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What makes red meat less healthy than seafood, after millennia of evolving to eat meat?
We are told that red meat is carcinogen; fish and white meat are not. What make us not "compatible" to red meat after thousands of years of evolution and meat eating, and yet seafood is opposite ?

Compatible is not a biological term in this case. We're compatible with red meat, and all the other good stuff, because we can eat it, derive nutrition from it, and survive long enough to reproduce. That's all it takes to be a viable member of the biosphere. Also, please consider that the Sun is a carcinogen too. Being carcinogenic does not disqualify it from being consumed by humans. Think cigarettes and barbecue.

Right. Even if compatible is not a correct term, I suppose the question is understood by everyone. Beside, you made a good example for my point : The sun is carcinogen, destroys tissues and we are exposed daily, therefore evolution drives the darker skin of certain race to counter that.

@Kenny - Please cite a reliable source that states red meat is a carcinogen. To my knowledge, it is not. What are co-carcinogens, though, are the products of grilling/frying/searing it over high heat. The same is true for grilling/frying/searing fish if there are any fat drippings (either from the fish, or from the sauce used to baste the fish. Since most fish isn't fatty, this is less of a risk.) Red meat can cause other problems, but a direct link

http://www.who.int/features/qa/cancer-red-meat/en/ "Red meat was classified as Group 2A, probably carcinogenic to humans" (limited evidence), and the fact that several renowned doctors in France recommend some friends of mine to stop eating red meat while treating cancers.

"We are told..." by people with quasi-religious agendas, like vegetarianism.  It's a good idea not to believe everything you're told without considering the source and/or looking for independent confirmation.

I've also voted to close because the question seems to be based on an incorrect assumption (that red meat is a carcinogen).

Sorry, but read meat IS a carcinogen that contributes significantly to colon cancer. Also, charred meat, as you mentioned, is a co-carcinogen. Kenny should not have to provide evidence for some of the minor details of his question. I have edited the question so that it makes more sense, but it seemed clear to me from the start.

If you read that article carefully, it supports my position quite clearly. There is no convincing evidence of a link, the only possibility is colorectal cancer, and who knows but that may be gut flora, etc. @KarlKjer - It is presumed to contribute to colorectal cancer. There is a great difference between presumption and fact.

@jamesqf True.But aren't all knowledge in the form of "we are told",or are you born knowing how to count? Second,human will never agree 100%, see round-earth fact. It's a good idea to take into account,not blindly,expert opinions in the fields we don't know when a large amount in that group agrees, especially in highly controlled domain like medical. Until agreed otherwise (e.g religion-never debunked, or slavery-agreed otherwise). Will you follow advices to treat syphilis according to the majority of medical advices now,or let it grow with a yet unproven chance of becoming superman later?

@anongoodnurse bolstering my point about "majority" against "convincing evidence". Even for agreed treatments, there is no 100% success rate. Clinical trial is always a statistical "majority acceptance amongst subjects". People are still debating if smoking is linked to cancer. That's because the number of known and unknown variables affecting health outcome is so huge, noone is certain and have to rely on "majority". Look at how we have thousands years of weather info and still cannot tell with certainty if it rains tmr. Talk about butterfly effect...It's a gray area and never definite.

The fact that there's no 100% success rate in treatment has absolutely nothing to do with causation. And, fyi, no one is seriously debating that cigarettes (or asbestos, or alcohol) cause cancer. Rain tomorrow? These are false equivalencies. They don't bolster your argument, they weaken it.

I beg to differ. First, about your argument Noone is seriously debating about the effect of cigarettes or alcohol, please refer to last month 's http://time.com/5376552/how-much-alcohol-to-drink-study/ "A New Study Says Any Amount of Drinking Is Bad". Wouldn't you call it debating over a 'fact' people seem to agree for years ? Aren't clinical study to prove a causation "Is drug A effective (more effective than drug B) for disease D ?" Rain tomorrow : ever noticed rain forecast tomorrow changes when it suddenly rain tonight ? The fact of raining today causes the chance of raining tmr to change.

@Kenny: No.  To use your example, we can deduce counting from observation.  WRT "we are told", it seems that there should be an obvious difference between "told" meaning the (repeatable & testable) results of scientific studies, and someone making up claims because it fits their agenda.  So where are the scientific studies showing that red meat causes cancer?  Whereas a couple of minutes with Google finds studies like this one https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4691673/ showing no overall difference between vegetarians & meat eaters.

Interesting question that reveals a very common misconception about evolution. Evolution is not the same as optimization or advancement. It is about selection. Cancer and heart disease mostly kill people AFTER they have had their offspring. Selection does not generally act upon post-reproductives. So anything high in fat, calories and proteins would be likely to help humans survive starvation, and live to reproduce. We do not evolve to beat the diseases of old age, and our genes can be 10,000 years behind present optima. We don't evolve to be happy, live long lives, or be nice, unless these things help more of our offspring to survive.


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What species of arthropod is in this picture?
I've found exactly one of these, dead, on my kitchen floor most mornings this past week.
It looks like a large flea, is about 1 cm long (picture compares it to a British 10 pence coin, approx. 24.5 mm in diameter) and 2 mm thick with a laterally flattened body.
I believe it to be of the order Siphonaptera, but am unsure as to what exactly it is.
Can anybody identify the exact species of this arthropod?
If it helps, I live in the South-West of the UK.

Doesn't look like a flea, to me. Fleas have saliently long hindlegs.

Don't worry, it is not a flea, nor is it an insect. Looks like a crustacean to me (like a pillbug), but I am not sure of the species.

This is an amphipod, or "scud" (think of a pillbug that's flattened side-to-side rather than top-to-bottom); they're usually aquatic.  Getting past that point will probably be difficult (impossible for me, as I don't know the British fauna of the group).

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In PCR what is the chemical makeup of the primer? DNA or RNA?
I'm thinking the answer is RNA. Is that right?

You could improve your question by editing it to add why you think/thought the answer was RNA.

Almost always DNA. While RNA is possible, it’s much harder to synthesize (and keep stable) and DNA results in a purely DNA result that won’t need to be replaced with DNA later.

PCR primers are short pieces of single-stranded DNA, usually around
  20 nucleotides in length.

You can read more about PCR on Khan Academy or Wikipedia.

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What is this aquatic organism in Fiji?

I found them under reefs in Fiji. The hand-like structures moved slowly. I was not sure if it was an animal or plant. I was not even sure if they were several individuals or it was a whole.
The part that was not hidden by the stone was about 50cm length. I did not touch them, since I was not sure if it was dangerous.

What size is this?

the part which was not hidden was 50cm length.  I did not touch them, since i was not sure if it was dangerous.

They seem like sea-cuecamber (Holothuroidea).

It is probably Holothuria leucospilota
Holothuria leucospilota is a medium-sized sea cucumber reaching a length of up to 40 centimetres (16 in) when relaxed but it can stretch to about a metre (yard) when extended.
Holothuria leucospilota is found in shallow water along the east coast of Africa and in much of the Indo-Pacific region. It is a common species on the north east coast of Australia where it is found on reefs and rocky coasts, often partly concealed under a boulder.
References
https://en.wikipedia.org/wiki/Holothuria_leucospilota

Please provide more explanation, links, etc., that help others understand why you think this is the answer.

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How have single-celled organisms learned to survive?
Upfront: I am a computer science student trying to understand evolution and its implications.
I've been pondering the concepts of evolution for some time, especially related to neuroscience / how the brain works / how to emulate brains. I wonder how single-celled organisms evolved at all. I know, they don't "think"; but once their ATP levels get low, they know they must find food to sustain their system, aka staying alive. This is probably no active decision, more like: "The enzyme concentration tells me to find food".
Question: Was the entropy just high enough that at some point those organisms had the property that finding food somehow is preferable to death? Edit: How can an organism perform something without "knowing" it needs to perform it?
I hope, this isn't a terribly stupid question.

Do you think the following is a good reformulation of your question: Not all responses to environmental stimulus are performed consciously. How can unconscious responses be made? How can an organism perform something without "knowing" it needs to perform it?

If the above is a good reformulation then note that 1) it is rather unrelated with the field of evolution (except by the extend that everything in biology is related to evolution) and 2) Any living organisms has unconscious responses to environmental stimuli (incl. humans). The question has no reason to be specific to unicellular organisms.

@Remi.b Yes, especially the last part of your suggested reformulation is better than my own question. I will edit my question accordingly.

@Remi.b I know, that this is not specific to single-celled organisms. I hoped, that by reasoning about simple life forms, one can deduce answers for more complex ones. If simple organisms "know" it is necessary to find food or procreate, more advanced organisms should know that too, right?

@Charles I see you have the same point as @Remi.b; at some point those organisms must have learned, that one response is better than another response to a specific stimuli. Is it just trial and error?

@Charles For me, it's just hard to grasp, that evolutionary forces (in the sense of natural selection and mutation) or entropy were "high" enough to allow enough variation in the first and succeeding generations of organisms to "figure out" the basic (and increasingly complex) processes of survival and the corresponding actions.

You would be better off retagging this as a question about microbiology, ethology, and possibly  neurology. the organisms don't need to learn anything the simplest behavior are entirely fixed the organism does not decide anything.  Its not a bad question it is just not very clear what you are asking without the discussion.

Nothing more than physics
Simple physics
If you drop a rock, the rock will fall to the ground. If there was a table underneath, the rock would stop its fall when reaching the table. Clearly the rock response to the environment but the rock does not need to be conscious (whatever you mean by "consciousness") of anything in order to response to the environment.
Explanations for a programmer
As you are a programmer, you will agree that when you do std::cout << 3+2 << std::endl;, nothing more than physics is happening so that the value 5 followed by a newline gets printed to the screen. It is relatively complex though. So complex as it may feel quite magical before having spend many hours learning about computer engineering.
You understand that if you write a, say, boids program, all that is happening is just a bunch of addition and multiplication (eventually a power). The program does not need to be "aware" of what it is doing (nor do the individual agent) in order to respond to the change of behaviour of a predator.
You could even write a self-learning algorithm and you would still accept that there is no consciousness involved but only very simple operations.
Biology
Living things are pretty much the same. They are relatively complex (more like a computer than like a rock) but essentially the same. Also, the response tot he stimulus is often (not always) adaptive as it has been selected. But at it's core there's nothing more than physics involved!
More info
If you want to learn more about the mechanism of living things in general, you might want to just open an intro book or have a look at an intro course such as Khan Academy > Biology for example.
You can as well pick a simple response to an environmental stimulus and study its mechanism. How about having a look at chemotaxis for example!
Note that you might also want to follow a short and introductory course to evolutionary biology such as Understanding Evolution for example.

Thank you for your answer and suggested readings! Maybe you are right with your first observation, that I concentrate too much on single-celled organisms. They are really just simple, biological state machines. As a computer scientist, it's just highly interesting to find out more about biological systems and how cognition evolved.

I understand your point that "it's just physics", especially with lower life forms. However, how do things change with, say, mammals? Or probably anything that has a nervous system with a lump of neurons acting as a brain? Then, those stimuli certainly influence the behaviour of the organism, but based on experience or other internal assessments of the situation, the chosen behaviour may be different.

Of course, the brain can also be seen as a very complex state machine, where neurons fire just differently after experiencing events ("learning"). Probably I should just do some reading to figure out how to better formulate my question about life and how the sum of these basic processes forms into something we call "intelligence" for higher life forms :)


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Abnormal Prolactin Level
I want to know what makes the balance of the Prolactin abnormal. Is that related to the presence of a nodule near the pituitary?

It could be, but this website is NOT for medical advice. If this is your personal condition, please seek a qualified medical professional. If this is a hypothetical condition, please clarify exactly how Prolactin levels are abnormal (hyper- or hypo-) and what you mean by 'nodule near the pituitary'.

The main abnormality in prolactin levels is hyperprolactinemia, meaning blood levels of prolactin above the normal range, not during pregnancy or lactation.
The major cause of these abnormal prolactin levels are tumors consisting of pituitary lactotroph cells--called prolactinomas--which secrete prolactin. This is generally corrected with synthetic dopamine analogues, as dopamine negatively regulates secretion of prolactin in lactotroph cells.
Here is a 2010 review with further detail:
http://joe.endocrinology-journals.org/content/206/1/1.full.pdf

Prolactin is a hormone which is produced by the pituitary gland.  Prolactin is named because it was found to be elevated in women who are lactating, its also produced by men and in elevated levels during sleep. Because of this, like many blood factors and hormones it probably has more than a single purpose.
When there is an abnormal growth from the pituitary gland, since the tissue produces prolactin, abnormal pituitary tissue can also produce extraordinary amounts of prolactin. I don't think this means that its a cancer, but its a sign that there is an unusual pituitary condition. It can even be the result of taking some drugs.
Most of these tests are from experience - we find that this happens a lot, but the causes are usually not understood well. Cancers in particular are quite unpredictable and can have many different properties from one case to another.  Pituitary tumors are the most common central nervous system tumors, so common they are found in autopsies 3-27% of the time, often never having been found previously.

I am not sure whether I understand your question right, but prolactin levels can be abnormal under several conditions like cancer, drug abuse, stress, breast surgery etc.
Its secretion is mainly controlled (inhibited) by Dopamine. Other hypothalamic factors like VIP, TRH, PRH etc. are enhancers.
Please specify your question for a detailed answer.


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The difference between "Hunger" and "Appetite"
When I am "hungry", I need something to eat physically. But what about "appetite"? I think it is a psychological phenomenon. Is that correct?


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Can Bioluminescence drive photosynthesis?
I'm trying to construct an anaerobic kitchen-waste digester at home.
The major output from the digester is methane - with a significant component of carbon dioxide. To scrub/reduce the CO2 I was thinking of passing the methane through a freshwater container charged with algae ... then it occurred to me to also think of introducing some bioluminescent algae to drive the photosynthesis & absorb some of the oxygen released by the other algae. Understandably this would be an unbalanced system.
But ... can bioluminescence drive photosynthesis?

Sounds like an interesting project. But why not just expose the algae to sunlight?

Also, what are you going to do with the methane?

Don't laugh. I forgot why I didn't want to expose the algae to sunlight ... To answer the second question - burn it!

This mainly depends on three things: The emission wavelength of the bioluminescence, the intensity of the bioluminescence and the optimum wavelength of the photosynthesis. I don't have actual numbers, but my educated guess is that the bioluminescence, even if the wavelengths fit, is way to weak to show an effect.

this is like asking if opening a refrigerator in the kitchen can cool the kitchen.  it can, but only if you spend a lot of energy.

@shigeta - No, opening a refrigerator in the kitchen can only warm the kitchen.  The more energy you put in, the warmer it will get.  You can cool the kitchen if you put the refrigerator half in the kitchen and half in some other room (or outside).

@RexKerr that was more or less my point.  the open freezer is a freshman thermodynamics talking point.  For the same reasons, you could never create a closed  bioluminesence photosynthesis cycle.

@shigeta - Refrigerators are reasonably efficient air conditioners.  The key is not how much energy you expend, it's the configuration of the heat cycle (i.e. cooling coils and open door not in the same room if you want to reduce the mean temperature in one room).  It's really not analogous at all--here the issue is that you need the methane processed, and providing light input (and methane as the carbon source) is one way to accomplish it.

@shigeta: (+: I did expect it to be unbalanced. Off-topic, the depth of these inter/co-dependent networks in nature make one revere that nature developed so. Imagine the number of broken branches of evolution & mutation that must have occurred to develop to our present day ....

Yes and no. Yes as in the energetics do work out and you will be going down a small but non-trivial driving force as long as you continue to provide the luciferin to the algae.
However, the wavelengths of light by which photosynthesis absorbs its energy are well defined and narrow. As a result, light sources for photosynthetic organisms have to be fairly strong and bright to cover the whole spectrum to provide the necessary light. As a result, your bioluminescent algae will also have to emit light at the desired wavelength to achieve a high photochemical efficiency and provide light to both Photosystem II and Photosystem I which have different wavelength requirements.

(source: gsu.edu)

"Marine species tend to emit light of wavelength between 440 and 479 nm (bluish), which is the range of greatest optical transparency of seawater." - http://www.quantum-immortal.net/physics/biolum.php
So it's in the correct wavelength range, but I'm with shigeta - it's not going all that efficient (unless, of course, there's the possibility for breeding brighter algae).

Curiously enough, this was the subject of a paper in 2013. The authors claimed to have driven photosynthesis by submerging some dark-adapted leaves into a solution containing a mixture of luminol, hydrogen peroxide and horseradish peroxidase (HRP).
They measure the levels of starch on the leaves produced in three different solution concentrations and bioluminescence irradiance levels.
As the leaves were severed from the plant I do not see much of a future in submerging leaves or an entire plant in this solution but it would be interesting see how algae would react. Also, I am very curious the luminol could potentially be injected in the plant, although this might be far fetched.
The link to the paper below:
https://pubs.rsc.org/en/content/articlelanding/2013/cc/c3cc45264f#!divAbstract

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What is this cloud of red pond creatures?
Today I came across a pond in the Netherlands where I noticed a cloud, for lack of a better word, of small red creatures swirling around near the surface of the water, as can be seen in this video:
https://youtu.be/ZQMox-bbJ9s
And here is a picture:

The surface was unfortunately quite reflective, but the motion is visible. The creatures were too small for me to see any structure to them with the naked eye. Some tadpoles can be seen in the video, which are much larger. They would swim straight through the cloud now and then, so perhaps the tadpoles consider the red stuff food. The entire cloud consisted of various dense clusters connected with less dense or thinner parts, as can be seen to some extent in the video, and its total size was perhaps 2 meters or so.
What was I looking at?

Can you kindly add some pics/screen-shots here too as: 1-) Not everyone can check a video link 2-) External links are prone to modifications or even deleting. Thanks!

Where were these pictures taken? Also,the video is too short.Try to get a longer one next time.

You don't say where this was, but my first suspicion would be some sort of algae bloom.

@JeffreyBarber it was in the Netherlands, I added it to the question. Are algae generally mobile?


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What mushroom species is this?
Found in garden ,Brisbane Australia at base of trees and amongst plants in open ground

you need a decent mushroom book m8. flipping through the pages of a well photographed book always leads to a close ID, and good ones have spore drawings too.

Could you describe the substrate they were growing on? For instance were there wood chips under the plants, or were the fungi growing on soil? Did you get any photos of the stipe (stem, if any) and a clear shot of the pattern of the gills?

These look like they fall under the description of 'gilled fungi with lateral or no stipe' (there looks to be a lateral stipe on at least some of the fruiting bodies), so it should be in https://www.fncv.org.au/wp-content/themes/field-naturalist/publications/fungi_in_australia/fia-8-pg-lateral-stipe.pdf. Crepidotus crocophyllus sounds like a close match, but the pictures don't seem to agree as closely...


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Species identification - What is this "bug"
The title says it all. What the heck is it?

Edit:
I found this on my car, in Kansas city.

Well, it's a spider. Other than that, can you post the approximate location you found the spider so we can narrow down the possible species?

After trying to dig through this list the closest I can get are the Araniella species, some of which are white. But the pattern of dots is wrong, and the leg lengths look wrong too.

@user137 I updated the question.

After conducting a small investigation, it would appear most likely that the spider captured in the attached photograph is an arachnid in the family 'Thomsidae' or 'Crab Spiders'.

Although the proposed genus of Araniella proposed above by user137 shares a superficial similarity to this family, thomsids generally do not construct webs to ensnare prey - I might hazard that the web on your car does not hold the same structure, as shown below, to that of an Orb Weaver Spider (Araniella).

From the available information it is challenging to propose a genus, let alone a species. Based on the location of the car, I may propose the sub-family Misumenoides or genus Thomisus.
The general characteristics of crab spiders are the ambush of prey as opposed to trapping prey; the inverted V-shape under the cephalothorax; and the sideways movement of certain species in the Thomsidae family. It is of interest to note that any member in the population could vary appreciably in colour.
Wikipedia article concerning Crab Spiders available from: https://en.wikipedia.org/wiki/Thomisidae
Britannica regarding Crab Spiders available from: https://www.britannica.com/animal/crab-spider
Information regarding Misumenoides is available from: https://en.wikipedia.org/wiki/Misumenoides

This answer makes sense. I grew up north of KC and saw several crab spiders, but I don't remember any white ones, I was also confused by the web, because I never saw crab spiders on any web at all. But the leg lengths look more appropriate for crab spider. If @Gogeta70 can provide more detail about size and behavior, that would help confirm the answer.

It stayed in the same spot on my car for over an hour. And the width of its long legs was about as wide as my thumb. Thanks for the answer!


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What's the difference in roles of GATA-2 and BMI-1 in guiding Hematopietic cells?
I've discovered that hematopoietic cells become lineage-positive (Lin+) and go down the path of becoming lymphoblasts and myeloblasts, and that both BMI-1 and GATA-2 are transcription factors that play a role in that.
What is the specific difference in the role of BMI-1 and GATA-2 in guiding a hematopoietic cell down either of those lineages?


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World population pyramid since 1800
I am interested in understanding how the global population pyramid has changed in the last couple of centuries.
I have two questions:
1) Has this been calculated? Are there estimates of population pyramids from the 19th century? Or from the beginning of 20th century? The earliest I have seen is 1950 (below).
2) If it hasn't been done, how can I construct it? It should be possible to model the population dynamics using birth and death rates (I would be surprised if this hasn't been done, as it has many applications outside of demography - e.g. economics).

I'm voting to close this question as off-topic because it is not a question about Biology in the terms of SE Biology.

@David: I have edited the question to emphasise the population dynamics aspect. Similar questions have received answers, e.g. here: https://biology.stackexchange.com/questions/36715/what-is-the-percentage-of-people-living-in-england-in-1500-ad-whose-lineage-is-s?rq=1

Also this one here: https://biology.stackexchange.com/questions/32981/human-population-growth-where-can-i-find-the-data?rq=1

Just because people answer questions that are not about biology sets no precedent. The site is adminstered by its users and not everything that should be is caught. I just call them as I see them. It will take another four like-minded reviewers to put your question on hold. They may not materialize.

Makes sense. Let's see how the others see it. And I would be of course happy to migrate the question elsewhere if anyone has ideas of a better fit.

Global seems like quite a far fetch to find out for one of us. It's therefore a research question, you would find out by searching for as old pyramids as you can find for various population types in the past and present and making an estimate of totally un-industrial types versus transition and modern types.

I am voting to close because it is a question of geography, not Biology.

@EOO The first post you link is clearly about population biology. The post you linked (which I asked), I agree, is arguably more about geography than biology.


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Can anyone help me identify this insect?
I'm trying to identify the insect below that I found in Edmonton, Alberta, Canada. Any help would be appreciated.

Where was it found?

Edmonton AB, Canada

Also, what type of environement was it found in? Forest, grass, in the basement, etc...?

it was flying in my garage while the door where open. I assume it's terrestrial but I'm not 100% sure


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Identification of an insect found in Edmonton, Alberta, Canada.
It's 8.5mm long found in front yard. Unusual wing shape. Sorry about the images: the insect is so small my camera was struggling.

Thank you but I'm looking for more specific answer,the species name or at least family


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Do plants sleep under ultaviolent rays?
I observed Phyllanthus reticulatus is sleeping during nights. I want to plant this species indoor under a UV device.  Do these plants sleep under ultraviolent rays?
(Sleeping means leaves are close to each other)

For this answer, I'm going to assume that by "sleep" you mean that it maintains a circadian rhythm/photoperiod. Recent unpublished research indicates that even protoplasts maintain their circadian rhythm under UV lights so the UV light isn't the problem. In order for the plant to "sleep" like you mention, the photoperiod needs to be maintained. The UV light needs to be on during the day and off at night. If you leave the UV light on all the time you would actually perturb the plant's photoperiod and it would be very unhealthy. Plant metabolism and photosynthesis requires both dark and light reactions. In summary...yes, the plant will sleep but you must maintatain the photoperiod by switching the UV light off and on.


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Can chain-linked genetic segment data be used to reliably assign unknown relatives to either the donor's mother or father?
I am analyzing DNA matching segment data, and I am trying to broadly group all DNA matches by my donor's parents.
Based on documented evidence, I can confidently identify "Person 'B'" as a familial match to my donor "Person 'A'" via a particular parent.
Is it probable that extrapolating the assignment of family members to each of the donor's parents by 2nd and 3rd step matching will yield accurate results?  I will explain my question more clearly below.
In my graphic below, persons 'A' and 'B' are known relatives via paper trail documentation.  "Person 'C'" shares common DNA segments with both 'A' and 'B', so I want to know if it is safe to accept "Person 'C'" as being related via the same parent as "Person 'B'" is to the donor without a supporting paper trail.
Furthermore, if it is indeed acceptable to identify person 'C' as being related via the donor's same parent, would it be safe to also assume that "Person 'D'", who does not match "Person 'A'" (aka the donor) or 'B'(the paper-trail linked relative to the donor) on the same segment as "Person 'C'" but matches the donor and person 'C' each on unrelated segments, is a genetic match via the donor's same parent?
Here's a graphic to illustrate my scenario described:

If, in the illustration, person 'B' was known to be related to 'A' via the donor's father's side, is it highly probable that person 'D' would also be related via his father's side as opposed to his mother's side?
For the purpose of this question, assume any direct descendants of the donor are excluded from the analysis, only ancestors and branching descendants (parents, uncles, cousins etc.) are included .

Much depends on how unique your "matches" are. If they are short matches of low-polymorphism stretches of DNA, they are not worth much.  I'm a bit confused about what you mean by "related via ... side" in your examples. Posting one or more possible or putative family trees would help clarify things.

I'm finding that the answer is no. At least without considering polymorphisms. I did this across the donors father's matches, and the result is that about 84% of the donor's DNA would have come from his father. So that's definitely not right.


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Identification of a bug, Anobium punctatum?
At first I feared that our old building was attacked by Anobium punctatum. But now, I'm not so sure.
Each week we find 2-5 of them around our apartment. What are they? and should we worry?
The bugs were found in our apartment in Denmark.
UPDATE Added Picture of Antenna

If you can get a photo with a clear view of the antennae, that would help.  At the moment, I'm thinking Dermestidae (Carpet and Larder Beetles, among others), but am not certain.  Mind, if I'm right, you DO have a problem, and WILL want them gone ...

+1 for a great and detailed photos!


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Can distilled / deionized / demineralized water "attack" teeth?
Demineralized water is claimed by some resources to be highly aggressive (due to their lack of minerals) and to attack all sorts of materials. From the World Health Organization website:

Demineralised water is highly aggressive and if untreated, its
distribution through pipes and storage tanks would not be possible.
The aggressive water attacks the water distribution piping and leaches
metals and other materials from the pipes and associated plumbing
materials.

Teeth are constantly going through remineralization and demineralization processes and demineralized water has neutral pH in room temperature which is positive for promoting teeth remineralization.
However I wonder if such water in practice rather promote demineralization when in contact with teeth by means of leaching of minerals from teeth to water due to their lack of minerals?

Interesting question.  My first thought is how does demineralised water "attack" materials?  Other web sites claim it, but I have not found one that provides a mechanism.

From a corrosion perspective , "pure" water is considered a problem for common pipe metals.

If you read your source all the way through, the answer would/should be, "Of course! It's pretty awful stuff!" If you search for reliable sources, you won't find too much literature on the subject, but you will find more on the effect of soft and hard water on health (soft = low levels of Mg/Ca; hard is opposite.) I'm not completely disagreeing with the author, but people need clean water however they can get it. I would not drink distilled water, mostly because it tastes awful, it's expensive, and I have access to safe drinking water. I doubt it's an idea liquid.

@User65535 - Water is a solvent. It will leach metals from metal pipes (like lead, causing lead poisoning) or other elements from other surfaces. If you want to know more, read about problems associated with reverse osmosis in home water treatment systems. Or study chemistry. Or something.

I’m voting to close this question because as other users have already indicated this: 1) lacks evidence of prior research, 2) is phrased as a personal medical question, and 3) is primarily a chemistry question. Please take the [tour] and consult the [help] starting with [ask] for details and [edit] or delete your question accordingly.

@tyersome For me the subject is pure curiosity. I've edited the question to emphasis it's relation to the biological processes, changed wording to "claimed by some resources" and to be more "neutral" (sound less like medical question).

Here is a list of mineral dissolution rates in pure water. they ALL dissolve, even quartz. The figure for quartz is 4 × 10−14 mol/m2s at 25'C:
https://pubs.usgs.gov/of/2004/1068/pdf/OFR_2004_1068.pdf
There's carbonate rocks and phosphate rocks including fluorapatite at the end of the study, it's quite complicated, although they do weather in pure water.
Rain is demineralized water which has had time to take in carbonic acid from CO2.
Teeth can actually become stronger and remineralize when the mouth has a pH of 7.5 or above. ref. Demineralized water contains no minerals though, so it will only erode the teeth.
Up to pH 9 is the highest range recommended by the health authorities locally where I live, and it's quite common to have tap water at pH 8 that leaves white residues on taps. It may be annoying, it's very healthy.
If the local water leaves limestone flakes, that's ideal for teeth. If it doesn't it's not very good. Fluorapatite has a pH of 4.5, it comes from fluorine toothpaste, it has higher acid resistance comparatively.


text:
Can a plant be induced to accelerate transpiration?
Just what the title states.
I wonder whether it is possible to fire a chemical switch - sort-of like injecting adrenaline in a human, to accelerate a particular process in a plant. For example, transpiration.

With high(er) temperatures, especially in drier air with a bit of breeze, a plant will transpire more. While not a chemical solution, it is indeed a mechanism that serves to cool the plant.


text:
Is stereo olfactory ability restricted to humans?
Most animals I see around seem to have two nostrils - humans, snakes, birds, fish .. and so on. From reading online I see that 2 nostrils provide a stereo olfactory effect. This stereo effect is caused by the difference in flow of air through the nostrils.
Does this stereo effect apply only to humans? Are there any animals that have a different number of nostrils? Say, more than 2, or less.

Moles and rats also smell in stereo (Catania 2013 and Rajan et al 2006), as do desert ants (link).  The latter is rather interesting, given that ants "smell" using their antennae, which suggests multiple sensory structures, not necessarily nostrils, are required for stereo olfactory ability.
EDIT: Hammerhead sharks have two nares and also stereo olfactory ability (here).  Dolphins have one spiracle, as do a number of other cetaceans.
It's actually not clear whether humans have stereo olfactory ability, (see edit below)  as the "stereo" aspect derives from having nostrils that are sampling from different spatial locations.  However, the research in the eastern mole suggests that this is not so far-fetched an idea, as their nostrils are not so far apart.
EDIT of EDIT: I take that back about humans: we do appear to have stereo olfaction.


text:
What is ear wax?
A human, at some time in life or the other, must clear the auditory canal. This is usually achieved using soft-cotton buds, or such similar device.
Where does this wax come from? What purpose does it serve? Is it really wax? Is it the inner fluid leaking out?

As quoted from the wikipedia page on Earwax:

Cerumen [earwax] is produced in the outer third of the cartilaginous portion of
  the human ear canal. It is a mixture of viscous secretions from
  sebaceous glands and less-viscous ones from modified apocrine sweat
  glands. The primary components of earwax are shed layers of skin,
  with 60% of the earwax consisting of keratin, 12–20% saturated and
  unsaturated long-chain fatty acids, alcohols, squalene and 6–9%
  cholesterol.

It's purpose -- further quoted -- is that it:

protects the skin of the human ear canal, assists in cleaning and
  lubrication, and also provides some protection from bacteria, fungi,
  insects and water

Some interesting (and stomach churning) earwax trivia:

In medieval times earwax, and other substances such as urine, were
used to prepare pigments used by scribes to illustrate illuminated
manuscripts.
The 1832 edition of the American Frugal Housewife
said that "nothing was better than earwax to prevent the painful
effects resulting from a wound by a nail [or] skewer"; and also
recommended earwax as a remedy for cracked lips.
Before waxed thread was commonly available seamstresses would use their own earwax
to stop the cut ends of threads from fraying.

in case  you want some more nitty gritty details: this boingboing post records some actual TLC of earwax (original link is off line). note the huge squalene/cholesterol ratio.http://boingboing.net/2006/08/08/scientist-analyzes-t.html

Gnarly! P.S.: Good news:  thanks to the invaluable Archive.org, we can view the original article here: http://web.archive.org/web/20060829233236/http://blog.tenderbutton.com/?p=187


text:
Does stress physically age our body?
Going by the assumption that stress eventually triggers a flight/fight response, and the subsequent realization that flight/fight puts the body in a system of readiness to use it's available resources (mental, physical).
Does it make sense to think that stress physically ages a person? I am specifically referring to characteristics identified with aging such as  bleached hair, telomere shortening, wrinkles around the eyes, etc.

The fight/flight situation, through activation of the sympathetic part of the autonomous nerve system, leads to secretion of catechol amines, i.e. adrenaline and noradrenaline. The effects of these hormones, if excreted continously or without real resting time, are thought to be bad for your health. If you recall the possible effects of those two substances (which are both similar to amphetamine, by the way), and look at what big studies have found about the impact of high blood pressure then you know the most important negative effect of stress, IMHO.
http://en.wikipedia.org/wiki/Sympathetic_nervous_system

Not sure that I am entirely convinced by this. Some studies have shown (looking for refs...) that stress can be an important stimulant of the immune system - i.e. hormesis.

This is no contradiction. The positive effects might be greater than the negative. Surely you cannot endure stress 24-7. So there must be a limit.

I didn't say there was a contradiction, but as you have just said it a clearly more complicated than saying stress=bad.

OK, I have differentiated my answer

@Poshpaws Long during stress actually triggers auto-immune diseases.


text:
Does all cells in individual has same mitochondrial DNA?
I read that genetic code is universal except for mitochondrial DNA.
However, I want to clarify (generally speaking, regarding humans especially):

does all mitochondria in the same cell have almost the same mitochondrial  DNA?
does all cells in a single individual have almost the same mitochondrial  DNA overall?
does all the siblings in one family have almost the same mitochondrial DNA overall?

Thanks :)

Are you asking about mtDNA in humans or in general?

@qeschaton humans :)

In a homoplasmic individual, all mitochondria is the same. Therefor will be the same amongst cells and between siblings/mother. Unless some mutation occurs. A homoplastic individual either has all mutated mitochondria or all functional mitochondria of the same type.
A Heteroplasmic individial (more than one type of mitochondria) mitochondria occur when a mitochondria has accumulated sufficient mutations. When a hetroplasmic mother has children, the siblings have varying ratios to each other and the mother.
When you produce oocytes, a selected number of mitochondria are transferred into each. During maturation, there is a rapid replication of mt-DNA, which can lead to a random shift in mutated DNA between the offspring and the mother. This is the mitochondrial bottle neck. Bottlenecks enforce mechanisms that omit cells or individuals, in this context mitochondria, ideally such that only the healthiest mitochondria are transmitted.

In a heteroplastic individual, different cells or populations can have varying amounts of of the mutant mitochondria (including complete homoplasmy).


text:
What is meant by Remote Diuretics & Remote Vomiting?
I have encountered the terms Remote Diuretics & Remote Vomiting separately or sometimes in association in various articles related to medicine.
But I am unable to find any reference to what they actually mean.
Can you help me understand these terms please?
Update
Examples:

Urine sodium less than 10 mmol/L indicates extrarenal loss of urine
  (remote diuretic use and remote vomiting).

link: https://www.ncbi.nlm.nih.gov/books/NBK470386/

Go to google and search for "remote diuretic" to get more references, some are:

It would be helpful if you provided some context such as a citation.

@BryanKrause i have updated the post

"Remote" can mean distant/far away, often in space but also in time (as in, the "remote past"). In just the search results you included in your question it is fairly clear that these sources are using the word "remote" to mean (relatively)"far away in time" or simply "not recent."
For example:

associated with remote diuretic use, therefore, diuretic effects were already washed off

Referring to diuretic use in the past, so there is not current diuretic effect but the secondary consequences are still present.
Note that these terms are quite uncommon in the literature, I get 21 results in Google Scholar for "remote diuretic" and 16 for "remote vomiting" and nearly all seem to be related to the specific context of hypokalemia.


text:
Paper saying that humans and animals are (mostly) the same age
I'm brazilian and today I've came across this news published in a religious brazilian site. It's about a recent study that says that 9 to 10 species on Earth today, including humans, came into being 100,000 to 200,000 year ago.
Also, according to the site, that study supports what the bible says about the origins of life.
I'm pretty sure it's creationist rubbish, but I couldn't understand the conclusion of that study. So, I wish someone would explain to me that conclusion in lay terms. And, taking the opportunity, I'd also like to know if the paper is peer-reviewed and realiable.
Thanks in advance.
Source: https://phys.org/news/2018-05-gene-survey-reveals-facets-evolution.html

What is exactly the claim that you want to have it confirmed or not? Can you please clearly write out a clearly defined claim for which we could work on to write an answer. For the moment, I am afraid the question is unclear.

I didn't ask for a confirmation of a claim but for the conclusion of the study (if there's one). I think my questions are pretty clear.

Do you want us to copy-paste their conclusion? Have you read their conclusion (see their section Summary and conclusion). Was there anything specific that was unclear to you from this section?

To answer your side question... Yes, the paper Stocker and Thaler (2018) has been peer-reviewed. It is published in the Journal of Human Evolution, which a journal of average to low impact.

The conclusion is too technical for my level of english. I'm not a scientist, but I like science, so I decided to try this board expecting that someone could explain that conclusion in plain terms. And to say whether the paper is reliable.

Is your question Can you please summarize in lay terms Stocker and Thaler (2018) for me?, then? If yes, you might want to clarify this in your post. You might want to add your level of knowledge in evolutionary biology too. For example, the paper talks about mtDNA, incomplete lineage sorting, genetic drift and population bottleneck. Do you know those concepts?

Can you just say if that study brings any implication to the evolution theory?

They key qualifier is living species, many living species have relatively recent origins, that is exactly what you would expect in an ever changing ever evolving biosphere. That is like stating that most cars on the road are less than ten years old, OK, but that's not really a surprising statement. If you plotted a bell curve of how old all current animal species are the bulk would be fairly recent geologically speaking. Species have a lifespan. The average lifespan of a mammal species is around a million years so simple statistics will mean most living mammal species will be less than half that. No one is surprised when you say most of the data points in a randomly distributed set fall within one-two standard deviations.
In fact based on back of the envelope calculations, if the average lifespan of a species is ~ 1 million years, and  we assume they are randomly distributed, (they are not, extinction events exist which would shorten it), then just based on the 68–95–99.7 rule, 95%  of living (at or below the mean) species should be less than 320,000 years old.
Now the paper itself is meaningless, it's justification is largely circular: define species based on mitochondrial mutation rate, (which of course is a time based calculation), then use that definition to say most species fall within a certain time period. You can change the number of mutations in your definition of species to fit your conclusion. Even a species has existed a single unfractured population for millions of years will count as a recent species by that definition. It is circular reasoning, made worse by using mitochondria, which are not undergoing recombination so variance is basically only controlled by generation time. If a population splits into two or remains a single population its mitochondrial variance will remain largely unchanged. Interestingly they exclude the groups (plants, fungi, ect) in which mitochondria undergo recombination.
Really the only conclusion you can draw from the article is  most journalists don't understand statistics or genetics.

I like the cars on the road analogy. If you used the same logic as the paper you'd be concluding that the automobile was invented sometime after 2000.


text:
What kind of caterpillars are these?
My niece found some caterpillars that we can't identify. Anyone know what these are? They were found in Massachusetts. The look kind of like Luna Moth caterpillars to me, but I'm not sure.

These are "the big kind" of caterpillars! :-)

Most likely it is Polymopheus moth caterpillar, known as Antheraea polyphemus  from the giant moth family.

yellow-green, and the setae become relatively less prominent with each molt. The translucent yellowish-green to green, full-grown (fifth instar) caterpillars are 60 to 75 mm in length. They have yellow mid-segmental lines that run from the sub-dorsal scoli (setae-bearing, wart-like bumps) touching the spiracles and to the lateral scoli on abdominal segments 2 to 7.

Reference

The species is widespread in continental North America, with local populations found throughout subarctic Canada and the United States. The caterpillar can eat 86,000 times its weight at emergence in a little less than two months.

Reference

The adult wingspan is 10 to 15 cm (approximately 4 to 6 inches). The upper surface of the wings is various shades of reddish brown, gray, light brown or yellow-brown with transparent eyespots.

Reference

Adult male moth

Adult female moth

These ones don't appear to have any setae at all, would the latter stage instars lose them completely?

@asgallant 'Older instars are yellow-green, and the setae become relatively less prominent with each molt. ' reference

Yes, I read that. I'm asking if "less prominent" could mean "not visible at all".


text:
Is the number of protons in the mitochondrion sufficient for ATP synthesis?
If the proton concentration in the mitochondrial matrix (based on its pH) is multiplied by its volume, the total number of protons in somewhere in between 2 and 8.

My question is whether this is sufficient for ATP synthesis, if 2–3
  hydrogen ions are required for each molecule of ATP synthesized.

My calculation is as follows:
pH = –log[H+]
The pH of the mitochondrial matrix is ca. 8. Thus, [H+] = 10-8 M (moles per litre).
If the mitochondrial volume is 0.2 μm3 this is equivalent to 2x10-10 μl = 2x10-16 litre
Using Avagadro’s number as 6x1023 it follows that:
Total number of protons in the matrix of a mitochondrion = 10-8 x 2x10-16 x 6x1023
= 1.2 (although other figures may give a value as high as 8).
If a pH of 6.8 is considered for the inter-membrane space along with a 0.1 fl volume, the number is 6.7 protons.
I found a paper where the question is adressed. First, the definition of pH at very low volumes is challenged, along with its measuring techniques. Second, it proposes novel mechanisms for proton availability in such situations.
(http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0045832)

Can you please explain how you got to the numbers 2 and 8? For the moment, the question is unclear as we have no idea what calculation you've made and what you misunderstanding is. Also, the number of protons in a piece of matter is not the same thing as the number of free protons.

The calculation is as follows: pH=-log [H+], in mitochondrial matrix around 8. Thus,  [H+] =10(-8) M. If a mitochondrial volume of 0.2 um3 is considered (as it has been reported), Then: 10(-8) M2.1x10(-16)L6.022x10(23), gives a total of 1.26 H+, for example. Similar numbers can be obtained when other reported mitochondrial matrix volumes are used in the calculation.

You should edit your post to include that calculation. While you're at it, try rewording it so that it's a clear question, instead of just a statement. It's an interesting point, though

This is a chemistry question. Not really a biology question. I think Chemistry.SE would be a better fit for your question.

@Remi.b I'm guessing the chemists would say it's a biology question, since it's about mitochondria. But, again, it needs to be a question before we can say for sure what it's about :)

I don´t know how to edit the post. The question would be: how is it possible that  the stoichiometry for ATP synthesis is 2-3 H+:ATP, when there are around 2-8 total H+ in the mitochondrial matrix?

There is an edit link at the bottom of the post. If you edit it with that info, I think it will be a good, answerable question. If nobody else answers it by the time I get home, I'll answer it.

@Mithoron, If you refer to the conversion between um3 and L, I believe that 1 um3 is 1x10(-15) L (dm3), 1x10(-12) ml (cm3), and 1x10(-9) ul (mm3)

OK, then it's at least not a matter of miscalculation, but still it's just about water and pH, so still general chemistry. More to the point, you could easily pick a small enough part of any highly diluted solution, where there would be no H3O+ at all, but statistically there would be probability of finding of H3O+ in a different moment directly related to pH. As far as your synthesis goes, there are a lot of more or less acidic protons in there, just waiting to be used.

I find "a lot" hard to calculate or discuss. Could you help me? Have you got any idea of how can I calculate such probability? I´m sorry if the question didn´t match the forum spectations. Still, I think that mitochondrial function IS a biological question, even though in this case involves some chemestry bases.

I have edited the question so that it is clearer. It should also make the unexpressed assumptions — addressed in my answer — more obvious. If I have changed your meaning, do say so, but try to keep things clear.

@David, thanks a lot. I added the numbers for inter-membrane calculation, and the reference to the paper I mentioned.

The question, as amended, can be summarized as:

If there are 2–8 protons in the mitochondrial matrix (as calculated
  from a pH of 8) is this sufficient for ATP synthesis, if 2–3 hydrogen
  ions are required for each molecule of ATP synthesized?

The initial deficiency in the argument was that it did not consider the inter-membrane space, and my answer was:

According to the generally accepted Mitchell Hypothesis, the generation of ATP in the
mitochondrion is due to an electrochemical gradient between the
mitochondrial matrix and the inter-membrane space.
This gradient is predominantly a pH gradient — the [H+] is
higher in the inter-membrane space than in the matrix
The flow of protons down this gradient is responsible for the
production of ATP.
The H+ gradient is maintained by protons being pumped across the inner mitochondrial membrane by the flow of electrons through the electron transport chain. (i.e. The H+ concentration is kept low in the matrix and high in the inter-membrane space, even though protons are continually flowing into the matrix.

i.e. For ATP synthesis to occur there is no requirement for a high steady-state concentration of hydrogen ions in the mitochondrial matrix — quite the opposite (as is reflected by the pH 8). A relatively high concentration of hydrogen ions is only required in the inter-membrane space — as is indeed found.
The amended question assumes a pH of 6.8 for the inter-membrane space, and calculates 8.9 protons to be in this compartment.
The poster still does not state specifically what the problem is — there is still a concentration gradient of hydrogen ions, and a vast body of experimental evidence shows that it is this gradient of hydrogen ions that drives ATP synthesis.
So the implied question does not seem specific to ATP generation, but to the concept of pH in cellular compartments of small volume. There is obviously something wrong here, and the paper quoted — which addresses this question — suggests some possible explanations:

That the pH measured is incorrect because of the methodology
That the hydrogen ions are not free but associated with negatively charged species (possibly phosphate ions) from which they may be released, as required.

The latter point had occurred to me before reading the paper. In summary:

The steady-state hydrogen ion concentration gradient is sufficient to drive ATP synthesis, with many hydrogen ions at any time passing through the membrane in one direction or another.
Many of the hydrogen ions in both compartments will be buffered in a manner that allows there release
The naive calculation is likely to be an underestimate because the pH in the inter-membrane space may be much lower.

If I were an ox-phos person I would know how many molecules of the ATP synthase complex there are per mitochondrion and the number of protons pumped into the membrane space per unit time. Such information would, presumably, bear on the problem.

Thank you for clarifying the question. Electrochemical gradient, as you mentioned it, relies on the CONCENTRATION gradient. The formula du=RTln(C1/C2)+zFdV, allows you to know if the transport is energetically favorable.and gives you a number for that energy change. The actual pumping however relies on the quantity, not on concentration. It is true that protons are pumped frome the inter-membrane space to the matrix, and that the concentration is higher there (about an order of magnitude).

My guess is that the volume of the intermembrane space will be smaller as well. But I will search the number to give you an actual quantity, to avoid subjective definitions, such as "small".

I´ve just find a paper that adresses this question, I leave it here in case anyone is interested:The Final Frontier of pH and the Undiscovered Country
Beyond
Wojciech Bal1
*, Ewa Kurowska1
, Wolfgang Maret2
1 Institute of Biochemistry and Biophysics, Polish Academy of Sciences, Warsaw, Poland, 2 King’s College London, Diabetes and Nutritional Sciences Division, London,
United Kingdom

@RosaliaMoretta — Your enthusiasm for a numerical approach to biology is admirable, but it is perhaps expressed in a manner other than expected on this list. As a poster your first obligation is to express your problem clearly. Your question still has an (unhelpful) title that appears at odds with your question, which is still not clearly explained. I will edit it slightly, but you need to correct the focus on the matrix alone, and present information on the pH of the intermembrane space. If the paper you mention is relevant you should summarize it and provide a journal reference.

@RosaliaMoretta I enjoyed your question, and this answer is excellent. Since you're new, let me point out what you should do when someone answers. Choose the best answer by clicking the little gray checkmark next to it (which turns it green). You should also upvote any useful answer when you have the upvote privilege. This answer should get both (an upvote and a checkmark).

I'm also surprised i was the only one to upvote the question... It's useful and quite clever

In view of the amendment to the question I have amended my answer, shortening the initial answer and adding to it in the light of the reference cited. I think @DeNovo for explaining the acceptance system, but suggest the poster should not be pressed to accept an answer she may not find satisfactory. I never taught or conducted research in the oxidative phosphorylation area, and am aware that there are people better placed to answer this question. But they are not on this list and it is August.


text:
Is the Insulin Receptor Considered an Enzyme?
Can we consider insulin receptor an enzyme? In other words, does the insulin receptor have enzymatic characteristics?

For a better understanding. you can refer to :
https://blog.udemy.com/types-of-enzymes/ http://www.diabetes.co.uk/body/insulin.html

Yes, the insulin receptor can be viewed as an enzyme, since it catalyzes a reaction -- phosphorylation of tyrosine residues on its substrates. But since the protein has multiple functions, it's probably better to say that the insulin receptor "has enzymatic activity", rather than "is an enzyme".
The notion "enzyme" is not restricted to catalysis of reactions involving small molecules, like those in central metabolism. The IUPAC definition of an enzyme reads: "Macromolecules, mostly of protein nature, that function as (bio)catalysts by increasing the reaction rates". So "enzyme" is a broad term, including catalysis of all chemical reactions. DNA replication, mRNA transcription, protein synthesis and posttranslational modifications all involve enzymes. Those enzymes that act on small metabolites can be called "metabolic enzymes" to clarify their function.

Insulin receptor tyrosine kinase, is for all intends and purposes an enzyme. It catalyzes the transfer of a Gamma phosphate from ATP to its substrates (a tyrosine), require divalent metal ions (Mg2+) and have maximal activity when bound to an activator such as Insulin. As such it is perfectly acceptable to call it an enzyme.

Also what other activities are you talking about? The insulin receptor to my knowledge bind extracellular insulin or closely related hormones, become activated and start phohorylation of intracellular substrates. Which substrates and adaptor proteins that are present and their concentrations are what determine downstream signalling.

@JeppeNielsen  I only meant that the protein has multiple functions since it is both receptor and an enzyme. I agree it's fine to call it an enzyme, but it can be useful to indicate that it's not only an enzyme.


text:
How are Thyroid Stimulating Ab destroying thyroid tissues?
I was reading about Graves' disease, which is an autoimmune disorder. I read a few books, including Endocrinology by Hadley and Levine, and websites where they mentioned that the antibody named TSAb (Thyroid stimulating Antibody) binds to TSH receptors and stimulates synthesis and release of thyroid hormones from thyroid gland. This results in the symptoms of Exopthalmic goiter or Graves' disease.
My question is how are these antibodies actually attacking the healthy tissues (which I presume is the tissue of thyroid gland)?
I've so far found no website explaining this part of the autoimmune disorder. I'd appreciate any information or references in this regard.

Have you searched PubMed?

Thyroid stimulating antibodies (sTRAb) don't destroy thyroid tissue. To the contrary, they have a TSH-like effect on thyrocytes and therefore lead to hyperthyroidism and thyroid growth resulting in goiter. The exception is Graves' disease with Hashimoto component. Here, the thyroid is also affected by cytotoxic T cells and antibodies directed against thyroid peroxidase, which gives rise to destruction of the thyroid. But even in this case, it aren't the sTRAb, which destroy tissue.
Perhaps healthy tissues refers to extrathyroidal tissues. Due to unknown reasons several tissues including skeletal muscle, heart muscle, adipose tissue and skin have TSH receptors, and they are affected by sTRAb, too. Hypertrophy results from cross-talk of TSH receptors with IGF-1 receptors in Graves' disease.
References

Dietrich JW, Landgrafe G, Fotiadou EH. TSH and Thyrotropic Agonists: Key
Actors in Thyroid Homeostasis. J Thyroid Res. 2012;2012:351864. doi:
10.1155/2012/351864. Epub 2012 Dec 30. PMID 23365787.
Krieger CC, Neumann S, Place RF, Marcus-Samuels B, Gershengorn MC.
Bidirectional TSH and IGF-1 receptor cross talk mediates stimulation
of hyaluronan secretion by Graves' disease immunoglobins. J Clin
Endocrinol Metab. 2015 Mar;100(3):1071-7. doi: 10.1210/jc.2014-3566.
Epub 2014 Dec 8. PMID 25485727.
Krieger CC, Place RF, Bevilacqua C, Marcus-Samuels B, Abel BS, Skarulis MC, Kahaly GJ, Neumann S, Gershengorn MC. TSH/IGF-1 Receptor Cross Talk in Graves' Ophthalmopathy Pathogenesis. J Clin Endocrinol    Metab. 2016 Jun;101(6):2340-7. doi: 10.1210/jc.2016-1315. PMID 27043163.
Yoo WS, Chung HK. Recent Advances in Autoimmune Thyroid Diseases. Endocrinol Metab (Seoul). 2016 Aug 26. PMID 27586448.

In an autoimmune disorder body tissues are not necessarily damaged, the immune system can also cause

Altered organ growth
Altered organ function

Grave's disease is a result of altered organ function causing hyperthyroidism due to hypersensitivity reaction.
It is hypersensitivity Type-V.

Instead of binding to cell surfaces, the antibodies recognise and bind to the cell surface receptors, which either prevents the intended ligand binding with the receptor or mimics the effects of the ligand, thus impairing cell signaling.

Wikipedia: Hypersensitivity


text:
What are the typical values of probabilities for nonspecific binding to an antibody?
I'm physicist by training, so please excuse me if I don't use the proper terminology.
I think there is a way to make a sensor that detects if a single antibody has caught something from the flow. So I'm trying to figure out if this would be a useful sensor, but this depends on how specific the antibodies really are.
When I ask biologists "How specific are antibodies?", they reply: "Very-very specific", but provide no values that I understand on microscopic level. But I am trying to make a quantitative estimation, e.g. for the following thought experiment:
Suppose I have attached an antibody to inorganic surface. It's an antibody for catching object X. And I flow blood over the surface, slowly. Suppose there's no X in this blood at all. But there are lots (maybe 1017, or some crazy number like that) of other stray particles flowing by this antibody every second, right? So, when one of these particles bumps into this one antibody, what is the probability that it would stick to this antibody? Is it really 10-17 ? Is it really so small?
And, in any case, how do I estimate this probability at least to 1-2 orders of magnitude?
Also, how do I estimate the "collision cross section area" through which an object has to fly to make an attempt to bind to an antibody? In other words, does it only have to touch it slightly, or bump into antibody in a hard and messy collision?
Does the probability of successful bind depend on the flow speed?
How would the values change if I take serum instead of blood?
Could you please point to some relevant papers, books or just keywords? I would very much appreciate any help.

You have to keep in mind antibody structures are complex as well as the antigens they bind to.  I think it really depends on an antibody with a specific structure (the binding site of the antibody, the sequences in its hypervariable site) that's being measured.  This is an older paper that touches on anitbody binding specificity.  http://pellegrini.mcdb.ucla.edu/Lab/publication_pdfs/M4Xl99-fulltext.pdf

The specificity of antibodies can vary. Also, the binding/unbinding rates can be different. You can look at 1977 Gillespie's paper on how to convert deterministic rate constants to reaction probabilities. For incorporating flows you need to formulate partial differential equations or corresponding stochastic models.

TL;DR Specificity of antibody can be not superb. It can give false-positive results in up to 90% of experiments. However, some essay are 90% specific.
That is an interesting question and there sure a lot of research done to understand specificity and strength of binding of antibody to its target.
First of all, let me say that antibody-epitope interaction is, as many biological processes, probabilistic process, which means it can go either way, however, after binding antibody need a lot more energy or time to "fall off". Direct contact is always required for establishment of non-covalent bond between antibody and epitope, because characteristic length of that interaction is very low (order or angstroms, 0.1nm and less). Point here is that you don't need to run antibody in stream, rather let is sit in solution with your sample or mix gently, random thermal motion will take care of them finding each other. In flow you will waste a lot of antibody, which is expensive.
I think that you can estimate probability of given antibody binding given molecule from their 3D structures, but this is extremely burdensome calculation. What you can do experimentally, I suppose, is label "right" epitope with red fluorescent tag, and every other molecule in your solution with green tag. Then run solution through column with antibody sitting on beads (as in chromatography), elute everything and compare green to red signal. Measuring accurately, this will tell you how much "junk" antibody picked out of solution.
Now, to numbers. Here Abcam talks about its antibody for progesterone. Molecules, closely related to progesterone, are recognized with 40-90% efficiency, compared to true-positive target (progesterone). But this is absolute-worst case scenario, because those molecules are so closely related.
On other note, antibody specificity is very important when essay is used, e.g. for HIV diagnosis. Here is nice page from U Penn, that discusses issues with specificity:

For example, in one study of 290,000 asymptomatic Minnesota blood donors donating 630,000 blood units, the false positive rate when both the screening and confirmatory assays were positive was was 0% per donation (95% confidence interval 0% to 0.0006%).
...
For example, in one study of asymptomatic Italian blood donors, only about 13% of donors with repeatedly-reactive EIA tests were confirmed to be HIV-infected on the basis of positive immunoblot. However, in a high risk population the false-positive rate can be much lower, as low as 1-3%.

I couldn't find any more precise data or studies. In biological imaging (my field) antibodies are split into "works" and "don't work, drop it" (aka high background) groups.

Your first statement is not always true: the specificity of antibodies can vary; some can be extremely specific. Also, in antibody based chromatography there is flow, however, the antibody is immobilized and it is the antigen that is flowing.

Specificity of antibody can be not superb 2) I could not find data :-( My antibodies are working nice for imaging. 3) In chromatography flow is pretty slow, I think. But yes, if you fish antigen out of solution, you don't waste precious antibodies

Clarify, when you say "antibody" do you mean a monoclonal antibody (where every antibody is identical, and therefore a pure population), or do you mean a polyclonal antibody (which is a mixture of antibodies that all recognize the same antigen, but may each be recognizing different epitopes on the antigen)? A monoclonal Ab (mAb) recognizes a single epitope.
Textbooks and supplier catalogs often act like Ab binding is absolute, as if you could not measure the three quantities: molar concentration of free antigen, molar concentration of free mAb, and molar concentration of bound antibody antigen complex. In other words, as if every antibody is fully occupied all the time, once the Ab encounters a molecule of free antigen.  But I think you can discern from the discussions and answers above that not all Ab are created equally.

In cases where people have measured this Kd (the dissociation constant) for a "tight" binding antibody the value is in the order of 10EE-14 or smaller (as I recall).  When we say tight binding we usually mean that the so-called off-rate is very slow, with a t1/2 on the order of hours. In a typical reaction the on-rate is usually limited by the rate of diffusion, and cannot be faster (but search for discussions of lac Repressor DNA binding protein finding its targets with kinetics that are faster than the rate of diffusion!)

The device you are describing (that detects binding events using fixed proteins on a surface and target proteins in solution) measures surface plasmon resonance, and at one point was available for purchase under then brand name BIAcore. It was developed by Mel Simon, at CalTech.
Finally, if your goal is an automated way to use antibody reagents to detect vanishingly small quantities of antigen in a complex mixture of fluid, you would do well to familiarize yourself with the radioimmunoassay (RIA), it can be exquisitely sensitive.  Keep in mind that all of these different techniques will have a lower limit of detection such that a negative result ("We could not measure any of protein X in the sample from this patient") always has to be considered with the proviso of "using this particular detection assay". So it is a type of confidence level.

I understand that you talk about false-negative binding. $K_d$ is about probability of false-negative binding — antigen is present, but antibody doesn't bind it despite being specific to it. What I'm asking is the probability of a false-positive binding — a probability that non-target particle will bind to this antibody. That is, a particle that is not the antigen this antibody is specific for.

Thanks for the links about BIAcore, but their methods don't count individual single particles. They measure the average signal over entire sensor surface, in an ensemble-averaging way. I'm talking about seeing a single bound particle - as in the detection scheme by Zybin et al.

authors: Михаил Беклемишев


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Chimeric Gene vs Fusion Gene?
According to wikipedia on chimeric genes:

These mutations are distinct from fusion genes which merge whole gene
  sequences into a single reading frame and often retain their original
  functions.

I am not totally sure I understand the statement. My interpretation is that a fusion gene is caused by a translocation of DNA in a single gene; therefore, it "retains their original functions". This is different from a chimeric gene where DNA from two or more different genes are translocated to a new location to form a completely new gene.
Is my interpretation correct?

A chimeric gene is formed from fragments of other genes whereas a fusion gene is formed from the entirety of other genes. Often in the literature you'll see the term fusion gene used for both cases.


text:
I am interested in Sociobiology. Which academic field should I study?
I like to study Sociobiology and evolutionary psychology. Which academic fields concentrate on these sciences in bachelor and master degrees?

I'm voting to close this question as off-topic because it is about career advice, not biology.

So to continue with what Remi B says, of course it is going to require quite a bit of chemistry for it all. Chemistry in sociobiology distinguished areas among each other, where even nuclear reading make a distinction for it all.

This could be reworded to be more oriented toward field of study/self education advice rather than career advice, It may be more acceptable then.

What fields are sociobiology and evolutionary psychology?
Sociobiology (aka. social evolution) is a subfield of evolutionary biology.
Evolutionary psychology is a subfield of both evolutionary biology and psychology. Evolutionary psychology is, for the moment, very theoretical without much (if any) empirical testing. For this reason, not only natural scientists
 and social scientists work on the subject but some philosophers have also contributed (such as Daniel Dennett for example).
How to become a researcher in one of these fields?
Biology.SE is not BiologyCareerAdvice.SE. We have way too few information about you to give reliable career advice anyway. Also, I am not trained in any way to give you carrer advice.
That being said, a priori, start with a Bachelor in Biology and follow up with a master in Evolutionary Biology. Because evolutionary psychology is very inter disciplinary, I would personally advice to go with whatever broad field of study attracts you most. If you are more into psychology than biology, please go with psychology. If you are more into philosophy than biology, then go into philosophy.
Short intro to evolutionary biology
For a very short intro course to evolutionary biology, you can have a look at evo101 by UC Berkeley.

Remi. Please discourage people looking for career advice on here.

@TheLastWord Yes, I think you're right. I added Biology.SE is not BiologyCareerAdvice.SE. We have way too few information about you to give any reliable career advice. Also, I am not trained in any way to give you carrer advice.


text:
Volley theory and sound amplitude/power
Assume a pure tone (single frequency) is listen, lets say 2 kHz. If I understand correctly the temporal theory (aka timing theory), in a cochlea neuron the action potentials create a signal that will have one spike for each single tone cycle with the exception of some gaps due to the minimal interval between neuron triggers.
Volley theory extends previous model to a set of neurons. The union of triggers in all neurons of the set will have at least one spike per cycle (with few exceptions). In other words, the base frequency of the signal composed as the union of triggers of all neurons in the set will be the same frequency than the one of the incoming sound.
My question is, if in this model the trigger intervals is used to encode the sound frequency, and taken into account that usual models for neuron activity only take into account intervals between action potentials (all-or-none), how sound amplitude (power) of the sound is translated to the nerve signals. That is, the differences in the nerve activity caused by two tones of same frequency but different amplitudes/powers, assuming frequency/volley model.

It's complicated.
The simplest explanation is that sound amplitude/level/loudness is encoded by the number of participating units, including off-best frequency cells that get recruited when amplitudes are high (the concept of 'tuning width' is helpful to understand). Loud sounds will recruit cells of a wider best-frequency range with high coincidence, for example (see Carney, 1994).
In some experimental paradigms, this hypothesis holds; in others, it does not. It is most likely that the perception of loudness is quite context-dependent and also depends on background, the presence of energy in other frequencies, and adaptation.
Similar to how absolute brightness is not all that perceptually useful (and therefore humans display incredible invariance over very wide brightness ranges), loudness is probably perceptually most useful in terms of relative loudness: sounds that are getting louder may be approaching, for example.
References

Carney, L. H. (1994). Spatiotemporal encoding of sound level: Models for normal encoding and recruitment of loudness. Hearing research, 76(1-2), 31-44.
Heinz, M. G., Issa, J. B., & Young, E. D. (2005). Auditory-nerve rate responses are inconsistent with common hypotheses for the neural correlates of loudness recruitment. Journal of the Association for Research in Otolaryngology, 6(2), 91-105.
Neuhoff, J. G., McBeath, M. K., & Wanzie, W. C. (1999). Dynamic frequency change influences loudness perception: A central, analytic process. Journal of Experimental Psychology: Human Perception and Performance, 25(4), 1050.
Relkin, E. M., & Doucet, J. R. (1997). Is loudness simply proportional to the auditory nerve spike count?. The Journal of the Acoustical Society of America, 101(5), 2735-2740.

"Best frequency" is not a term related to the place theory? It applies also to volley one?

@pasabaporaqui They aren't really competing theories anymore, rather the one that predominates depends on the frequency range you are considering. Certainly people can still argue which is important for some of the intermediate frequencies, but that's more a niche argument. But in principle, louder sounds will induce synchronous volleys over a wider 'place' on the cochlea. Not even an extreme proponent of volley theory would try to argue that the cochlea is not tuned in space.


text:
VC06 neuron of c.elegans
My understanding was that all neurons and their synapses of worm c.elegans are already listed.
As source of this map I'm using following databases (both should contain same information):
Connectivity Data
Database of Synaptic Connectivity of C. elegans for Computation
In both databases, neuro-motor neuron VC6 (aka VC06) has no synapses to any other neuron. This is surprising for me.
Is connectome of this animal finished? If it is, are these two databases up to date? Finally, if answer to previous questions is "yes", any explanation about this "isolated" neuron ?


text:
Fungi growing in pH 1 FeCl₃ solution
I have a FeCl3 tank that I use to dip spruce wood in. After 2–3 weeks a fungus appears in the tank and it keeps growing with time. The fungus has a white colour and is spread throughout the whole tank. It looks like mainly on the surface but its everywhere in the fluid.
The FeCl3 solution has pH 1 and that doesn't change with time.
Can anybody tell me what it might be? What's the best way to make sure it doesn't occur anymore?

I would suspect an iron oxidizing extremophile bacteria not a fungi. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5023253/


text:
Epistasis: Why should a recessive allele be a hypostatic gene?
Let us take the example of Recessive epistatsis, an epistasis in which a double recessive gene mask the phenotypic expression of alleles  of another locus.
(adapted from: An Introduction to Genetic Analysis)
An example from the same book:

In  plant blue-eyed Mary (Collinsia parviflora), the biochemical pathway is as follows:

The w and m genes are not linked. If homozygous white and magenta plants are crossed, the F1 and F2 are as follows:

Complemention results in a wild-type F1. However, in the F2, a 9:3:4 phenotypic ratio is produced.
This kind of interaction is called epistasis, which literally means “standing on”; in other words, an allele of one gene masks the expression of the alleles of another gene. In this example, the w allele is epistatic on m+ and m$^1$. Conversely, m+ and m can be expressed only in the presence of w+.

Interpretation & Question:
The gene product of m$^+$ is needed to form blue pigment from magenta. On the other hand, in the absence of w$^+$ allele (i.e. w w genotype), no magenta (precursor of blue) is formed so the phenotypic expression of m$^+$ allele(s) is masked. Now, what has m got to do here? $^1$ It is not encoding anything.
Note:
On referring other books I found they do not suggest a hypostatic gene to be recessive (as $m$ has been considered here).
My idea of recessive allele is that one that due to loss-of-function mutation either produces a non-functional variant of the protein or the same protein at a lower quantity.
Has recessive allele been considered an hypostatic allele here considering that it might be able to code normal functional protein at a lower rate?

Scope of answer:
Which concept should be followed? Why (ideally with citation)?

I'm confused, what exactly is your question?

@canadianer Edited. If there are still issues, please point out the concerned paragraph.

It's called recessive epistasis because the recessive allele w masks the phenotypic expression of m+ and m. I don't understand this part: Now, what has m got to do here? It is not encoding anything.

If you see the flow chart m+ is responsible for the conversion of magenta into blue and not the product of m (something consistent with other books explaining epistatsis, in this case recessive epistatsis), so is my question.@canadianer

Does this help? I'm still not really following you. 1) The phenotypic expression of the m locus is dependent on the w locus. This is why the w locus is epistatic over the m locus. It is called recessive epistasis because the homozygous recessive genotype w/w prevents the phenotypic expression of the m locus. A w/w organism will be white regardless of the alleles at the m locus. 2) The m allele is considered recessive to the m+ allele because two m alleles are required to show a phenotypic effect. When a w+ allele is present, the organism will be blue unless there are two m alleles

'In this example, the w allele is epistatic on m+ and m' -m according to the dig. and as you said has no contribution to blue pigment then why its phenotypic expression has to be masked? (I can't put it in any better way)

Let us continue this discussion in chat.

In this example, the $w$ locus is epistatic on the $m$ locus or, in other words, the phenotypic expression of the $m$ locus is dependent on the $w$ locus. It is called recessive epistasis because the homozygous recessive genotype $w/w$ prevents the phenotypic expression of the $m$ locus. A $w/w$ organism will be white regardless of the alleles at the $m$ locus.
Now, to get to your question, consider the situation where the organism is $w^+;m^+$:
$$\ce{white \stackrel{w+}{\rightarrow} magenta \stackrel{m+}{\rightarrow} blue}$$
You can see that the phenotypic expression of the $m^+$ allele is a blue colour. Next consider a $w^+;m/m$ organism:
$$\ce{white \stackrel{w+}{\rightarrow} magenta \stackrel{m/m}{\nrightarrow} blue}$$
You're right that, at a molecular level, $m$ likely codes for some defective enzyme. But, in the case of epistasis, it is important to consider its expression at the level of phenotype. The phenotypic expression of $m/m$ is a magenta colour.  Finally, look at a $w/w;m/m$ organism:
$$\ce{white \stackrel{w/w}{\nrightarrow} magenta \stackrel{m/m}{\nrightarrow} blue}$$
Despite having the $m/m$ genotype, which should give a magenta colour, the organism will be white because of epistasis. In other words, the expression of the $m/m$ phenotype is dependent on the $w$ locus.
I hope that answers your question. Let me know if I still misunderstand or something needs to be explained better.

In the context of this textbook, m is simply an allele that codes for a non-functional protein product. The protein product of m is incapable of converting magenta pigment into blue pigment.


text:
Is the size of the genome across species roughly the same?
Chromosome number differs across species.
Is the amount of DNA comparable between organisms, just being split into smaller chunks in those species with more chromosomes, or do species have different genome sizes? If so, does the genome size correlate roughly with the complexity of the species?

Please clarify your question. As it is written now, you ask multiple, very broad questions.

To briefly answer all four of your questions: no, no, yes, and kind of but not really. If you narrow it down a little more there are great answers to this question.

@Resonating - now, see why comments are bad as answers? I think I can make a good case for "yes, yes, yes, and not really".

There are exactly two questions: do different species have the same genome size and, if they don't, does size relate to complexity. This is pretty straightforward and can be well answered in a paragraph, which is hardly broad.

I guess you're right. I retracted my close vote and removed my comment.

I would call this a homework. It is quite well known that genome sizes are different between different species.  You may edit the question to add more details if you really wanted to ask something more than this. In general what you intend to ask should be clear in the question.

@anongoodnurse Comments are terrible as answers, that's why we have answers. I sometimes can't resist, though :( Too broad questions get too short answers. I'd like to read your case for your first yes though, if you'd like to drop it in chat for my edification?

I'm not voting to close but think it would benefit from a good edit

Chart of C-values (the mass of DNA in a single haploid cell); there is no logical order to the groups:

[source]
Base pairs in haploid genome (some examples):

Escherichia coli (bacterium): ~4.5 million
Caenorhabditis elegans (nematode worm): ~100 million
Homo sapiens (we all know what these are): ~3 billion
Pinus taeda (coniferous tree): ~22 billion
Prorocentrum micans (single-celled algae): ~245 billion

From these data we can conclude:

Different species do not have the same genome size.
Genome size is not correlated with complexity. Organismal complexity can be hard to define but, qualitatively, I think we can all agree that a human is more complex than a single-celled alga. And yet, humans have a genome that is 80 times smaller. This is known as the C-value paradox. Note, however, that this paradox has been resolved after it was found that the genomes of most eukaryotes contain a large proportion of non-coding and repetitive DNA.

Further reading:
The C-value paradox, junk DNA and ENCODE by Eddy SR
Eukaryotic Genome Complexity by Pray L

It is already mentioned by canadianer that genome size differs between organisms. But what about complexity?
First we should define what complexity is: complexity can be defined as number of different cell types that a multicellular organism can produce, with the same genome. Yes complexity does not correlate with genome size. However, it seems to correlate with number of genes. According to Kauffman, the number of cell types i.e. complexity is linearly correlated (direct correlation) with the square root of number of genes.

Though Kauffman says that complexity increases with DNA content, which is not actually true, it is certainly possible that that complexity is correlated with number of genes. The book is a little old and certainly molecular and cell biology has seen a lot of progress in this time. However, theoretically higher number of distinct genes should produce more complex phenotypes which Kauffman justifies using his NK-model. This assumption has again been disproved. The catch would be that exact duplicates/polyploid genes should not be counted as different genes. Moreover metabolic genes should also not be counted (plants/bacteria have a higher number of functional metabolic pathways). Organismal complexity arises because of the complexity of gene regulatory network which in-turn is dependent on the number of regulatory genes. NK model also in a way assumes regulatory genes (i.e. genes that can interact with each other). Surely complexity cannot arise out of nothing. I can't find the data for this at the moment but the theory is quite strongly plausible.
Another point I would like to add is that complexity need not only mean spatial complexity. Complexity can also be temporal.

 Reference:
    Stuart A Kauffman (1993) The Origins of Order, Chapter 12

That graph seems quite outdated. Man, for instance, doesn't have ~600,000 genes (or am I reading it wrong, I can't imagine an estimate that high in the 90s). Also, the selection of organisms isn't exactly inclusive. Plants are conspicuously absent. It would be interesting to see the comparison done with contemporary estimates and a broader range of species. From what I've read, complexity and number of genes don't correlate.

@canadianer I agree and I said that this is outdated. However, number of unique genes can theoretically (perhaps also in real) give rise to complexity. It is also intuitive that with increased functionality, you need a bigger repertoire of genes. The complexity of gene network also matters, though. I must also indicate that metabolic genes would not play a role and it is the regulatory genes that would matter. Complexity cannot just arise from nothing (if it has no connection with genome whatsoever). I'll add this to the answer.

I can show the facts here.
Human:
total length: about 3,000,000,000
coding genes: about 50,000 (included predicted ones)
3,000,000,000/50,000=60,000
Chromosome number: 23
Zebrafish:
total length: about 1,400,000,000
coding genes: about 36,000 (included predicted ones)
1,400,000,000/36,000=38,889
Chromosome number: 25
Fruitfly:
total length: about 1,400,000,000
coding genes: about 19,000 (included predicted ones)
1,400,000,000/19,000=73,684
Chromosome number: 4
Saccharomyces cerevisiae:
total length: about 12,000,000
coding genes: about 7,000 (included predicted ones)
12,000,000/7,000=1,714
Chromosome number: 16
http://useast.ensembl.org/Homo_sapiens/Info/Annotation
http://useast.ensembl.org/Danio_rerio/Info/Annotation
http://useast.ensembl.org/Drosophila_melanogaster/Info/Annotation
http://useast.ensembl.org/Saccharomyces_cerevisiae/Info/Annotation

and how do these numbers answer the question? The answer is in there, but it would be good to end with a concluding few sentences addressing the question.


text:
Is flowers nectar secreation influenced by bees/pollinators?
Nectar secretion by flowers is influenced by many environmental factors e.g. water supply and air temperature [1].
My question is: do bees (or any other pollinator) influence it too?
I can imagine every bee's visit takes away a certain amount of nectar from the flower. Then following the flower nature, it should produce nectar again (if there are the right conditions, e.g. enough water).
[1] https://www.jstor.org/stable/2468960

In short, yes, it seems many flower species have mechanisms to replenish nectar after removal. For example, in Luo et al. 2014 Journal of Pollination Ecology,  9 of 11 species of plants they studied in the Colorado Rockies showed significant additional nectar production after some nectar was experimentally removed. Furthermore, the magnitude of this behavior was greater for flowers known to be heavily visited by bees:
https://www.researchgate.net/publication/268523373_Stimulation_of_flower_nectar_replenishment_by_removal_A_survey_of_eleven_animal-pollinated_plant_species

Hi Michael. Please provide some summary or other form of support from the source you provide. Simply adding a link without an explanation or summary is not acceptable on this stack site. If the link goes dead, this post literally becomes useless. Please update accordingly to avoid having it downvoted or deleted. Thanks!