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Origin of term ‘confluency’ in cell culture
Since as long as I have been doing cell culture, the word confluency has been used to describe the percentage growth of cells or area covered by them. However, no dictionary that I have found uses this word. I was wondering if anyone could reliably state where the meaning comes from or how the association began, and truly what it means. I don't believe I can post this on another Stack Exchange  because the word doesn't have even a resembling meaning in the dictionary. Cell culture is such an integral part of cell biology, medical research and biological manufacturing. And this term is an integral part of cell culture. I was surprised to be unable to reliably verify its meaning.

I think that's a fair and sensible guess.

Besides the etymologic explanation that @aandreev gave, in cell culture this term is commonly used to describe the density of adherent cells and it is used as a measure of their proliferation. It is usually combined with an estimated (or counted) percentage, so 10% confluency means that 10% of the surface the dish or flask used is covered with cells, 100% means that it is entirely covered. The cells grow twodimensional on the surface of the flask in this case. The picture below (from here) illustrates different levels of confluency:

The level of confluency is important as the cells change their growth with changing densities. Low density cells (10-20%) usually grow slower than 50% confluent cells. If the plate is complete grown by cells, they tend to grow much slower again. This influences their genetic program, behaviour in experiments and transfections.
As @Roland pointed out it is important to say that confluency is not a hard measure, but rather an estimate of the cell density. Different people will get different estimations, but the trend should be the same.

Chris thank you thorough answer, any thoughts on the etymology of the word as used here other than @aandreev above?

@rhill45 Confluence means coming together. It actually does not mean how dense the culture is but this word has been used for several ages now for what Chris has said in his answer. Perhaps this term came from Dictyostelium (this is a wild wild guess)

@rhill45 I think aandreev's answer about the etymology is right. I don't know any other.

This is good answer. I would add though that the % confluence (area covered) is actually pretty hard to estimate by eye, since cultured cells often change size and conformation as they grow more dense. Different people typically give different estimates from the same image (I'm not sure that last one is 90%, for example :)  So confluency numbers are rather unreliable.

@Roland Thanks, this is a good point. I will add it.

@rhill45 — for the record, I think that is not an etymology, as I explain in my comment to the answer in which it occurs.

con- (com-) is prefix that usually means "togetherness", joining. Root fluency/fluent comes from latin fluere, to flow.
Source: Google's definitions for con- and fluency (information scraped from OUP).

Although this is a reasonably analysis of the meaning of the two components of the word confluency it is not a definition from any dictionary as the word does not occur in any dictionary. In my opinion it is invalid as etymology (the origin of a word and the historical development of its meaning) as the word is either a corruption of confluence or (more likely perhaps) a recent formation from the adjective confluent. Neither of these words are derived from fluency in English as explained in note [2] of my own answer.

The word confluency is a variant of the word confluence, although this variant only appears with any frequency in the context of cell culture [1]. The word confluence itself appeared in the fifteenth century and is derived from the Late Latin confluentia meaning “a flowing together” [2]. In English it was initially used for the flowing together of two or more streams, but acquired a large variety of more figurative meanings [3].
The word confluence (but rarely confluency) occurs in various biological contexts in the first half of the twentieth century [4], but the first example I can find in relation to monolayer cell culture is in 1961 [5], although the term confluent appears in the 1950s [6]. The form confluency seems to have appeared at about the same time as confluence [7]. Since the 1960s both forms have been used by different authors, currently with comparable frequency [8]. Some authors employ either one or the other exclusively, others use confluency when indicating a percentage designation and confluence to indicate the absolute concept — or vice versa [9].
The reason that confluency is not defined in general dictionaries (or even in the Oxford Dictionary of Biology [10]) can only be surmized. None of the online dictionaries I have consulted [11] give the cell culture usage as an example of confluence, suggesting that its use is less frequent than in other technical contexts, where the meaning is similar. With this usage of confluence not being thought to merit separate mention (irrespective of the importance or otherwise of cell culture) then the need to define an alternative form would not have arisen.
It should be added that there is there is a Wikipedia entry for confluency [12] but, despite its title, this uses the term confluence in its definition:

“In cell culture biology, confluence refers to the percentage of
  the surface of a culture dish that is covered by adherent cells. For
  example, 50 percent confluence means roughly half of the surface
  is covered, while 100 percent confluence means the surface is
  completely covered by the cells, and no more room is left for the
  cells to grow as a monolayer.”

Notes
[1] The hits reported by a Google Book ngram for the word confluency between 1800 and 1954 were analysed individually, as journal results from ngrams often have erroneous dates. There was one example (1829) of its occurrence before 1900, and 13 before 1950, about half in relation to vaccines or biological phenomena.
[2] The etymology of confluence given in the online etymological dictionary is:
early 15c., “a flowing together, especially of two or more streams,” from Late Latin confluentia, from Latin confluentem (nominative confluens), present participle of confluere “to flow together," from assimilated form of com “with, together” (see con-) + fluere “to flow” (see fluent).
I would emphasize that the word confluence is not a compound formed in English by adding a prefix to the word fluency, but derives from the compound word, confluentia, already evolved in Late Latin (i.e. by the sixth century).
[3] The Oxford English Dictionary quotes an early instance of the extension of the meaning of the word confluence (1606) as “In this confluence of so many prosperous successes”. A variety of examples, appearing to come from the fields of politics, philosophy and mathematics, can be found in the Cambridge Dictionary online for its second definition of confluence, “a situation in which two things join or come together”.
[4] This can be seen by going to the websites of some of the older biological journals (e.g. Journal of the National Cancer Institute or the Journal of Experimental Medicine) and searching for the word confluence.
[5] 1961 Yearbook of the Carnegie Institute of Washington (p.66).
[6] For example W.R.Earle (of Earle’s saline) uses it in a paper on the growth of fibroblasts in 1951, and T.T.Puck  (of Puck’s saline) uses it in a 1958 article in Experientia. The earlier use of confluent (also of 15th century origin) in relation to monolayer culture suggests that the word confluency, rather being a corruption of confluence, may have been formed from the adjective — perhaps in ignorance that a noun form already existed.
[7] Königsberg et al. (1960) J. Biochem. Biophys. Cytol. 8 333–343.
[8] There seems to have been division at the outset. In the US, Harry Eagle and Renato Dulbecco used the term confluency, whereas Howard Green and George Todaro used confluence. What one might refer to as the Glasgow school always used confluence: John Paul) at the Beatson Institute and his student Ian Freshney, both authors of influential books on cell culture. The more recent frequency of use may be judged from a Google ngram for “cell confluence v. cell confluency”.
[9] Searching for confluence in the Journal of Cell Science and examining recent issues brings up results for both confluence and confluency. This recent paper uses confluence exclusively both as an absolute concept and as a percentage, whereas this recent paper, for example, uses confluency exclusively in both absolute and numerical senses. Another paper refers to confluency, but to 70% confluence, but exactly the opposite is found in this paper which refers to confluence, but 70–80% confluency. Some papers — e.g. this alternate at random. The editors of the journal obviously do not care.
[10] The Oxford Dictionary of Biology has nothing between the entries for cone and confocal.
[11] Collins, Chambers, Cambridge, Lexico or Merriam-Webster.
[12] Wikipedia entry for confluency.

If this seems a little over the top, it was my time that was spent. I don't think it was wasted as demonstrates how one can use search indexes of various sorts to try to trace the history of biology. This overturned my previous view of the term which I had expressed in a previous answer that I decided to delete.


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How Fast can the Electrochemical Gradient on a Neuron be Reestablished?
The electrochemical gradient of Na+, K+, Ca2+, and Cl- between the inside and outside of a neuron is vital for its function. When a neuron fires, this gradient reverses. How long does it take for the gradient to be re-established?

Does this answer your question?: https://biology.stackexchange.com/q/57064/27148 Gradients don't reverse during an action potential, only permeabilities chance substantially. Yes, a few ions do move and pumps are needed to restore concentrations, but it's very few ions.

Also https://biology.stackexchange.com/a/76167/27148

Thanks for the clarification. Although I knew the voltage change, I didn't realize how few ions are actually needed to cause that change. If you post an answer saying the same thing I'll pick it as correct.

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Which will produce more oxygen? A few large trees or a greater number of smaller plants?
In a given area A, we have two choices -
(i) we can plant maximum number of trees (which are larger in size) possible in A, say m
OR
(ii) we can plant maximum number of plants (which are smaller in size) possible in A, say n
(evidently m will be smaller than n)
Which choice will yield more amount of oxygen?
It can be assumed that the total number of leaves capable of Photosynthesis is N and is same for both the cases.

The largest amount of Carbon-di-Oxide to Oxygen conversion in the world is done by single celled ocean phytoplankton (I think I saw in some documentary)

Hard to plant them on land, though :-)

I once read a study (but I don't remember the reference) that shows that you need a diversity of plants of different size to maximize the rate of oxygen production. I think, the rational behind this observation is that having a diversity of plant size increases the surface contact between leaves and air.

Welcome to Biology S.E! If you need additional assistance, please visit The Help Center. This looks like it maybe a homework question; if it is then please show any work you have already done or what you think the answer may be.

@Remi.b It could also reduce intraspecific competition.

@L.B. I don't see from which angle it appears as a H.W. problem to you. I thought of this question long back, as an optimization problem. But I could not think of a solution, since I thought I lacked some specifics which might be important inputs from biological view-point.

@DevashishSingh Okie, my apologies! I was concerned that it was due to the wording.

one word, algae.

It's hard to generalize, you need to experimentally determine it.

Ignoring parameters such as:

Leaf shapes
Difference in photosynthetic efficiency due to other metabolic factors
Unequal illumination of leaves
Nutrient content of the soil

Photosynthesis rate of a plant1 depends on the [total number of leaves] × [surface area of a leaf].
Assuming that a tree occupies same ground area as a shrub, there will be same number of trees as shrubs.
A tree is taller and can bear more number of leaves and if we assume that the surface area of the leaves are similar between trees and shrubs then the tree would carry out more photosynthesis.
However you say that the number of leaves is the same; in this case both will carry out same amount of photosynthesis (the shrub may outlive the tree though, as the latter won't be able to support its huge size with same level of photosynthesis as the shrub).
A note on phtoplanktons and algae: One reason amongst a few for why they are efficient at photosynthesis is because the number of photosynthetic cells per volume is higher in them.

1 I am using the term plant to denote all plants. Big trees are called trees and small plants are called shrubs, for convenience.

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What would the RBCs of someone heterozygous for sickle cell anemia look like?
Would half of the RBCs look normal, and the other half sickled?
Or would all of the RBCs have slight deformation/sickling?
Thanks!

The peripheral smear in a patient with sickle cell trait typically appears normal (see Cecil Medicine Ch. 166). Each cell has only 30-40% HbS, and so the polymer that causes the sickling doesn't usually occur.  You can find some examples online of smears with target cells and maybe one sickled cell, but these are the exceptions to the rule. This is one of the reasons a smear is not a good screening tool for sickle cell trait.
To clarify, RBCs in the blood of a patient with sickle cell disease aren't all abnormal either. See this smear from this case published on the NEJM blog:

Again, this is sickle cell disease, not trait, and you see many normal RBCs, even from this patient (honestly, it's not clear whether this is that patient's smear, but this would be typical). In sickle cell trait, the smear would likely be normal (image from webpath tutorial at the university of utah):

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Can you eat cancer cells without risk?
Afaik GMO products are not a real risk to health of course if they do not contain toxins.
But how about cancer cells? Like say rhabdomyosarcoma which is more or less a muscle cancer found also in cows.
Likewise, meat breweries use stem cells, but wouldn't cancer cells just grow faster?

Cancer cells themselves are not effective transmissible agents of disease in humans. Unlike infectious pathogens, there is not a suitable receptor for adhesion at an exposed or accessible site, a suitable environment for replication, and adaptions for immune escape by the tumor cells. There are exceptions in other species: tasmanian devil, dogs, and clams. Importantly, in all of these cases, transmission to another species has not been demonstrated. Eventual transmission to another clam species may be more likely to occur, though, because, unlike vertebrates, they are not known to have a self/non-self recognition system.
Humans, though, do have a self/non-self recognition system.  Even if we ignore the requirement for receptor binding and invasion, consider what happens when cells from another species, and even another human, are surgically implanted. Without immunosuppression, these non-self cells are rapidly attacked and destroyed.
With immune suppression and surgical implantation, though, you can see transmission of cancer. Donor-related tumors in transplant patients are still rare, though the low frequency of transmission may be due, in part, to screening. The fact that we see this at all demonstrates the significance of transmission route and immune escape.
Cancer cells do, of course, metastasize within a single human individual. In order for a tumor seed to successfully metastasize it does need to evade the immune system, find an environment suitable for replication and adhesion. This, however, requires tumor associated cells, non cancerous cells that regulate the microenvironment to make it favorable for growth and replication. You can read about them in Hanahan and Weinberg's 2011 review.
The requirement for tumor associated cells and a permissive microenvironment might be why, in a problematic series of experiments at Sloan Kettering in the 50s, when subjects were inoculated with tumor cells, the procedure resulted in growth of the new tumor, recurrence after excision, and death in some cases where the subject had pre-existng cancer. Transplantation into healthy subjects (yes, they did this) resulted in nodules that spontaneously regressed. This experiment has since been interpreted as evidence for immune system control of transplanted tumor system in healthy individuals, as compared to growth and progression in a receptive niche in a cancer patient. In this example as well, you have eliminated the need for a natural mechanism for adhesion and invasion, and these are same species cells.

HeLa cells (which are of course derived from a cervical cancer) have actually been injected into humans to see if they would grow; they grew briefly but were promptly rejected. Similarly, surgeons have on occasion accidentally stabbed themselves and inoculated themselves with the human tumors they were operating on.
Injecting human cancer cells is a far greater risk than eating non-human cancers, and even in that case the risks seem to be very low.
There have been rare cases of people with profoundly suppressed immune systems (organ transplant recipients) allowing a transferred tumor to grow, so (though of course the risk there is vastly higher than merely eating a cell) it's not completely impossible.
Pragmatically, it's very likely that everyone who's eaten, say, chicken has unknowingly consumed some chicken tumors.


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Polar renal scarring in pyelonephritis?
Why does infection and scarring occurs at poles in Vesicoureteric reflux but not in Obstructive pyelonephritis?

It is said in Robbins that, it is due to polar papillae being flattened or concave unlike convex lateral papillae, but why is it not the case in obstructive pyelonephritis?
Also why polar papillae are not convex?

It's more an issue of the extent of reflux than anything else. If you look at the data on scarring, you'll see that grade III and IV VUR present with lateral scarring as well. So, any pyelonephritis that is associated with gross dilation of the ureter and collecting system will give diffuse scarring. Mild dilation, you'll get scarring where the reverse flow goes first. I can't answer the question about why the reverse flow goes to the poles first. The authors of the paper I linked have their own speculation. Robbins has another. Neither have evidence on the mechanism.


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Why don't allergies cause fever?
Allergy
To my understanding, an allergy is a hypersensitivity of the immune system causing a substance in the environment to be identified as pathogenic by the immune system while it is not pathogenic. During an allergic reaction, the immune system triggers histamine, which triggers an inflammatory response just as if the allergen was a pathogen. The resulting symptoms of an allergic response is similar to the symptoms of a cold but without fever.
Fever
To my understanding a fever is an increase in body temperature driven by the body through production of pyrogens, most often in response to a pathogen. This response might be adaptive for various reasons that I am not too interested in discussing here.
Question
According to NIH, an allergic response never causes a fever. Given that the fever is not directly caused by the pathogen but rather is caused by the body, why do allergies not cause fever?
The fact that allergies don't cause fever give me the weird impression that the immune system somewhat "understand" the allergen is not pathogenic otherwise the immune response would be the same in the case of an allergen or a pathogen.
Un-educated guess
Allergic responses implies the firing of IgE. IgE are typically involved in response to parasites such as helminths. Could it be that pathogens leading to an immune responses mediated via IgE never yield to fever. Why would it be the case?
Plasmodium falciparum (which causes malaria) is a pathogen who causes an immune response involving IgE (according to the wikipedia). Malaria's symptoms include high fever (according to Mayo Clinic). Now it would be possible that the pyrogen would be of external origin (not produced by the body but by the pathogen) or it is possible that several immunoglobulin are involved in response to P. falciparum. The same logic hold for Fasciola hepatica (an helminth; common liver fluke) who also causes fever and is who's infection lead to the firing of IgE.

The short answer seems to be that fevers help combat microbes (a term I take herein to include viruses for brevity), which aren't a part of the threat addressed in an allergic reaction. While there's not a full consensus on which benefits, if any, a fever brings to the response to microbes, both humans and other warm-blooded vertebrates fare better with infections when a fever is present.
Fevers appear to mobilise leukocytes and enhance their phagocytosis while suppressing endotoxin effects (see Craven, R and Hirnle, C. (2006). Fundamentals of nursing: Human health and function. Fourth edition. p. 1044) and proliferate T cells (see Lewis, SM, Heitkemper, MM, and Dirksen, SR. (2007). Medical-surgical nursing: Assessment and management of clinical problems. sixth edition. p. 212), rather than mobilising basophils.
Higher temperatures are also more damaging to at least some pathogenic cells than the body's own, as they are typically smaller with higher relative surface area. Note this also explains why fevers wouldn't be as natural a response to such large parasites as helminths. (Even their cells, being eukaryotic, are comparable to human cells.) It is unsurprising that IgE would be a more specialised response, found only in mammals.
On the subject of malarial fever, for which the pathogen is relatively large because it is eukaryotic, there is ongoing research into both the mechanism and function of this fever. It seems to be Plasmodium itself that creates and presumably benefits from the fever, not the host. I'll discuss the evidence in a moment, but note this means the "endogenous fevers follow suspected small pathogens" hypothesis is unthreatened.
According to this 2013 paper, the timing of such ruptures may (I stress may; the paper discusses the uncertainty around a number of ideas about this) serve the function of controlling the time at which the immune response is most active, so the reproductive cycle is unaffected. According to this 2007 paper, the malarial parasite's hemozoin causes the disease's characteristic fever following erythrocyte rupture. The same paper mentions that the timing of the fever has been used as a diagnostic criterion for malaria, and the 1927 Nobel Prize for Medicine was awarded for the now discontinued treatment of syphilis with a malaria-induced fever.

By the same logic, the body doesn't need to "combat" peanuts, pollen, or cat hair with an inflammatory response, yet it does for people with allergies to those things.

@mgkrebbs I'll admit the immune system has to be imperfect whatever explanation one advances, but I think the evidence suggests allergens are mischaracterised as poisons or toxins rather than as pathogenic microbes.

@J.G. I don't think this answer adds much beyond the background already contained in the question - can you provide some citations?

In light of the reference-seeking notice (whose posting I welcome), I've edited my answer to directly reference the relevant primary literature, although in some cases this is a book or a possibly paywalled link.

@BryanKrause Whether or not my answer "adds much beyond the background", I think any answer needs to see the real question to be not "Why do allergies that don't warrant fevers still happen?" but "Given that allergies are clearly a mistake, why aren't they the same kind of mistake they would be if they were feverish?" Adverse reactions to vaccines, which can be feverish, are the microbe-detecting mistake type.

Malaria, which is caused by a helminth, is causing high fever though. I edited my question to add some info on the subject in the "un-educated guess" section.

@Remi.b Since when is Plasmodium a helminth? I can find any number of interesting papers on the interaction between infection types in their shared regions of prevalence, but no evidence Plasmodium is a helminth.

Sorry, I corrected that. According to wikipedia, an infection by P. falciparum lead to the firing of IgE. I wrongly concluded that Plasmodium was an helminth. I added the common liver fluke who is a helminth and cause fever (according to wiki).

@Remi.b I've added a discussion of malarial fevers to my answer, but I couldn't find anything useful on the possible causes of fevers in liver fluke infections. My guess is this may have a different cause again, possibly linked to bile duct infection.

@BryanKrause Please review whether recent edits have addressed the concerns of the notice you posted. I'm sure there's room to improve this answer further, but I'm not sure what, if anything, still needs a reference or citation added.

@J.G. I still don't feel like your answer addresses the actual question in the OP, it's mostly about why fever is useful against some pathogens plus some added speculation. I'll remove the notice, however, because the notice is only meant to draw attention to a lack of references.


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Evolution of the haplo-diplontic life cycle
From wikipedia > Biological Life Cycle:

haplontic life cycle - the haploid stage is multicellular and the diploid stage is a single cell, meiosis is "zygotic".
diplontic life cycle - the diploid stage is multicellular and haploid gametes are formed, meiosis is "gametic".
haplodiplontic life cycle [..] - multicellular diploid and haploid stages occur, meiosis is "sporic".

To my knowledge, all mammal species are diplontic. It might even be true for all vertebrates (but I am not sure). In plants and in fungi, there is a much greater diversity of life cycle however. In many (all?) bryophytes for example, the sporophyte (the diploid phase) is multicellular and its life is completely dependent on the gametophyte. This diversity of life cycle lead to the following question:
What drives the evolution of the relative time an organism spend in the haploid vs in the diploid phase of the life cycle?

This post comes as a follow up to @JAD's comment here

I appreciate that English is not your first language, but at 60k you can surely come up with a clearer title and question. How can “relative importance” evolve (either in English or French)? Are you sure your question can’t be rephrased to something like “What determines the relative…”?

By "relative importance", I was referring to the ratio of time spent in the diploid pahse over the time spent in the haploid phase (or the same ratio but in terms of number of mitosis). I chose "What drive the evolution" to clarify my question was about the evolutionary pressures and not about the physiology. I made a few edits but please feel free to edit it yourself if you can improve language and clarity.

I’d rather you do it yourself. I’m sure you’re able to. The title can be simplified because it’s just a title. Think about the question. Two sentences is often the solution.

I just want to report the finding of one paper here. I don't know much about the rest of the literature and can't comment on it.
Otto et al. (2015) investigate this question in sexually reproducing organisms. As I understand it, they assume that the amount of time spent in on phase of the life cycle is proportional to the amount of selection happening in this phase. With a theoretical model Otto et al. (2015) showed that there is a sexual conflict over the length of the haploid phase. Mothers favour a longer haploid phase while fathers favour a shorter haploid phase. The outcome of the model depends upon who is in control of the length of this phase.
For mothers, producing a baby is often costly (see Bateman's principle). As such, the mother might want to ensure that its baby has high fitness. In the haploid phase, deleterious recessive alleles are no masked by their dominant counterpart and hence can be purged out of the population. A long haploid phase, therefore allows purging of deleterious alleles and make the diploid phase more resistant which is in the mothers interest.
Among fathers, the evolutionary pressures are different. Fathers evolve to mask mutations carried by their haploid gametes (e.g., by provisioning with diploid gene products), causing their sperm to be more competitive. As such, a father has interest that the haploid phase is short.


text:
What is (roughly) the net charge of the DNA in an average human cell?
I was wondering about what general range for the net charge of DNA in human cells is in Coulombs.  I imagine that kind of thing would be hard to measure but could be approximately calculated/estimated.  Could you approximate it by taking the average number of base pairs in the human genome and multiplying it by the charge of a phosphate group?  Would you have to multiply by two as well because there are two phosphate groups attached to each base pair?

That reasoning seems to work for Harvard's bionumbers database. They use a charge of -2 per base pair, and then estimate the linear charge density as 2e / 0.34 nm, where 0.34 nm is the length of a base pair. There are approximately 3.08 billion base pairs in the human genome, so you could run the same calculation: $2e \cdot 3.08 \cdot 10^9 = 9.86 \cdot 10^{-10} C$.


text:
Is it possible to contract the plague by kissing a wild chipmunk?"
I watched  this cute video and I came to conclusion that the lady in the video is putting her life in danger. She kisses a wild chipmunk.
As I know, they have fleas, and fleas have a black plague. Am I right? But maybe the risk of infection in contact with just one chipmunk is low?
How dangerous is such behaviour?

Very dangerous. Cute videos rot the mind (of those that watch them).

I suggest replacing the question title with the one you're actually asking: "Is it possible to contract the plague by kissing a wild chipmunk?"

I was going to vote close for opinion-based, but apparently this is actually a risk: https://www.cdc.gov/plague/resources/PlagueEcologyUS.pdf

@Armatus Yes, transmission risks are generally well studied and not opinion based. If you get a VTC as opinion based itch, hold off for someone who has specific knowledge

@DeNovo "As I know" is a signal phrase for opinion basis, but as you can see I do double check

@Armatus a quick search is not always a good way to tell whether something is or isn't opinion based. Be wary of the opinion based VTC, which is often a "not my field" VTC.

@Armatus this was a great suggestion!

The causative agent of the plague, Yersinia pestis, can be indirectly (via a flea vector) or directly (via exposure to infectious fluid or a bite) transmitted by rodents. In the western United States in particular, Y. pestis is endemic, and ground squirrels, prairie dogs, chipmunks, and woodrats are important reservoirs (see Cecil Medicine Ch. 320). US National parks have signs warning against feeding squirrels and chipmunks for this reason. You can read more about it in a national park brochure . Chipmunks and squirrels indirectly and directly transmit a variety of other diseases as well, including Tularemia (Cecil Ch 319) and various tick and flea borne encephalitides.

Can you also tell how dangerous is it for that lady? I mean except for kissing the chipmunk, she doesn't seem to be a poor medieval peasant. Not even a poor modern day folk. Maybe if she is generally clean, such cute act poses a low risk? And if she contracts plague, how doomed is she? I wonder how much darkness lurks in this cute video.

@user46147 Y. pestis infection is treatable, though it can cause loss of limb or death, especially if diagnosis is delayed. It's not a common disease. There are a few thousand cases globally every year. Exposure to the chipmunk is a risk factor, regardless of whether she is a medieval peasant or royalty, and it is a risk factor for more than just the plague.


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When you have your gallbladder removed, how does it affect bile flow into your small intestine?
Cholecystectomy, or surgical removal of the gallbladder, is an extremely common operation around the world. The gallbladder is typically viewed as a storage organ for bile produced by the liver, but is not necessary for life.
The classical teaching from digestive physiology is that bile is stored in the gallbladder and then released in a pulsatile fashion from the gallbladder in response to nutrients/hormones in the intestine during a meal. The major function of bile for digestion is to solubilize dietary fat so it can be digested by digestive enzymes in the small bowel.
When you don't have a gallbladder and there is no storage of bile, how does that affect bile flow into the intestines? Has anyone ever examined the effects of gallbladder removal on the release of bile from the liver? Is bile continuously released by the liver or is there still pulsatile release in response to intestinal nutrients?

Bile is stored, concentrated, and acidified in the gall bladder. Schwartz Principles of Surgery ch. 32 has a good section on this. After recovery from an uncomplicated surgery, the loss of the gall bladder does surprisingly little (other than, usually, resolve the symptoms of gallstones). This was a bit of a surprise to the medical community when the first cholecystectomy was performed in 1882, and it remained a controversial procedure for some time.
There are a number of studies on the effects on bile flow and the overall cyclic release, reabsorption, and return to the liver of bile via the portal vein called enterohepatic circulation.  Animal and human studies demonstrate compensation by the liver, bile duct, and the sphincter of Odie. Overall bile flow is reduced, there appears to be greater release into the intestine during fasting states, and there do appear to be changes in the composition of bile, but, most importantly, enterohepatic circulation is still pulsatile, in response to a meal, as you can see in the figure below.

Both solid lines are subsets of bile acids, measured in the serum of cholecystectomized patients in a classic 1978 study. The shaded areas represent control (not cholecystectomized) patients. These measurements suggest that enterohepatic circulation still follows a pulsatile pattern after cholecystectomy.

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text:
How does a bacterium age without cell division?
If somehow a bacterium, let's say E. coli, is engineered in such a way that it loses the formation of ftsZ ring (or other ways that inhibit cell division), and if other conditions are optimal for bacterial growth, then will the bacterium grow without cell division? If so, how long will it live? And how will it age?

what do you mean by bacterial growth without cell division? I didn't know that was even possible.

You need to be more specific about your definition of "growth". Many mycelial Actinobacteria   develop and replicate without undergoing cytokinesis for long periods of time, but they evetually break into separate cells. The strict classic definition of bacterial growth implies cell division.

Your question is a bit open-ended (of the kind "given an imaginary situation X, what will happen?") . Such questions attract answers that would be based on guesses and opinions rather than actual facts. If you add some more details then the question may become answerable.

If you post about bacteria, please be aware that the singular is bacterium and the plural bacteria. I appreciate this is not self-evident as it is Latin, not standard English, but it's not that hard. I've corrected it in your posting.

First of all, the growth of a bacterium is associated with an increase in cell biomass.So if a bacterium is restricted from replicating it does not grow. Coming to your later parts of the questions about how long will it live and will it age;
Yes, a bacterium would age irrespective of its ability to replicate.According to The Free radical hypothesis, all organisms age due to random deleterious events, oxidative damage by ROS produced during normal metabolism. It has also been found that cells undergo irreparable damage which can also lead to cell death eventually.
A complete review on bacterial ageing:
http://www.ias.ac.in/article/fulltext/reso/017/04/0347-0364


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Does pepsin digest plant protein?
This may sound trivial, but...
Protein is sourced from plants and animals. Pepsin and HCl digest meat (animal protein). Does pepsin also digest plant-based proteins?
I took a look at few articles online and this. None seems to explain what I am after.

What you probably are missing here is that plant proteins are fundamentally indifferent from animal proteins; both are polymers of amino acids, and pepsin just breaks these polymers into oligomers (or monomers).

@another'Homosapien' in this case, can we say that amount of the pepsin is required for plant protein cleaving is less than of meat and may I know why?

well, you can't really answer this question without including a lot more variables. To say at the simplest level, enzymes are catalysts, so digesting both plant proteins and animal proteins requires quite similar amount of pepsin. Again, this is the simplest one you can get, the more details you add, the more complicated it gets.

Yes, pepsin does digest plant proteins also. Pepsin is a protein and its job is to cut other proteins (also known as polypeptides) into smaller pieces. Proteins are made of amino acids and there are 20 amino acids found in proteins. Pepsin cuts the bond between two amino acids to break the protein into smaller pieces. When pepsin encounters a tryptophan (Trp), tyrosine (Tyr), and/or phenylalanine (Phe), it cuts the bond between that amino acid and the one next one, as shown below.

image source
Proteins from plants contain these amino acids so pepsin can cleave plant proteins.


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What is the function of epidermal ridges on human fingers (that produce fingerprints)?
What function is served by the epidermal or capillary ridges on human fingers, the supposedly unique impressions of which are known as fingerprints?

In this case, it seems that @canadianer successfully identified some positive selection-based answers. But, honestly Mark, I would read my neutralist answer too... too often people "expect" a selection-based answer, when most of the time the answer is simply neutral.

So that I can my phone's fingerprint sensor! Just kidding. ;-)

It's not just humans that have fingerprints, they're also present in many of our closest relatives and have separately evolved in Koalas and North American Fishers.

It should be noted that fingerprints may not be considered as a reliable unique identifier as they once were. http://www.naturalnews.com/044876_fingerprints_law_enforcement_forensic_science.html And also that some farmers and some old people can have rubbed out fingerprints.

I find it ridiculous that so many questions like this ask "what is the evolutionary reason…". You could ask whether "whatever is the technical term to describe the feature of the skin that you are referring to" (and it is not fingerprint — do a little work before posting) has any function. But to assume that every feature of an organism is selected for is an intellectual blind alley.

@StephanBranczyk: Natural news dot com is not a trustworthy source. Google "quackwatch naturalnews".

Fingerprints no longer uniquely identify people. http://www.nbcnews.com/id/5053007/ns/us_news-security/t/fbi-apologizes-lawyer-held-madrid-bombings/#.WMngMW_yu70 You could say fingerprints suffer from hash collisions (computer science and cryptography).

I like the new title, it focusses on the general trait rather than a specific patterning of some finger, X

I found many plausible claims that fingerprints increase friction. However, the following article claims, at least under their experimental conditions, that fingerprints actually decrease friction with smooth surfaces by reducing contact area.
Fingerprints are unlikely to increase the friction of primate fingerpads.

It is generally assumed that fingerprints improve the grip of primates, but the efficiency of their ridging will depend on the type of frictional behaviour the skin exhibits. Ridges would be effective at increasing friction for hard materials, but in a rubbery material they would reduce friction because they would reduce contact area. In this study we investigated the frictional performance of human fingertips on dry acrylic glass using a modified universal mechanical testing machine, measuring friction at a range of normal loads while also measuring the contact area. Tests were carried out on different fingers, fingers at different angles and against different widths of acrylic sheet to separate the effects of normal force and contact area. The results showed that fingertips behaved more like rubbers than hard solids; their coefficients of friction fell at higher normal forces and friction was higher when fingers were held flatter against wider sheets and hence when contact area was greater. The shear stress was greater at higher pressures, suggesting the presence of a biofilm between the skin and the surface. Fingerprints reduced contact area by a factor of one-third compared with flat skin, however, which would have reduced the friction; this casts severe doubt on their supposed frictional function.

That said, the author does later discuss their potential role in gripping of rough or wet surfaces:

So why do we have fingerprints? One possibility is that they increase friction on rougher surfaces compared with flat skin, because the ridges project into the depressions of such surfaces and provide a higher contact area. Experiments on materials of contrasting known roughness are needed to test this possibility.
A second possibility is that they facilitate runoff of water like the tread of a car tyre or grooves in the feet of tree frogs (Federle et al., 2006), so that they improve grip on wet surfaces. Though there is evidence that friction falls on fingers coated with high levels of moisture (Andre et al., 2008) it is possible that it falls less quickly on fingertips than on flatter skin. Once more, suitable experiments could test this idea.

There seems to be more consensus on the idea that fingerprints are useful for tactile sensation. The following are just some articles which discuss this.
Effect of fingerprints orientation on skin vibrations during tactile exploration of textured surfaces.

In humans, the tactile perception of fine textures is mediated by skin vibrations when scanning the surface with the fingertip. These vibrations are encoded by specific mechanoreceptors, Pacinian corpuscules (PCs), located about 2 mm below the skin surface. In a recent article, we performed experiments using a biomimetic sensor which suggest that fingerprints (epidermal ridges) may play an important role in shaping the subcutaneous stress vibrations in a way which facilitates their processing by the PC channel. Here we further test this hypothesis by directly recording the modulations of the fingerpad/substrate friction force induced by scanning an actual fingertip across a textured surface. When the fingerprints are oriented perpendicular to the scanning direction, the spectrum of these modulations shows a pronounced maximum around the frequency v/λ, where v is the scanning velocity and λ the fingerprints period. This simple biomechanical result confirms the relevance of our previous finding for human touch.

The role of fingerprints in the coding of tactile information probed with a biomimetic sensor.

In humans, the tactile perception of fine textures (spatial scale <200 micrometers) is mediated by skin vibrations generated as the finger scans the surface. To establish the relationship between texture characteristics and subcutaneous vibrations, a biomimetic tactile sensor has been designed whose dimensions match those of the fingertip. When the sensor surface is patterned with parallel ridges mimicking the fingerprints, the spectrum of vibrations elicited by randomly textured substrates is dominated by one frequency set by the ratio of the scanning speed to the interridge distance. For human touch, this frequency falls within the optimal range of sensitivity of Pacinian afferents, which mediate the coding of fine textures. Thus, fingerprints may perform spectral selection and amplification of tactile information that facilitate its processing by specific mechanoreceptors.

This paper also asserts a reason for the elliptical nature of fingerprints:

In humans, fingerprints are organized in elliptical twirls so that each region of the fingertip (and thus each PC) can be ascribed with an optimal scanning orientation.

The first paper shows that fingerprints decrease friction when gripping dry acrylic glass, but I guess there wasn't much dry acrylic glass in the environments where fingerprints evolved. It might be quite different when gripping rough or wet surfaces. (But for all I know there might be plenty of research on that as well.)

@Nathaniel Much in the same way that slick tyres are better than anything on dry tarmac, but you'd want treads on rough or wet terrain.

Would this mean that people without fingerprints could be measured to have less sense of touch than those with?

@Nathaniel I agree. As I said, their experiment is not exhaustive, but literature on this subject seems hard to come by (at least in my admittedly brief search).

Clarity on the TLA: PC, in "and thus each PC", please.

Just a gentle push and you're in 10k club! Congrats ;)

Extensive amount of research, I've learnt a lot from this. Particularly on the final quote TQ

To balance the debate, from a neutralist evolutionary perspective...
There does NOT have to be a direct selective pressure for a trait's contribution to an organism's expressed phenotype.

Three alternative, neutral, explanations:

"Hitch-hiker" traits: It (the trait) could be a by-product of a more necessary component whose function is directly associated with survival. E.g. we have hair, and it happens to have a colour, the colours perceived in the specific pigmentation of our hair are not strongly selected, one way (blonde) or the other (brunette), at least as significantly as the functionally essential properties of the hair itself: to keep our ancestors nice and warm. This brings us to...
Ancestrally Inherited Vestigial traits: once evolved, they can take a long evolutionary time "to get rid of". This accounts for traits we still express phenotypically, yet whose original functional purpose is obsolete today. For example, the Coccyx and our defunct visual sensor, a more optimal design is found in squid eyes: the retina should be ahead of the vitreous gap to avoid blind spots, a "glitch" we mammals have to still deal with. Echidna, still laying eggs? That's soo last-epoch...
Neutral Evolutionary Regimes: mutations whose inheritance patterns are heavily driven by a force known as genetic drift (wiki). Long story...

Side Note
A most remarkable trait, in my opinion, is found in the blind cave fish. Why does this fish have eyes, when it can't see?
Have a guess: which of the answers listed above is true: 1., 2. or 3.?

Related topics:

Is there a name for the evolutionary loss of vestigial structures?

EDIT/s:

2017-03-17: Correction (kudos AliceD): I mixed up reasoning about the mammalian eye example, floaters was not the suboptimal trait, it was blind spots. No blind spot in cephalopod eyes.

In response to your cavefish question, without guessing ;) http://biology.stackexchange.com/questions/34466/is-there-a-name-for-the-evolutionary-loss-of-vestigial-structures/34471#34471

I think in this case, neutral evolution is highly unlikely, because of the convergent evolution of fingerprints in other species (e.g. Koala and North American Fisher) which appears to be linked to their lifestyle and habitat but it's still important to consider other explanations.

@JackAidley You still need to make sure there's no other trait that is linked to fingerprints that's the actual result of convergent evolution, with fingerprints being just a common side-effect of that.

@JackAidley, I would argue that you're missing a key facet about fingerprints: their large variability in, at least, Human populations... You need to be sure what you mean by "finger print", a specific patterning? Because if maximum friction was the evolutionary "end game", surely we'd all have gecko hands?

@JeffreyBosboom, feel entirely free to edit that in the bottom of the answer following the "---" markdown symbol. Search: "Pending correction of mammalian eye example."

Mammalian retina location is a very bad example. It does serve it's purpose so it's promoted. The fact that better solutions exist is meaningless to the evolution process. Switching to a better solution would require un-evolving vision first - that just aint gonna happen. Same with vas deferens being looped over the pubic bone, pointless but "we've invested too much in this solution to scrap it now".

@Agent_L. touché. I agree to you on some level, but "meaningless", is a bit harsh right? What I meant, is what I agree with you on, essence being: Natural Selection is a "blind watchmaker" -- Dawkins. See: https://en.wikipedia.org/wiki/The_Blind_Watchmaker. Care to edit my answer?

Why wouldn't a squid eye have floaters? You could mention the absence of a blind spot in squid eyes

@AliceD: touché, EDITED. I mixed up my optimal design reasoning in mammalian vs. cephalopod eyes.

Glad I could help. +1

@hello_there_andy No, I believe "meaningless" is the right word here. Evolution literally doesn't care that objectively better solution exists somewhere (unless another species can outcompete you thanks to that solution). I don't think there is a reason to evoke Dawkins either, he's needed when someone can't grasp the basic concept of evolution and people participating in this discussion seem to have no problem with that.

@hello_there_andy There is no "grand blind watchmaker concept" to realize, the very basic idea of evolution is that grand concept. Blind watchmaker is just a way to explain it, an "evolution for dummies" story. We are not dummies here, please don't treat us so. Dawkins is controversial figure even among evolution proponents, because he's dangerously close to preaching science like just another religion. And I don't agree evolution is a bad watchmaker, it's a very good one. Because it's better to release a successful product that works than spend too much resources on unneeded improvements.

Nothing to add but: "Let's see if your cavefish still has eyes in a million years! :) ) PS: There's a newly discovered cave loach. It's awesome.

@Kara more importantly, let's see if we if we can adapt to a hotter climate, low oxygen levels, and competition with an expected H.sapiens population size of 12 Billion by 2039!


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How many generations does it take for one species to become a new one?
First lets consider that a species is a group of individuals that can reproduce by breeding fertile offsprings.
It's usually said that evolution takes a very long time. Lets say that 1000 generations are required for species A to evolve into species B.
Which species would generation 999 belong to, A or B ?
If A then it means that there was no evolution in 999 generations and that the entire evolution is going to happen in a single generation from 999 to 1000.
If B then which specie does generation 998 belong to ?
etc etc
In the end it seems to me that if there is evolution it can only be instantaneous, but that requires many improbable things, one of them being that the spermatozoids and ovules of species A contain DNA of species B !
How does that work ?
EDIT this is not a duplicate I'm not asking what a species is I'm asking what is the genetic process of evolution, how do we move up in the evolution tree.

In short, the concept of species is a subjective one and is not objectively defined. You should have a look at How could humans have interbred with Neanderthals if we're a different species?. While your post is not directly a duplicate of the linked post, your question(s) are being answered in the accepted answer of this other post. I am therefore voting to close as duplicate. If you think your question has not been answered in this other post, please let us know

Btw, the singular of "species" is "species", not "specie".

The observed minimum within animals is three generations. ---- While the question is marked as a duplicate, the answers differ between "How many generations does it take for one specie to become a new one?" and different from  "How could humans have interbred with Neanderthals if we're a different species?"; ------  For the former the answer would be: The observed minimum within animals is:       Three generations. Lamichaney et al. Science, 2018: Rapid hybrid speciation in Darwin’s finches

@tsttst there are plenty of cases of hybrid speciation (single generation) i plants especially.

@Remi.b good point; and there is also at least one synthetic specification in Drosophila; intended to stay close to natural evolution in animals and thus close to the previously linked question - which has an excellent answer about general themes of evolution

The word "species", in the biological sense, is both singular and plural. The  only meaning of the word "specie" that Chambers gives is "coined money". Please edit your question to reflect this so that others do not copy your error.

"Species" is to a considerable extent a human construct.  There are numerous examples of groups which are considered different species because they are reproductively isolated from each other (e.g. the hybrids between native & introduced trout in the Sierra Nevada/Great Basin).  So essentially what makes a new species is a group of biologists agreeing that it is a new species: http://www.bbc.com/news/science-environment-42103058

Your question is like asking about the color spectrum. A wavelength of 530nm is green; a wavelength of 580nm is yellow. So let's say it takes 60nm of wavelength change to go from green to yellow. What color does a wavelength of 579nm have, green or yellow? If it's green, then does the color shift in a single nm difference of wavelengths? If it's yellow, what color is 578nm, etc?
The answer in this case is, 579nm is yellow; so is 578nm. 570nm is more ambiguous; some people might say it's yellow, others think it's greenish-yellow, in some contexts it might look clearly green. And so on along the spectrum; the reality is that there is no hard boundary between "green" and "yellow". There are colors that are clearly green, colors that are clearly yellow, and there is a difference between those two, but there are also plenty of intermediates that are a bit like green and a bit like yellow, and those intermediates are what you go through when you go from green to yellow. There is no definite point everybody can agree on where a single shift happens.
It is the same thing with species. A species is a group of organisms that interbreed to produce fertile offspring, but "interbreeding to produce fertile offspring" isn't a on/off thing. Organisms are more or less fertile. What if organisms from two groups interbreed and produce offspring, and only half of those offspring are fertile? Or they have half as many offspring as couples within the two groups have?
The reason species are an important concept, and can be distinguished visually as being like each other and unlike members of other species, is that within a species there is widespread sharing of genes over the generation, as individuals breed with each other, but they don't share genes with other species. Meaning species will evolve as a unit; changes that happen within a species will spread between individuals of that species, but won't spread outside of it.
But because sharing genes isn't an on/off thing, you could have 100% of genes being shared from one population to another (then they're clearly the same species), or 0% (then they're clearly not), or 90%, or 70%, or 10%... That's where you find the fuzzy boundaries. The races, strains, varieties, sub-species, all those different words to describe populations that are different but aren't outright different species. And the debates on whether different groups are different species or not in the first place, in the cases where it's really ambiguous.
And the same thing is true of evolutionary change in general. You don't have a mammalian carnivore that isn't a cat, and then bam! a cat. You have a mammalian carnivore that isn't a cat (or dog, or weasel... but kind of like any of those in various ways. Like generic carnivore-ish), then a mammalian carnivore that's a bit more like a cat or a dog (and another one next to it that's a bit more like a weasel), then a mammalian carnivore that's even more like a cat (and others that are even more like a dog, and even more like a weasel), then a mammalian carnivore that's clearly feline but isn't a cat, or a lion, or a tiger; it's a different species of feline that doesn't exist today, and also looks more generic-feline-ish than any modern feline. Then there's a feline that's more like a cat (and others around it that are more like a lion, and a tiger), but also clearly isn't a modern cat. Then there are felines that are really like cats but a bit different from modern ones and it's hard to tell, maybe we should extend the definition of "cat" to include them? And then bam! a cat. But that cat isn't clearly a Jungle Cat, or a European Wildcat, or a domestic cat, or any modern species; it's its own "archaic cat" species. And then there are cats that are more like Jungle cats, or more like domestic house cats...
Also don't confuse the creation of new species with evolutionary change in general. Over the long term they are related, because once two groups are different species then they will change through evolution in independent directions, and they will end up looking different from each other as well as from their common ancestor. But over the short term you can have speciation with very little morphological or genetic change (you just need two groups that used to interbreed, to no longer do so), or morphological/genetic change without speciation (if all the change happens within one group).
Both speciation and genetic/morphological change can happen within a single generation, but usually happen over much longer timescales. But there is no hard rule for how long that is; as far as speciation goes, if groups aren't prevented from interbreeding in some way then they will keep breeding with each other and can stay a single species indefinitely (whether individual from generation 10,000 could interbreed with individual from generation 1 is a different question, but it's not like it's a situation that happens). As far as evolutionary change goes, natural selection means species change to adapt to their environment. Once they're adapted to it, if it happens their environment never changes then natural selection will push them to stay the same as they are, again indefinitely. In the real world most environments change over time so organisms do change more often than not, but just to illustrate that the timelines are a product of circumstance, not an intrinsic feature of evolution itself.

Ring species are a great example of how fertility can vary even within a single species, and just how vague the concept of species is. Penguins are another a great example since some species can successfully crossbreed in the wild.

Species is a hard concept to really pin down but your definition is fine for animals and most plants.
If the only distinction we make is their reproductive success, and we know g1000 is the only generation that is part of species B and it is unable to reproduce with g999 then something must have happened when g1000 was born that makes all members of g1000 unable to successfully reproduce with all members of g999. The most likely scenario is geographic or temporal isolation, they must have migrated into another area or their mating season went out of sync with g999. In that case the real speciation happened in one generation, from g999 to g1000.
If on the other hand we know g1000 is species B and g1 is species A, but we haven't decided if g2 through g999 are part of either A or B then the possiblity exists that g2-999 are intermediate populations. Using the temporal isolation example again imagine g1 has mating season from Feb-07 to Feb-16, g100 has mating season Feb-08 to Feb-17 and every hundred generations the mating season shifts one day, then g1000 has mating season Feb-17 to Feb-26. This means there is no way for g1000 to reproduce with g1 simply because they never have sex but g1000 can reproduce with g100 and up. This is the closest explanation we have for speciation, any obvious differences between species come only after many generations of isolation.
Regarding DNA, all species are related and all related species share a lot of their DNA. The closer their relation, the more DNA they share. Even humans and grass both have the genes that allow us to get energy from sugar. So yes, all cells of species B will contain DNA from species A, there is just a tiny difference that is just big enough to keep them from breeding. This could be mating season differences, but also incompatible genitals or one of the species has become allergic to the other, or anything else you can think of.

Welcome. Can you add sources to allow other users to background read on your answer?


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Bird identification: Warora, India

These photographs have been taken in Warora, India. Could someone please help identify this bird?

This is a pond heron or paddy bird. The de-facto source for identifying Indian birds is Birds of the Indian Subcontinent by Richard Grimmett, Carol Inskipp and Tim Inskipp. The book is remarkably complete and contains the vast majority of species found in the Indian Subcontinent.


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Resource to obtain listings of tissues that different viruses infect
I am working on a project that involves analysis of viral DNA sequences. I'd like test hypotheses about issue specificity. Ideally I'd be able to get a table of virus/strain names with a column in it for something like 'tissue tropism' which would equal neurons/nervous system, liver, epithelia, etc etc. Does anybody where I could find this?
I so far haven't located it www.viprbrc.org which seems to be molecular bio info like domains, dna sequence etc.
I also found this paper paper which has data in the ideal format but is limited to analysis of RNAseq data and to healthy subjects.

Tried viralzone?

Animal viruses? Vertebrate viruses? Mammalian viruses? Human viruses? Please clarify.


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Is there a biological neuron that spikes in response to hyperpolarizing currents?
As some background I've been building Electrophysiological models of neurons, and in the process stumbled upon a model, that in all respects is biologically plausible, but has a bizarre property I didn't think happened in nature. It spikes in response to hyper polarized currents.
My particular model has only one ion channel which is has similar properties to Hodgkin-Huxley's transient sodium channel. It has one activation gate and one inactivation gate.  The reason I only use a single Ion Channel was I was exploring If I could create a minimal spiking neuron with just a single channel. The answer is yes, but has different properties then I expected.
Basically when I inject a hyper-polarizing current it spikes and depolarizing current causes it to stop spiking.
I know that Depolarization block can occur, my current isn't that High, in fact its no current produces no spikes. It has a normal rest potential around -55 mV and Fires upward to about +40 mV.
Also note that If I change the parameters around I get a more normal neuron that spikes in response to depolarizing currents. So the property must be somehow related to the ion channel kinetics.
The question is: Are there biological neurons that spike when hyper-polarizing currents are injected?

This is a very interesting question and I hope it is well-received. Welcome to Biology S.E. if you have questions or need assistance, please visit The Help Center.

Could you tell us a bit more about the model? Does it follow Hodgkin&Huxley kinetics? Which types of channels are included in the model? Did you model a specific neuron?

@AliceD. I added some description of the model, hope that helps? I wasn't sure if it was allowed to post the entire equations that reproduce the equations, but I am more asking if the behavior is seen anywhere in nature.

Search for "rebound excitation" or "rebound spiking".

Short answer
Action potentials are always generated after a depolarization step.
Background
Action potentials are generated by prior depolarization of a neuron, typically by the action of an excitatory neurotransmitter. An action potential is per definition a sharp depolarization, followed by a somewhat slower re-polarization step. The most important step in an action potential is the activation of voltage-gated sodium channels (VGSCs). VGSCs open when the membrane potential exceeds a certain voltage upon depolarization (Liu et al. 2012), in turn initiating the depolarization step of the action potential. Hence, action potentials are always generated through depolarization.
The only ion channel I am aware of that may mediate a hyperpolarization-induced cation influx resembling that seen in VOSCs is the hyperpolarization-activated cyclic nucleotide-gated (HCN) class of channels. The associated current (Ih) is a non-specific cation flux (Na+, Ca2+). The HCN channel opens when the membrane potential hyperpolarizes. Thereby it generates a relatively small positive, depolarizing influx current. it is mainly involved in setting the frequency of pacemaker activity in, e.g., thalamic relay neurons that are involved in the oscillatory cortical activity characteristic of slow-wave sleep. However, Ih itself does not elicit spikes, it generates excitatory postsynaptic currents (EPSCs) associated with excitatory postsynaptic potentials (EPSPs), but not full blown spikes (McCormick & Pape, 1990).

Model evaluation and recommendations

Perhaps you identified EPSPs as action potentials? They are not.
Your resting membrane potential is very high (depolarized) - a more typical value is -70 mV.
VOSCs are opened at around -50 mV, hence your resting membrane potential is awfully close to action potential threshold. Any small perturbation leading to a bit cation influx will trigger action potentials. With a bit of stochastic leak currents included, a spontaneous spiking neuron is what you get. Ih (-like) activity may also set the stage for your out-of-the-ordinary observation.
Suggestion - lower your resting membrane potential to a more conservative value (-70 mV) and check the difference between EPSPs and action potentials. If you look at the following figure you can see that at your chosen resting membrane potential you are hovering between EPSP / actin potential threshold. A bi-stable situation results.

Action potential versus EPSP. Source: What when and how
References
Liu et al. BMC Neurosci 2012;25:2-9
McCormick & Pape. J Physiol 1990;431:291-318

Hey, did you check the chat room?

Thanks! It definitely helps. I got too caught up in the mathematics of the equations, and this helped me realize my parameters, where not in a biologically relevant range.

I was doing some more research and stumbled upon this paper here by Dr. Izhikevich that describe neurons as a system that can exhibit resonance. The author built a model that he calls the resonate and fire, which is a linear piece-wise model of a neuron.
The interesting thing, and why I bring it up, is it can respond to a "two inhibitory pulses, that if timed correctly will cause the neuron to fire. but neither inhibitory pulse alone can cause the neuron to fire.
Following some of the citations in the article (found here), apparently thalumus neurons can exhibit resonance and thus theoretically can fire in response to the right frequency of input. However it is important to note that they thalamic neurons are close to threshold, and are not receiving the double inhibitory input that Izhekivich talks about in his paper. The second paper uses a ZAP protocol.
A Zap protocol is injecting a Sine wave into a neuron and slowly change the frequency linearly in time.
$$I_{ZAP}(t) = \sin((\omega_0+\omega t) t) $$ where $\omega_0$ and $\omega_1$ are constants.

Not sure If I was allowed to answer my own question after accepting someone else's answer, but figured that this was relevant and useful to others.

You may answer your own question for sure! It is actually encouraged. However note that your question was on examples of real neurons and both cited papers are on models. +1 for your elaboration though :)


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Why is oxygen needed for the electron transfer phosphorylation?
I understand that oxygen is the acceptor of electrons and hydrogen ions during the electron transfer phosphorylation, the last step off the ATP-producing aerobic respiration.
But why?
Aren't there any other alternatives for this acceptor? Oxygen is already recognized to have several harmful effects to cells - wouldn't another molecule be a better choice?
Why does it even require an "acceptor" to accept the electrons and hydrogen ions? What would happen if they were left alone?
I apologize if my question was due to my ignorance in basic chemistry or biology, but do please point it out and explain it to me. Thanks!

Some what related: http://biology.stackexchange.com/questions/452/what-does-the-human-body-use-oxygen-for-besides-the-final-electron-acceptor-in-t

Aren't there any other alternatives for this acceptor?

Not that we're aware of. Every other alternative requires an anaerobic environment - which means small, and often less efficient.

Oxygen is already recognized to have several harmful effects to cells - wouldn't another molecule be a better choice?

When we're talking about a molecule's fit there are many things to consider. Primarily its electronegativity, as that determines its stability, ability to accept and donate electrons, protons, and its ease of acquisition given plentiful amounts in the environment.
Molecular Oxygen is comparatively stable to a lot of di-atomic molecules, and comparatively reactive to others. It's in the butter zone for the act of being the terminal acceptor.
Let's think about Fluoride: Almost all of it is bound up in rocks with other elements. It's not available everywhere. It might be an alright candidate if we could eat rocks, but it also replaces minerals in our bones and teeth. Yes, you're familiar with this - but too much leads to fluorosis - where too much of the calcium compound is replaced, and it ends up making the bones and teeth much weaker.
Alright, let's think about Nitrogen - Very stable, pretty good electronegativity, abundant... but a little too stable. Yup, it's a gas, it's everywhere, and we can't use a lick of it. It's so stable that it's basically inert. The only reason rhizomes and other beneficial bacteria can use it is because they're in a controlled environment away from oxygen with significantly different biochemical processes which produce much less energy (and probably wouldn't be able to support large multicellular organisms that are as active as we are). So, Nitrogen is out.
Carbon? Nope, as an ion it's dangerously reactive, and as anything else it's too stable. Plus, we're carbon-based! If we used carbon as the terminal acceptor then the proteins handling the electrons would have to be even more exotic and filled with other elements to prevent them accidentally gobbling up the electron and becoming useless.
Sulfur? Not electronegative enough for human purposes, unfortunately. It wouldn't act as a terminal acceptor unless our bodies seriously oxidized it; and any oxidized molecules floating around would be more dangerous than molecular oxygen floating around. Plus most sulfur is bound to minerals as well - not abundant unless you're in the ocean.
Oxygen is both incredibly abundant and easy to perform the chemistry with. More reactive molecules are usually not abundant and tied up in the Earth's crust and could be more dangerous.
Less reactive molecules tend to be so non-reactive that we can't do anything with them, and if we could force them into a state where they would be reactive they tend to be violently reactive or require very specific environments that we can't reproduce on a scale necessary to be as mobile as we are.
Oxygen is not perfect, but it's a good fit.

Why does it even require an "acceptor" to accept the electrons and hydrogen ions? What would happen if they were left alone?

Same thing that would happen if you clogged a pipe or hose. Once all of the electron acceptors on the transport chain are full, movement stops. The electrons won't be magically absorbed by other parts of the proteins making up the chains, and while there might be errant reactions with other molecules, you'd be lucky to get a whole ATP molecule out in a day - assuming you could magically stay alive.
In reality, Cyanide poisoning is precisely what you're asking, and will kill you very quickly.

Ah, so electrons with their energy pumped out become useless clogs in the phosphorylation pipeline, and the oxygen molecules are right there for removal. Thank you for this easy explanation.

Aren't there any other alternatives for this acceptor?

Yes, there are multiple other acceptors used by anaerobic bacteria. Iron is probably the most common other acceptor used by a range of organisms in a range of environments but others are used as well, such as sulphur.

Aren't there any other alternatives for this acceptor? Oxygen is already recognized to have several harmful effects to cells - wouldn't another molecule be a better choice?

No, Oxygen is a very good acceptor. It's highly electronegative which makes the process highly efficient, and it's also abundant in the environment since its created by photosynthesis. This has two consequences: firstly, there's plenty around to use, making it a good choice (obviously) and, secondly, cells need to deal with the harmful effects of oxygen regardless of whether they're going to take advantage of it.

Since oxygen was late on the scene it could be that reducing it was originally a method of detoxification.

Is there even an "electron transfer phosphorylation" process in anaerobic respiration? I thought it was glycolysis-only, then instant reduction.

@GreekFellows: It depends on the anaerobic process you're thinking about. In anaerobic respiration there is a terminal receptor and electron transfer; however the majority (I think) of anaerobic energy production is not respiration but rather the shortened process you are thinking of.


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Is there an animal which does not have any kind of symmetry?
Bilateral symmetry is a common feature of animals, and starfish have rotational/circular symmetry.
But is there any animal that has no symmetry?

Symmetry on what scale? Whole organism only? even animals (like some sponges) with no bilateral or radial symmetry in their larger body plan may still have some degree of symmetry in their histology.


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Histidine aromaticity
I understand that the imidazole ring in histidine is aromatic. I also realize that it retains its aromaticity when protonated.
I am wondering why this is not mentioned at all in basic text books such as Lehninger? Also, across the web there are a number of places claiming that histidine isn't aromatic in all cases.
Another reason I am a little confused is, if protonation doesn't alter the aromatic nature, then why is histidine such a weak base?

This is one of my favorite charts demonstrating the complexity of amino acid properties:

http://www.jalview.org/help/html/misc/aaproperties.html
Histidine is probably the most complicated amino acid in this regard (just compare how many circles it falls into).  But don't undersell cysteine and methionine: those sulfurs exhibit some surprising behavior, especially when coordinated properly.  Cysteine, of course, forms disulfide bonds, with methionine occasionally functioning as a methyltransferase.
Biochemistry textbooks make some oversimplifications because presenting the full messiness of these classifications is pretty confusing. Lehninger is the worst about this, especially when presenting math.  Voet and Voet is probably the most reliable about presenting this complexity. I still think Lehninger is a better teaching textbook overall (I was first taught biochemistry from the 3rd edition), but I also recall spending a week being confused about a topic before someone pointed me at V and V and I realized Lehninger was oversimplified to the point of being wrong, in that case.

Diagram is nice and informative +1 :)

@Dexter I also like the diagram. Do you agree these are improvements? 1. "Tiny", rather than "tiny". 2. Instead of blue, green, and grey as the main colors and blue (twice, which is confusing) and brown (which is so dark as to make reading the black print difficult) that are hard to distinguish, howabout the big three being the light primaries ie red, green, and blue? Then the overlaps would be more clear (and have intrinsic interest). 3. How about distinguishing medium/big/huge? As it is leucine and tryptophan are lumped together. 4. Removing the "Charged" ellipse, since it adds nothing.

Contd. 5. How about representing size by position, e.g. distance from the center of the "SMALL" oval, or from the center of the diagram as a whole? That way, the ranking by size could be made clear, and even the actual magnitudes of the size. 6. How about something more precise than "small" and "tiny". Does it refer to volume, mass, number of atoms, or something else?

I am wondering why it is not mentioned at all in basic text books such as Lehninger?

Books are not flawless.

Another reason I am a little confused is, if protonation doesn't harm the aromatic nature, then why is histidine such a weak base?

Pyrroles have a weak basicity because of delocalization of the electron lone pair of nitrogen. It is the lone pair of nitrogen, in amines, which gives it basicity (Check Lewis bases and acids) .
In imidazole, the other nitrogen (N-2) has a free lone pair and does contribute to its basicity. As you pointed out before, imidazolium is a stable moiety and imidazole is a much stronger base than pyridine, although it is a weaker (pKb ≃ 7) base than lysine (pKb ≃ 10.5) and arginine (pKb ≃ 12.48).
Imines are generally weaker bases than amines because the sp2 hybridization of the former gives them a more s-like  character; this causes the lone pair to be held more tightly to the nucleus thereby reducing the basicity. Also, the C-N(2)-C angle is constrained (small) because of the planar ring. This again leads to a more s-like character.
The strong basicity of arginine is because of the guanidium group.

The imidazole ring in histidine is indeed aromatic. But "aromatic amino acid" does not usually mean "amino acid with an aromatic ring". Rather, it indicates one or more particular chemical properties, such as high absorption at 280nm, or, better, its metabolic pathway.
Histidine as a stand-alone amino acid is a weak base, but this is mainly due to the amino group and acid group that every amino acid has. The imidazole ring itself has a neutral pKa.

I was referring to the basicity of the side chain itself. Why is its pKa neutral?

i dont think there is a term called neutral pKa.
pKa of water is ~15.7. pKa of imidazole is ~14 which makes it slightly better acid compared to water but poorer acid compared to carboxylic acids.

@WYSIWYG: I was referring to the deprotonation of the acid conjugate, physiologically more relevant. pKa≃7. I agree that 'neutral pKa' is a misnomer.

The reason why it's mostly referred to as basic is because the non-protonated nitrogen in the ring has a lone pair that it actively donates in several biochemical reactions. Lone pair donator = Lewis base

Hi and welcome to Bio.SE! This is more of a comment on the protonation rather than the aromaticity. Once you get more reputation you'll be able to make comments. If you want to expand your answer, see these tips on writing a good answer.

Consider it as an amino acid with "pro-chiral auxiliary" properties instead of broadening the entire molecule as aromatic.

Welcome to SE Biology. You may not have noticed that this badly confused question was posted almost ten years ago, and the poster has not been on the site in the last eight. If you think that the description "pro-chiral auxiliary" is an important general contribution to the topic, then you need to explain what it means. I am a native English speaker, have a degree in Chemistry, and have taught biochemistry for many years. The phrase means nothing to me.


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How much do crocodiles eat?
How much do crocodiles eat? The closest I found to an answer was on German wikipedia, where it says that adult nile crocodiles eat "only about 50 full meals a year." While interesting, without knowing what a full meal is this is meaningless. So how much does an adult crocodile actually eat?
I think relevant other questions in this context are:

Do all adult crocodiles (or even all crocodilia) eat roughly the same (corrected for body mass)?
Some crocodiles apparantly eat fruit and seeds on a regular basis*, is this is a relevant part of their caloric intake or just a "vitamin supplement"?

*paywalled article, I only read the abstract

re the close vote: a) I've added the additional questions because I don't think one can answer the question meaningful without at least adressing them (but could be wrong) b) a comment why exactly the vote to close would be appreciated.

fwiw, english wikipedia on crocodilia states "10-20% of what a lion needs" witht this paywalled source: http://onlinelibrary.wiley.com/doi/10.1111/j.1469-7998.1986.tb01518.x/abstract someone with access could use this maybe?

full meal= bloating with days of digestion


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How much solar energy required to produce enough food for a herbivore?
Just curious, how much solar energy can power an (herbivore) animal? Specifically, is it enough sunlight on Mercury (4 to 10 times brighter than on Earth) to "feed" a zebra? Will it be sufficient at 10x more effective photosynthesis? Notwithstanding lack of atmosphere, water being buried deep and other minor problems, of course :)

BMR is the amount of energy an animal uses just by being alive. BMR is proportional to the mammal's mass. More precisely, BMR is proportional to the mammal's mass to the power of 3/4. A 0.1 kg mammal has a BRM of 10 kcal/day. Using the aforementioned proportionality, a 600 kg mammal (average mass of a cow) will have a BMR of 6800 kcal/day.
This means that a cow would need about 6800 kcal of energy per 24 hours (1440 minutes) to survive.
The amount of solar energy reaching the earth’s atmosphere is 0.00194 kcal per square centimeter per minute. Since, according to you, there is 10 times the amount of sun in Mercury, there should be 0.0194 kcal per square centimeter per minute hitting Mercury.
0.0194 kcal per minute for 720 minutes (counting only day - since there is no sun during the night) equals 13.968 kcal per square centimeter per day. At this rate, the sun has to hit an area of 486 cm squared to harness enough energy for the cow.
In summary:

The average cow needs about 6800 kcal per day to survive (BMR)
On Mercury, the sun generates 13.968 kcal per square cm
Which means, the sun has to hit an area of 486 square cm

In one sentence:

In order to power a cow on Mercury, the sun has to hit an area of 486 cm for 720 minutes.

To learn more:

https://en.wikipedia.org/wiki/Kleiber%27s_law
http://www.ase.org/resources/measuring-number-calories-sunlight

According to wikipedia's [phoyosynthetic efficiency] (http://en.wikipedia.org/wiki/Photosynthetic_efficiency) a typical plant will convert about 1% of solar energy into chemical energy. But if our chlorofylled cow utilize sugar cane's 8%-efficient photosynthesis, then deal with overradiation, we get 6075 sq. cm area needed. Since day on Mercury is very long, we can require cow migration toward zenith, doubling energy production and eliminating 40% loss on photo-respiration. Finally, we got 1735 sq cm to light up. 40x43 cm, fine.

any thoughts on How much energy do small spiders expend when they are just waiting for their web to vibrate?


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Why don't we breathe nitrogen when it makes up most of the air?
Why don't we breathe nitrogen while it makes most of the air?
Why do we always tend to breathe oxygen, not hydrogen and nitrogen?

I'd argue that we do "breathe" all those gases. Air that we inhale (at sea level) is about 78% N$_2$, 20.9% O$_2$, 1% argon, and smaller percentages of CO$_2$, neon, methane, etc. So all those gases are going into the lungs with every breath in.
We take up oxygen preferentially because we have hemoglobin to bind O$_2$. When hemoglobin binds the oxygen, it upsets the balance and pulls more oxygen across the alveolar membrane. This is aided by pulmonary circulation which carries the blood away. Here's a demo of the diffusion process.

Nitrogen dissolved in the blood and pressurized during an underwater dive can, during a return to the surface, bubble out of the blood, just like the release of pressure opening a bottle of a carbonated drink causes bubbling.  In human divers, it can causes the painful  and potentially lethal condition called decompression sickness or "the bends".

You seem to be saying that nitrogen does not get absorbed into the blood. Are you, in fact, saying that? I came here because I am trying to learn whether humans can survive with trace quantities or even no nitrogen in the atmosphere.

I would argue that your argumentation isn't correct. Saying we have hemogobin to transport oxygen is like saying we have amino acids to build proteins. Your answer describes how the oxygen gets transported but not what the actual goal of this transport is. This is mainly because  oxygen is extremely electronegative and therefore important to form water  during oxidative phosphorylation

Completely agree with @RickBeeloo,  this answer gets the causality all wrong. We don't breathe O2 because we have hemoglobin --- we have hemoglobin because we breathe O2!

Animals use oxygen as a chemical energy source because oxygen gas can react with many other compounds to form oxides, which releases energy and happen spontaneously.
Both carbon and nitrogen can be made to react with oxygen, but otherwise they are pretty inert.  So of all the gasses in the air present at over a fraction of a percent, oxygen is the only one we can use for energy.
Nitrogen gas itself (N2) is incredibly chemically inert; N2 requires energy input into it to react chemically.  Biometabolism relies upon a chemical release of energy.
If we had ammonia gas (NH3) in our air it would be a great redox source of energy... taking energy from the ammonia could produce N2.   N2 takes a lot of work put into it to get the nitrogen out for other uses.
Hydrogen (and sulfer) are both possible substitutes for oxygen in the role of redox energy source, but are normally pretty small components of our environment.  On another planet they might well be the basis of biometabolism.
Of course the fact that plants can use carbon dioxide to fix carbon is a different case of biology using a gas out of the air.  Its the defining quality of plants!
The energetics of using CO2 is endothermic - it requires energy input. They have to use sunlight to get the energy to utilize this energy and its very costly energetically.  Animals can afford to move and grow because they use oxygen while they eat plants.

I wouldn't call oxygen an "energy source". It's an electron acceptor.  But the rest of the first sentence, "because oxygen gas can react with many other compounds to form oxides, which releases energy" is spot on. +1

try doing without it for a few minutes and see what happens to your energy :) combustion engines, forest fires and thermite reactions could also be called 'electron transfer' reactions. People falling off of tall buildings could also be called 'release of potential energy events' but also i wouldn't expect the use of language to conform to freshman chemistry just because there is different language for the same thing.

@shigeta, superb answer. I know you tried to keep the answer simple for our benefit, but could you please edit the answer to include the relevant scientific concepts (an equation perhaps). What does inert mean in chemistry? Does it mean for example that a chemical reaction involving an inert element/compound has a higher activation energy? Gracias.

ok @AgentSmith i made an effort though discoursing into freshman chemistry is something i typically try to avoid

@shigeta, ok, arigato gozaimus. A quick question. What makes a molecule reactive as opposed to inert? Is it the electron configuration? Also endothermicity is a good explanation.

Sure.  @AgentSmith its about the electron configuration around the nucleus of a given charge.  this is one of the foundational bases of chemistry.  some chemicals react, others do not.  why is a pretty deep question... far beyond a single answer here. https://www.coursera.org/learn/intro-chemistry this course is free at the moment

Nitrogen is much less reactive than oxygen.  Indeed, if I haven't totally forgotten my long-ago chemistry courses, most chemical reactions involving N2 are energy-consuming.  Thus you get nitrogen compounds produced by lightning, in auto engines, and other places where there's a lot of energy to spare.
Oxygen reactions, OTOH, are energy-producing.  You might think instead of fire: most organic stuff will burn (if dried), but it only combines with the oxygen in the air, not the nitrogen.
PS: Indeed, many nitrogen compounds take so much energy to create that they are explosives.  Ammonium nitrate, nitroglycerin, trinitrotolulene (TNT), even the potassium nitrate (saltpeter) used to make gunpowder.

You can focus on the fact that dinitrogen (N₂) is very stable and is not a good electron acceptor. Many anaerobic organisms can use metal ions as electron acceptors instead of oxygen.

There are two parts to this answer, and several answers have addressed one or both aspects but I figured I'd put it all in one place.
1) We use oxygen for a purpose that nitrogen is chemically useless for
2) While there is a different purpose we might want to use nitrogen for, it is something that is difficult to evolve (only bacteria have done it) and we can manage without.
Explanations:
1) We use oxygen because our metabolism uses it for energy. Our metabolism derives chemical energy from the breakdown of complex carbon molecules; this doesn't happen on its own and you need very reactive molecules to interact with those complex carbon molecules and break them down. All organisms do this step-by-step, using successive "electron acceptors" to basically strip electrons off of simpler-and-simpler molecules and thus break them down. Molecular oxygen is the most reactive molecule and greedy electron acceptor out there, and allows organisms that use it to get the most energy possible out of a given carbohydrate. That's why aerobic respiration is so useful, and that's what we use oxygen for. Molecular nitrogen has completely different chemical properties; it isn't that electronegative (i.e. greedy for electrons) at all. There are other molecules that can be used as electron acceptors, and are used in various forms of anaerobic respiration: nitrate, sulfate, carbon dioxide... but molecular nitrogen isn't one of them.
For various kinds of anaerobic respiration, see :
https://en.wikipedia.org/wiki/Microbial_metabolism
2) There IS a purpose for which one could use molecular nitrogen, which is to use it to build nitrogen-based molecules that our body depends on - like DNA, RNA and proteins, which basically do everything in a living organism. No organism uses molecular nitrogen as a source for these; it's much easier to use organic nitrogen compounds like nitrates and ammonia. It can seem silly that such compounds are so limiting, when nitrogen makes up most of the atmosphere! This is less of an issue for carnivores since we get all of our nitrogen needs from eating nitrogen-filled animals, but it's a huge issue for plants. The need for such compounds (and, to a lesser extent, phosphates) is why agriculture needs fertilizer. So why can very very few organisms break down molecular nitrogen ? Because it is a very stable molecule; if you've done chemistry you might know that the two nitrogen atoms in the nitrogen molecule are connected by a triple bond, which is very strong and hard to break. This may be a big reason why the metabolism to break that bond evolved only in bacteria, and all Eukaryotes get by using the bacteria themselves (nitrogen-fixing plants), absorbing nitrogen-filled organisms (carnivores, carnivorous plants - it's the reason they're carnivorous!) or getting by on the organic nitrogen that naturally occurs in the ground thanks to nitrogen-fixing bacteria.
https://en.wikipedia.org/wiki/Nitrogen_fixation
As an aside, the fertilizer humans make uses the Haber process, which converts molecular nitrogen in the atmosphere to ammonia. If you look at the Wikipedia page by the way you'll get an idea of how hard it is to break that triple bond, between the catalysts and the high temperatures and pressures... But through that process you could argue that humanity as a species does "breathe" nitrogen.
https://en.wikipedia.org/wiki/Haber_process
So basically, tl;dr:
1) we don't need to breathe nitrogen
2) if we did our bodies still wouldn't because it's really hard to do; no eukaryote does it, except maybe humans themselves but only through technology.

The bond in oxygen molecules is high energy, and ready to undergo an energy-yielding reaction with other molecules like sugar.
The bond in nitrogen not chemical useful to us...other organisms use energy to "fix" nitrogen to make energy rich nitrogen compounds that we can use.

As others have pointed out, we do breathe atmospheric nitrogen but we cannot do anything useful with it.
The problem is that the triple-bonded N2 is very unreactive and almost all animals and plants cannot convert it to anything else. Humans do not have the ability to reduce it to NH3, for example, but is would be great if we could.
All forms of life need nitrogen. It is necessary to make protein and DNA, for example. It is also very plentiful. N2 constitutes about 78% of air by volume, but it is in a form (N2) not usable by most forms of life. And therein lies the problem: in order to use atmospheric nitrogen, it needs to be 'fixed', ie converted to a form available to 'normal' metabolic transformation.  This is usually taken to mean that N2 needs to be converted to NH3.  Very few forms of life have the ability to do this.  The 'fixation' of N2 is also a great industrial problem.
As outlined by Rozenn Keribin, the first artificial process to successfully 'fix' N2 is the Haber-Bosch process, which was developed in the early part of the 20th century, and uses a metal catalyst and high pressures to achieve the following transformation:

N2 + 3 H2 → 2 NH3

This process remains the main industrial source of NH3 today, and is a 'mainstay' of the fertilizer industry. During the First World War, it was also an source of NH3 for the production of ammunition by Germany. For his work in this area, Haber was awarded the 1918 Nobel prize in Chemistry, a (controversial) honour that has surely stood the test of time.
Biological N2 fixation is an amazing story, and I'll restrict the discussion to an amazing enzyme: nitrogenase. This enzyme catalyzes the ATP-dependent reduction of N2 to NH3
(I will not deal with  leguminous plants, which can also 'fix' N2 using a symbiotic relationship with bacteria in root nodules, as I do not know enough about it).

In nature, [the] ability to fix N2 is restricted to a small
  but diverse group of diazotrophic microorganisms that contain the enzyme nitrogenase (Burgess & Lowe, 1996)

One type of nitrogenase (that contains molybdenum) catalyzes the following reaction:

N2 + 8 H+ + 8 e- + 16 ATP → 2 NH3 + H2 + 16 ADP + 16 Pi

Let's analyze this one: that's an eight-electron reduction that uses 16 ATPs just to make two  NH3 from one N2 !
Nitrogenases may be classified into 3 general types depending on metal content: Molybdenum nitrogenase, vanadium nitrogenase and iron-only nitrogenase. (All forms contain iron).
Biological nitrogen fixation was discovered by Martinus Beijerinck and t Hermann Hellriegel.  In addition, Beijerinck discovered that tobacco mosaic disease was caused by a virus.  Neither received a Nobel prize.
Ref
Burgess, B,K. & Lowe, D. J. (1996) Mechanism of Molybdenum Nitrogenase
Chem. Rev. 96, 2983−3011

The other answers seem to be missing the role of oxygen in oxidative phosphorylation, as an organism with aerobic metabolism we use oxygen for its electronegativity. Basically, as we break down glucose energy is released in the form of free electrons, these are "transported" for use in the oxidative phosphorylation to create new ATP which is our main form of energy storage. Oxygen eagerly accepts these free electrons at the last step of the oxidative phosphorylation and binds with H+ to form H2O. See here.
So without oxygen there would be an accumulation of electrons, stopping the oxidative phosphorylation and forcing us to break down glucose in the (less efficient) anaerobic manner.

Basically when air fills our alveoli, by the process of diffusion, only oxygen in the air is taken into the blood stream while the other gases along with the waste CO2 is exhaled. So you do breathe in nitrogen, but it is exhaled as it is by the body. The whole process of the respiratory system is explained here with diagrams.

Nitrogen and CO2 are also taken in. All gases dissolve and diffuse across the alveolar membrane