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Identify a lone bone (jaw including teeth) found on a beach at Trouville-sur-Mer (France) in 2018
Found this on the beach at Trouville-sur-Mer in France, on 11 May 2018. It was laying in the sand, close to a trash can. Considering the strong smell of sand within the skeleton, it must have been near the sea for a very long time.

What species is this from?
Also posted on other identification websites and fora:

https://www.inaturalist.org/observations/14323892
https://observation.org/waarneming/view/160056539
https://forum.waarneming.nl/smf/index.php?topic=431852.0
http://www.nhm.ac.uk/natureplus/message/115302/

The length of the bone (the piece remaining) is under 12 centimeter.
The height of the only easily removable tooth (the smallest remaining one) is under 25 milimeter.

Old pictures in sunlight (all in low resolution & without measure bar):
Click the images for enlargement.

Update of 22 July 2018 (most in higher resolution & with measure bar):
This new set of pictures is archived at Wikimedia Commons.

Jaw with teeth (lone animal bone) found on beach of Trouville-sur-Mer in France on 11 May 2018, length smaller than 12cm, side A, photographed on 22 July 2018 - Image 1 of 3

See Wikimedia Commons for a higher resolution.

Jaw with teeth (lone animal bone) found on beach of Trouville-sur-Mer in France on 11 May 2018, length smaller than 12cm, side A, photographed on 22 July 2018 - Image 2 of 3

See Wikimedia Commons for a higher resolution.

Jaw with teeth (lone animal bone) found on beach of Trouville-sur-Mer in France on 11 May 2018, length smaller than 12cm, side A, photographed on 22 July 2018 - Image 3 of 3

See Wikimedia Commons for a higher resolution.

Jaw with teeth (lone animal bone) found on beach of Trouville-sur-Mer in France on 11 May 2018, length smaller than 12cm, side B, photographed on 22 July 2018 - Image 1 of 2

See Wikimedia Commons for a higher resolution.

Jaw with teeth (lone animal bone) found on beach of Trouville-sur-Mer in France on 11 May 2018, length smaller than 12cm, side B, photographed on 22 July 2018 - Image 2 of 2

See Wikimedia Commons for a higher resolution.

Jaw with teeth (lone animal bone) found on beach of Trouville-sur-Mer in France on 11 May 2018, length smaller than 12cm, top side, photographed on 22 July 2018 - Image 1 of 3

See Wikimedia Commons for a higher resolution.

Jaw with teeth (lone animal bone) found on beach of Trouville-sur-Mer in France on 11 May 2018, length smaller than 12cm, top side, photographed on 22 July 2018 - Image 2 of 3

See Wikimedia Commons for a higher resolution.

Jaw with teeth (lone animal bone) found on beach of Trouville-sur-Mer in France on 11 May 2018, length smaller than 12cm, top side, photographed on 22 July 2018 - Image 3 of 3

See Wikimedia Commons for a higher resolution.

Smallest remaining tooth from jaw (lone animal bone) found on beach of Trouville-sur-Mer in France on 11 May 2018, height smaller than 25mm, side B, photographed on 22 July 2018 - Image 1 of 2

See Wikimedia Commons for a higher resolution.

Smallest remaining tooth from jaw (lone animal bone) found on beach of Trouville-sur-Mer in France on 11 May 2018, height smaller than 25mm, side B, photographed on 22 July 2018 - Image 2 of 2

See Wikimedia Commons for a higher resolution.

Can you do a close up shot of the teeth from above, so we can see the crown layout, that is one of the main ways to identify mammal material.

Sasquatch for sure :p.

@John I have now added new pictures, including the teeth from above.

It would be great to have a scale bar in the photo, so that the size would be easier to determine. However, by the shape of the teeth, I will propose that it is the back half of the jaw of a pig. Here is an image from the National Maritime Museum:

This one is from Vanuatu and has a rather elaborate mesial portion of the jaw, but the teeth look very similar. It's virtually impossible to know the bone's age or species, however.

Thank you for your answer. Yes, posting these images on Identification apps/websites/fora, I also became aware of the usefulness of a scale bar. Within a couple of weeks, I can take high-resolution pictures with a scale bar. --- Do you think any conservation archive, museum or researcher could be interested in analysing or conserving the specimen? How would I be able to find such an interested party easily?

without knowing what rock it came out of there is not a lot that can be done scientifically with what you have. Although someone might be interested in trying to figure out where i eroded out from. Contact the nearest natural history museum.

I agree with @John. Without additional provenance information, it's not much use scientifically. However that does not mean that a local museum would not be interested in it for display.

@kmm I have added new pictures, which show the bone with teeth from above and also feature a scale bar. Please update your answer if appropriate.


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Why can't the mutation for this simple pedigree be X-linked recessive?
http://ocw.mit.edu/courses/biology/7-012-introduction-to-biology-fall-2004/exams/finalprac.pdf
For question 7a on pages 10-11 of the above link, why can't the mutation be X-linked recessive?
The solution says "An autosome, because individual 6, a male, has 2 alleles." However, can't individual 6 just have a wild type X-chromosome if he inherited a Y-chromosome from his dad and a wild type X-chromosome from his mom? Also, if he is heterozygous for this trait, it also seems from the DNA fragment analysis that he expresses both alleles; how is this possible f the mutation is recessive?

think about what the genotypes and phenotypes of the third generation (i.e. individuals 5-8) have to be if it was a x-linked recessive gene...remember that x-linked recessives will be manifest in all males and only females who happen to get a recessive X chromosome from mom and dad

Say X is dominant and x has the recessive phenotype. Couldn't the layout be: XY (grandfather), Xx (grandmother), XX (1), xY (2), Xx (3), XY (4), Xx (5), XY (6), XY (7), xY (8)? Or is the reason why we know individual 6 has both the dominant and recessive alleles is because of the DNA fragment analysis- because there is a 1000 bp fragment and another sequence that was cut into 600 bp and 400 bp fragments?

This cannot be X-linked recessive because of the picture of the gel that has been shown.
If it were x-linked recessive, then person 6 would be completely clean from the gene mutation since he is male. If that were the case, he should only be showing two small bands at 600 bp and 400 bp since he has only one good X chromosome.
However, his gel column shows a 1,000 bp fragment, which means that one of his genes was not cut by the Nhe1 enzyme. This implies that that one gene is being vut (hence the 600 bp and 400 bp fragment) and one gene is uncut (hence the 1,000 bp fragment). Since person 6 has two genes, and males only have one X chromosome, this must be an autosomal disease.
This is also reinforced by person 5, who has the same column as person 6. Person 6 also shows an uncut and cut gene by Nhe1. Since their dad has the disease, and neither of the children have the disease, it must be recessive in nature.
Person 7 has two normal genes (hence the two thick bands at 600 bp and 400 bp) and person 8 has two recessive genes (hence the one thick band at 1,000 bp). Their parents must both have a recessive trait for this to happen.
Hope this helps! Let me know if anything is unclear

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Portal Systems in Humans
I was reading about nephrons in my physiology book when i came across this-
The efferent arterioles and peritubular capillaries technically constitute a portal system
But according to Wikipedia, renal portal system is absent in mammals. Can someone please explain this contradiction?
Edit 1: Could it be that humans are an exception to the case and do contain a renal portal system?
Edit 2: When we were discussing this in class, the my lecturer did say, "They are like portal sytems."
Why is human renal portal system not considered a portal system? Although, it connects two capillary beds (efferent arterioles and peritubular capillaries)
Edit 3- Some sites do say that the capillary beds that connect generally belong to different organs. Could this be responsible for exclusion of human renal portal sytem?

I think it is a semantic disagreement. Your physiology book says "technically", which suggests that the author knows the renal capillaries are not the same kind of "portal" system found elsewhere. Humans are not exceptional mammals.

@kmm point taken, but what differentiates it from a portal system?

You should ask your lecturer why they say "are like a portal system" and not "are a portal system". The distinction seems to matter to them. I don't care much for semantic details.

Unfortunately, my lectures on the topic have already ended and currently it is our prep time for the examinations. I know this to be just another semantic disagreement but I am curious to find out why.

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How did Shulgin take cognizance of the dosage of a new substance?
We know that Alexander Shulgin synthesized MDMA, 2C compounds and several other tryptamine derivatives and phenethylamines. But how did he find out that the average dosage of an unknown compound is X mg? For instance, if I synthesized a new psychoactive compound, how could I find out the dosage?


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What´s the role or function of the homologous arms in a donor template in a knockout/knock edition via Crispr-cas9?
I have to make an exposition in my university about Crispr-cas9 edition and I have some questions about the method. In the knock out/knock in technique is used a plasmid containing the DNA that codifies for the Cas9 protein and guideRNA and a Donor template that has a gene for puromicine resistance, and a DNA that codifies for a fluorescent protein and "left homologous arm" and "right homologous arms". My questions is What's the fuction of the homologous arms?Furthermore what's the role of the Loxp(look at the image)?
The method is described here   http://www.origene.com/assets/documents/CRISPR-CAS9/CRISPR_manual.pdf   (page 5-10)

This is not the CrispR/Cas9 system but the LoxP system which works differently.

It is there to facilitate homologous recombination and thereby a knock-in. See http://biology.stackexchange.com/q/29735/3340

@ Chris This plasmid can be part of the CRISPR based knock outs, the LoxP sites are there to recycle the marker if you want to do successive knock outs


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Effect of respiration on Arterial pressure
I am trying to explain the effect of respiration on arterial pressure.
I am looking preferably some visual way to show it.
How can you show the effect of respiration on arterial pressure?
I am thinking some kind of figure which has the respiration rate and arterial pressure.

I did a Google image search for respiration AND "arterial pressure" and found lots of graphs including one at http://69.36.35.38/accp/pccsu/update-evaluation-intravascular-fluid-status-critically-ill-patients?page=0,3 which may be what you are looking for

@AlanBoyd Your article is about venous pressure (outside of the topic).

Keep scrolling until you get to Figure 4.

@AlanBoyd I added two pictures about thing below which I think present the thing. What do you think is the most appropriate one?

Alan's pointing picture is this

I found this picture better

but not sure if it is exactly the level respiration to the arterial pressure.


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How does Mupirocin affect in staphylococcal infection?
I found this sentence confusing
Transitor carriers of staphylococcal infections 70% because of mupirocin i/n.

Mupirocin is drug which affects some way.
I am not sure if the statement means inner neuronal.
I am little confused by the abbreviation i/n.
What is the point of the sentence?

This comes from the usage of the Mupirocin: Its an antibiotic, which is used topically (on the skin, its not taken in form of pills). It binds specifically to the isoleucyl t-RNA synthetase in gram positive bacteria and Streptoccus and Staphylococcus and is used to fight intranasally (that what i/n stands for) infections with these bacteria. It inhibts the introduction of isoleucine into proteins. More informations can be found here.


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Is this necrotizing skin infection caused by Staphylococcus aureus?
A 5-year-old boy returns from summer camp with several minor cuts and abrasions on legs. He has fever
and extensive cellulitis, subcutaneous tissue and muscles are involved. Necrotic tissues were surgically
reomoved and broad spectrum antibiotics were used. Which of the following microorganisms usually
causes necrotizing fasciitis?

a. bacillus cereus
b. clostridium tetani
c. A-group streptococci
d. Micrococcus sp.
e. Staphylococcus aureus

It is so severe that I started think that Staphylococcus aureus is possible.
My previous answer was A-group streptococci, but I disagree with it now.
What is causing the case?

if broad spectrum are being given chances are that it will be staph aureus because nowadays resistance to multiple antibiotics is being found in it.

@biogirl broad spectrum antibiotics are the standard first step in treating just about any infection.

@terdon You are right.I just thought that  because the question specifically states "broad spectrum" it may hint at staph aureus.I may be wrong.

At the moment, I am not sure what is the right answer. I am wondering still between C and E.

It is not mentioned in the question about the time period, how long it took that the surgeon was done from  the incident. If it was done very fast after incident, then I would pick Staphylococcus aureus. However, I do not understand its pathology yet.

I still cannot find any reason for C, since it is not pneumonic. The fever is only related to the symptoms of necrosis. Staph aureus is related with post-operative wounds which may imply that also minor cuts and abrasions can cause it. So most support goes for Staph aureus at the moment.

Murray says that the answer is C for cellutitis and necrotizing fasciitis in a table, but I have found no explanation. I want to understand why.

@Masi Have you read the article on Necrotizing fasciitis on wikipedia ?

Yes, but my books cover the topic much better and deeper. They say that the answer is C by empirical evidence.

Staphylococcal infection is more likely to cause abscesses and Streptococcal infection is more likely to cause cellulitis. It is not clear how a 5 year old did not get medical attantion till he got to this serious state. Why was culture not done? Surgical removal of necrotic tissue due to cut and bruises? doesn't tally with cellulitis. Incision and drainage is a standard proceedure for absecesses, is that what was done? Is this a hypothetical question?

I do not know. I hope it is.

No. It is caused by A-group streptococci. Source Murray and empirical evidence.


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Salbutamol's Pathways of Interaction and Classification
Salbutamol is a very commonly used direct-acting β2-agonist.
This suggests me that it is sympatholytic.
However, it has sympathomimetic pathways, see PubChem for Sympathomimetic.
I am trying to think the group of Salbutamol.
Sympathomimetic or sympatholytic.
How can you classify Salbutamol into a group?

An agonist works with the receptor: a substance that initiates a physiological response when combined with a receptor; in the case of salbutamol (or albutarol in the US) they activate the beta-2 receptor on the muscles surrounding the airways. They are also known as sympathomimetics, as they imitate β2 adrenergics.
A blocker (or antagonist) is one that that blocks the action of endogenous catecholamines; for that reason, they are also called sympatholytic: antagonistic to or inhibiting the transmission of nerve impulses in the sympathetic nervous system.
It appears you have experienced a simple confusion in terms. Salbutamol/albuterol is definitely a sympathomimetic, used extensively on asthma and COPD.
Pharmacology and Therapeutics of Bronchodilators

You seem to be right. I read this A short-acting beta-2 adrenergic agonist as beta-adrenergic antagonist which is false. Thank you for excellent answer!


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Quick overview of how to capture microscope images of histology plate or fluorescent plate
I am looking at these two:

I would like to DIY take photographs of plant and animal cells using a cheap microscope such as this:

I don't know too much about microscopes or the techniques to do the staining, but that is what this question is about. I would like to know briefly what is required (tool-wise and material-wise) to capture images like the two above.
For fluorescent microscopy images, wondering if I actually need a fluorescent microscope, or if I can make do with a regular optical microscope. If I need a fluorescent one, wondering if there is anything else needed, like special lighting or special materials for tagging the cells, which seems like it might require extra stuff like centrifuge and who knows what else. In that case I would just like to get a sense for how complicated it is to do fluorescent microscopy.
For the histology slides, wondering generally what it takes to do that too, if I can get by with a regular microscope.
Generally wondering what equipment is required to accomplish these two images.
So far I have a DSLR camera and am imagining a basic optimal microscope with a DSLR adapter, and perhaps some basic dies that I would just drip into the slide (don't even need a pipette). That just shows my simplistic understanding, maybe fluorescent microscopy requires advanced biotechnology of some sort, which is sort of what I'm wondering, what the basics are.

For fluorescent microscopy images, wondering if I actually need a fluorescent microscope, or if I can make do with a regular optical microscope.

You need a fluorescence microscope. You need to be able to excite your sample with a narrow wavelength of light, and then image a different wavelength of light that is emitted. You need mirrors, emission and excitation light filters for that. You also need to understand the process. If you don't, having software to do the 'thinking for you' such as overlaying the different color channels is a nice thing, but then it's another requirement.

If I need a fluorescent one, wondering if there is anything else needed, like special lighting or special materials for tagging the cells, which seems like it might require extra stuff like centrifuge and who knows what else.

Samples can sometimes have autofluorescence (e.g. the chitin that makes up the cuticle of insects is autofluorescent) but most samples are not. Almost always a fluorophore is used to stain the specimen for something. These can be cheap or very expensive, depending on what you want to stain. This really depends on your sample and how it is prepared. And know that most 'good' samples' are dehydrated or are treated by chemical fixation, which requires chemicals you cannot usually find at a local pharmacy. It depends on how ambitious you want to get as an amateur microscopist!
Also, you won't need a centrifuge.

For the histology slides, wondering generally what it takes to do that too, if I can get by with a regular microscope.

You can get by with a regular upright widefield microscope for sure. If you perform the sectioning well (making thin slices of your sample) then even basic microscopes will produce fascinating images, provided your lighting is good. It helps to have a condenser or a nice lamp and some thin and clean glass slides for well illuminated images.

Maybe fluorescent microscopy requires advanced biotechnology of some
  sort, which is sort of what I'm wondering, what the basics are.

It requires a little bit more optical work. I would stay away from it unless you are serious, because it takes quite a bit more work and equipment to make it minimally workable. Normal microscopy is certainly a lifetime of fun if you have the desire to find interesting samples and work to make them good for imaging.
Addendum: the principle of fluorescence microscopy is quite simple but aligning everything is actually quite difficult if you are an amateur with no specialized tools. Here is the principle only, notice how the input and output must be aligned and the small objective lens has to transmit both excitation and reflected light:

And here is an example of a basic lab stain for two elements of the cytoskeleton (actin in red and microtubules in green) and a DAPI-type stain for nucleic acids (that shows you the DNA-rich nucleus in blue). The crispness of the image really depends on the use of at least two or three lasers (not epifluorescent illumination, i.e. "lamp nearby") to produce the necessary and specific narrow excitation to separately image the different channels. The light detectors are in black and white (for increased resolution), and only in post-processing are they color-coded to make the image pretty.

For a start I would begin with the basics! Pollen, cells on the inside of your cheek, blood, a single onion layer (...is a monolayer of cells, perfect for imaging), anything else you find and can think of! And find yourself a nice stain, or a nice dye or ink that is partially permeable. The world is your proverbial oyster at this point.

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My hand was stabbed with a pencil tip 10 years ago - why is the graphite still visible?
I, and multiple people that I know, have permanent marks (up to 30 years) from a graphite pencil puncturing the skin. The palm of my hand still shows a very clear mark where my hand was punctured by a pencil 10 years ago in school.
Why/how does the graphite remain in the skin indefinitely?

Perhaps your question has the same answer as this one: http://biology.stackexchange.com/questions/36712/why-do-tattoos-persist-if-body-cells-are-regularly-renewed

I had to join just to say that I have a pencil tip mark in my knee that I've had for 40 years!

I had the same thing happen to my leg. I think it eventually went away, but it was definitely many years.
I am going to go with the Tattoo answer. The way tattoos work is that Macrophages in the skin phagocytose the heavy metals in the inks. Because the heavy metals do not interact with Toll-like receptors, or any of the other pathogen receptors that macrophages have on their cell surface, they do not induce a transcriptional signal into the nucleus of the macrophage to induce it to chemotax out of the dermal tissue and into the lymphatic system, so they just sit there. The YouTube channel Smarter Every Day actually has two interesting videos on tattoos Tattooing Close Up and How Laser Tattoo Removal Works.
Macrophages are long lived, so unless they receive transcriptional signals to get them to move out of the tissue they are in, they will just sit there, and if they happened to have engulfed the heavy metals in tattoo ink, or the graphite from a pencil jab, then they sit there with a vesicle filled with that compound. As graphite is pure carbon, I wouldn't worry that much about it, but it is also not not in a form that the body can use, so it will persist. If eventually the macrophages are induced to move, they will likely take their contents with them, which is why tattoos fade over time.
It also is likely that the graphite was taken up by several macrophages in the region, in particles large enough that they cannot be cleared and remain visible, but not so large that the macrophages could not phagocytose them.

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Nucleoside analogs that cause mutation
I'm confused with this explanation in my book:
2-aminopurine is incorporated into DNA in place of adenine but can pair with cytosine, so an AT pair becomes a CG pair.
This sentence seems odd to me. It says that adenine is replaced with 2-aminopurine, but can pair with cytosine. And the AT pair turns to CG pair. Does it mean that 2-aminopurine substitute adenine, and then it works like cytosine to bind with guanine?? Because 'AT pair becomes CG'. But it says 'but can pair with cytosine', which one is going to bind with cytosine??
I've Googled on this but couldn't reach to a clear explanation about this. Can someone please explain to me how this analog works or rephrase the sentence in my book? Thank you.
The book that I'm referring is Microbiology: an introduction 10th ed. By tortora, funke and case. Page 229.

Welcome. If you could give the title, edition, and page of the book you are using, someone on the site may have it and can reference it. Without seeing everything else in the chapter, I am going to take a stab that Aminopurine basepairs with cytosine, then when the DNA repair mechanism finds aminopurine in the DNA, it will cut it out. When it does that its template will be the C, and it will replace aminopurine with a G.

Such a mutation can also occur when the DNA is replicated. http://biology.stackexchange.com/questions/26022/gt-transversion-vs-tg-transversion

I am not sure if this will help to clarify Base pairing and mutagenesis: observation of a protonated base pair between 2-aminopurine and cytosine in an oligonucleotide by proton NMR.

Thanks for the links but those are beyond what I'm learning now.

If you feed bacteria 2-aminopurine then at some low rate it gets incorporated into into the DNA instead of adenine during DNA replication. In other words there will be a base pair between thymidine and 2-aminopurine.
Two things could happen:

DNA repair could detect the unusual base and attempt to correct. If the 2-aminopurine is excised then adenine will be inserted--no mutation. If, however the thymidine is excised then sometimes a cytidine will be inserted. This gets resolved below.
During the next cell division the replication machinery will sometimes incorporate a dC across from the 2-aminopurine. Then in the following cell-division a dG will be incorporated across from the C, so what used to be an A-T base pair has become a G-C base pair (eventually).

Oh!! @mdperry, I've got it!!!! Thank you so much!! And I've 2 questions. I'm wondering if that cytosine form a complementary pair with guanine, then what about 2-aminopurine, since it's a semi conservative replication, we shouldn't leave 2-aminopurine hanging there correct? Would it pair with a new cytosine again?

And another question. This tortora text said that 5-bromouracil would pair with cytosine (if it's not being fixed by DNA pol) but what the Brock's book said it actually binds with guanine. Which one is correct? Or 5-bromouracil actually capable of pairing with both of them?

@Theresa Re: fate of nucleoside analogs incorporated into DNA, I don't actually know how long the modified base persists, but I have read papers where one entire strand was labeled, and the analogs could be detected 10 or 20 cell divisions later. If I understand correctly, the 2-AP can form base pairs with either dT or dC in subsequent rounds of DNA replication.

Re: BUdR (bromouridine deoxyribose--that is what you are referring to?) I am not familiar with all the details, but off the top of my head, you would not expect to find U in DNA, only in RNA (ordinarily). Since T pairs with A in DNA, it follows that U pairs with A in RNA. In RNA double-stranded regions rU can also form base pairs with rG, as long as the Br atom does not disrupt this U=G pairing I would naively assume that dU (and by extension Br-dU) can base pair with dG. A dU=dC base pair would be quite unusual since they are both smaller, pyrimidines.


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Explaining the simpson's diversity index
In my biology class, we were trying to compare the biodiversity of two site. In doing so, we were instructed to use the Simpson's Diversity index as follows:
$$ \frac{\sum_i n_i (n_i - 1)}{N (N - 1)}$$
Where $n_i$ is the total number of organisms of a particular species; and, $N$ is the total number of organisms of all species.
We were given a method to calculate the index in a class that required almost naught mathematical understanding for the purposes of the experiment. From what I have read, the Index calculates the probability that any 2 randomly selected organisms belong to the same species, and it is thought that the closer the result is to zero, the more diverse the region is.
What I can't understand, is the math behind the index; for example: why is it multiplying n by n-1? And how is this better than dividing the sum of all the organisms by the number of species?
I'm in Pre-Cal, so when explaining, please do so with minimum emphasis on "advanced" math terms.

Welcome to Biology.SE. Wiki might help a bit.

For the following answer, assume we have two communities of size 4. Community 1 has two organisms of species A and two organisms of species B. Community 2 has three organisms of species A and one organism of species B.
The probability that two randomly selected organisms belong to the same species
In this example, for either community, the probability that two randomly selected organisms belong to the same species is the sum of the probability of selected two organisms of species A and two organisms of species B. In other words:
P(selecting two of the same species) = sum(P(selecting two of species X))

Where we sum over all species present (in this case, species A and species B)
The probability of selecting two organisms of species X is the probability that the first organism is species X times the probability that the second organism is species X.
The probability that the first organism is species X is simply:
P(first organism is species X) = nX/N

Where nX is the total number of organisms of species X and N is the total number of organisms in the community.
The probability that the second organism is of species X is:
P(second organism is species X) = (nX-1)/(N-1)

Because we are sampling without replacement, we subtract one from each value as we are now sampling from a community that is missing one individual (the one we first sampled).
The probability that two randomly selected organisms belong to species X, is then the sum of the previous two probabilities:
P(Selecting two of species X) = nX/N * (nX-1)/(N-1)

or
P(Selecting two of species X) = nX(nX-1)/N(N-1)

Then, to get the probability that two randomly selected organisms belong to the same species, we sum the above equation for all species. Summing over all species will give us your first equation.
In this case, for both communities we sum over species A and species B.
P(Selected two of same species) = [nA(nA-1)/N(N-1)] + [nB(nB-1)/N(N-1)]

P(Selected two of same species) = [nA(nA-1) + nB(nB-1)]/N(N-1)

For community 1, this comes out to 0.333. For community 2, it comes out to 0.5, accurately representing that community 1 is more diverse.
Why can't you take the total number of organisms and divide it by the total number of species?
The point of the Simpson's biodiversity index is not just to represent the total number of species in a community, but to portray how spread-out organisms are among the species; a community in which one species dominates and the rest are rare is considered less diverse than a community with the same number of species that has a roughly even number of individuals per species.
In the case of our two communities, the total number of organisms divided by the total number of species will give us the same number (4/2), not accurately representing that the communities do not have the same diversity (they have a different spread of organisms)

While this answer resolves the question of what Simpson's biodiversity is, it does not answer why it reflects diversity. Particularly, it is better to demonstrate the index is minimum when all species have equal number of organisms and the index reaches maximum when all organisms belong to only one species.

That's an estimator for Simpson index,
$$ \sum_i p_i^2 $$
where $p_i$ is the probability that $i$-th species is sampled.
This is sum of the probability that two independent samples are from the same species.
There are multiple ways of estimating this quantity from observations $n_i$.
When $n_i$ is small,
$$\hat{p} = \frac{n_i}{N}$$
is unbiased but has high variance, and plugging it in $\hat{p}$ to the definition would also have high variance. (Note that this is equivalent to sampling with replacement.)
If one uses sampling without replacement formula,
$$\hat{p^2} = \frac{n_i}{N} \cdot \frac{n_i-1}{N-1}$$
then, the resulting estimator is
$$ \sum_i  \frac{n_i \cdot (n_i - 1)}{N \cdot (N - 1)}$$
Note that both estimators converge to Simpson index for $N \to \infty$.
But of course, there aren't infinite number of samples, usually.


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Is there a database of cell images?
We're working on an algorithm for processing images of cells, similar to but much more basic than Cell Profiler, and we are looking for a large database of cell images to test our software. Can anyone point us in the right direction? We found the Cell Image Library immediately, but it seems almost empty.

Possible duplicate of What are good sources of free-to-use images and diagrams and http://biology.stackexchange.com/questions/38774/open-database-of-medical-images and dataset of microscopic images before and after staining

The ATCC website has a bunch of images of cells in culture.

@AMR those are not duplicate questions. I vote to leave open as it looks like a valid question to me.

@AliceD That is your call, but all three have links to cell image libraries. The point of flagging as a duplicate question is also to show where a simple search of the stack would have yielded acceptable answers to the question. Answer in first link leads to Wellcome Images which has a large set of cellular images of all types. The second link had this comment https://www.nlm.nih.gov/NIHbmic/nih_data_sharing_repositories.html and the third is pretty much an identical question, with the sole exception that they did not specify it was for bioinformatics.

@AMR - admittedly, I didn't check the answers in your links, but then, as far as I understand SE's policy, I don't think questions should be closed because the answers are out there as sidelong answers posted to unrelated questions. If that would be so, a great many questions could be marked as duplicate.

There is a yearly contest on cell tracking organized by the IEEE International Symposium on Biomedical Imaging, and the associated data sets are freely available.
See for example: http://www.celltrackingchallenge.net/

I've actually answered my own question. The creators of Cell Profiler mentioned a database of biological images which they used to benchmark their software, and it appears to be available at http://www.broadinstitute.org/bbbc/


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Calories burn rate calculation — scientific studies
There are many online calculators for measuring walking/running/bicycling calories burn rate. They differ in input parameters like some might need my weight as well as height and some don't. Almost none take into account duration of the exercise (and this is crucial in my opinion).
So my question here is: Where are these formulas (used in these calculators) coming from? Any scientific studies perhaps? Are they reliable?
Also I would like to know what is the most accurate method available for measuring the burn rate (I'm only interested in the scientific part, not going to do this myself).

This might be off-topic on this hub, also asked here http://fitness.stackexchange.com/questions/18730/calories-burn-rate-calculation-scientific-studies

If you are measuring a rate (calories burnt per until time) why would the time matter - are you suggesting that  the rate varies over the period of exercise?

Small note: burning calories is a wrong terminology because (a) Calorie is a unit of energy (basically heat); burning calorie is like saying lifting kilograms (doesn't make sense unless you say how many kilograms) and (b) Nothing is burnt in the body.
As per the second law of thermodynamics amount of storage energy consumed $\geq$ amount of work done. Whether or not fat is used up is a different question altogether.

Disclaimer: Not my field but I'm doing my best.
We often measure the calories consumed indirectly by measuring the quantity of oxygen consumed. As we have a reserve of ATP(ATP is a molecule, a stock of ATP is some kind of battery of our body) in our body, at very short term the oxygen consumption is not necessarily perfectly correlated with energy use but at a longer term it works perfectly fine. Seek for further information on the Citric Acid Cycle to understand why the oxygen consumption is directly related to the energy created (which is itself at a long enough term directly related to energy use). If I am not mistaken a bunch of seconds should probably be a long enough term (time to consume all ATP at the start of an important effort) but I would appreciate if someone could give a reference for that.
For small animals we often put the animal in a chamber and calculate the energy consumption by measuring the volume of CO2 that they expire. For this purpose we have to measure the volume of CO2 at the entrance and at the exit (of the chamber) to measure the difference. For humans, we often put a mask on the face of the "cobaye". We allow him to breath normally without doing any effort for a while and then we ask him to run/bike/whatever on a home trainer.
I don't know much about such studies but it is important to 1) know the variance in energy consumption in the population for a typical exercice 2) understand that lab condition probably differ in various ways from person-to-person real life condition (no wind, no dust, stress of the experimentator, discomfort of the mask, ...).
As I have no idea concerning the variance in the population I cannot tell how representative are the summary values that we can find on many popular websites but I would tend to think that given the experimentation, these numbers has probably been fairly accurately measured.


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(Non-expert-question) What exactly do chloroplasts do when they "convert light into chemical energy"?
Disclaimer: This question is kind of sprayed over biology, chemistry and physics.
Anyway, I had to learn more about photosynthesis recently, and although it is quite complex, I think I got it - except for one thing: Everywhere it is basically just said, that chloroplasts convert light energy into chemical energy. But seemingly no one is interested in how they do it. I couldn't find an explanation after some googling. Not even Wikipedia had something for me (at least nothing I was able to sort out of the technical jargon).
So my question now is: What exactly happens in this process? It'd be good if the answer wouldn't include to much jargon, because I'm not really experienced in the field. (Just the usual knowledge and a little more due to being interested in science in general).

The overall process is photosynthesis, the chloroplast is the structure that accomplishes this in most photosynthesizing organisms. You'll find a description in any Biology text. Here's a reference with diagrams to illustrate the role of the chloroplast: https://www2.estrellamountain.edu/faculty/farabee/BIOBK/BioBookPS.html

@bpedit Thanks, that is already a little more information. It states In the Light Dependent Processes (Light Reactions) light strikes chlorophyll a in such a way as to excite electrons to a higher energy state. In a series of reactions... But it doesn't mention what these reactions are. The electrons gain more energy, but that's only part of the answer.

Your question is broad. Please narrow it down to a specific issue.

@WYSIWYG You did notice that there is already an accepted answer which provides exactly the information I asked for, right? And I don't think that the question is too broad. "What exactly happens when the light is turned into chemical energy" is quite specific I think. What would you have needed to understand it better?

@Namnodorel just because there is an accepted answer it does not mean that the question itself is very good. Perhaps you got your answer but to a general reader the question and the answer should be coherent, understandable and useful. "What exactly happens when the light is turned into chemical energy": you can find an entire book chapter on this topic. You can go into great level of detail; people are still doing extensive research on mechanisms of photosynthesis. You should therefore clarify what exactly you are looking for. The question should be clear and explicit.

Moreover, the currently accepted answer is very basic (I am not saying it is bad). If you were actually seeking such an answer then you are expected to do some research yourself. This kind of basic information (in fact more details) can be found in Wikipedia or similar resources. Whenever you say "I searched so and so" you should clarify what you found there and why was it not satisfactory (or not understandable) so that people can focus their answers on the points that you actually need to understand.

@WYSIWYG Well, what I found was just "Chloroplasts turn light into chemical energy" which I mentioned in the question. I had no idea what happened to do that, so I couldn't ask for the exact reactions or what happens to the electrons, because I couldn't be sure if it would be important/fill my knowledge-gap. Maybe that would be irrelevant, and I'd get an unsatisfying answer? What I meant with the accepted answer is that it is exactly what I looked for, so how could I have made it more specific so you know that I mean exactly that?

@AlwaysConfused Okay, I can see that. Better now?

I see you've given this a try, so here's a synopsis hopefully appropriate to both your current knowledge level and curiosity.
Light excites electrons in chlorophyll to a higher energy. Higher energy means less stable, those electrons want to return to a state of lower energy. The chloroplast is structured in such a way that the electrons, instead of just plopping back to the lower energy state in the chlorophyll to liberate the light they just absorbed, are handed off to another molecule. As the electrons get passed off to other molecules, they lose energy. All of this is taking place on a membrane within the chloroplast. The energy being "lost" by the electrons is harnesed to pump hydrogen ions across that "thylakoid" membrane in the cholorplast. The increased concentration of H+ within the thylakoid space is another form of energy that can do work. The work done is the creation of ATP.
We're not done with those electrons yet. They get passed off to yet more molecules, losing energy again in each hand-off. This energy is used to create additional energy-rich substances that will power the creation of energy-rich organic molecules in a process termed the Calvin Cycle. The Calvin Cycle, which creates the sugar G3P from inorganic CO2 from the atmosphere, also takes place within the chloroplast.
So, the chloroplast is a multi-talented factory for the conversion of CO2 into sugars. These sugars provide both energy and carbon, in a useable organic form, for other processes in the plant. Chloroplasts also contain DNA. This, and other evidence, suggests that chloroplasts, like mitochcondria, were once free living organisms that got co-opted by other organisms and now exist within cells in a mutualistic association (the Endosymbiont Theory).

Thanks a lot, finally a good explanation ^^ I'll probably need to think multiple times over this to fully understand it, but it is something to work with :)


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Allele frequency question
You are heterozygous at locus A. Both of your alleles, A1 and A2, have a 10% allele frequency in the population. If you are one of 22 people in a room, how many people do you expect to share a locus A allele with?
I come up with 6.8, working like so:
22 people = 44 locus A alleles in the room = 4.4 A1 alleles and 4.4 A2 alleles at 10% frequency.
I have one of each, leaving 3.4 of each allele to the rest of the room. So, looking at both alleles, there are 6.8 shared alleles out there.
My answer assumes that these alleles are all in different people - I don't know how to account for the probability of someone else having two of them. So I know I am wrong already. Is that last step all I'm missing, or have I gone wrong in a more fundamental way?
(Context: This was a question on a grad-level immunology exam. None of us students could agree on the answer afterwards, and the confused wording (I rephrased it above) made us strongly suspect the professor doesn't have the right answer either, so we wanted to see what the answer actually is for when the exams are graded.)

Gotcha, will edit it in.

My first inclination for a problem like this is to address it by enumerating all the possible permutations the two alleles a random individual could have, and multiplying the two allele probabilities (frequencies) to get the combination's probability. Using the given frequencies, the remaining allele (set), call it $A3$, has freqency 0.8.  Because the two alleles of an individual are independent, there are nine possible permutations: one of $\{A1,A2,A3\}$ for the first allele and one of $\{A1,A2,A3\}$ for the second.  One can then just sum the probabilities for the cases of interest.
But for this particular problem, there is an easier approach.  What we are interested in is all individuals who have at least one A1 or A2 allele.  This is the same, though, as all individuals except those who have no A1 nor A2 alleles, or, stated another way, those having A3 and A3.  Therefore:

$f(A3|A3) = 0.8\cdot 0.8 = 0.64$
$f( not(A3|A3) ) = 1 - f(A3|A3)  = 0.36$
$expected( not(A3|A3) ) = 21\cdot f( not(A3|A3) ) = 7.56$

This is of course the same as noting that in the first exhaustive enumeration that there is just one case excluded from the group of interest, calculating its probability, and knowing that all the others must sum to the complement of this probability.  Sometimes using the complementary set out of the full enumeration is an easier way to the answer.
Note: Remi's answer shows a slightly consolidated form of the exhaustive enumeration approach.  The earlier numerical discrepancy in that answer was just due to arithmetic or typos.

Thanks for the correction (+1). Small typo is now fixed.

@Remi.b, the final result is also wrong: 7.77 vs 7.56.

And also because I multiplied the probability by 22 instead of 21 (as the question says that "you" are one of the 22 people in the room). Thanks

Same as @bpedit but stated a little bit differently.

You are heterozygous at locus A. Both of your alleles, A1 and A2, have a 10% allele frequency in the population. If you are one of 22 people in a room, how many people do you expect to share a locus A allele with?

There are 5 possible genotypes that could share at least one allele with "you" A1|A1, A1|A2, A2|A2, A1|A3 and A2|A3, where A3 is the allele (or set of alleles) which frequency is $0.8$. Under Hardy-Weinberg assumptions, the frequencies of each of these genotypes are

$f(A1|A1) = 0.1^2$
$f(A1|A2) = 2 \cdot 0.1^2$
$f(A2|A2) = 0.1^2$
$f(A1|A3) = 2\cdot 0.1\cdot 0.8$
$f(A2|A3) = 2\cdot 0.1\cdot 0.8$

which sums to $4\cdot(0.1^2) + 2(2\cdot 0.1\cdot 0.8)=0.36$.
As the frequencies of both A1 and A2 are $0.1$, the frequencies of each of the three mentioned genotypes are all $0.1^2$. Therefore, the expected number of individuals that share at least one allele with "you" at this locus is $21\cdot 0.36 = 7.56$ people.
Why did we need Hardy-Weinberg assumption to make this calculation?
This section comes in reaction to @Atwo comment below.
To give you the intuition for why you need H-W for this calculation. Imagine all A1 where in heterozygous A1|A2 (and therefore same for A2), then the only other genotype that would share an allele with you are A1|A2 genotypes that would be present at frequency $0.2$. And therefore the expected number of people the share at least one allele with you in the room would be $21\cdot 0.2 = 4.2$ people.
For exercise, I would like to invite the reader you to repeat the same calculation for a case where all A1 and A2 alleles are only found in heterozygous A1|A3 and A2|A3.

Thanks! It looks to me like this solution requires no assumption of H-W equilibrium - is that correct?

It also require the H-W assumptions in order to calculate the genotype frequencies (in bullet points) from allele frequencies.

Gotcha. In that case can you make anything of the original exam question, which I posted as a comment on the previous answer?

Of course. Simpler and more elegant than my approach since it more easily accommodates the A1/A2 individuals.

@Atwo Please have a look at the added section that address more fully your comment about the role of H-W assumptions into the calculation.

Instead of computing this complicate sum, what about computing the expected value of the number of people $(A_3,A_3)$ : it is $21\times 0.8^2=13,44$, and the expected value of the number of people you share at least one allele is $21-13,44=7,56$

@Thomas Yes, this is the way mgkrebbs used which is computationally easier, I agree.

I've never done one like this, here goes.
First, remove yourself from the room, just 21 people to consider. You're right that you have to account for the homozygotes. Let's represent the A1 allele with p. All other allele frequencies represented by q. (Sorry I don't yet know how to format properly)
p = 0.1, q = 0.9
The genotype frequencies in the population are represented by:
p^2 + 2pq + q^2 = 1
We're interested in the p^2 + 2pq part. It represents the genotype probabilities of having either one or two of the A1 allele.
0.01 + 2(0.1)(0.9) = 0.19
That's the frequency of individuals in the population with at least one A1 allele.
0.19 * 21 people = 3.99 people
Ditto for the number of people with the A2 allele. These should be additive giving you 7.98 people. BUT, Some people would have both the A1 and the A2 allele. I think we need to subtract that from the 7.98. If this is true, the calculation is easy.
2(0.1 * 0.1) = 0.02 chance of a person having both A1 and A2
The 2 is because there are two ways of achieving this (A1/A2 and A2/A1).
0.02 * 21 people = 0.42 people
7.98 - 0.21 = 7.56 other people in the room with at least one A1 of one A2 allele.

I like it (me using A1/A2 instead of p/q shows how rusty I am), but I guess I am curious about removing yourself from the room at the start. There are, in fact, 22 people in the room. Your calculations are for a room of 21 people and produce the incorrect frequencies for a room of 22, especially given that the genotype of the 22nd is known. Or am I being led astray by my intuition here?

Can you share alleles with yourself? Sharing suggests "with others". I'd read that prof the riot act if they use 22. You said you paraphrased, perhaps the original wording makes 22 feasible.

Ouch. I edited the final answer to say OTHER people in the room.

Thanks, I understand you there. The actual question without the paraphrasing was: "The frequency of HLA-B alleles [there are 100s] ranges from <0.1% to 10% [we didn't learn any frequencies, hence the info here]. What is the maximum expected number of people in this room that share an HLA-B allele with you?" There were 22 people in the room. Can you make any headway on that (notably, no H-W equilibrium), or is it hopeless?

Ah, that doesn't seem to implicate "you" as one of the population to share. So substituting 22 for 21 seems fair.


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What does factor VIII have to do with thromboplastin formation?
I've got the following question and I'm afraid that the question doesn't match with the answer...
Factor III (rather than factor VIII) is known as thromboplastin or tissue factor and it makes sense that the factor III deficiency is related to thromboplastin formation. Isn't it?
What does factor VIII have to do with thromboplastin formation?

The question refers to factor VIII, not factor XIII.

Typo. My mistake. Thank you for the attention.

Have you done any research, for example, looked at Wikipedia for the function of Factor VIII? If so, please explain in more detail why you're still confused. Thanks.

@GerardoFurtado thank you for the attention, it was corrected. I'm a non-native English speaker and it may happen, I'm sorry for that.

@anongoodnurse Regarding to research, I did a lot, and also discussed with my friends on Whats-app group, I came here as a last resort. We have a confusion about this question. I'm confused because the factor III by itself is thromboplastin and since it's absent, then we don't need to talk about absence of factor VIII which interrupt thromboplastin formation (and by the way it is by itself not so clear, because factor III takes place before factor XIII works), I hope I explained myself well.

I am so confused... Why are you referring to FIII? The question is about FVIII (deficient/defective in hemophiliacs and patients with Von Willebrand syndrome.)

Indeed I referred to it as well, but just as possibility of a typo in the original question (FVIII instead of FIII). One of my thought was that FIII by itself is the problem of thromboplastin formation because FIII is thromboplastin. But as I said I don't reject the possibility that the question is about FVIII and I just don't know why the official answer is thromboplastin formation in this case.

As far as I can see from OMIM https://omim.org/entry/134390 there are no hereditary conditions associated with FIII deficiency so I think it unlikely that it is a VIII/III typo. I agree with @GerardoFurtado, if the asterisk is indicative of the 'correct' answer then this is a mistake in the question (or actually in the answer to the question).

Thank you for the additional information. One of my classmate claims that  Thromboplastin is involved in the conversion of prothrombin to thrombin and therefore the answer is thromboplastin ("it needs factor xa to do the conversion but it needs need also factor VIIIa to aid in the conversion"). Honestly, I still don't understand.

@UbiquitousStudent Is the formation of thromboplastin a step in blood coagulation?

"Thromboplastin (TPL) is a plasma protein aiding blood coagulation through catalyzing the conversion of prothrombin to thrombin." (wiki)

@UbiquitousStudent Okay. So if the answer is C, what is the question?


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Exocrine system + endocrine system =?
What is the title name for endocrine system + exocrine system?
In another language that I speak they are called "secretion system" but in English the term secretion system is different and it is about proteins in Gram-negative bacteria.

Since it would be a collection of all glands I would call it as Glandular System same as vascular system which includes blood vessels.

Thank you for your comment. Based on this article, it seems that glandular system is a synonym for endocrine system. Isn't it? https://fmidr.com/glandular-system/

I don't think so because, in one of the heading it has written Endocrine system in a bracket beside glandular system, which can be interpreted as endocrine is a subset of glandular system. Thats my view. Try google ngram

Ok, after some searching and activation of my logic, I accept it. You can write it here as an answer of course.

We can coin our own term too.

As long as in any publication or communication you define your meaning of "glandular system",, it seems like a pretty reasonable term to use for convenience. As far as a conventional term already established in the literature, I'm not aware of any.


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Does animal fat and meat contributes differently to our body?

Is animal fat harmful to our body or is it harmful if the amount eaten exceeds a certain amount?
I have heard fat is more concentrated than protein. If I am correct then we can get more energy from fat. Then why is fat not desirable?
Our ancestors used all the parts from their hunt, even the fat. How did it work for them?
Would eating fat be beneficial for an athlete? (May be for different purposes: power, endurance or building muscle)

Have you read the Wikipedia article on Fat?  It has literally all of the answers you are seeking.  However...
1: Every single thing is bad for you if you get too much of it.  Animal fat, sugar, water, you can over-do it on anything.  Fat can be bad for you but it is definitely required.  In particular, "Vitamins A, D, E, and K are fat-soluble, meaning they can only be digested, absorbed, and transported in conjunction with fats. Fats are also sources of essential fatty acids, an important dietary requirement."  Fat does a host of other things, as mentioned in the article.
2: Fat is indeed a concentrated store of energy, but there's more to life than just energy.  Protein, like other nutrients, are required for life.  Protein happens to be particularly important, providing the structure for all our cells, is required for muscle growth, and provides amino acids, which are needed to make other proteins in your body.  Proteins are used as hormones, cellular messengers, immune receptors, so on and so forth.  You couldn't live without protein.  Energy, while concentrated in fat, could come from elsewhere.
3: It worked just the same for them as for us.  I will add, however, that our ancestors did not necessarily use every part from every animal, and these days, we actually use every part of many animals, just not always for food.
4: Sure?  Energy is good, but protein is probably better.  "Athlete" is a vague term, as strength-training and endurance activities are very different from each other.  Protein is probably better for strength, carbohydrates are probably better for endurance.  But you can ask over at https://fitness.stackexchange.com/.


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Examples of subvarieties and forms in botany or other biological nomenclature?
So I found a fairly complex Rhododendron subgenus to subsection classification list, and despite there being genus > subgenus > section > subsection > species > subspecies > variety > subvariety > form, the only parts that seem to make up a name when things go beyond the species level is picking the last one after that (so subspecies, variety, subvariety, or form). So we have examples like Capsicum annuum var. glabriusculum or Rhododendron campylogynum var. leucanthum.
https://en.wikipedia.org/wiki/Infraspecific_name
You can also have the cultivar epithet added after species.
So my question is, is it always genus species [possibly one deeper]? Or are there any other situations I missed? Also, it sounds like you can insert arbitrary number of levels between the ones you are taught in grade-school (kingdom / phylum / class / etc.), you might insert a few layers there when necessary like phylum > subphylum > superclass > class sort of thing. Like for family we added 4:

Superfamily
Family
Subfamily
Tribe
Subtribe

So in the end it might be something like this, or even more!?:

empire
kingdom
superphylum
phylum
subphylum
superfamily
family
subfamily
tribe
subtribe
genus
subgenus
section
subsection
species
subspecies
variety
subvariety
form

So from 7 to about 20 levels! They don't make that obvious in your initial pass at learning this. Do I have the naming system correct then? If there is anything below the species it gets a 3rd item in the name. If there is anything between genus and species, that is ignored in the name.

Binomial nomenclature is the name for the formal naming of species in "Genus species" form. Genus species should always be a unique identifier (also see Are All Taxonomic Groups Uniquely Named?), so this is the "official name" of a given species.
However, as you've pointed out, sometimes after a species is described it is found useful to differentiate between subspecies or smaller varieties, especially in agriculture where artificial selection has taken one native species and transformed it into many cultivars that have become so distinct from each other that they'd hardly be considered the same species had they been discovered that way in the first place (and very unlikely to evolve those discordant traits naturally without some of the reproductive barriers that lead to speciation).
Note that all of these designations are somewhat arbitrary, besides their order. They are all just a way of imposing a categorization for the convenience of humans in describing relationships between different living things.
Some more reading:
https://en.wikipedia.org/wiki/Phylogenetic_nomenclature
https://en.wikipedia.org/wiki/Evolutionary_taxonomy
https://en.wikipedia.org/wiki/Taxonomic_rank
How could humans have interbred with Neanderthals if we're a different species?
Usage of "lineage" over "species"
Why is traditional rank based taxomomy considered by some as logically inconsistent with phylogenetic knowledge?
Difference between Category, Rank and Taxon
Imagine life as a very, very big tree. You can call a part the "trunk", that's pretty well-defined. That might be the original common ancestor of all life, or perhaps all eukaryotes, or perhaps all vertebrates; you can choose where you want to start. The leaves, also, are relatively well-defined. Those are the species. But some leaves have a complex shape and you might even debate when a leaf is one leaf and when it's actually a collection of leaves. In between, though? We use some names for tree parts. Limbs, branches, twigs, etc. But if you want to get into more detail, you may eventually find yourself needing a word to describe something between a branch and a twig, and then sometimes between that thing and a proper twig, etc. There is no real behavior of the universe that is based on these classification points, it's just convenient to draw a line somewhere to say "okay, I want to talk about all parts of the tree past this branch, so I'll give them a name". Nothing constrains the tree of life to grow in any particular pattern where there are a set number of branches between particular extant species; you can easily have leaves that grow directly out of the trunk and serve as their own branch, their own twig, etc.

Does NCBI not use the new PhyloCode system then?

@Lance I have no idea, I assume PhyloCode is some sort of new standard? See https://xkcd.com/927/ and also note that just because there is a standard does not mean it is not ultimately arbitrary in some fashion. For example, the length of a meter is both entirely arbitrary and also exactly the distance light travels in 1/299792458 of a second. Of course, a second is also an arbitrary unit of time, even if it is also precisely 9,192,631,770 periods of the radiation corresponding to the transition between the hyperfine levels of the unperturbed ground state of the 133Cs atom.

(from https://en.wikipedia.org/wiki/Metre and https://en.wikipedia.org/wiki/Second )

The rules may be different for zoological names, but for botanical names:

Is it always genus species [possibly one deeper]?

This is governed by the International Code of Nomenclature for algae, fungi and plants, Article 24.1, and the answer is yes, the name is always genus species [connecting term infraspecific epithet].
The Code provides the following example:

Ex. 1. Saxifraga aizoon subf. surculosa Engl. & Irmsch. This taxon may also be referred to as Saxifraga aizoon var. aizoon subvar. brevifolia f. multicaulis subf. surculosa Engl. & Irmsch.; in this way a full classification of the subforma within the species is given, not only its name.

Here, the name is "Saxifraga aizoon subforma surculosa" (where subforma can be shortened to subf.), and it is common to list the authors who described that taxon (here, Engler and Irmscher). However, that taxon is placed within a hierarchy of variety, subvariety, and form, which may be listed if the full classification is needed.
One consequence of this is that no other subform within Saxifraga aizoon may have the epithet "surculosa", even if its classified in a different variety, subvariety or form.

It sounds like you can insert arbitrary number of levels

Also yes. Article 2 states, "Every individual organism is treated as belonging to an indefinite number of taxa at consecutively subordinate ranks, among which the rank of species is basic."

If there is anything between genus and species, that is ignored in the name.

Correct, if you're naming a species or infraspecies, only use the genus, specific epithet, and infraspecific epithet.
You can, of course refer to those intermediate ranks if you need to, such as Primula section Dodecatheon.


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Do individual mammal hairs absorb water?
In my look into the world of shaving I've seen claims that it is better to shave after a shower because the hairs will absorb water and soften, making the shave easier. Likewise, I've seen it claimed that natural hair brushes (i.e. boar and badger hair brushes) should be soaked before use. My question is: do the hair fibers actually absorb water, presumably thickening in the process, or does the water just adsorb onto the surface (maybe lifting the scales in the cuticle) meaning you can wet hair in aggregate, but it doesn't soften when soaked? Especially, is there a side-by-side comparison of a single hair under a microscope before and after soaking showing what happens?

Researching this answer took me to some strange literature, but it appears to suggest a little bit of both (at least for human hair, which is porous, implying that some water can suffuse through the cuticle into the cortex). For example this paper looks at the impact of this effect on drug testing.
There's also a few papers in cosmetics science journals describing various elements and effects of increased hair porosity, but I was unable to find one primary citation which characterised the trait.


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Does natural selection select for randomness in development?
In a podcast with Sean Carroll and Liv Boeree they discuss a result from game theory that the optimal strategy in the face of incomplete information can require random decision making. For example, without more information (e.g. the robot that uses high frame rate video and fast movement to see what the human is picking and quickly pick what beats it), the strategy in rock-paper-scissors that cannot be dominated is to choose which one your going to do randomly with equal probability.
We know that situations where there is not one optimal strategy exist in biology. Examples: male vs. female, side blotched lizards, E. Coli (produce toxins and defense vs. just defense vs. neither).
Now, in most of the examples above the source of the randomness is entirely from sexual reproduction (meiosis). The only example I can think off the top of my head of where this isn't the case is for crocodiles (maybe only some) where the sex is fixed by the temperature the egg is at during a certain stage of its development. In a sense, for them, sex selection is completely non-genetic but is done as a response to a stimulus.
My question is this: are there examples of genes that control development in a non-deterministic way (i.e. are there genes that by their presence will produce a trait with some probability greater than zero and less than nearly 1)?
I think genes that can be switched on and off in response to relevant environmental stimuli shouldn't count (e.g. the development into a queen for a honey bee). I'm just interested in whether there are genes that function in a highly random fashion and if natural selection has lead to such genes being produced (something like the presence of gene X causes trait Y with 30% probability, all other genes being equal). I add the qualifier "highly" to the randomness because these processes are ultimately always going to have some randomness from thermodynamics, and our cells go to a lot of effort to mitigate that randomness in most situations.

X-chromosome silencing/inactivation is inherently random (in all mammals), but can only lead to a phenotype in the case of heterozygous genes on the X-chromosome. Would that fit what you're looking for?

@Nicolai I don't know. Isn't that random on a cell by cell basis, leading to a mosaic expression? Although, you raise an excellent concern: how would the gene's activation be coordinated across the body? Maybe if the activation only lead to a particular trait if it was activated in a particular tissue, then yes, that would work.

Yes, you're right that the randomness is cell-based and leads to mosaic expression and that happens so early that it afaik affects almost all cell types, so I'm not sure if it would be possible (or at least probable) to have a specific phenotype in a given tissue.

@Nicolai It is. See: calico cats. https://en.wikipedia.org/wiki/Calico_cat It's just a question of if an entire organ or tissue (e.g. the adrenal glands) can express one or the other, that I don't know.


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Why do some animals have 8 Limbs (e.g. Spiders, Octopuses)?
Octopuses have 8 tentacles, spiders have 8 legs.
Is there something special about 8? It seems like an animal that needs 360° mobility has 8 legs.

@Kevin, "octopuses" is better form although octopi is used under the mistaken assumption that the word is latin. If you want to be pedantic, it should be octopodes or octopoda since it comes from Greek. See here for a nice discussion.

cool topic, it led me to this page: https://www.echemi.com/community/examples-of-animals-with-12-28-legs_mjart2205252409_313.html

No, there is nothing special about eight legs. You have species with two legs (humans), four legs (most mammals), six legs (insects), eight legs (spiders), ten legs (lobsters), and many more legs (millipedes, centipedes).

@PaulA.Clayton I am not sure what it means to have 360 deg. motion.  All organisms use 360 degree motion.  One could argue that radially symmetrical organisms lack a preferred "head" direction, but spiders and octopuses are not radially symmetrical.  Why would a spider be more 360 degree motive than a crab, a mouse, or an insect?

@KennyPeanuts, I think both the OP and I, in my previous comment, were laboring under a misapprehension. 180 degree vision and motion would be more correct. A spider has eyes situated all around its head, allowing for 180 degree vision. The lack of a specific "forward" direction in this species would indeed indicate a greater ability for 180 degree movement. Not so octopuses though, I agree.

I suppose that octopodes (and really all animals, but especially those that swim and fly) have 41,253°² motion, not 360° motion, because they exist in a three-dimensional world.

First of all, it's wrong to assume that an organism "needed 360 mobility" and therefore ended up with 8 legs, as the question implied. That would be a misunderstanding of evolution.
No, there is nothing special about 8 legs. Might as well be 6, 10 or 12. Take note, it would have to be an even number all organisms you mentioned are bilaterally symmetrical.
However, for these organisms 8 limbs were obviously something special. But independently, as they aren't closely related - octopusses are molluscs and spiders are arthropods. Maybe octopusses have 8 limbs because it gives them the best moving speed and agility while not expending too much energy. It's always a delicate balance.
The difference between an insect (6 legs; 3 segments), a spider (8 legs; 4 segments) and a lobster (10 legs; 7 segments) - all of them athropods - is in the number of leg segments. By the way, molluscs aren't considered segmented so they don't fall into this category.
When it comes to the difference between 8 and 6, You don't know did spiders "get" an extra leg segment or did insects "lose" one in order for the legs to be less of a burden during flight.
Interestingly, evidence suggests insects are the last to appear in the evolutionary family tree. Spiders also seem to have ended up with 8 legs by reduction as opposed to addition.
To answer the question "why do some animals have 8 limbs" - they have an even number of limbs because they're bilaterally symmetrical. The exact number of limbs in molluscs is a balance of energy consumption and fitness, as always, and the number of limbs in arhtropoda is the same thing, and my personal opinion is that spiders didn't go beyond reducing the number of their limbs to 8 for some reason - maybe because with 6 they were less efficient in walking the spiderweb.


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Gas from bacteria that's not methane
Is gas produced by bacteria always mainly methane? Or, are there bacteria out there that produce some biogas composed mainly of hydrogen, natural gas, propane, butane?

synthetic biology is working hard to produce such things, but they aren't found naturally in significant quantities I think.

note that methanogens actually use $H_2$ that is generated by other bacteria.

Isn't natural gas mainly methane?

Microbes can produce several gasses other than methane.

All microbes produce $CO_2$ through the oxidation of reduced carbon

Additionally some metabolic pathways produce other gases.

Photosynthetic microbes produce $O_2$
Sulfur reducing bacteria can produce $H_2S$ (as @ohcanada points out)
Denitrifying bacteria produce $NO$, $N_2O$, and $N_2$
Fermenters produce $H_2$ (as @mart indicates)

There may be others that I am not thinking of but these are some of the major players...

Good answer. Although fermentation can produce carbon dioxide too.

@JackAidley indeed they do... thanks.  I edited the answer.

Well, some bacteria can produce Hydrogen Sulfide gas. For example, Proteus and Salmonella. The presence of $H_2S$ producing bacteria is actually clinically significant and we have a way to test for this, which is via the use of TSI (Triple Sugar Iron) media.
Assume you set up the test correctly, $H_2S$ producing bacteria will generate dark deposit within the media.
In the clinical setting, there are other choices beside TSI, such as SIM media and API20E.

Thanks sviter! This is actually my first time using Stackexchange so I'm still trying to familiarize myself about the word format here.


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Serotonin - Does being aroused make you sleepy?
My Psychology text book says Serotonin causes "Sleep, arousal levels and emotion"
Does this really mean that when you are being aroused, Serotonin is released, which in turn makes you sleepy? If so, what evolutionary benefit would that have??

This can be answered by reading the Wikipedia article on serotonin, which has a nice list of functions.

I've always wondered whether heightened serotonin was responsible for socially accepted phenomena such as post-coital tiredness and "morning glory"...

You do realize that Arousal does not have anything to do with sex unless you expressly use the adjective Sexual to modify arousal From Medical Dictionary Arousal 1. a state of responsiveness to sensory stimulation or excitability.
2. the act or state of waking from or as if from sleep.
3. the act of stimulating to readiness or to action.

According to this article [1], serotonin (5HT) inhibits sexual arousal:

Dopamine is generally facilitative to male sexual
behavior; however, 5-HT is regarded as inhibitory.
Antidepressants of the selective serotonin reuptake
inhibitor class (SSRIs, including Prozac and Zoloft)
impair ejaculatory/orgasmic function and frequently
inhibit erectile function and sexual interest as well.

However, serotonin can also facilitate erections:

Systemic administration of the 5-HT1B receptor agonist
anpirtoline impaired ejaculation in male rats. On the
other hand, stimulation of 5-HT2C receptors with mCPP
impaired ejaculation but facilitated erections in male
monkeys, suggesting an increase in parasympathetic
influence.

Serotonin release also causes sleepiness after ejaculation in males (source):

5-HT is released in the LHA at the
time of ejaculation and promotes sexual quiescence during
the postejaculatory interval

There are many signalling molecules used by the human body that have a different effect depending on the cell type they are detected by and the receptor type they activate.
I would also like to touch on your question about evolutionary benefit. Evolution does not care about you after you have reproduced. As long as an individual reproduces, evolution is "happy". For example, you think falling asleep after sex is counterproductive on the evolutionary scale? What about Mantises where the female will sometimes eat the male during or immediately after copulation. Falling asleep seems like a pretty small thing compared to that (source):

Although the praying mantis is known for its cannibalistic mating process in actuality it only occurs 5-31% of the time. Especially in laboratory conditions of bright lights and confinement, the female is more likely to eat the male as means of survival. "In nature, mating usually takes place under cover, so rather than leaning over the tank studying their every move, we left them alone and videotaped what happened. We were amazed at what we saw. Out of thirty matings, we didn't record one instance of cannibalism, and instead we saw an elaborate courtship display, with both sexes performing a ritual dance, stroking each other with their antennae before finally mating. It really was a lovely display". (7) There is one species, however, the Mantis religiosa, in which it is necessary that the head be removed for the mating to take effect properly. (5) Sexual cannibalism occurs most often if the female is hungry. But eating the head does causes the body to ejaculate faster. (3)

Anything that makes an individual less likely to reproduce will be selected against. Things that happen after reproduction do not affect the survival of the species and will not be subject to selective pressures.
References

E. M. Hull, J. W. Muschamp, S. Sato, Physiology & Behavior 83 (2004) 291 – 307

Arousal does not have anything to do with sex unless you expressly use the adjective Sexual to modify arousal From Medical Dictionary Arousal 1. a state of responsiveness to sensory stimulation or excitability. 2. the act or state of waking from or as if from sleep. 3. the act of stimulating to readiness or to action.

@AMR if you don't know what a word means, look it up in a regular dictionary, not a medical one. Here are a few: 1, 2, 3, 4, 5. Note that every one of them includes sexual arousal as the primary or secondary meaning of the word. In English, with no other context, arousal will always be taken to mean sexual arousal.

@AMR still, your rather aggressive comment urged me to check my guess and change my answer to be based on fact, rather than guessing. Happily, my guess wasn't far off the mark. Thanks.

It is a very small aspect of what neuroscience terms arousal. The use of the word in the context of the quote cited by the OP has nothing to do with arousal in the sense of sex and is used to describe activity during a wakeful state. You are sophisticated enough of a member to know the distinction and instead of pandering to the question you should have correctly described the use of the broader use of the term in a scientific sense and as it was likely used in the context of the textbook.


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Molecules and human memory
Has it been demonstrated that the memory of human brain is just connections between neurons, not "long" molecules such as RNA or proteins?

The idea that memories could be stored as RNA or proteins is an old one.  It got a lot of attention decades ago when James McConnell did a number of experiments where he conditioned planarian flatworms to respond to certain stimuli, ground them up, fed them to worms that hadn't gone through the conditioning.  He claimed to have observed that the worms fed conditioned worms learned to respond to the stimuli faster.  This supported the idea that memories were just RNA or proteins, and thus survived the grinding up process.  His results were not readily reproducible, and so the idea fell out of favor.
There have been a number of studies at this point that have been able to look at the firing of individual neurons and shown that there are unique patterns that respond to different stimuli, for example Category-specific visual responses of single neurons in the human medial temporal lobe. So I think it is pretty well established that there are certain connections between neurons that are critical, sometimes even individual neurons.
That doesn't necessarily rule out that there are unique RNA or proteins in those specific neurons, and they are what's actually storing the memory.  I'm not a neuroscientist, but I think the biggest argument against such a storage system is simply the speed with which you can recognize something.  When you see a face you know you nearly instantly recognize the person, and have a flood of memories about that person.  If the memories were somehow stored in RNA or protein structures, I think it would take much longer to somehow "read-out" that data from the molecular structure.  The only thing that really works that fast are the action potentials in neurons.
An interesting comparison might be made to the system in our bodies that DOES have molecular-based memory, the immune system.  When you get sick with a cold you've never been sick with, your immune system doesn't immediately recognize the antigens that come from that virus.  Through the process of somatic hypermutation, your body produces B- and T-cells that have protein receptors that recognize the viruses and the cells infected by the viruses and go and kill them.  A small subset of the T and B cells that have the molecular recognition of that cold become 'memory' cells.  These memory cells that go into a quiescent phase, waiting around until the next time that cold infects you.  But that time they 'remember' it immediately, and you don't get nearly as sick, if at all, because the genes for those recognition proteins are stored in the memory cells.  The activation of immunological memory cells takes a long time as compared to remembering a face, or some other normal memory function, so such a molecular system couldn't be responsible.

cf. http://biology.stackexchange.com/questions/2875/can-rats-pass-on-memories-of-a-maze-to-their-offspring

ah, thanks, I thought I remembered there were some old papers on rats but couldn't find any reference.

The study with the cannibalistic planaria has never been replicated, after many attempts.


text:
Is there a correlation between brain size and amount of sleep?
As far as we know, sleep seems to be the part of the daily cycle when executive functions are resting and memories are fortifying. Many, but not all, of the functions that become dysfunctional upon sleep deprivation seem to be situated in the frontal lobe or associated with the neocortex.
My question is whether there is a correlation between percentage of the day spent sleeping and brain size (either the whole brain, or a part of the brain such as the neocortex or frontal lobe). How do other species correlate compared to us? Either in absolute brain size, or in brain size relative to body size.

I'm closing this question as it is cross-posted on CogSci already at http://cogsci.stackexchange.com/questions/6440/is-there-a-correlation-between-brain-size-and-amount-of-sleep

@MadScientist not sure, they're complaining about the cross-posting over there too and neither one has an answer. I'm not sure which site is a better fit. Darko, could you please modify your question  to fit the different communities more specifically?

Changing the question would not alter the outcome and as such is stupid. But ok. Since the question is more specific towards the correlation between species, I will leave it as it is here. Cognitive scientists have nothing to add to that. I will edit the Q on CogSci to make it a better fit.


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What is the cause of the spots on this leaf?
On a hiking trip to the Alps I found trees whose leaves showed those spots you see on the picture. I am curious about what the cause is.
Higher resolution pictures of front and back side.

This site is not for specific medical or botany advice.  Please consult your local botanist for a specific diagnosis.

I was just kidding

This is a "Tar Spot" disease usually found in Europe and North America. It mostly affects the Maple tree leaves. Tar spot is caused by 'Rhytisma acerinum' a plant pathogen fungus. This pathogen does not seem harm to tree but disturbs the leaves as it finds a suitable condition in summer with bit of wetness. It enters the leaves through stoma and then creates yellow lesions of various sizes over the leaf area which later gradually turns into brown-black tar colored spot. It reduces the photosynthesis process of leaves and thus creating more wide dark spots on the leaves. After sometime the leaves will fall.
Entire detail is available in the Wikipedia link with the detail of the pathogen. (Add some more info if you find this detail not enough)


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(How) can a pink grasshopper exist?
I saw this foto on Reddit recently:

Is this possible? How can a grasshopper become like this? Is this just natural genetic mutation?

Genetically modified... or naturally mutated... I doubt the natural part though - given the number of genome research out there...

Looks like a Katydid, not a grasshopper, and googling pink+katydid will get you many hits

Pink individuals of the katydid species Amblycorypha oblongifolia are a relatively uncommon but natural phenomenon with a long history of research.
It looks from popular press accounts (Science Friday, Scientific American) that the pink coloration may be caused by a dominant allele, and is only rare because of a high selection pressure against pink individuals (i.e. they're much less good at hiding among leaves, and are eaten before they can reproduce).

Photo by Richard Whitby, via flickr.com/blueboat2 (cc-by-sa 2.0)

I thought I could find a pink praying mantis, but couldn't. Orchid mantis's do come in a variety of colors, and sometimes a pinkish. Since mantids are grasshoppers and katydids are related, it's not farfetched that similar genes could control coloration in all these insects.

Can't edit the comment, mantid's aren't grasshoppers, should read ..."mantids and grasshoppers..."

Any idea, what kind of pigment is involved?

Side-question: if you were to breed with solely pink individuals, what are the odds of the offspring to be pink as well?

@StevenRoose the odds are very good – check the SciAm link where they have results of just such an experiment, looks like it's about 3:1 odds to 7:1 odds that the offpsring will be pink.


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Is it possible to perfuse chemicals into brain after removal from body?
I've read studies where fixatives (eg glutaraldehyde) have been perfused into the brain while it is still inside the skull. I would have thought that this could also be done after the brain is removed, provided all the veins/arteries are connected to a perfusion machine. Is this possible, and are there any major obstacles?

Of course it is possible to perfuse an organ once it has been removed from the body. It is probably unwise to do so with the brain as the delicacy of the structures and high levels of lipids make rapid fixation necessary and difficult. I think the major obstacle is the speed at which the brain could be removed with arteries intact and then perfused as ultrastructural changes occur rapidly once ischemia (oxygen deprivation) begins.

The main obstacle would be connecting all of the arteries to a perfusion machine.
 The neurovasculature is complex, and begins branching prior to entering the brain, therefore it is easier to do in situ. With a larger brain, the meninges and skull are also important for supporting the brain stucture. If unfixed brain is removed from the skull, it will begin to deform and collapse under its own weight. For fixation, especially, it is much safer to fix in situ and remove post-fixation.


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Identifying very tiny worm
i couldn't take a picture because i get rid from it as soon as posible. Because i thought maybe it was a bad parasite.
But i draw a picture of it at my computer. But my picture not very accurate because it was very tiny to see what it actually look like. and i cant remember all of the characteristics of it.
It is very tiny about 5 mm in length. and maybe almost 0.1 mm thick. I assume that yellow thing is head, because of movement directions is towards that way. To move, he elongates its own body then holds to surface with its own head, then let free its other ends grasp from the surface simultaneously shrinks to shorter length maybe half of its elongated length. than repeats whole process.
It was shrinks and elongates to move
it was moving like its got very soft body. and it was becoming significantly thinner when elongates.
Sometimes looks like checking surrounding surface with his head. Seem like it tries to navigate.
finally I must describe how my picture could inaccurate: it was very tiny i cant see his body parts exactly. i guess i see a tiny structures appears like his 2 pair back leg and 1 structure ball like thing attached to end. But this structures possible thickness are micrometers so i also thought that structures could be attached dust particles. And i also saw structures like this at the front end, but it was so tiny, i cant even drew because i see just barely but cant figured what was it like.
only im sure about its head and white-ish neck.
it is elongated at the picture.
So picture is representing what i see. but not %100 accurate. due to reasons i described.
i hope my questions description is enough and isn't improper.

I think without an actual picture it's going to be nearly impossible to identify. Species identification is very difficult and often depends on details that aren't initially important. But I can tell you that if it has legs, it is not a worm.

@BryanKrause yes imposible but i was hoping to get a general idea like a family or genus guess rather than exact specie.

Interesting question, and probably a little bit hopeless. I don't see how anyone could give an answer without a lot if guessing. Maybe you should remove the inchworm image, since that just seems confusing if it wasn't really "inching". As @BryanKrause says, it's not a worm if there ar legs. But a lot if insects have larva that are a bit worm-like. Maybe try googling videos of different larvas? I'm guessing fly larva of some sort. How does this hover fly larva look? https://www.youtube.com/watch?v=gkU8YHpuAtw

@picapica now i watched this video and it is so close what i see, especially about movement type. But my things was more thinner at the body. Tomorrow ill google about relatives of Hover fly, thanks for the video.

Was it an inchworm? It fits the description, as well as the 2nd picture.

no. sorry i guess i didnt clearly asked. 2nd picture doesnt represents it. 2nd picture just here to describe how it moves. thanks for answering.

1st picture is represents it with high but limited accuracy.

but maybe it is very far relative of inchworm. but two things doesnt fit to inchworm. Inchworms body is too bigger than it.and mainly inchworm bends  not shrinks like what i see.


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identify this plant
location: trabzon (turkey) can seen in rural areas, in woods and in some gardens.

In the American South will call that Poke Salad.

Looks like pokeweed (Phytolacca americana):

Source: https://nature.mdc.mo.gov/discover-nature/field-guide/pokeweed

Source: http://ribbonsandlines.blogspot.com/2012/09/september-at-cape-may-point-nj.html
Per wikipedia:

Pokeweed is native to eastern North America, the Midwest, and the Gulf
  Coast, with more scattered populations in the far West. It is also
  naturalized in parts of Europe and Asia.


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Would it be correct to state that any biological difference between the sexes has to be found in the Y chromosome?
If the reason Why Men Don't Listen and Women Can't Read Maps is genetic, then one of the genes in the Y chromosome is to blame and in theory could be identified.
Correct or incorrect?

If it was genetic then the answer is almost certainly yes, but I would think it is more likely due to hormone differences.  Ultimately hormone's are regulated by genetics, but other things can influence them as well, for example tumours, or drugs and many other environmental and epigenetic influences.

check this post. It covers some aspects of what you are asking.

There are two main flaws in your reasoning: 1) you are assuming that male autosomes are equal to female autosomes, which is not necessarily true and 2) you are assuming that such complex traits are monogenic which is definitely false

@Chris why would the answer be yes? See Amroty's answer below and also consider that very few traits are monogenic. I see no reason to expect such differences between the sexes to be confined to the sex chromosomes.

@terdon, I agree with Amory's answer.  I meant if we assume that genetics is the only reason for the difference between males and females (which is the silly assumption made in the question), and considering the somatic chromosomes are selected randomly independent of gender, only the sex chromosomes can account for the difference.  However, that is not to say that the sex chromosomes don't regulate the expression of other genes on other chromosomes, giving rise to gender differences.  So I agree other chromosomes can contribute to gender differences.

...(continuing) other genes can contribute, but they can be present in both males and females, but are just expressed differently.  The reason for their difference in expression is because of the differences in the sex chromosomes that ultimately regulate the other chromosomes.

Here is a book that will probably interest you (it is not published yet)

"Blame" is a strong word.  The human Y chromosome has only a few dozen protein-coding genes.  One of the most important, for males anyway, is SRY, the sex-determining region.  This is a transcription factor that is responsible for modulating the expression of other genes; those genes need not be on the Y chromosome.  SOX9 for example is itself a transcription factor, is upregulated by SRY, and is found on chromosome 11.  Most of the genes associated with maleness are found elsewhere.  Moreover, once the testes form, they can be potent secretors of hormones that cause a number of physical changes.  So is SRY to blame, or SOX9, or the testes?  It depends on how direct you want your genes to be.  If you're blaming SRY you're not wrong, but at that point you might as well blame fate.
Oh, and there are epigenetic differences between the sexes.  You could also make some arguments about the Xist gene responsible for X-inactivation in females.

Imagine a culture where girls are chastised for taking risks, and heavily punished when they take risks and fail, but where boys are encouraged to take risks, and praised highly when things work out their way.
Wouldn't you expect that when put in a situation where such individuals are supposed to make a high stakes action based on risk assessment, that those girls would show much higher stress levels than the boys would?
Big biological difference, having nothing at all to do with the Y chromosome,or genetics at all.  Just the environment.

Good point! It is good to add on Armory's great answer that part of the differences between sexes are due to the fact that both sexes do not live in the same environment (social environment) and this is especially noticeable in humans that have a great culture and (unfortunately) big social considerations of what is a female and what is a male and how they should differ.


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Why are humans and almost every species on earth symmetrical?
I admit I'm not very learned on the subject of evolution, I just started researching it for myself about a week ago. One of the things that I don't understand is why humans and almost every other animal/bug/fish etc. on earth has a symmetrical body. What advantage does this have for the survival of the fittest? It must be quite important, since it re-occurs so frequently and early in the evolutionary family tree.

Related Question: http://biology.stackexchange.com/questions/5588/why-is-most-life-symmetrical-externally-but-not-internally/

Only Bilateria (http://tolweb.org/Bilateria/2459) are bilaterally symmetric like humans. Millions (billions?) of other eukaryotes and  prokaryotes (by whatever names they are going these days) are not symmetric.

still a fair question - perhaps change to: "why are humans and most animalia phyla symmetric - bilateal?"

This is not a duplicate, the other question is about lack of internal symmetry, not the evolution of symmetry in general.

@kmm.. there are others that are radially symmetric too.. some unicellular organisms also have an axis of symmetry..

@WYSIWYG Good point. I assumed bilateral symmetry because the OP asked about humans.

Come to think about it: Almost every vehicle that human beings have designed is bilaterally symmetrical, exlternally at least. Symmetry makes coordinated movements simpler. This is just a thought.

[If we are talking about animals, there is a number of types of body symmetry: asymmetry, radial, bilateral, spiral, rotational, glide and metameric symmetries. Bilateral and radial are the two basic types, which served as main classificatory character for animal mega-systematics in the past.]
It's assumed that body symmetry is associated with general environmental gradients.
Animals with (elements of) radial symmetry have one dorso-ventral axis which echos only one environmental gradient: substrate/water column, depth etc. Besides this polarity, resources/signals/danger may come from any direction. Imagine a Hydra polyp with its foot attached to a waterweed and its tentacles surrounding the mouth on the opposite end and expecting the victim to come from any side.
Body of bilateral animals possesses the same dorso-ventral axis and yet another polarity, orthogonal to it: the anterior-posterior axis. This axis is conjugated with the gradient created by locomotion: the anterior margin of the body is likely to encounter something new first. This principle lies in the basis of cephalization: most bilaterial animals have more or less shaped "head".
Evolutionary changes in body symmetry are thus thought to be associated with changes in life-style, e.g.:

there is a hypothesis that cnidarians were originally bilateral (and many of them still show some degree bilaterality), but lost it after becoming sedentary.
non-walkers echinoderms originated from fully bilateral animals and later acquired their famed pentameric radial symmetry (were they originally fully sedentary like modern stalked sea lilies?). This symmetry, however was again distorted towards secondary bilaterality (not matching the original plane of symmetry) in endobenthic forms: sand dollars and some holothurians.
worms like nematodes or priapulids are dwellers of viscous media, similar in all directions: dorso-ventral gradient of environment in this case is absent or weak. Though the original bilateral symmetry is very clear in their body plans, signs of radial symmetry prevail in some organ systems, including the general vermiform appearance. Thus, nematodes combine triradial (head sensilla, pharynx), biradial (musculature) and bilateral (nervous system, genitalia, tail) symmetries.