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Why are butterflies drinking blood?
According to this video, butterflies sometimes drink blood. Do they have the organs necessary to digest blood? I thought they eat only salts and nectar, which are easy to digest compared to proteins.
@aandreev
100mg/dL is the human blood sugar content (I assume it is similar in other animals). Afaik. sugar energy density is about 4kcal/g. A butterfly is about 1g of weight, which means 1mL if we count with water. So it can drink around 0.5mL of blood. That means 0.5mL×100mg/dL×4kcal/g = 0.002kcal = 8.4J. The top butterfly speed is about 12 mph, so I think we can count with 6mph by an average butterfly, which is about 2.7m/s. So it needs 1/2×1g×(2.7m/s)2 = 0.0036J kinetic energy to move and 1g×9.81m/s2×1m = 0.0098J potential energy to keep the 1m height of flight. I think we can guess that it loses this kind of energy in 2secs, which means it needs 0.0134J/2s = 0.0067W power to fly. So the 0.5mL blood means 8.4J/0.0067W = 24925s = 21min of flight time, which is not much compared to nectar (30g/dL$, $2500J$, $100h). Ofc. this is just a very rough estimation (the real flight time is probably much lower) based on data coming from non-scientific sources, but I think you can see the difference.

For salt content I think. Not sure enough to answer but blood is full of nice things besides calories.

calories in blood are glucose

@aandreev I edited the question.

what about salts though?

@aandreev Find evidence and send an answer. This is how science works. :-) http://scholar.google.com

check http://en.wikipedia.org/wiki/Hematophagy

I am quite sure blood contains far far more than just glucose. Most of the compounds in blood (proteins, lipids) can all be oxidised.

@MarchHo Ofc. they can be used to produce energy, but can a butterfly digest proteins and fats?

I didn't watch the video so I don't know if this was mentioned. Butterflies will exhibit a behavior called mud puddling which occurs mainly with male butterflies [1]. Puddling is when butterflies seek out moist surfaces in order to consume the fluid. Butterflies will puddle in soil, dung, carrion (rotting flesh/meat), etc. Boggs and Jackson claim that puddling falls into two categories which aren't mutually exclusive [1]:

scarce nutrients for example sodium
competitive exclusion of males or young individuals from flowers

But we can see blood isn't the only option for puddling. Basically anything that provides moisture and nutrients will do.

This competition for flowers is very new to me, I did not know that butterflies can fight each other. :-)

@in3rno I choose you Butterfree! Use Sleep Powder on the other Butterfree! Seriously though, I would assume they use the same tactics as birds...minus the beak stabbing, and vocalizations?


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Are there any de-novo genome assembly programs for HADOOP?
I have access to a small (approx 20 nodes) cluster that has HADOOP running on it, and I need to do some de-novo genome assembly. I'd like to ask is anyone knows of any program that can do this on a HADOOP cluster. Cloud based stuff is not an option right now, unfortunately, so I need something that I can deploy on our cluster locally. Thx in advance.

You can try CONTRAIL and CLOUDBRUSH...

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How can I align more than 2 sequences locally?
ClustalW and Omega of EBI and Blast of NCBI, both globally align sequences. Smith waterman of EBI aligns sequences locally, but works with just two sequences. How can I align more than 2 sequences locally?

You have to do it pairwise (there is no other option).
You can do that with BLAST or even SSEARCH (Smith-Watermann). If you have a fasta file of your sequences then do this:

make index of your sequences using makeblastdb -dbtype nucl -in <yourfastafile> -out <yourdbindex>
Run BLAST with your <yourfastafile> as input and <yourdbindex> as database with desired parameters. This will do a pairwise alignment between all sequences

Similar strategy can be used for SSEARCH.

I just use GUI based software and sites. what are these codes?

@StackUnderFlow This is the command to run blast in commandline (UNIX terminal or Windows command prompt). blast does not have a GUI or even if there is one, I have never used it. It is much better to write commands (it saves RAM and also allows you some automation)

The various web-based BLAST tools are basically a GUI for BLAST.

@terdon Ohh yes that's true but they don't give much controls.

More than you might think. The NCBI blast lets you set things like e-value, gap penalty, match/mismatch scores, low complexity filtering. That's more than enough for 99% of uses.

Even Water (in EBI itself) is Local alignment tool for multiple sequence alignment. Also in BLAST you get bla2seq which is also used for pairwise alignment. In any of these tools  you just have to enter FASTA sequences (any number you want) or any sequence with > sign and run it against the subject (database or your required sequence).
If you want to see the results for all the alignment in one screen, a tool like BioEdit would be ideal.
I hope this is helpful, I'm not an expert in bioinformatics so feel free to correct me :)

Thanks but those tools are for pairwise alignment but I need a multiple alignment tool which locally align sequences

I use Jalview, that is a small program written in Java. It is simple to use and can do many many things. It's web-service based and it has 7 different services built in just for sequence alignment. You can load your sequences from many file formats, or get them by reference id. It's really a small swiss-army-knife. I really recommend to take a look at it. It's available on http://www.jalview.org/.
EDIT:
I might have missed the local alignment part earlier, but I did some research and found that MULAN (MUltiple sequence Local AligNment and conservation visualization tool
) may be what you're looking for.
PMC article of Mulan, and the manual for Mulan.

Thanks and where is Multiple local align in jalview?

@StackUnderFlow Jalview may not have what you need but I edited my answer and found Mulan that might suit your needs.

jalview is not for local alignments.

Yes, I know that's why I edited my answer, but maybe I'll delete that part, so it won't be misleading.

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By what mechanism does Risperidone swell breast tissue?
There has been much talk of the anti-psychotic drug Rispeirdone causing un-natural breast tissue growth as well as galactorhea (milk production). Especially in young men and boys.
What is the mechanism of this drug that is causing this? Is it actually introducing some amount of female hormones into the male's body or is just causing increased production of them?

There is a class-action lawsuit against the makers of this drug (a.k.a. Risperdal) because of it causing breast development in men and boys. So the answer is yes.

The edit is much better. +1 and retract close vote.

Risperidone prevents dopamine from acting on the pituitary gland by blocking dopamine type 2 receptors. One of dopamine's effects on the pituitary is to suppress prolactin production. In patients taking risperidone, prolactin production thus increases and prolactin levels in the body are higher than normal. In younger males, this can result in abnormal growth of breast tissue and even milk production.
See e.g. Melkersson, K. I. (2006). Prolactin elevation of the antipsychotic risperidone is predominantly related to its 9‐hydroxy metabolite. Human Psychopharmacology: Clinical and Experimental, 21(8), 529-532.

Could you add a reference for this?


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Hydrogen peroxide decomposition and catalase uses
All google searches have simply returned more info on catalase. I'm looking for a catalyst that isn't found inside living organisms which  can break down H2O2. Looking for any resources to look at, or just examples of other catalysts.
Side question since I don't want to clutter with a new thread.
Can catalase be used for anything other than the decomposition of h2o2?

https://en.wikipedia.org/wiki/Hydrogen_peroxide#Decomposition - you're looking for non-biological catalysts so you should ask on Chemistry SE

@Mithoron yea I suppose, I just received this question in bio class so I thought there might be some relevance.

Manganese(IV)oxide can be used as a catalyst to speed up the decomposition of hydrogen peroxide

A reference would be appreciated Hamza.


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CRISPR Knock in
Using the CRISPR/Cas9 technology, it is possible that after inducing a DSB with the Cas9 endonuclease guided with an RNA designed by the user and using a template DNA, get a desired Knock-In (KI) by homologous recombination.
I have read that for desired KI-s that are less than 200 bp, a olygonucleatide should be enough as template. On the contrary, if the desired KI is bigger than that, a plasmid vector should be used.
Is that information accurate and correct? and, where is the upper limit for the KI length?

Successful knock-in of 1000 bp and 500 bp has been done before. ncbi.nlm.nih.gov/pmc/articles/PMC5307959/


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Telomerase as cancer target
There are a lot of publications, starting from 2000, about using telomerase for targeting cancer cells (it is upregulated in more than 80-90% of tumor cells). Specifically using its promoter (hTERT). In all publications, researches talking about the success of this approach.
So my questions,  why there is no use of this? What is the problem? I read a lot of articles - and didn't find an answer.
http://scholar.google.com/scholar?q=telomerase+suicide-gene+promoter
http://www.spandidos-publications.com/ijo/21/3/661  (one of the newest)

The study you linked to uses cell cultures; there's a big difference between introducing genes in cultured cells and in whole organisms. Also, telomerase is expressed by some non-cancerous cells in adults.

@canadianer, thank you. But in studies that I read, they wrote that the targeting is really good, and has a really little affect on healthy cells - much better then chemotherapy. So the delivery is the main problem...?

Delivery of a transgene would be a problem currently. Delivery of some inhibitory drug could be easier.

Thank you. If you want to write an answer - I will choose it.

With help of canadianer (thank you) I think I found the right article, so just want to share.
This study not talking specifically about telomerase, but about the same approach of using promoters that are upregulated in tumors - exactly what I looked for. Published in 2014.
http://symbiosisonlinepublishing.com/genetic-science/genetic-science03.pdf

However, the therapeutic approach in humans is limited by
  low efficiency of delivering the suicide genes and concerns regarding
  safety. Thus the number of clinical trials in human patients has been
  limited and treatment benefits observed modest. An intensive research
  effort is necessary to overcome these obstacles and turn suicide gene
  therapy into real benefit for our patients.


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Why does a human's field of view narrow when moving faster?
A relative of mine is a driving instructor and he regularly likes to bring up that the field of view narrows noticeably when driving at higher speeds.
Is this true, why is this so and does this apply for other species as well (for example, leopards, who are widely known for their fast speed)?

Do you have a citation for this other than the anecdote? I did not notice this effect when looking out of the window in planes and high-speed trains, which travel much faster.

@MarchHo Sorry, I don't have a reference, updated the question. But as per airplanes, no object is actually moving fast in your field of view, as everything is far away.

I mean when looking at the runway moments before takeoff, or a parallel set of rails.

I believe your cousin is referring to what is usually called 'tunnel vision'

stuff on sides of your FOV are moving faster than in the center (right in the center speed is zero, actually). At some speed things on sides will just be a complete blur. Try looking from the window of moving car on hills far away and on the road barrier close to you: same thing for driver

I totally concur with @aandreev - the field of view is a constant (bar any medical issues) and will not change when moving about at any reasonable speed (at the speed of light things might change :-). Attentional focus (subjective percept) may change at high speeds, and physical retinal image slip indeed changes with visual angle as aandreev suggests.

Perhaps it has something to do with adrenalin discharge?


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Why is the opposite of plantar flexion called "dorsiflexion"?
Why is the action of flexing the foot so that the toes move anteriorly/superiorly (i.e. in the direction opposite that which they move during plantar flexion) described as "dorsiflexion?" In the same vein, why is the top surface of the foot called the "dorsal surface?"
If anything, the action opposite to plantar flexion moves the foot in the ventral direction, doesn't it? And surely if you've ever seen a human in the anatomical position, you can see that there's nothing dorsal about the top surface of the foot - it's superior, perhaps, but by no means dorsal.

It comes by logical extension of the hand... which side of the hand is the front side? In many languages, the back of the hand is called the back, dos in french for example means the back.

Anatomical terms must be able to fit a wide variety of organisms, from insects to fish, dogs, horses, chimpanzees to humans. That's why the terms are sometimes confusing to people who are thinking only of bipedal humans.
In anatomy, the dorsum is the upper side of animals that typically run fly, swim or crawl in a horizontal position. In vertebrates the dorsum contains the backbone. In such an animal the "ground side" is the ventrum.
Due to varied orientation on quadrupedal mammals (where the term is more appropriately used) the "back"-side of the hand, the "top"-side of the foot and the upper surface of the tongue are referred to by the term dorsum.

Does this picture help? Note the dorsal surfaces of the body, muzzle, feet.
In anatomy, the sole of the foot is called the plantar surface. The top of the foot is called the dorsum of the foot. (Imagine us walking on all fours like apes.) Therefore when you extend your foot, it's called plantar flexion; when you flex your foot upwards towards your head, it's called dorsiflexion.
Similarly, the arteries feeding the bottom of your foot form the plantar arch. Those feeding the top are the dorsal artery (or the dorsalis pedis).
Because anatomy must describe other animals than ourselves with other orientations, it must be consistent. In a quadruped, the dorsum of the tongue and the feet do actually point to it's "back" surface. See the picture below:

Lynxes have big paws, so it's more obvious that the surface facing the backbone is appropriately called the dorsum of the paw/foot. This picture is particularly interesting because it shows three degrees of dorsiflexion and one paw in full plantar flexion.
In humans, the "back" is actually the posterior surface, because we are not primarily in a horizontal orientation. The ventral surface is called "anterior". Thus we speak of the anterior chest wall and the posterior chest wall, not the dorsal and ventral surfaces, although those designations would still be entirely correct.

I mean, I get that all of that is true. The question remains - why would you call the top of the foot the "dorsum"? Some anatomist at some point in time must have figured that there was a good reason to call the top of the foot the "dorsum", and what I'm hoping to find out is what that reason was.

It is because anatomy must describe other animals than ourselves with other orientations. In a quadruped, the dorsum of the feet do actually point to the back.

Minor nitpick: The dorsum of gorillas' hands do not point to their backs

@March Ho - They do if the hands were splayed out. As I said, it's meant for quadrupeds: think cats and dogs, etc. Obviously, it has to be able to fit kangaroos and gorillas as well. The bigger problem comes with elephants and hoofed animals, I should think.

@anongoodnurse Ah, that's what it is - I wasn't thinking about how the feet would be positioned on a quadruped.

Anterior and posterior is described in the upper limb based on anatomical position. In human anatomical position the palms face forward, so it becomes anterior. I think this would translate to ventral.

Enlightening explanation, But being philosophical,  the surface at the top of the foot is a surface, not a stick with a point, so it doesn't point. And if you did look at the the surfaces as pointing in some way, then both surfaces of the foot are nearer the front/belly of the animal than the back/vertibrae. .  You could say the foot is parallel with the front and back, and  the surfaces correspond, and in that sense the top of the foot corresponds to the back and the bottom of the foot to the front.

@barlop - you can philosophize till the cows come home; that won't change the nomenclature, which I thing is based on clarity, consistency (an iguana's foot really does stick out like a stick) and function, not personal views; those are too variable.

@anongoodnurse all feet are stick like, n an iguana or any four legged animal's feet don't point towards its belly or back.And if u wanted to talk of where the dorsal surface points to,well,if u put a little spaceship on the dorsal surface of the foot and travelled up,you'd hit the front of the animal,not the back.So if the surface points anywhere, it points to both the front and the back of the animal,and the front first.So I don't think it makes much sense to talk of where feet point if you're talking about a surface and ignoring the surface it points to first when saying what it points to.

I suppose what one could say is the foot and back (in that diagram / the default position for a quadruped) is parallel and if you were to write in a top and bottom, and have 2 planes for the foot and 2 planes for the torso all parallel, then the planes can be said to correspond in that 2 planes, one on the foot and one on the back, could be said to be nearest the top(the so-called dorsal/posterior), and 2 nearer the bottom(the chest and what in humans would be the fleshy part of the foot), would be the ventral/anterior planes of that body part..

Although the other 2 answers are accurate and well thought out, I just wanted to answer this with a bit different focused response.
Two things to note:

In general, one should think of flexion as decreasing the angle of a joint (see here, here, here, here, here, here or here for reference). From Saladin's 2015 Anatomy textbook$^1$:

Flexion = a joint movement that , in most cases, decreases the angle between two bones.

Put differently,

Flexion refers to a movement that decreases the angle between two body parts.

As the other linked answers have aptly described, the superior surface of the foot is referred to as the dorsal surface (dorsum meaning "back"), and the inferior surface is referred to as the plantar surface (from Latin plantaris, from planta meaning "sole").

Given these two pieces of information, we can understand why the terms dorsiflexion and plantarflexion are used:

Dorsiflexion = decreasing angle between dorsal surface of foot & anterior side of of the leg.
Plantarflexion = decreasing angle between plantar surface of foot & the posterior side of the leg (or, more realistically, between the plantar surface and coronal plane of the leg).

From University of Michigan:

A transverse axis through the ankle joint allows a pair of actions similar to flexion and extension at the wrist joint.
The analogous action to wrist flexion is one that would tip the sole of the foot downward, increasing the angle between foot and leg. The usual term for the increase in such an angle would be extension, but in order to emphasize the relation between foot and hand, this action is instead termed plantar flexion .
The action similar to extension at the wrist would be a tipping of the upper surface (dorsum) of the foot toward the anterior surface of the leg. However, this would decrease the angle between the body segments, and action usually termed flexion. Since the term, plantar flexion, has been used for the opposite action, this is now referred to as dorsiflexion.

$^1$ Saladin, K. S. 2015. Anatomy & Physiology: The Unity of Form and Function. Seventh ed., McGraw-Hill, New York, NY. 1248pp.

While this makes sense superficially, it doesn't hold up universally, because there is more than one relationship to body parts. If in one position one angle is decreased, the corresponding angle(s) will be increased. It makes more sense (to me) if flexion (etc.) is described by position rather than by angles. We don't describe abduction as increasing the angle of the arm to the ribcage. (At least I never heard of this either in anatomy class or surgery or neurology of any other study in which anatomy is used.)

Ah, but it does hold up universally. Flexion/extension are very often defined as "increasing/decreasing the angle of a joint" (e.g., see references above or see often used Saladin 2015 textbook). Adduction/abduction are different because they refer to movement of a body part away/toward the midline of the body. They are not in reference to angles, per se. However, since flexion/extension are relevant to all different parts of the body, it is better to define them generally as increasing/decreasing angles of joints in general.  (cont.)...

(cont)...And yes if you increase/decrease any angle, you have to do the opposite (decrease/increase) its adjacent complementary (or supplementary) angle. But even though that adjacent angle is always present,  it  is more relevant  for the given muscle's  antagonistic  partner and not relevant to the muscle moving. That does not disqualify these valid definitions of these movement terms.

I think the angles thing is throwing you off. But remember, we're talking about angles of individual joints. That's why flexion/extension differ from abduction/adduction, which refer to movement relative only to the midline of the body.  Regardless, I'm addressing the definitions and origins of these terms -- I'm not making this stuff up :p. I'm surprised you've not heard of extension/flexion being defined or used in this way, but I would think my answer doesn't deserve a downvote because this is the way these terms are often defined.

I do understand all that you're saying. But, I have never - and I've been a doctor for decades - seen it defined in this way (therefore "...this is the way these terms are often defined" is not true to my knowledge.) You obviously have. It's just less clear cut to me.

Huh, weird. Yeah,  I've been teaching  human A&P at  the University level for over half a decade and this is what we're  teaching  up and coming doctors / health professionals. This  was the way I was taught a  decade ago myself.  It's as general of a  set of definitions/explanations as I've seen.

I don't know how to explain it either. I asked my son (finishing med school in May) if he was ever taught the way you identified, and he said no, never. Maybe it's a geographical thing?

Well, I found a number of universities and textbooks using a quick search (see the 7 new sources cited in my answer) that support the "decrease joint angle" definition. So it's a fairly common way to define flexion (though, I'll admit I only found US examples). I also provided a directly quoted explanation about dorsiflexion/plantarflexion to my answer to provide additional support. Although defining these terms this way was not true to your knowledge previously, I hope this overwhelming evidence can convince you that it's very common and valid and true.

I can't argue with evidence.

I just realized you thought I downvoted you. I didn't; I upvoted you. If I could share this bounty with you, I would be very happy to. Your answer is excellent.

@anongoodnurse Ha no worries. I actually didn't think so. Our extended chat convo was simply me kicking into teacher mode. Thanks for the compliment :). glad we were both able to provide informative answers to this Q -- always great when a Q gets multiple good answers :D. [woww neat bounty, where'd that come from??. I could put in a feature request ;p]

Only fair to give you the larger part of the bounty since your answer is better than mine. :) I had forgotten about this until recently.

@anongoodnurse whoa! What a surprise. Thanks a lot :) ! Glad to share that bounty with you -- our answers compliment each other well

Dors/dorsum in Latin simply means "back", and it is rather normal and reasonable to use the equivalent term in English with regard to the extremities (hands and feet), see "back of my hand".
It is medical convention to refer to the non-gripping surfaces of the feet and hands, as well as the upper (towards the brain) surface of the tongue as "dorsal".
My best guess for the etymology sequence is that all the terms were borrowed from Latin anatomical books written by Roman and Greek doctors (Dioscorides, Galen) which named the anatomical structures in normal language (back/dorsum, stomach/venter, sole/plantarum) and these terms were then fixed into modern medical terminology as jargon.
Caveat: I could not find any citation for the etymological sequence, but it seems a rather reasonable explanation to me.

Yes, I am aware that "dors" or something like it is Latin for "back". For the hands, this makes sense, since the non-palmar surface of the hands faces dorsally in the anatomical position. The same is not true of the feet. Are you saying that calling the top of the foot "dorsal" is because it is homologous with the dorsal part of the hands?

@senshin Saying that it is due to homology would be at best a speculation. What I am saying is that in many languages, the non-gripping surface of the extremities are referred to as "back" (eg English as above, and Chinese "手背，脚背"). Therefore, I believe the Latin name is just an extension of this naming convention.

I suspect that the etymology might derive from the fact that much of the scholarship of medieval and renaissance Europe was written in Latin.

In the same vein, why is the top surface of the foot called the "dorsal surface?"

I don't think the above answers are correct -- they do not really address the question of why the top of the foot is the dorsal surface, and why the surface of the hand opposite to the palmar surface is dorsal.
The reason why the top of the foot is dorsal is due to how the body develops embryologically. See the below figure:

Figure taken from Dr. Ann-Judith Silverman's human development notes, Columbia U. See: Human Dev Notes
The dorsal side of the upper and lower extremity begin on the dorsal/posterior surface of the body. However, during the 6-8th weeks of development, both the upper and lower extremity will turn medially, so that the originally dorsal surface is now anterior/ventral.

The position of the human foot by human anatomical convention dictates that the human foot is perpendicular to the human body in a standing position, such that the rest of the human body (including the hands with the palmar surface facing forward) , but except the foot, will conform to the anterior or ventral plane versus the posterior or dorsal plane. The foot, at conventional anatomical position will have its own plane, consistent with the same reasoning such that the top of the foot is the dorsum, while the underside is the plantar surface (more correct), or the ventral surface (less acceptable due its confusing orientation).
The plane of reasoning for the entire human body at anatomical position above ends at the distal junction of the tibio-fibula with the tarsal bones, such that the human feet will have its own surface plane directly perpendicular at 90 degrees to have its own 'dorsal' and 'ventral' surface.
The feet as such is in a special position compared to the rest of the human body's plane surfaces to warrant its own. Thus by convention, one may acceptably hear 'antero-flexion' or 'dorsi-flexion' of the foot, but not 'supero-flexion of the foot' which sounds sort of disagreeable.
The same way, oppositely, it is customarily said the 'plantar-flexion of the foot' which is more accurate (rather than infero-flexion or ventro-flexion or postero-flexion of the foot which sounds quite confusing)

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What happens to the precursor protein's signal sequence after it is cleaved?
Where does this signal sequence "go" after it has been cleaved by signal peptidase and what is its next function?

Doesn't that entirely depend on the protein? This is too broad.

I think specification of the question (example protein perhaps) may indeed help.

For example, a transmembrane protein in the ER with a N-terminal signal sequence. Are there molecules or proteins that transport the signal to other precursor proteins or does it remain in the membrane of the ER?

After cleavage, the signal sequence is generally thought to be degraded by intramembrane proteases (since it is embedded in the endoplasmic reticulum membrane). For at least some proteins, the signal sequence is further processed and released into the cytoplasm or ER lumen.
Martoglio B. 2003. Intramembrane proteolysis and post-targeting functions of signal peptides. Biochem Soc Trans 31:1243-1247

When translocation continues, the signal sequence’s c-region appears in the ER lumen and becomes accessible to signal peptidase, which cleaves the signal sequence from the pre-protein. The latter is further translocated into the ER lumen, while the liberated signal peptide is usually not detected in assay systems, implying rapid degradation. In a cell-free in vitro system with ER membranes from canine pancreas, we reported several years ago that after cleavage by signal peptidase, the liberated signal peptide is transiently embedded in the lipid bilayer and undergoes further processing to be released from the membrane.

The activity of released signal sequences is not entirely known and only partially characterized for some proteins. The following review discusses some functions of signal peptides after cleavage:
Martoglio B, Dobberstein B. 1998. Signal sequences: more than just greasy peptides. Trends Cell Bio 8(10):410-415
The signal peptide of bovine preprolactin and HIV gp160 can bind calmodulin.

…the signal sequence of bovine preprolactin, which consists of 30 amino acid residues, is cleaved by signal peptidase and then further processed by an unknown signal peptide peptidase (SPPase; Fig. 4) … This signal peptide fragment resides initially in the membrane and, after a chase period, is released into the cytosol. Once in the cytosol, the signal peptide fragment binds to calmodulin in a Ca2+-dependent manner. A signal peptide fragment derived from HIV-1 gp160 also binds to calmodulin when it is released into the cytosol … With their n-regions having the potential to form a basic amphiphilic α-helix and their hydrophobic C-terminal region, they are similar to other calmodulin-binding domains. Calmodulin is a small, acidic protein involved in the regulation of many cellular processes controlled by Ca2+-dependent signalling pathways. It is possible that binding of signal peptide fragments to calmodulin influences Ca2+/calmodulin-dependent cellular signal-transduction pathways. Further studies are required to elucidate the physiological consequences of interactions between signal peptide fragments and calmodulin.

The signal peptides of MHC class I proteins are presented to NK cells by MHC-I (with HLA-E alpha chain). This allows monitoring of MHC-I expression, which is often disrupted in virally infected or cancerous cells.

Peptides presented by classical MHC class I molecules represent the broad spectrum of peptides generated by the proteasome. In contrast to this general use of peptides, only a very specific signal peptide fragment is presented by so-called nonclassical MHC class I molecules (HLA-E in human). These molecules monitor the presence of classical MHC class I molecules by presenting a signal peptide fragment derived from HLA-A, -B or -C to natural killer (NK) cells (Fig. 5b). NK cells destroy cells unable to activate inhibitory receptors specific for MHC class I molecules.

This book section discusses the function of signal peptides in some viruses:
Kapp K, Schrempf S, Lemberg MK, Dobberstein B. 2009. Post-targeting functions of signal peptides. In: Protein Transport into the Endoplasmic Reticulum, Zimmermann R.


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Medical Uses of toxic venom
One interesting thing I recently learned is that venom has medical uses that can actually save lives! But from what I see so far this either applies to venoms from creatures that are not fatal to humans or that only proteins or enzymes from these venoms are what is being used medically.
Are these proteins or enzymes themselves fatal to humans or is this just a misrepresentation of the fact that venoms can save human lives?
EDIT: To clarfiy, while I realize venom is harmless in lower doses, I also read the following :
Enzymes from cobra venom may be instrumental to finding cures for Parkinson's disease and Alzheimer's disease.
An enzyme derived from copperhead venom could be used to treatment for breast cancer.
What I was not sure of was whether the enzyme by itself was toxic or they were just extracting a non-lethal element of the venom to use medically. Can this enzyme alone of venom administered in large enough doses be fatal?

Can you specify to which venoms you're referring? Can they not do both under different circumstances? I hardly think anyone is trying to misrepresent anything.

Maybe I am understanding your question wrong, but venom is only deadly when given in a certain amount. From that point of view, everything can be lethal, even water. This makes the first part of your question shaky. For example, digitalis extracts can save live-threatening heart failure, but in large amounts it can kill. Further, proteins in snake venom are the chief toxins as far as I know. So the second part of your question is unclear. In all, I think the question needs to be specified before it can be answered.

You should narrow it down. For example just talk about cobra venom. Different venoms act differently; some are enzymes others are not.


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Reconstruction of wildlife distribution based on poorly-sampled data
cross-posted to Signal Processing, Cross Validated, and World Building Stack Exchange
Hi, I thought I'd also put this here in case there are any field biologists with ideas on the matter.
Problem: After reading a series of fantasy novels, I noticed that the biosphere in that world made no sense. To clarify, this is a world where despite magical occurrences, the world itself is almost entirely non-magical. 'Alternate history magical realism,' perhaps. i.e., unlike, for example, Harry Potter, in which almost all plant and animal species mentioned are fictitious and magical, this series uses real flora and fauna. This allows me to extract information about the fictional world's environment based on the distribution of these animals, by assuming that similar animals will live in similar climates on Earth and in the fictional world.
Ignoring the likelihood that the original author did not put enough thought into worldbuilding to make this a necessarily reasonable endeavor, my idea for how to proceed was as follows:
As maps exist of the fictional world, and the path of the characters can be plotted, I hoped to mark every mention of a specific plant or animal in the text, along with the location of the characters when it occurred, and from this reconstruct a plausible distribution for each species. I've created a theoretical example (in photoshop), for illustration:

where the red dotted line represents the paths of various characters, the orange, green, and blue splotches represent the true distribution of the species; the stars, triangles, and circles represent the locations at which a species is mentioned; and the brown, green, and blue lines represent the reconstructed contours of the distribution.
Is there a method to do such a reconstruction? It sounds a bit like a Monte Carlo analysis, but I figured I should check... (It also sounds rather like the magical programs detective shows use to plot serial killers' locations)
Note: It should be clear from the problem statement that just because a species is not mentioned at a specific location does not mean that it does not exist there. i.e., a sample at a specific location returning only 'A' - 'Bill and Jeff saw a lemur.' - does not exclude the possibility of 'B' and 'C' also at that location, but not sampled. Just because the text may specifically say that Bill and Jeff saw a lemur, and doesn't mention any other flora or fauna doesn't mean we should assume that they are in a universe devoid of anything but the occasional lemur.
Final Thoughts: Ideally, the analysis method would further:

take into account the coverage of the paths, and not assume that (in
the example above) nothing exists in Mexico or northern Canada, just
because there are no samples taken there. Remember that samples can
only be taken along paths.
take into account edges, in this case coastlines. If A, B, and C are
land animals, it does not make sense that a reconstruction of their
distribution would include water, even if their range surrounds a
lake or something.

Sorry for the long-winded explanation. Any thoughts?

I'm voting to close this because it is not a biological question.

This is not a biological question though these kinds of measurements are performed by ecologists. It is mostly about placing sensors and tracking movements. Even if the question was on-topic it is not clear what you want to ask.

I think the question is valid and voted to keep open, even if the background is purely hypothetical and without any direct connection to real-life biology. The problem of inferring species distributions from species occurrences is a common problem in ecology, and this question is dealing with exactly that.

@terdon - so this should be deleted then?

I don't get why this question is closed. Yes, the background is hypothetical, but the actual problem is embedded within ecology and population biology. And to say that this is "only" dealing with methodology does not make sense, as long as we allow questions on sequencing, PCR, BLAST etc, since these methods/lab techniques aren't "biological questions", only methods to observe biological features or to estimate biol. parameters. Which is the case here as well, but this deals with another level of biol. organization. The Q could be reframed though, to put less emphasis on the fantasy parts

The problem of how to infer species distributions from scattered species occurrences is common in ecology, and there exists a number of methods to construct distribution maps. As a start, you should have a look at Species Distribution Models (SDMs) using regressions models or Maxent, and the paper by Elith et al (2009) is a good starting point and a standard reference. SDMs using maxent is now a common approach, which integrates species occurrences as point data along with environmental layers (e.g. temperature, moisture and topography) to predict species distribution maps, and this can also include absence data or "pseudo-absence" data (randomly sampled data from a region of interest). The maxent software is described and can be downloaded here: http://www.cs.princeton.edu/~schapire/maxent/
A common criticism against distributions produced by Maxent is however that they ignore e.g. species interactions, and they only considers the species occurences and the environmental variables that has been included in the model.
In your "Note", you touch upon the issue of detectability, which is an important issue that has received much attention recently. The problem is largest when you only have presence data, and to have real presence/absence data is preferable. Even if you don't have real absenses (the species has been searched for but not found), an estimate of sampling effort in different areas is still very useful, since this means that you can at least evaluate whether absenses is due to "real" absense or lack of sampling. In your case, the movement paths of characters could be used as a measure of spatial "sampling effort". The main issue with detectability in studies of distribution of species trends is if there is trends or bias in detectability, which means that apparent changes over time or patterns in distribution might be due to differences in detectability and not real differences between areas or over time. This could for instance be the case if observers are more likely to spot a species in one type of habitat (open savannah) then in another type of habitat (closed forest). Useful starting points for issues of detectability are Dorazio (2014) (technical though) and Kery et al (2010).


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Can someone link me to resources on the efficiency of sticky end ligation?
I really would like to know if sticky end ligation could potentially be performed with very high efficiency, and which factors influence that.  However, I can't find any papers on the subject, even though I'm sure they exist.  I was hoping someone would know of some literature.

What exactly do you want to know?

I want to know if there is literature that shows that sticky end ligations occurs without indels and that sticky end ligation can be done with around 80%+ efficiency.

The best resource for troubleshooting ligations I found (and use frequently) is this NEB page.  That is assuming you've already referred to the instructions provided with the enzyme you're using.   In my case it's T4 Ligase, again from NEB.   It's helpful to check the FAQs and the references listed on that page.    Also, you can make use of their Molar Calculator tool on Ligation setting (see more from first link).
Good luck with high efficiency!

To measure the frequency of indels at the ligation site you can use a vector with a unique restriction site in the lacZ gene. With a colorimetric assay you can count the number of white cfu. Perfect ligation in-frame yields blue cfu

Welcome to Bio.SE and thanks for sharing your answer. Please avoid using acronyms and unintelligible jargon. I have a biochemical background (ages ago since last using it admittedly) and frankly I don't understand this answer.

Yes, this is entirely understandable.

Altought it it is could be more digested, I think that the response is not unanderstandable: it refers to the prototypical "blue-white assay" using the LacZ gene, which encodes beta galactosidase and this digests X-gal making bacterial colonies blue.(the word "cfu" stands for colony forming unit)

He is poposing to digest with restriction enzime this gene and check after ligation the % of blue/white colonies (of course after restriction and ligation E.col are transformed).If all ligation process happened without introducing any indel, the gene should be functional and the colonies blue, and the % of blue colonies serves as a readout of efficiency

I guess I want to know what the maximum possible efficiency of religation is.

The enzymatic reaction requires adenosine triphosphate as a co-factor, and Mg++ (as well as a dilute buffer). The substrate is double-stranded fragments of DNA possessing 5' phosphates. Blunt ended DNA fragments can be ligated to each other, and this reaction is enhanced by adding polyethylene glycol. However DNA with complementary overhangs are ligated much more efficiently. The reaction is at least trimolecular (2 DNA ends + 1 protein) so the reaction volume affects the concentration and therefore the rate. So how long do you want to let the reaction proceed?


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Proteins in Milk, Oat , Eggs and Soy
I have read that there are proteins in oat which are similar to those in soy, milk and eggs. I know nothing about biochemistry, and I'm struggling to decipher the info i find..
the closest Ive got to an answer is albumin - which i believe to be a group of proteins, all present in the above?
Can you be intolerant to albumin? or a derivative of?
a simpilar version of the question - what is the name of the protein(s) found in milk/oat/eggs and soy, if any?
the reason for my question, my daughter has a milk/egg/oat (protein) intolerance and I'm just interested to find out if its a particular protein (or group of), or if its an intolerance to random things.
Many thanks!

Say, wouldn't this be better at chemistry.SE?

@MARamezani Cross posting is not frowned upon by the SE devs

Hmm, I've nothing but to say thanks @MarchHo! Still, this question asks about proteins that exist in milk, and egg, and oat, mainly. Let's leave it to see how it plays out. Unless an answerer directly points at intolerance issues that can rise, with referring to something other than what chemistry can answer, this question will be off-topic.

@MARamezani proteins are biomolecules, allergies are a biological mechanism, why would this be better on Chemistry than Biology?

Allergies are often caused by the immune system reacting to a part of a specific protein, therefore it is in fact a specific protein in the food that is causing the allergic reaction to occur.
Milk allergies are caused by casein and whey (Source: Mayo Clinic)
Oat allergies can be caused by avenin (Source: EJCI)
Soy and egg allergies are caused by their respective albumin proteins. Additionally, egg lysozyme can also cause allergy. (Source: Cleveland Clinic, Food Allergy)


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How does a sperm cell die?
What causes an animal sperm cell to die? Does it die somehow from being outside its original environment?
I've studied the Wikipedia page
 on sperm and I see a lot of information on what makes up a sperm cell, but can't quite figure out its lifecycle and exactly how it dies.

Seppuku; for the vast majority of cells that don't make it to the egg, upon realizing it has failed at its one and only task in life, the sperm cell takes its own life and dies in shame.

So most cells require growth factors and survival factors to stay alive in an organism. Cells which stop receiving survival factors, such as sperm, undergo a process of programmed cell death (PCD) called apoptosis. Some cells will also undergo necrosis, or autophagy, among other types of PCD. Lachaud et al. performed a study in 2004 on the contribution of apoptosis and necrosis in ejaculated sperm. They make note in the intro that from other literature that we see some hallmarks of apoptosis like externalized phosphatidylserine, fragmented DNA, etc. despite inactivated nuclei and a small cytoplasm. Their data notes that ejaculate sperm cell death mainly occurs from necrosis, however, because sperm themselves lack the ability to initiate apoptosis. However, in the testes, there's data to note that apoptosis plays a role, and the presence of apoptotic spermatozoa in the ejactulate may be result of the inititation of apoptosis by factors which still inside the body. Apoptosis of spermatozoa in the testes is currently under investigation in male infertility, and damage in cryopreservation.
Just to give you an idea of the difference, necrosis is a much messier outcome derived from physical factors, or those factors external to the cell. Apoptosis is organized, controlled, and modulated by cellular signals.


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Stretching and compressing bones
The Young's modulus of elasticity when a bone is stretched is : 16×109 and when it is compressed, it is 9×109 N/m2. That means, change in length will be more if you compress a bone as compared to stretching it.
What is the biomechanical reason behind this ?

I really don't know anything about this but it doesn't seem surprising that a material would have different tensile and compressive properties. I don't think there necessarily needs to be a biological reason for this difference in bone, though it's likely because of my naivity on the subject.

@canadianer hi ! In my textbook, they have cited different values of Y (tensile and compressive )only for bones ,for other materials - there is only one Y.

Citing your source would help to answer.
In order to test an elastic modulus, you need to apply some non-zero strain. If the strain is infinitesimal, then compression and stretch modulus will be equal. But if it is finite, then there can be a difference due to the structure of the material.
In bone, I believe porosity will provide most of the dissymetry between compression and extension: at small scales, the material can rearrange using the pores without much deformation. Whereas in extension, there has to be some deformation of the osteons.
In other living tissue, the difference can be due to filamentous proteins: if you compress them, they buckle (form loops) without much resistance. If you exert extensive stress, once they are stretched tight they will resist any further extension. (Think of what a piece of string would do, it's very similar)


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Can anti-aging cream work?
I have a friend who told me that anti-aging cream cannot work to reduce wrinkles as it only penetrates x amount of skin layers and can never make a long term effect. Me not knowing much about how penetrative skin actually is, I was wondering if anyone knows if this is true and if anti-aging products are only working like a temporary moisturiser?

Welcome to Bio. Your first sentence "...not based on whether anti-aging products actually work..." does not match with your concluding question: "...if anti-aging products are only working like a temporary moisturiser...". Be specific - what do you want to know? I certain compounds can penetrate deeply enough, or whether anti-aging creme is bogus?

@AliceD Hi, you're right, I wasn't being clear. I've just removed the first line.

You mean anti-aging cosmetic cream in the sense that they remove wrinkles etc.? These cannot work, as they are not allowed to go deep into the skin, otherwise they would be classified as medical drugs. As such they would need licensed by the regulation agencies, undergo extensive testing and so on. These creams are mostly useless beyond moisturizing the top skin layer.

@Chris Yes that's what I mean. When you say "not allowed to go deep into the skin" do you just mean that the cream physically cannot penetrate that far down?

@SaturnsEye Yes, that's what I mean.

@Chris Why can they get away with selling such a product then :/

I have once been told that if the effects of anti-ageing cream were to be real, then one would need a doctor's certificate to buy one. In other words, companies building these products are not allowed to make products that work otherwise nobody would be allowed to buy the products. But it might be totally wrong.

Because their claims are vague enough and it doesn't do any harm.

Since there are different formulations for anti-aging creams, it would be helpful to focus on the specific compound or combination of compounds.
According to a comprehensive literature review done in 2007, certain compounds (Vitamin C, alpha-hydroxy acids, Vitamin A, Vitamin B derivatives, and botanicals) have had varied success in literature demonstrating anti-aging efficacy with Vitamin C and alpha-hydroxy acids being the better candidates.
Vitamin A/retinols have been shown to reduce wrinkles in some studies but no large studies have been conducted to show efficacy, Vitamin C has been shown to be the most effective (statistically significant improvement in texture, wrinkling, etc.) and alpha-hydroxy acids have been shown to increase collagen density, for example among other improvements.  A lot of these and other compounds have had positive or encouraging results replicated in literature, on mostly animal and human cell models so whether they actually have a significant effect on a large group of people needs to be looked at but to assess whether or not they actually "work" depends on what issues of skin damage as a result of aging one is targetting, the severity, the age at "treatment" and whether you're referring to over the counter or prescription-strength.
Huang, C. K. and T. A. Miller (2007). "The truth about over-the-counter topical anti-aging products: a comprehensive review." Aesthet Surg J 27(4): 402-412; quiz 413-405.


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Is there a database of known riboswitches?
I'm looking for sequences and annotations of known riboswitches, but so far I haven't found a resource that actually fulfills my requirements. The best database I found so far is Rfam, which has entries for many riboswitch classes. The biggest drawbacks of Rfam for my case are that it doesn't contain any information about the expression platform, only about the aptamer. I'd like to know if a riboswitch is translational or transcriptional, and where the terminator/Shine-Dalgarno sequences that are regulated by the switch are. Another limitation of Rfam is that I can't easily see which sequences are validated biologically in some way, and which are just predicted.
Is there a database of riboswitches that also contains information about the expression platform?


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What is the difference between myopia and hyperopia?
In myopia the lens is bending the light too much even in the most relaxed state. Thus the image is produced in front of the retina. If the object comes closer  the lens just adjusts a bit less than a healthy eye and the myopic subject is able to see clearly.
Why is the hyperopic eye not able to do that? If the object is far away, could the lens not just bend a bit more to elicit normal vision? So, why is the Myopic eye able to adjust its focus, but the Hyperopic not?

Short answer
Myopic eyes can still focus on nearby images as the lens needs to relax a bit more than in a normally-sighted person. However, objects far away cannot be focused, because in a complete relaxed state (for distant objects), the lens focuses the image in front of the retina. Hyperopic eyes cannot focus on nearby objects as, at a certain close distance, the lens reaches maximum accomodation (maximum roundness) and objects cannot be focused any longer.
Background
Myopia or near-sightedness is a condition of the eye where the light that comes in does not directly focus on the retina but in front of it, causing the image that one sees when looking at a distant object to be out of focus, but in focus when looking at a close object. Often the eye ball is too long, or the cornea has too much curvature (Web MD).
Hyperopia ("over-measured sight") or farsightedness, is a defect of vision caused typically by the eyeball being too short, or a lens that cannot accomodate/become round enough. It causes difficulty focusing on near objects (wikipedia).

Source:Monroe Publishing


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C. elegans are either male or hermaphrodites, but why aren't there any females?
From my understanding C. elegans are mainly hermaphrodites but are occasionally males to increase genetic variation. Why is it that random females aren't born instead to achieve he same goal (genetic diversity)?

The evolution of self-fertile hermaphrodites is thought to be a specialization that occurred several times in the nematoda. For example, most of small, free-living soil nematode species related to C. elegans are male/female. C. briggsae, which last shared a common ancestor 80 myr ago is also male/hermaphrodite, but I believe their ancestor is thought to have been male/female.
At the developmental level, the first germ cells to mature in the somatic gonad develop as sperm and then the Germline switches over to make oocytes.

Re: the origin of spontaneous males in a culture. This occurs due to non-disjunction during meiosis of the XX Germline. About 1/700 times a nullo-X germ cell is randomly generated. Fertilization then results in an X0 embryo, which develops as a male. To get an actual female C. elegans you would need a genetic mutant that interrupts spermatogenesis.

C.elegans makes use of an X0 sex determination system, so there is only one sex chromosome (X), which only allows for two sexes (XX and X0) as 00 is not viable.


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Immediate Early Genes during sleep
In Neuroscience 3rd ed by Bear et al. on page 607, immediate early genes are described as related to changing synaptic strength, yet have decreased expression during sleep. The explanation given is that "learning and memory formation are largely absent in [sleep]." But that seems somewhat counterintuitive as LTP occurs during sleep.
What is really going on here?

memory consolidation is highly prominent during sleep. What do you define by memory formation? The gain of new information?

I think it is indeed important to note the difference between consolidation and formation. Serotonin and epinephrin levels (both important for memory formation) are very low during sleep, so the synaptic pathways being modulated by LTP are probably not very active. Just speculating here, but perhaps this is even a mechanism to focus LTP on pathways from events in the near past by minimizing 'present' pathways of the same form.

As @Sleepses suggests, there are theories that memory consolidation involves the pruning of synapses resulting in the lowering of net synaptic "weight" while asleep in order to improve the signal to noise of new memories and to prevent acquisition saturation.


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Can reptiles digest grains?
As a caretaker of a turtle, I sometimes struggle understanding the logic behind the inclusion of corn, soybean, and wheat meals in reptile food, such ingredients seem truly aberrant from what a reptile would naturally be exposed to. Nevertheless I am aware of the biological and chemical similarity between most organisms, so I wonder whether that will help reptiles, especially omnivores with an eclectic digestive ability, to digest these compounds.
I'm looking for legitimate studies on reptile digestibility; anecdotal experience or advice is supplementary if present.

This is not a yes / no question. Many tortoise eat plants (veggies and fruits) while some turtles eat fish too. Snakes are basically predators and do not dwell on plants neither do most of the lizards. I think if a reptile is capable of digesting plant food in general, then it should be able to digest preprocessed grains as well.
Edit:  As for whole intact grains I'm unsure, as canadianer pointed out in comments section, intact grains are hard(er) to digest. /end of edit/
I found this article where scientist fed alligators with a mixed diet in various setup. The diet included corn too and the 'gators responded well in terms that they could use carbon-hydrates.

Recently, we (3) have demonstrated that hatchling alligators benefit from and apparently do utilize some dietary carbohydrate.

Don't make the assumption that being able to digest some plant material means that the organism can digest all plant material. Whole grain is notoriously hard to digest for many animals.

Yes that is true, but the OP asked about wheat in reptile food which I assume is preprocessed and as such can be digested. Nevertheless you're absolutely right in your comment, I did not express exactly what I meant to write / say. My bad, I'll edit my answer.

Ah yes, you make a good point. The original question did in fact specify wheat meal, meaning it has been processed.


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Is the amount of blood that flows through every vein and artery per minute really a constant?
I was listening lectures from Mark Saltzman via Open Yale Courses. Now, if I did not understand him wrong, he said that the amount of blood that travels through every vein and artery in our bodies per minute is a constant. Five liters of blood go through the aorta every minute, and since the blood circulation is a closed system, also every other vein/artery must pass that amount of blood per minute. Is this true? How could I (mathematically) show that it is true?

I found the video you have seen at https://youtu.be/It_cV56Dxtk and watching from about 40:00 I can not recognize what you are stating here, more on the contrary though. I suspect you misunderstood him, or can you refer to an exact statement?

I think he is referring to the Bernoulli's principle which states that the sum of kinetic energy, potential energy and the internal energy due to pressure, is constant.

I think the question is not whether the blood flux is constant in time, but rather in space: if 5L/min is the flux through aorta (in given physiological conditions), then at the same moment 5L/min will cross the capillaries. This is volume conservation, for a closed system filled with an incompressible fluid, see this sketch:

If 5L are pushed through the main pipe, the same volume needs to be pushed through the system downstream of it.
Then comes the fact that the system is not perfeclty closed, and some water (and solutes) will "leak" in and out, as @inf3rno points, so this is only approximatively true. Another limitation is that vessel walls are actually elastic, so a change in vessel radius does occur during blood flow. However I believe it is a fair approximation.

It is ofc. not true, because it is not a closed system. The kidneys filter blood and excrete water and other compounds (which are reabsorbed or go to urine), the sweat glands remove water and salts. By drinking daily 2 liters (the total blood volume is about 5 liters) of fresh water and salts are absorbed from the intestines to the circulation, by eating just the opposite happens. Every cell has aquaporins which are responsible for water transport, so they can dilute the blood for a while, if necessary. The spleen can withhold red blood cells (before injury) which reduces the blood volume. The white blood cells can leave the circulation. By inflammation water leaves the vessels because of increased permeability, and so on...

Nope. All blood flows in the body can change at any time(more or less).
If the heart rate and blood pressure, etc, is constant the amount of blood that travels through the aorta is constant, yes. But there is far more capacity in the arterial and venous systems for the actual amount of blood flow there normally is. Veins and arteries contract and expand to route blood flow to different parts of the body, so the amount of blood flowing through any particular artery can change without changing the aortic flow.
A good example of this: Vasomotion. It happens all the time in your hands (sometimes it's even visible as patches of red/white skin. On my hands they're a little smaller than the head of a thumbtack) on the order of minutes. fMRI is a neat technology based around watching brain blood vessel changes in flow as a proxy for activity.
All the flows through all your arteries don't even have to sum to the aortic flow, due to compliance(a fluid dynamics term. essentially, the aorta or other arteries/veins can 'inflate' so more blood is flowing in than is flowing out. Then later they 'deflate' and more blood flows out than in. Arteries tend to be more compliant because they have to be springier to deal with heartbeat). There are also osmotic effects where fluid leaves the arteries and becomes lymph, which then later drains back into veins. It's not a huge effect but it's there. If you measure total blood flow through the aorta and then total blood flow through all the capillaries, there will be less total blood flowing through the capillaries. Not much less( 10% at the most) depending on blood salt and blood vessel position and whether you count the kidneys, etcetera etcetera.
So: the amount of blood that passes through a given artery given the aortic blood flow is not fixed. The amount of blood that passes through all arteries given the aortic blood flow is much closer to fixed, but even that can be different(even if you're not bleeding). And if you were asking if the amount of blood that flows through the aorta is constant, that's absolutely not true. That can vary through the heart rate, the contractility of the heart, the venous return pressure, the overall blood pressure, and a bunch of other things that very slightly affect flow rates.

The amount of blood flow is not constant in general.  As you exert yourself, your heart rate and therefore blood flow increases.  Furthermore, individual vessels dilate or constrict to increase or decrease flow by modulating their resistance to flow.
Your circulatory system is closed however, so all of the blood leaving the heart must eventually come back to it.


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Are both (partial) copies of DNA transcribed in S and G2 phases of cell cycle?
For a little less than half the cell cycle, a significant number of genes are represented twice (just before dividing).  Does the cell differentiate between these DNA in any way or are transcription rates limited by the amount of polymerase anyway?

I can't unequivocally say, at least without further literature review, that both sister chromatids are transcribed equally everywhere, especially since the cell does have mechanisms to differentiate between the old and new DNA strands (such as methylation state). It would be conceivable to expect, however, that the same regulatory factors that were present before replication have the same effect on newly synthesized DNA as they did on the old. Here are some electron micrographs showing transcription from both chromatids at some locus.
McKnight SL, Miller, OL Jr. 1979. Post-replicative nonribosomal transcription units in D. melanogaster embryos. Cell 17:551-563
Here you can see RNA (solid line in schematic, b) of increasing length branching from both sister chromatids (dotted line):

A similar image but this time showing the replication fork (arrow):

This image shows RNA free gaps (arrows) in a single transcription unit, which are symmetrical between the two chromatids:

From which they conclude:

The observation that fiber-free gaps often occur at symmetrical positions on sister chromatid transcription units suggests that the two identical transcription units respond similarly to the mechanisms that control RNA polymerase chain initiation. These cannot now be specified, but could include the local supply of RNA polymerase or other controlling molecules.


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What level of cellular radiation is harmful for humans?
What level of radiation at the frequencies used by the cellular network(1-2 Ghz) is harmful for human health?

This cellular network means mobile phone? Is it electromagnetic radiation?

Yes, I mean it, mobile phone network, like gsm, CDMA, LTE and all...

Addition to the previous answer

First you need to understand how radiation causes cellular damage.
EM waves like γ-rays, X-rays and high-energy UV (in certain molecules even visible light) can knock out the electrons from the atom and create an ion and free radicals by breaking chemical bonds. This term — ionizing radiation is not used for low energy UV and visible light because these waves can only ionize a few types of molecules and are not ionizing in general. Moreover X-rays and γ-rays can dislodge even inner electrons which UV and visible light cannot (High energy γ-rays can also lead to the nuclear reaction of pair production). These ions that are formed are reactive and can attack other molecules (DNA/proteins etc) around them. DNA absorbs UV and this can cause DNA lesions such as dimerization of adjacent pyrimidines (via a cyclobutane bridge). Both reactive ions and pyrimidine dimers can cause cancer; the former is most frequent in melanomas which happen because of solar UV. Since UV cannot penetrate very deep, they affect mostly the skin (See here).
IR, with energy lower than visible light does not have sufficient energy to cause electronic transitions. But it can cause vibrational transitions such as bond stretching and bending. Microwaves have even lower energy and can only cause molecular rotation. Both IR and microwaves because of their property to make molecules move, generate heat.
Continuous usage of mobile phones can cause discomfort but only because of their heating effect. They can by no means cause cancer and even though mobile phone radiation is classified as a potential carcinogen (IARC Group 2B) perhaps because of the pressing allegations of certain factions, they do not have sufficient energy to cause DNA damage.
If you ask me if mobile phone radiation can be harmful to human health, then I would say yes, they can be potentially harmful with prolonged usage but in no way as harmful as to be causing cancer. I would say that it is as harmful as wine :P

One thing to note is that close proximity to cell tower microwave transmitters can and will give you radiation burns, due to the wider range of harmonics. The GSM band runs at 1800MHz, from which the first subharmonic sits inside a range (~915MHz) that is known to excite water molecules in the same way that an industrial microwave does.

Afaik. radio waves don't have enough energy to cause anything similar to the damage ionizing radiation (gamma rays) does.
What it can cause is probably heat damage similar to microwave ovens.

According to the United States Food and Drug Administration's Center for Devices and Radiological Health, a U.S. Federal Standard limits the amount of microwaves that can leak from an oven throughout its lifetime to 5 milliwatts of microwave radiation per square centimeter at approximately 5 cm (2 in) from the surface of the oven.[52] This is far below the exposure level currently considered to be harmful to human health.[53]

http://en.wikipedia.org/wiki/Microwave_oven
Advanced Measurements of Microwave Oven Leakage - http://www.arpansa.gov.au/pubs/emr/microwave.pdf

According to the article referenced by wikipedia a 35 W/kg SAR level (caused by a 30 mW/cm2 leakage) can raise the tissue temperature with 1.5°C, which probably does not any serious damage. I guess from this you can count the radiation intensities - you are interested in - to any frequencies.


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What is the relationship between radiation and evolution?
There is always a certain amount of background radiation present, for example due to ionizing radiation from the sun and other stars. Also certain materials like granite may emit relatively large amounts of radiation.
Ionizing radiation may cause mutations in the DNA (Gevertz et al, PNAS 1985). Mutations, in turn, may lead to altered phenotypes. Altered phenotypes and survival of the fittest are key to evolution and formation of new species.
What is the (relative) contribution of background radiation on the formation of new species?. In other words, is background radiation a critical component in evolution and would the course of evolution have changed substantially when there would be no such background radiation?

Welcome to bio.SE! Sorry for the skepticism, but... this question may be too broad. Spontaneous mutations (due to e.g. radiation) may indeed lead to beneficial traits and hence formation of new successful species. However, evolutionary biology is a big discipline and radiation contains many potential candidate particles. Are you talking background radiation, cell phones, UV light, nukes...

Sorry so unclear.  I'm curious about natural radiation  ie elements, stars, etc., and if it is essential to biology in the broadest sense?  Would the lack of radiation have a negative/positive impact on evolution?

Thanks for explaining. I took a bash at re-wording your question and voted to re-open it. Feel free to roll back or change when it does not reflect your initial question. However, it its previous form the question is not suitable for Biology.SE as it needed editing.

Welcome. I suppose one could come up with estimates of how much "background radiation" influence the mutation rate. The link between mutation rate and speciation is not an easy subject though. I vote to re-open but I think it is good to accept answers to "how much different would the mutation rate be if there were to have no "background radiation"?".

This might be an interesting start to an answer.

I realize that this is broad, but I think it is important for people to understand, and I would like to officially answer this as I find that I often get questions that seem to come from the largely incorrect understanding that evolutionary change is driven by external insults like radiation rather than damage caused by replication errors.

This is more on the historical side, but concerns about the effects of radiation were major drivers in the development of evolutionary genetics in the mid-twentieth century, particularly via the work of H. J. Muller. Muller and Theodosius Dobzhansky had very different views of the role of standing genetic variation because they studied very different types of variation: radiation-induced mutation in the former case and chromosomal inversions in the latter.

Thank you for the edit.  Your edit is exactly the question I wanted answered.  Do I change the question now?

Is background radiation a critical component of evolution? No, it most certainly is not.
The DNA replication and DNA repair mechanisms aren't perfect and errors happen without any external cause or catalyst. You could say mutations happen on their own. There are mutagens that also cause DNA damage or mutations, but they're merely affecting the DNA replication in a negative way, causing it to err more often.
So, the effect of background radiation isn't the key here, the key is that the biological processes of DNA replication and repair are not infallible, although radiation does increase the error rate (the rate of mutation) just like many other mutagens do.

A few points for looking deeper into this question:

Radiation is not the only extrinsic source of mutations. One that has to be necessarily mentioned alongside the radiation is the exposure to chemicals - via smoking, drinking and food consumed. These are not necessarily industrial chemicals - e.g., many things found in soil will find their way to water and to the organisms.
For multicellular organisms one has to distinguish somatic and germline mutations. The former are relevant for the evolution of cancer tumors (which can be viewed as generations of cells), but this is not what we usually mean by the evolution, since this does not affect the offspring of the organism as a whole. In other words, to affect the evolution the mutations must happen in the egg/sperm cells.
Now we are down to the question raised by @DanHorvat: whether the rates of errors during replication are higher than those due to radiation. The former vary wildely among the organisms (e.g., $10^{-4}$ per nucleotide per generation in HIV, but $10^{-8}$ or less for human). The effects of radiation and chemicals may vary depending on the surrounding environment, time period in question, etc.

Thus, I would say that there is no a general answer to this question, although one may certainly compare numbers for a specific organism.


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Comparing gene expression levels between control and disease at different time points
I have a data set with expression levels of a list of genes, measured in replicate at two different time points between two groups; a control group and a disease group.
I want to identify the changes in expression between the two groups, however I'm having some trouble on formulating how best to do this. For example, if I have $[C_0]$ and $[C_1]$ as the control group measured at $t=0$ and $t=1$ respectively, and $[D_0]$ and $[D_1]$ as the disease group, I had tried to do:
$$\frac{([D_1] - [D_0]) - ([C_1] - [C_0])}{[C_1] - [C_0]}$$
I feel like a fold change would be appropriate, however it doesn't seem to make any sense logically for the genes where $[C_0] = [C_1]$ or $[D_0] = [D_1]$.
Could anyone suggest an appropriate ratio or measurement? This is straightforward enough when it's simply comparing between C and D, (e.g. you just find $\frac{D}{C}$), however I'm not sure how to treat the different time points.

The gene expression profile may change at different time points between the two groups; you should decide what you actually want to measure. If you want to see if the diseased group is different from the control then you should compare them at every time point. For most situations you would need to compare just their steady state behaviour.
Imagine a diseased individual who shows some physiological differences at certain developmental stages compared to the control but in the end turns out to be perfectly normal. So what matters in most cases is the steady state and not the transients.
However if you are interested in the change in expression then you should compare ([D1] - [D0]) with ([C1] - [C0]). This will tell you if the dynamics of the diseased and the control samples are similar or not.
There are issues with fold changes. Though they are decent measures, you cannot really apply a t-test with fold changes (normalizing to 1 is a different thing).
You can do another t-test between [C1] and [C0] (similarly for D). This would tell you if the diseased or control population changes its expression at time t=1 or not.
AFAIK you cannot compare the dynamics and the values simulatenously. What you should test depends on what you are interested in.


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Barr body Giemsa staining
Not all the female cheek cells show Barr Bodies when stained with Giemsa stain? Only 30 to 40% female cells show Barr Bodies. Why?
Our Experiment:
We washed mouth twice with listerine to reduce bacteria count, then scraped cheek cells with moistened ear bud then smeared that on clean glass slide. then air drying the smear we fixated it with methanol, then after air drying we applied thin layer of giemsa stain and after 15 minutes drained and washed off extra stain. the cells were stained and we could see the nucleus but nobody could see barr bodies. it was an experiment in our undergraduate lab and nobody could identify barr bodies in female cells. very few samples had barr bodies.

Please describe how you did the experiment and attach a picture

we washed mouth twice with listerine to reduce bacteria count, then scraped cheek cells with moistened ear bud then smeared that on clean glass slide. then air drying the smear we fixated it with methanol, then after air drying we applied thin layer of giemsa stain and after 15 minutes drained and washed off extra stain. the cells were stained and we could see the nucleus but nobody could see barr bodies. it was an experiment in our undergraduate lab and nobody could identify barr bodies in female cells. very few samples had barr bodies. i will attach pictures soon

I think the issue here is the image is a 2D representation of a 3D object. It may well happen that the Barr bodies are below the Geimsa stained nucleus.
This is the same reason we don't see peripheral nuclei in all muscle fascicles in a muscle cross section.

Rinsing mouth with tap water and than distilled water is enough, listrene is not needed, use 95 % ethanol instead of methanol, repeat experiment with  Wright's stain and carbol fuchsin. Only 40% females show barr bodies.

This is an interesting experiment description but it doesn't answer the question why Barr bodies are only found in 30-40% of the cells.


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What are the positive effects of wrongful antibiotic use on a viral infection?
I categorically accept that bacteria differ from viruses; so antibiotics DON'T help in viral infections. I also read this and this; so no need to explain this. I've read about the negative effects (eg exacerbation of antibiotic resistance); I ask only about the positive effects here, and NOT for reasons to exploit antibiotics for infections not due bacteria.
Yet I myself have witnessed that some people with viral infections feel better after wrongly taking antibiotics? and so asked about this first on Cognitive Sciences SE.
Initially, I suspected only some placebo effect, but this enlightened me on the side benefits of antibiotic consumption for a viral infection and motivated this question, now that my original question on psychology has revealed the relevance of biology.

There are indeed antibiotics which have immunomodulatory side-effects, these are mostly from the class of macrolide antibiotics (erythromycin, clarithromycin, roxithromycin, azithromycin) and to some degree from the tetracyclines. Beta-lactam antibiotics (as Penicillin or Ampicillin) have not been shown to be immunomodulatory, but they are among the most commonly used. See reference 1 for more details.
The biggest effect has been shown on pulmonary diseases such as cystic fibrosis or diffuse panbrochiolitis (see reference 2).
Although the exact mechanism of action is not known, Macrolides are know to downregulate the inflammatory cascade and that the reduce the strong cytokine expression of some viral infections. However, these regulatory effects are relatively weak if you compare them to the anti-inflammatory properties of corticosteroids. So the question here is if the advantages are really sufficient compared to the problems, which an unnecessary use of antibiotics may cause. See reference 3 and the references in the paper for more details here.
Antibiotics may be useful to fight bacterial secondary or superinfections which accompany a virus infection.
References:

Immunomodulatory Properties of Antibiotics
Macrolide activities beyond their antimicrobial effects: macrolides
in diffuse panbronchiolitis and cystic fibrosis
Macrolide Therapy in Respiratory Viral Infections


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Are Whales More Intelligent Than Humans?
Are Whales smarter than Humans?
Their brain size leads me to think so.

possible duplication of http://skeptics.stackexchange.com/questions/2948/does-brain-mass-have-any-correlation-to-intelligence

related: Is life expectancy linked to intelligence in animals?

I think this is impossible to answer without clearly defining what "smart" means, in some way that is valid across species.  I would bet that whales do poorly on standardized IQ tests for example ;)

I'll say this: If one were presented with both brains and asked which one belonged to a god-like being, seems like 9 out of 10 people would say the one on the left. I find arguments like, "What do we mean by intelligence?" boring. We know: Memory, reasoning ability, etc. If some animals begin to approach human intelligence, why must whales and every other candidate intelligence necessarily squeeze between apes and men?

The "wiring" of the brain is more important than the actual size. If only size would matter that basically humans would be rather unintelligent beings ( many many animals have larger head and brain than us). Intelligence is more related to the complexity of the brain (number and size of different brain components) and the number of connections between neurons. We humans are intelligent because we have high complexity compared to our brain size, our brain has more grooves therefore higher surface than a whale brain. So even though whales are quite smart they're not as smart as us.
EDIT: After getting a few comments I felt I need to clarify my answer, so here it comes: as pointed out by user137 humans have much higher brain-to-body size ration than whales and this is very important. What I was trying to explain (yet failed for the first time it seems), that mere physical size / volume is not that important. The level of development and complexity is that matters the most. Many parts of the human brain is found in lower order animals as shown in the image below:  (taken from http://en.wikipedia.org/wiki/Brain
The surface to volume ratio matters because the higher ratio implies a more complex brain structure. So while whales have a higher surface in absolute value (approx 2-3 times) yet their brain is larger by approx 5-6 times ( lots of comparison data here), thus we have higher surface/volume ratio (i left the ratio part out on my original answer). In the accepted answer on the question linked by Bez it is said that more grey matter in frontal lobe correlates with IQ. Now since grey matter is made of neuron bodies and (fewer)axons, this is quite straightfoward --> more neurons = more connections = higher complexity. But all that comparison was made between humans. So brain size differences between different individuals of the same species may contribute to individual qualities. Comparing mere physical brain sizes of different species is not straightforward because of different brain development levels and brain structure.

I might also be useful to check the wiki pages about brain and brain size
http://en.wikipedia.org/wiki/Brain
http://en.wikipedia.org/wiki/Brain_size

It's useful to think about brain size relative to body size. Whales and elephants have much larger brains than humans, but have even larger bodies to go with them. The large bodies probably cost more "brainpower" because of the extra sensory input and simply having more body to control.

I think being able for fine movement requires far more brain power. Basically all land mammals have the basic senses more or less, so just being big does not imply more sensory input. By this logic tall people would be smarter because bigger body--> more sensory input --> more brainpower.

This section on brain and body size is probably a little clearer than my previous comment. Sperm whales have large brains, about 8kg, but have bodies of about 57,000kg. Humans have brains of about 1.5kg and bodies about 70kg. The brain to body ratio for humans is much larger than it is for whales or elephants. While this does not directly correlate into intelligence, it is at least a useful measurement across species. Trying to apply it within a species ( tall vs short humans ) is not appropriate.

Ahh, okay I misunderstood.

Does our brain have a larger surface- the picture doesn't seem to support this. Further, in your answer you first say size doesn't matter and only complexity does - and then you conclude size does matter because surface matters?

plus the answers in the linked question by @Bez do not support your claims

I left a bunch of reply comments earlier, then decided to edit my answer and delete my comments. I hope this clarifies what I'm trying to say.

In any comparison of intelligence, the most important question is how are we going to define intelligence? The typical inclination is: intelligence is what is required to do the things that we admire as difficult intellectual feats. More generally, intelligence is what it takes to do things that humans do. Making comparisons between species is inherently difficult & limited by our species centered narcissism.
An orca has a brain 5-7 times larger than a human brain. The majority of that brain mass is in the frontal lobes- the part of the brain associated with higher cognitive processes (relatively little is involved with motor processes).
Brains require a lot of energy. Nature doesn't like waste. Whales would not have evolved such huge brains unless they were beneficial (& being used)
Consider the image associated with this link:
How your brain sees your body: Meet the cortical homunculus
https://io9.gizmodo.com/how-your-brain-sees-your-body-meet-the-cortical-homunc-5670064
Much of our brain is devoted to hands.
Whales don't need to use their immense brain power on hands (that they don't possess). Therefore they're using it for something else. I wouldn't be surprised if that something else is more complicated ( perhaps more intelligent) than we can imagine.

Welcome to Biology.SE! While you have an interesting perspective, your answer lacks supporting references for most of the claims you make. Without those references this is indistinguishable from opinion and is unlikely to be well received. ——— Please take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site and then edit your answer accordingly. Thanks!


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Help identifying what this is in Crayfish gills?
this is my first time posting here. I was in my Zoology lab doing a dissection on a Crayfish when I noticed these hairlike structures within the gills. They were very "snappy" and fine, and would break off if I pulled hard enough. I put some on a wet mount under a dissecting microscope, but my Lab prof and the parasitologist could not identify it. We put it under a compound microscope and thought maybe it is an animal but we couldn't definitively say it had no cell well. My profs thought it was an animal, with setae, but I would really like to know what it is
Edit here are the images:

Were the hair things coming off the central tubes paired? It almost looks like they are, but I'm not sure.

I had to concede on this one after a lengthy query. If we had a look at either end of whatever it is it'd make identification a tad easier.

My best guess would be Trematoda which is a fluke worm that infects mollusk. I would think this is the larval stage of cercaria which is free swimming and develops in the mollusk and then moves on to infect others.
Here are some different images of a cercaria:

In this YouTube video you will see what is known as a "Rat King" which is just a ball essential of Trematoda. Here is a screenshot

It would be nice that the images from the question have some scale. The first picture of a trematode cercariae has a view of 0.267 mm across according to the source. From the average size of trematode cercaria, perhaps it's a little too small compared to the 'hair' structure on the (visible fine structures of) crayfish gills?

@SYK If you click edit, you will find the sources to the images. There was no scale provided. I just made do with what was available. The size of the rat king is appears to be an equivalent size.

@dustin OK, not that your image is not cool. I was just looking at the seemingly identical image at http://www.networlddirectory.com/blogs/permalinks/7-2006/parasites-form-the-thread-of-food-webs.html

I know this post received a bounty 4 years ago, but I really am not at all convinced this is a correct answer...

@theforestecologist if you read the first sentence I wrote, I state it is a guess. With the available information giving, that was my best guess.

You asked this question 4 years ago, but i randomly noticed this only now. Whell, that not parasite, not Rat King or someting. This is "setobranchies" - crayfish's cleaning organ. They struggle when crayfish move his legs, and cleaning gills from dirt and sand. I hope this information may be usefull for you, even so many years later

Welcome to Biology.SE! Your answer is plausible, but you are much more likely to get a positive response if you explain why your identification is correct. Specifically, please [edit] your answer to add discussion of key features that led you to this conclusion and supporting references or at least validated images. Without this your answer is indistinguishable from opinion. ——— You may also wish to take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site. Thank you!


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What are the lower and upper hearing limits of the human ear?
I am looking for the loudness limits, expressed in decibels, for the human ear.
Google and Wikipedia is only giving me the frequency limit that the human ear can receive, but I cannot find mention about the decibel limits.
Related question on acoustic frequency: why-do-humans-hear-better-between-2khz-and-5khz

Decibel limit for what? The lowest discernible sound? That depends on frequency, age of listener, etc. The level at which damage occurs? What kind of damage? The level at which deafness occurs? How quickly are you talking about? Seconds? Minutes? Instantaneously? Basically, please [edit] your question (don't respond in the comments) and clarify what exactly you're looking for. Otherwise, this question may be closed as "Too Broad" or "Unclear What You're Asking".

i am not asking in frequency limit, i want answer in decibels, db.

I edited your question to improve its clarity

ok why you removed word decibel in the question.

I didn't, just in the title as loudness is pretty much by definition expressed in dB. Also - write @AliceD before you ask for clarification to ping me

sorry, thank you, for making my question more clear

Short answer
Hearing threshold is 0 dB SPL at 1 kHz, and pain threshold is around 125 dB SPL at that frequency.
Background
Loudness thresholds depend on acoustic frequency (pitch), as depicted in the following figure:

Loudness contours in human. Source: Stanford Uni
When expressed in dB sound pressure level (dB SPL) the threshold of pain is approximately 125 dB SPL. The lower bound peaks at a hearing threshold of about -5 dB SPL at 4 kHz (maximum sensitivity). Outside that frequency, hearing sensitivity declines (and threshold hence increases).
Note that dB SPL references to a sound pressure of 20 µPa = 2 × 10−5 Pa. This sound pressure corresponds to the hearing threshold at 1 kHz and is hence defined as 0 dB SPL. (Stanford Uni).

Further reading
Why do humans hear better between 2kHz and 5 kHz

but you haven't mentioned any number between this and this is the decibel limit for human ear.

I did, and it's in the graph. Now in the short answer as well.

@KlaytonThomas - since you are new here - if the answer is to your liking and sufficient please accept it by clicking the check button on the left and/or upvote it. If it is not what you were after, just let us know :)

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


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How animals know which is carnivorous and herbivorous?
Deer ran away from tiger or cheetah, but not from giraffe or zebra.
where did deer learn this?
How animals know which is carnivorous and herbivorous?

Tinbergen's famous goose/hawk paradigm and subsequent work would be a good place to start.

They probably don't know and probably don't need to. They tend to run away from potential danger and predators in the same evolution environment because those who don't run away will have fewer offsprings that exhibit similar behaviors.
If an animal suddenly sees a predator that his ancestor has never seen before, then it may not run away from it, to its own detriment. Dodo Bird thought humans were harmless.

It is definitely not that easy and the answer will depend on the species of interest. There is probably an important part of culture. There is also probably various reaction depending on the smell or the color of the animal  that is perceived that might be adaptive. One cannot make a general case saying "they just run away from anything".

I agree, deer just do what deer do when they see a predator. To imply that they know or are conscious of their actions carries a huge burden of proof. In fact they are almost certainly acting unconsciously in order for the reaction to be fast enough.  It sounds silly but that's what evolution and natural selection pressures do. There probably were many kinds of deer that didn't run from predators, and they died at various times in history, and we don't call then deer now.

@ebrohman: Yet this "run away" reflex is not what you observe in nature.  If you come upon a deer while out hiking, as I often do, it will often stand and look at you, apparently evaluating whether or not you're a threat.  If you live within a game refuge, as friends of mine do, they don't even bother to run from humans, as they usually do where hunting is allowed.  So it seems that, at least with larger mammals, there is a good degree of learning in threat recognition.

@jamesqf humans aren't the deer's natural predator so I don't think it's surprising that some deer do not flee when they see a human. Humans may hunt deer now but that's more recent in terms of evolutionary time scales. The predators that deer evolved alongside of run on all fours, or fly (large birds of prey).

In zoology, the word "Naive" means an animal which is suddenly put into a terrain/ecosphere which its evolution has not prepared it for, or when a new animal arrives which can destroy the terrain/ecosphere. For example, if an island has no predators, then the animals on it would have no sense of fear and thus not be prepared if a predator suddenly comes along. That is how the dodo became extinct - because it was not scared of humans. Source

Higher predators usually have the eyes in front of their head to see stereoscopically and judge distance visually. Prey usually has eyes on the side of the head to visually analyze the most possible area, giving up stereoscopic distance information.
This puts human in the predator, carnivorous category. That being said, I am not sure that it is used by animals to judge unknown species.

Hello! Might be better suited as a comment. As you said ("I am not sure that it is used by animals to judge unknown species"), you don't actually answer the question.


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How did birds become so intelligent?
I have seen a Discovery Channel video of a bird throwing stones in a pot to raise the water level so it is able to reach and drink it.
A similar experiment in this paper from Current Biology shows the same phenomenon under controlled conditions, and is documented in this video.
This clearly illustrates how intelligent these animals are may well be more intelligent than many mammals. For example, the regular domestic dog will definitely not push stones in a bucket of water to quench his thirst.
How did crows, and perhaps birds in general, became so intelligent, and even more intelligent than many mammalian species?

Birds are animals and, as far as I know, there is no basis for your claim that they are the most intelligent.

@KlaytonThomas - I edited this question as well, but you should try to find an image, a link to a movie fragment or other source illustrating the claims you make on crows increasing water levels

Using a movie scene as an example is not an accurate form of asking a question. However, I have indeed seen documentaries detailing how intelligent crows are. I suggest you youtube it and find a suitable documentary clip.

@TheLastWord - I agree movie clips are not the best thing, but in this case I doubt there are scientific articles that support the claim

some one added "movie fragments" in my question not i, actually i seen this video in discovery channel.

I edited your question as I was expecting it to be put on hold. I voted to re-open as I like the question, but I am afraid it may be too vaguely defined. Give it a thought how to improve it and make it more approachable for folks here.

You should really define what you mean by intelligent... for instance a dog can bring you the newspaper, which a bird can't do.

The basic raise-the-water-level experiment described in this paper has been subsequently repeated and extended with a number of corvid species and also with human children; it is known as the Aesop's Fable Paradigm.

@Corvus Yet another apropos name :P