find a good answer in the literature.

Endocytosis can happen through several processes, such as clathrin coated pits or caveolae. Do you have one or the other in mind?

Sorry, yes, I was mainly thinking about clathrin-mediated endocytosis. We can focus on that one.

Endocytosis (specifically you asked about clathrin-mediated endocytosis) is indeed an energy consuming process. the coating of the vesicle may be "spontaneous", but the pinching off of the vesicle, the uncoating of the clathrin, and the transportaion of the vasicle inside the cell all require ATP/GTP hydrolysis.
Dynamin - dynamin forms a spiral around the neck of the vesicle, and uses GTP hydrolysis which in order tighten the coil around the vesicle neck causes it to break and results in the pinching off of the vesicle from the parent membrane.
The uncoating of the clathrin is also ATP/GTP consuming. proteins such as hsp70 chaperon and auxilin is thought to be involved in the ATP hydrolysis. the uncoating process starts after the pinching off of the vesicle.
the tranportation of the vesicle will also cost energy, proteins such as the Myosin family are considered to transport endocytic vesicles into the cell, and use ATP hydrolysis.
Dynamin - Wiki
Myosin  - Wiki
Uncoating process - Molecular Biology Of The Cell ed.6 p.701

Thank you for your answer. I asked this a while ago... Eventually I got a similar answer to yours on Reddit. It seems clear that energy is required for pinch-off and later processes, but perhaps the previous steps can occur spontaneously.


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How should lentil roots grow in a microgravity system?
I recently executed an experiment in which I collocated 20 lentil seeds in independent Petri boxes with an agar agar solution, all of it located in a clinostat (a slowly rotating device used to simulate microgravity conditions, where they rotated perpendicularly to the ground (gravity). The objective was to see in what direction did the roots grow under the effects of microgravity, since geotropism didn't have a fixed direction to head to. At the end of an entire cycle, the forces (gravity in 360°) applied to the seeds would turn out to be equally strong, in opposite directions, so it would come down to nearly zero.
However, after many executions, without having any functional problem with the clinostat, the seeds simply didn't grow roots while being in the agar agar in the Petri boxes. I tried different agar agar solutions, different concentrations, more & less quantity so that the seeds would have a thin air layer; and I also added copper sulphate to prevent fungi from appearing, also varying its concentration. Afterwards, I tried using an already germinated seed so that the radicle had direct access to the solution and to the air layer. Nevertheless, after several executions, only a few seeds grew their roots and I din't find a concrete explanation for this experiment not being successful.
I expected having the roots in the experimental group to grow in many different directions, not being constant. As in the other hand, I expected the control group to grow roots in the same direction, going downwards, being in the same system (clinostat) without having the rotations going on.

I am looking at an old study on soil symbiotes that used lentils on agar, their method is described as {Surface-sterilized (1 min in 70% ethanol and 3–5 min in 3% NaOCl) and pregerminated (48 h on 1% water agar)} if that helps.

It sounds like your first issue is with seed germination. I am assuming you are doing a seed sterilization. You may want to try allowing them to imbibe water for about an hour after the sterilization process, and then wrapping them with aluminum foil and placing them in a fridge for a day or two. I've done this with Medicago, which is another legume. However, not sure if it works for your lentils.
The root may also have trouble developing given the micro-nutrients in the media. I am curious what recipe for media you are using, as the amount of agar may also affect the ability for these roots to penetrate the media. I have had trouble germinating legume seeds when there were 100+ seeds in a plate as they inhibit each others growth.
It's hard to give a clear answer, but try optimizing your seed sterilization protocol and media recipe and best of luck!


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Boiling A frog in a sous vidè bath
So if i were to use a sous vidè water bath and a frog and slowley raised the temperature say 1 to 2 degrees a day would they survive harsh boiling water through thermoregulation

How will it survive energy depletion?

could you perhaps provide a bit more context for asking this question?...

No.
No higher order organism has enough proteins that are stable at 100 degrees C to survive. Proteins denature at higher temps and all cellular functions that depend on them cease.
Some thermophillic bacteria have evolved proteins that are stable above 100 degrees C over eons of evolution.


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Why does the mass increase in this question?
So, on 'http://filestore.aqa.org.uk/sample-papers-and-mark-schemes/2016/june/AQA-BL3HP-QP-JUN16.PDF', question 1.b., they show a partially permeable bag of glucose solution, in a less concentrated solution. Since sugar is more dense than water, why does the bag get HEAVIER, when there's more sugar, and less water?

Hint: the bag is partially permeable, but to what?

You try to explain why you find it surprising that the bag would get heavier but I still don't understand your reasoning. I don't see how you go from the density of sugar and water and how much of them there is in the bag, to being surprised the bag is heavier. Maybe you could give more details on the logical connections there?

@DevonRyan If it's not permeable to sugar molecules, then is the amount of sugar inside and out remaining the same? If so, and water is going inside the bag, then the bag is swelling. Does diffusion do this? Make things swell? My understanding was that you couldn't create pressure this way.

@RozennKeribin If you replaced the sugar in the bag with water via diffusion, the bag would be lighter. My understanding is this what is happening in the bag. Why is it becoming heavier?

@Piomicron thank you, your question makes more sense that way (you might want to edit your question to include that reasoning). I think you have it right in your answer to DevonRyan: the bag is permeable to water but not sugar. Could you elaborate on the objection "my understanding was that you couldn't create pressure that way"? Is there a specific source you are basing this on?

@Piomicron: Osmosis :)

@DevonRyan hey, I thought we were making them work through the answer and not just giving it! :p

@RozennKeribin I still expected Piomicron go from "osmosis" to why it'd result in the phenomenon, but point take :)

The reason that dialysis bag A and B will get heavier is due to water diffusing into the bags in order to bring the sugar concentration on both sides of the membrane to an equilibrium. Likewise bag C and D will get lighter as water will diffuse out of the bags in order to bring the system as close as possible to equilibrium. Water diffusion is also called osmosis and can be studied closer here: https://en.m.wikipedia.org/wiki/Osmosis


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Hemoglobin oxygen affinity curve
I have a general understanding of the Bohr effect, and that Hemoglobin's affinity for oxygen will shift depending on the conditions of the lungs and tissues. However, I'm struggling with the following question; I feel as though I'm getting caught on the less-than-ideal answer choices, but I want to make sure I'm not missing a basic principle that could reason this answer more clearly.
Q) Which of the following best describes how a shift to the right in the dissociation curve results in more oxygen delivered to tissue?
A) The distance between the curves at 100 mmHg is less than the distance at 40 mmHg
B) The distance between the curves at 100 mmHg is more than the distance at 40 mmHg
C) On the right-shifted curve, Hb will pick up more O2 in the lungs
D) On the right-shifted curve, Hb will pick up less O2 in the lungs

My reasoning for choosing A is less-than-ideal: let me explain. First, I've been taught that a good rule-of-thumb for oxygen affinity is that Leftward shifts are related to the lungs, while Rightward shifts are related to the tissues. Therefore, because the answer choices C & D refer to right-shifted curves and the lungs, they can be eliminated. However, I'm not convinced this "rule" is so absolute - I can imagine that the curve can shift left & right within the tissues and the lungs. For the sake of argument though, I'll assume the rule works and eliminate answer choices C & D. Then, I can also eliminate answer choice B because it's not a true statement. As a result, I arrive at answer choice A. However, I don't feel as though it quite answers the question. Can anyone please provide some insights as to my reasoning, and/or perhaps what I'm missing? Thank you!

This is just a guess, but does the pH play a role in the answer? As the CO2 levels increase, the pH will drop, so it makes some sense that in tissues with high metabolism, they will release more CO2 and the pH will be lower. Because the hemoglobin can't hold as much O2 in these more acidic conditions, the bound O2 is released near the tissues that make the most CO2.

Comment: this question is a bit confusing, since none of the answers seems to directly explain how a shift to the right in the dissociation curve results in more oxygen delivered to tissue. Therefore, we'll try to choose the least wrong option...
This answer came out a bit long, so here's a TL;DR for you. I chose

 Option A

and here's why:
Although not stated explicitly, the pH in question is most probably the blood pH (this is a rather well-known graph from biochemistry undergrad studies). It shows that when blood pH drops or rises, the amount of %O2 saturation of hemoglobin deviates from the norm accordingly.
First of all, regarding your rule-of-thumb, it might be misleading in this context, since it may be true in both normal conditions and pathological conditions, depending on the site of measurement:

Under normal conditions, general blood pH is around 7.4 (7.35-7.45), blood pH in the tissues is around 7.2 (due to increased pCO2 resulting from cellular metabolism), and blood pH in the lungs is around 7.6 (due to the release of CO2 in the lungs for expiration, which results in lower pCO2 in the lungs) - see this reference and its references.
Under pathological conditions, general blood pH may rise above 7.45 (alkalosis) or fall under 7.35 (acidosis), regardless of the site of measurement [reference]. This means that a dissociation curve under abnormal blood pH value does not necessarily relate to normal conditions in a certain body site, but may also relate to a pathological condition in which blood pH is abnormal in general.

I believe the graph represents the latter situation, i.e. how hemoglobin behaves under the pathological states of acidosis (lower blood pH = right-shift) and alkalosis (higher blood pH = left-shift) compared to the normal state, since it depicts the change in %O2 saturation over the physiological range of pO2 and the curve is continuous (a depiction of blood pH only in the tissues or the lungs would not have resulted in a curve, since pO2 does not change significantly in each site, certainly not over the physiological range).
Now let us consider the possible answers:

Option A - The distance between the curves at 100 mmHg is less than the distance at 40 mmHg. This seems to be true in it's own right. However, other than describing the situation, it does not explain explicitly anything. It essentially says that the difference between oxygen release in the tissues is more pronounced than the difference in oxygen binding in the lungs, when comparing normal blood pH and acidosis. We can infer that if the right-shifted curve is below the normal and left-shifted curve, it means that less Oxygen is bound in the tissues (and also everywhere else, since this trend is consistent), i.e. Hemoglobin is less saturated, i.e. more Oxygen is released in the tissues in a state of acidosis than in any other state.
Option B - The distance between the curves at 100 mmHg is more than the distance at 40 mmHg. This is merely the opposite of A, and therefore is untrue by the same amount that A is true.
Option C - On the right-shifted curve, Hb will pick up more O2 in the lungs. This is a bit trickier. This option suggests that when pH is lower-than-normal (acidosis), more Oxygen will bond to Hemoglobin in the lungs. However, by observing the graph, we can see that the right-shifted curve is always below the other curves (both the normal and the alkalosis curves). This is also true in high values of pO2, which are present in the lungs. This renders this statement incorrect in itself, and it also does not explain why more oxygen is released in the tissues.
Option D - On the right-shifted curve, Hb will pick up less O2 in the lungs. Based on the analysis of option C, it should be rather evident that the opposite must be true. That is, if the right-shifted curve is always below the other curves, including in high pO2 values, then under this condition Hemoglobin is bound to pick up less oxygen in the lungs than in any of the other conditions. Therefore, this statement is correct, but it does not explain why more oxygen is released in the tissues.

According to the section titled The influence of pH on oxygen-hemoglobin binding in this excellent reference, "the presence of a low pH locks it [hemoglobin] in an unreceptive state, preventing it from binding oxygen molecules". This means that Hemoglobin's affinity to oxygen will be reduced, so that more oxygen will be released (in other words, less will be bound) in the tissues and less oxygen will be bound in the lungs. The two "less" in the previous sentence are in accordance with the curve of pH=7.2 being below the other two curves over the entire range of pO2. I highly recommend reading the above reference through and observing the figures.
To sum up, none of the possible options is satisfying enough, but option A seems to be the least wrong or unrelated to the situation described, so I would choose it.


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What are the features on a microscope one needs in order to do lab work?
By lab work I mean urinalysis, blood work(live as well), fecals, cytologies, histologies and all other.
I have read(partly) a book(from 2002) on lab diagnostics and the author did not mention anything about diagnostics. I've spent a lot of time searching on google as well and I did not get anything.


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Source of journals collecting titles of scientific publications regarding clinical trials with dogs fed medicinal herbs
After some time researching on the web, you can find a lot of websites telling you that some herbs may have or have specific properties(unfortunately most seem to be "advertised" as if they were wonder drugs), but none or few give references to specific titles of papers.
Another alternative is the pub med website but papers don't seem to pop up regardless of any search words.
Where is all that research information posted?

NCBI tends to be a good one. While this isn't about dogs, they have the effects of mint on exercise. However I did find an article about ginseng and dogs here, here, and here. To find the dog article I typed "NCBI ginseng dogs" into Google.

For a lot of "alternative" medicine there are only claims but not serious scientific studies have ever been conducted. Look at Pubmed, if you don't find them there, they are most likely not existant.

Check the databases mentioned in this post with right keywords.

Thanks to all, don't know if it matters but, I was looking for research on something that is anti-inflammatory such as turmeric.


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Are there any fruits that rely on dispersal of their seeds using excrement?
Are there any fruits that have seeds which can survive the digestive entirety of an animal's digestive system and remain germinable once passed on in animal excrement?
Perhaps this is the primary function of all seeded fruits and I'm just fundamentally unaware of the intended biological processes. If so, then why do poisonous seeded fruits exist?

Yes, many. A common example is the fruits containing capsaicin (e.g., hot peppers): this compound is an irritant to mammals but does not affect birds. This adaptation seems to have evolved to discourage consumption of the fruit by mammals, whose digestive systems damage the seeds, and to encourage consumption instead by birds, which distribute the seeds effectively.

Seeing as the main premise of your question is completely wrong (meaning that loads if not all fruit can survive the digestive system of an animal), I am voting to close as unclear. Please do some research (just glance through a wikipedia page or something) and ask something a bit more specific.

@terdon https://biology.meta.stackexchange.com/questions/2961/voting-to-close-a-question-as-off-topic-because-it-is-based-on-a-faulty-presuppo

@canadianer yes, but my vote wasn't because the premise was wrong but because, given that the premise was wrong, the question is unclear. I mean, the question in the title can be answered by "Yes, most of them" but I don't think that's very interesting to the OP.

That's really kind of the point of having fruit in the first place. Why would the plant waste valuable nutrients just to feed animals? That doesn't mean that all fruit seeds survive the digestion of all different kinds of animals, of course, but the whole purpose of a fruit is to be eaten or carried (a lot rarer) by animals for dispersion.

Yep, almost all fleshy fruits rely on being eaten - even some non-flowering plants like juniper bushes and yew trees do too. The process works like this:

Animal eats fruit
Animal digests fruit except for the seeds, which are designed to survive the process
Animal deposits seeds in its excrement.
Seeds grow, now a long distance from their parent and with a free helping of manure to get them started in life.

To answer your confusion about toxic fruit, let's consider holly berries.
A bird can eat holly fruit with impunity, while a human or a horse would end up seriously ill. This is because birds tend to swallow their food whole - this combines with their ability to fly makes them prime vehicles for seed dispersal, while humans and horses thoroughly chew their food, which risks damaging the seeds, rendering them useless.
To this end, holly fruits are packed with toxins that are harmless to birds but cause anything else severe discomfort, discouraging them from trying that again.

reagrding your second last paragraph: Viscum would be another prominent example..


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Are there any traces for evolution in modern humans over the last 100 years?
I ask that because I had a biology class and my teacher said something about a bone in the back of the head that apparently every male has, and for some reason, in the last 20-25 years, its started to fade away and so even though my father has the bone I don't. Or when I was still in high school, and I had to do X-rays for braces the doctor told me that I don't even have wisdom teeth? Are those traces of evolution or are they just random mutations?

Re: "Are those traces of evolution or are they just random mutations?" These two options are not mutually exclusive.

Your biology teacher was quite misinformed if that is what they told you.

Spotting evolution over only 4 generations would be very difficult. You certainly wouldn't see an entire bone disappear in that timeframe, though it might be slightly smaller in average people today than it was several generations ago. Over the timescale you're describing, the only real option is epigenetic changes, which might not be permanent enough to "count" as evolution.


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Is the amount of cholesterol the body produces affected by how much cholesterol you take in with food?
In the past I've been told multiple times that if you don't eat foods containing cholesterol, your body will increase its production of cholesterol to balance out the lack of nutritional cholesterol. On the other hand, if you eat sufficiently much cholesterol, the body will adapt its production of cholesterol in the other direction.
What evidence is there to support this statement?

Here's a study in which they measured a decrease in endogenous cholesterol synthesis after various amounts of dietary cholesterol: Dietary Cholesterol Feeding Suppresses Human Cholesterol Synthesis Measured by Deuterium Incorporation and Urinary Mevalonic Acid Levels (Arteriosclerosis, Thrombosis, and Vascular Biology, 1996):

The objective of this study was to measure the response of cholesterol
  biosynthesis in subjects to three different amounts of dietary
  cholesterol: 50 (low), 350 (medium), and 650 (high) mg cholesterol per
  2800 kcal. Individuals with low (n=7), normal (n=12), and elevated
  (n=11) plasma cholesterol concentrations consumed in random order
  solid-food test diets (15%, 55%, and 30% of energy as protein,
  carbohydrate, and fat, respectively) at each dietary cholesterol
  level. The three diets were consumed for 4 weeks each, and each
  dietary phase was separated by a 4-week washout period. During the
  final week of each diet, 0.7 g D2O was given per kilogram of body
  water and deuterium incorporation into the erythrocyte cholesterol
  pool was measured for 24 hours. Urinary mevalonate levels were also
  determined in samples obtained during two consecutive 24-hour periods.
  Both techniques provided measurements of whole-body cholesterol
  biosynthesis. In all subjects the cholesterol synthesis rate as
  measured by deuterium incorporation was significantly lower (P<.05)
  after the transition from low- to medium- and low- to high-cholesterol
  diets. Urinary mevalonate excretion decreased after the change from
  the medium- to high- (P<.05) and low- to high- (P<.01) cholesterol
  diets. Although correspondence between the two methods was poor, they
  both indicated some suppression of cholesterol synthesis by dietary
  cholesterol. The response of cholesterogenesis to different amounts of
  dietary cholesterol was related to the rate of synthesis under
  depressed conditions of the low-cholesterol diet. These findings
  indicate modest downregulation of synthesis in response to dietary
  cholesterol in humans, independent of plasma cholesterol levels.
Metabolic responses to increased dietary cholesterol potentially
  include reduced endogenous synthesis, decreased absorption, and
  increased biliary excretion of cholesterol.

In some people, who are cholesterol hyperresponders, dietary cholesterol does not effectively suppress endogenous cholesterol synthesis, so it results in elevated blood cholesterol levels (Comprehensive Biotechnology, 2011). In one study, a decrease in dietary cholesterol intake resulted in a decrease of blood cholesterol in hyperresponders but not in hyporesponders: Endogenous cholesterol synthesis, fecal steroid excretion and serum lanosterol in subjects with high or low response of serum cholesterol to dietary cholesterol (Clinical Nutrition, 1986):

In this study we addressed the question whether hypo- and
  hyper-responders to dietary cholesterol differ with regard to the
  flexibility of endogenous cholesterol synthesis after changes in
  cholesterol intake. Whole-body cholesterol synthesis was measured as
  faecal excretion of neutral steroids and bile acids minus cholesterol
  intake. In addition, we determined serum concentrations of lanosterol,
  a precursor of cholesterol and a possible indicator of cholesterol
  biosynthetic activity. The study was carried out with 2 hyper- and 4
  hypo-responders; these subjects had shown a consistently high or low
  response of serum cholesterol to a decrease in dietary cholesterol in
  two previous experiments.
The subjects received controlled high- (on average 697 mg of
  cholesterol per day) and low-cholesterol (109 mg/day) diets for
  periods of 4 weeks in succession; cholesterol was the only dietary
  variable. The two hyper-responders again showed a significant decrease
  in serum cholesterol. There was essentially no decrease in serum
  cholesterol in three of the four hypo-responders. The decrease in
  cholesterol intake caused an increase in cholesterol synthesis in five
  out of the six subjects.

In conclusion, in most people, dietary intake of cholesterol does not increase blood cholesterol levels because of decreased absorption and endogenous synthesis and increased excretion of cholesterol.

Some info about the mechanism would be interesting and not  off topic, I guess: "because of decreased absorption and endogenous synthesis". How is cholesterol intake downregulated, by enterocytes?

Your question asks if/how "the body will adapt its production of cholesterol".
Literally, any cell - that should include the hepatocytes of the liver - of "the body" produces cholesterol, as it is an essential part of the membrane (of animal cells, by the way, by a factor of 100 more so than of plant cell walls), and it should be empirically well ascertained that there is adaption of cholesterol production to dietary input (reflected, especially, by delivery of cholesterol by - so called "remnants" of cholesterol transporting lipoproteins and chylomicrones, which may very much seen as a regulatory system that balances production between specialized cholesterol producing cells, i.e. especially hepatocytes of the liver and adipocytes of the tissue).
However, refering to any mechanism your question may be about, there are still open questions. See quote below, last sentence.
Here's the only pertaining quote I found.
Takizawa, Cellular control of cholesterol:
"When cells are faced with low cholesterol levels, they respond by increasing the gene expression of proteins that stimulate biosynthesis of cholesterol, such as HMG-CoA reductase, and proteins that increase the uptake up cholesterol from the external environment, LDL receptor. These genes contain a common upstream regulatory element called the sterol response element that binds a transcriptional activator, called the sterol response element binding protein.
When bound to the element, the binding proteins turns on transcription of downstream gene. So, a key question is how the cell regulates the binding of the binding protein to the response element and how that regulation is sensitive to cholesterol levels."

This question has also been answered on MedicalSciences.SE:

"The net daily synthesis of cholesterol is equal to the amount of cholesterol lost in the feces minus the dietary cholesterol"
The body synthesizes an amount approximately equal to the amount it absorbs
Source: Balancing Cholesterol Synthesis and Absorption in the Gastrointestinal Tract David E. Cohen, M.D., Ph.D.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2390860/

copied from this answer https://medicalsciences.stackexchange.com/a/17712

Duplicating answers from elsewhere on StackExchange is okay, but make it abundantly clear that this is what you are doing. Additionally, I would much prefer some level of original content to be added especially when it isn't the same person answering both questions. This answer also doesn't really add much that isn't already in the existing answer here.


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Are we going against nature?
Nature selects those who leave more progeny (reproductively fit) according to natural selection. But nowadays we are going in for family planning. So are we in a way going against Nature?

I'm confused about what you're asking. Can you please clarify? For example, are you asking if we are becoming less fit?

Your brain is a product of evolution; so technically whatever you decide to do is pretty much natural. Please clarify your question or else it would be put on hold.

Are you suggesting that Homo sapien development is some form of supernatural progression?

I mean to say that nature selects those who leave more progeny according to Darwin.But as we are now going in for family planning, we are going against what Darwin said.So how will we be selected by nature and exist thereafter

I think yes. In most cases we( man ) is against the nature .

If the "more progeny" claim was true, codfish would rule the universe.  Sarcasm aside, you might note that it's SURVIVING progeny that matter.  If your species produces more progeny than can be supported by the environment (food supply &c), then most of them will die.  See Malthus.

Issue in the post
The question is based on a false dichotomy between what is natural from what is not. This non-existence of the concepts of natural vs artificial is a matter of analytical philosophy, therefore your question is non-sensical for philosophical reasons.
Some insights despite above issue
In several species that have advanced cognitive abilities, there are traditions and culture. This culture may affect the number of offspring that individuals will have. This effect exists in humans for sure. There is nothing unnatural to it (but again it depends what you want to call natural and artificial)!
In a comment you say

I mean to say that nature selects those who leave more progeny according to Darwin.But as we are now going in for family planning, we are going against what Darwin said.

There are at least 2 issues here
Misrepresentation of evolutionary biology as being Darwin's saying
Evolutionary biology is so much more that Darwin's work. Of course Darwin was a very important scientist that contributed a lot to evolutionary biology but summarizing any saying from this field of science to Darwin's saying is very downgrading for evolutionary biology.
It feels like nature is an active character
In saying nature selects those who leave more progeny, it feels like "nature" would be some kind of character that actively chooses those that leave more progeny. This is wrong. Genomes that leave on average more copies of themselves will tend to become predominant in the population. Selection is just the consequence of fitness differential and not a choice that is made by looking at fitness differences. If you are unused to the term "fitness" as used in evolutionary biology, please have a look at the wikipedia link. This term is completely different from the concept of body-building in sport.

You might want to have a look at Understanding Evolution by UC Berkeley, a free online very introductory course to evolutionary biology.

@user31223 You already accepted the answer but I would like to attract your attention to the fact that I edited the answer to add some information about a comment of yours.


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Genetic pros or consequences of children born to parents of mixed nationalities?
I've gleaned a potentially flawed impression over time that a more diverse gene pool should, in theory, result in healthier progeny. Something about dominant genes promoted over recessive genes..
As a result of the above, I always assumed I should favor a mate from another region if I want to have children, thus hopefully ensuring the children have a diverse mix of DNA bits to assemble out of.
I'm an American male (almost 38), and by a curious chance I find myself dating a Russian female (almost 29) who is in a US PhD program. We've been together a little over a year, and we've discussed marriage/children. So far so good.
However there's an observational wrinkle.. She sometimes associates with a local group of Russians and I tag along. Not long ago at a gathering with several young families, of which I think many are mixed-national (Russian and American), I was discouraged to observe what I thought was a disproportionate number of children with various disorders. If memory serves, there were 2 or 3 autistic and one down syndrome child out of about 11 or 12 kids of the same age.
[It might be worth noting that this is a church group. Church might provide a kind of social safe-haven that allows these families, particularly the children, to socialize with fewer concerns. As such it might make sense to see them in greater numbers.]
Anyway, suddenly I'm doubting my prevailing assumption about genetic diversity and wondering if there is a correlation between autism and the children of parents of mixed nationalities.
In this article, I read:

In the studies conducted in Nordic countries, a statistically
  significant 58% increased risk of autism was observed among the
  offspring of mothers born abroad.

So I find myself vexed. Is there a propensity for genetic challenges in children born to parents of mixed nationalities?
(FWIW I realize our ages dip into another risk factor, but I'm specifically asking about regional genetics.)

Related: Does it make sense to classify all humans in a single species?

Did you read the rest of that article? The authors suggest many alternative possibilities for the effects they observe:

Several hypotheses have been postulated, including the idea that fathers with social disability potentially due to a genetic mechanism associated with autism may be less able to find a spouse from their own country and may therefore find a wife from a foreign country with whom to have children91. More likely, Gillberg et al.91 suggested that women born in another country may not be immunized against the common infectious agents in the country in which she gives birth and may therefore be more susceptible to relatively innocuous infections which may increase the risk for autism. Other possible explanations include a potential role of maternal stress due to the demands of residing in a new country, particularly with limited social support, or stress resulting from the experience of emigrating, perhaps due to economic or social factors. These hypotheses do not explain the relationship with maternal place of birth seen in a cohort study of children born in California between 1989-199416, which showed a 40% decreased risk of autism among the children of women born in Mexico as compared to California. The association between maternal immigration and autism risk requires further examination in other areas of the world to examine whether the relationship can truly be generalized.
  Gardener et al., 2009

(emphasis mine)
In addition to these factors, note that p-value for that trend was only .06, and although there are a lot of problems with basing conclusions on fairly arbitrary p-values, a p-value of .06 suggests that differences of the magnitudes observed would often occur by chance. I'd say it's an area of open study, but it is quite a leap to jump to a conclusion that mixed nationalities result in higher incidences of things like autism from 1) the observation of a very small cohort of 12 children and 2) this other study which suggests many alternative possibilities for what is a small and possibly insignificant effect.
There are two main benefits for populations to avoid becoming inbred. The first is that there may be many deleterious alleles with low-incidence across a whole population, but you have a very high likelihood of producing a homozygous recessive offspring with a close relative. The second is overall maintenance of genetic diversity across a population, which could be important if suddenly exposed to a new disease, for example.
However, it is also possible for outbreeding depression to occur, which is a reduction in fitness after mating genetically distant individuals. However, outbreeding depression usually occurs either when fitness of some variable is low at intermediate values: for example, high fitness for small or large animals, but not for medium-sized animals, perhaps due to slightly different niches within the same species. Outbreeding depression can also occur when there is sufficient genetic separation between two individuals such that their whole protein milieu has evolved on a different background, such that alleles that cause no problems in either population alone are incompatible with alleles in the other population.
This previous answer here on Biology.SE talks about the lack of evidence for outbreeding depression in humans and a bit about why. Briefly, there is simply not the type of disparity in fitness conditions or sufficient genetic variability within humans for either of those situations to occur.

The site has apparently queued my upvote, but you got me--I skimmed the article and missed those alternate theories. However, would it not be true that statistic (58% increase) describes the mere condition that the mother was an immigrant...and the correlation does not regard why, which the alt theories then consider? Maybe it can be immunization and/or maybe it can be stress...or even something else, but the fact is, being a female immigrant was still the common denominator...no?

@user31840 That's my understanding - the point, though, is that being a female immigrant is likely to be correlated with all of those other factors, and based on our understanding of not only the unlikelihood of outbreeding causing autism (for the reasons I state later) as well as the poor relationship between autism and purely genetic causes, those are much better explanations than outbreeding, especially because, like the other answer I linked notes, there isn't really any evidence for outbreeding depression in humans in any circumstance.

Given a couple of centuries of European immigration to the US (and presumably a good deal of intermingling of European peoples in previous millenia), could mating between a (mosty caucasian) American and a Russian really be consideed outbreeding?

@jamesqf Yes I'd agree that intermingling and immigration means there are very few groups of humans that are truly isolated from each other over an appreciable number of generations, although I don't think there is a specific definition for outbreeding, or inbreeding for that matter, it's all relative.

@Bryan Krause: I think you possibly could find such groups, depending on how much isolation is enough.  Say Japanese and the !Kung people of southern Africa, or Inuit and Australian aborigines.  But any two populations of mostly European descent, no.

@jamesqf Exactly why I said "very few" groups - those are all fairly special cases. However there are also some groups of European descent that are slightly isolated from other Europeans, including some Amish communities or Ashkenazi. The other point I was making is that inbreeding and outbreeding don't have specific definitions, it's all relative.


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Why are sushi proteins called "sushi"? What are the origins of this name?
Does anybody know why complement control proteins (also short consensus repeats) are called "sushi" proteins? Is there any special reason for their name?

Hi Welcome to Bio.SE. Your question could use a tad more context to demonstrate that you've tried answering this on your own. We always ask that the asker provide evidence of prior research. See here. Thanks.

People who discover things have some small reward in being able to name it whatever they want within reason. There's a moth with donald trump like hair which was named after him, and some proteins have incredible names (my current amazement is with the sonic hedgehog protein.) Sometimes - after a while - the names are changed if particularly ridiculous. Sometimes not (luciferin is a prime, imaginative example.)

@anon Biologists, in particular, like to be clever/creative with how they name things, but it has gotten them in a bit of trouble in the biomedical area. It turns out that when patients have some kind of debilitating disease, it doesn't go over particularly well when the doctor starts trying to explain to the family what causes the disease, and some protein or gene with a funny name is implicated. There have been movements to change some of the real zingers that arise most often in clinical cases, but inertia has gotten in the way (plus some resistance from those of us with a sense of humor).

@CodyGray - Yep. Am following the controversy around sonic hedgehog and personally think, out of respect for the devastating illness it is associated with, it should be changed. But I might feel differently if I were the biologist involved. In this case, though.... I would not have named it sonic.

@anon Oh, you had cited Sonic Hedgehog, but I didn't realize you already knew of the controversy surrounding it. The reason for the "Sonic", though, is that this is actually the fourth protein in a class of developmental-patterning proteins. The others are named after real species of hedgehogs: Indian hedgehog, desert hedgehog, and moonrat hedgehog. So it's not like someone just pulled the name completely out of the blue. No one ever talks about it, but I don't think those affected would feel much better telling them they had a defect in their moonrat hedgehog gene, either. :-)

@CodyGray - :) Thanks. I do understand the natural progression, but knowing the disease associated with it does (or should, imo) have some bearing on the name. For example, if there were a group of proteins called "camper proteins" that caused serious mental handicaps, I would not like to see one named happy camper, no matter how humorous that is. But, it's not in my hands, I'm glad to say.

@anongoognurse I believe the naming preceded the discovery of the diseases it caused.

Note that most (all?) of these names come from experiments in Drosophila. That the human homologs kept the same name is another issue. And if you think sonic is bad, consider sevenless, son of sevenless, junk (JNK)  and smack, mothers against decapentaplegia (mad), the list goes on. Drosophilists are kinda weird :P

@anongoodnurse: I think you may be mistaking the source of the name "luciferin".  It's from the Latin for "light bearing", and only (sort of) coincidental that it also happens to be a name for the devil figure from Christian mythology.

@terdon - Wow, I had no idea how... unusual some of those names could be.

@jamesqf - Please don't get me wrong; I love the name 'luciferin', and always have from the beginning. I admire wit (Wilde, Burns, Pope, etc.), and wish I had more of it. But it would surprise me if the researchers who named it were oblivious to the name of the mythological fallen angel.

@anongoodnurse: Not oblivious, no, but also not directly referencing it.  To name a luminescent protein "light bearer" seems obvious.  See also "luciferase", and remember that an old word for the common match was "lucifer".

Because their shape reminded researchers of rolls of Sushi (Ichinose et al, 1990):

These repeats were initially called GP-I structures because they were first identified in $\beta_2$-glycoprotein I. More recently, they have been called short consensus repeats or sushi structures because of their shape.

I thought it would be cool to add in a quote here from the paper, giving the explanation of the name in the authors' own words. Then I realized the paper you cited is merely a review that claims "More recently, they have been called…sushi". Following the next sentence is a citation to this paper, but that one never uses the word sushi. I'm curious if you know who the first author to use this term might be.

@CodyGray No idea. A lot of these terms enter the lexicon in labs and at conferences before they ever reach the literature.

Rumors of free alcohol offered in research conferences are completely untrue. I swear!

@terdon You're going to the wrong conferences, mate ;)

Special thanks for @JackAidley and also thanks for all the other comments.
I surmised that the explanation would refer to the shape of proteins, but I couldn't find any source which would tell me so. I also thought that it might be attached  to some kind of background story - my own example with precomplex Bötzinger - its name comes from Bötzinger wine served at the symposium in Heidelberg when discovery of this structure was first presented. You can never be 100% sure when it comes to weird names in science and their origins. Examples are numerous.
Once again, thank you very much!

@jack maybe. I don't really remember, it's all a bit of a haze. ;)


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Requirements for ability to reproduce
In my (albeit basic) biology classes in the past, we've learned about how, to reproduce, two organisms must have the same number of chromosomes. This has been verified by a few other websites I found. So- I've heard about various genetic disorders in which people can have fewer or more chromosomes than usual. For example, if a person had tetrasomy, they would have two extra chromosomes (48 in total). Chimpanzees also have 48.
Therefore:
If, hypothetically, a person with tetrasomy and a chimp's sex cells were combined, would it create anything?
If not, what are the other requirements for creating a baby organism besides the parents having the same number of chromosomes?

You seem to be more interested in the ability to mate with another individual than to reproduce. A lot of the reproductive efforts out there does not involve any mating (asexual reproduction). You might want to clarify that in your title. Also, you might want to highlight in your title that you are interested in differences in chromosomal number among the two mating individuals.

Can you please link to the few other websites [you] found?

The ability to produce offspring has more to do with the compatibility of the chromosomes than the number. This is why hybrid species (such as mules) are able to survive (but are infertile). If you want to learn about why hybrids are infertile here is stackexchange question about.
Although, this would all be dependent on weather gametogenesis could occur with the tetrasomy. But as seen here with Down syndrome, it can be successful.


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Artificial Hormones of human body
Can hormones of human body created artificially even i mean the hormones just consisting of bio chemicals and nothing else?

Human insulin was the first hormone to be artificially made by recombinant DNA technology and marketed  by Elli Lily.

Do u know why only insulin is possible until now not other hormones?

Other hormones have also been made using rDNA technology. Some of which I'm aware of are HCG and GnRH used for Induced breeding of fish. Now humulin synthesised is not exactly the same as natural human insulin it varies in certain amino acid sequences.

Its just out of curiosity that can new hormones be created for the body in order to perform new functions ?


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Gene expression for mouse feeder cells (inactivated MEFs)
I'm looking for a paper with gene expression data for mouse feeder cells, inactivated by gamma radiation or mitomycin C. Ideally I'd like RNA-seq data but I'll use microarray data if that's all there is.
I've spent quite a while looking (in GEO, Google Scholar, PubMed, etc) with no luck. Any leads would be appreciated.


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What does it mean to have a Y-DNA Haplogroup "R-M512"?
I did a DNA test to learn about my origins, but the results are highly technical.
I see I have a Y-DNA Haplogroup R-M512 and a mutation (zero marker in DYS448). I Googled these terms and came across a bunch of technical papers, but I don't have the expertise in Genetics to make much sense of them.
I wonder if one of you can shed light on this?

Normally Humans inherit from each parent one sex determine Chromosome. If you have a XX chromosome pair you are female. If you have a XY pair you are male. Therefore the Y-Chromosome get only passed on from father to son. The Chromosomes itself consist of DNA. The DNA consists of base pairs in which an A only pairs with a T and a C only pairs with a G. The Y-Chromosome has about 57 million of these base pairs. DNA is normally relative stable but from time to time only one of these base pairs randomly changes from a C-G base pair to an A-T base pair. This phenomenon is called a pointmutation. So imagen two brothers. One has the unchanged Y-Chromosome of their father the other has one this pointmutations. So the descendants of the one Brother have the same Y-Chromosome, with exception of the pointmutation, the same Y-Chromosome. This is called a Single Nucleotide Polymorphisms (SNP). In the millennia the Y-Chromosomes acquire more and more of these SNPs. One combination of these SNPs is called a Haplogroup. By the amount of SNPs and the kind of them you can reconstruct which Haplogroup descended from which one. You have the Haplogroup R-M512 which is a rather old one (https://upload.wikimedia.org/wikipedia/commons/d/d4/R1a._Info-19.05.2014.jpg) and could be found in great area. M512 is actually the name of the last SNP that defines your Haplogroup. Here some people had write down which Haplogroup they belong to. By the ethnicity of the name you can assume how far it is spread ( https://www.familytreedna.com/public/R1a?iframe=ysnp ).
Another Name would be R1a1a. Maybe these papers help you more to understand the nomenclature ( http://www.ncbi.nlm.nih.gov/pmc/articles/PMC155271/ http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1288547/ ).
Short tandem repeats (STR) are small DNA sequences that repeat multiple times.  On the Y-Chromosome these STR can be referred to as DNA Y-chromosome Segments (DYS).  DYS448 has the sequence AGAGAT  with 20 to 26 repeats. Here ( http://cstl.nist.gov/strbase/ystrpos1.htm ) is visualized where actually  it is located on the Y-Chromosome.  In your case the laboratory was not able  to measure any repeats.


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How does DNA from sperm fuse with DNA in egg?
I see this statement all the time "half of our DNA (23 chromosomes) are from mom and 23 are from dad". Fine, but which chromosomes in our nucleus are from each parent? When I think of nucleus (before interphase), I imagine a total of 23 unique chromosomes and 23 copies of them. In the first cell after reproduction (zygote), does chromosome 1 from mom align with chromosome 1 from dad? When zygote divides (after S phase) do you now have 4 copies of the same cell? Since choromosome 1 from mom and dad is the same.
What role does crossing over play in all of this.
I have done lots of reading but nothing is helping me connect the dots.

By "23 copies of them" I mean the "copies" that we receive from one of the parent. So in our nucleus, we have our whole genome X 2 (except Y chromosome, which is only once).

First, to clarify on the number issue and parental origin of the chromosomes. For the moment, disregard crossing over. Then, you would begin with an adult somatic cell in the growth phase, having 46 chromosomes, two of each kind, that is, 23 pairs (assuming sex chromosomes to be of the same kind, including the case in males). Then, in the S phase, each chromosome replicates, creating exactly similar sister chromatids, each of these sisters being similar to the single chromosome the cell had in growth phase. Each of these chromosomes with two chromatids, sends one to each daughter cell, making the daughter cell exactly like their parents. In meiosis, after this step, one of each kind of chromosome separates into a gamete, so that instead of 23 pairs, each gamete has only 23 chromosomes, one of each kind. On fusion of two gametes, you would have the original configuration again.

Crossing over, just means that when the two chromosomes of a particular kind separate during meiosis, they exchange corresponding material. If no crossing over happened, the gamete would either have one of the two same-kind chromosome, or the other. But due to crossing over, you create a different set of genes on these two chromosomes, different from the ones fond elsewhere in your body. So if say two chromosomes of the same kind have genes $ABC$ and $DEF$, if no crossing over happened, the gamete would have either $ABC$ or $DEF$. But crossing over makes possible combinations like $AEF$, or $DEC$ etc.


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How to increase contrast with only a top entry specimen holder
My question is: If my microscope had a top entry specimen holder, instead of a side entry holder, what additional option(s) should I have to increase the contrast with the same constraint that I only have a single objective aperture? Why would this option work?
Any ideas are welcome. Thanks in advance!

What is a top entry specimen holder? What kind microscope is it?

If your doing EM you can ignore, out of my area of know how :-(


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Why have whales and dolphins not evolved to have gills?
It seems at first glance that it would be an evolutionary disadvantage for a sea creature to have to come up to the surface on a regular basis in order to breathe, so why are there animals (e.g. whales and dolphins) which still need to do so?
If there is some advantage to breathing from the air instead of using gills, why haven't animals such as sharks (or indeed fish in general) evolved to do this instead?

Ever heard the expression "there's more than one way to skin a cat"? Living in the ocean does not require gills to breathe, it's just one of the suitable adaptations. Questions like this are near impossible to reasonably answer because the answer is simply "because they didn't evolve gills."

Just to be sure; are you aware of the evolutionary history of whales (i.e. their phylogenetic relationships)?

I don't know many of the details, but I seem to recall that they actually evolved from land animals, is this the primary explanation for why they still lack gills?

@Cliff Whales and dolphins are not just land animals; they are mammals (in fact they are phylogenetically related to hippopotamus). Gills are not present in higher animals.

@WYSIWYG I'm aware of this, but my question is why is this the case?

@Cliff and the answer is: just because that's the way things happened.

@Cliff It is because whales would require too many mutations to restructure their respiratory and cardiovascular system to develop back gills whereas they could survive in an aquatic environment with lungs and few mutations. The likelihood of selection of that many mutations without an obvious advantage is too less.

Another part of the answer is that it's probably a lot more difficult to re-evolve gills than to evolve the simple streamlining &c that is necessary to become air-breathing aquatic mammals.  There'd also seem to be no real pressure/advantage, since air-breathing whales, dolphins and so on are pretty successful top-of-their-food-chain creatures.

Looking at deepsea fish with gills, they tend to be sluggish and at a bare minimum of activity/expenditure due to the utter lack of oxygen at depths whales are known to frequent. So you have these enormous marine mammals, with enormous concentrations of myoglobin packing literal tons of oxygen, it elicits a much greater capacity for hunting etc. at greater depths. There are advantages to lungs in whales.

So first off, during development mammals produce pharyngeal arches, same as fish. Fish development turns them into gills, mammalian development into ears and parts of the jaw. It isn't too much of a stretch to assume that aquatic mammals with slight alterations in their expression patterns during development could revert to developing gills. I think the best answer is what @Kendall suggests. Gills are a pretty inefficient means of obtaining oxygen, and considering the amount of oxygen that a warm-blooded mammal needs to consume, oxygen efficiency would out select expression to form gills.

While the subject is different, the origin of your misunderstanding makes your question very similar to Why don't mammals have more than 4 limbs?

I marked the question as duplicate but did not expect my vote only would be sufficient to close it. I don't think I can undo it now.

I think you're looking at this the wrong way.
Animals evolve to fill niches. Many, many land animals returned to the water as a place to live, including:

whales, dolphins, porpoises, seals, sea lions, walruses, manatees, dugongs, otters, hippos, pygmy hippos, crocodiles, sea snakes, sea turtles, river turtles, river snakes, etc. etc. etc.

Their success in this environment points to no need whatsoever to "evolve" gills to be better suited. Without the interference of man, there would be yet many more of them.

Not to mention penguins (and should we count diving birds like ducks?), and in prehistory the ichthyosaurs, plesiosaurs, pliosaurs, mosasaurs, and probably more that I can't remember.  Becoming an ocean-going air breather seems to be a pretty successful ecological niche.

Gills are a really inefficient means of obtaining oxygen, while you have some cold-blooded creatures on your list, warm-blooded animals have an oxygen requirement that probably could not be supported by gills. Also, we have pharyngeal arches during development. Our developmental pattern produces ears and parts of the jaw, and fish get gills. I think it is less about no need than it would be unsustainable for a warm-blooded organism to try and supply its oxygen requirement with gills.

@AMR - you may have a point there! My point is that evolution is influenced by selective pressure, not "(un)common sense." Land animals returning to the sea started with lungs, and kept them. Fish started with gills, and kept them.  You state, "it would be unsustainable for a warm-blooded organism to try and supply its oxygen requirement with gills." (The great white predator seems to do fine. It is still about niches in my mind. However...) If you could add an answer that covers your point, the OP might get all the information they need.

Welcome to evolution.
Just because the idea is great, the path obvious (in our minds), does not mean it will happen.
Evolution works by random mutations followed by selection to weed out nearly all phenotypes that are less successful than the original.
So you need both the mutations and right selection environment.
So while gills on a sea going mammals is a great idea. The path towards that is not an easy outcome without some form of intelligent design. You see those gills arches fishes have to support their gills... well the tetrapod lineage has since re-purpose those bones to make several structures such as the thyroid gland, part of the jaw, the larynx, and the bones in mammalian ear. https://en.wikipedia.org/wiki/Branchial_arch
So a whale that simply reconverts to gills, would be without a larynx (mute), or inner ear (bad hearing) and parts of the jaw (Can't eat). So you can see alot of other work will need to be done to make such an animal work. And if this process is left to nature, each intermediate must also work successfully in some environment.
Such are the constrains of evolution.
However if intelligent design were available. No problem. It can be done. We can ignore temporary lowered fitness, and work with a desired outcome in mind.

Natural selection can only choose from the diversity available. Sometimes there are physiological or other constraints that prevent a solution we think should be optimal to arise. For instance, insects are the most diversified group of animals, but there are no marine insects. Why? It seems their respiratory tract (a tracheal system) can't deal with salt water. Or we can think of flying as something very advantageous, but flight has only evolved four times (insects, pteurosaurs, birds and bats; or five, if we include our flying machines). So "you can't always have what you want".
The precursor of gills can yet be seen in the early stages of mammal embryological development (they lead to the channel that allows you to unclog your ears by swallowing). But to turn them back into fully functioning gills would take so many mutations and the re-adaptation of so many working systems, that it's not a much viable option for large animals such as cetaceans. Remember that the gills first formed in the very first, very small vertebrates, and slowly acquired it's present shape we see in bigger fishes.


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What part of the body holds the most pain receptors?
What part of the body holds the most pain receptors or is likely to cause someone to feel the most intense pain?
I thought it was the eyes but I can't find that source anymore.

try looking at the a map of the postcentral gyrus, that will tell you which parts of the body have the most sensory neurons. I would guess the hands if I remember the homunculus right.

@John - The cornea is many times more sensitive than the fingers, with excellent reason (we use our hands to work with.) Imagine three grains of sand being rubbed between two fingers. Now imagine them getting dropped onto your cornea.

There is anecdotal evidence that the cornea is indeed the most sensitive tissue. Just think of it: our eyes well up with tears when slicing an onion. A tiny insect who flew into our eye feels enormous, and a corneal injury, say a scratch, can leave us severely compromised for a number of  days. Luckily, the cornea has rapid healing powers.
The cornea is so sensitive that part of determining the amount of brain injury one has sustained is by measuring the corneal reflex. The way this is done is to take a cotton swab and pull off some cotton fibers and twist them into a tiny tail (so to speak), and tough the cotton fibers to the cornea. If there is no reaction, that's a bad sign.
The Sensitivity of the Cornea in Normal Eyes
Evidence-based guideline update: Determining brain death in adults
Report of the Quality Standards Subcommittee of the American Academy of Neurology


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What is the present tense verb form of apoptosis?
For example, if I want to say something along the lines of "this signaling pathway causes a cell to go through the process of apoptosis", but I want to shorten the phrase "go through the process of apoptosis" to one word, what would that word be? I've been saying "apoptose" so far but I'm not sure if that's correct.

Apoptosise? I think most people would just phrase it as you have.

Personally, I would say "undergo apoptosis" being both shorter and not risking coining new word forms.

According to Google Scholar, there were ~40000 hits for "apoptose" and ~120k hits for "undergo apoptosis" in published literature, both of which had significant numbers of high-impact articles.
Therefore, it is clear that both expressions are sufficiently used in literature for either to be used.
Personally, I would say "undergo apoptosis" being both shorter than your original phrase and not risking coining new word forms.


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How far does eardrum move?
Sound waves move human eardrum back and forth, like the peak to peak excursion of speaker driver, how much is it though? Ofcourse this movement depends on sound pressure, frequency and even location on eardrum, the edge moves less than center just like rubber surround around driver diaphragm.
I am interested in center of eardrum, the part of it that moves the furthest. The SPL is 100db at the eardrum and I would like to know how far it moves at 20 Hz and 20 KHz. I know this is hard question without specific answer becose every person have different eardrum but I believe there must be some rough average, some decent estimation about how much is it.
Is it micrometers? Is it nanometers? Or does it exceed 1 milimeter?

Tympanic displacement measurement (TMD) is a well studied field using hi-tech tools (i.e. stroboscopic holography), and complex units:
Vm = volume displacement in nl nanoLiters.
μm/pa (UDTF) = Linear tympanic membrane displacement is known as the umbo displacement transfer function.
The graph on the left gives you a value of 0.8-0.6 = 0.2 microns:

The graph above can be seen as resonances in an images sequence of stroboscopic holograms of tympanum (cool name to call your band) https://i.sstatic.net/fD6E9.jpg
According to this graph a 94dB sound wave gives you 0.1 micron displacement and a 100dB sine wave gives you 2pa, 0.2 microns.
https://i.sstatic.net/O7nQL.jpg
The first research document on google gave me a volume displacement from -120 to -700 nl.
1000 nano Liter = 1mm3
So the TMD volume displacement when very loud can be 1-2mm3, and eardrum rupture probably occurs from 10 to 100 mm3.
There are even muscles in the ear that can modify the way that you hear, i.e. the stapedius muscle which protects against low fequencies, and perhaps which can focus your eardrum elasticity modulus to let hear different frequencies, perhaps conciously? fascinating, I don't know.
See also pages describing elastic measurement of the eardrum, energy transfer by the tympanum by the cone, through these two google search phrasings: "eardrum response measurement" and "tympanic membrane displacement measurement"
Here is research comparing the eardrum to microphone design which is written easily.

This was best answer I ever got here on Stackexchange, the whole thing you wrote is treasure saturated with the juiciest most valuable information. I never knew this TMD field exist nor did I ever heard about stroboscopic holography, I will study these things passionately, big thanks com.prehensible.

Cheers man, it's a very cool topic can do some YT videos from this kind of research. I design synthesizers so I am a fan of waves, sometimes on the DSP forums here.

I want to ask just one very important extra question, is that 0.2 micron at 100db with or without the ear gain? I ask becose the ear canal and outer ear can boost frequency around 3 KHz by up to 20db, thats 10x the pressure. Was that 100db measured at the ear drum or somewhere else before the ear gain happened? Wasnt it some dead body test where they cut out the middle ear and the outer ear was gone?

Yes for the dB graph: a uniform unit sound pressure was applied to the outer side of the tympanic membrane. https://springerplus.springeropen.com/articles/10.1186/2193-1801-2-527


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What is official term for contraction induced muscle "vibration"?
I can activate my tensor tympani muscles at will, it makes me hear rumbling bass sound becose the muscles "shiver / "vibrate" when contracted. Also when I put cleched fist to my ear I can hear it too. I read all muscles make makes this rumbling low frequency sound when contracted.
I wanted to study this thing but I run into the problem becose I dont know how is this muscle vibration officialy called. I dont know what words should I type to get relevant search results. I dont want anything about shivers, tremors or other stuff, I just want to know how is the normal muscle "rumble" called.

you may be able to post an answer to What causes “ear rumbling”?


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Most sensitive hearing human ever measured?
The Fletcher Munsen curve shows the lowest spl that humana can hear is -6db around 4 KHz.I assume this curve is average obtained from measuring many people.
My question is,what is the most extreme hearing in terms of threshold spl ever measured? What person holds the record for most sensitive hearing?


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How does the Platypus grow before it eats?
From this fascinating documentary on monotremes it is mentioned that the Platypus is born less than 1 cm in length, but has doubled its size by day three when it begins to nurse. How does the animal grow before feeding?
Surely by conservation of mass there must be some alternate process by which materials are being processed and absorbed by the young animal. Does it absorb nutrients from the air or surrounding environment? Sucking on dirt? Osmosis?

Plausibly, it could grow by intake of water (much like seeds germinating into seedlings). No citation so left as a comment.

The video is quite old and they knew a lot less about the species then.  They probably had to make some guesses.  Any modern reference I find doesn't mention any waiting period before nursing.
It seems to me that were this the case it would be very explicitly studied by now as it would be a real oddity for a mammal.  And we love platypus oddities.
Interestingly, the platypus doesn't actually have teets to be suckled on.  Instead the milk is expressed through their skin and into grooves on the belly that the newborns can drink from.

This doesn't really answer the question.

Why was this downvoted? Is it inaccurate?

Maybe I didn't state it clearly enough but the answer is "it does not".  There is no record of this in any literature I saw, other than the aged documentary provided in the question (with no explanation of the very odd physiology).


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Is bacillus strain 2-9-3 really 250 million year old?
I've read that in the last decade (I believe) some scientists discovered a microorganism, which they dubbed bacillus strain 2-9-3, in a crystal of salt that they think is 250 million years old and that started replicating when put in favorable conditions.
Is this really an example of the longest surviving life form?
Could someone confirm this is true and scientifically validated and provide some info and references that can be understood by non specialists. I'm a telecommunications engineer so I can understand general scientific approach and I have a basic understanding of chemistry and biology, but no formal or specific training on the subject.

Disclaimer
I was unaware of 2-9-3, but performed a simple internet search which brought up a an open-access paper from 2001 refuting the claim, and nothing more recent, suggesting that the refutation was valid. I mention this both to make it clear that although, like the poster, I am not an expert in the topic one can get considerable mileage through standard search techniques. (I do acknowledge that it does help if you know you can get access to papers through a University Library, open-access or not.)
Refutation
The claim was actually made nearly two decades ago in a paper by Vreeland et al. in Nature 407, 897-900. The date is relevant because at that time full-length sequences of bacterial genomes were only just appearing.
The paper refuting the claim is entitled “The Permium Bacterium that Isn’t” by D.Graur and T.Pupko and was published in the journal, Molecular Biology and Evolution 18 1143–46 (2001).
The authors put forward various indirect arguments for doubting the claim but they based their refutation on sequence comparison between so-called Bacillus permeans (2-9-3) and other bacteria. The first argument was that the 99% similarity of B. permeans to a contemporary halophilic bacterium, previously known as Bacillus marismortui, subsequently renamed Salibacillus marismortui, implied a relatively recent divergence from the latter. To rebut the argument that S. marismortui had also been trapped in salt for millions of years until recently a comprehensive comparison with other bacteria was conducted resulting in the phylogenetic tree shown below which was incompatible with the bacterium having not evolved in the last 250 MYr:

An independent analysis by Nickle et al. in Journal of Molecular Evolution 54, 134 (2002) came to a similar conclusion.
I am not expert enough to judge the methods of determining rates of evolution and relative distances between species, but it would appear that they are accepted by those in the field.


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What are hot spots on human body?
Recently I have just discovered that a certain amount of the mobile phone frequency can be absorbed by human tissues.
For example, this is the SAR info of iPhone 4s:

Head: 1.180 W/kg 1 g
Body: 0.491 W/kg 1g
Hotspot: 0.491 W/kg 1 g

http://en.wikipedia.org/wiki/IPhone_4S
so hotspot means a hot spot on human body right?
Then question is:
What are hot spots on human body?

"Hot spot" does not refer to anything on the human body, but   testing while using the phone's "Personal hot spot" feature: http://support.apple.com/kb/ht4517 See also the documents on "RF exposure info" at https://apps.fcc.gov/oetcf/eas/reports/ViewExhibitReport.cfm?mode=Exhibits&RequestTimeout=500&calledFromFrame=N&application_id=134990&fcc_id=%27BCG-E2430A%27

I think hotspot in that context means the highest exposure amount as this document shows (https://apps.fcc.gov/eas/GetApplicationAttachment.html?id=1544448), which comes from the reference the above wiki page provided.

@ Bez, i don't think so, hotspot mean "if iPhone works as a WiFi hotspot" & the Wi-Fi hotspot can generate WiFi electromagnetic radiation). I opened a WiFi last time & I suddenly feel a litle bit of uncomfortable when sitting next to it so i have to turn it off. (http://www.radiationtalk.com/info/wifi_radiation.php)

The author has listed the Specific absorption rate of radio frequencies and asked about hot spots which is not something associated with the human body and is a mobile phone technology (to my knowledge). The question is just wrong and the author has not made relevant efforts to understand the topic before placing the question.

I vote to keep open. The question is reasonable and easily answerable:"Hot spots" in this context does not refer to anything on the body).


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What are the naming conventions for mutations of proteins?
I have been reading about Maltose Binding Proteins. Mutant forms of the molecule seem to be named MalE_ where the _ represents a number, for example MalE36 or MalE50.
Please can someone explain the naming convention for this? i.e. what does the 'E' stand for? Does the number refer to the amino acid that has changed?

I know that usually both amino acids and the position are named, for example BRAF V600E means an exchange of valine against glumatic acid at position 600 of BRAF.

What your example is referring to is the change in the glutamic acid (E) amino acid (AA) residue, which is in position 36. This is denoted so that people/scientist would know what has been changed and usually there should be another letter after that number such as Y, which is tyrosine, to denote what it has been changed to, if it is a substitution. Then there is the delta (∆) symbol to denote deletion, and usually a number range e.g. 36-50 or just a number e.g. 70 appears after it to denote if a protein has been truncated in a certain AA range or if the entire protein from that AA is truncated, respectively. Sometimes (quite often now a days) the delta symbol is followed a protein domain name such as SH3 or RA to denote that a protein domain has been deleted and people use all sorts of naming variations for a protein that has been altered from its native sequence, which can be confusing!!
These are just some conventions, which isn't documented very well and you just figure them out when reading a few papers but I would welcome any edits for a good source for protein change annotations.
EDIT:
Since as pointed by Alan Boyd response, MalE is an E. coli gene encoding Maltose Binding Proteins, then my answer will not apply for any protein AA changes as correctly pointed out and elaborated on in Alan Boyd response.

MalE is the gene that encodes the maltose-binding protein in E. coli. If you look at the genotype of any E. coli strain you will see similar nomenclature. Everything in the answer from @Bez is correct, but in this case the E has nothing to do with glutamate.
The numbers are probably just arbitrary numbers that were assigned to the individual mutations, but you would need to provide a link to a source before this could be confirmed.