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Why is menstruation in wild animals not a disadvantage to organismal survival?
When I watch wilderness specials for more than a few minutes, I notice a familiar pattern: predators are depicted as being alerted by the scent of blood. Wounded animals seem to make the best prey and predators seem to have a heightened awareness for the smell of blood.
It would seem that it would then be a disadvantage to evolutionary survival for female organisms to menstruate. How do females of a species not attract predators to the signal of menstrual blood?
Do female organisms in the wild actually menstruate? If so, is there a difference in the composition of menses that does not alert predators? How would this not at the very least give predators an idea of the general vicinity of the female?
If wild animals excrete their menses, do they have ways in which they are able to mask the evidence of its release or are they somehow internalizing the tissue so that they are not released?
If female organisms in the wild do menstruate, then why is this not a survival disadvantage?

Most mammals reabsorb the endometrium (estrous). I believe only primates actually menstruate.

In addition to the rarity of menstruation in animals, it's worth noting that menses are only about 50% actual blood, the remainder being tissue and mucus. The smell is probably distinct and unlikely to be confused with wound blood. A menstruating female is also neither pregnant nor nursing very small offspring, and is therefore more resistant to predators. Why follow a scent signal to a prey species that's both healthy and adult? That's the opposite of what you want to do as a predator.

Thanks to the other answer for pointing me in the right direction with some references. It seems that two biologists in the early 1990s had a back-and-forth over this topic in The Quarterly Review of Biology.1,2
A statement of the problem:

The function of menstruation is a central enigma of mammalian, and especially primate, reproductive physiology. Each cycle the uterus builds a glandular epithelium with a high secretory capacity and an elaborate microvasculature, only to reabsorb or void it with the menses if implantation does not oc-cur. Why does the endometrium not maintain a steady state of readiness for implantation by the blastocyst? What is the selective advantage of cyclical regeneration and regression?1

One hypothesis2
In  1993, Margie Profet hypothesized that menstruation is primarily advantageous as a defense against pathogens transported by sperm. During mammalian insemination, she stated, bacteria from the male and female genitalia cling to sperm tails and are transported to the uterus. Menstruation, triggered by the abrupt constriction (causing necrosis of endometrial lining) followed by dilation (causing shedding of said necrotic tissue), forces loose not only the endometrial lining but sperm-borne pathogens contained therein. In addition to shedding the uterine tissue harboring these bacteria, menstruation delivers immune cells to the uterine cavity, triggered by the mechanical pressure exerted via the shedding of endometrial lining.
In this 50 page (!) article, Profet also points out that other mammals with covert menstruation take advantage of some of these same benefits, as the immunological stimulation includes phagocytosis of pathogens by cells that may be expelled in cervical/vaginal mucous. Further, proestrous  bleeding (i.e. that preceding ovulation, 180 degrees off from the human cycle), which occurs in some mammals (domestic dog, coyote, etc), seems to serve a similar function.

If not eliminated prior to estrus, these tenacious pathogens might otherwise attach to incoming sperm during estrus and ascend the oviducts.

As to why humans and other primates are subject to overt bleeding in contrast to other mammals, she lays out a theoretical argument that selection pressure to menstruate should increase with decreasing per-cycle “fecundability” (the probability of pregnancy) because copulation not followed by bleeding risks infection. In contrast to, e.g., mice (98% fecundability), humans have some of the lowest fecundability rates, primarily due to “concealed” ovulation which de-couples copulation and ovulation. (Contrast this to most mammals whose females have a defined estrous period during which they are receptive to male sexual advances; the data for the existence of such a period in humans are controversial, and sexual behavior is driven primarily by “higher” social, environmental, and cognitive cues.)
A different view1
In response/objection to this paper, Beverly Strassman in the same journal published an article outlining an alternative hypothesis about the potential adaptive value of menstruation. She proposed a hypothesis based on energy conservation:

[T]he uterine endometrium is shed/resorbed whenever implantation fails because cyclical regression and renewal is energetically less costly than maintaining the endometrium in the metabolically active state required for implantation.

Her research determined that, in its regressed state (i.e. s/p endometrial shedding), oxygen consumption in the endometrial tissue is markedly declined, nearly sevenfold. Although this would seem to be a trivial component of whole-body metabolism, she argues otherwise:

Metabolic rate is at least 7% lower, on average, during the follicular phase than during the luteal phase in women, which signifies an estimated energy savings of 53 MJ over four cycles, or nearly six days worth of food.

Her argument shares with Profer’s the implication that mammals with lower fecundability are more likely to menstruate. In those with high probability of pregnancy at every cycle, the energetic benefits of ridding the body of the need to support endometrial lining (relevant only in the absence of pregnancy), are decreased. Her hypothesis also predicts the larger volume of menstrual shedding in humans and chimps in contrast to other mammals related to the increased uterine size relative to the female body (a ratio that is largely determined by the especially large head of the human fetus).
Conclusion
As noted in the comments, only primates have overt menstrual bleeding. The adaptive benefits have been variously explained, and it is probable that there is more than one operative explanatory model. Whatever the small decrement in survivalship incurred by the intermittent and uncontrolled depositing of blood in the wild, it is apparently outweighed in these species by the processes described above.

References and Notes

1. Strassmann, Beverly I.  The Evolution of Endometrial Cycles and Menstruation The Quarterly Review of Biology, June 1996; Vol. 71, No. 2 pp 181-220.

2. Profet, Margie. Menstruation as a Defense Against Pathogens Transported by Sperm. The Quarterly Review of Biology, Sept 1993; Vol. 68, No. 3  pp. 335-386.

Note: Your comparison to urine and feces is an interesting one. Perhaps a vaginal sphincter would be a good idea…..were it not for men and babies….

Another view is that high host of pregnancy (e.g. brain development) is driving menstruation (it is worth to remove substandard zygotes): http://aeon.co/magazine/science/pregnancy-is-a-battleground-between-mother-father-and-baby/ and http://www.quora.com/What-is-the-evolutionary-benefit-or-purpose-of-having-periods. This way it explains why it makes sense for primates, but not - other mammals.

I found a nice write up elaborating what @PiotrMigdal is talking about - reddit

It is a very nice question.
From wikipedia:

Though there is some disagreement in definitions between sources, menstruation is generally considered to be limited to primates. Overt menstruation (where there is bleeding from the uterus through the vagina) is found primarily in humans and close evolutionary relatives such as chimpanzees. It is common in simians including Old World monkeys and apes and New World monkey, but variably expressed in prosimians, being completely lacking in strepsirrhine primates and possibly weakly present in tarsiers. Outside the primates it is known only in bats and the elephant shrew.

This other wiki article says:

Many have questioned the evolution of overt menstruation in humans and related species, speculating on what advantage there could be to losing blood associated with dismantling the endometrium rather than absorbing it, as most mammals do. Humans do, in fact, reabsorb about two-thirds of the endometrium each cycle. Strassmann asserts that overt menstruation occurs not because it is beneficial in itself. Rather, the fetal development of these species requires a more developed endometrium, one which is too thick to reabsorb completely. Strassman correlates species that have overt menstruation to those that have a large uterus relative to the adult female body size

I just cite two wiki articles but it is probably worth going through some more reading in order to give a more complete overview of the selection pressure underlying the evolution of menstruation in mammals and especially in primates. In the first paragraph above, wiki cites 5 articles. From the title of one of those, it seems that menstruation is also a defense against pathogens transported in sperm. I hope someone will give a better answer than mine.


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Is Sugar a stimulatant or a weak sedative?
Quite often, I have heard the remark that children become hyperactive when high amounts of sugar are consumed.
But common websites suggest that sugar is a sedative, and the hyperactivity in children is more likely caused by 'artificial dyes and preservatives'. (http://curezone.com/forums/am.asp?i=1444631)
So, is Sugar a stimulant (for adults and children) or is it a sedative? Is there any conclusive research to validate this theory?

Can you tell us which websites do claim this?

better ask at skeptics.SE

@edition Sorry, but this page is not a source to be trusted. As Jeremy already answered, this is pseudoscientific bllsht.

thanks for the clarification, but you wanted a website :)

The idea that 'dyes and preservatives' cause hyperactivity dates back to this '76 paper by one Dr. Feingold. Despite being disproved neatly in 1978, it's still around.
As far as sugar goes, I recommend this review paper covers both the arguments for and against sugar causing hyperactivity, as well as 12 double-blind placebo controlled studies showing sugar has no effect on children's actual behavior.

What about sedative effects? Is there a paper in that context? And what about adults?

I couldn't find anything testing specifically sedative effects. I don't see a plausible mechanism and 'no effect' means no effect, hyperactive or sedative. If you can think of a reason why something would be psychoactive only in adults, let me know, but I feel comfortable generalizing from children to adults here.

Could you provide a summary of these arguments? It's better to have the answer here rather than on another site which is behind a paywall (not everyone has institutional subscriptions)

source: Stack Exchange

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

sort: votes


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Are triglycerides fat?
I have a quick question: Are triglycerides essentially what we call "fats"?
I've tried reading up on it but there seems to be some conflicting information.
Thank you.

I think "fat" is a word that maybe it is not too recommended to use in an organic chemistry context. What I understand as fat is those "yellowish" and solid compounds, like margarine.
In a chemical context fat is often confused with the lipids, which are (be the definition broad) the amphipatic compounds, mainly composed by carbon and hydrogen and that fall in two groups, the ones that can undergo saponification and the ones that cannot. this is consequence of having or not the FATTY acids (C-H chains ended in a carboxy group).

If the fatty acids have a double bond in their C-H chain they are called insaturated, and are often liquid at room temperature. The ones with no double bond are saturated, and are SOLID. If you accept my definition of "fat", saturated triglycerides YES would be FAT, but the others would be not. Thats what I think, but I am not 100% sure

Fats include free fatty acids and their compounds with glycerol: mono-, di- and triglycerides.
In a cooking context, fats refer to solid fats, and oils to fats that are liquid at room temperature. Most of them contain triglycerides.
Fats belong to a broader group--lipids--, which are substances that are usually not soluble in water and usually soluble in certain organic solvents, such as ether or acetone. Besides fats, lipids include sterols (cholesterol, plant sterols), waxes, lipid-soluble vitamins (A, D, E, K) and steroid hormones (aldosterone, corticosterone, etc).
Examples of complex lipids are phospholipids, glycolipids and lipoproteins.
Fats and lipids are often used as synonyms. However, you usually say dietary fats and blood lipids.
http://www2.chemistry.msu.edu/faculty/reusch/VirtTxtJml/lipids.htm
http://biology.about.com/od/molecularbiology/ss/lipids.htm

As far as I know fats are solid lipids while oils are liquid lipids in (I guess) room temperature. So saturated triglycerides are usually fats, and unsaturated triglycerides are usually oils.
This is because saturated and trans-unsaturated fatty acid chains are linear while cis-unsaturated fatty acid chains are curly (non-linear). Forces between linear chains are stronger that's why they are solid after a length.

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Is carbohydrate an important part of phospholipid?
My professor tells us that carbohydrate is an important part of phospholipid, but phospholipid is composed of Choline, Phosphate, Glycerol and two Fattyacid, and I don't think even one of them is carbohydrate.
What's wrong with my statements?

Question: What is a fatty acid and which elements do you find in it?

Similar question: what are the elements in glycerol?

@Chris Sir, fatty acid is a kind of lipids and I find C,H,O in it.

There you have the carbohydrate part you are looking for.

@Chris fatty acid is also carbohydrates? I don't think so. It's not in the textbook. Lipids and carbohydrates are completely different.

No, but the fatty acids have a carbohydrate tail.

@Chris do you mean hydrocarbon tail? And phosphoinositol would have something similar to a carbohydrate as its head group.

Phospholipids have lipids, of course, but those are bound to glycerol, a 3 carbon carbohydrate that is usually derived from glucose.  Glycerol is the only carbohydrate (or even carbohydrate-like) part of the phospholipid.

@JasonPatterson Thanks, that's the right answer I am looking for! Would you mind write this as an answer?

Your thinking is correct based on typical carbohydrates, but glycerol, the backbone of the phospholipid, is a 3-carbon carbohydrate that is usually derived from glucose.  It is not a sugar, but it does fall into the general class of polyols (aka sugar alcohols) that are a type of carbohydrate.
A carbohydrate definitely is an important structural part of the phospholipid, but your instructor probably should have been more clear in describing why that is the case; I can definitely understand your confusion here.

There's nothing wrong in your statements!
Maybe your professor was talking about glycolipids, that are lipids (also phospholipids) with a carbohydrate attached; they can be found on the outer surface of all eukaryotic cell membranes. They are important because they work as a recognition site for specific chemicals or for antibodies.


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Definitions of robustness and canalization
The concepts of robustness and canalization are fashionable today in the biology literature. However, I am not sure of their definitions and I am not sure either that all authors actually use the same definition.
I am therefore asking here for a the definitions of these terms or for a short review of the common definitions of robustness and canalization. How do different authors define these words? I am particularly interested in...

The differences between robustness and canalization (canalization seems to apply more in developmental biology than robustness who seems to be a more general concepts)
At what level do these concepts apply? To populations, to genotypes, to both, ..?
How does the concept of adaptation link to these definitions.
How does the concept of plasticity fits in opposition of the concepts of robustness and canalization?

As canalization is defined in your question (also in wikipedia) it means robustness.
Semantically it is possible to differentiate the two.
Robustness of a system refers to its sensitivity to perturbations. In other words small differences in parameters would not affect the steady state of the system (parameter changes in a physically plausible range would not lead to bifurcations).
By system I mean a set of entities connected to each other in a defined fashion. For example an ecosystem in which different species are connected to each other by interactions of the food chain. At steady state a system configuration (for instance- 10 foxes, 100 rabbits, 10000 grasses, 1000 honeybees etc) remains constant over time (that, however, doesn't mean it is static). Or in case of development a system may be the body defined by a set of certain phenotypes.
Canalization/channelization refers to mechanisms that make the system follow a certain trajectory. So if you see it mathematically canalization keeps the trajectory dictated by a  given set of eigenvectors. In case of development you may call mechanisms such as dosage compensation, functional compensation by isoforms, parallel metabolic flux channels etc as canalizing mechanisms.
So in contemporary usage we can call a system robust (a property of a system) whereas we should address mechanisms that help to preserve trajectories as canalizations. The final aim of canalization is to render robustness to the system but it is not the only mechanism that is responsible for robustness (for e.g. the steady state may just be independent of certain parameters).
Robustness is a property of the system and is dependent on how the different entities of the system are coupled and what their interaction parameters are (rates etc).
You should note that these are parlances that are adopted by different groups in the scientific community and may perhaps mean the same thing- this is merely my attempt to remove redundancy of terms by the means of semantics.
Now, plasticity is a different concept altogether. Plasticity is in a way opposite to robustness. This means that the qualitative nature of the system can change if certain parameters are tweaked. However, the system should still maintain its stability. In a stable system mild perturbations from steady state will result in system going back to that steady state - like a ball in a well. However, a system may inherently allow for multiple steady states (like switches), and depending on certain parameters the system can be in either of the states (but if pushed too far then the system can go to another stable steady state). This is called multistability.
NOTE: some people also use the term plastic to mean "responsive". The above definition may not be exhaustive or the most perfect.

THanks for your answer, it is already very informative although I am still a bit confused. When you say that robustness is a property of a system, do you mean it is a property of genotypes, populations, both, ..? Robustness is the property of a system to always produce the same phenotype while canalization is the mechanism of this system that yield to the production of always the same phenotype. hum... Did I get it right? What do you call trajectories when you say that canalization preserves trajectories? Thanks a lot for your help.

Are you aware of an article that directly compares the definitions of these two concepts?

No I haven't read an article which compares them.

There are several subconcepts within the concept of robustness. Several definitions exist for all of these concepts and I am just suggesting one variant of the possible definitions below.

Mutational robustness

Might be defined as a function of the mean and variance of the distribution of mutational effects.

Environmental robustness

Might be defined as the opposite of phenotypic plasticity. Here, plasticity is not only defined as adaptive plasticity. Plasticity is any phenotypic change induced by an environmental change. Environmental robustness might therefore eventually be defined as the inverse of the slope of the reaction norm.

Developmental robustness

Might be defined as the variance of phenotypes that a given genotype produces in a given environment.

From Gilbert and Epel (2009), page 384, Canalization is developmental robustness.
In Biology, those concepts almost always refers to genotypes. Rarely do they apply to populations or ecosystems and when they do the definitions are often quite different.


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Bacterial Cell Problem
A microbiologist has discovered what she thinks are two new types of algae. The first cell
(Organism 1) appears cubic and is approximately 1.5 μm long, 1.5 μm wide and 1.5 μm deep.
The second (Organism 2) is rectangular and 2 μm wide by 5 μm long by 2μm deep.
a.  What is the surface area/volume ratio of each organism?
b.  Which organism will find it more difficult to interact with surrounding environment (receive nutrients, excrete metabolites etc.)?
c.  How will this organism cope with the reduced capacity to interact with environment?

In respects to question A.

V of Rectangular organism= (V = L x W x D)
Surface Area= (L x W)
Im assuming these simple rules still apply to organisms concerning minuscule measurements.

Im assuming for question B., that the molecule with the smaller dimensions will have the most difficult time interacting with its environment, due to the fact that it has a smaller perimeter with less channels & ports.
I am completely lost for problem C.

Any insight Would be awesome. Thanks all !

The surface area of a rectangular prism is not length times width. Questions B and C are related to the ratio you calculate in A.

Woops. I mean A=2(wl+hl+hw)*

B. Higher surface to volume ratio allows better interface with environment.
C. To increase surface area the cell can form processes such as microvilli.


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Regarding the kingdom Animalia, which phylogenic tree is more common: Molecular Comparisons or Body-Plan Grades
In the picture below, which I obviously do not own:

it depicts two different phylogenic trees, one which is based on molecular comparisons and another one which is based on body-plan grades. My question is which is more common or accepted in the current Biology world?
Image reference: http://www.zo.utexas.edu/faculty/sjasper/images/32.12.gif

Molecular comparisons are more reliable. BTW ctenophora has been identified as a sister clade to both porifera and cnidaria.

@WYSIWYG Correctly speaking Ctenophora are a sister group to Porifera+Placozoa+Cnidaria+Bilateria

@har-wradim .. yes you are right.. missed it..

I will say that classification using body plan is more common. Because animals show extensive morphological and anatomical diversity which makes it easier to classify. That's why in our high school we learn classification based on body plan. These also form the basic attributes and general characters of a phylum. So learning classification is also helping us determine general characters.

Long story short, use sequence information if you can.
The long story long:
Sequence information and the trees generated from them are strictly more reliable than morphological characters. For instance: sharks are pretty much the same shape they were millions of years ago, but they've been accumulating genetic differences 'invisibly' that allows us to group the different kinds of shark accurately. Where genetic data is unavailable (paleontology as a rule, certain kinds of field taxonomy where it's cheaper to code the morphological features of each new beetle than sequence them all) morphological trees are still used. So in terms of which tree type is more common: It depends.
In terms of which tree type is more accepted, it's genetic data by a landslide. Genetic data by and large is much less affected by homologous structures and convergent evolution. In addition, it works on species that all look pretty much identical (imagine trying to code hundreds of bacterial species that are all closely related). Using highly conserved cellular machinery, trees for very distant species can be constructed. Using unconserved noncoding sequences trees for very closely related individuals trees can be constructed with a reasonable degree of accuracy.
Some examples: Mitochondrial Eve would be impossible to date with morphological characters. There's just not enough morphological variation between humans.
Opabinia is a really good example of how hard it is to classify things based on shape, especially when they're a weird shape.
Something you can do yourself: Human  and Thermodesulfator(seq) are about as morphologically distinct as two living things can be. One is you, and one eats carbon dioxide and breathes sulfate and hydrogen. It lives at the bottom of the sea and would be more at home in a cup of hot coffee than outside it. Nevertheless, the two species show ~50% sequence similarity using 16S, twice as much as would be expected by chance and easily enough to classify a third thing as more closely related to one or the other. Try it yourself if you like.


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What are typical values for bone mass in humans?
I wonder what are typical bone mass values for adult males and females? And do they change significantly with workout and diet?

I wonder what are typical bone mass values for adult males and females?

This seems hard to find. The only value I could find is on Bionumbers at it says that vertebrates compact bones have a mean density of 2 mg/cm$^3$ [1]. However in medical practice two scores are used to indicate the ratio between tested bone density and ideal bone density [2, 3] and absolute values are uncommon.

And do they change significantly with workout and diet?

Bone mass is mainly influenced by genetic factors. Only up to 25 % may be influenced by environmental factors such as diet and exercise [4].
Among the medical conditions that influence bone mass, osteoporosis is the most frequent especially in women. Other conditions are: hyperparathyroidism, glucocorticoid therapy, other bone abnormalities and fractures [2].

References:

Brian Cotterell, Fracture and Life, Imperial College Press, 2010 p.77 bottom paragraph via http://bionumbers.hms.harvard.edu//bionumber.aspx?id=108642&ver=2
Bone density. (2014, September 15). In Wikipedia, The Free Encyclopedia. Retrieved 17:08, September 29, 2014, from http://en.wikipedia.org/w/index.php?title=Bone_density&oldid=625737182
http://www.niams.nih.gov/Health_Info/Bone/Bone_Health/bone_mass_measure.asp
http://www.niams.nih.gov/Health_Info/Bone/Osteoporosis/bone_mass.asp

it is really hard to find absolute values. maybe because it is hard to estimate, or maybe just because total mass is irrelevant for medical interest. my motivation was actually a bit off-topic, I wanted to know if my body composition estimator scale gives reasonable values.


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Biology Experiment Data (Hodgkin-Huxley)
I'm doing research into the Hodgkin-Huxley Model from an electronics/mathematics perspective and I'm looking to find actual numerical results from experiments on squid axons. I want to compare the results of the experiments to the curves produced by modelling the equations in MATLAB.
My problem is, that while there are an abundance of resources discussing the equations and methodology of the experiments, I am having great difficulty finding tabulated experimental data (not just numbers generated from modelling the equations).
As I am coming from outside the field of biology I would like to know are there sources of quality numerical data for these types of experiments? In particular I am looking for the data for Potassium Conductance vs Time, here is the plot from the 5th paper in their series of publications that earned them a Nobel prize:
Hodgkin AL, Huxley AF. A quantitative description of membrane current and its application to conduction and excitation in nerve. The Journal of Physiology. 1952;117(4):500–544.

You are looking for raw data? I suspect that none of these has been published. You could try to contact the authors and see if you can get hands on them. But I wouldn't be too optimistic.

There are various programs that can help to extract numerical data from graphs, I'd try something like this on the figure you posted. It is very unlikely that numerical data is easily available for such old experiments. The other option would be to look for very new papers about the subject, it is much more likely that such data is available for new papers.


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What is the difference between a fixed substitution and a single nucleotide polymorphism (SNP)?
I recently read a report that stated "We found 430 fixed substitutions […], with an additional 34 single nucleotide polymorphisms (SNPs) fixed within individual patients." What is the difference between both terms?

I'd need more context to be sure but what makes you think that the substitutions were only a single nt? Also, that sentence could be read as having found 464 SNPs, of which 430 were fixed.

It would be important to read the original paper.

If you look into a certain population, you will find mutations (for example SNPs) in some ratio with the wild-type allele. When a mutation reaches fixation, it will be the only allele, reaching 100% penetrance in this population. See here for more information.
In the context given I would interpret it in the way that a total of 464 SNPs were found, 430 of these were in fixation (so can only be discovered when comparing them to another population) and 34 SNPs which haven't reached fixation and thus cannot be found in all members of the population.

Fixation is a process when one of the polymorphic alleles becomes fixed in the population gene pool due to genetic drift or natural selection and ceases to be polymorphic anymore. Therefore fixed substitution and SNP are two absolutely different concepts. So, the term “fixed single nucleotide polymorphism” seems to be oxymoron as it bears a contradiction. To calculate the real number of fixed substitutions at least one individual from another distant population or closely related species is needed.

Welcome to Bio and thanks for your answer. Could you add sources, links or citations to your answer to allow users to read the backgrounds?


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What is the evolutionary explanation for bat's echolocation
The bat's ability for echolocation is amazing (so are other the abilities of other animals). I was wondering how all of it came to be.

This is an interesting question.

https://www.youtube.com/watch?v=Z_E3zxx2l9g < might not take much

The main reason for bats to "develop" their echolocation system was the avalability of an almost empty niche: Hunting insects at night. Birds are not able to hunt without light and here is where the bats come in. They are able to hunt at night and also to live and orientate in environments where they are protected over the day: Caves. Bats at night are also protected from predatory birds.
There is are a few interesting sources if you want to dive deeper into the stuff:

The evolution of flight and echolocation in bats: another leap in
the dark
Echolocation in bats
Evolutionary aspects of bat echolocation

Not a major issue, but owls and nightjars might disagree with your assessment of birds' ability to hunt insects at night.

They still need some light - bats can hunt in total darkness.

They developed this ability because there was an empty niche? So what, they hired an MBA to find a market opportunity and set an R&D budget? There are lots of "niches" in the animal kingdom - your answer doesn't explain how they are evolutionarily determined and filled

This happens in the usual way: Mutations occur and don't have a negative effect. At some point they prove advantageous, which put selective pressure on mutations which lead to a better adaptation of this new niche. So for example (speculative here) bats were able to navigate better because of mutations in their hearing. This led to a shift of their hunting habits more to the evening, which resulted in the survival of more bats better adapted to this (because less got caught by predators, more food was available etc.). This led to a further selection of animals adapted to this kind of living.

the question isn't "does mutation occur" but:  how did this particular mutation occur?  Randomness isn't a sufficient answer.

Why isn't randomness a sufficient answer for you? Mutations occur randomly, some of the proof advantageous, some are neutral, some negative.

I think your answer would be enhanced if you extracted some of the deeper results from your sources.

Remember, evolution says things don't initially develop "for a reason" -- they develop at random, non-harmful mutations are kept in the gene pool, and eventually a selection event occurs (opportunity to exploit another food source or avoid a hazard) which selects for the mutation in some subset of the population. Over the kind of timescales evolution works on, that's enough to take something that is harmless, turn it into something that is just barely useful (though not necessarily for what it's now used for, eg feathers), and then continue to randomly vary it so it works better or differently or whatever.
Echolocation by itself isn't so remarkable -- we generally can tell about what size room we're in by listening to the echos around us. It's focused echolocation that was a breakthrough.
Late addition: In fact, it is possible for humans to learn to echolocate well enough to get an accurate picture of their surroundings. Some blind individuals have demonstrated this under MRI imaging of their brains. It's not common, but this may be because not enough respect has been given to the technique -- just as ASL was not respected until deaf linguists were able to explain why it was so much better than the alternatives.
So maybe what's special about bats is not the ability, but their reliance upon it.
https://en.m.wikipedia.org/wiki/Human_echolocation

It would be frat if you provided some references for your response.

References: The keyword to search for is "punctuated equilibrium".


text:
What percent of your blood can you lose before you need a transfusion
Losing a little blood is okay. If your a normal healthy person, and got into an accident, how do they know if you need a transfusion or if you'll be okay? This is hypothetical.

You may find http://whqlibdoc.who.int/publications/2010/9789241599221_eng.pdf and http://www.compliance.iastate.edu/iacuc/policies/docs/blood-collection-guidelines.pdf useful.

Typically transfusions are indicated for hemoglobin < 7 g/dL (for adults normally: 12-15 grams per deciliter [1]) or < 8-10 g/dL if there is cardiac disease where diminished oxygen carrying capacity cannot be compensated by increased cardiac output.
The answer above is theoretical because there is no accurate way to measure blood loss in the clinical setting - it's usually a mess.
The most useful parameter to assess intravascular volume in the immediate term is blood pressure. Again, the actual number is variable but a 30% drop from baseline in the acute setting is bad.
Another less acute indicator of hypovolemia is urine output (normal is .5-1 ml/kg body weight/hr, dropping below ~35 ml/hr therefore is an indicator of hypovolemia.)[2] Hypovolemia is often corrected with sterile saline fluid and adding packed red blood cells only as needed to keep hemoglobin in the above required range, unless someone is actively bleeding (trauma, bleeding ulcer, etc.) in which case "whole blood" (or packed red blood cells, fresh-frozen plasma and platelets) is given.[3]
[1] McPherson: Henry's Clinical Diagnosis and Management by Laboratory Methods, 22nd ed.
[2] Oliguria &  Volume Depletion
[3] Fluid Resuscitation and Volume Assessment

Welcome to biology.stackexchange. Can you please expand your answers with some references and also explain the parameters you name? It is then easier to understand for people who are not specialized in the field.

I'm confused about the last sentence - whole blood? I took a look at the paper cited and don't see that, nor have I heard of it. Blood isn't generally stored that way. Perhaps you mean packed RBC + platelets + FFP....but that's different from "whole blood."

@Susan - One can order units of whole blood, but yes, FFP + packed red cells + platelets is more readily available and easier to transfuse. see http://clinicaltrials.gov/show/NCT01227005

What percent of your blood can you lose before you need a transfusion

According to Wikipedia: starting with Class III (more than 30 % of circulating volume loss), hemorrhage requires transfusion.

Class I Hemorrhage involves up to 15% of blood volume. There is typically no change in vital signs and fluid resuscitation is not usually necessary.
Class II Hemorrhage involves 15-30% of total blood volume. [...] Volume resuscitation with crystalloids (Saline solution or Lactated Ringer's solution) is all that is typically required. Blood transfusion is not typically required.
Class III Hemorrhage involves loss of 30-40% of circulating blood volume. [...] Fluid resuscitation with crystalloid and blood transfusion are usually necessary.
Class IV Hemorrhage involves loss of >40% of circulating blood volume. The limit of the body's compensation is reached and aggressive resuscitation is required to prevent death.

Of course this applies to a healthy person. If suffering from anemia or other blood conditions, smaller amounts of bleeding may require transfusion.

how do they know if you need a transfusion or if you'll be okay?

In most situations it is hard to estimate how much blood was lost. So in medical practice some indicators are used. These include (according to Puget Sound Blood Center):

hemoglobin / hematocrit ratio and/or values lesser than 7 / 21
small hemoglobin correlated with clinical signs (symptomatic anemia)
low O$_2$ saturation
acute blood loss of more than 30 % (when it can be observed)

But how can the doctor tell when the patient has lost that much blood?

@anongoodnurse a significant drop in blood pressure, along with a commensurate increase in heartrate, is often used as a "back of the envelope" measure of blood loss.

@MattDMo - My point is that the OP asks, in trauma, "how do they know if you need a transfusion or if you'll be okay?" This answer gives no indication of how the trauma doctor would assess this.

@anongoodnurse I agree.


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Does applying sugar to the tongue taste buds releave sugar withdrawal symptoms?
I found several online articles discussing sugar withdrawal symptoms that people experience after cutting back on large sugar intake.
http://healthyeating.sfgate.com/refined-sugar-withdrawal-symptoms-9911.html
http://www.growyouthful.com/remedy/sugar-addiction-recovery.php
One question that came to mind, was the following: If one experiences a sugar withdrawal, what happens if they apply sugar to the tongue, but do not digest it? Does that trick the brain into stopping the sugar withdrawal, or is it far more complicated than that?

It's not clear to me that "sugar withdrawal" is a real medical condition, despite what a newspaper and a site pushing low-carb diets might say.

Theoretically if you could somehow activate the G-protein-coupled receptors (GPCRs) corresponding to sweet stimuli without absorption of the sugar into the bloodstream than it may be possible to "trick" the brain. (See this review to learn more about how taste signaling works). However, the process of absorbing sugars into the blood stream begins in the mouth (see this question), so testing your idea would be nearly impossible.


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Short, concise, practical manual for doing experimental biology
I am am physical scientist working in biology, and have recently started doing experiments. I would like a manual akin to "Numerical Recipes", but for the lab: straight forward, easy instructions on how to do the (100) most basic biology experiments - PCR, cloning, etc. I realize that a lot of these depend on kits, and specific equipment, but it seems like there still should be something that would give you the outline of how to do these experiments. Does anyone know of a resource like this?

Kits are often a good way to do a basic procedure, but don't use them as black boxes, and learn how to make the buffers and buy the reagents individually because you can often save money doing it that way instead of buying more kits. Also allows you to modify the procedure to fit your research.

Molecular Cloning is updated and in its 4th edition.  Every lab used to have it.  Its comprehensive, but really no book could be complete.

Along with @shigeta's answer, I'd highly recommend Springer/Humana Press's series Methods in Molecular Biology, which started out as just a single collection of protocols (as I recall...) and is now a series of 1208 books, published between 1984 and 2015. There are a ton of protocols available online at places like Springer Protocols and Cold Spring Harbor Protocols, as well as at many locations across the 'net, with varying degrees of accuracy, reproducibility, and clarity. As you mentioned, you can do just about every molbio assay with a kit nowadays, and the manufacturer's websites (like Qiagen's) are often great resources, and frequently (but not always) include some scientific background as well, if you want to go back to the literature. There are also sites (some independent, some sponsored) that cater to specialized areas of research. For example, I work in immunology, and the Human Immunology Portal is a pretty good resource for basic and advanced protocols and assays.
So, there are quite a number of digital resources available, which I actually prefer because there is a greater chance that they are kept up-to-date, and will have new technological advances much more quickly than they are likely to show up in a revised edition of a book. Best of all, most of the online resources are free, and if you have academic access through your institution, you may be able to access some of the pay sites as well, such as the archives area from Cold Spring Harbor.


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Are the cpli and ctli tests time senstive(i.e. is it needed to test right away in order to get accurate results)?
I'm sending the blood samples to a lab and this takes some time until the actual testing.
Some information on the tests.
TLI : http://www.vcahospitals.com/main/pet-health-information/article/animal-health/trypsin-like-immunoreactivity/405
CPLI : https://www.vetstream.com/canis/Content/Lab_test/lab00522

From doing a bit of research, I quote

The various analytes have different stability in serum. Serum TLI and
  PLI are stable for up to 2 weeks at room temperature. However, serum
  folate shows limited stability at room temperature. Therefore, serum
  samples for folate analysis should be kept at 4ºC for not longer than
  48 hours, but freezing is preferred. Furthermore, folate is light
  sensitive and samples should be stored in the dark or wrapped in foil (reference).

So, it should be fine if the tests are conducted in two weeks.


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What is a good source that will help me classify protists?
I am a 15 year old that enjoys looking at the micro world. The only issue that I have is that I can't find a good online source that will help me classify the name of the micro organism that I'm looking at. Does anyone know a place that will help me do this? Thanks in advance.

You can have a look at Cavalier-Smith's classification of protists.

@WYSIWYG: it's pretty old

@har-wradim Any free sources?

If you need an overview of higher taxa than this scheme from Wikipedia seems be a good starting point (see also the papers they cite).

@har-wradim: could you turn your comment into an answer? It seems to be helpful.

While not comprehensive, the Portal to Protistology has many resources for exploring the diversity of protozoa. I especially recommend their videos that are really fascinating, focus on distinguishing features of different protists, and may be helpful for identification to some degree. But given your interest you should just explore all the pages on the site, check out the books they recommend (e.g. the Illustrated Guide to Protozoa), and see what is useful for you!

Since no one else decide to post anything that was put in the comments as an answer I decided to.
There is an excellent article from Wikipedia on the subject, found Here. It was also recommended in the comments that you should read the sources provided.
I also found this PDF to be quite helpful, Nebraska Med.
I hope this helps!

There is a CBOL working group that categorizes protists based on genomic sequencing and barcoding. Here is a link to their publication: CBOL Protist Working Group: Barcoding Eukaryotic Richness beyond the Animal, Plant, and Fungal Kingdoms

No offense, but I don't think a casual teenage biologist has access to high-throughout sequencing technology


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What makes living beings alive?
To clarify, I'm not asking about the common properties of living organisms, such as reproducing and having a metabolism, etc. What I'm curious about is, what is the difference between organic molecules and actual living beings?
For example, if a person's heart stops beating, they are technically dead, but all the chemical compounds and molecules are still there.. I guess another approach to this question would be "If we bring together all the atoms of a living being in the same exact arrangement, would that new thing be alive?"

organic compounds are carbon based molecules. Living being contains several properties, some of which you have named!

I don't think you can ignore the common properties of living organisms (or the definition of organism) if you want to talk about life. Someone whose heart has stopped is no longer alive because they can't deliver oxygen to their cells any longer for metabolism to occur.

@anongoodnurse I understand that, but what separates what was alive just a minute ago from the dead state of it? I just can't wrap my head around how these seemingly ordinary chemical compounds get together and do things with a purpose (which is to not die and to reproduce I guess).

The minute a critical component stops functioning, the organism dies. That's why the definition of organism counts. For a highly complex organism, it has to be that organism, not all the cells which make it up. This can go on and on. If the cell membrane integrity of a single celled organism is lost, it dies. But what if enzymatic processes are still going on before cell lysis? Is that protein alive? No, it's not. Similarly, a person's death is not negated by how long it takes for all of his cells to stop metabolizing.

@anongoodnurse That's a pretty good explanation. Thanks a lot


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Whats the difference between voltage gated and ligand gated neurons?
How are they similar and how are they different?

Is this a homework question? If so, please read our homework policy. Essentially, we require that you attempt to answer your own question as much as possible, explaining your thinking on the matter and where you are stuck. We will not answer homework question without any effort on the questioner's part.

no... ... ... .

There is no such thing as voltage gated or ligand gated NEURONS. I believe what you are refering to are what is known as voltage gated and ligand gated ion CHANNELS. Each neuron has both types of channels in their cell membrane.
Voltage gated ion channels open in response to voltage (i.e. when the cell gets depolarized) where as ligand gated channels open in response to a ligand (some chemical signal) binding to them.
Both types of channels are critical for proper activation of the post synaptic neuron. The pre synaptic neuron releases neurotransmitters into the synaptic cleft, these neurotransmitters then bind to the ligand gated channels, thus activating them. The ligand gated channels open up and allow the influx of sodium, which depolarizes the cell. This depolarization activates nearby voltage gated ion channels, which open up and let in even more sodium. Voltage gated sodium channels open up one region at a time, the previous region providing enough depolarization to activate the next regions voltage gated channels. This effectively allows the action potential to propagate through the cell.


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How many proteins are synthesized in human body throughout life?
My idea to calculate this is:

Define up to what age will do the calculation. (for instance 60)
Determine how many cells born and died up to that point in life. (by type of cell)
Determine how many proteins are synthesized in the cells life. (by type of cell)

Points 2 and 3 are not constant throughout the life of the human body. To calculate this data I need a function.
After obtaining all the data: complete calculations of addition and multiplication.
The question is not about mathematics, but about useful data to make these calculations. Another approach would be welcome too.

Related question.

Also related, protein turnover.

you will probably want to take a mean lifetime of human cells - some of them are very slow growing and life practically forever, others relatively short - just a few days.  (blood cells and male gametes for instance).  the amount of protein synthesis would also similarly vary.  a single cell type with good measurements would be good to see..

Just to add another factor, there are many proteins that are often recycled and persist for quite some time.  I would be impressed to see some solid arguments on this.  I think you might have some luck by trying to break down to average masses of the various tissues, but I believe this will be quite a challenge.

Hmm. Maybe measuring mRNA content can help to estimate the speed of protein construction. It is a hard question btw...


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How does an embryo know where to grow limbs etc
For example you have a cell or already a bunch of cells. Those cell(s) divide and after several week you have a grown organism, for example a human with limbs, several different organs etc.
However, how do cells know where up, down, left, right etc. is?
I know left and right can be defined clearly in physics, for example by the Wu experiment verifying parity violation really occur.
However how do cells define those directions? What are the mechanisms for them to grow into a certain direction and tell other cells to attain a certain property?

See Human embryogenesis and Prenatal development on Wikipedia.

You may want to look into "Evolutionary - Developmental Biology", which deals with how an embryo develops into a grown organism.

Thus, by combinatorial specifying the identity of particular body
  regions, Hox genes determine where limbs and other body segments will
  grow in a developing embryo or larva. A paragon of a toolbox gene is
  Pax6/eyeless, which controls eye formation in all animals. It has been
  found to produce eyes in mice and Drosophila, even if mouse
  Pax6/eyeless was expressed in Drosophila.

In short, there's a sequence of gene activations that progressively map body into different regions. At first, there are just 3 regions (head, body, tail), then these get broken down into more and more finely defined sections.
You can think of these sections as GPS coordinates for the body. A gene combination at a certain point means that a limb will grow there.
You can look into "Sonic Hedgehog" gene, which allowed scientists to produce fuzzy growth on a fruit fly head.
The most interesting thing is that every living creature is mapped/built using the same toolbox of genes. The genes that define where a fruit fly wing is also define where a human arm is.

Embryonic cells "know" where they are relative to each other by chemical signals, same as in adults. These molecules are known as morphogens (specific examples include the sonic hedgehog and β-catenin). The amount of morphogen in a region of cells determines which gene gets turned on and thus what it develops into. And the amount varies by how far they are from the source of the morphogen. Though AFAIK, scientists don't fully understand their mechanisms yet (like how they are dispersed, how the different concentrations are kept rigidly, etc.).
As for arms, etc., the earliest cells are unspecialized (stem cells). They "define" which becomes what early on by how they are arranged. Remember that their "up, down, left, and right" is relative to them, not to their surroundings. The first multicellular hollow ball of stem cells, the blastula, separates into distinct germ layers during gastrulation - the ectoderm, mesoderm, endoderm. Each of these layers develop into something different upon further division. What develops after that is basically a worm, composed of a series of repeating "segments" (somites) with a distinct head and tail area. Somites are initially undifferentiated. The job of determining which segment becomes what falls on Hox genes. So that for example, one segment becomes the head, another becomes the arm and pectoral girdle, another becomes a rib+vertebra, etc. Hox genes are arranged in clusters within the DNA relative to which gets expressed first. The first hox gene is for the head for example, while the last is for the tip of the tail (the tipmost segment of the coccyx in humans). Though these clusters themselves are often repeated into a kind of redundant failsafes. This page from the University of Utah explains it pretty well. It helps if you view embryogenesis as more or less echoes of evolution in fast forward.

I wanted to add some helpful references. The 6th edition of the Gilbert Developmental Biology textbook is available on NCBI bookshelf. It's a bit old (2000), but much of the information is still relevant. You can search this textbook for specific terms but not browse.
There is also a collaborative science/fashion project between the Storey sisters, called Primitive Streak, which documents the early stages of human development.
For any given developmental process, there are a number of genes being activated and/or inactivated at that stage that determine how and when structures grow. Events can determine axes too; for instance, the dorsal/ventral axis of the embryo is determine by how the embryo blastocyst implants in the uterine wall. The left-right axis of the body is determined by the direction that fluid travels through a structure called the node, which is directed by hair-like structures called cilia. If nodal flow is backwards, your internal organs will switch sides, called situs inversus.
Back to the limb example... in tetrapods, or animals with 4 limbs, the area where limbs emerge is based on Hox gene expression, and whether or not it will become a forelimb (arms) or hindlimb (legs) is determined by either Tbx5 or Tbx4 gene expression, respectively.
The proximal-distal axis (proximal = towards the trunk; distal = away from the trunk) is determined by FGF gene expression, which induces formation of a structure called the apical ectodermal ridge (AER).
The anterior-posterior axis (head to tail) is determined by Sonic hedgehog gene expression in a region called the zone of polarizing activity (ZPA).
The dorsal-ventral axis (back-front; or back of the hand/arm - palm/inside of arm) is determined by the Wnt7a gene being expressed on the dorsal side.
The outgrowth of the limb is determined by Hox gene expression.
Digit (finger) formation is dependent on cell death between the fingers - hands start webbed, kind of like ducks, and then genes such as the BMPs cause cells between the fingers to die.
Terms to look up for more detail, since I don't have enough street cred here to post more than 2 links yet:

Snapshot Summary: The Tetrapod Limb (Gilbert book)
apical ectodermal ridge (AER)
zone of polarizing activity (ZPA)
situs inversus
Hox genes

That node-flow ciliar thing causing situs inversus is so amazing!

yea the hox genes are essential for the the specification of the location but the actual growing of the limbs are determined by a series of protein and other factors. proximal limb contains fgf(fibroblast growth factors) wnt(look up wnt pathway) and high levels of retonic acid where distal limbs shows high fgf's high wnt and little to none RA. the sonic the hedgehog gene talked about in the other answer has to to do with the anteriorizing(up)/posteriozing(down) of the autopod(digits, carpals). as to dorsal ventral wnt would be the culprit

Can you please work on your answer and also add some references to it? At the moment it's hard to understand without basic knowledge of the field.

I concur with @Chris: with some elaboration here and there and the necessary citations this could be a great answer

why would i have to cite topics that i have learned through school, it is a topic that i am familiar with as far as elaboration sure what exactly would you recommend i elaborate on.


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PSI-BLAST website algorithm parameters
http://blast.ncbi.nlm.nih.gov/Blast.cgi
In this website, when I want to apply the psi-blast algorithm on a sequence, under the section of algorithm parameters , what does PSI-BLAST threshold mean? The question mark says it means that:

Set the statistical significance threshold to include a sequence in the model used by PSI-BLAST to create the PSSM on the next iteration.

Another parameter is there called pseudocount. Did not understand that too. Could not understand what this means, someone please explain in simple language.

PSI-BLAST is an iterative algorithm. Each cycle it uses a model (the position-specific scoring matrix, or PSSM) to search for sequences matching the model, next updates the model with the sequences found, and then runs the search again with the updated model. That P-value controls which of the sequences found in each iteration should be included in the new model (i.e. only include those sequences satisfying the P-value).
Regarding the pseudocounts, this is a value to be added to each column in the PSSM. The reason is to avoid zero count entries, which may give problems later. But as the help suggests:

Pseduocount parameter. If zero is specified, then the parameter is automatically determined through a minimum length description principle (PMID 19088134). A value of 30 is suggested in order to obtain the approximate behavior before the minimum length principle was implemented.

It is probably OK to leave the default option unless you have some reason to change it.


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Is chloroplasts per cell indicative of the photosynthetic power of a plant?
Plant-A has on average N chloroplasts per cell. Plant-B has on average M chloroplasts per cell. If N > M, is plant-A more efficient in turning carbon dioxide into oxygen? Also, is it possible to see chloroplasts with a standard bright-field microscope?

You can say that but chloroplasts do not have uniform morphology across different species. Moreover some organisms such as red algae have chloroplasts of different origin.
Real indicator would be lets say number of chloroplast ATP synthases and/or light harvesting photosystems; these can be perhaps indirectly approximated by the total surface area of the thylakoids.
But for all practical purposes and comparison between not so distant species density of chloroplasts is a decent enough approximate for photosynthetic power.
About turning carbon dioxide to oxygen:
You should note that the source of oxygen is not CO2. Oxygen comes from photolysis of water; this is the initial step in the electron transport chain (ETC) in chloroplasts. The ETC results in production of ATP and NADPH; the latter is used in the Calvin-Benson cycle to fix CO2 to sugar.
So photosynthesis and carbon fixation, though associated in chloroplasts are basically different biochemical processes. Theoretically as long as NADPH is provided a plant should be able to fix CO2 [this is just my guess].
It is difficult to observe internal structure of chloroplasts with normal bright-field microscope but you can count them easily at 40x magnification. See here.

As @wysiwig already pointed out the different morphology of chloroplasts is something that is hard to come by. This influences the amount of chlorophyll in these organelles which is the key for photosynthesis. So it is very difficult (to impossible) to compare chloroplasts of different plants as they differ pretty much. There is one paper from 1929 which goes into detail here:

The relation between maximum rate of photosynthesis and concentration
of chlorophyll.

However, there is a paper which studies the photosynthesis rate in connection to the number of chloroplasts when manganese ions are a limiting factor. Manganese is part of the active center of the Photosystem II in the photosynthesis. So without maganese, photosynthesis is not possible.
The article finds the number of chloroplasts in cells approximately reduced to the half compared with leafs without maganese-deficiency. Testing the photosynthesis capacity of these leafs, they find that the photosynthetic activity in the manganese-deficient leaves is reduced by about 40%, which fits nicely to the reduction in chloroplast number. They do not find other significant changes in the biochemistry of the photosynthesis in these plants, so is the ratio between chlorophyll a and b not affected, and also the ability to transfer electrons is not affected. The findings are presented in this paper:

Reduction in chloroplast number accounts for the decrease in the
photosynthetic capacity of Mn-deficient pecan leaves


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About sharks and how they find fish
Other than olfactory senses do sharks use some kind of sense that uses electromagnetic waves? Is this similar to an electric eel? I saw a book with the cover statement 'Sharks never get cancer'. IS this possible or just 'quackery' ? Could being constantly 'bathed' in some kind of electromagnetic field cause pre-cancer cells ( that are already unstable) to be 'disrupted'?

Sharks do get cancer.. See also, "Shark cartilage, cancer, and the growing threat of pseudoscience". Contrast, this nonsense.

Oops, the link was wrong: Shark cartilage, cancer, and the growing threat of pseudoscience

I didn't say it was 'sense or nonsense'. Notice I asked if this was just quackery? But is cancer in sharks rare? What about electric eels, do they get cancer; is it rare? I read on wikipedia there is a biological paradox related to whales. They obviously have alot more cells than humans yet they don't get cancer as much as a random process would 'cause' if cancer causes are 'random'. Is this true? Why is cancer in the Heart rare?

Sorry, I didn't mean to imply that you were endorsing that view; just making an observation about the available literature on the topic.

Thank you for the response but what about my other questions?

I don't know the answers, sorry. I think that's probably best left for the answer space rather than comments anyway.

Sharks sense their prey with the normal senses, they see, hear and smell them.
They have a remarkable sensitive sense of smelling, which enables them to sense highly diluted traces of prey. They can also use their smelling to determine the direction where a certain smell comes from. This is achieved by the timing in which the senses arrive in different parts of the sharks nose. See references 1 and 2 for more details.
While sharks have eyes which are similar to that of vertebrates, they have an additional reflective tissue called "tapetum lucidum" behind their retina, which reflects the light back and therefore raises the sensitivity of the eye. It seems that a lot of shark species are either colorblind (because they only have rod cells but no cones) or they had only one kind of cone cells which allows them only to see one color. For sharks it is obviously more important to detect objects than to see colors. See references 3 and 4 for more details.
The sense of hearing of sharks is also highly sensitive and is able to detect sounds from far away. See also references 5 and 6 for more details.
The most interesting sense of sharks is their electrosensory organ. This is also called Ampullae of Lorenzini which is a number of sensory cells along the head and which are able to detect the weak electric fields that exist around living animals. This sense only works on a very short distance. See references 7 and 8 for more details.
Finally sharks have the so-called lateral lines (which are present in most fish), which is an organ which detects movements and vibrations in the water around the shark. See the Wikipedia page for more information.
And for the sake of completeness (already quite nicely answered by @Susan in the comments), sharks do get cancer. All cures which are made from shark and claim to be able to treat cancer are pseudoscientific nonsense. This also endangers many shark species as they get radically overfished. See references 9 and 10 for more details.

References:

Smell and Taste
The Function of Bilateral Odor Arrival Time Differences in Olfactory
Orientation of Sharks
Microspectrophotometric evidence for cone monochromacy in sharks.
Vision and a Carpet of Light
Hearing and Vibration Detection
Functional anatomy of the auditory system in sharks and rays
The Shark's Electric Sense
Electroreception
Mythbusting 101: Sharks will cure cancer
Shark cartilage, cancer and the growing threat of pseudoscience.

Excellent information. Is cancer in sharks rare? If an animal has some type of 'function' like the Ampullae of Lorenzini that 'uses' weak electric fields could this de-stabilize pre-cancerous cells that are already unstable to some extent.

As far as I am aware, cells are not destabilized by weak electromagnetic fields. This is different for high energy, but then we are talking about denaturating proteins.

Are they de-stabilized by microwaves or M.A.S.E.R.s?


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What's the difference between growing cells in culture and cloning them?
The wikipedia page on Hela cells refers to George Gey being able "to isolate one specific cell, multiply it, and start a cell line." Later it says, "In 1955 HeLa cells were the first human cells successfully cloned."
What's the difference between multiplying the cells and cloning them? How is multiplying not cloning?

Clones are genetically identical daughter cells from one parent cell. So when you start you culture from one cell, all new cells are clones of this cell.
The first three cells (red, green and blue) undergo clonal expansion.

If you multiply cells in cell culture you usually start with thousands of cells, as this can be seen in the second part of the figure. These cells are not genetically identical, as they individually collect mutations. So the daughter cells of each "starter cell" (a lot of them) in the mixture are technically clones, but the whole culture is not seen as clones. See also the Wikipedia on this topic.

Ok, makes sense. So when the Wikipedia article refers to "isolating one specific cell" and multiplying it, is that just cloning?

Yes, that would be cloning. If you make a very high dilution of a cell suspension so that you can grow cells on a solidified growth substrate, then every daughter cells which derives from a single cell is a clone.


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How many RNA-binding proteins can simultaneously bind on a single mRNA?
Typically, how many RNA-binding proteins can simultaneously bind to a single mRNA?
Or said differently, how many "binding sites" does an mRNA have?
What order of magnitude?
I am interested in RNA granules like stress granules or P-bodies. They contain, inter alia, mRNA and RNA-binding proteins. I am not a biologist and I didn't come across this information so far in the related literature.

In what kind of cells? Bateria or eukaryotic cells?

Both kinds can be of interest to me, as long at is relevant to RNA granules.

See this paper. They have studied RBP-protected sites in the entire human transcriptome by RNA-protein crosslinking followed by RNAse digestion and sequencing: PIPseq.
Figure 1 of the paper shows distribution of protein protected sites in RNAs. They also correlate it with different regions of mRNA and its expression.
They show number of protein protected sites (PPS) per transcript but that is not a proper metric in my opinion. The number should be normalized with transcript length so that you get density of protected sites. From figure 4 (see below) you can roughly estimate that average PPS density is close to 0.6 which means that 60% of any RNA is expected to be protein bound.

Figure 4

Other points to be noted:

Highly translated mRNAs will have multiple ribosomes on their CDS and
are likely to be more protected.
Sequestered RNAs in stress granules will also have high density of PPS
Footprint of different RBPs will be different. So number of proteins that can bind to a mRNA will differ between different RBPs.

Further reading:

http://dx.doi.org/10.1186/gb4153
http://dx.doi.org/10.1016/j.cell.2012.04.031
http://dx.doi.org/10.1016/j.molcel.2012.05.021

HTH :) You can also have a look at ribosome profiling -  sequencing experiments.

@David I added some more links to studies on RBP binding sites


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Fruit colour related to the dissolving of pectin
What does the dissolving of pectin have to do with the colour of a fruit?

During ripening, pectinases are produced which break down pectin and render it soluble. Color change is also associated with fruit ripening.
Hence the correlation.

So there is a correlation but no causation?

yes as it seems. Both are an effect of ripening. Chloroplasts differentiate and lose chlorophyll and other metabolic changes cause pectin hydrolysis along with other things such as increase in sugar content etc.


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What's the evolutionary reason behind decussation?
A bunch of stuff in the human nervous system decussates. Optical information inputs from the eyes cross over in the optical chiasm. Multiple sensory and motor pathways cross-over before ascending the spinal chord or within the brain stem.
What's the current hypotheses being explored for justifying this anatomical phenomena?

Related: http://biology.stackexchange.com/questions/3807/why-do-the-two-hemispheres-of-the-brain-control-the-opposite-sides-of-the-body/3835#3835

I don't think it is a clever thing to group all types of decussation and look for a general explanations. I would tend to think that different decussation have different explanations. It is like asking what are the hypothesis to explain evolution of body size. There is no general answer to that but only a list of case specific impact of different factors on body size (see this post). Consider the two case-studies 1) "why does left brain controls the right part of the body" and 2) "Torsion in gastropoda" as examples of how different explanation applies to different decussation.
why does left brain controls the right part of the body?
See @shigeta's answer to this post. It is very interesting.
Torsion in Gastropoda
Torsion in Gastropoda is an interesting case. In this lineage individuals undergo some torsion during their development. This wikipedia articles say:

Snails are distinguished by an anatomical process known as torsion, where the visceral mass of the animal rotates 180° to one side during development, such that the anus is situated more or less above the head. This process is unrelated to the coiling of the shell, which is a separate phenomenon. Torsion is present in all gastropods, but the opisthobranch gastropods are secondarily detorted to various degrees.[13][14]
Torsion occurs in two mechanistic stages. The first is muscular and the second is mutagenetic. The effects of torsion are primarily physiological - the organism develops an asymmetrical nature with the majority of growth occurring on the left side. This leads to the loss of right-paired appendages (e.g., ctenidia (comb-like respiratory apparatus), gonads, nephridia, etc.). Furthermore, the anus becomes redirected to the same space as the head. This is speculated to have some evolutionary function, as prior to torsion, when retracting into the shell, first the posterior end would get pulled in, and then the anterior. Now, the front can be retracted more easily, perhaps suggesting a defensive purpose.
However, this "rotation hypothesis" is being challenged by the "asymmetry hypothesis" in which the gastropod mantle cavity originated from one side only of a bilateral set of mantle cavities.[15]
Gastropods typically have a well-defined head with two or four sensory tentacles with eyes, and a ventral foot, which gives them their name (Greek gaster, stomach, and poda, feet). The foremost division of the foot is called the propodium. Its function is to push away sediment as the snail crawls. The larval shell of a gastropod is called a protoconch.

You can find more information there


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Open Source Variant Caller comparable to GATK Haplotype Caller?
Is there a Variant Caller comparable algorithmically and in performance to GATK Haplotype Caller but Open Source Compliant (non-restrictive use)?

You could also try asking on http://biostars.org.


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How do I put on a labcoat?
Let's assume I am wearing a labcoat for two reasons:

Prevent the various bacteria, proteins, skin cells and substances on my clothes and my skin from contaminating my experiments.
Prevent various dangerous things from the experiment getting on me, and ruining my clothes or endangering my health (eg. toxic chemicals, pathogenic bacteria, ecotropic virus, etc)

A labcoat is an imperfect, but valuable barrier against such hazards. Perhaps a droplet of some Nasty Substance™ ends up flying towards my arm, but instead of getting on my exposed skin, hits my labcoat.
However, what happens when I take off my labcoat? My gloves, which have just been in contact with lots of Nasty Substance™, go through the sleeves of the coat, possibly smearing the substance all over the inside of the fabric. When I put on the coat again the next day, now my skin is in contact with these smears.
I could remove my gloves before taking off the labcoat, to avoid this smearing. But this time, I have to touch the labcoat with my bare hands as I remove it. Remember the Nasty Substance™ that was stopped when it splattered on the outside of the fabric instead of my skin? What if I know end up touching that?
I know that for truly dangerous conditions, there is specialized equipment and detailed procedure. Even at BSL2+, traditionally disposable labcoats are required, rendering the issue somewhat irrelevant. So let's assume the highest level below that, BSL2, as the context for answers.
In short, what is the correct way of putting on and taking off gloves and non-disposable labcoat when working in BSL2 conditions?

I use a labcoat when working with RNA or Iodine-125. I always do labcoat first, then gloves. When taking the coat off, I remove gloves first, then labcoat. This is usually sufficient, but if you're working with stuff nasty enough to matter, the coat won't provide protection for long. If it's acid, get the coat off ASAP before it soaks through. If it's biological you probably should have been working in BSL3 or 4 conditions. If you're working with something bad enough that a few drops on your labcoat will hurt you, your labcoat is not proper protection.

Wear two sets of gloves.  First, use nitrile gloves, not latex for this. 4mm or thicker is a specification I would recommend to avoid tearing.  Latex will bind too well to itself and tear easily with increased friction etc (same logic behind not using two condoms).  Also, use a coat with an elastic cuff on the sleeve.
So here's the breakdown

Put on first set of gloves
Put on coat over gloves.  Decon if needed for application.
Put on second set of gloves.
Science
Take off second set of gloves.
Decon as needed for your health
Take off coat
Take off first set of gloves

I can find sources for this, but I've been doing ABSL2 and BSL3 for a while, and they always go through this in safety training.
Edit: My internal nagging to site got the better of me, so some examples that recommend double gloving:
http://oehs.vcu.edu/chemical/labsafe/perchloricacid.pdf
https://extranet.fhcrc.org/EN/sections/ehs/hamm/chap3/section6.html
http://orsp.umich.edu/policies/um/committees/BRRC/ADDITIONAL_PRACTICES_revised_8_7_14.pdf
http://ehs.columbia.edu/carcmutguide.html
I could go on, but I think you get the idea.

I would say that double gloves are overkill for BSL2. Above that level I would agree, but they are causing some problems and inconveniences, too. So I would do lab coat first, then gloves and vice versa. And make sure that you put the lab coat in the laundry regulary or when something get spilled on it. It is also a good idea to have some (probably older) clothes in the lab available for changing if necessary.

@Chris I agree it's a bit overkill, but it is the correct way to handle the scenario described.  It can also be used in BSL2 conditions where there are chemical concerns on top of biological ones.  I think the "I'm worried about a drop" scenario is only likely to be an issue with chemical concerns (but is actually unlikely altogether).  I would be curious to know if there are more users of BSL3 and higher or chemicals which require double gloves. I lean towards chemical, but that's just a guess.

I would say it really depends on the chemicals. Chloroform breaks through almost all gloves used in the typical biology/biochemistry lab, phenol gives a little more time.

The National Academies Press publishes reports on lab safety http://www.nap.edu/search/?term=Lab+safety PDF downloads are free. Chapter 1 of Safe Science; Promoting a Culture of Safety in Academic Chemical Research reads like the script for a horror movie of what can and does go wrong in and academic lab setting.


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Just how dangerous is ethidium bromide?
A common precaution for preparing EtBr-agarose gels is to add EtBr only after the gel solution has cooled somewhat, because EtBr is a dangerous mutagen. Supposedly, adding it to a hot liquid allows EtBr vapors to get into the air and everyone's lungs, where it can act as a carcinogen.
In addition to this are commonly seen special procedures for handling EtBr vials and gels (fresh nitrile gloves, avoid contaminating other work areas, special waste disposal rules).
However, there's also some saying that EtBr isn't all that mutagenic and all this care is over the top.
What's the reality? Just how dangerous is EtBr, especially in amounts used at a typical biological lab? How long does the danger persist? Are even trace amounts hazardous (for instance, touching a "clean" pipette without changing gloves after working with EtBr)?

I've heard that you shouldn't put EtBr in hot agarose to prevent degrading the dye in the heat.

I also believe you loose intercalate abilities if you break it down with heat.  Thus I don't think the risk is vaporized EtBr in the steam.  It might be a carcinogen/mutagen given that it intercalates DNA so well, but I think it's toxic effects are more substantiated.  With proper PPE you are at little risk.  I certainly wouldn't bathe in it.

Cows are injected with the stuff in quantities thousands of times higher than are used in a lab without any ill effects.  That said, you're probably not a cow, so you might as well wear gloves.  Being overly cautious isn't going to hurt anyone, and contaminating someone else in the lab because you're not concerned about what is probably a very low level risk is inappropriate.

Oh it is not that dangerous as its current image. Pouring hot gel has another problem too; it damages your gel tray and combs. I guess EtBr is not that volatile (MP=260 deg C) that it will fume in a hot gel @ 70deg C.

I usually find the treatment of Ethidium bromide in the lab widely exaggerates the true dangers of this chemical.
It is not really toxic (the LD50 is 1.5 g/kg bodyweight, as a comparision NaCl has a LD50 of 3 g/kg). It has also only been shown to exhibit mutagenic potential to bacteria after it had been treated with liver extracts. This means that some of the metabolized products of EtBr in the liver are mutagenic, but EtBr itself not. See reference 1 for details here. It is also not classified as a cancerogenic substance by the regulation bodies (for example see the National Toxicology Program of the US on Ethidium bromide).
As already mentioned, it is used to cure Trypanosoma infections in cattle (reference 2). Here up to 1 mg/kg bodyweight are given, with no signs of toxic or other adverse effects. The typical concentration used in the lab to prepare gels is 1 μg/ml. It works as a drug by interfering with the mitochondrial DNA (changing it to the Z-form, which is not available for replication). See reference 3 for details. Ethidium bromide also acts as a Topoisomerase I inhibitor as other chemotherapeutic drugs. See reference 4 for more details.
Additionally, EtBr is negatively charged and cannot enter cells or the nucleus, since cannot pass the membranes. I would wear gloves and also apply the usual safety rules when working with gloves (do not touch anything you don't need to touch, especially things like door knobs, keyboards or phones as you might spread contamination) dispose your gloves when not needed anymore and you should be fine.

References:

Detection of carcinogens as mutagens in the Salmonella/microsome
test: assay of 300 chemicals.
Comparison of isometamidium chloride and homidium bromide as
prophylactic drugs for trypanosomiasis in cattle at Nguruman, Kenya.
A low dose of ethidium bromide leads to an increase of total
mitochondrial DNA while higher concentrations induce the mtDNA 4997
deletion in a human neuronal cell line.
The geometry of DNA supercoils modulates the DNA cleavage activity
of human topoisomerase I

The dangers of this compound are wildly exaggerated but like @chris said, the dangers aren't completely known. I wouldn't recommend shaving with it. I think the deep red color actually is what  heightens people's curiosities and fears most.

I wouldn't recommend this either - and I recommend wearing gloves when handling it. But besides that, irrational fears and actions are really not necessary.

Inspired by Jason Patterson's comment, I looked up "ethidium bromide cattle" and found a blog post about ethidium bromide toxicity. Apparently ethidium is routinely used to treat sleeping sickness in african cattle at 1mg/kg without ill effects. All data concerning ethidium toxicity comes from in vitro tests that may not apply to in vivo use. You should still wear gloves, but don't freak out over it.
The blog post had some references, but most are dead links now. Here is the only working link left. Here's a review article on dye therapy for parasites.


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How does fluorouracil inhibit pyrimidine synthesis?
I was reading in my pharmacology textbook about fluorouracil, and my book mentioned that fluorouracil is an antimetabolite whose function is to inhibit pyrimidine synthesis. However, I was curious to know how exactly does fluorouracil accomplish this. Is this drug involved in a specific mechanism that enables it to prevent pyrimidine synthesis? If so, how?

Your cells produce thymidine by converting uridine using an enzyme called Thymidylate Synthase. 5-Fluorouracil irreversibly inhibits this enzyme.
Here is the structure of 5-Fluorouracil:
Here is the mechanism the enzyme uses to make thymidine:

It looks like the enzyme forms a bond to the uridine ring through a sulfur. 5-Fluorouracil probably inhibits the reaction at the next step because fluorine is much more electronegative than the proton it replaced. This makes it harder for the electrons on the double bond in step 2 to attack the folate. Might also inhibit step 3 because the fluorine won't want to give up its electrons to reform the double bond. Because 5-fluorouracil is stuck to the enzyme's active site, the enzyme can't perform its given duty of converting uridine to thymidine. Because you can't use uridine in your DNA, your cells don't have enough thymidine to copy the DNA and replication is slowed. If thymidine supplies are low enough, cells might die.


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Mutation-Selection-Drift Equilibrium
mutation-selection-drift equilibrium is one of the most important concept of population genetics. I could easily find the calculations for mutation-secltion equilibrium and for mutation-drift equilibrium but not for mutation-selection-drift equilibrium.

mutation-selection equilibrium
At mutation-selection equilibrium the expected frequency $p$ of a given allele is
$$p ≈ \frac{\mu}{s\cdot h}$$
, where $\mu$ is the mutation rate, $s$ is the selection coefficient and $h$ is the coefficient of dominance.
mutation-drift equilibrium
At mutation-drift equilibrium the expected frequency $p$ of a given allele is
$$p ≈ \frac{1}{4N\mu+1} $$
, where $N$ is the population size.
What is the allelic frequency at mutation-selection-drift equilibrium?

I think this paper might be relevant. From what I can see they derive an analytical approx for deleterious allele frequency in MSD equilibrium.http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1894624/

Drift doesn't change the expected frequency of alleles. In your equation for the mutation-drift equilibrium, I don't think that $f$ is an allele frequency -- it's the homozygosity.

"expected frequency f of a given locus is" are you sure this is correct? do you mean frequency of an allele rather than locus? According to Charlesworth & Charlesworth it should be $q^*$ which is the equilibrium frequency of $A_2$ the mutant allele

(I'm concerned with the definition not the notation - I've seen $f$ used elsewhere)

Oh I missed your comment for some reason. You are right "frequency of a locus" makes no sense. I corrected it. Also I replaced $f$ by $p$ as $p$ (or $x$) are more often used to represent allele frequency. Thanks

Maybe I wasn't clear in my previous comment -- I also was talking about the definition, not the notation. Your mutation-drift equilibrium equation is for the homozygosity at a locus, not the frequency of an allele. Drift does not change the expected frequency of alleles. So your first equation is valid for mut-sel-drift equilibrium... with one caveat: the actual equation you wrote down is just the strong selection limit of the exact equation, so if drift is too strong it won't be valid.

Oh I got the point. Can you develop your comment into an answer by clearly stating what are the expected homozygosity and allele frequency under the different scenarios of mutation-selection balance and mutation-selection-drift balance? Thanks a lot.


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Are the DNA codon mappings arbitrary?
I am a Biology novice so I apologize in advance if I state anything incorrectly....
My question is, are the DNA codon mappings arbitrary? I understand that the DNA code is made up of codons which each consist of 3 base pairs. There can be 64 codons which map to 20 amino acids (some are duplicated and others act as stop codons). So was there a reason why one particular codon mapped to one particular amino acid - or is the mapping completely arbitrary?
Thanks!

"the assignment of codons to amino acids seem to be an advantageous one (most likely not the optimal one)" - so why didnt the optimal one appear at random ?

The code is for RNA, not DNA. As a novice you need to understand this basic point.

There is no reason for why a certain codon came to represent a certain amino acid. But some reason is attributed to similarity of degenerate codons. Usually the degenerate codons only differ in their last (third) nucleotide. The corresponding first anticodon in tRNA usually bears a modified nucleotide such as inosine which can (promiscuously) pair with A, C and U.
You can see the wikipedia page on wobble base-pairing.

Evidence suggests that the correspondence between DNA codons and amino acids (i.e. the genetic code ) is not random. A good place to start with this interesting topic is the Wikipedia article about the genetic code, in particular, about its origin:

Many hypotheses on the evolutionary origins of the genetic code have been proposed. Four themes run through the many hypotheses about the evolution of the genetic code:

Here I summarize the four themes (adapted from wikipedia).

Chemical principles governing specific RNA interaction with amino acids.
Biosynthetic expansion. The standard modern genetic code grew from a simpler earlier code through a process of "biosynthetic expansion".
Natural selection has led to codon assignments of the genetic code that minimize the effects of mutations.
Information channels: Information-theoretic approaches models suggest that the genetic code originated as a result of the interplay of the three conflicting evolutionary forces: the needs for diverse amino-acids, for error-tolerance and for minimal cost of resources.

Other models combine some of these hypothesis.
Selected references:

The genetic code is one in a million. Freeland SJ, Hurst LD. J Mol Evol. 1998 Sep;47(3):238-48.
Selection, history and chemistry: the three faces of the genetic code. Knight RD, Freeland SJ, Landweber LF. Trends Biochem Sci. 1999 Jun;24(6):241-7. Review.

I see your point and have read some articles in this direction too. So as you say rare amino acids like Trp have less codons. But why a certain codon came to represent an amino acid is in my opinion a chance event. Just like any evolutionary process

So it sounds like there are a bunch of theories on how this codon to amino acid mapping came about - but none of these are supported by specific evidence - its all speculation. Is that correct?

@WYSIWYG, yes, evolution is random. But here the point is that some outcomes are more advantageous than others. In this case, the assignment of codons to amino acids seem to be an advantageous one (most likely not the optimal one) based on several considerations.

@MichaelScott, the many research papers on this topic present supportive evidence. As with any research trying to demonstrate the past, it is very difficult to find irrefutable evidence.


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How do animals handle light refraction in different media?
For a human, when diving underwater, everything is blurry because of the water's different refractive index compared to that of air, which we are accustomed to. How do animals, like turtles, seals or penguins, handle that difference when changing the medium? Are they nearly blind at surface and can focus underwater or the other way around? Can they adapt to different refractive indexes on the fly? How?

I guess that they are optimized for one particular environment. In the other they might have to rely on other senses.

It is more complicated than this, but... I don't think it has as much to do with the refractive index of water but rather the shape of our corneas and the loss of this shape advantage under water, for if the eyes are protected by goggles, one can see quite clearly underwater (much the same as a camera can, as the shape of it's lenses are not affected). Any change in the shape of the cornea changes the way light passes through the eye, and results in a change in vision. The following is from Ch. 9 Optics of the eyes of marine animals, from Light and Life in the Sea:

This is different for penguins (and turtles): the surface of their eyes, the cornea, is not as much vaulted as for humans (it's much flatter), and the lens is much rounder (meaning the shape can change more than our relatively flat lenses can), so the difference between air and water is not so big and the light isn't refracted too strongly. Also, the ciliary muscles (not to be confused with the pupillary muscles) holding the eye's lens (behind the pupil) are stronger, increasing their accommodation, so a penguin has a sharp sight in the water. Or as stated in A Survey of Vertebrate Strategies for Vision in Air and Water

Whereas the cornea is usually the major refractive element of the terrestrial eye, it is of little or no refractive consequence to an aquatic vertebrate.

See the difference in these four vertebrae groups (the first is man, the second is fish, the third is whales (similar to penguins) and the fourth is sirenians - manatees and dugongs)1:

Penguins.info
[1] Comparative anatomy and physiology of vision in aquatic tetrapods

This answer is great and seems feasible. Thank you!!! So in a nutshell: The effect of light refraction in different media is only a problem for beings with very convex corneas an flat lenses. Does this mean that e.g. Penguins have a sharp sight inside and outside of the water because of their ability to bend their lenses much more than humans could do. Thus, making their visual system far superior. Or are there some disadvantages with a flat cornea-design?

No, you have it precisely correct. Their lens does all the work. They can see well in or our of the water because their cornea has little to do with their vision.

Nice answer.. But the refractive index does have a role and the convexity of the lens as you rightly explained corrects for it. I had read about fish's highly convex lens but was not aware of diving animals having a flexible lens.


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Why proteinase K doesn't degrade itself?
Can anyone tell me why proteinase K doesn't degrade itself?
If possible please provide me the source.

Are you asking about in vitro or in vivo?

According to invitrogen proteinase K does undergo autolysis, but that some leftover fragments still have protease activity. The solution should be stored at -20C, this low temperature is probably the best way to prevent autolysis. If you're using the enzyme to digest protein at 37C, you'll just have to deal with losing the proteinase k during the reaction and make sure you add enough to destroy the target protein before the proteinase is depleted.

Proteinase K is sensitive for autolysis. The enzyme is stabilized by the presence of calcium ions (which bind to the protein). Absence of calcium promotes autolysis of the enzyme and also reduces the half life of the enzyme activity. The most likely reason why most researchers never notice an substancial effect of autolysis is that this takes around 48h to get noticed, while the most proteinase K digest take only a few hours. For details read the following paper:

The enzymatic activity of proteinase K is controlled by calcium


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What equation to compare protein isoforms in a Western Blot?
The protein isoforms I am interested in comparing appear as distinct bands on the gel I have already run. I have an Excel sheet with optical density measurements I obtained using ImageJ; it looks something like this:
Lane    Iso1       Iso2       GAPDH
1       149.06     194.646    893.08
2       832.654    494.473    148.335
3       49.998     490.539    147.361
4       29.347     208.53     120.652

For the other proteins I've analyzed so far, I've been computing fold-change relative to my loading control, GAPDH, with the following equation:
Fold-Change = Log2(Protein/GAPDH)

I'm not sure how best to compare my isoforms to each other and considering the following two equations:
1. Fold-Change = Log2[(Iso2/GAPDH)/(Iso1/GAPDH)]

2. Fold-Change = Log2(Iso2/Iso1)/GAPDH

I've already computed both of these values for all my samples, graphed them and found that the resulting graphs look pretty different. Which of the two equations do you think is a better way to compare the relative quantities of these proteins?
Alternative equations are also welcome.

Are your lanes replicates ?

No: each lane was loaded with a different sample.

Now see, the problem here is that in the first equation your GAPDH normalization factor is lost. So finally there is no normalization.

Could you explain more fully how the normalization factor is lost?

Oh, now I see that dividing the numerator and denominator by the same value cancels that value's impact on the final answer.

In my opinion you should use this formula:
$$ \frac{\text{log}_2(\text{Iso}_1/\text{Iso}_2)}{\text{log}_2(\text{GAPDH})} $$
This will normalize the relative fold differences between the isoforms with the loading control- GAPDH.
Since both numerator and denominator are log transformed they are in comparable domains unlike the formula-2 that you mention in your question. This is just a modified formula-2.