text:
Why can’t plants prepare their own water?
Water is needed by every living object. If plants have developed that property of theirs to prepare their own food from simple molecules, why can't they also prepare water?  Oxygen are present in the atmosphere in bulk!
Or more generally, why isn't any living system capable of generating water and using it for itself?
Is it because, the plant does not want to make something that is already available to it in excess? Or is it because water is needed by the plant in excess but food is needed by it in a relatively small amount, so it is just built up in such a way that it does not prepare those things which are needed to it in excess?

Hydrogen is not present in the atmosphere in bulk; if it were, when you lit a match the air around you would explode in flame. Most of the hydrogen in air is in the form of water vapor.

@BryanKrause, Thanks for the comment but I disagree with you.  The air doesn't explode because of Nitrogen. You see, P, Mg, Na etc are present in much much smaller amounts than H but then also, they are used very effectively!

Right, because the atmosphere is mostly nitrogen and oxygen, just about everything else is present in trace amounts only. You said hydrogen is present in the air in bulk: citation please? I would also like to know what gaseous forms of phosphorus, magnesium, and sodium you have around you.

@BryanKrause, on some research i found out that I was wrong. Hydrogen is not present in bulk but in quite small quantities which can be compared to Mg,Na etc. But, Oxygen is present in bulk! Why can't the plant take advantage of that?

Water is H2O - you can't make water with only oxygen. There is way way more water vapor in a typical atmosphere than there is free hydrogen.

Exactly @BryanKrause . Okay, i got an idea. So, a plant does not prepare it's own water because water is itself present in excess in the atmosphere , just like it is useless for the son of Bill Gates to go to a job to earn some money?

Somewhat. It is just extremely more practical to get water from the ground, or in some rare cases, from the atmosphere. (Maybe this goes with your Bill Gates analogy) But there is also no practical way for a plant to synthesize water from the atmosphere - plants need to use a LOT of water, way more than things like nitrogen, potassium, etc, and the ingredients just aren't there.

So @BryanKrause , are plants built in such a way that they prepare things which are needed by them in small amounts but they just don't want to prepare those things which are needed by them in excess?

Water is also quite abundant. Life evolved in water

Assume you are any living thing. You have the option of drinking water from a river, or painstakingly extracting and purifying trace elements from the upper reaches of the atmosphere. What would you pick?

Hydrogen is not present in the atmosphere in bulk (the original question stated it was); if it were, when you lit a match the air around you would explode in flame. Most of the hydrogen in air is in the form of water vapor. Water is H2O - you can't make water with only oxygen. There is way way more water vapor in a typical atmosphere than there is free hydrogen.
It is just extremely more practical to get water from the ground, or in some rare cases, from the atmosphere. But there is also no practical way for a plant to synthesize water from the atmosphere - plants need to use a LOT of water, way more than things like nitrogen, potassium, etc, and the ingredients just aren't there.
To clarify a bit though, there are reactions in plants that produce water: plants use cellular respiration just like animals do, but the source of this water is oxygen from the atmosphere plus sugars synthesized by the plant - those sugars originally required intake of water, so there is no net production of water for the plant.
It isn't an issue of plants "wanting" to do anything. The big thing that plants make for themselves (that animals do not) is by their ability to turn atmospheric carbon into sugars and carbohydrates via photosynthesis. Everything else is either A) not particularly distinct from other organisms, or B) depends on the plant species. Even nitrogen fixation isn't really done by plants, but by microorganisms, some of which have symbiotic relationships with some plants.
The general rule is that organisms have roughly 3 ways to get the things they use from the environment, in order of efficiency: diffusion of things that are in high supply in the outside environment (depends on the particular environment but might include oxygen from the air, salts in the ocean, water in some contexts), using pumps to transfer desirable things into the organism directly or indirectly by utilizing established concentration or electrical gradients, including osmosis - note that these processes occur in digestion as well, and finally, synthesis. Synthesis can be expensive, depends on the development of very specific enzymes, and requires component parts to be available, so when the other options are available there is not much selection pressure to develop synthetic machinery. Water is incredibly abundant on Earth, and even where it is rare, it is present in the environment in more accessible ways than are the ingredients.
There are some organisms that produce enough water through metabolism that they do not need to drink; plants would not be included in this category because they need to use water to produce the products that the metabolic water would come from. However, the source of water in these reactions is not gaseous hydrogen and oxygen, but produced from cellular respiration.

Please answer my edited question, sir.

@AaryanDewan You should not edit a question to make previous answers to the question invalid - edits should only be for clarification or spelling/grammar issues. That said, I believe this answer still addresses your edited question. Please let me know what your specific issue with this answer is: which part of your question is left unanswered?

The last paragraph. Is this a general rule which is visible in most living organisms? ( humans and other animals excluded )

@AaryanDewan See my edits.


text:
Why is contractile vacuole absent in parasitic protozoans but present in free living protozoans?
I know that contractile vacuole helps in osmoregulation of protozoans and some nitrogenous wastes are also excreted through it. Since contractile vacuole plays an important role in protozoans, why is it absent in parasitic protozoans? I could not find the logic behind this.

No, you are wrong. Parasitic protozoans too have contractile vacuole, for example trypanosoma.
Also Wikipedia says:

Not all species that possess a contractile vacuole are freshwater organisms; some marine, soil microorganisms and parasites also have a contractile vacuole

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

sort: votes


text:
Isn't heritability more important to genic capture than just genetic variance?
Rowe & Houle (1996) give two criteria for the selection of costly female choice:

Condition dependence of sexually selected traits
High genetic variance in condition

Regarding heritability, they wrote,

comparisons based on heritability are misleading, as Fisher's fundamental theorem of natural selection shows that the response of fitness to selection depends only on the additive genetic variance, and not on other components of variance.

However, the magnitude of environmental variance should matter for the selection of female choice for sexually selected traits, since the more environmental variance means the less likely offspring of fitter males will be fitter themselves and the less likely females should be to incur costs to mate with fitter males.  Am I not correct?  Is this an oversight on their part?

I would suppose they talked about genetic variance for fitness while you are expecting them to refer to genetic variance for female choice. Fisher's fundamental Theorem stands right when talking about the genetic variance for fitness, not for another phenotypic trait such as female choice. Do you think you were mislead by this confusion? Note: I have not read the paper.

Their paper is intended to explain the evolution of female choice.

Possibly relevant: the breeder's equation can be written in two different ways. for a given selection differential (covariance of trait with fitness), response to selection is proportional to heritability. But for a given selection gradient (regression of trait with fitness - i.e. the covariance divided by the total trait variance), response to selection is proportional to additive genetic variance. Between the two versions, you're just shunting the V(P) denominator between the two right hand quantities. See https://biology.stackexchange.com/a/52250/26665

Since the regression of fitness with itself is just 1, the response to selection of fitness is proportional to additive genetic variance (that's kind of like a discrete version of Fisher's Fundamental Theorem)

But ya I see your point - if e.g. horn length is condition dependent, but condition has high environmental variance, then shouldn't horn length be less correlated with fit genes? So shouldn't the same amount of "horn-length preference", get you a smaller fitness benefit for your children?

Like you're right, females aren't directly selecting for fit genes, they're selecting for a fit phenotype which may be strongly or weakly correlated with fit genes

Thank you, sir.  These comments are helpful.  They seem to be equating the benefit a female receives from choice with response of fitness to selection, which I do not understand.

@David Bahry, I appreciate your time.  That was very helpful.

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


text:
Hardy-Weinberg for triploids
Problem:
A certain species has somatic cells with ploidy 3n (the organism inherits
three sets of homologous chromosomes from each of three parents). At a certain locus, there are three possible alleles A 1 , A 2 , A 3 , which are
completely dominant in the order A 1 > A 2 > A 3 . The proportion of organisms
exhibiting traits A 1 , A 2 , and A 3 are respectively 0.614, 0.306, and 0.08. In
addition, the proportion of organisms that are completely heterozygous
(genotype A 1 A 2 A 3 ) is 0.18. Which of the following are allele frequencies of A 1 , A 2 , and A 3 , respectively?
Answer Choices:
A. f(A 1 ) = 0.5, f(A 2 ) = 0.3, f(A 3 ) = 0.2
B. f(A 1 ) = 0.3, f(A 2 ) = 0.5, f(A 3 ) = 0.2
C. f(A 1 ) = 0.3, f(A 2 ) = 0.4, f(A 3 ) = 0.3
D. f(A 1 ) = 0.6, f(A 2 ) = 0.2, f(A 3 ) = 0.2
E. f(A 1 ) = 0.7, f(A 2 ) = 0.2, f(A 3 ) = 0.1
Correct Answer:
A
Solution:
No clue. I'd guess that the solution follows a hardy-weinberg model for polyploids. For simplicity, I will refer to A1, A2, and A3 as x, y, and z, respectively.
(x + y + z)^3 = x^3 + 3x^2y + 3xy^2 + y^3 + 3x^2z + 6xyz + 3y^2z + 3xz^2 + 3yz^2 + z^3
Given that z^3 = 0.08, shouldn't z (A3) equal the cube root of 0.08 = 0.43?
That doesn't match any of the answer choices, so I will assume that my steps were incorrect.
Any suggestions?

First, although it only speaks about cases of diploidy, you might want to have a look at Solving Hardy Weinberg problems.
Information given to us
The question gives the same names to the phenotypes than to the alleles which si rather confusing. Let's call the three possible phenotype $P_1$, $P_2$ and $P_3$. We know that the frequencies of these phenotypes are
$$f(P_1) = 0.614$$
$$f(P_2) = 0.306$$
$$f(P_3) = 0.08$$
Compute phenotype frequencies in terms of allele frequencies
Let, $x$, $y$ and $z$ be the frequencies of the three alleles, $A_1$, $A_2$ and $A_3$ (I chose those names to fit with the equations you wrote). The whole difficulty now is to express $f(P_1)$, $f(P_2)$ and $f(P_3)$ in terms of $x$, $y$ and $z$. You should try yourself before looking at the result. Start with $f(P_3)$, it is the easiest.
Here is the solution for $f(P_3)$

 $f(P_3) = z^3$

Here is the solution for $f(P_2)$

 $f(P_2) = y^3 + yz^2$

Here is the solution for $f(P_1)$

 $f(P_1) = x^3 + 3x^2 (y+z) + xyz + xy^2 + xz^2$

Once, you have done that, you have three equations with three unknowns and you just have to solve them. Make sure at the end that $x+y+z = f(P_1) + f(P_2) + f(P_3) = 1$.

I've tried to do that. z^3 = 0.08. z = 0.43, which isn't correct. Maybe f(P3) should equal 0.008 instead of 0.08?

Indeed. Something is wrong in the possible answers or we misinterpreted the genetics basics as the explanation of dominance is a little unclear. If $f(P_3) = 0.008$, then some other phenotype frequency must be adapted so that that sum up to one. In any case, the other phenotype frequencies are made so that the corresponding allele frequencies don't match! So, I very much think I did not interpret the genetic basis correctly. Stating  completely dominant in the order A 1 > A 2 > A 3 is not sufficient unfortunately. IMO, the question is undefined.

Well that's a shame! Thanks for the help, regardless.


text:
Do all polygenic traits involve epistasis?
Consider the following statement

All polygenic traits involve epistasis.

I think its true because polygenic traits involve several genes interacting together to result in a certain phenotype and if one of these genes is altered, the resulting phenotype is different.

Eh, I guess you could talk like that? But I think it'd be unusual and confusing. One thing is that in quantitative genetics, you don't usually talk about eg. a "gene for being x feet tall"; you only talk about a "gene for being x feet tallER" (than you would be otherwise, with the competing allele). If you talk like that, then only if the latter acted non-additively with other loci would you say there was epistasis.

eg. Suppose that in your population A's are always a foot taller than a's; and that there are also other genes affecting height. In this case, for the trait of being "1 foot taller" there isn't epistasis; for the trait of being "5 feet tall" there is. Quantitative geneticists generally talk in terms of the former.

A polygenic trait is a phenotypic trait for which the variance in the population is explained by two or more loci. Epistasis is a case there is a statistical interaction between several loci on the value of a phenotypic trait.
The several loci underlying a polygenic trait might be purely additive (no interaction) and therefore a polygenic trait does not necessarily involve epistasis.

This is a sort of weird question, because it is so vague, but it is still important because quantitative genetics seems incapable of giving a coherent answer even for people with PhDs.
The idea of "additivity", for instance, is a statistical rather than biological concept. It was first applied to quantitative genetics by Fisher in his 1918 paper, and it comes down to a neat trick developed for predicting the phenotypic correlations between relatives (what we would now call "heritability"). Fisher showed that if you assume that genes are roughly additive/independent in their contributions to traits, that makes the math much simpler for calculating heritabilities. He goes on to argue that the approximation works ok as long as you let the number of genes tend to infinity.
More recent research, notably by Peter Visscher and co, suggests that the additive approximation is in fact pretty good for all measured human traits for which there is data. So, this would argue against a big role of epistasis.
The problem with all this is that there is no reference to biology whatsoever. Anything that happens in a cell is governed by interactions, e.g. epistasis. When two proteins work in the same pathway, their genes have an epistatic relationship. So, anything that happens in a cell is entirely dependent on epistasis. In fact, in highly controlled experiments where you can directly measure the epistatic component by measuring all possible genotypes, you generally find that epistasis is a really important component of variation, because additivity is just a best guess at the sum of all epistasis effects in a sample population.
Visscher and co have argued back that while all this epistasis stuff could be interesting, Occam's razor means that additivity is probably good enough for the purposes of quantitative genetics. Yet more recent work has suggested that you in fact improve predictions a bit if you consider pairwise epistasis, so it's very much an active field of research.
In summary: this is a question that sort of depends on where you fall on the experimentalist-to-statistician continuum, with the experimentalists saying it's all epistasis because look at their data showing epistasis, and the statisticians saying that additivity is probably ok on its own because look at the quality of the predictions. Epistasis is important if you care about things that happen inside of cells and organisms but not so much if you just care about easy phenotypic predictions.


text:
ID flying insect found in Belgium
I live in Belgium, and I've just witnessed a weird looking wasp/fly flying around in my room. Here's a picture:

So, what's this? It's still in my room, just chilling there. It zooms like a wasp, and flies VERY FAST. You can see white vertical stripes on his upper body, and then golden vertical patches. I couldn't get the camera to focus, so it's not really full-hd.
[Edit (better picture)]

Welcome to Biology.SE. You should add a descriptive of the size (or an object for size reference on the picture).

I have to disagree.  Horseflies are in the Tabanidae family, and I really suspect this is a hoverfly (the Syrphidae family).  Please see my answer below.

This is a hoverfly! Specifically in the genus Helophilus.  A lot of species of hoverflies exhibit Batesian mimicry of wasps/bees, as we see here, while they mainly feed on pollen and nectar.  So please, don't worry about it trying to bite you.
As far as species go, I think it is probably a Helophilus trivittatus.  I am basing that on location and a lot on the banding patterns on the thorax as well as the markings on the prominent terga.  Here is a picture below for you to compare.

It looks like a horse-fly

What is a horsfly?
Horse-flies (Tabanidae) represent a family in the order of Diptera that are distributed world-wide. They are large flies that fly quickly. Adults feed on nectar while females feed on mammals blood (including humans). When they sting, it hurts much more than a mosquito! You probably want to get rid of it before going to bed!
Wasps (Hymenoptera) vs flies
You thought about a wasp because you saw a pseudo-pattern of yellow bands on the abdomen I suppose. It is actually easy to tell it is a fly (Diptera) because (1) it has only two wings, (2) it has very big eye and (3) Hymenopterans have a thin waist while diptera don't. Another noticeable trait that should make you think of a horsefly is that it flies very fast. Note by the way that hoverflies have a very distinctive pattern of black and yellow bands but are flies and don't sting.
What species?
I don't know! But someone on this website will probably be able to find out.

As the OP noted, horseflies can indeed fly very fast. Actually, they are the fastest flying insect on earth! The speed of the male horsefly is attributed to Jerry Butler, an entomologist at the University of Florida, who once got a male Hybomitra to chase a plastic pellet fired from an air rifle; "Which it caught in midair and dropped," Butler says. From the speed of the pellet, he calculated the fly was going at least 90 miles per hour (145 km/h) at the beginning of female pursuit.

It's not a wasp. Wasps have a thin waist.
It's a fly, and flies can indeed be fast.
I would not bet on Tabanidae, but on Sarcophagidae instead, because your fly looks less hairy than what I'm used to for horseflies, and because of the striped pattern on the thorax, but it may well be some other family.


text:
examples of chromosomal aberrations with lack of sexual chromosomes?
Are there any examples in animals where individuals survive having no copies of their sexual chromosomes?

In humans the Turner syndrom is a disease that occur when the carrier is X0 (has only one sexual chromsome, the X chromsome). But it does not answer your question I guess!

Are you talking exclusively about nullisomic during the diplontic phase of an organism? Otherwise before Turner syndrome occurs in the diploid individual, one gamete (haplontic phase) has to be nullisomic for a sex chromsome.


text:
Detecting a Fasting State in the Body via Lasers
I was just wondering wether it would be possible to detect if the body is in a "fasting" state, via lasers attached to the body. If it is possible, what sort of laser would be needed?

If by a fasting state, you mean blood glucose levels, researchers seem to think it is feasible. See for example Pleitez et al. (1) and Guo et al. (2). Their designs both utilize infrared IR laser light to measure glucose levels in the skin.


text:
Is excretion always necessary?
I know we defecate or/and urinate to rid ourselves of toxins and excess undigested food. If I was somehow able to get exactly what my body needed to function.
Let's say that I create a pill (or something) that provides the body with literally and exactly the nutrients and hydration it needs, would there still be a reason to carry out excretion?
Do humans or any animal, absolutely have to excrete?

I'm not sure I understand the question because it is slightly unclear as it stands. But I think you're asking about a reasonably interesting and answerable topic; how much of our waste is from processing food and drink. A lot of your feces is bacteria, archaea, yeasts, fungi, viruses, and cells from your body. A fully fleshed out answer for this question could be useful, but we need a few edits!

@James yeah sorry. I have a basic understanding that we pee/poop to remove excess vitamins and toxins, so am just wondering if I have the most perfect diet ever, is there still a need to pee/poop? I'll try and think of how to edit this. I guess most broadly, why do we pee/poop?

Yes; there are byproducts of metabolism and maintaining the body that must be excreted, which has nothing to do with taking in unneeded nutrients. For just a few examples, urea is produced normally as part of the constant building and break down of proteins, but must be excreted, the brown color of feces comes from the breakdown of red blood cells, and a substantial weight of the feces is gut bacteria, some of which are necessary for proper digestion of some of the nutrients you take in.

Hm, that's interesting. So given the fact that I have perfect nutrition thnaks to MiraclePill, would my feces generally be the same amount/weight/etc? You mention substantial weight is due to gut bacteria, so would I expect to poop just as often as now, but just not defecate as much (volume wise)?

"Total parenteral nutrition" is the medical term for full IV feeding - this is not perfected to the "miracle pill" level and typically not used long term, but you can use this to try to find the information you are looking for. I couldn't find an ideal reference for you, in part because patients fed IV are usually quite sick, and in particular they often have serious bowel issues, hence the IV feeding. Just searching around I saw some anecdotes that suggest defecation still occurs but the quantity is reduced - not clear if this is because of frequency or the volume of individual stools.


text:
How long do fishes survive in a milk environment?
Suppose you placed a fish, a goldfish for example, into milk instead of water. How long could you expect the fish to survive?
Would it die due to lack of oxygen? Is there any other factor that could cause the death?

Why not a trout?

I am voting to close this thread because no previous research attempt is shown. You can't just come, ask a three line long question as if you were on the net. This goes against this forum's strict rules

@Algae — Unfortunately, in practice, you can't vote to close until you have more points (aka reputation). But I did it on your (and my own) behalf. However it's an old question, and, like the goldfish, dead by now.

I can't support this answer with scholarly articles. But it's an interesting question if you think of milk as highly polluted water.
Water from a tap (which is what goldfish usually live in) is 'fairly pure', with the naturally occurring minerals sodium, calcium, magnesium and potassium respectively in highest concentrations (varies by location.)
Milk, on the other hand, has not only a much higher mineral content, but also has fat, protein, carbohydrates, and white blood cells as 'pollutants'. In fact, whole cow's milk is only ~87.8% water.
Looking at calcium alone, the concentration of Ca in water is about  3 mg per 100cc, or .003%. Milk has .13% Ca, or 130 mg per 100cc. Since Ca is a major player in nerve and muscle function (in humans, a very relatively mild increase in serum Ca causes tetanic contraction of muscle), my guess is that the poor little fish would not be able to maintain normal serum Ca levels for long. It would die of inability to move fluid over its gills, that is, it would suffocate even in the presence of dissolved oxygen. Not to mention that the gills would also be coated to some extent by fat (3.5%), protein (3.8%) and other 'gunk'.
How long would it last? Probably not more than a few minutes.

Thanks for the answer. Now I can do some more reading about the effects that the presence of these minerals have on fish.

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


text:
First infection of malaria
As I know Plasmodium falciperum survive in either a host animal, human or mosquitoes.
But how does malaria come to infect either of them initially?
I am interested in knowing evolution of malaria. How it infected first mosquitoes when neither human nor any other mosquito was infected?

Could you provide some clarification of your question? Are you wondering how malaria evolved a multi-host life cycle? Or are you more concerned with how malaria is transmitted between a new host-vector cycle?

@hamilthj i know malaria resides either in mosquitoes or infected bitten animal, question is how it infected first mosquitoes , where did it come from

Great, I'd suggest clarifying that in your question to highlight your interest in the evolutionary origin of malaria


text:
Carbohydrate diet and dental health
I read that human started carbohydrates rich diet after adopting agriculture before that meat was main energy source which has comparatively less carbohydrate. High carbohydrate started destroying human teeth.
Would a keto diet (high protein fat) diet and low carb diet reduce cavity in teeth?

Where's your reference for the claim?

@GrahamChiu http://www.businessinsider.com/growing-crops-human-cavities-increase-2016-3     there are plenty other sources on google

Please run an English spelling check (and preferably a grammar check too) before posting. They come free on web browsers. You should at least check that the five words of your title are spelled correctly. And pay heed to @GrahamChiu. You need to cite your sources for assertions in your question. It is not enough to say there are plenty on Google (by which I assume you mean the web). If you cite them we can judge their quality. Are they papers in a peer-reviewed journal or just quack health site?


text:
Limit of muscle atrophy
I read that lack of action leads to muscle atrophy , I experienced same when I had a cast for hand fracture. So how far this atrophy go, who decides minimum size of muscle due to lack of activity, for example in coma patients.
Which part to brain or body signals muscle atrophy and upto what limit it should go?


text:
PCR master mix contents
I am running PCR reactions with different sets of degenerate primers and I want to know what should go into the master mix

My usual master mix:

DEPC water
PCR buffer (-Mg)
25mM MgCl2
10mM dNTPmix
cDNA

On ice I add my forward and reverse primers to the appropriate PCR tubes, add master mix to each PCR tube, then right before I pop them into the thermal cycler I add taq and mix.

Is this a proper way of doing it? I get product but I'm thinking maybe I can improve it by changing what I add to the master mix. For example, is it better to add taq instead of cDNA to the master mix and then add cDNA before I start the PCR? Is it okay to add both cDNA and taq to the master mix together?

I always add the Taq to the mastermix. First it makes the handling easier and it avoids pipetting steps which can cause contamination and can also be forgot. Then the enzyme is very stable and will even tolerate room temperature without problem. Since we are going to heat this 30-40 up to 95°C, so this is clearly not problematic. Since the reaction mix is cooled, you reaction will not start. And even if it does, there wouldn't be much amplification due to the low temperature.
I usually add everything which is the same for all reactions to the mastermix (this can include the DNA as well). If I use more than one DNA I split the mastermix in half. This way you are not going to make different pipette errors for the template, which is especially important for realtime-PCR. I usually dilute the primers slightly so I can pipett bigger volumes (simply use a part of the water used to balance the PCR reaction). You can also premix primer pairs, if you want, I have never seen problems doing this.


text:
Excercise and fitness in old age
I have seen so many news and study online, saying exercise keeps body healthy in old age and keeps us fit? how is this possible normal tear and wear will become more with activity hence more mutation hence more loss. Why exercise help?
Tear and wear means lots of regeneration in our body, regeneration will lead to mutations, no regeneration is perfect, hence more regeneration's, more risk of bad DNA.

Simplistically, the body repairs itself, and in reaction to the repair, often makes itself stronger.

@jamesqf - I wish that myth were put to rest where it belongs!

@anongoodnurse Specifically which myth?

@jamesqf repair means mutations

@murmansk: I really don't understand what you mean by "repair means mutations".  Do you mean accidents leading to imperfect repair?  In any case, it seems as though you're arguing from what you think SHOULD be happening, and ignoring a mountain of observational evidence that "it just ain't so".

@jamesqf - Repair does not leave things better. Healed fractured bone does not become better than unfractured bone (it's worse) unless it's fixed with titanium. A scar does not become stronger than the surrounding skin; it's weakened and less organized than normal skin. Etc. Otherwise sports injuries would never be devastating, etc. That's why studies are done on factors that improve healing.

@anongoodnurse: Yet when you stress a muscle by e.g. lifting weights to the point of exhaustion, it becomes stronger.  Likewise with aerobic exercise: stress heart & lungs, and they increase their capacity.   And (as you point out in your answer) when you stress bone, it becomes stronger.  Of course you can carry this stress/repair too far, to the point that it causes damage, but (at least to me) that seems less risky than idleness.

@jamesqf - My reaction was not to stress (I agree with that); it was to your comment, "the body repairs itself, and in reaction to the repair, often makes itself stronger."

If repair happens means there is duplication of cells and as I understand no replication is perfect, hence it will cause deleterious mutations, reason we get old and die or we get cancer

@anongoodnurse: So it seems that what we're differing about is not the process, but the language used to describe it.

@murmansk: Except for the observed evidence that a sedentary person who does not undergo that wear & tear of the stress/repair cycle is highly likely to die much earlier than one who does, and is likely to suffer from many diseases while they're still alive.  So however much you may like your theory, there is abundant evidence showing that it's flat-out wrong.

Not all "wear and tear" is bad. I will provide only one example. Trust me, I can provide many more, but I think one is sufficient to answer your question.
Exercise (against resistance, e.g. even gravity) is known to strengthen bones, for example. The stronger your bones, the less likely they will break as a result of a fall. While that sounds kinda "meh", it's incredibly important in the elderly, because once they sustain a fracture, their activity level falls dramatically for fear of sustaining another fall/fracture. Because of this, they have a decrease in muscle mass, a decrease in lung capacity, a decrease in cardiac fitness and an overall acceleration in decline of motor function, as well as a decreased quality of life.

Low-impact fractures, commonly called fragility fractures, have even higher mortality. Older patients with injuries from a fall have five times the mortality that their same age colleagues have from injuries from MVCs (motor vehicle accidents.) Five-year survival after an osteoporotic hip fracture is similar to that of patients with breast or other cancer. Almost one in 13 (7.5%) of those with fragility fractures will die within 90 days of fracture.* ...A fracture can be a devastating blow to an older adult’s health and independence, decreasing functional status and quality of life permanently. While some may recover their independence, half of older adults will require home health care in the 6 months following a fracture, and many will have long-term functional decline.

"Wear and tear" is good for muscles, bones, the heart, the lungs, balance, proprioception, and a number of other systems which help to prolong life, as well as the quality of life.
*Mortality is mainly with regards to hip fracture.
Fractures in Older Adults


text:
Is it possible to lose weight doing brain exercise?
According to this article human brain consume a comparable amount of energy with skeletal muscle. So is it possible to do some brain exercise (calculate something in mind etc.) instead of physical exercise to lose weight?
More specific questions:

Is it theoretically possible?
Is there any real-life example?
What kind of brain activity require more energy?
Pros and cons (brain exercise vs. physical exercise)

There have been several studies that show that even physical exercise itself isn't that good at causing weight loss unless you work out at athlete levels; dietary intake is much more important. Health.SE would be a more appropriate place to address that, however. As far as the brain, most of the energy the brain uses goes to just maintaining brain activity, metabolism doesn't change much during waking hours. Having seizures might cause a bit more energy use but I wouldn't suggest that for health.

only way to use serious calories is by upping heart rate to 100 - 140.

No The amount of calories the brain consumes is basically the same whether it is doing anything or no. Best case only about 3% increase in calories consumed by the brain or about 50 calories per day, which is miniscule and most studies do not even show that much.
Additionally buring calories is only important for weight loss once consumption is controlled. It is too easy to out eat any amount of exercise.
https://www.scientificamerican.com/article/thinking-hard-calories/


text:
Calculation of Respiration Fluxes in Terrestrial Ecosystems Based on Total Respiration (RT)
Overview
Researchers have been studying a temperate grassland ecosystem with the view to understand it's current status with regard to carbon inputs and outputs and to identify whether the grassland is currently a sink or source of carbon.
Investigation:
The aim of this investigation is to calculate different respiration components within an ecosystem with the energy fluxes within a terrestrial ecosystem consisting of:
Energy Fluxes

GPP = Gross primary productivity
NPP = Net primary productivity
NEP = Net ecosystem production
NEE = Net ecosystem exchange
RT = Total respiration
RA = animal respiration
RS = soil respiration
RM = microbial respiration

Query
I have answered the questions below to the best of my ability but with much confusion (see calculations below).
Am I on the right track? Am I calculating these respiration components correctly?
If anyone is able to help here, your advice and input would be deeply appreciated.
Many thanks!
Table 1: Flux values for temperature grassland

Respiration Components to be Calculated: My answers to the questions
1. Researchers measured the total ecosystem respiration (table 1;
    figure 1) as RT = 1300 g/Cm-2/yr-1. What is included in this total
    respiration?
Rs and Ra are not to be included in this calculation because they are part of the heterotrophic respiration system and they cannot be added to plant respiration.
The respiration components incorporated into RT =1300 g/Cm-2/yr-1 is Rp = 800 g/Cm-2/yr-1 (plant respiration), leaving 500 g/Cm-2/yr-1 to
be designated to roots, shoots, and microbial respiration.
2. The researchers measured soil respiration as  Rs = 900 g/Cm-2/yr-1 and estimat3e animal respiration above ground as RA = 50 g/Cm-2/yr-1. Calculate the respiration values for plant shoots (R,p-s), plant roots (R,p-r), and microbial activity (R,m).
Calculations for respiration components (Table 1; Figure 1)

Fig 1: Visual reprsentation of respiration fluxes

Can you give your reasoning for why you did the calculations as you did?

Hi Oosaka, After doing some really dumb calculations, I went back to the drawing board and tried again. I think these calculations are much improved and all respiration fluxes add to 1300. Is this answer correct? Many thanks if you can offer any helpful advice. Thank you again, you have been wonderful!

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


text:
Why do cells divide (or copy themselves)?
What I know
I learned about cells (not too much, but I've studied them a little bit. So don't feel offended when I say something which isn't really true. If something I write is wrong, please correct me (if it's not too much of effort).
Question
Imagine the first cell on earth.
Why would this cell "think" of dividing itself? How would a cell come up with the idea of dividing itself? The process of dividing itself isn't that simple, so ... how could that be? I don't really see a reason for devision from the "standpoint of a cell".
One of the solutions would be, that there's an intelligent creator, but I want to know the answer from the point of view from science.
Layman explanation would be appreciated
Just don't go too deep in the answer, I really just want to know if there is a solution to my questions. And if scientists really found out something, please just give me a very (VERY VERY) easy explanation.

There are two different points in your post. 1) Intelligent design. It has been explained thousands of times throughout the net why this pseudo-science hypothesis makes no sense. 2) Why did cells evolve to replicate. This second is IMO a good question (the answer of which lies into the existence of external causes of mortality). You should narrow your point down to this element I think.

As a sidenote, you might want to follow some very easy and very introductory course to evolutionary biology such as Understanding Evolution by UC Berkeley for example.

ok, I changed the question. I really just was wondering how that could be, because as I studied the cell, this question came to me, and my teacher couldn't give me an answer.
Thank you for the link!

I think this is as much a question in philosophy of biology and metaphysics as it's in biology alone. You might also be interested to look in this SE question in the philosophy section-http://philosophy.stackexchange.com/questions/15596/why-is-it-necessary-to-survive/41102#41102 . There I gave a brief answer from both philosophical and biological point of view that might be related to your question. If you are interested in the broader perspective of your question you may check it out.

if I have an ocean with two things one that copies itself and one that doesn't, and I wait a while, then I am more likely to have more of the first because it, you know, makes more of itself. Thus there are many of the first and few of the latter. certain chemicals copy themselves, certain strands of RNA are a good example as are some prions. It's like asking why stick in a fire want to catch fire, there is no want it's just chemistry.

You're assuming that a cell somehow came into existence and then began to replicate. The situation is most likely the opposite: there were self-replicating molecules (perhaps RNA, nobody really knows) long before there were cells as we know them today.

"One of the solutions would be, that there's an intelligent family of creators" - thought of that too?

The "Why" question
Why do organisms replicate?
Given that there is (extrinsic and also eventually intrinsic) sources of mortality, organisms that did not replicate just ended up disappearing. Those that did replicate eventually ended up giving rise to important lineages.
In other words, replication occurs because those who did not replicate disappeared. It is also because unique instance of things may disappear that you regularly backup your computer (if you do).
The "How" question
By what mechanism did early replication occur?
You actually did not really ask about it but here are a few words anyway.
The mechanism by which first replication occurred are mainly unknown as it is hard to investigate specific processes that occurred such a long time ago. The field that studies the origin of life is called abiogenesis. You might especially want to read the section on Self-enclosement, reproduction, duplication and the RNA world. You might also want to read about Autocatalysis.
I am afraid that a summary of existing hypothesis on early reproductive systems are 1) out of my capacity and 2) would hardly fit into the wish to receive a very (VERY VERY) easy explanation.

Good answer; the others seem to overshoot the simple observation of what happens when one molecule reproduces itself and another doesn't.

There are two issues with your question that both lead to potential answers.
First, the assumption that there was ever "a first cell" is wrong. Life in general occurs in populations; if there's one of something then there usually are others. And the same is true in chemistry; usually if you have a certain molecule in a certain place there are probably others there too (that got there in the same way the first one did), and they're all having similar reactions (because similar molecules behave in similar ways). As abiogenesis, the general term for the development of life from non-life, involves complex chemistry resulting in self-replicating systems resulting in life as we know it, all of those principles would apply there too.
Second, the assumption that the first life was a cell is likely wrong (except if God created life, and started with a cell, or some other such ad-hoc idea of course). Life is partly defined by self-replication, and self-replication is also what allows the optimization of systems for specific purposes via the processes of biological evolution (which requires, and is a consequence of, imperfect replication); meaning that as soon as you get a self-replicating system you're well on your way to having life - and the first cells as we know them likely developed quite far along that process, because they already are quite optimized.
In this perspective, the answer to your question is that there was never an issue of "the first cell" "deciding" to "replicate" - the first life replicated by definition - and whether it was a cell or not is a completely different issue.
As to how the first life "decided" to replicate - replication is a chemical reaction, it's not like modern DNA "decides" to replicate, it is a chemical reaction that occurs when the conditions make it inevitable. Biologists currently do not know what the first self-replicating molecules or systems were and how they replicated without the complex mechanisms that allow the chemical reactions that make DNA replicate, but the assumption is that it was a chemical reaction that happened for the reason chemical reactions happen - the components and conditions are such that following the laws of physics results in the chemical reaction happening. For what it's worth though it should be noted that while DNA cannot do anything outside of the mechanisms of the cell, the same isn't true of RNA; in fact small sequences of RNA can pair off on their own in solution, and it is generally thought that RNA came before DNA in the development of life.
Abiogenesis is an unanswered question of science, but if you want more ideas of what biologists think might have happened you could look here:
https://en.wikipedia.org/wiki/Abiogenesis
Otherwise I can't help but mention my favorite hypothesis of abiogenesis, which I find most exciting and (to my layperson eyes) convincing, and more importantly illustrates how "the first cell" could have been a fairly late step in the development of life. Here is a video of one of its originators talking about it:
https://www.youtube.com/watch?v=gb7pZyks_HE
Basically those researchers started out looking at the energy of the chemical reactions that make the building blocks of life, and figuring out how natural reactions could generate that energy. They found that the conditions that occurred in hydrothermal vents were conducive to such reactions:
http://journalofcosmology.com/Abiogenesis107.html
In more recent papers they connect this to comparisons of existing cells to try and figure out which features the Last Universal Common Ancestor of all life had, and putting those things together they build a fairly coherent picture of the first "organisms" developing inside pores of the material of hydrothermal vents, involving chemical reactions that produced complex molecules which promoted the production of further such molecules (including proteins, enzymes and RNA that can both self-replicate and promote the creation of proteins),  and the development of membranes not so much as a protection from the outside world but to maintain the energy difference between inside and outside the pores ("proton gradients") that further promoted the reactions in question, and bacteria and archae being the result of two independent events of cells "breaking off" from the porous rock and becoming free-living.
http://nick-lane.net/wp-content/uploads/2016/12/Sousa-et-al-Phil-Trans.pdf
Here is a figure from that paper:

(And this goes a bit to my first point about there not having been a single first cell - you can see in this hypothesis there would have been many pores/reactions occurring along proton gradients/groups of complex molecules reacting in positive feedback loops/self-replicating systems/membranes forming/cells breaking off/etc at any one time, making it more likely for any one "step forward" (in quotes because it's only a step "forward" in hindsight; at the time it would be a variation among others) to occur somewhere in that population).

this is nice answer but energy is not always associated with the emergence of Life. See for example here- https://en.wikipedia.org/wiki/Dissipative_system an article about what scientists call dissipative structures. They too can consume energy and self-organize but would you consider them alive? Actually the big question concerning your post really is: Can there be Life without cells? And if the answer is not, then the OP has a point about equating Life with cells.

@YordanYordanov I never said "life DID originate without cells", I said "life COULD HAVE originated without cells" (well ok to be fair I said it LIKELY originated without cells, which is still less absolute than what you're claiming). OP started out assuming that the first life was a cell; this is a valid assumption if we know that life cannot exist without cells, as you say, but it isn't a valid assumption if we don't know that, which is the point I was making. Also, I don't see how your comments about energy relate to things I said in my answer.

Actually if you want to know more how difficult it is to actually define Life and why all those who favor one or other property to define Life have so much problems defending their point of view here are 2 papers related to the subject-http://www.google.com/url?sa=t&rct=j&q=&esrc=s&source=web&cd=3&ved=0ahUKEwjutJqR29bSAhXG6xQKHSn3C_sQFggnMAI&url=http%3A%2F%2Fspot.colorado.edu%2F~boonind%2FCleland.Life.synthese.pdf&usg=AFQjCNGkPTHYezOUG7D2_aajhmclkpq5Pg&sig2=rj31QVZo9Ge-BYKuNIel5Q

and http://quod.lib.umich.edu/p/ptb/6959004.0006.001/--proper-activity-preference-and-the-meaning-of-life?rgn=main;view=fulltext . They make an excellent example of the difficult (both philosophical and scientific) of prescribing Life to anything. I guess you should check them out. My argument is you can claim anything about Life at this point of development of science. What we know for sure is that Life is within cells but this doesn't mean we can prove Life is possible without cells. If you ask me (for my subjective opinion) then I would gladly agree viruses are alive,too

But the scientific community won't back me up 100% because as I say-"There is NO definition of Life, yet." at our current level of development of science. Therefore the only case for Life we can all agree on is cells and the OP has the right to ask his/her question in the manner it is asked, but the claim that Life is defined by self-replication is not valid in the context of modern attempts to define Life because as, I show you, we have no universal definition of Life yet, So how can you claim what defines Life we have no definition of it?

@YordanYordanov Neither of those papers seem relevant to abiogenesis. The first is closest but is about applying the definition of "life" in a general enough way to include potential extraterrestrial life (which the author is right that we currently don't know enough to do), not about the intermediate steps that would have led to modern Earth life. The second is purely about definitions; again, not useful for abiogenesis where the parameters are already well-defined in the sense those philosophers are thinking of.

@YordanYordanov I am not talking about a universal definition of life, and neither is OP. We are talking about how life started on Earth. In this context it's true that defining "life" is a matter of boundaries, and it's also true that "self-replication" isn't the only possible place to set the boundary (that's ignoring that the boundary WILL be fuzzy, and will be so even if we use "self-replication" as the boundary) (...)

my point is that if we have no universal definition of life and we can claim only that cells are the definitely alive, then the OP's question is justified in the way it's asked but at the same time the argument that Life begins with self-replication is not justified because as you can see in the papers it's still a matter of debate which is the property that defines Life so your point of view of equating Life with self-replication isn't justified. Can you understand me?

@YordanYordanov  ...but the justification I gave for using it is a good one: self-replication, aside from being a definition of life, also defines the point at which the process of biological evolution starts; in other words, the point starting from which the features that develop are the result of evolution (and the optimization that implies) and not only abiotic processes.

I understand your point but setting boundaries arbitrarily isn't possible without some deeper understanding of what the phenomenon which you put inside the boundary is. And we don't have that for Life, yet. This is why you can't "just use" self-replication for the definition of Life. The only thing you can use for sure is a cell because everyone agrees cells are alive. Otherwise I can put up the argument that even a hurricane (e.g. dissipative structure) is alive if it can self-replicate. Do you agree hurricanes are alive?

@YordanYordanov "Can you understand me?" I understand you fine, you are simply wrong and confusing definition games with scientific enquiry. "All modern living things have this feature" is not a good justification for "the first living thing had this feature", because the development of life would have been gradual, i.e. would involve intermediate steps between life and non-life, i.e. would involve entities that had many but not all features of modern life, i.e. we cannot affirm that a feature occurring in all modern life implies it existed in the first life, or worse defines a boundary.

Let us continue this discussion in chat.

@YordanYordanov Two last points: first, I don't know how you can claim I "just use" self-replication when I have justified this choice twice now and you have addressed the reasons for that choice neither time (I addressed in my previous comment why "is a cell" is way more arbitrary a criterion for setting the boundary). Second, please read Sousa et al, or look at the diagram, and tell me by what criterion you call the free-floating stage "alive" and the immediately previous stage "not alive".

@YordanYordanov I have to leave, I'll be in the chat in half an hour or so.

Here is a story,
Lets imagine that we go back a long long time ago.
Lets imagine a bunch of cells. Some divide. Some do not. And every so often a cell gets randomly damaged from UV light, toxic chemicals or just gets eaten by another cell.
So what happens.... cells that divide soon out number cells that do not. And in say 1 years time, all cells that you find are cells that divide.
And this is why cells divide. A self replication machine soon outnumbers a non-self replicating machines by virtue of being able to replicate.
There is no thinking required. Also no intelligent design is required either. Anything, any random mutation that makes the self replicating machine work better, even a little, will soon cause that better more efficient revision to out number the original version.
It isn't intelligence so much as water flowing down hill.
In fact that this is how some man-made ribozyme are made. A scientist first makes hundred of millions random RNA sequences. Then feed the mixture into  a test for activity. If activity occurs the molecules is copied by RNA dependent RNA polymerase. And more copies are made... and since RNA polymerase makes many error... you have a mutation rate. The products go through another round of selection. And so on.
And when the scientist comes back later in the week... they have an efficient ribozyme. Did the scientist design this molecule.. some intelligent design? Nope. There was next to no intelligence in the design of RNA. In fact said scientist wants to study this mixture of ribozymes and find how they work.
In nature that test is simply survival. Being around as long as possible to replicate as much as possible.
The experiment I am describing is a generic experiment to demonstrate how the RNA world could develop. Several examples
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2652413/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4390851/

can you show the paper where this experiment is described. Can you provide some references? I mean the artificial rybozome experiment.

First of all, there are cells that don't divide. For example, the nerve cells of mammal's central nervous system are shown to be very long lived and the rule is they don't divide through time. The same is true for most of their muscle cells, but yet, the point you infer is correct-cells do replicate, otherwise all the cells would have died of old age by now and the Earth would be lifeless. Therefore, the answer to your question is more in the line of the answer of the question: Why do there are always cells which want to divide? Do you agree?
Now, I have one question in the philosophy section that you may find relevant to yours. It's here. There I ask about the relationship between the ability to "act on your own" which is defined as agency there and the notion of choice-e.g. the ability of anything to move into different states in a non-deterministic way. I will cut down the philosophical terminology and give you the short answer I made for myself after reading and discussing this question in the Philosophy SE. Basically, the cell doesn't have a choice other than choosing to replicate. Yes, I know this answer may seem very hard to grasp but you need to think of the cell not as a free will creature as you are but as a kind of "computer" which has instructions in its "program", e.g. DNA when and where to replicate and when and where to stand still. So it has agency (the ability to choose) but it doesn't have free will on its own like you or I have. Just like a computer can't really choose what to do-it's its program that tells it what to do.
This is the answer to your question-there isn't such a thing as a "standpoint of a cell" because it really does not have free will. If it has no free will it can't have a "standpoint". Just like computer can't have "standpoints", too. It divides because it's programmed to do so. It only appears to us the first cell had any choice what to do and what not. The reality is the cell is nothing more than your computer with Windows OS. If Windows say-divide, it will divide (if of course, it was able to). There is no choice for the cell to divide or not. It's just what its program is. So, until there are cells programmed to make more copies of themselves which program their descendants to make more copies of themselves there will be cells dividing because the program is self-replicating. And just like any other computer virus until the hard drive (e.g. the environment) provides it with the means to reproduce-it will do so. Can you understand me?
P.S. If you however, kind of "translate" your question as to why the first cell had this "program" to replicate, then the answer lies in chemistry, not in biology. There is this thing called chemical evolution. It literally mean the origin of the "drive to reproduce" which eventually became the "drive" to divide was a direct result of the interactions between chemical, not biological reactions. And chemical reactions are deterministic, e.g. they have no free will. A reaction just can't possibly choose to occur, or not to occur. It happens under the natural conditions of the environment and when chemical evolution was eventually replaced by biological evolution the cause of the first became the cause of the other, too. This is how to explain the origin of the "will" of the cell to replicate and as you can see everywhere around you this "cause" is pretty much still in action everywhere. I hope you can get my point.


text:
Can you use a microscope without an eyepiece?
Can you use a microscope without an eyepiece?

Do you mean without a camera too and looking straight into the tube?

yes I do mean that.

Yes, sort of. I tried it just now - take the eyepiece out and look down the tube.  However, the view area is smaller, and you lose the magnification of the eyepiece.

Yes, you can. I have a microscope where the data can be transferred to a screen on a computer instead of going to the eyepiece. This microscope has both an eyepiece and the option to redirect the image to a screen. However, I also have a microscope with a screen only. So, I suppose you can have a microscope without an eyepiece.
I have never come across a microscope that has neither an eyepiece nor a camera but I don't know whether it's possible or not.

You might want to edit your answer to address the OP's answer to my comment under the question.

Surely you have taken the eyepiece (or the camera) out of your microscope?  I think with most the eyepieces just slide in - mine works that way.

@jamesqf I have not taken the eyepiece out. It arrived without an eyepiece, just with a screen.

A microscope composed of a single lens is called a simple microscope. In fact you can use an objective or just the eyepiece, as a magnifying glass. Antonie van Leeuwenhoek's microscope's were simple microscopes.

Source: Wikipedia
In contrast, compound microscopes (by far the most common type nowadays) are composed of two or more lenses. I would argue that their benefits compared to simple microscopes include:

Multiplicative magnification arising from the combination of lenses.
Ease with which the objectives can be interchanged independently of the eyepiece offering different magnifications.
Easier to achieve an ergonomic design.
Advanced illumination setups, such as phase contrast.
Cheaper to provide stereoscopic vision and achieve parfocallity with two low-magnification lenses that are able to be focused independently than having two high-magnification lenses.
Some eyepieces additionally correct for aberrations.


text:
I need some forearm bone motion pictures
I would like to know how my forearm bones move inside my forearm when I'm twisting my hand. (Also, it would help to see the hand bones action too). "twisting hand" means to me the motion in which the rest of the body is in place except the hand which turns from upside up to downside.
I have the intuition that the bones inside my forearm move between themselves to make my hand twist, but am not sure if that is true.
I would like pictures of the forearm bones before and after twisting. Animations would also be great of course.

I replaced the "I want" and similar expression (that give of answering to the request of a dictator) by "I would like" and other more appropriate expression. In the same logic, in your comment under the current answer i would remove the I will accept your answer if you clarify that [..] part of it. Of course, I don't think you feel like giving orders. It is only a matter of expression. You might as well not be a native english speaker. (I am not either).

@Remi.b yes, thank you for editing, I was experimenting with language. He fulfilled my request and now I gave him his prize. And yes, I'm not native english speaker.

Here is a basic image. Palm up is called supination and is the resting (anatomical) position. The radius and ulna sit parallel. When the forearm is in pronation, the radius crosses the ulna.
You can feel this yourself. Put your fingers on the ulna and move the palm into pronation and supination. You will not feel the ulna rotate. Only the radius pivots during this movement. The wrist is not involved in this movement.

The ulna is unable to rotate at all, because its olecranon process is locked into a groove on the distal end of the humerus. If you put you fingers on your bony "elbow" (olecranon process) and pronate/supinate your hand (without flexing/extending your elbow), you will not feel you ulna moving.

Suppose I rotate my forearm as described, from pronation to supination. My ulna rotates around itself? I see the radius moves, but I want to know if the ulna rotates around itself. I will accept your answer if you clarify that in your answer.

Thank you very much, this is indeed the info I needed! Please feel useful :).


text:
Difference between feral and domesticated honey?
Is there any significant differences in composition (and/or taste) between the honey of wild ("feral") honeybees versus that of domesticated ones used in beekeeping?

I think your question is on-topic but just for info cooking.SE might also have been a possible place where to ask this question.

Domesticated bees are often used to fertilize crops, so their honey consists mainly of nectar from a single type of flower: e.g. clover, orange, alfalfa, blackberry, and more.  Feral honey (or honey from garden hives) presumably comes from a mix of whatever flowers happen to be growing around the hive.

@Remi.b Not so sure, since when it comes to cooking, wild honey can be pretty hard to come by!!! :-D


text:
Definitions of hermaphroditism, dioecious and monoecious?
What is the difference between these terms "monoecious","Hermaphrodite".
my lecturer says hermaphrodite is a zoological term and monoecious is botanical term, but in contrary to it, in my textbook both of these terms are used both botany and zoology.
So what is the actual difference?

Below are definitions that I've seen; there may be less strict definitions under which monoecy (the noun form of 'monoecious'). and hermaphroditism would be the same thing.
Dioecious: Although rarely used for animals, one could say that human are dioecious because each individual produces only one type of gamete. In a dioecious species, some individuals are males and others are females.
Monoecious: In monoecious plants, individuals carry both males and female flowers but not flowers that can produce both female and male gametes.
Hermaphrodite: Hermaphroditic plants have flowers that can produce both male and female gametes.
Then, there are many other fancy terms such as dichogamous, gynomonoecious, subandroecious, heterostyly or androgynomonoecious! Plant mating systems are fantastically diverse and complex!
More information
Some of these terms are defined in The Evolution of Sex Determination, which is very pleasant to read. For shorter articles, consider Barrett 2002 or just Wikipedia > plant reproductive morphology or Wikipedia > dioecy (the noun form of 'dioecious').

According to "Plant Identification Terminology: An Illustrated Glossary" (Harris & Harris, 2001):
The main difference is the frame of reference. "Monoecious" refers to a whole plant having both male and female parts, while "hermpahroditic" refers to an individual flower having both male and female parts.
Hermaphroditic:

With pistils and stamens in the same flower; bisexual; monoclinous; perfect

Note: "Perfect" = with both male and female reproductive organs (stamens and pistils).

Monoecious:

Flowers imperfect; the staminate and pistillate flowers borne on the same plant

I will caution you that different sources use "bisexual" inconsistently to refer to either instance.


text:
Autosomal genes expression occurs from both alleles simultaneously
Based on my understanding of Knobil and Neill's Physiology of Reproduction.
For the vast majority of autosomal genes, expression occurs from both alleles simultaneously. In mammals, however, a small proportion (<1%) of genes are imprinted, meaning that gene expression occurs from only one allele (some recent studies have questioned this assertion, claiming that the number of regions of parent-of-origin methylation in, for example, the human genome, is much larger than previously thought).
I'm confused, why would expression occur from both alleles simultaneously? Ex. if it was "Rr" - the expression would only occur from "R", as opposed to both alleles simultaneously?

Definition of dominance and recessivity
By definition, an allele is dominant over another allele if the phenotype of the homozygotes for the dominant allele and the phenotype of the heterozygote are the same but not the ones of the homozygotes for the recessive allele. In other words, let $p_{ab}$, be the phenotype of an individual with alleles a and b, then

$p_{rr} = P_1$
$p_{rR} = P_2$
$p_{RR} = P_2$

, where $P_1$ and $P_2$ are two phenotypic describer.
Note btw, that very very few traits have their variance explained only by the genetic variance, even fewer are explained only by variance at a single locus and yet even fewer have a locus that show a simple dominance / recessivity pattern.
Expression
If needed, please check gene expression.
The fact that an allele is dominant over another does not mean that the other allele is not being expressed. In fact, it does not say anything about the molecular mechanism by which this dominance pattern is achieved. It is possible that in some cases, if the recessive allele was not expressed at all, then the resulting phenotype would be $P_3$. It just so happen that most of the time, both alleles are being expressed.
Imagine for example a case of a locus coding for a black pigment. Let's consider haplotypes that where the gene is missing (copy number variation). Let's refer to such haplotype with 0. 00 are white. 0r individuals are light grey. rr individuals are grey. The allele R causes the expression of a lot of pigments so that both rR and RR individual are indistinguishably black. The allele r is still being expressed in heterozygotes rR even the phenotypes of rR and RR individuals are the same.

So both genes are being expressed  as in "Rr", but because "R" is dominant, only, "R" is demonstrated via the phenotype.

Yes, by definition of R begin dominant, the phenotype of Rr is the same of RR but r might be expressed (or not). See added example at the end of the post.

Note btw, that very very few traits have their variance explained only by the genetic variance, even fewer are explained only by variance at a single locus and yet even fewer have a locus that show a simple dominance / recessivity pattern. WHAT DOES THIS MEAN?

What part of this sentence is unclear to you? You should maybe check the word 'locus'. You probably should need to have a look at the post Why is a heritability coefficient not an index of how “genetic” something is? that offers an intro to quantitative genetics to get a sense of why I am talking about variance.

thanks asked a new question with my interpretation of the terms.

why would expression occur from both alleles simultaneously?

Why wouldn't it?  What mechanism do you propose and have evidence for that would cause one allele to not be transcribed, based only on the phenotypic outcome of its expression?


text:
What are the total number of alleles for a single trait?
Humans receive a copy of gene from both parents and each gene has an alternative form called allele. Does every person possess two genes and four alleles for a single trait?

To fully answer your question it would take an entire course of molecular genetics and quantitative genetics. I will be only very brief and will let you seek for more information on your own.
Basics of molecular genetics
You are confounding gene copy and allele. As we are diploid, we have two copies (I am ignoring here sexual chromosomes and mtDNA) of every locus. This is true for genes too. We have two copies of each genes. Now, we may or may not have the same allele at these two copies. If we have the same allele at both copes, we are homozygous, otherwise we are heterozygous at this locus.

You might want to have a look at the post Do men and women have the same number of genes?

Now, each chromosome is made of two sister chromatids (although this number varies depending upon the stage of life cycle). The sequences at the two sister chromatids are exactly the same, so you can't have different alleles at two sister chromatids.

You might want to have a look at the post What is the relationship between DNA molecules and the chromosomes?

Basics of quantitative genetics
Of course, a single phenotypic trait is not necessarily mapped out by a single locus. There are usually plenty of loci involved (see Quantitative Trait Loci, epistasis and eventually pleiotropy). There is also other source of phenotypic variance than genetic variance such as environmental variance for example.

You might want to have a look at the post Why is a heritability coefficient not an index of how “genetic” something is?

Ok ,but I can't get your point .As there are two copies of one gene each from father and mother and we have an allele for every gene copy so, combining these we got two genes and four alleles .?Can we?

We receive one copy of every locus (or gene as you seem to get stuck with this term) from each parent. If these two copies differ, then we have two different alleles (heterozygous), otherwise we have only one type of allele (homozygous). In some life stage of the cell cycle, each chromosome is made of two identical chromatids. When this is the case, there are 4 copies of the gene but never more than two different alleles.
You really seem to use the term "allele" when "gene copy" should be used. Think of an allele as a pokemon card. When you ask someone "do you have Pikachu?", you're not asking whether the person has the exact same card that the one that is in your deck of cards. Alleles are the same! So even if you have 2 copies of a given locus (that is two pokemon cards), you might or might not have two different alleles.
You also use the term "gene" where it would be more correct (or more general) to say "locus". You should check out the definition of locus.

Ok ,but I can't get your point .As there are two copies of one gene each from father and mother and we have an allele for every gene copy so, combining these we got two genes and four alleles .?Can we?

@RabikJohn See edit

By two copies of gene you mean that there is a pair of alleles which we receive from our parents?Like in pea plant diploid cells have a pair of alleles for each gene Rr Yy or Tt?

I just insist to use the term gene copy and not allele because the two gene copies we receive might be the same allele. I feel like I am repeating the same thing over and over. I am sorry if it does not help.

Genes are sequences of DNA that do specific things (typically, that get encoded into proteins).
Chromosomes are long DNA strands that contain, well, DNA, and some sequences of that DNA are genes.
Those genes occur in specific places along the chromosome, just like the word "genes" occurs in specific places in this sentence (second and fourteenth word, namely), and if you copy-pasted this sentence they would be in the same places in the copy. This means two ways of recognizing the same gene in two copies of a chromosome are its sequence (which might not be identical if there are copying errors, but will be very close), and its location in the chromosome.
There is a bit of an ambiguity there; sometimes we use the word "gene" to refer to a literal sequence of DNA that forms a gene, but sometimes it refers to the more abstract concept of the same sequences that occur at the same locus in different people and do the same thing.
It's a bit like people can talk about "a Harry Potter book" and refer to the literal paper-and-ink book on their shelf, or they could be talking about the abstract stories in the Harry Potter series.
If you see a DNA sequence with ATCG and it's labeled as a "gene", it would be the first one. If people talk about "we've found the gene for Parkinson's", "how do we recognize the same gene in two copies of the chromosome", it will typically be the second one. And because the sequences aren't always identical you can have similar sequences of DNA, in the same place, that do basically the same thing, so they're "the same gene" in the abstract sense, but they do it differently from each other. Those can be thought of as variants of one another, and those variants are called "alleles".
In the Harry Potter analogy, alleles are like which of the six Harry Potter books we're talking about. So if you have two Harry Potter books in your library, The Philosopher's Stone and The Prisoner of Azkaban, you wouldn't count it up and say you have four books: the two Harry Potter books, and The Philosopher's Stone, and The Prisoner of Azkaban. You would understand that "Harry Potter books" is a general term that refers to a certain kind of books, that have enough in common that they can be considered "the same" in the sense of all being one series, and that this specific kind of books comes in six variants. You can't have "a Harry Potter book" that isn't also one of the six specific Harry Potter books that exist (I bet there are more now but let's ignore that for the analogy).
Also, if a person has on their bookshelf two copies of The Prisoner of Azkaban, do they have one Harry Potter book, or two Harry Potter books? It depends on whether we are talking in an abstract or a concrete sense. They have two literal paper-and-ink books on their shelf, but they have only one Harry Potter story.
Similarly, every person has two copies of a gene, i.e. a certain DNA sequence at a specific place, or "locus", on the chromosome, and if we're talking about literal DNA sequences we'd say they have two genes, but if we're talking about the more abstract concept we wouldn't say that. Usually when people talk about genes they're talking in the abstract sense, and thus talking about different sequences at different places on one chromosome, not copies of the same sequences in different chromosomes. Kind of like if someone asked you how many book series you own, you wouldn't count your paperback and hardcover copies of the same Harry Potter books as two series.
So to answer your question "Does everybody possess two genes" -> yes, for one sense of the word "gene", but it's not necessarily the one you meant.
As for the alleles, just like your two HP books aren't four just because they also have a specific title, people don't have four alleles because they have two copies of a gene and those copies are each a specific kind of that gene. People have one or two alleles, depending on whether the two copies they have for that locus are the same allele or two different ones.
By the way, it is not true that every gene has one variant called an allele (or, put in a better way, that every gene comes in two variants). Some genes don't vary much at all between people, so there's only one allele for the human race and everyone has the same one, while others have tons of alleles. But every person will only have one or two of those alleles, unless they have more than two chromosomes.

Thanks,I think I got it know .Are you trying to say that we have two copies of genes on every locus(of homologous chromosomes) but one gene can have homozygous allele or heterozygous allele so at one locus we can only have one allele so combining alleles of both locus we came up with just two alleles for two copies of genes ?

You are phrasing things in an unusual way so it's hard to tell! You say "two copies of a gene in every locus" as if "locus" is the abstract concept of a place on a chromosome, but then say "both locus" as if talking of the literal place on each copy of the chromosome. We have only one gene at each literal place on the chromosome where that gene is (just like you can have only one first word in a sentence), and because there are two copies of the chromosome that means two copies of the gene for each locus (where locus=abstract concept "that place on chromosome 2 where gene A is found").

@RabikJohn Also, a gene "having homozygous or heterozygous allele" is strange phrasing because "heterozygous"/"homozygous" isn't about the gene. Like a sock in a drawer isn't "matched" or "mismatched"; it's a person wearing a pair of socks, and them being the same or not, that makes that pair matched or mismatched for this person. A gene has alleles, i.e. variant forms it exists in. People have two copies of the gene, each in one of those variant forms. If the two copies are the same variant(allele) the person is homozygous for that gene; if the two copies are different, they are heterozygous.

I confused you because I was confused myself about itI don't know what does actually mean to have two copies of genes on homologous chromosomes? I always think it might be like that one locus on mothers chromosome will have a gene and father's chromosome will have the same gene on same locus but with different alleles and when they combine to form homologous chromosomes then we will have two copies of genes for every locus  but I can never understand how does two homologous chromosomes with two different alleles (as ithink they have) express a single trait ?

@RabikJohn The way genes express traits is very complicated, and not really about chromosomes. Chromosomes are about packaging the DNA so that it can be duplicated in reproduction. Outside of reproduction DNA is transcribed into proteins, which do everything in the body. This transcription has several intermediate steps, which can involve "amplifying" genes (making many copies to make more proteins), silencing them, etc. So what it means to have two alleles depends on the genes and traits involved. Sometimes if you have two alleles means you have two types of a certain protein.

If we  have more than two alleles for a single trait then the protein product produced depends on both alleles or an intermediate protein product is formed ?And can you tell me something about location of genes on homologous chromosomes?

@RabikJohn With "more than two alleles for a single trait" do you mean "more than two genes" (i.e. the trait is affected by many sequences at many places on one or more chromosomes; any of these sequences can have variants that are different or not on the homologous chromosome)? Because again, no human has more than two alleles of a gene, unless they have more than two copies of a chromosome. If you are heterozygous for a gene I think the typical case is for both proteins to be produced; for example the sickle-cell gene, heterozygous carriers have both normal and abnormal red blood cells.

Yes ,by more than two alleles I mean two genes,As there can be only two alleles for a single trait so these two alleles can be different on homologous chromosomes as( I think you are saying) then these two "alleles" are present on "homologous chromosomes" I mean to say one gene is present on one chromosome out of homologous chromosomes or an allele is present ?


text:
By what mechanism can two chromosomes fuse?
What condition(s) would likely exist which could cause 2 chromosomes in the newly fertilized egg of a placental mammal to fuse? Assume this is more likely than having the same chromosome pair fuse in an individual egg, as well as an individual sperm.

Chromosome fusions (as well as fissions and other changes) usually take place during cell division or pairing, therefore, it's very unlikely that two chromosomes will fuse in an already fertilized egg. If they do such, this egg would probably be aborted.
One factor that may lead to chromosome fusion is loss of thelomeric sequences (telomere = chromosome extremity) (O'Sullivan and Karsleder, 2010) - but probably not in an fertilized egg.

As I trashed a recent answer of yours, I felt like I had to show myself nice by adding a reference to this answer! +1


text:
Does the body have specific mechanisms for healing burns, or is it general purpose stuff?
I burned my thumb lighting sparklers (fireworks) a few nights ago. I've been pleased with how it's healing, and have been especially impressed because it's not a scenario that really could have come up in our evolutionary history. Then I started thinking that fires are not that common in nature. This prompts the question: do our bodies heal from burns using burn-specific techniques, or do they just follow general “procedures” for repairing damaged skin?

general applies to many specifics.


text:
What species of butterfly is this? Picture taken on 9-18-2018, near Helena, Mt

Butterfly picture taken on the 18th of September 2018 at an elevation of 1800 meters (6,000 feet) near Mount Helena in Montana, USA.

To me it looks like one of the tortoiseshell butterflies (genera Aglais and Nymphaiis) - but I could not tell which one :/

Oh, and just to be certain: I guess "Helena, Mt" is "Helena, Montana, USA"? It might not be obvious to everyone in this international community :)

Yes, Helena, Montana, USA.

That is a California Tortoiseshell google[https://www.butterfliesandmoths.org/species/Nymphalis-californica]


text:
If an insect becomes upside down, do they have mechanisms to turn themselves right side up?
This question is mainly applicable to beetle's and cockroaches. If I flip them so their legs point upward, they usually squirm around and wiggle trying to come back upright. Sometimes they succeed, and turn right side up again; sometimes they don't. Do insects have any built in mechanisms to unflip themselves.
I was unable to find any sources, but I believe they should, since insects climb stuff, and they may land inverted if they fall, so a mechanism might've been evolved to unflip themselves.

Why don't you consider their attempts to come back upright as a mechanism to do so? If they are having difficulty, it might be because artificial surfaces provide an environment they have not experienced over evolutionary time: that is, very flat surfaces, with no debris around for traction.

Why don't you consider their attempts to come back upright as a mechanism to do so? I could attempt to fly, although I'd die if I tried, since I have no mechanisms (wings, hollow bones) to fly.

Pinging @BryanKrause

@Pritt Air is not the natural fluid for us to fly, you would fly if you change the fluid to water( that is swimming). Hope u understand the analogy.

You seem to have skipped the second half of my statement. I think your question is a bit like putting a human on glare ice, perfectly smooth, and asking them to try to run. Then, when they slip and fall, you ask "Do mammals have mechanisms to keep themselves from falling while running?"

But @BryanKrause insects getting flipped isn't an artificial phenomenon is it? It could happen as an insect climbs a wall and slips down. It could happen anywhere on Earth's landmass.

I'm suggesting that the beetles and cockroaches you see are probably only struggling because you have them on a very flat surface. In natural environments there are almost always going to be other things around to grab on to.

@BryanKrause I'm led to this sort of thinking. Human civilizations (with flat floors) has been here for centuries. Insects have been regularly invading human settlements due to the great abundance of food there. Given that insects have short lifespans, haven't they evolved mechanisms to unflip themselves? (P.S. I believe cockroaches are more commonly found in human settlements rather than in the wild, correct me if I'm wrong.

https://biology.stackexchange.com/questions/3278/why-do-cockroaches-flip-over-when-they-die The answer to this question suggests healthy cockroaches flip back no problem.

Thank you @BryanKrause . Would you care to write all you told as an answer so that I can accept and upvote it? It would also mark this question as resolved.

Well, many insects have developed ways to right themselves when they get turned over.
One of the more interesting families are the Elateridae, or click beetles: so named because they press their prosternum and mesosternum against each other which causes pressure. That pressure is eventually released causing a "clicking" sound and springing the insect upward (or away from predators).

You can see an additional video of a click beetle doing so here.


text:
Can you tell the name of this spider?
This image has been posted on the Wikimedia Commons

This spider is about 3~4cm long. It was found in the middle of tomatoes plants in a garden, in the center of France, Clermont-Ferrand. Photo taken in the early days of August. It would be interesting to specify the species on Wikimedia Commons.
Please let me know if you need other information.

Apparently, Americans aren't the only ones to use their currency as unit of length $\ddot \smile$. I changed the unit from "2 € coin" to "cm". I edited a few other things. I am not sure what you meant by specify the species on Commons though, so I left it unchanged.

Thanks. You're right. Commons refers to the Wikimedia fundation site where the image is hosted. These images are often used as illustrations on the different Wikipedias so that adding the specie in the description would be a great added value.

This is a wasp spider (Agriope bruennichi)
See here: Wasp spider
The link leads to a German Website showing the belly side of a wasp spider
Or see here: Wasp spider II


text:
"50% of the variance in antisocial phenotypes is the result of genetic factors" means what?
How can i understand the following sentence:

Overall, the conclusions reached by these studies have been highly consistent in showing that approximately 50% of the variance in antisocial phenotypes is the result of genetic factors.

Is it saying genetic factors have a weight of 50% in the total influences on antisocial behaviour?
Source: "Natural born killers: The genetic origins of extreme violence" by Christopher J. Ferguson , Kevin M. Beaver

In a population the phenotypic variance can be caused by several underlying variance including the variance in the environment and the genetic variance (among others). The fraction of the phenotypic variance that is caused by the genetic variance is what we called the heritability in the broad sense. The fraction of the phenotypic variance that is caused by the additive genetic variance is what we called the heritability in the narrow sense.
So the sentence

50% of the variance in antisocial phenotypes is the result of genetic factors.

can be rephrased as

Antisocial phenotypes have a heritability of 0.5.

The concept of heritability is useful as it gives us an idea of how well selection can act on the changing the frequency of phenotypic traits in the population (see How to interpret the breeders equation?). Please have a look at Why is a heritability coefficient not an index of how “genetic” something is? for more information.

Let's look at the context surrounding the sentence you referenced.

A rich line of behavioral genetic research has analyzed samples of kinship pairs (e.g., twins) to estimate the proportion of variance in antisocial phenotypes that is due to genetic influences. Results of these studies, which have been based on thousands of sibling pairs, have pointed to the inescapable conclusion that genetic factors are implicated–at least to some degree–in the etiology of violence. Precisely how influential genetic factors are, however, is difficult to garner when examining single studies because heritability estimates wax and wane from study to study based on sample characteristics and methodological differences. A number of meta-analyses (Ferguson, in press; Mason & Frick, 1994; Miles & Carey, 1997; Rhee & Waldman, 2002) and literature reviews (Moffitt, 2005) have thus been conducted as a way of summarizing the findings from these extant behavioral genetic studies. Overall, the conclusions reached by these studies have been highly consistent in showing that approximately 50% of the variance in antisocial phenotypes is the result of genetic factors.

So as you said, he's basically saying that genetic factors influence antisocial behavior.  He's saying that 50% of the deviation from what would be expected based on environmental and social factors can be accounted for by genetic hereditary traits.

Sources:

Aggression and Violent Behavior, Volume 14, Issue 5, September–October 2009, Pages 286-294


text:
Fear in elephants
It has been noted that elephants trained for war, as was done occasionally in earlier times, have still shown a tendency to panic in battle much more often when compared to a war horse trained for the same purpose.  However, is this due to an innate quality of elephant behavior, or a result of poorer training methods due to humans simply having less experience training elephants than horses?  Are elephants naturally more fearful creatures than horses or other beasts of war?

Do you have any reference on the fact that elephants are having a higher tendency to panic than horses in the same situation?
Elephants were much more involved in the fight, than horses, since a horse rider would never run into the middle of the battlefield, but elephants were used in the first rows!

I doubt if a comparison between these two animals in war situation is in order. These two animals serve different roles.
Here is a reference to an article in Wikipedia on War Elephants. Elephants have been used in war for thousands of years pretty effectively till the enemies discover their weakness and use it to their advantage. Making the elephant panic is one of the ways to counter them. Here is a list of methods from the above article:

Elephants had a tendency to panic themselves: after sustaining painful wounds or when their driver was killed they would run amok
One famous historical method for disrupting elephant units was the war pig......
At the Megara siege during the Diadochi wars, for example, the Megarians reportedly poured oil on a herd of pigs, set them alight, and drove them towards the enemy's massed war elephants. The elephants bolted in terror from the flaming squealing pigs.

It is for sure that many horses also panic in war situations. However a panicked elephant can cause more havoc than a horse. It appears that to prevent a panicked elephant from running amuck back into the ranks

The driver, called a mahout, was responsible for controlling the animal. In many armies, the mahout also carried a chisel-blade and a hammer to cut through the spinal cord and kill the animal if the elephant went berserk.

In recent times elephants in temple festivals in india do occasionaly panic and run amuck when the high explosive fire works are set of. However most of the elephants seem to tolerate it.

authors: Андрей Беньковский


text:
How can fruit flies and mice share the same gene that says to build an eye if they evolved separately?
I saw a documentary where they inserted the gene of a mouse that basically is the starting "build an eye" command into a fruit fly, and a fruit fly eye grew. My question is, if eyes of different types of animal had different evolutionary beginnings (I don't know much about arthropod eye evolution, but for a different example, as I understand it, cephalopod eyes evolved from skin cells while vertebrate eyes evolved from brain cells), then how is it that the same gene controls the growth of two such evolutionary different eyes?

Both fruit flies (Drosophila) and mice (Mus) are classified  under Bilateria.
The presence of such a highly conserved sequence in both species suggests that they share a urbilaterian ancestor who also used a similar gene to turn on eye formation (not create the whole eye, just start the process).
Even though the structure of insect and mammalian eyes diverged evolutionarily after the common ancestor, the switch that starts eye development worked so well there was little need to change it.  I suppose one could say that it remains backwards compatible.

Okay so to clarify one point, going back to the example of cephalopods, which are also Bilateria, if one eye evolved from skin and one eye evolved from brain tissue, how can they have the same origin of the eye? Was the brain and skin part of the same thing in the common ancestor?

Yes, in a way.  The outermost layer of a gastrula, the ectoderm, gives rise to both skin and neural tissues.

So the first bilateral animals had a mush of quasi-skin neurons for an eye or what?

Perhaps something like we see in the chiton, not quite an eye but definitely light-sensitive.  But as a soft-bodied animal without the mollusc's shell, there was usually very little left of early bilaterians for fossil records. Another intriguing example of the skin--brain conection is the parietal eye still seen in some ampibians, fish, and reptiles.

The documentary was probably talking about Halder's paper in Science (Science, Halder et al., v.267). If you'll read the abstract (especially the bottom part) You'll notice that the gene is a control gene that is responsible for starting a chain of interactions at the end of which the real fly-specific 'eye-building' process begins. Basically this is like using the same kind of electrical switch to turn on the light in your room (mouse) or an air conditioner (fly).

I understand that part. My question is how is it that they both use the same genetic switch if arthropod and vertebrate eyes had completely different origins? Wouldn't they each have their own unique switch?

To extend the metaphor, in evolutionary history it wasn't a light or an air conditioner, but something much simpler, like a bare light bulb or something. The light bulb needed to be upgraded, but the switch was fine.

So the gene that was implanted from the mouse to the fly is called a homologue/homeotic/hox gene which doesn't actually build the eye it just switches on the genes that build the eye. The reason that this worked is because hox genes are found in most or all multicellular organisms. In terms of evolution this is most likely evidence for a common ancestor.

thanks for your effort... can you add some references with hyperlinks so that others can follow you answer?


text:
Batch several sequences for absent restriction sites
I have a collection of about 120 7kB sequences I would like to check for ether a list of specific restriction sites, or what restriction sites might be absent in all of them.
Is there a app or library that can do this?
So far I've only found systems that can do 1 or 2 sequences at a time.
Possible workaround:
Right now I'm trying to concatenate all the sequences together (about 850Mb) and then using Bio.Restrictions methods of the Biopython libraries.  As I kept running into memory overflow problems, I'm refining the search make a new RestrictionBatch based on 4-5 enzymes that are absent and introduce-able into 3-4 test sequences.
Even then I'm running into crashes, which will probably mean that I take the complete set and test over five or so combined strings.
Before I completely go re-inventing the wheel, can anyone let me know of something that already does this?  I don't really care about the language, we have Python, .Net, Java, R, and MatLab "covered" across the lab.

Why can't you read in each sequence one at a time, and use regex's to see if the recognition sequences are in there?

@swbarnes2 I can, but that seems only practical so long as I keep the restrictionbatch small. Vs a real test of hundreds of enzymes is that practical?

How long do you think it takes to search for 100 regex sequences in one string?  I don't think it will take long.

@Swbarnes2 that's backing out of using Biopython, but something we're considering. The actual full library we have is about 1200 enzymes, many of which with wildcards. I wanted to make sure something like that didn't already exist before we build it