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Why do sulfur compounds smell?
Many of the compounds of sulfur have a strong odor.  Hydrogen sulfide from rotten eggs, the mercaptans of a skunk, the odor compounds in onions and garlic, the bitter taste of brassicas (cabbage, Brussels sprouts, collard greens, and similar plants) are all sulfur compounds.  What is it about sulfur that makes this so common?

I think most sulfur compounds are toxic (given a certain concentration). The ability to smell or taste sulfurous compounds therefore protects us, since we can avoid them.

I was once told by a professor that rotting food releases sulfur compounds and we evolved to find their smell repugnant to avoid eating such food. Don't know if it's true, but it sounds plausible.

canadianer got it, sulfur 's stronger smell is not something intrinsic to sulfur,  we evolved to be better at detecting sulfur becasue we are very vulnerable to the bacteria in spoiled meats. And sulfur compounds are good indicators of rotting meat. Humans have not had the time to evolve the specialized immune-digestion pairing of carnivores.

Bitter taste has less to do with sulfur than the PH of the food in question, bitters is basically biological detection of alkali ph.

(I've noticed dogs are attracted to rotting organic matter.) @John immune-digestion pairing of carnivores?

Dogs (or at least the wolves we bred dogs from) like most carnivores have adaptations of both the immune system and digestive system to handle the bacteria in rotting meat. things like a much more acidic digestive system and more specialized immunological response. http://www.jwildlifedis.org/doi/abs/10.7589/2016-07-162

Related: Why do cyanide and arsenic smell like almonds and garlic, respectively?

Nice question! It would, obviously, be a long answer if I talk about all types of sulfur compounds here. So I will take up just 2 examples to explain this.

Thiols: when we talk about sulfur compounds with foul smell, thiols (mostly) come to the top in the list. Thiols (R-SH) are a class of compounds famous for their smell. Some examples of thiols include:

compounds in onion and garlic (see this answer for more details).
a mix of compounds responsible for the smell of skunk's spray (Anderson et al, 1975)
(R)/(S)-3-methyl-3-sulfanylhexan-1-ol found in human sweat
(Methylthio)methanethiol found in male mouse urine

Some biologically important examples would include coenzyme-A, glutathione and cysteine. However, not all thiols have fowl smell. For example, furan-2-ylmethanethiol provides the aroma of roasted coffee while grapefruit mercaptan gives grapefruit its characteristic scent. You can see a complete list here.
After seeing some examples, lets come to the main point i.e. why thiols have such foul smell. Thiols are decomposition products of proteins. When amino acids, like cysteine and methionine, are decomposed, thiols are one of the last things to form. This would explain why it becomes important to smell and avoid them (you wouldn't want to eat a dead and decaying mammoth, and a blind hunter might not be able to tell if he has found a decaying mammoth if he can't smell such compounds). As a side note, this also explains why organic acids have sour taste and smell. Compounds like glucuronic acid, citric acid, oxalic acid, lactic acid, butyric acid, acetic acid, etc. are all decomposition products (if you know how vinegar is made traditionally). This is why your body tries to get rid of them (I saw that in a video, if you eat things with foul smell and sour taste (it was a Japanese dish probably), you'll suffer nausea and vomiting since your body will do all it can to prevent its harmful effects). See this Wikipedia page for more info.

Hydrogen Sulfide: H2S, or hydrogen sulfide, is another compounds famous for its smell. It smells like rotten eggs, and indeed it is because H2S is what rotten eggs release. The basic reason why H2S smells so bad is again the same. Hydrogen sulfide is one of the final products of proteolysis during decomposition (see same Wikipedia article). But there is another cause why H2S has such foul smell (and why I didn't just stop at thiols): H2S is itself toxic.

H2S has many biological signalling functions, similar to NO and CO. These include:

H2S serves as endotheium-derived relaxing factor (EDRF) and endothelium-derived hyperpolarizing factor (EDHF). In short, it acts as smooth muscle relaxant and vasodilator. It also increases the response of NMDA receptor and facilitates long term potentiation in the brain.
it is converted to sulfite by thiosulfate reductase, and further to thiosulfate and sulfate by sulfite reductase, in the mitochondria. Sulfate is excreted in the urine.
it acts on ATP-sensitive potassium channels in smooth muscles, and does the blood vessel-relaxing work in smaller blood vessels.
it blunts, reverses and promotes healing of diverse inflammatory reactions. A full list is available on this Wikipedia page.
the most pronounced effect of H2S is much similar to that of CO. It also binds to the iron in the mitochondrial cytochrome c oxidase and other mitochondrial cytochrome enzymes, thus preventing cellular respiration and causing death.

This would explain why external source of H2S would be so harmful since, being biologically such an active molecule, its amount needs to be controlled strictly. Now, if you want to know why decaying bodies would be dangerous, this Wikipedia article would be a good starting point.
EDIT: The bitter taste of some vegetables is because of a type of compounds called glucosinolates found in some plants. These compounds dissociate upon eating to form isothiocyanate and are thought to be a part of the plants' defense system (see this answer for more details). Interestingly, a similar type of compound, cucurbitacin, found in Cucurbitacae plants, does not contain sulfur, yet it is responsible for the bitter taste of these plants.

Nice answer, but here is a tip: instead of using this ugly mhchem package formatting, like $\ce{H_2S}$, which changes the font style, just use a good old HTML sub tag, like this: H2S. HTML tags don't work here at the comment, but if you put that in the answer the HTML tag will work. Try it, it's way better.

A paper was published about this in 2016: https://pubs.acs.org/doi/abs/10.1021/jacs.6b06983 Apparently the OR2T11 receptor detects thiols and requires copper to work. Also, it's interesting to note that SO2, which is not a thiol, is also quite easy to smell. You smell SO2 from burnt matches, gunpowder (e.g. fireworks), and some other sources. Evolutionary, I suppose it might be the most common chemical sign of fire that isn't also a normal part of the atmosphere, unlike CO2 and H2O, which are the main products of combustion, and carbon is not a gas, though you maybe can smell it as smoke(idk).


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Is there a reliable estimate of the number of cells on Earth?
A quick Google search didn't turn up any reliable sources. An awkward Cosmoquest thread gives a rough estimate of 10^25 to 10^32, but this is just a bad extrapolation of the number of cells in a human body. Also, I recently learned that we don't even know the number of cells in humans to good precision.
Has anyone ever made a serious attempt to figure this out? If not, does anyone here want to make a quick calculation?

Do you want to count human cells, animal cells or really ALL cells (including bacteria & archea), because these are different orders of magnitude & difficulty

@Nicolai All cells, anywhere and in any organism.

All eukaryotic cells or do you count bacteria as well? Do you count viruses?

All cells, including bacteria and other prokaryotes. Viruses are not cells so they don't count.

I'm voting to close this question as off-topic because it relates to the Guinness book of records, not biology.

@david although this question is off-topic, I don't think it is related to Guinness book in any way :P

@another'Homosapien' — A manner of speaking. You might also term it a "Freak Show" question. This sort of question is asked for no reason other than to be able to respond "wow". It is the very antithesis to science.

I disagree strongly with the people saying this is off-topic, or that it is simply a "wow-factor" question. I think knowing at least an estimate of the number of cells on Earth is important to understanding the environment we live in and just how rare multicellular life is.

I also disagree strongly with those disparaging this question. I think it is an excellent one. I think the burden should be on those who want to avoid answering it to explain why they don't think ecology and evolution have any important extensive properties.

Okay so I looked around a bit, and there are surprisingly few papers related to this question.
This paper is the best I cold find, but it's almost 20 years old. There's also this one, which slightly updates the other one, but they both focus on bacteria. For those the total number is estimated to be somewhere in the range of $10^{30}$.
For humans the latest published number is $3.72 \times 10^{13}$, so even with a few billion in total ($10^9 \times 10^{13} = 10^{22}$) we probably don't even matter for the total cell count. Since smaller more abundant animals have a much lower number of cells, they probably don't matter either.
Now to the only thing I'm not sure about: plants
The number of plants on earth is really elusive, only more elusive is the number of cells per plant. This study claims around 3 trillion ($10^{12}$) tree's on earth. Since tree's are bound to have (many) more cells than humans, we're probably getting closer to the number of prokaryotic cells by now (I guess the number of 'tree cells' will be somewhere around $10^{27}  - 10^{30})$.
So far I didn't find anything about grasses or other plants (neither numbers nor cell counts), so it's really hard to say whether these matter or not.
This study seems to give an average number of cells per growth ring in tree's, but I'm not sure how to get a number of cells / tree from that.
In total the estimated number of bacteria ($10^{30}$) is probably a good measure for the number of cells on earth. Even if plants manage to come to that level, the order of magnitude will probably not change (by much).

It doesn't seem that surprising to me that there are few papers on unanswerable trivia.

About $10^{30}$ prokaryotes (Whitman et al. 1998).
It is an extremely vague estimates of course! Not that every eukaryotic cell contain about $10^3$ mitochondria, so of course eukaryotic cells would have to be negligible in counts even if you consider only the mitochondria. I don't know if Whitman et al. 1998 counted bacteria but it does not change much given the accuracy of their estimate.

Highly related posts

How many organisms have ever lived on Earth?
How many eukaryotes are there on Earth?

$10^7$ is way to low for the number of eukaryotic cells. There are ~7 billion ($10^9$) humans on earth, and we definitely have a large number of cells to multiply with that.

Very minor edit suggest: proCaryotes would be proKaryotes . I could not save the suggested edit because the warning message tells "edit must be 6 character at least. Is there anything else to improve?" Spaces are not getting counted. I don't really have anything else to improve.

Thanks for your help. Indeed, $10^7$ was an estimation of the number of species from M. Lynch. I rewrote the number without thinking. I removed the estimate.

Thanks for your help. Indeed, $10^7$ was an estimation of the number of species from M. Lynch. I rewrote the number without thinking. I removed the estimate.

source: Stack Exchange

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Text Book Recommendation: Organic Evolution
I was wondering if anyone could point me in the direction of any text books on organic evolution? I have recently become interested in the subject and would like to know more. I think an undergrad level book would be a good place to start, but if you would like to recommend any graduate level books it could also be helpful.
I have a background in mathematics and modeling using mathematics. I have also taken a genetics class and an intro to cell biology class as well as read some papers on both subjects. Any help would be nice.
update
I was looking for a higher level discussion on the mechanisms of evolution. A better term to use might be evolutionary biology.
Sorry for the confusion I was under the impression that "organic evolution" was a common term.
Thank you for your time.

Do you mean 'evolution of organs' or 'natural evoltion', or something else with organic evolution ?

Please clarify what you mean by "organic evolution".

Thank you for the help Remi.b I will look in to the books you have recommended.

Organic Evolution - Definition
'Organic evolution' was a common term. It is just rarely used today. Today, we just say 'evolution' or 'evolutionary biology' when referring to the field of study of 'evolution' (or of study of 'evolutionary processes').
Book recommendation
Math oriented
As you are used to work in applied mathematics, you'll definitely be interested in an intro book to population / evolutionary genetics. Population genetics is the mathematical basis of evolutionary theory. You will find recommendations at the post Books on population or evolutionary genetics?.
For you, I'd recommend Population Genetics: A Concise Guide as a start (or another one presented in the first section of the top answer to the post I referred to above). If then, you like coalescent theory (branching process), you might want to look at Coalescent Theory: an Introduction or some other more specialized books.
Not Math Oriented
Maybe you'll want something more introductory with much less math such as the Evolution: Making sense of life by Zimmer and Emlen or Evolution by Futuyma. These books are classic textbooks for intro class to evolutionary biology in Bachelor. These books will have the advantage to present you some other subfields of evolutionary biology such as the diversity of life, reading phylogenetic trees, ecological relationships and many other things that the books of population genetics don't go over.
Most common fields of math used in evolutionary biology
The most common fields of mathematics used in evolutionary biology are system dynamics, game theory, approximation theory, probability theory, branching processes and diffusion equations.

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Why does something taste less sweet after eating something else that is sweet?
Why does something taste less sweet after eating something else that is sweet, especially if you don't drink water in-between.

Welcome to Biology.SE! What research have you done before asking it here?

It happens for food of any taste, not only sweet.

It's a general flaw (IMO bad design) in organic/neural sensor frameworks where inputs tend to be measured relative to previous experience rather than absolute quantitative.
This happens with weights as well. There have been plenty of experiments where people are asked to pick up a heavy weight and then a light weight, then record/estimate the perceived light weight. The next day, they pick up a medium weight and then the same light weight and record the perceived light weight.
The 2nd recording turns out "heavier" because of relative perception.
Suggestion: Computer-mediated nerves designed to measure in absolutes.

Ugh, I can't disagree with you enough about it being a 'flaw.' Sensory adaptation is almost certainly a feature, not a flaw, and is incredibly well preserved across senses and species.

Downvote an otherwise fine answer just because you personally disagree with 1 part of it? pathetic... if relative measurements are a feature, perhaps all the measuring instruments you use should use relative measures, everything from weighing scales to CPU Hz configuration and the speedometer in your vehicle. While you're at it, perhaps your electricity and water meters should use relative measurements so you get a ridiculously large bill if your neighbor uses those utilities sparingly. Precision is a virtue, and mechanical precision is something that everyone should aspire to.

Have you considered that organisms aren't solving the same problems that machines are? I'm not saying relative measurements are good for all things, I am saying they are useful in biology. I'm downvoting because I think your answer is wrong, because it contains no references or explanation the process, and doesn't even contain the word "adaptation" which is the term given to this process in sensory systems.

"Precision is a virtue, and mechanical precision is something that everyone should aspire to." - Citation needed.

If your keyboard ever stops typing the precise keys you press, I'm going to laugh. While relative measurements might be good enough for primitive animal life, modern civilized society requires mechanical precision. Example consequences of lack of precision: missing your highway exit and ending up in the wrong town, accidentally putting lower amounts of food/drink in commercial packages and bottles (infuriating customers), and screwing up a recipe because you couldn't measure the ingredients straight.

When your brain starts receiving non-adapted sensory information, I'm going to laugh. While precise, invariant measures might be good enough for machines and computers, biological organisms need filters that make relevant information salient. Example consequences for not filtering out unnecessary information: not being able to operate a car at all because you are dazzled by the sun and unable to adjust, deafened by the roar of the road that you can't ignore, distracted by being bombarded by dozens of odors from your own body, the air coming in from outside, and the upholstery.

"When your brain starts receiving non-adapted sensory information" It could be part of what's informally called "human 2.0". Some machine learning frameworks and programs filter or transform data in a way that doesn't use relative measurement yet makes it vastly more useful, such as a database view or a numeric array transform. Filtering out sunlight is handled by the eyes rather than in the brain. The road doesn't roar, and even if it did you would be able to hear everything else by mentally "subtracting" the background noise. You obviously have no clue what you're talking about.


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What is the necessary criterion for the maintenance of signaling honesty?
Zahavi's (1975, Journal of Theoretical Biology) handicap principle held that the cost associated with a signal is integral to ensuring that signal is accurate, since dishonest signals would be too costly to bear.  Grafen (1990, Journal of Theoretical Biology) held that in order for signal honesty to be maintained, the signal must be differentially costly, such that it is more expensive for lower-quality individuals.  Getty (2006, Trends in Ecology and Evolution) disputed this:  "Here, I show that (Grafen's) most well known and
influential result (‘the marginal cost of advertising.
should be greater for worse males’) [6], which is widely
interpreted as a proof of the handicap principle, is based
on a simplifying assumption that does not generalize to
signalling in sexual selection. I show that the general
criterion for reliable signalling can be interpreted to mean
that higher quality signallers must be more efficient at
converting signals into fitness and that, in sexually
selected signalling, higher quality signallers can be more
efficient in spite of higher marginal costs."
Nevertheless, Biernaskie, Grafen & Perry (2014, Proceedings of the Royal Society) wrote, "It has long been a challenge to test for the relevant costs of
animal signals [2,17,18,25,42]. This is because, as stressed
above, the modern view of costly signalling theory does not
necessarily imply that observed signals will be costly;
instead, the key prediction is that a given signal size will be
differentially costly for low-quality individuals [2,13,17,31]."  The criterion of differential costliness continues to be invoked despite Getty's critique of it.  So, my question is, what is the criterion necessary for the maintenance of signal honesty?
Note:  This question asks about the maintenance of costly signals that could theoretically be faked, not so-called index signals that cannot be faked.


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Why is the cough reflex triggered when we hear others cough?
Very often, I see a "chain reaction" in people coughing in an exam hall. One person coughs and many follow. It's not necessarily the person closest to him who coughs, it can be someone sitting far away. This doesn't just occur in this setting but also in other situations, such as in public spaces. I was wondering if this is a reflex which has evolved over time as a means of protecting our body from pathogens and harmful chemicals in the air.

https://en.wikipedia.org/wiki/Mirror_neuron


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Is olfaction same among different individuals?
For instance if I smell the fragrance of a rose, well it smells like roses (little bit sweet).  But is that smell the same for other people?
Because we also have different voices, why not have different olfaction.

The substance that you smell is very likely the same as other people (the smell receptor on the nose react to the same chemical), however how your brain reacts to a certain smell is very likely different to other people - so the perceived smell can also be different

@Nicolai thank you! Can you move your comment to the awnser box so I can accept is as an awsner?

Humans generally have the same set up of olfactory receptors, since they are encoded by genes (there likely are minor differences between people, since there are a lot of these genes). Therefore chemically or physically  all humans can smell the same substances.
However, how a smell is perceived depends also a lot on how the brain reacts to a certain smell (or rather the activation of certain olfactory neurons). Therefore individual people can perceive the same chemical substance a different way - how different depends probably strongly on previous experiences.

Humans actually have a wide diversity in the range of odors they can detect. [1],[2] The variations are dependent on a number of factors, including age, sex, pregnancy, training, and individual genetics. [3],[4],[5],[6]
A significant source of genetic variation in olfactory function between individuals comes from the fact that quite a few chemical-sensing genes have in recent evolutionary times become defective in some gene variants while remaining functional in others.  An individual's inheritance of a particular combination of functional and nonfunctional olfactory receptor genes gives the individual an personalized combination of smelling sensitivities. [1]
[1] Menashe, I., Man, O., Lancet, D. and Gilad, Y., 2003. Different noses for different people. Nature genetics, 34(2), p.143. PDF
[2] David G. Laing, Richard L. Doty, Winrich Breipohl, eds., The Human Sense of Smell, Springer Science & Business Media, 2012, p. 312.  Image
[3] Odor - Wikipedia
[4] A.B. Marin  T.E. Acree  J. Barnard, Variation in odor detection thresholds determined by charm analysis, Chem Senses (1988) 13 (3): 435-444. DOI: https://doi.org/10.1093/chemse/13.3.435
[5] Darren W. Logan, Do you smell what I smell? Genetic variation in olfactory perception.,
Biochem Soc Trans. 2014 Aug; 42(4): 861–865. doi: https://doi.org/10.1042/BST20140052
[6] Simon Makin, Sense of smell has a genetic flavour, New Scientist


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Organ of ingestion in lice
I want to know that what the name of the organ used by lice for ingestion is? (also please explain if possible). In my research, I got this wiki page that didn't help me out. Then I found this link which says that it sucks blood and pumps up that with a tube so, I want the specific name of that organ.

What louse are you interested in? Human head louse? Louse is a pretty big taxon/group.

human head lice @Tytoalba

Okay. Can you do some research specifically on it? A good set of keywords would be 'head louse feeding'. If you don't find your answer and share the things you found, your question is likely to be reopened for answering.

new edits up in the discription, you must check that out @Tytoalba


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How Plausible is Restoration of Cryonically Preserved People?
I fear death (so much that I'll prefer a year/few of torture over death), and plan to sign up for cryonics. I would like to know how plausible it is, why the answer would be so, and if possible how many years away would revival be.
Thanks.
I have read a lot of articles on Alcor, and done several hours of research since yesterday. Mainstream Science seems to assign infinitesimal probabilities against, it, but the guys at Alcor (and other Cryonic institutes like Cryonics.org think they've got a case). It seems theoretically possible to me, but I don't want to but into too much hype—so how plausible is it?

Not even the "world's leading cryonics company" wants to give any kind of estimate. http://www.alcor.org/FAQs/faq01.html#patients

I've browsed their FAQs; I want information from a non biased source.

I think @skymningen's point is that if even the biased source isn't promising anything, the plausibility is vanishingly small.

You browsed their FAQ, was there any data? Have they accomplished a successful freeze/thaw? Do they have stability data? Safety data?

Vitrification of a Rabbit brain and devitrification was done, and the brain was successfully preserved in perfect condition (they didn't bother reviving it though.

Largely implausible, mainly due to damage from freezing. This type of damage even happens when food is frozen (although flash-freezing decreases it).
More feasible approaches for avoiding death would include machine-replacement parts, lab-grown transplants, neural backups, and regenerative gene modifications. I'm surprised no one has considered studying hibernation and how to add similar genes to humans that would enable hibernation.

They don't freeze people—they vitrify. Freezing damage doesn't happen. Downvoting for not bothering to acquaint yourself with the process before condemning it.


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How to form biological metallic tissue?
There are numerous popular articles claiming that the wasp Apocrypta Westwoodi Grandi features an ovipositor tipped with zinc. You can find such an article here. You can watch an impressive video here. Beyond that, I have found information on the genus to be sparse.
Yet my question is, how metallic tissue can be formed. The popular article claims actual zinc was detected. It seems unlikely to me, these creatures consistently find a source of zinc to feed from, so as to deposit zinc in their tissue. Even so, I don't understand how this zinc can be made to deposit at a specific point. The article clarifies:

With an x-ray detector and the electron microscope, they discovered the presence of zinc. It was only on the tips of the parasitic fig wasp’s ovipositors. Gundiah said, “We see it very consistently only at the tip and not anywhere else.”

I am no biologist, but, to my feeble understanding the only alternative is that the so called zinc is actually synthesised by the body as a protein normally is. Surely no atomic reactions could take place in the wasp! :-p  Even teeth are mostly Ca5(PO4)3 OH, Calcium is found in plenty of our foods. Phosphorus is present in meats. But zinc? I totally don't understand it!

I'm not aware of body synthesising ions de-novo.

I don't know about non-trace amounts of zinc but iron is common, and Iron reinforced tissues exists, things like beaver teeth and scaly foot snail shells which are made of iron reinforced enamel and iron sulfide respectively.

@Ludi You may not be aware but zinc is an essential mineral for all plants and animals (not certain about all bacteria), as are several other metal ions.

@BryanKrause exactly. Of this I wasn't aware. Now, due to Gillian's answer, I did some research. Before I thought it was extremely rare. Embarrassing, since I was a physicist, but what can I say...

Related: Why are there no organisms with metal body parts, like weapons, bones, and armour? Or are there?

First and foremost, it looks like the original article is slightly less dramatic:

Parasitoid ovipositor tips have a higher content of the transition metal zinc compared with the cuticle elsewhere on the ovipositor

So a 'higher concentration' isn't quite the same as 'tipped with'. It looks like they are describing a higher numbers of metal ions, rather than pure metal:

The presence of transition metals in insect cuticle and mandible is hypothesized to increase material hardness to permit cutting through hard substrates with minimal wear

There are many examples of organisms using inorganic chemistry to make materials. The overall topic is called biomineralization and you even mention teeth - which is hydroxyapatite (not really organic chemistry!).
However, a pure metal like zinc is unusual, I think. There are examples such as the snail that has an iron pyrite 'armor' or even the iron nanocrystals in ferritin.
More spectacular examples include the bacteria that produce gold particles

As a result, Au
  detoxification is mediated by a combination of efflux, reduction, and
  possibly methylation of Au-complexes, leading to the formation of
  Au(I)-C-compounds and nanoparticulate Au0.

Where Au0 is pure gold. I don't know of any other examples of pure zinc in organisms, but there is a nice review here of zinc biochemistry.
When you say 'synthesise' I assume that you mean 'deposit'.

I am not a biologist or chemist so my (faulty?) understanding is that the wasp has to eat zinc to deposit it. Otherwise it has to somehow produce it, which I cannot imagine. My other assumption was that substances based carbon are called organic, with some historically motivated exceptions.

@Ludi - Sure, they certainly have to eat it, as organisms are not known to synthesise elements! You are right that most compounds with carbon in them are 'organic', but "Ca5(PO4)3 OH" is a calcium compound, with no carbon.

@gillean oh, gosh, what a stupid mistake! Anyway, it is clear we can get Calcium and Phosphorus from some foods. But where the heck would a wasp get Zinc?

@Ludi Most foods will have small amounts of elements that we tend to think of as rare - zinc, molybdenum, iodine, etc. It's actually quite common to find zinc in biochemistry, as they are used in a "zinc finger" that binds to DNA - of course, that's just a single atom

Maybe you put that in the answer, unless I am the only simpleton who doesn't know it ;)

@Ludi: Just to make things clear: the wasp only needs to consume some substance that contains zinc atoms, not actual bits of metal, right? So the molecule containing a zinc atom doesn't need to behave like pure or even concentrated metal at all. From the Wiki article on Zinc Compounds: A very large number of metallo-enzymes contain zinc(II). Also many proteins contain zinc for structural reasons.


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How do fish maintain razor sharp teeth?
I was watching a program about Barracuda - they have a front tooth that is supposed to be razor sharp.  My kitchen knife goes blunt if I use it for long periods without sharpening.  Sharks keep on growing new teeth but barracuda don't.
How do fish like Barracuda maintain a tooth that is razor sharp?
Edit News article on how sharp the tooth is
http://www.dailymail.co.uk/news/article-1348152/Barracuda-attack-breaks-womans-ribs-forces-boyfriend-seal-punctured-lung-hand.html

Added wiki link to your post. Adding links to content improves readability for curious and/or competent users, experts and those reviewing your posts.

Fish replace their teeth over time as needed. Thus, they don't maintain the sharpness of individual tooth, they just replace it. This is a passive process not a conscious process.
Source: Barton, M., & Bond, C. E. (2007). Bond's biology of fishes. Thomson.Pg. 414-415.

@cup feel free to accept the answer


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What does it exactly mean to sequence the genome of a species?
Since all organisms are different from each other - that is, we all have different alleles, some SNP, microsatellites, etc. -, what does it exactly mean, for the genome of a species, to be sequenced? I understand what it means for an organism's genome to be sequenced, but I don't really get what it means for a species.
I'm quite confused about this. Thanks in advance for the help!

Sequencing a "species" builds a reference genome that is considered to be a good "representative" of the species. Of course there will be genetic variation between the reference and healthy specimens in practice (usually SNPs), however it should be minimal.

+1 for a concise answer, but saying the variation is "minimal"...


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How many kg of seed can one expect from 230 kg of cotton fiber?
So I'm working with data from recent cotton harvest from a seed company. They're more interested in cotton seed than the fiber itself. I'm trying to come up with seed yield numbers for an array of cultivars but the data I was given came in kg of harvested fiber. Excluding any changes between cultivars due to genetics,
Does anyone have an idea of how many kg of cotton seed I can get from a given yield of cotton fiber?
Kind regards,

That would be a great question for Agriculture&Farming.SE (still suggested in Area51 and quite far from having its won site though).

According to this document (pdf) the rate is around 700 lb seed per 500 lb of fibre.
seed = 1·4 × fibre
230 kg fibre ≅ 320 kg seed
(Strangely, the rate has fallen over time.)

That is strange…

Curious, it has indeed. 230 kg of fiber in our case yielded 226 kg of seed.


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Why aren't there more Ash-Red pigeons?
My favorite color pigeon is Ash-Red, but I don't see a lot of them.  I figured it must be a recessive phenotype, but when I googled it, I found out it's dominant.  So why aren't there more Ash-Red pigeons around?
Edit: I'm in North America.
Edit 2: This website from the University of Utah is where I learned that Ash-Red is the dominant phenotype.

"I don't see a lot of them" is a bit of a vague statement. Have you checked whether there is some data available that shows that population levels for Ash-red pigeons are low in North America? It could simply be that the pigeons are more timid than other species or that the particular micro-enviorment you live in (it's an assumption here) is not suitable for Ash-red pigeons.

Good point!  Searching for specific numbers of Ash-Red pigeons in North America actually helped me find a book with a really good answer to my question... thank you!

Welcome to Biology.SE
Assumption
I will assume it is true that the allele causing a ash-red plumage is dominant over all other alleles. Note however that you should cite your reference when making such claim in your post.
Dominance and allele frequency
Phenotypes associated to a dominant allele A aren't necessarily more common than the phenotype of the recessive allele a. It all depends on the allele frequency. If the dominant allele is at low frequency then both AA and Aa (both displaying the dominant phenotype) are at low frequency (esp. AA individuals) and most individuals are aa and show the recessive phenotype.
Learn more
You might want to read about Hardy-Weinberg rule with this post for example.


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What biological process was taking place?
A tub of a side dish, either tomato salsa or baba ganoush (eggplant), was left in a plastic bag for several months.  The plastic bag was not airtight, but was wrapped somewhat tightly around the tub.  Although it was supposed to be stored refrigerated, it was not (it was stored at room temperature).  It also was not supposed to be stored for such a long duration.
When the bag with the tub inside was eventually handled, it was noticeably hot.
What biological reaction was taking place that would generate that kind of heat, especially after months of storage?

Exothermic bacteria such as routinely found in compost piles! http://compost.css.cornell.edu/physics.html

As outlined in my comment, I hypothesise it must have been the growth of exothermic bacteria. As the name suggests, these produce heat. An especially interesting phenomenon concerns the danger of fire erupting from moist hay, as the bacteria feed from it and dry it simultaneously! This is outlined here. A memorable quote from that article:

Dry hay (stored at 15 percent moisture or less) is safe for long-term storage. However, if the hay has become wet the quality has been permanently changed and the potential fire hazard from spontaneous combustion increased.

The same principle underlies the heating of compost, about which you can read in greater detail here.
Most astounding I found the post dealing with the possible contribution of exothermic gut bacteria to our thermoregulation.
As of now, I don't know about the basic mechanisms by which these bacteria generate heat, but the abstract of this article implies that heat absorbing bacterial growth is extraordinary.
I myself have forgotten everything about chemistry, but from the comments below I gathered that what happens is similar to the oxidations of sugar. You can read examples here, which demonstrate that these are exothermic.

The mechanism is that they are essentially "burning" the organic compounds for energy, just like your own cells do, it's just that they are doing so fast enough to create a lot of heat.

Why is it a tautology? I guess my point was that there isn't any special mechanism, it's just from metabolism. I suppose maybe what you mean is "what is the mechanism by which they can continue to generate so much heat without simply sterilizing themselves."

I meant burning in the sense that the end reactions are converting carbohydrates into CO2 and water. Although the path of reactions isn't the same (and much slower), the products and thermal output are the same as if you lit the pile of hay on fire. So yes, oxidation.

@BryanKrause ok that makes perfect sense!


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What is this white/translucent with brown back, larva/worm creature I found, in the UK, on my lettuce?
I'm in United Kingdom, East Anglia. I've just started to grow lettuce in my back garden, taking my first harvest today, I found one of these creatures:

They have a distinctive brown/white mark along the top of their behind. The black dot appears to be its front, as it scouts with that, and moves in that direction most of the time. This is about 10mm long, give or take 50% depending on how stretched out it is.
They appear to have transparent skin, as I think we can see its organs in there. It moves almost peristaltically (similar to a worm), but with direction, not just flapping around, and seems to like the undersides of things.
They're not particularly segmented, though they have those tiny, tiny ridges as you can see. And there are no legs or meaningful features to speak of on its underside. They were also slightly sticky, with a white-ish secretion.
I have since looked and found a few amongst the other lettuce, which all look incredibly similar to this. Usually hiding inside the outer leaves, but not exactly an infestation (yet!). They don't seem to be on any other plants at the moment. There's no evidence that they've eaten any leaves, or anything, currently.
I have done a lot of searching and attempts to identify, but I can't for the life of me find this online. My amateur guess is some sort vermiform fly larva, but it could be anything from a baby caterpillar to a worm, for all I know. Any help in narrowing it down, or especially in finding out if I should be worried for the plants, would be helpful.

It's a kind of hoverfly larva (don't know which one, maybe Episyrphus balteatus), they eat aphids on cabbages.
Image on wiki commons

Hi Claudia, welcome to Bio.SE & thanks for providing a response to this question. Though I agree that your answer appears to be a valid guess, it really comes across as just that: a guess. What we're looking for in this SE community are answers that are well-supported and descriptive. Please [edit] your answer to provide details (i.e., why your answer is right and what characteristics led you to your conclusion) and either citations or links to reputable support for your answer. Our goal is to educate others, so the more info you give the better.

Editing your post will surely result in more positive response from our community. Please see How do I write a good answer? and suggestions for writing [tag:species-identification] answers. Thanks!

I think this answer is right, so I've added a link to a picture. Feel free to roll back if you disagree.

They indeed really look like "maggots": fly larvae (number 15 in the "section 2" figure: https://entomology.ca.uky.edu/ef017.
These ones look to me like Drosophila larvae, but much larger than the common laboratory fruit fly, so they are probably a different genus.
Maybe they are simple housefly larvae, like in this video: https://www.youtube.com/watch?v=F6TcIybY7Qo

Thanks for the interesting link, but could you explain why it is nr 15 and not nr 16?

@RHA, I'm familiar with the typical shape of a fly larva (number 15). Admittedly, I'm not familiar with the aspect of aphid predator larvae (number 16), which could have very similar features. The description for number 16 mentions "they tend to have green tinged bodies" while for number 15 it mentions "a cream to white body", which better matches the photos given in the question. I would not exclude number 16, though.

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


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Small jumping bugs inside Swiss flat
Saw these bugs inside the flat I'm renting (Switzerland), but I really can't figure what kind they are. What I can say about them:

They can do small jumps (up to 5cm I would say). It doesn't seem to be for locomotion, but as a means of escape when I try to catch one.
Size: about 1.5mm for the "big" ones. There are of various sizes down to 0.25mm for the really tiny ones (approximately; never managed to get one without crushing it). They behave much the same as the big ones (including the jumps) and are whiter in color.
They don't seem to live as a colony or in a nest (or I simply didn't find it), but sparsely on the wood floor, often near the baseboards. Found some on the walls, but those were the exceptions. They don't seem to like the bathroom.
Rather delicate; can easily be crushed.
Seem more active in the evening and at night, but don't mind going out during the day.
I live alone, without pets, but I don't remember having been bitten. I guess they don't feed on blood.
Seem to have long antennas (about half their body size) and small wings.

Side note: the flat is on the 3rd floor of a recent building (finished 14 months ago). I'm the first tenant.
An exterminator came and quickly classified them as some kind of flea. He put some pesticide on the baseboards, and their number is now quickly decreasing. But I'm still curious.
My first thought was "fleas" (because of the jumps), but I deemed them too squishy and not "vampire" enough for that. Also, I don't think that (what I assume to be) the young ones should be able to jump.
Then I thought "springtails", but I didn't see any furcula (granted, I don't have a good eyesight) and I don't think they are supposed to have wings.
One of them was nice enough to jump on some tape.
Top (on a ruler):

Front/Side:

Also, blowing on it (to open the wings):

Youtube video of one of them

They're definitely not fleas despite what the exterminator said. Fleas can REALLY jump, don't have wings and aren't easily squished. But I've no idea what sort of insects are found in Switzerland, especially in homes.

You must be mistaken. The Swiss are very, very clean.

I've resized the images to reduce the amount of scrolling. You can still click on them for the large version, but feel free to rollback if you want.

I believe these are some sort of Psocoptera, "booklice", even though they don't really jump much. Could it be that they ran or flew a little bit instead? I won't try an identification of the species, but in general booklice like damp places and most of them aren't considered serous pests.
Example of a booklouse:

Slender legs and antennae, wings, and general appearence close to your specimens.
(Image from Wikipedia)

Yep, this is the one! That would be a Dorypteryx (domestica or longipennis) then, I guess? I can't tell if they are jumping or flying, I will try to record and upload a video next time I corner one of them.

See this question, this question and this question for other posts about psocids...

@theforestecologist Yeah, this seems like a recurring thing. I guess this sort of question could be closed as a duplicate? But species identification is pretty hard to find answers to by searching if you don't know what to search for, so they'll probably keep coming.


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How do I find samples/patients in TCGA (the cancer genome atlas) that had radiation therapy?
I want to correlate the expression of a gene (for sample the KRAS gene) with survival and if the patient received radiation therapy using any suitable TCGA (the cancer genome atlas) dataset. However, I have so far been unable to figure out what patients have received radiation therapy.
Any suggestions?

The process is slightly painful but here is how you do it.
Go to UCSC Xena, then launch the browser, hit the Visualize tab, pick your cohort of interest, then in the next menu pick phenotype, and then type radiotherapy in the box and pick the radiotherapy related columns you want. Then, once it has loaded the annotation bar, you can hit download and the downloaded spreadsheet will have this information along with the TCGA barcodes. As for clinical data, https://www.synapse.org/#!Synapse:syn7343873/wiki/412112 is a very good pancancer source.


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Are nastic responses growth responses?
I know they are non directional movement responses, but like tropic responses, does their movement involve growth?


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What does endochorous dispersers means?
In an article (Guerrero and Tye, 2009) it talks about endochorous dispersers.
Guerrero, A. M., and A. Tye. 2009. Darwin's Finches as Seed Predators and Dispersers. The Wilson Journal of Ornithology 121:752–764.

The highest proportions of feces containing viable seeds were of Small
  Ground Finch (G. fuliginosa) and the ‘‘insectivorous’’ species
  Woodpecker Finch (Camarhynchus pallidus) and Warbler Finch (Certhidea
  olivacea). These two may be more important endochorous dispersers than
  other species that eat more fruit but are better seed predators.
  Intact seeds were found in 23% of fecal samples; 50% of the samples
  with intact seeds had viable seeds.

I've looked on google and found nothing...
Do you know what that means?
It seems it relates to mast-fruiting plant species.

I found the definition here, which is a cool package in R:

animal - all vertebrate dispersed seeds, without distinction between
  attached(epichorous) and ingested (endochorous) dispersal of seeds


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Can you identify this Illinois wasp?
I live in northern Illinois and had these guys appearing in my room. No facial markings and they seem non agressive.
About 2cm in length with off white u shaped markings below it's waist and a single white line a few segments down.

It looks to me as Potter Wasp (or mason wasps), the Eumeninae, are a cosmopolitan wasp group presently treated as a subfamily of Vespidae, but sometimes recognized in the past as a separate family, Eumenidae.
Since there is no more info provided and image is not sharp I cannot be 100% sure.

The post displays info about its size now which was previously hidden due to improper usage of markdown.

The online Canadian Journal of Arthropod Identification has an issue covering the Vespidae of northeastern North America (PDF available here: http://biologicalsurvey.ca/ejournal/bmc_05/pdf/bmc05.pdf), with Illinois as a limital point; if you have a stereoscope available and are willing to take a specimen (freezing will work, if you don't want to use poisons), you will get a species name from that work.


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How does evolution get around the combinatorial problem?
Imagine a combinatorial tree showing all the possible arrangements of nucleotides. Some arrangements are functional, meaning they can be plugged into a cell and create a living organism capable of reproducing. Some arrangements are nonfunctional, meaning they can't sustain any living system at all.
In evolution, new information is created as the result of what are essentially an accumulation of copying errors. My question is, would the ratio of functional to nonfunctional arrangements have to be relatively large  so that enough genetic information can arise in response to natural selection? If so, what scientific studies have led biologists to conclude that this combinatorial space is rich with functional arrangements. If it isn't necessary please explain why.

The ratio is incredibly low with almost all possible combinations being nonfunctional. If you have, by chance, a functional combination, evolution is extremely conservative and works in a step-wise trial-and-error manner, usually not taking large steps in the space of possible sequence combinations. If no one else answers your question in greater detail, I will provide an answer in the coming days.

What exactly do you mean by "genetic information"?  Are you thinking of some Shannon entropy-type thing, or do you just mean new genetic variants that increase fitness?  Please clarify.

No, with some caveats. First, about the actual value of the ratio: it's probably tiny, with almost all possible genetic sequences failing to lead to living organisms.
Why does this not make evolution impossible? Each sequence can have billions* of neighbors in sequence space. If even a very small number of those are functional, evolution can proceed. More importantly, the functional sequences are clustered in sequence space. If you pick 3 billion nucleotides randomly, you'll get nonsense, but if you mutate a single nucleotide in a human you'll most likely get a perfectly good human.
There are interesting open questions here, though, especially regarding the origin of life, and whether natural selection tends to drive populations to regions of sequence space that are especially dense with functional sequences.
*Just looking at point mutations. Including the full mutational spectrum gives many more.

would the ratio of functional to nonfunctional arrangements have to be relatively large so that enough genetic information can arise in response to natural selection?

Evolution does definitely not explore all possible combinations of a DNA. It just try things out. Of course a new gene is not necessarily recreated from scratch. A gene often get copied and then the two copies can diverge (this is called neo-functionalization).
So, no not the all possibility space is explored but this is in no way a trouble. It is not like a mutation would cause a whole brand new sequence out ov the void and hope for it to be beneficial. A path is being taken through this possibility space.

"would the ratio of functional to nonfunctional arrangements have to be relatively large so that enough genetic information can arise in response to natural selection?"
Yes it is very large. Because most mutations are synonymous mutations.
Take a look at the part about the degeneracy of the genetic code.
Another reason, and this one only helps evolution move on is called gene duplication. Many proteins in a genome are duplicated, meaning there is some redundancy involved. If we delete one protein, the fitness of the organism may/may not be affected but survival won't be affected. One example that comes to mind is Histone H1 (because I studied about it a bit). To clearly affect a change we need to delete at least three H1 genes, any less and one of its variants act as replacements.
Bonus answer, evolution does not always lead to the best possible combination, it leads to functional combinations.

I am not the down voter. But I think the first part does nothing to explain a large fraction of functional arrangements. It merely simplifies the problem to a smaller number of arrangements, but we don't know the ratio of functional ones among these!


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Where to begin studying Biology in earnest, with preferably free sources?
I am a biology enthusiast and would like to study Biology in earnest. I have basic knowledge of biology (high school level) and some extended knowledge of small animals, mainly about mammals as I am naturally interested in them.
So I would like to start studying veterinary and Mammalogy first.
I would prefer free sources for studying since I have little money available.

Welcome to Biology S.E. I would recommend to have a quick look at the  tour (https://biology.stackexchange.com/tour), learn about Biology S.E and earn your first badge.

Okey Johhny will do now. EDIT: Got it :)

I think if you can narrow down your areas of interest a lot more, answering the question will be easier, other wise this question is too broad. (I have found that non-specialised, general  biology sites meant for open learning are not great, lack precision.) Narrowing down your areas of interest to something like Evolution, Genetics (if you are into mammals, may be Zoology, or if their behaviour, ethology) will get you good answers(recommendations).

Thank you for response what I am interest in Veterinary itself but for now I will start with Mammalogy I guess :)

Coursera may have some stuff you can use. https://www.coursera.org/learn/becoming-a-veterinarian/lecture/rS68J/teaching-learning-veterinary-medicine You can buy old mammology and vetinary  textbooks, you will likely find some free pdfs of them if you look in the right places. You may need to study up on college level biology first however. .

[Khan Academy > Biology][https://www.khanacademy.org/science/biology] is very good. It offers a good broad introduction to the main fields of biology. It does not talk about mammalogy or veterinary though.

@Remi.b I have found some factual errors at places on Khanacedemy videos especially ones made by Sal Khan (talking about biology videos). So I think grabbing a book is better than learning from these videos.

I have modified your question. You want free stuff. Open source means (more or less) that the code or original material is not protected by copyright and can be modified and redistributed.  You are not interested in this.

Considering books, I guess the Campbell is the best place to start in biology, but it's really a general biology book and it's not focused on mammalogy, even if there are some chapters dedicated to animal physiology and animal diversity... you can probably find it in a library if you don't want to buy it, and there exists a pdf version as well. I hope it helps somehow. :)

Before getting into veterinary and mammalogy, you might want to start with the basics. As many people have mentioned, Campbell and Reece is one of the best textbooks to start a foundation in biology. If you live near a public library you might find a 6th or 7th edition to borrow. Amazon has a few 7th editions for cheap as well. Although it is an introductory biology book, it will give you a wonderful tour of cellular and molecular biology that will make it much easier when studying animal physiology (which they also covered in the later chapters to a limited extent).
Free Biology Text Books:
Boundless Biology: Boundless is a company that has many free textbooks for high school level biology to help teachers in have a free online textbook.
I have also found a list of free biology text books here that might be of use.
Free Mammology Textbook:
As part of a National Science Foundation Grant, the Northwest Center for Sustainable Resources created *Introduction to Mammology*. It is a free textbook that was developed for a two-year Wildlife Technology program. It also contains information related to the lab portion of the program, but you can skip those and focus on the material.
Free Online Coursework:
Coursera: A few people have already mentioned Coursera, which is a Massive Open Online Content (MOOC). Here, you can find many courses across a wide range of biology topics (and others!). You can enroll in a course (for free) and many times they come with accompanying free textbooks as well (at least that is what I have experienced).
edX: Another MOOC that was started by Harvard.
Khan Academy: Another great website for explanations of certain aspects of biology. As Tyto alba stated, there are some errors in the videos.


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Detect which antigen binds to IgE
Assume that a patient has chronic hives (itchy) on the skin. I understand that he has an antigen, which binds to IgE and eventually triggers histamine release, causing an allergic reaction. So is there any method to detect which molecule/antigen has bound to his IgE? (can we capture it with like what we do to obtain a 3d protein/molecule structure?)

Have you any idea how much work is involved in determining 3D structures?

@David I've seen some method to determining 3D structures here but i haven't tried it my self ( I'm just a student learning theory ): https://pdb101.rcsb.org/learn/guide-to-understanding-pdb-data/methods-for-determining-structure. - "The protein is purified, placed in a strong magnetic field," I'm not sure how many copy of purified protein is needed to determine their structure. Is that possible if I extract these IgE-antigen complex from 5cc blood, purify and determine 3d structure like that?

3D structure determination is a complex expensive specialized procedure that can take months or years. It is not something that can be performed routinely or even purchased commercially. Labs that do this kind of work choose the proteins to work on with great care because of this, the main criterion being biological interest. They live by their resulting publications.

@David  I've never known about that. Thank you very much for this precious information. So this mission is very hard to archive even it may possible in theory. I hope to see a method that widely available on the market on near future.

From what I understand most allergies are detected by a scratch test. from the link below:
"A skin prick test, also called a puncture or scratch test, checks for immediate allergic reactions to as many as 40 different substances at once. ... After cleaning the test site with alcohol, the nurse draws small marks on your skin and applies a drop of allergen extract next to each mark. He or she then uses a lancet to prick the extracts into the skin's surface. A new lancet is used for each allergen. ...About 15 minutes after the skin pricks, the nurse observes your skin for signs of allergic reactions. If you are allergic to one of the substances tested, you'll develop a raised, red, itchy bump (wheal) that may look like a mosquito bite"
More information on scratch tests can be found here:
http://www.mayoclinic.org/tests-procedures/allergy-tests/basics/what-you-can-expect/prc-20014505
After a quick google search,I found a paper from 2014 [1] that seems to speak to the essence of what you are asking, link below.
http://www.tandfonline.com/doi/abs/10.1586/14737159.4.4.539 [1]
In the paper above they propose using a protein microarray technology to find allergies.
I am not sure if there is any way to extract the igE-antigen complex from the patient. But I think it could probably be done with the microarray technology. Although it would be cool to see a picture of the complex.
I hope I have helped answer your question.
[1] Harwanegg, Christian, and Reinhard Hiller. "Expert Review of Molecular Diagnostics." Taylor and Francis Online. Expert Review of Molecular Diagnostics, 09 Jan. 2014.

Thank you for sharing your knowledge. +1 for this answer because your answer covered the only possible method that I've known to predict antigen by skin prick test and microarray. But i won't mark this question as resolved because I would like to see a better method, what happen if an unknown antigen present on our body that skin prick test and microarray cannot recognize it?


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Has human evolution currently stopped?
Due to the advent of social networking and dating sites, it is now possible for almost anyone to find a potential mate. Therefore, there is not as much of a pressure based on physical characteristics or even intelligence anymore. Society does not present the same pressures as was historically present in nature to find food and avoid being killed by predators and potential mating rivals. Almost all alleles regardless of their characteristics are passed on to the next generation through someone or another and attractive traits are no longer chosen above deficient ones. The only exception often being conditions such as dwarfism, Down Syndrome or Parkinson's Disease where the recipients of disadvantageous alleles choose to remove themselves from the gene pool.
Therefore, does this mean that human evolution has been halted due to an absence of natural selection?
My question differs from "Has human medicine stopped humans evolving?" because my post focuses on societal and cultural changes as opposed to medical changes.

"My question differs from "Has human medicine stopped humans evolving?" because my post focuses on societal and cultural changes as opposed to medical changes."
Still a duplicate because the answer is still that humans continue to undergo strong natural selection, so it doesn't matter what you speculate is preventing natural selection, it isn't stopping natural selection. If this question is considered not a duplicate, you could then ask if Sugar-frosted Wheaties are stopping evolution, and then if bleached hair is stopping evolution ... doesn't matter since the premise is wrong.

If the premise is wrong then respond by answering. Just because 2 + 3 and 7 - 2 have the same answer they are not the same question.

The questions are different clearly

On top of the two posts marked as duplicate, you might also want to consider the post Is there evolution in humans since the first homo sapiens sapiens

No charlie they really are not, the question boils down to are humans still evolving and the answer is yes. All the speculation does not change the fundamental question. It might not be an exact match to the two marked questions but Remi's linked question is identical, even to the timeframe.

"Due to the advent of social networking and dating sites, it is now possible for almost anyone to find a potential mate." - Citation needed.

Evolution is an attribute of complex adaptive systems, it is a mistake to consider it as just a biological phenomenon. Human physiology, culture, society, economics and the environment, and so on, are all examples of complex adaptive systems, and interdependent (actually not separate). Evolution is inherent in the system, it never ceases.


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What is bilateral symmetry in "bilateria", an actual symmentry
Wikipedia defines bilateria as :

animals with bilateral symmetry, i.e., they have a head ("anterior") and a
  tail ("posterior") as well as a back ("dorsal") and a belly
  ("ventral"); therefore they also have a left side and a right side.

By symmetry, I understand that divisions of the body along some plane be similar. Now, if you have a head and tail, isn't the horizontal symmetry lost (head and tail look different) ? Similarly, for a vertical division, a different looking belly and back also destroys symmetry along this axis.
An organism whose head and tail are exactly the same (you can't even make out if something is head, and the other, tail), is perhaps "actually" bilaterally symmetrical (along the horizontal axis).
What am I missing here ?

You are missing that "bilateral symmetry" does not mean "the divisions are the same on some arbitrary plane" it means "the divisions are the same on one specific plane".
That specific plane for animals with bilateral symmetry is on the mid-saggittal plane that divides the body into left and right. You won't get symmetry if you bisect in any other plane. If you do get symmetry in a different plane, then you are no longer talking about bilateral symmetry but rather some other type of symmetry, such as radial symmetry, spherical symmetry, or biradial symmetry.
Note also that although many animals do not have perfect bilateral symmetry in their internal organs (humans, for one), they are still considered to be bilateral symmetrical, because the bilateral symmetry is the main organizing feature of the whole animal.

Horizontal axis is a meaningless term.
Bilateral literally means bi=two Lateral=side, so one plane (two halves) of symmetry comparing sides, the symmetry is in comparing right to left.
having a front and back create alone (no top and bottom or left and right) would create something like radial symmetry.  add a diffrence in top and bottom and you get bilateral, in which left and right are the only plane in which one side mirrors the other. Consider this image. An organism where you can't tell one end form the other would be a sponge things with no symmetry or spherical symmetry, symmetric across all possible planes.
Horizontal axis could mean anything, it could mean three different things(symmetrical top to bottom, symmetrical front to back,  or symmetrical left to right) that's why we use terms like bilateral. So you need to qualify what you mean by horizontal. Horizontal is not an axis it is a plane, and I know of nothing symmetrical along that plane (top vs bottom).


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What would happen to the body if it suffered no injuries?
In this (super cute) animation: 'Jinxy Jenkins & Lucky Lou' (youtube), the girl, Lucky Lou, is shown to be so lucky, she seems to have never suffered an injury. This is, atleast, what I get the indication of at 1:26 when she looks at her hand in a mixture of confusion and awe.
And this got me thinking, what kind of applications would it have for a human body, to live to about 20-25 without having ANY injuries happen to it? And I mean NONE, not even muscle aches, scraping of hands or knees, no nothing.
I may be wrong in this, but I have perhaps been led to believe that when an injury occours, whilst the body repairs itself, it also goes through some steps to toughen the injured area.
Would the body be noticably more fragile, or would it have virtually no effect?

It is a myth that injuries toughen your body. Broken bones and scars are not stronger than the original, and neither is any other injury beneficial. Have you heard the saying, "Whatever doesn't kill you makes you stronger"? That's optimistic nonsense. Sometimes what doesn't kill you leaves you paralyzed.


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Question about the consequences of non-random mating and allele frequencies
I just began studying population genetics, and I don't understand something that is written in my lecture:

Consequences of non-random mating:

More homozygote and less heterozygote individuals in the population
Allele frequencies are constant (not in case of negative density dependence)
Genotype frequencies change

What I don't understand is the second point. If the genotypes' frequencies change, shouldn't the frequencies of alleles change as well? Furthermore, I don't really understand either how this is supposed to be linked to a negative density-dependence case...
Any help is welcome! :)

Out of context at least the small piece of text you cite is very poorly phrased and partially wrong.
First, you should have a look at Solving Hardy Weinberg problems. Take your time and read that post... Done? Good.

More homozygote and less heterozygote individuals in the population

This is wrong as non-assortative mating might be disassortative mating where individuals are attracted to individuals of different genotypes.
However, it is true that population structure will cause excess of homozygotes. This is called the Allee effect. The loss of heterozygosity due to population structure is equal to twice the variance in mean allele frequency among those populations. These details sounds a bit too advance for your needs though so I won't go any further.

Allele frequencies are constant (not in case of negative density dependence)
  Genotype frequencies change

Constant over what? Change over what? Not over time necessarily (at least not unless some other assumptions are being made).
I guess what is meant is that if in a given generation mating is not random (due to population structure for example), then you expect the same allele frequency as if it was random but not the same genotype frequency. If it is not clear why, you should probably reread the post "Solving Hardy-Weinberg problems"

Much further discussion in both english and french on @AlissaDeschamps misunderstanding can be found here.

Thanks for your answer! I read all the post about Hardy Weinberg and solved all the problems, but now I still don't understand why the allele frequencies should be constant under non-random mating, and I don't understand either how re-reading the post is supposed to help since Hardy-Weinberg is assuming random mating... I imagined a situation where there would be non-random mating (such as positive assortative mating) and a change in genotype frequencies, but I got a change in allele frequencies as well... So, could you please help me a little bit more? Thanks in advance!

I think your issue has to do with the phrasing (but I am not sure). The allele frequency is the same whether in a given generation mating was random or not. It does not mean that the allele frequency is constant over time. If mating is not random, then the H-W expectation won't hold and genotype frequencies won't be that easy to extrapolate from allele frequencies. But it does not change the allele frequency in any way different than if matin was random (assuming there is no selection at least).

Let me know if that helps and don't hesitate to keep going with further question to narrow down to what is unclear to you.

Thanks a lot for the help, again. However, I'm now more confused than before. If it does not mean that the allele frequency is constant over time, then what does "allele frequencies are constant" mean at all?... (I'm now considering trying to answer the question "what are the consequences of non-random mating" without looking at my lecture, since it became so confusing to me... but if you're ok to help me again, well, it would be welcome and greatly appreciated.)

Totally out of subject, but I just visited your website, looked at your CV and noticed that you studied in Neuchâtel :) That's the city I come from and I'm studying biology in Fribourg... le monde est petit! ;)

Let's continue in chat...


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Branch length in phylogenetic trees
I know this is a very basic question, but it is not too clear to me what is the unit of measure of branch length in phylogenetic trees.
I have come to understand that it is usually expressed in number of substitutions/site/some unit of time.
What is that "some unit of time"? Generations?
Does it depend on what method of tree construction I am using (NJT, MP, ML)?
Thank you for your time.

It does depend greatly on the format, in some diagrams it is meaningless and just created by what is necessary to make the tree visibly clean. Make sure the diagram intends for it to mean something first.

@BeatriceBaldi See the chat for ongoing discussion.

When you estimate a phylogenetic tree, be it by likelihood, parsimony, or distance (like NJ), the lengths will be given in units of substitutions per site, with no time information. For example from here:

The units of branch length are usually nucleotide substitutions per
  site – that is the number of changes or 'substitutions' divided by the
  length of the sequence (although they may be given as % change, i.e.,
  the number of changes per 100 nucleotide sites).

To transform these lengths into a time scale, further information is necessary. For example assuming that the molecular clock is valid, or instead using relaxed clock models that describe how each branch length l=r x t can be decomposed into a rate r and a time t. Since in many cases the rate is not constant along the tree (i.e. the clock is not valid), an inferred phylogenetic tree is not ultrametric (i.e. the sum of branch lengths from the leaves to their MRCA is not constant).
There are software packages, most notably BEAST, that explicitly model a strict or relaxed clock for you, and then can return the branch lengths in arbitrary time units. "Arbitrary" means that the numbers by themselves do not have special meaning, and will reflect your choice for instance of the prior. In which case they can represent year, million years or generations (http://beast.bio.ed.ac.uk/faq#Evolutionary_rates_and_time_scales).

I think it is important to separate the proxy used to estimate time with time itself. There's two solutions to the answer either "time" or "it depends upon the methodology used". However, in the second case one will note that whatever statistics is being used it is always a proxy for time. One will also note that many tree are being build as a congruent of various proxy so that the branch length are the best possible estimates of time. The overal goal of the tree representation is the time from lineage to their MRCA.

The branch length unit of a phylogenetic tree is always "substitutions per site" (the only info we have from sequences alone). No discussion there. Pls check the books by Felsenstein, by Ziheng Yang, the timetree resource, or the manual of any tree inference program. To interpret as time, usually you're assuming a (strict) molecular clock. In this case you are in fact claiming that the rate is constant (then branches are proportional to time). The lengths are NOT the best time estimates unless the sequences do follow a strict clock. (tests for clock-likeliness use this very fact BTW.)

How about phylogenetic trees based on phenotypic data and carbon14? Do you think it is wise to consider that there is no universal meaning to the length of a branch in a tree as it depends on the technic rather than saying that the length of the branches express some proxy for time?

I can't comment on wisdom, I am only answering the OP's question. Morphological data has the same interpretation as sequence data, and also need a model to disentangle rates and times, since the lengths describe only their product. I am happy to explain more through the chat. (By your comment on carbon14, for fossil ages, maybe you are thinking about "total evidence approach" and other dating methods? They are based on relaxed clock models.) And yes, there is a universal meaning for branch lengths -- that is my answer.

Let's continue in chat...

Thank you and @Remi.b your answers and chat were both helpful! What I was looking for was exactly what you said, that in all those methods of tree reconstruction that I mentioned (starting from sequence data), the branch lengths given are in units of substitution/site. Then of course, to have information about "absolute" time, we have to apply a molecular clock (be it strict or relaxed) and a calibration point (be it fossil data or biogeographical events). That way we can calculate time as branch length/mutation rate.
Thank you both so much, it's great to find such a helpful community!

This answer is mainly inspired by a long discussion in the chat with @LeoMartins.
Branch length represents some measurement of lineage divergence
Branch length represents some measurement of lineage divergence. The actual measurement depends upon the type of data considered. For genetic data, it is generally (if not always) a number of substitutions. In any case, those measures of lineage divergence are not a priori design to be best estimates of time, however they are often good proxy for time and often interpreted as being measurement of time.
Cases of meaningless branch length
Be careful that some trees use branches only to represent evolutionary relationships but do not convey meaning via branch lengths.
Total evidence approaches
More and more often, we make consideration of "total evidence approaches" (e.g. Arrigo et al. 2013) which can use sequence data, fossil data and morpho data to form a consensus and offer best estimate of lineage divergence.

This is a good, generalized response that remains unbiased in perspective. +1.

The length of branch indicate time in years (or whatever standard objective unit of time). It would make little sense (although one could argue that it'd be interesting to look at) to build a tree of life where time is in generation as the generation time varies so greatly among lineages.
It is important to not confuse the mean of estimating the length of a branch to the length of the branch itself. For this I will just give you two technics used to estimate such branch length.
Number of substitutions
Now, we estimate this time based on a number of method. One of them is the number of substitution at neutral sites. The number of substitution at neutral sites over $n$ generations is equal to the mutation rate $\mu \cdot t$. That's a classic result, it is due to the fact the there are $2 N \mu$ mutations at each generation, each of them having probability $\frac{1}{2N}$ to fix (given they are neutral) and therefore the neutral substitution rate is $\frac{2N\mu}{2N}=\mu$.
So, using substitution rate we can estimate the number of generations and by estimating the generation time, we can estimate real time (in years).
Most of the time the length of the branches are simply the number of observed substitutions but as not all phylogenetic trees are made from such data, one must consider the branch length in phylogenetic trees in general as being measure of time.
Fossil data
Other methods exist to estimate the length of branches such as fossil datation for example. Here we directly estimate the time in years, not in generation first.
It is important not to confound the mean of estimation of time with


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Tumor-suppression, cell differentiation, and apoptosis: How do macroevolutionists justify dismissing such strong evidence for intelligent design?
Consider the 20 kilobase TP53 gene named for its massive initially-believed 53 kilodalton protein product (later found to be 43 kilodaltons - see https://en.wikipedia.org/wiki/TP53).
Something that complex and of that length doesn't just "happen" on its own. Considering there are 2^40K unique DNA strings of that length (enumerating every permutation), you could easily spend orders of magnitude more than the age of the universe waiting. Simply put, the odds of randomly generating that are none for all practical purposes.
Also consider apoptosis - where a cell recycles itself when it detects too much damage.
The principle of "survival of the fittest" would intuitively rule out the development of apoptosis - there's no reason for a cell or species to develop that feature on its own because that would damage its ability to replicate. Survival of the fittest would actually encourage cells to proliferate as tumors, because they're preserving their genomes and eating everything else out of existence.
The only logical conclusion is that apoptosis and tumor-prevention was purposefully built-in through intelligent design. There's no way that mutations alone could "figure out" that self-recycling (taking one for the team) would increase fitness. Even if 1 pre-tumor cell in a complex life form suddenly decides to recycle itself, chances are that dozens of other pre-tumor cells disagree (sinking the whole life-form). In the absence of that, the pre-tumor cell that recycles itself never survives to hand that ability on.
Additionally, it's even more implausible for mutations alone to "invent" apoptosis mechanisms and 20 kilobase mutation/damage scanners purpose-built for them.
Then you have cell differentiation. Take for example a simple 2-cell system where both cells are joined together and are specific-purposed for different tasks. If 1 of them cells breaks, the other one can't survive on its own. Obviously, decreasing a cell's survivability wouldn't increase its fitness, considering all the types of disasters and damage that could split the 2-cell system.
From a fitness perspective, you would expect any cell to retain the ability to take over the tasks of a different cell type suddenly found to be in short supply, however that often doesn't happen in more complex life forms. Mammals in particular are notorious for relative inability to regenerate large amounts of damage. The only logical conclusion is that the different cell types were purpose-built (read: intelligently designed) to work that way.
With that mountain of evidence for intelligent design, how do macroevolutionists continue to justify fooling themselves?

"The principle of "survival of the fittest" would intuitively rule out the development of apoptosis" - Apoptosis is a normal part of development of multicellular organisms, and is entirely consistent with the concept of selection. For multicellular organisms, selection does not act only at the single-cell level but at the level of the entire organism. There is a mountain of evidence for evolution, not for intelligent design, and arguments for intelligent design, including yours, are either based entirely on religion or based on a misunderstanding of evolution.

umm.... why am I being accused of basing my argument on religion? considering I never even mentioned religion in the original post. All of my arguments were based on basic arithmetic and logic, something that most computers and STEM majors would be proud of.

I'm voting to close this question as off-topic because it is not a question in the terms of SE Biology but an opinion/rant pretending to be a question. It is a clear abuse of this site.

@user1258361 No, your argument falls under the latter of misunderstanding evolution. See Remi.b's answer which is making exactly the same point.

@David I disagree that the post should be closed, because posts like this can often generate good responses, like the one Remi.b posted. I fear that closing posts like this without a robust refutation seems a bit like censorship and there is benefit to engaging to some extent. Not all such posts are acceptable, of course, but this one contains many easily refuted points and demonstrates a clear misunderstanding of selection and evolution as a whole.

@BryanKrause — Please re-read the introduction to SE Biology to refresh your understanding of its purpose and what constitutes a good question. That is what determines whether a question is off-topic, not whether you think someone has made a good point feeding the trolls.

@David "general questions about biological concepts" - Isn't evolution and selection a biological concept? I know, my first reaction to these types of posts is a face-palm, but it's nice to have good answers to point to in the future to refute these types of arguments. That's my opinion, I understand yours, and I disagree. There has been disagreement in the community as a whole, too.

@BryanKrause — I am away from my desktop, so chapter and verse will be delayed. But it cuts no ice to say "there is disagreement" when the purpose and mores of the list are perfectly clear.

@BryanKrause — for the record (as you already know) I have expressed my arguments on meta

@BryanKrause Questions about biology and evolution are of course not off-topic. Troll questions spreading intelligent design and which are obviously not interested in the answer (see the comment on Remi.B's answer) are off-topic, should be closed and not answered.

You are mixing up a bunch of different subjects so that your question is very broad. The post should be closed as too broad.. I will just briefly say a few words about each misunderstanding and hopefully you'll be curious to further your understanding in each of these subjects.

The principle of "survival of the fittest" would intuitively rule out the development of apoptosis

Yes, there is. You are confusing germ lines with soma line.
A cell does not proliferate. It will just do whatever it has to do to all cells in the testes and ovaries (if we're talking about a mammal) to proliferate. Just like a worker ant can commit suicide, a cell can commit suicide. There is no contradiction between the existence of cell apoptosis and the theory of evolution.

Additionally, it's even more implausible for mutations alone to "invent" apoptosis mechanisms and 20 kilobase mutation/damage scanners purpose-built for them.

Clearly, life does not explore all of these possibilities. It only explore a little subset of it. But it does not do that by randomly picking sequence from this gigantic set of possible sequences. New sequences are created via "small modification" (actually such modification can be rather important in reality) of previously existing sequences.

Obviously, decreasing a cell's survivability wouldn't increase its fitness, considering all the types of disasters and damage that could split the 2-cell system

Same issue as above, you need to learn about the soma line germ line differentiation. It will then bring you to the field of social evolution (evolution of traits that affect other's fitness) but you'll probably have to start with an intro to evolutionary biology before going into the field of social evolution.

From a fitness perspective, you would expect any cell to retain the ability to take over the tasks of a different cell type suddenly found to be in short supply

Just google why do cells specialize, you'll get tons of hits.

With that mountain of evidence for intelligent design,

There exist no evidence for Inteligent Design mainly because Intelligent Design does not do any falsifiable and testable claims

how do macroevolutionists [..]?

The macroevolution / microevolution distinction is not used very often in evolutionary biology actually. Today, it is a distinction mainly done by religious extremists to attack the theory of evolution based on a logical fallacy called argument from incredulity

how do macroevolutionists continue to justify fooling themselves?

Maybe you should learn a little bit about science and evolutionary biology before calling scientists fool :)
This sentence suggests that you have an opinion and will not reconsider it based on evidence but I might be wrong here. Maybe you'll be able to rethink your representation of the world based on what observation of this world are being made. Good luck!
Want to learn about evolutionary biology
Understanding Evolution by UC Berkeley is a short very introductory course to evolutionary biology. You should have a look at it.
On Biology.SE, you might want to have a look at the post Is evolution a fact?.

Please don't feed the trolls.

Your post has more holes in it than a rag. The original question specifies 2^40K strings (K=1000) which you obviously failed to read. "A cell doesn't proliferate" -> that already violates the principle of survival and replication. A non-intelligent cell has no way of knowing the consequences of unlimited exponential replication. "Life only explores a subset of possibilities" Weakest argument ever. There is no way for a blind random process to selectively explore a subset of possibilities short of failing everything else - in fact the existence of such a subset implies intelligent design.

Indeed, I missed the K but you could remain polite when pointing it. For the rest, obviously, you are opinion-based and will refuse any evidence, so there is really no point about talking any further. I will be happy to help you learn about evolutionary biology when you'll be ready to learn. FYI, I (like several other users of this website) am researcher in evolutionary genetics and know a thing or two about evolutionary processes. Following @David's advice, I will not react any further unless you show good will to learn. Cheers,

@user1258361 I've actually never seen a rag with a hole in it.


text:
Why are bruises not lethal?
Given the following:

bruises are caused by minor trauma which breaks blood vessels beneath the skin, causing bleeding
the mechanism by which bleeding stops is clotting
blood clots inside the body have an unfortunate tendency to get into the bloodstream and cause blockages, leading to severe problems such as strokes or heart attacks

why is it that people don't die from bruises?  What mechanism does the human body have to keep this from happening?

In addition to the serious answers which are given below, I'd like to point out the real reason bruises are not lethal is because our clotting system is beautiful and borderline miraculous in every way.

I would note that clotting around a bruise or similar injury is a reaction that was "learned" in the process of evolution, and it exists precisely to protect the body from further damage.  No doubt, during the evolutionary process, there were times when a mutation made things a bit worse, but over a few hundred million years it got sorted out.

Your question can be answered without any factual knowledge: Because of evolutionary pressure. To some individuals minor trauma is life threatening. Until recently they did not tend to survive long, let alone procreate.

blood clots inside the body have an unfortunate tendency to get into the bloodstream and cause blockages, leading to severe problems such as strokes or heart attacks

This statement is primarily true only for blood clots within blood vessels, especially in the veins. When you are talking about bruising, you are talking about clots outside of the vasculature.
When a blood clot occurs in an artery, it can block that artery or break off, flow downstream, and block some smaller distal vessel. These events are most severe when they affect crucial organs like the brain and heart ("stroke" or "heart attack"), though of course any organ can be damaged in this way. However, blood clots in arteries can't ever directly affect a tissue that is not distal from where the clot starts, because they can never pass through capillaries or travel backward.
When a blood clot occurs in a vein and is dislodged, it can follow the increasingly larger venous system back to the heart, where it can cause a pulmonary embolism (blockage in the lungs) or, via a patent foramen ovale, travel to the left-side circulation and end up anywhere, including the coronary arteries or blood vessels of the brain. Similarly, clots that form in the venous return from the lungs to the heart or in the left side of the heart itself can travel anywhere (except the lungs) and create a blockage.
For a clot outside the vasculature, for it to have an effect somewhere else systemically it must re-enter the vasculature. This is simply not possible in most situations, because the vessels involved are very small, and during bleeding the blood is flowing out of vessels: there is no pressure gradient to push the clot back into the vessels.
In more severe cases of injury where major vessels are involved, clotting in those major vessels can indeed be a problem, but not for common occurrences of bruising.
(see also @anongoodnurse's answer that contains a good clarification of what exactly a bruise is, as well as how there are risks from very serious bruises but not the same way the original question implied)

"...travel to the left-side circulation and end up anywhere, including the coronary arteries or brain" How would a blood clot get past the blood-brain barrier?

I don't mean that it could actually enter the brain, or any other organ or tissue for that matter, but rather that it could close off circulation to the brain; that's what an embolism does.

I also want to point out that the blood-brain barrier really just refers to the special regulatory interface between capillaries and actual nervous tissue in the CNS that prevents a lot of molecules from entering the brain that can more freely do so in other tissues. There are lots of blood vessels all in and through the brain (as a whole organ) that are exposed to the same circulation as the rest of the body.

"bleeding the blood is flowing out of vessels: there is no pressure gradient to push the clot back into the vessels" Doesn't the heart both push blood away and pull blood in, so wouldn't there also be a negative pressure trying to draw clots back in?

@IshouldchangemyUsername There isn't any negative pressure anywhere in the vasculature relative to the outside.

@IshouldchangemyUsername: To elaborate: during diastole -- when the heart refills, which is not the same as "pulling blood in" -- there is still pressure. When your doc tells you you have a 130 / 80 blood pressure, the lower number is the pressure during diastole -- pressure above ambient. So, as, Bryan said, the vasculature is always under pressure.

@DevSolar That is true about the heart refilling, but the 130/80 number is arterial pressure, the 80mmHg is for arterial diastole. On the venous side, there is very little oscillation (right by the heart there are some effects on pressure from atrial systole and the mechanical motion of the heart) and much lower pressure (~10-20mmHg). Instead, the veins on constantly "full" and a bit distended. The connective tissue and the muscles in the veins hold a constant pressure on the blood, a lot like a stretched balloon would, and this is the pressure that refills the heart.

@Bryan Krause's answer is quite correct. I just want to clarify what a bruise is, because I think you have a misconception of what happens.
There are bruises (blood leakage into tissue because of damage to capillaries) and there are hematomas (a collection of blood in a tissue caused by breakage of either many capillaries or normally a larger blood vessel.)
A capillary is small. As an analogy, imagine someone injects a small amount of blood, say, .5cc, under your skin with a very fine needle, but leaves the needle there. The blood will spread out as much as it can over time. The blood does not need to clot; only at the level of the injured capillary does the blood need to clot. So if the fine needle represents the capillary, the .5cc of blood won't clot then go back up into the needle; it can't happen. It's stuck in the tissue (the extracellular fluid of the skin.) A tiny clot near the tip of the needle will stop more blood from pouring out. No problem. No bleeding to death.
Since the blood has nowhere to go once it spreads out, the blood cells die in the tissue, and heme degradation begins. Initially the blood is reddish, then reddish blue, then dark purple, followed by purplish-brown, to brown-greenish, to yellow, to normal.
A hematoma is a collection of blood that can't spread out because it is unable to penetrate the tissue very well (maybe there's a fibrous capsule in the way.) The blood will stay there and will eventually clot, but it can't get into the end of the fine needles (capillaries) or the bigger needle (arteriole). The body doesn't work that way. Hematomas are eventually broken down by the body as well, but it takes more time, and often there is a residual "scar" in the tissue where it was. That's why sometimes you feel a little bump forever afterwards where you had a really bad bruise.
Bruises - really bad bruises - can cause major damage if there is insufficient or no clotting factor, but not because clots form and kill us, but because the bleeding doesn't stop and if it's bad enough, one can bleed so much into a tissue that the swelling can cut off the blood flow into the tissue (e.g. see compartment syndrome).

I would like to add a point which I feel others have missed: our body already has a safety system to prevent such a thing from happening, called fibrinolysis.
Obviously, this system is not solely for degrading clots that might have come into the bloodstream, but this is an important part of all of its functions. The main character here is plasmin: a serine protease (just like trypsin) whose function is to degrade blood proteins, including fibrin clots. It is synthesized by the liver and secreted into the bloodstream in an inactive form, namely plasminogen. It comes with two levels of safety systems. In the zymogen form, it is in the closed form i.e. the active site is hidden and inactive. When it encounters a blood clot, it gets a conformational change and exposes its activation site. Now, enzymes like tissue plasminogen activator (tPA), urokinase plasminogen activator (uPA), kallikrein and even factor XII convert it into its active form (by breaking a peptide bond between Arg561 and Val562). This two level safety system helps in preventing unnecessary activation of plasminogen (since both the zymogen and its activators are flowing in the bloodstream).

So what prevents it from chewing off all the blood proteins? The secret: its inhibitors are also flowing with it in the bloodstream. Plasmin is inactivated by proteins like $\alpha_2$-macroglobulin and $\alpha_2$-antiplasmin. Plasmin cleaves $\alpha_2$-macroglobulin at the bait region, causing a conformational change. In the resulting $\alpha_2$-macroglobulin-plasmin complex, the active site of plasmin is hidden so that its efficiency is greatly reduced. This conformational change also allows the clearance proteins to bind this complex and let it get out of circulation. You can see the Wikipedia article to know more.

This is all factual, but bears no relation whatsoever to the OP's question. The point of our answers was that it is impossible for a clot to enter the bloodstream the way the OP proposed. This is an answer that might support the OP's faulty supposition.

@anongoodnurse I have supposed that the OP did not take blood vessel size into consideration while asking the question. I don't think just telling why it would be impossible for clots to reach capillaries is enough, if there is something to add, it must be added, and that is what I did; just in case the OP would become curious about how any clot is removed eventually. Anyways, the OP has already selected an answer, so my answer can be taken as a bonus point too.

This answer is IMHO the best... it explains the exact mechanism needed to prevent all of the blood from clotting up. Without this mechanism any minor wound would be lethal.

I think fibrinolysis should be included in a complete answer. Not all injuries producing bruises behave so that the clotting would be fully outside the capillaries. Hemostasis includes fibrinolysis.

Bruises usually damage capillaries (think of them as being side roads well away from the expressway and major routes). Just as closing down a few side roads in a lightly populated suburban or rural area a mile away from a major interstate is unlikely to cause a backup/traffic jam, blood clotting in capillaries at a bruise shouldn't generate dangerous blockages.

I don't think this analogy works at all. Blood clots aren't like closing a road in the abstract; rather, they're a blockage on the road that can break loose and move around. But there isn't any sort of blockage like that on the road network.