text:
Why do humans suffer anxiety when they view "Trypophobia trigger images"?
When you type Trypophobia Trigger Images in google, you see a variety of images with irregular lumps and bumps among some more gory images.
Many people report that these images induce phobia like symptoms of anxiety.
Why do we get anxious when exposed to these images? What advantage is there to be had from this response?
I find the reasons like this ABC news report on ants and spiders. But still didn't get it any info from it.

I've made some edits to clarify and narrow down the question so that it was at less risk of closure. Interesting question +1.

Can I post this in Cog sci community or not required? Thank You for editing to my question.

Generally, it's courteous not to cross post. If there is something you want more information on from my answer, let me know.

When I searched "trypophobia trigger images" in Google Images, most of the hits that I got were trying to show rotted flesh with maggots and such crawling out of it, as opposed to merely "lumps and bumps".  Is Google showing you something different?

@Nat That was my edit. From Wikipedia "Trypophobia is a proposed phobia (intense, irrational fear or anxiety) of irregular patterns or clusters of small holes or bumps." The term is somewhat commandeered by online communities that post freaky or gross images.

I have no reference or anything, only a guess: seeing those holes alone didn't trigger me anything, but when I see "human skin photoshopped with lotus seed", the very first thing that comes to my mind is: what if it happened to me!?, and then comes the anxiety (although I'm already used to such images). I think human has tendency to think something bad that may happen to themself that make them anxious.

@AndrewT. I also have no references, but I definitely agree. Any time I see one of these images, I'm reminded of a bug I learned about that lays its eggs in human skin. If I saw someone with lotus-seed-skin, I think it'd be in my best interests to go nowhere near them; considering natural selection, it seems likely this fear was evolved to help our ancestors avoid diseased individuals.

I guess one possible explanation is that some people's brains associate those irregular holes or bumps with illness. I don't feel any fear or anxiety, but I do have a slight "yuck" response.

My student created a neural network for recognizing trypophobia triggers: https://github.com/grzegorz225/trypophobia-detector

@PiotrMigdal The network achieves ~90% accuracy. Which images from the normal group showed up in the 10% false hits? Or did it seem random?

@James Usually ones people would mistake as well (e.g. from https://www.reddit.com/r/trypophobia/, but to low res after rescaling to have visible features; or from a "neutral" dataset, but actually being trypophobic). Only other "bad" set of examples was bushes/trees (which can be fixed by putting more of them in the "neutral" dataset). I encourage students (there were 6 of them) to do some write-up, as the results (and other finding) was interesting (and going beyond my expectations). Side note: try neural style: https://deepart.io/ (face as image, lotos seeds as style). A texture phenomenon.

Trypophobia is not a recognised specific anxiety disorder (Washington Post). It is worth mentioning that anyone can have a phobia to anything, this is merely a question of whether many people associate these spatial patterns with anxiety. Nevertheless, the response of individuals to these images can be quantified (Le et al., 2015). Ultimately the findings show that a response of trypophobia is not correlative with anxiety. Note that here we are discussing anxiety in a phobia response test. Typically anxiety manifests as sweating, dizziness, headaches, racing heartbeats, nausea, fidgeting, uncontrollable crying or laughing and drumming on a desk. This is not merely feeling uncomfortable.
One hypothesis was that these images had irregular spatial patterns that cause revulsion. A study found that in nature some animals and plants may use this patterning as a warning mechanism and that it is associated with poisonous animals  (spatial pattern quantification of 10 poisonous animals versus 10 control animals p=0.03), and indeed spiders were among those that use irregular patterns (Cole & Wilkins, 2013). Note that this hypothesis was presented in a psychology journal so the evolutionary mechanisms remain, in my opinion, not fully explored and scrutinised.
Hover over the below yellow box to view a lotus seed head, which has typical irregular spatial patterning presented in the 2013 study.
This image is often reported as inducing trypophobia.

Answer: In summary, humans do not reliably feel anxious when viewing these images. It also remains unclear why some people do get anxious or uncomfortable when viewing these images. It is perhaps to do with an aversion to some potentially harmful animals, but evidence remains scarce.

I am very much irritated by seeing the image you posted in the answer, I had to close the image with my hands to approve the answer just to click it.

@user48898: But it doesn't affect me at all.

Pictures like this make me feel physically sick, not just anxious.

As a third response class: I don't find the patterns irritating in a manner that makes me feel at all anxious, but I do find them distracting. They draw my gaze if they are in my peripheral vision and set off a "that's odd" feeling that I need to make at least a small amount of conscious effort to ignore. I assume I am subconsciously trying to find a pattern to satiate that part of us that feels safest once everything is understood.

LOL that's so weird - never noticed it before. I don't feel anxious or sick or anything, but as soon as I hovered over the image and saw it, I had a quick "Ewww" reaction as if I'd just put my hand on something gross. Only lasted a second, but it's still neat to realize the reaction is there.

Having no references to provide but basing on my reaction to images provided in this answer and answer of gemesyscanada I would argue that it is not the pattern of spots which makes it so gross but rather assumption that it is holes which look like they have been eaten out by something. I have negative response to the image of a flower from this answer, but I have absolutely no problems looking at the salamander from gemesyscanada's answer.

The image in this answer made me feel anxious but the lizard with the yellow spots did not.  It may be connected to arachnophobia, the spots make me think of spider eyes.

I wonder if reactions to the specific example of a lotus head are influenced by well-known fake images of lotus heads misrepresented as botfly larva in human skin.

And here I didn't think I had a reaction to these images... now my chicken tastes weird and I've lost my appetite. Thanks.

Coincidentally, the only reason I have an issue with the lotus seed is because of a hoax that floated around the internet a few years ago about a skin-eating disease, or bugs that crawl out of skin, or something like that, and they merged an image of a lotus seed with a womans nipple to make this hideous...  Thing...  Ever since then, I can't look at a lotus seed without seeing that image in my head.
Luckily for me, it has not affected my ability to view nipples.

@jamesqf: Not only do I agree with you, I would go further and say I find this particular shape/texture aesthetically pleasing. I might doodle a plant-like set of irregular holes like that. Clearly I should be careful who I then show that to. I'm not sure what the difference is - I have spent some hobby time crafting computer-generated textures and other artwork like fractals, not sure if that has skewed my appreciations. I generally find pictures of mold/slime/debris unattractive, but not the kind of texture in the image.

@SGR Here I am discussing anxiety in a phobia test scenario. Sweating, dizziness, headaches, racing heartbeats, nausea, fidgeting, uncontrollable crying or laughing and drumming on a desk are all common manifestations of anxiety.

@Kevin Krumwiede: Perhaps I have no reaction (other than mild curiousity) to the image because I've never seen those "well-known fake images".

As someone who is very disgusted by this kind of image, I think it is a caused by an association with maladies like burns, infections, and especially parasites. It is difficult for me to even describe this without feeling a bit nauseated, but it is hard for me to see things like that without picturing it being my, or someone else's, skin. Or that it is crawling with parasites. I don't have any particular source for this because it's from my own experience.
It isn't entirely unreasonable that this would be a biological defense because if you saw an animal with an area of perforated skin (also hard to even write) it would be a good idea to not touch it since this could indicate bacterial ulcers or a skin infection. If you saw a patch of ground with tiny holes all over it, it might not be a good idea to sit there as this would probably indicate burrowing insects such as termites were present.
Another thing that confirms this for me is that when trolls edit these patterns onto a human it has the worst effect, and nearly makes me vomit. As this article notes, also from its author's own experience, these types of images are some of the worst for Trypophobia. There have been some studies finding that the response is similar to our reaction to danger, rather that just disgust. From my own reaction to these images this seems to be accurate.

Please add some references to your answer.

I have created an account just to upvote this answer. I have exactly the same responses to this images as Paul S. I would theorise the same way Paul S does, images like that give me associations of flesh/substance crawling with larvae and insects, which I would consider dangerous. Places with holes like that give me association of the above mentioned creatures living there which would also be dangerous to approach.

Also, +1 for “feeling nauseated” (so many people use “nauseous” incorrectly).

+1 on this, espeically for the photoshops on these patterns. I don't suggest looking at if these pictures do bother, but if you're curious, the Suriname Sea Toad evokes similar revulsion.

Welcome to Bio. Thanks for this interesting answer. However, it seems more like a collection of personal thoughts. Could you generalize this answer,  and lift it to the population level, and add sources?

I'm not sure what I would cite since I am talking about my own feelings on it as someone on which the mentioned patterns have the mentioned effect.

I realize I could add references to infections and parasites that would cause these kinds of patterns on a creature, but for reasons mentioned in the answer, I really don't want to search for those references.

@PaulS I agree with AliceD & anotherHomosapien. Without sources, your answer is anecdotal in the first and final paragraph and speculative in the second paragraph.

Ok, what do you want me to add, specifically?

Why do you think it is an association with burns and parasites? Since not everyone has the same reaction, you cannot assume disgust is a reasonable response underpinned by a defence mechanism (see Triskaidekaphobia for an example of a phobia that has no clear advantage/defence). I'm also interested; what are these troll images and where can we see them? Is there any evidence that your opinions aren't yours and yours alone? Currently, I'm tempted to flag this as a comment since currently, it is mostly opinion, but I feel like if it can be justified, the community finds this answer valuable.

"Why do you think it is an association with burns and parasites?" Because that's what it brings to mind when it makes me feel nauseated. "I'm also interested; what are these troll images and where can we see them?" I am not interested in searching out images that nauseate me in order to provide links, I would rather you just delete or downgrade my answer if no one else knows what I'm talking about.

@user1264176 your personal experience and concurrence with PaulS does not add any weight to the answer. Any answer cannot be based just on feelings/personal experiences and guesses. We need authoritative answers that cite valid references.

@James well, actually OP has provided search terms for image.google.com search which are even bold "Trypophobia Trigger Images" which kind of makes me wonder if you have read the question.

@user1264176 There are >300,000 images. On the first few pages, some have images overlayed on skin, but in a massive variety. Some are images of pasta. They do not make me personally uncomfortable, yet OP is unable to even google a reference for the images that upset them the most. Without clarification, citation, and expansion, this answer certainly amounts to "I think those images are gross too!" and since the answerer has expressed no interest whatsoever in improving the answer, I think it should be removed.

@James I have made an edit to this answer because I don't have enough points to make a separate answer. I tried to add references and prove Paul S hypothesis about nausea feeling while looking at these images. Unfortunately, it was rejected. From my search - there is no research in this area, so we can only hypothesise.

@user1264176 I thought your edits looked good, but it doesn't look like I can accept edits without more points. I could manually change some of them later, but I'm not sure why they were rejected.

@James "answerer has expressed no interest whatsoever in improving the answer" It's more that I'm not aware of any definitive work on the origin of human emotion. I only said I don't want to add images meant to trigger Trypophobia, but I'll add in some references to people citing similar reasons if that helps.

@PaulS According to one of the reviewers "This edit deviates from the original intent of the post. Even edits that must make drastic changes should strive to preserve the goals of the post's owner." So if you feel like you want to add my sources and explanations please feel free to do that (+ maybe adopt them to better fit your answer)

BTW, after reading the articles on jordantrudgett.com and psychologicalscience.org, for the sake of science I have tried to look up all of the images from the authors' list. I got quite bad response only from lotus seeds and maggots removal, all the rest, like octopuses, frogs, frozen peas and rocks give me either no response at all or slight feeling of danger (in case of rocks where something can hide). From this I make a conclusion that I don't have phobia per se, and my responses are more related to danger of creatures living in those holes. This is approximately what I have written in edit

@PaulS I wasn't asking for a reference that humans have emotions. I am mainly interested in references supporting your idea about contaminated flesh & food. I know of one researcher working on this, but cannot find any published articles. What you've ended up citing is 1-a blog post and 2- a press release about one of the articles from my answer, which you have misrepresented since it doesn't explore your hypothesis at all. The community clearly likes this answer, and I encourage you to expand it so we can remove that banner.

The "That's Odd" feeling is real. And now I understand the term "trypophobia" as a specific example of a more general aversion response which seems common in nature, and might even be hard-wired in the neural-circuits of many animals.  The brightly coloured and mottled/spotted patterns found on various insects, amphibians and reptiles may represent more than just simple camouflage.  I recall a large black salamander I found which was covered by yellow spots - I recognized it as a local species, not rare, but when I noticed it, despite my interest and curiousity, I felt a clear sense of "weird - ugh - yuck".  Now this salamander lives under rocks, under leaves, in rotted-wood, and so on.  The existence of the bright yellow spots are not likely related to helping it hide.  Why would it evolve such a bright pattern, given its typical habitat?  It may be the spot-pattern itself is a weapon, as it seems to provide the creature with a way to trigger a "yuck - leave that ugly thing alone" response in humans, who could be potential threats to the small, slow-moving and otherwise quite defenseless salamader.    The pattern of spots on the lotus-seed head seem to be similar to the spot pattern on the salamander.  The aversion-response in humans has almost certainly evolved as a protective mechanism to keep us from being poisoned, stung, bitten or burnt when young children. But it is also possible this response is not "hard-wired" at all, but is learned.  Once stung by a brightly-coloured wasp or hornet, the child quickly learns to avoid handling this type of creature.
And the harmless salamander's bright yellow random-spaced spots simply mimic
the colour-coding of more effectively hostile agents.
It is possible the aversion to random spotted bumpy/lumpy surfaces may be related to a similar learning phenomenon.  We encounter stinking, rotted flesh, and already have the evolutionary systems in place to detect that rotted meat should not be eaten - it smells bad.  Really bad.  And so, other creatures have an opportunity to evolve displays which - if they mimic the appearance of the rotted flesh - can benefit by the associative trigger of the visual appearance of the rotten flesh, and the chemical response from the smell.   If the smell creates a powerful aversion response, the linkage that mammals - not just humans - might make to the visual appearance of the bad-smelling thing, might provide an opportunity for creatures to evolve mechanisms that can take advantage of this situation.
This linkage of stimulus-response, and the ability of the stimulus-response mechanism to be transferred to a different, associated response is well understood - Pavlov's dogs, for example, which learned quickly that the ringing bell meant feeding, and so would salivate when they heard the bell ring, without having to smell the food.
It is also possible the trypophobic response some humans feel, is simply learned, the way many phobias appear to be.  The work of B.F. Skinner (creator of the "Skinner Box"), showed that behaviour could be "conditioned", and virtually any stimulus could be made to be associated with any response, given sufficient time, opportunity and intensity of the conditioning effort.
I suspect if a behavioural economist offered to pay $100 for each yellow spotted salamander a person could catch, the typical human would very quickly encode a different internal response to the appearance of the salamander's bumpy, spotted appearance, and it would certainly not be an aversion response.

Welcome!!! Gemesyscanada to Biology Stack exchange. Please can u provide references to support your statements or for further reading on the topic. You can visit help center for more details.

Excellent answer Gemesyscanada. @Mesentery I am puzzled by this robot like obsession by some on stack exchange to feel compelled to point out technicalities in an otherwise excellent SE answer. Here's a first time poster that has posted what I discern as an excellent answer. And your criticism is more likely to scare him away for nothing. If you want to add refs feel free to edit his answer!

@curious_cat I just requested him to provide references, I didn't criticise him. I just wanted to give him an idea how the site works by guiding him to the help center. How can u feel that I scared him. Can u point out any threatening word in my comment, that if u don't provide references ur answer will be deleted.

@gemesyscanada Apologies, if u found my comment in anyway rude or threatening.

@Mesentery My point is that not every answer needs to have explicit references in it to be a good answer. So long as the point is not very esoteric or controversial it seems counterproductive to stick to a pedantic instance on references. Often a knowledgeable commentor may have enough time to give you a good answer but not enough to search and add for references.

@curious_cat If this answerer tries to answer an other question which need references, then the first who reviewed the post will be blamed for not guiding the newcomer, therefore it is essential to guide newcomers to the help center. As I said in my above comment, I just requested him. And the mistake I made was not to thank him for his contribution to the site.

@Mesentery Fair enough. I rest my case.

Welcome to Biology. It's a nice answer and thank you for your contribution. However, I second the comments from James & Mesentery that references, or sources are considered as an essential component of any answer.


text:
Why do we laugh?
Why is it that the reaction we get from absurdity is laughter? Everyone does it, even babies. Is there a reason why it is our instinct to laugh when we see or hear something absurd/humorous

I don't mean to be flip (well, not too flippant anyway), but one of the most profound things hidden in a Calvin and Hobbes strip - and there were quite a few profound things hidden in C&H - had to do with the evolution of a sense of humour, This is the strip I'm referring to: http://imgur.com/s0fZX

That is brilliant

There is a really good TED talk on this.

@biogirl is talking about this - https://www.ted.com/talks/sophie_scott_why_we_laugh?language=en

The book Inside Jokes by Hurley has the only idea for why humor and laughter evolved I have heard that actually made sense biologically, Including why it is so rare, it is only valuable to very intelligent species as a way to internally assess credibility of beliefs.

Like so much of biology, we just don't know!
I'll preface this answer by disappointing you; this answer doesn't entirely answer your question. That's because this is a pretty big mystery in research and a fascinating topic. I'll start with a couple of quotes that maybe explain why!

"If you search on the Web of Science database for papers on the emotion of fear, you’ll get back 6,477 published papers. Search for papers on laughter and you’ll get a paltry 175."

-Sophie Scott 2015
In other words, the lack of research into laughter possibly is because research usually tries to solve a problem. Generally, laughter isn't perceived as a problem and is relatively seldom investigated. Notably, there is a symptom called the Pseudobulbar affect. It describes someone that laughs (or cries) uncontrollably.

"Analysing humour is like dissecting a frog; few people are interested, and the frog dies of it."

-Elwyn Brooks White 1941
Why do we (as humans) laugh?
The consensus in the community of researchers seems to be that we laugh because it strengthens human social connections.
Counter-intuitively, it's not always because we find things funny. The linked article implies that although it's not exactly clear why we laugh, laughter is a form of seemingly non-deliberate social interaction that doesn't interrupt or replace speech, but adds to it. We laugh in addition to talking.
The evolution of laughter.
As you mention in your question, even babies laugh. Laughter is clearly not unique to humans, let alone human adults. Most social mammals laugh and there are lots of studies on ape laughter and a niche field in "rat tickling" which studies laughter in rats. Jaak Panksepp even found that rats can be bred that love to be tickled! That article also discusses the science surrounding laughter and the links laughter has with increasing neurogenesis. This implies that laughter emerged a long time ago even on an evolutionary timescale and contributes in a very real way to the wiring of our brain. It's not clear why this happens.
There is a popular but unfounded theory put forward by the philosopher John Morreall that laughter originated as some sort of group "the danger is over" signal after the flight or fight response.
Going back a step; what is laughter?
To fully place laughter in the context of our social constructs, we must first understand what laughter is. Unanimously, all types of laughter are non-verbal expressions of emotion (and above there is a reference to how laughter fits in around language, enriching it). These positive non-verbal auditory signals have been shown in primates to be involved with mirroring the emotions of others. At a higher level, there are different types of laughter in our social world ranging from Schadenfreude to laughter based off of specialist interest, all of which seemingly have different triggers, varying numbers of potential participants, and social purposes.
Another question is raised as people can interpret the authenticity of laughter. This study found that people can very easily perceive an inauthentic "polite tittering" from an "explosion of mirth". This highlights that why-ever we laugh, laughter has a complex and under-appreciated social underpinning in humans that we don't yet understand.
Personal views
To me at least, laughter may be the result of primitive non-verbal emotional communication and lie-detection; part of the intra-species evolutionary arms race of big-brained social mammals in terms of altruism and lying. For example, I would laugh, and I would gauge the state of you by seeing if you laugh too, and then I can act on how I think you feel; be it altruistically or selfishly. You would need to be able to tell if my original laugh was testing you, or genuine.
With that tool as a basic premise, one can imagine how such a wide variety of functions arose from a simple two-party status check.

If it's a social interaction that doesn't explain why we laugh when on our own (and often feel better for it!)

@Jez To counter that: it's usually much easier to find things funny when in a group.

@Jez Sophie Scott describes having problems in an anechoic chambre whilst trying to record isolated laughter from individual people laughing on their own.

@SmallLegend I just wish there was a review or something so that we laugh because it strengthens human social connections. can be referenced.

It is not known for sure. But I find Hurley and Dennett's theory very convincing.

Our brains are engaged full time in real-time (risky) heuristic search, generating presumtpions about what will be experienced next in every domain. This time-pressured, unsupervised generation process has necessarily lenient standards and introduces content - not all of which can be properly checked for truth - into our mental spaces. If left unexamined, the inevitable errors in these vestibules of consciousness would ultimately continue on to contaminate our world knowledge store. So there has to be a policy of double-checking these candidate beliefs and surmisings, and the discovery and resolution of these at breakneck speed is maintained by a powerful reward system - the feeling of humor; mirth - that must support this activity in competition with all the other things you could be thinking about.

I realize that the writing style is dense, and the quote requires some knowledge of their assumptions, so here is an explanation.
Pre-pre-explanation: What is a mental space?
A mental space is one of the modern assumptions of how humans organise the knowledge in their heads. I won't spend time explaining how it differs from other assumptions such as scripts. It is probably best introduced by thinking of fiction. When you watch Star Trek, you can easily think within the "Star Trek universe". You know that within this world, it is possible to beam up people, that money doesn't matter but dilithium crystals do, and so on. Your head holds a description of this world, and you can do logical reasoning to infer things which are true within this world.
A mental space is such a "world" within our head. It is rarely as elaborate as the Star Trek world. It is just a compartmentalization of our knowledge of our surrounding world, such that we can hold contradicting views of the world at the same time. This is useful, for example, when we consider whether we should hurry up for work: we can conjure up a mental space representing our day if we arrive at work on time, then a contradicting one where we arrive late, and compare them.
Pre-explanation: Why we find things funny?
Our heads are constantly carrying around innumerable mental spaces, some we actively think about, others buried in memory. And all the time, we are learning new information, which may or may not be true. It is in our best interest to incorporate true information into appropriate mental models (a mental model is a complex of theories which explain to us how something works), and discard false information. For example, when a Star Trek episode introduces the Tribbles species, we have to incorporate the information that Tribbles exist as true in our "Star Trek canon" mental space and possibly our "What I'd do if I were a Starfleet officer" mental space, and keep it as false in all other mental spaces.
What Hurley and Dennett are proposing is that our brains know how to evaluate information for truth value (or at least consistency with a mental model). This job is, like most jobs in the brain, too computing intensive for the conscious mind. But when it gets done, the conscious mind has to be informed about the computation result. This information arrives, as with all other conclusions of the unconscious computation, in the form of a feeling - in this case, the feeling of mirth. So, if you find something funny, it is a sign that the mental space you just built (which contains this "something") is incongruous and should be abandoned as untrue.
Explanation: Why we laugh?
We are social animals. It will frequently happen that we are all receiving the same new information from outside as our herd comrades. And out in the jungle, we frequently evaluate new information as being a possible danger. Is this rumbling a tiger? When a herd member has computed the signal and his sense of mirth has told him that the "this is dangerous" mental space is internally inconsistent, the automatically triggered laughter will inform other herd members that the situation is safe and they can relax. This is what makes laughter contagious and pleasant (although they have additional arguments for "pleasant" - basically, a reward without which we wouldn't be inclined to go through the resource-hungry heuristic computations).
Summary

We feel something is funny when we consider a proposition which turns out to be untrue,

especially also when we consider a potential danger and it turns out that we are safe.

We laugh when something is funny as a signal to others that "things are not what they seem to be",

especially that a danger we may all be evaluating is not dangerous.

Arguments for the above theory
I only had the space here to present the content of the theory. For the arguments why they believe this theory to hold, and how it compares to multiple competing theories, please see their book. It is a truly fascinating read.
Hurley, M. M., Dennett, D. C., & Adams, R. B. (2011). Inside jokes: Using humor to reverse-engineer the mind. MIT press.

Truly insightful, never thought of it like that. Thank you sir

I'm confused. You started with a philosophical description of the mind and then concluded that because we are at ease when we hear laughing that there is some sort of pavlovian response that makes us feel safe when laughing. Perhaps I am oversimplifying, but the argument feels circular and very unscientific. Expanding from one of your points, there is an interesting point about jokes being funny because they don't match expectation. I think it was Ricky Gervais who first put that to paper.

To clarify on why this seems like a circular argument: The conclusion is it's own evidence. The premis is not empirically tested and the essay on the mind relies on assumptions, misconceptions, and oppinions aside from being heavy in anecdote. Your reference is about our sense of humour, which is not necessarily the same as laughter as most of the other answers tackle. Sorry to be so blunt; I do think that this is an interesting answer to read, it's just that I don't see the value in using "fluffy" descriptions in neuroscience, particularly when it's implied as set-in-stone fact.

@GoodGravy of course I couldn't replicate all the arguments of a whole book here. Sure, the theory comes from philosophy and is based on pure reasoning without any direct "empirical testing" as usual in neuroscience. But in the book, it is applied on many jokes and different humorous situations, and is shown to fit better than the other existing theories, including the old oversimplified "don't match expectations". Also, the premise from which it starts is the best we have. Theories about "do we think in scripts, frames, cognitive spaces", etc. are established and tested as far as we can.

Oh, and another thing: there are no arguments in my answer, except the one connection from humor to laughter. I needed this space to simply explain the claim of the theory. I did not attempt to reproduce any of the evidence for it - if somebody can do this in a reasonable length of text, I am not this person. The book I am speaking of uses 3 pages to explain the above, and another 370 to present arguments for it. So of course you won't feel convinced of the theory being true just by reading this answer - don't expect this, or take it as evidence that the theory is not true.

@rumptscho People have seldom investigated laughter because it's not a "problem" to be solved rather than because it's impossible to test. To leap to philosophical reasonable hypotheses as the absolute truth before we have pushed the limits of empiricism seems premature. This isn't exactly theoretical multi-verse physics yet, it's just messy neuroscience! As you say, the mind-space theory fits many humorous situations; Platos world of forms fitted really well too. Remain skeptical until there is conclusive data. Why should we be afraid to say that we don't know?

@GoodGravy 100% of science is simply hypotheses which best fit what we have observed so far. Nothing in science is proven as the absolute truth, that's the point of it. This is why have the theory of evolution, not the gospel of evolution. Also, looking at a branch of science which does its empiric research differently than yours and declaring it "not empirical" is short sighted. To sum it up: I am not afraid to say that we don't know much about laughter and humor. Neither is the author of the book I cite. But I am convinced that we have a good, stable theory here, not idle musings.

Science is hypothetical, but not all hypotheses are scientific. The multi-verse is an unscientific hypothesis for example (hence my reference to it). But I do not think that the science of laughter has reached that point since it remains scientifically testable. There is if anything too much data (hence it's messy).

In the case of laughing, there has been barely any research on this data. As it stands, the hypothesis you present is unscientific as it cannot be tested; it sounds contextual, abstract, and verbose. I hope I'm not coming across as short sighted, I'm trying to be pragmatic; "how do we test what laughter is?" rather than "Laughter might be X." Why settle for that hypothesis when there are scientific hypotheses available in the field? This answer doesn't reflect any uncertainty in the same way your comments do.

@GoodGravy First, how do you know that this hypothesis is unscientific, when you don't know either how it was derived, nor what scientific evidence there is for it, and how much it incorporates the findings you referenced in your own answer? You are making assumptions without having the information necessary to judge. Second, "this answer doesn't reflect any uncertainty"  - why? The first thing it says is "It is not known for sure". And the second says that the rest of an answer is a theory I have found convincing after having read the argumentation its authors have for it.

Conceptual blending, & other cognitive semantics aren't testable & are more akin to metaphor. I've seen it recently in computer development, and essays in cogsci, but not biology. If a study shows mental spaces are used in brains, or if they are linked to laughter, using experimental data please share it (my cursory search didn't come up with anything). I thought your first line is refering to laughter, not mental-spaces? You go on to assuredly discuss mental spaces before laughter again. It could be clearer I suppose.

Why do we laugh?
The leading research on why we laugh is done by Robert Provine. He has even written several books on the topic. His theory is that laughter was a primitve form of communication that evolved. For example,he and some graduate students listened in on average conversations in public places and made notes. And in a survey of 1,200 "laugh episodes," he found that only 10%-20% of laughs were generated by anything resembling a joke. The other 80%-90% of comments that received a laugh were dull non-witticisms like, "I'll see you guys later" and "It was nice meeting you, too."[1].
Reason
One reason could be is that it is to make other people nearby feel good and charismatic. It is used to show you like them. It is a social signal[1,2 3]. What would support this is the fact that laughter occurs more in social situations in front of a person[4].
Another, more older hypothesis is thaf the first human laughter may have begun as a gesture of shared relief at the passing of danger. And since the relaxation that results from a bout of laughter inhibits the biological fight-or-flight response, laughter may indicate trust in one's companions. Again, this is a type of social signal.[3] Plus, this may be the reason why laughter has evolved to be contagious. Again, the fact that laughter occurs in a social situation supports this hypothesis as well.
Note that laughter isn't just a human phenomenon. It is also a mammal thing. As @GoodGravy mentioned, rats do laugh when they are tickled. But also primates laugh, especially when they play. Also, this is a social situation.[2, 4]
Summary
In short, laughter is a more primitive, ancient form of communication. We laugh as a social singal, not to say something is funny. Humor is not always the cause of laughter. It has to do with social situations. It is to show support and liking for the people around you. It is to make the atmosphere more charismatic and happy.
Really, the point I am trying to get is that laughter is a primitive form of communication in social situations to show support and likeness to others.
Your question is a great one and I enjoyed researching on this topic.
References
[1] - http://www.webmd.com/men/features/why-we-laugh
[2] - https://www.ted.com/talks/sophie_scott_why_we_laugh?language=en
[3] - http://science.howstuffworks.com/life/inside-the-mind/emotions/laughter2.htm
[4] - https://postmediavancouversun.files.wordpress.com/2009/03/extra1.pdf

@SmallLegend if you like it, you can upvote and accept my answer... If there is anything on this subject you want to know, I can continue researching and add more details..

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text:
How can I find the mRNA sequence for a specific prokaryotic gene?
What I want to find out is the start of the transcription for a specific gene, how long the UTR is before the actual coding sequence starts.
I've looked at various databases like NCBI Gene, Refseq or a specialized one like PRODORIC. But none of them actually contain the mRNA sequence or any information about the untranslated parts of the mRNA. Just the coding sequence itself.
Is that kind of information simply not annotated for many bacteria? I'm not looking at model organisms like E. Coli or B. subtilis, but I would have expected some information to be available.
Is there a database where I can find the actual transcript sequences for prokaryotic genes?

I haven't been able to find that kind of information anywhere. Finding the genomic context is "fairly easy" but the transcription information is much harder to find. You'll probably will have to find transcription elements yourself.

mRNA specific queries
Add this to your NCBI query: AND mrna[filter]
If it's not available in major databases it may not be known.
However mRNA data can be obscure to find even in those major databases but it should be there. I would be surprised if that is the case, however since you're not working with model organisms there may well be nothing available.
When looking for a transcript gene, NCBI have some tips that you can see here for searching their database. #8 might be relevant to you as it's a way of filtering exclusively mRNA records.

If there is no UniGene cluster for this gene and organism, perform a
  search in the Nucleotide database with the gene name, product name, or
  symbol. Include the organism in the search to find the most relevant
  results and filter for transcript sequences, for example: Cytochrome c
  AND bullfrog[orgn] AND mrna[filter].

Predicting mRNA
Basic: ExPasy DNA translation tool
Advanced: regrna 2
Assuming that advanced querying doesn't reveal what you need you might be able to make some useful predictions before taking it to the lab. There are a handful of other predictive tools that can maybe help you out if that's the only option available. I can't get my head around exactly what information you have as an input. Assuming you have the DNA sequence, I would start with the obvious choice: the ExPasy DNA translation tool.
I would then say that regrna 2 might be able to steer you in the right direction regarding more subtle translational elements.

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text:
How to perform a DNA structural alignment in pymol
How can I "fit" two DNA structures having different nucleotide sequences in PyMol?
I would like to use the structure of a DNA-binding protein in PDB (1h9t), which is bound to DNA in the PDB file, and fit a longer DNA built in silico with a 3D dart (haddock.science.uu.nl/dna/dna.php).

Welcome to Bio. Perhaps a link would be helpful, or some background info about your experiment.

Hi @Claudio and welcome to Bio.SE! I've hopefully shown you how to align DNA quickly in PyMol, but I'm not sure if you even need to for Haddock docking.

Aligning in PyMol
PDB ID 1h9t contains a structure of both a DNA and a protein. It starts as one object.
Before we perform an alignment, we need to separate your DNA from the protein.

Show sequence (click the S at the bottom right).

Highlight all the "residues" from the chains X and Y (these chains contain each strand of your DNA) in the sequence bar at the top.

Use the GUI to extract selection to new object (it's a faff doing this by terminal I find).

Rename new object (automatically named obj01 probably) to DNA1, or whatever you prefer.

Load your new, unaligned piece of DNA (I used fetch 1BNA).

Pymol uses the CEalign algorithm to align structures in 3D space. You can call it using the following command:
cealign DNA1, 1BNA, object=aln

Output:

Another 3D alignment software I really like is the Dali server.
Haddock
Haddock doesn't care if two molecules are aligned pre-analysis assuming you are submitting each DNA separately alongside a protein for binding analysis. This is because it tries a huge variety of orientations. Here is a list of things that you do need to do to your pdb before submitting to HADDOCK

And don't forget (like I did) to colour properly and raytrace (ray) the figures before putting them anywhere important!


text:
Protein binds to DNA and just stays there, what will happen next?
If I hypothetically make an inactive version of Cas9 or ZFN (that will bind to the DNA but does not apply the cleavage reaction). What will happen after the protein bound to DNA? Will it be stuck in there forever and disrupt the transcription/translation process? Or will it be self-unbound after a while?

All binding reactions are reversible. The binding and unbinding (association and dissociation) are usually in equilibrium. How much of the protein is bound to the DNA and how much time a single molecule spends in the bound state depends on the kinetic parameters. In case of the non-catalytic Cas, the protein may inhibit transcription if it is bound at the promoter. In fact, such inactive variants have been developed and used for targeted inhibition of transcription (Himeda et al., 2015).
If the CRISPR-Cas is blocking a binding site for a transcriptional activator, then the degree of inhibition would depend on the competition between the activator and the CRISPR-Cas-inhibitor for the binding sites. This competition would be dependent on the kinetic parameters as well as the concentration of the competing species.
Similarly, you can design proteins/RNAs that can bind to mRNAs (at RBS in prokaryotes or Kozak sequences in eukaryotes) and inhibit translation.
Another interesting fact: CRISPR-Cas system has been engineered to work like transcriptional activator, as well (Didovyk et al., 2016).


text:
Could below zero decibel environment cause arrhythmia?
While this topic has virtually no real life application and has never been examined due to obvious reasons, it is quite intriguing to me.
I've read a lot of speculations and claims about the world's quietest room (-8.7 decibel at Orfield Laboratories in South Mineapolis) including loss/deterioration of hearing, hallucinations etc. What I was wondering about is if any of the human self-preservance reflexes would kick in once an individual hears his own bodily fluids and organs expanding/retracting? Since, as far as I know, there aren't any scientific proofs or thesis on this subject, what are your thoughts based on your knowledge on regular body functions and reflexes?
Third-party links: TheDailySwarm's post, CBC's post, Quora's post

Can you include a reference to the speculations and claims that you've read? This makes it easier for others to fill in.

What are you referring to when you say "self-preservance reflexes"?

@MCM I was thinking of the involuntary actions a body makes when it detects a danger (e.g. removing extremities from a heated surface, increasing blood circulation to preserve BT in cold environment) so I was wondering if hearing your own heart-beat would cause your body to classify it as endangered state and try to adjust the pulse which could cause arrhythmia.

This question is better suited for skeptics SE.. As far as I understand, lack of auditory stimulus shouldn't interfere with any visceral function. People might feel depressed and heart may react to the psychological state but there cannot be any reflex here

@WYSIWYG I think its on-topic here as well - if there are potential effects and mechanisms they are clearly within the field of biology.

But the problem is, like I wrote in the question, that there exists no research on this topic, so any discussion would be pure speculation.

Since we are used to hearing sound it would not be very pleasant to be in complete silence. Hearing has not evolved to report the somatic state, but to merely perceive the environment. So my best guess is that this effect (if it exists) is purely psychological.

What makes you think that ".. an individual can hear his own bodily fluids and organs expanding/retracting"? in silence?


text:
Is there a way to measure ATP usage in the brain similarly to fMRI?
Is there a way to measure ATP usage in the brain (or anywhere else) similarly to how fMRI works (measuring changes in iron resonance in oxygenated/deoxygenated blood)? Is there some sort of similar signal that can be used for ATP?

I'm pretty sure this doesn't exist. If it did, that would be awesome.
The following is 100% pure speculation with nothing to back this up at all (as a disclaimer).
Phosphorus-31 (the stable isotope) is NMR active, which means that you could theoretically use an MRI machine to visualize phosphorus. A quick google search shows scientists attempting to use phosphorus MRI for visualizing bone structure.
I don't really know much about MRI, but I do know some about small molecule NMR, which is based on the same principles. This is a pretty cool paper showing phosphorus-31 NMR used to measure ATP synthesis.
Maybe in the distant future it could be possible to use phosphorus-31 MRI to visualize ATP/ADP ratios in various tissues, including the brain. But that would be some amazing sci-fi stuff.


text:
X Linked Hardy Weinberg Equilibrium Problem

In a given population under Hardy Weinberg equilibrium, 40.0% of men have hemophilia. What is the probability that a random man and random woman will have a daughter with haemophilia?

I think the answer is 16%, but the answer given is 9.6%. According to  Hardy-Weinberg principle, p2 + 2pq + q2 = 1. In order to inherit the disease, the mother must either be a carrier of have the disease, which occurs with probability 1-q2 = 0.72
Therefore, the odds of having a child with the disease is (0.84)(0.4). Since it asks for the probability of a girl, the total must be divided by two, so the answer is 0.168
Where am I wrong?

I think it is a case of the wording in the question: 'will have a daughter' still means we must consider all the offspring in ou probability. This means we must look at all the children they could have an including boys and girls and the probability that the daughter has haemophilia (with all of your working). If they had said: What is the probability that a random man and random woman's daughter has haemophilia? your answer would be correct, as we would have excluded the males from the offspring (as a conditional probability) which you had done correctly.

I make it 8%. Here is my reasoning.
The gene is X-linked.
40% mutant males, so freq(mutant allele) = p = 0.4, and freq(wt allele) = q = 0.6
To get a mutant female we have to have a mutant male parent, probability = 0.4
Of these matings one half will produce a female offspring so 0.4*0.5 = 0.2
i.e. 20% of matings derive from a mutant male and produce a female offspring.
Now look at the female mate:

probability(mutant) = p2 = 0.16
probability(carrier) = 2pq = 0.48
probability(wt) = q2 = 0.36

so our 20% of matings that have the potential to produce a mutant female offspring partition as:

mating with a mutant female: 0.2 x 0.16 = 0.032 mutant female offspring
mating with a carrier female: 0.2 x 0.48 = 0.096 of which:
0.048 mutant female offspring
0.048 carrier female offspring
mating with wt female: 0.2 x 0.36 = 0.072 carrier female offspring

(sanity check - 0.032 + 0.096 + 0.072 = 0.2)
Thus the probability of random mating producing a mutant female is 0.032 + 0.048 = 0.08 (8%)
Incidentally there is another way of thinking about this. Note that the H-W frequency of mutant females in the population is 16%. One of the assumptions of H-W is random mating. So the probability of a random mating producing a mutant female = p(female) * p(mutant if female) = 0.5 x 0.16 = 0.08
So - where have I gone wrong?

I get the same result. These type of questions can throw people off very easily, apparently including the people writing the answer keys!

In a given population, 40% of men have hemophilia – an X-linked recessive disorder. What are the odds that a random woman and a random man from that population will have a daughter with hemophilia?
Hemophilia is X-linked and recessive, so the frequency of males having the disease = q. So, q = 0.40. To determine the frequency of the dominant allele in the population, use…
p + q = 1
p + 0.4 = 1,
p = 0.6
Use these allele frequencies to calculate the genotype frequencies in the females using the Hardy-Weinberg equation:
            P2 + 2pq + q2 = 1
            0.36 + 0.48 + 0.16 = 1
Now use these frequencies in two separate Punnett squares
1)  All of the offspring from a homozygous recessive woman and a hemophiliac man will have hemophilia. Thus, (0.16)(0.4) = 0.064. Half of these offspring will be daughters, so 0.064/2 = 0.032
2)  Half of the offspring of a cross between a heterozygous woman and a hemophiliac man will have hemophilia. Thus, (0.48)(0.4)(.5) = 0.096. Half of these offspring will be daughters, so 0.096/2 = 0.048.
3)  Add the two possibilities together, so 0.032 + 0.048 = 0.08, or 8%

Frequency of allele for Haemophilia (q) = 0.4
Frequency of normal allele (p) = 0.6
Cross between Heterozygote female and hemophiliac male
by punnett square:
Probability of hemophiliac daughter = 0.5
P(hemophiliac male) = 0.4
P(heterozygote female) = 2pq = 2 × 0.4 × 0.6 = 0.48
P(hetero female+hemophiliac male+hemophiliac daughter) = 0.5 × 0.4 × 0.48 = 0.096
Hence 9.6%

In a given population, 40% of men have hemophilia – an X-linked recessive disorder. What are the odds that a random woman and a random man from that population will have a daughter with hemophilia?
Hemophilia is X-linked and recessive, so the frequency of males having the disease = q. So, q = 0.40. To determine the frequency of the dominant allele in the population, use…
p + q = 1
p + 0.4 = 1,
p = 0.6
Use these allele frequencies to calculate the genotype frequencies in the females using the Hardy-Weinberg equation:
            P2 + 2pq + q2 = 1
            0.36 + 0.48 + 0.16 = 1
Now use these frequencies in two separate Punnett squares
1)  All of the offspring from a homozygous recessive woman and a hemophiliac man will have hemophilia. Thus, (0.16)(0.4) = 0.064. Half of these offspring will be daughters, so 0.064/2 = 0.032
2)  Half of the offspring of a cross between a heterozygous woman and a hemophiliac man will have hemophilia. Thus, (0.48)(0.4)(.5) = 0.096. Half of these offspring will be daughters, so 0.096/2 = 0.048.
3)  Add the two possibilities together, so 0.032 + 0.048 = 0.08, or 8%


text:
Can someone identify this mushroom?
I found this monster on my lawn in New Hampshire USA, with a pileus that measures about 8.5 inches across. My mother has threatened to eat it unless I can demonstrate that it's poisonous, so any help identifying it would be greatly appreciated. I should mention that the mushroom is a slightly richer more brown than the fluorescent lighting suggests.
My best guess so far is an armillaria of sorts.

Cheers!

I doubt it is an armillaria. They usually grow in groups at the trees or dead strunks and have a darker centre. But being  European, I am unfamilair with American species. Depending how fond you are of your mother, I would strongly advise against eating an unidentified mushroom.

Do not eat any mushroom unless it is fully identified.  The results of a mistake can easily be fatal.

mgkrebbs is absolutely right. Some more information that might help with the ID is details of substrate it was growing on (or an in situ photo) and a spore print. That may be enough for an expert to ID it.

This is most likely a member of the genus Amanita, judging by the vellum traces on the cap, remains of a ring (2nd photo, under your thumb), free white gills.
What we are missing for a better id is the base: is there a volva, a bulbous end...? Please dig out your mushrooms instead of cutting them off.
Also, the colour is significant: are there pinkish tinges (-> A. rubescens?) or is it just brown?

Good shout. It think it looks a lot like Amanita porphyria

I don't recall any pinkish tinges. In any case since I haven't given enough information for an exact id, and the general consensus that it is most likely an Amanita, I will accept this as an answer. Thank you!


text:
Is neurogenesis essencial for learning?
So I read that our brain produces 700 new neurons in the hippocampus every day and that if we perform cognitive demanding tasks, eat omega-3 or exercise (other things?) it can produce even more neurons.
What happens with this new neurons? Say I'm learning some new skills, what role do those new neurons play in the process? Is it possible to learn without neurogenesis?
Edit: I'm interested in this topic (eg: brain, hippocampus, learning). Where can I learn about this from the basics? What classes teach this in college?

No, neurogenesis is not necessary for learning (assuming you are talking about adult neurogenesis: of course you need to generate neurons sometime in development to even have a nervous system).
Easily the most-accepted theory for learning and memory is that learning happens by changes in the strength of synapses, the connections between cells. The strengths of these connections are also often referred to as "synaptic weights." The primary mechanisms for this learning are long-term potentiation and the related spike-time dependent plasticity, as well as the guiding principle of Hebbian learning often stated as "cells that fire together, wire together."
Briefly, long-term potentiation or LTP describes the increase in post-synaptic receptors that occurs under certain conditions: this is what increases the efficacy or strength of certain synapses. One of the key conditions is that LTP tends to occur at synapses that causally contribute to making the post-synaptic cell fire.
Adult neurogenesis primarily occurs in a few localized area of the brain (Zhao et al.,
 2008). Although it is possible there is neurogenesis outside of these areas, it has not been demonstrated conclusively and is certainly not sufficient to be necessary for learning in a normal, uninjured adult brain.
Neurons born in the subventricular zone continually replace olfactory receptors, which have a relatively short lifespan, probably evolved due to their constant exposure to all sorts of potentially damaging external compounds entering the nose. These cells do have to undergo some "learning" processes to integrate into existing networks, but that isn't what you would colloquially think of as learning in general.
The best candidates for cells that actually impact learning to some degree are the new neurons born in the subgranular zone of the dentate gyrus in the hippocampus. The hippocampus is indeed an important structure for certain types of learning, but new neurons aren't necessary for this learning. Although it is still somewhat unclear what the roles are of the new neurons in the dentate gyrus, it is thought that they contribute to the primary roles of the dentate gyrus, which are to help distinguish between similar patterns of activity (Deng et al., 2010), also called "pattern separation."
Two other hypotheses are that adult neurogenesis helps to encode timing information in memories because the new neurons only participate in new memories, or that they allow for incorporation of novel stimuli once the older neurons have been conditioned and tuned only to stimuli that have been experienced before (Aimone, et al., 2013). There is evidence for all of these hypotheses but none of it is conclusive, and all may be true to some degree.
There are many different types of learning and these different types of learning can occur in different brain regions, most of which do not demonstrate any substantial adult neurogenesis. Often people think about associative learning with operant or classical conditioning. There is also episodic learning: remembering events that have happened (this is the type most closely associated with the hippocampus, where perhaps neurogenesis plays some role). There is also motor learning, and several types of learning in sensory systems like habituation or sensitization. Therefore, it is important to understand that learning isn't just one thing, and although the mechanisms can be related they are not always the same.
How to learn more: I can tell you about courses at institutions I have been affiliated with, but of course these could vary between schools. Learning and memory is usually at least part of a systems-level undergraduate neuroscience course, which is often the second of two overview courses in neuroscience. The most common time for students to take such a course would be as a second-semester junior or a second-semester first-year graduate student, because there is prerequisite knowledge in physics, chemistry, molecular biology, and physiology. There are also graduate-level courses in the molecular mechanisms of learning and memory, and theoretical neuroscience courses that cover the computational considerations of learning and memory rather than just the biological mechanisms. These types of courses might be available to a senior-level undergraduate as well.
Of course you can also read some of the review papers I have included here and follow the references they cite for original research, as well. The Aimone review is particularly readable and has some very excellent illustrations for a novice, and also extensively covers the regulation of neurogenesis by behavior and environment.
References
Aimone, J. B., Li, Y., Lee, S. W., Clemenson, G. D., Deng, W., & Gage, F. H. (2014). Regulation and function of adult neurogenesis: from genes to cognition. Physiological reviews, 94(4), 991-1026.
Deng, W., Aimone, J. B., & Gage, F. H. (2010). New neurons and new memories: how does adult hippocampal neurogenesis affect learning and memory?. Nature Reviews Neuroscience, 11(5), 339-350.
Zhao, C., Deng, W., & Gage, F. H. (2008). Mechanisms and functional implications of adult neurogenesis. Cell, 132(4), 645-660.

Plenty of AI and machine learning frameworks can learn incredibly quickly, yet they have no neurons and some of them make no attempt to mimic neural networks.
If rote memorization (the simplest and crudest form of learning) is considered learning, then you could even argue that a computer "learns" when you install a new program on it.
So the answer to your question is no.
Even if you aren't accepting computer learning as an example, any half-decent immune system can "remember" previously encountered pathogens and this doesn't appear to rely on neurons.

I think it's pretty clear the OP was asking about learning in the brain...


text:
What is this arthropod?
It is approx 2cm long and was discovered in house after a bush walk & BBQ at Riverside Garden Reserve in Mandurah, Western Australia. It has 6 legs.
Thanks! :-)

Welcome to Biology.SE. I edited your question slightly for improved readability. Please feel free to further edit.

It's almost certainly a beetle larvae/grub of some sort, but I'm afraid I don't know what species!

Lyn, I took the liberty to reedit your post to improve presentation.


text:
Anyone know what this bug is? (Southern California)
I found it in Southern California on the fringes of the Mojave Desert. They seem to have nests similar to ant hills but don't look like any ant I've ever seen. They seem to have shown up within the past week or so and have their nests near some big red ants (Camponotus castaneus I believe) though the ants don't seem to be eating them. They are around the same size as the little black ants (Monomorium minimum), but unlike ants they seem to get blown around by the wind. There were hundreds of them around and had several apparent nests. They were also climbing all over a wood fence nearby. I was able to get a picture, hopefully it is clear enough to make out the bug in. You can see a few of them on the gray rock.

The only thing I could think they might be is some kind of termite or something. Are they harmful, and if so, how would I deal with them?

They seem to be true bugs (Heteroptera) nymphs, they have long antennae, an oval shaped abdomen and the wings are not fully developed yet.


text:
What are mouse LS cells?
I have seen the term "mouse LS cell" used in several papers now, but I haven't found an explanation for the origin of these cells (for example, this paper).
What are mouse LS cells? What is their origin (besides coming from mouse!)?

Not an easy question, but I got some references about it.
Mouse LS cells are Fibroblasts growing in suspension culture, the paper in reference 1 has this paragraph in its Materials and Methods section:

This cell line seems to be in culture since the 1940s, as the reference to Sanford, Earle and Likely, 1948 suggests. Digging up this reference (number 2 below) tells a bit more about the isolation:

The cells of this study were from Earle's strain
  L (6), which originated from normal, subcutaneous,
  connective tissue of an adult C311 strain
  mouse.

Reference 6 in the Sanford et al. paper is:

EARLE, W. R.: Production of malignancy in vitro.
  IV. The mouse fibroblast cultures and changes
  seen in the living cells. J. Nat. Cancer Inst, 4:
  165-212 (1943).

which gives no further details. It is a methodic paper which analyzes the conditions necessary for cell culture - interesting on a historical point of view, since the techniques where developed at that time. The full PDF is linked in reference 3.
About the name I need to speculate a bit, but since the original cells where named "Strain L", and LS cells where derived from there to grow in suspension, it might translate into Strain L Suspension cells.
References:

The Uptake of Amino Acids by Mouse Cells (Strain LS) During Growth
In Batch Culture and Chemostat Culture: The Influence Of Cell Growth
Rate
The Growth in Vitro of Single Isolated Tissue Cells
Production of Malignancy in Vitro.


text:
Would I expect salt precipitate on fibres of DNA in a NaCl water solution?
I just recently conducted an experiment in my biochemistry class where we had to add DNA to distilled water, isotonic saline and 2.5M NaCl. I noticed different physical aspects depending on the solvent, but I'm not sure how I would categorize them. Here's what I saw:

Distilled: fibrous precipitate, cloudy liquid
Isotonic: Honestly barely noticed a change here? Maybe I wasn't looking hard enough
2.5M: salt precipitate at the bottom and fibres

I know DNA is polar so solubility should increase as the polarity of the solvent increases. But to my recollection what I saw in 2.5M saline vs distilled water did not differ much. However, there is always the possibility that I could have made some experimental errors that led to inaccurate observations.
So, can someone help me deduce the solubility of DNA (simply soluble/not soluble) in each of these solvents, or refer me to a paper I can read? Thanks in advance!

Do you have any pictures that might help us gauge exactly what you saw? Here is a related Q&A on DNA solubility in water

https://imgur.com/a/Apbps this is what I saw when I added distilled water to  the  2.5M NaCl (final conc of 0.16M), but other than that no photos! And I will refer to that discussion for water, thank you :)


text:
What would happen if a cell is poked by a fine needle?
I had seen this question in an exam:
A living cell has a protoplasm which is water based and demarcated by a lipid bilayer membrane. If a cell is pierced to 1/5th of its diameter with a very sharp needle, after taking the needle out
(a) no effect will be observed.
(b) protoplasm will leak out from the hole made by the needle for a few minutes until the cell heals the wound.
(c) protoplasm will keep on leaking out till the cell is dead
(d) the cell will burst like a balloon.
I understand that the answer is option (a) as the cell membrane will reseal itself after getting pierced.
But my doubt is that if in the question 1/5th was replaced by 1/2 or by any number greater than 1/2, will the answer be different.
Or in other words, I want to know whether the number 1/5 significant in this question.

This is a homework question. Unless you show that you made an effort to solve the question yourself it is likely to be closed. Please look here on how to properly ask homework questions.

Depends on the diameter and the shape of the needle, and the hydrostatic pressure inside the cell.

I don't believe the edits satisfy the need for an attempt at an answer, there's no effort or justification, therefore I don't think it should be reopened

@rg255 Why not? The OP is asking what (to me) appears to be a valid question about the fraction of lost cell membrane that results in cell death.

Because there is no attempt to work out an answer and is homework

Generally speaking, there is no effect in microinjections.
This is relevant in the real world example of micro-injections. A video of a pronucleus injection can be seen here, or here is a more thoroughly explained procedure involving cloning. As you can see in the video the membrane, almost no effect will be observed - molecular dynamic simulations show that the membrane can spontaneously reform from fragments in the tens-of-nanoseconds timescale.
1/5 refers to  the question "is the needle small enough?"
The question does include the term "1/5", which is a bit unusual. I guess they want you to recall a specific piece of information about the correct ratio size of needle should be. Here is a video of a microinjection at approximately that ratio. However the exit hole is unintentionally filled with the inserted material and cannot close immediately. The cell disappears out of frame before we can confirm the hole is closed.
Cell diameters are very variable
Cell sizes vary greatly.

From using these values, assuming a cell is a sphere an oocyte has a diameter of approximately 196µm, whereas a neutrophil has a diameter of 8µm. It's a bizarre question given this range because usually micro-needles are between 0.5 and 5 µm diameter in length, except in the case of oocytes where larger needles are used (according to wikipedia). I don't think this is relevant, and it is just arbitrarily picking a needle size that wouldn't completely maul the cell!


text:
A biological system to measure time
First of all I am a physicist, so I apologise for my non-existent understanding of basic biology. However, I have what I think is an interesting question and this seems like a good place to ask it...
I’ve recently been thinking whether there is a way to measure time using biological processes. In other words some system, a characteristic of which can be correlated to elapsed time. One example I can come up with is counting the number of divisions of a cell. I guess this can be done, but will most likely be highly inaccurate…
So this is my question: Do you know of any papers even tangentially related to the idea of a biological system that can be used as a clock?
Any ideas will be greatly appreciated!

I don't think circadian rhythms are accurate enough to be used as a clock.

What kind of time frame do you want to measure time on? If you want centuries / millenia / millions of years, you can look at the accumulated mutations in the noncoding sections of DNA; it's how we measure how long it's been since the last common ancestor of related species.

Fascinating question, thanks for asking! Welcomg to Bio.SE!

@Orange_Striped_Gecko I was hoping for minutes (or even seconds).

There are lots of biological clocks, or clocks made of biological components. The circadian clock is an important, though complicated, example. There are excellent engineered clocks that form some of the neatest examples of systems / synthetic biology. See for example Elowitz & Leibler's "repressilator" (link, link). The basic idea in all of these is to have gene regulatory circuits with feedback that lead to oscillation of the gene expression dynamics. Books on systems biology, or Philip Nelson's Physical Models of Living Systems (aimed at physicists), are good places to read more.

Thanks! I will look into this.

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


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How is the probability of a sequence occuring with BLAST calculated?
What is the probability that a given nucleotide/amino acid sequence will occur in the whole database program BLAST searches in? How this probability is calculated?

According to BLAST documentation statistics of local sequence alignment, when doing database searches, is done

by treating the database as a single long sequence of length N.

N is therefore a sum of all sequences with varying sizes from a given database.
Underlying assumption is that

query is a priori more likely to be related to a long than to a short sequence, because long sequences are often composed of multiple distinct domains.

To calculate the probability, we need to choose a scoring scheme (for ungapped example: choose a mismatch penalties), which for a query sequence gives us a statistically significance score $S$. Expected number of alignments with score of at least $S$ follows Gumbel extreme value distribution:
$$
E = Kmn\cdot e^{-\lambda S}
$$
where m is query length, $n=N$ and $K$ and $\lambda$ are distribution params.
Again, according to docs and its references, probability of finding at least one such seq would be $P=1-e^{-E_{(N)}}$, where $E_{(N)}$ is E-number for concatenated N-sequence and query sequence.


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How did people's liking of ceremonies evolve?
Habitual group activities are prevalent across many animal species, particularly in mammals, especially in primates.
However, I do not see any evolutionary benefit of this. 'Ceremonies' take time, and in many cases seem to exert more energy than they reap. Note at this point I am not talking about hunting groups, but rather about group activities that serve a purely social purpose (mourning is a  good example of this and is present in elephants, chimpanzees, bonobos, and probably more). This costs significant amounts of resources, time, and energy which apparently could be better spent hunting, foraging, traveling, mating, or grazing.
I'm interested in finding a timeline, and explanation, of why and how this phenomenon of higher social rituals (perhaps using mourning as an example) evolved throughout the mammalian kingdom.
A cursory google revealed nothing about how this 'liking' of interaction evolved.

I'm voting to close this question as off-topic because this is an anthropological question.

We'll need an accurate definition of rituals in order to answer this question. For the moment it is too broad. Do you restrict rituals to social traditions? Do you include personal habits and obsessive behaviour in rituals? You posted several links (without much explanation), you should probably report what you read so far, that would help.

Questions about the evolution of human behaviour are on-topic to my opinion.

@AliceD The question is about evolution, and as far as I know, evolution falls firmly within the realm of biology. Perhaps it would be better on a anthropology Stack Exchange, but one does not exist.

@Remi.b Okay, I re-wrote the question. Do you have any ideas to further improve it?

Thank you the question is much improved this way, I retracted my close vote. Note however, that the question is not so much about evolutionary genetics but fall within the field of "evolution of traditions/culture", or more broadly speaking "evolution of memes" also called "memetics", which is a field that has been created by biologists but in its current state is in between biology, sociology and philosophy. I think the question is on-topic but will appreciate to see what the others say. Might be a bit broad also...we'll see.

the question in it's present form does not have a biological perspective, the user thinks it is, but it's really more of a question of how did our cultures take the shape that they have today. What you can ask is why is our behaviour different from that of other animals, and how has it come to be so...

@KoustavPal What do you mean it doesn't have a biological perspective? Is there not some evolutionary advantage to ceremonies? Is that not biological?

no the evolution of ceremonies themselves have no biology, but neural development does, I'm not making myself clear. Ceremonies are our inventions, for instance mammalian males are generally polygamous, traditionally that has been so, in came the church and instituted monogamy, then in 19th century a few mistresses on the side were fine, and in the 20th century feminism started to pick up the pace and again we reverted to monogamy. So where is the evolutionary part of ceremonies. I will also point this out, the basal character of humans have not changed.

you would still prefer to sleep inside a closed space facing the point of entrance, why do you think that is?

@KoustavPal This is very far away from any biology particularly if you start talking about specific rituals from your own culture. For example, weddings in western culture have changed dramatically over the last century as media & adverts changed the concepts of a wedding. These are not biological evolutionary timescales.
Bird models are often used to study social dynamics, and primate studies often turn up habitual social group activities. Starting there might narrow down your question. Elephants have been observed mourning their dead too.

@KoustavPal I'm not asking how ceremonies evolved, as like you said, that would be cultural. I'm asking how the liking of ceremonies in general evolved. Given that this liking has existed for a very long time and is observed in other species, this seems genetic and biological.

@GoodGravy You might want to see the response I gave to KoustavPal.

Now I understand. You frame the question with in a very cultural-centric way. I'll try and suggest an edit.

@Kyth'Py1k I have made some major edits to the question so feel free to roll back, but I think the question is back on topic. It still remains vague. If you can better define a "ceremony" or restrict it to mourning, then it will probably be specific enough to re-open.

@GoodGravy You made a good edit. I'm not sure how to make it less vague without taking away from the meaning of the question. I could try to narrow the question down to a specific ceremony, for example burials, but this would only give an answer to one small part of the question. I'll do this if you do not have any better ideas, though.

@GoodGravy Okay, I asked a new, more specific, question.

Perhaps customs (and culture as a whole) arises to some extent as a result of relationships between individuals of the same species. For example, I think a good example of a custom is how elephants bury their dead. This does not benefit the surviving elephants in any noticeable way, and is a "waste" of energy and time. If customs do arise because of a group dynamic, then there is clear evidence supporting that social behavior in higher organisms (chimpanzees, dolphins, etc.) does increase fitness.
However, this speculation is based upon the idea that customs are a natural result of social interaction. As to why these customs arise, perhaps it is because it enforces the group dynamic over the participating individuals.

I don't think elephants bury their dead, it's just that they appear to hesitate to move on from a dead elephant. Happy to be proven wrong!

"...They then began to throw leaves and dirt over the body and broke off tree branches to cover her." I stand corrected!


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How to use swiss-mod to predict the secondary structure and 3D structure of a protein?
I'm trying to predict the protein secondary and 3-D structure for the sequence [Q1NN20] and need some help getting the ball rolling.
I'm getting confused with how and when to use Jpred, swiss-mod, and PDB. So far, I got the sequence from scanprosite, put it into swiss-mod, but what next? When does jpred come in?

I've tried to provide a general answer, but could you provide more specifics about the type of protein you have, and why you want to model it. Why are you using swiss model and jpred?

3D structure.
Use the PDB to identify structures that are similar to the one you have found (you can use BLAST to search the PDB). A 30% match or above is usually acceptable, and multiple alignments are of course useful at lower match scores. If structures exist that are similar enough, you can use homology modelling to generate a 3D structure (this is what the SWISS-MODEL server does, and I think it automates the BLAST alignments from PDB). If there are no similar structures, you can resort to ab initio modelling if you have a reasonably straight forward globular domain, otherwise you might need to draw in additional expertise.
There are so many specific factors that need to be taken into account for a project like this. Depending on what the model will be used for, different questions are relevant.
Secondary structure.
You will need a few different secondary structure predictors to make it convincing and then you will need to check that your secondary consensus matches your 3D structure. If they don't match you need to think about "why not?"
If there is a difference it usually indicates that some 3D interaction is involved in the folding, so your 3D model usually trumps the sequence structure predictions, but do check your 3D structure against the secondary structure predictions.
Secondary structure prediction is more useful when a 3D structure is not available and modelling one is not an option.

Metaserver runs several methods for you and runs consensus analysis (and a bunch of other stuff). I'd start there.

That's a good one to start with, but ultimately will still be "trumped" by modelling (from a good alignment).

Swiss model is an online tool for modelling protein tertiary and Quaternary structure using evolutionary information. J-pred and Swiss model both are pretty straight forward tools which requires only the sequence. Swiss model requires searching for a template and based on which the protein will be modeled further.J=pred is exclusively used for secondary structure prediction.

So when i'm using Jpred, I get a bunch of 'hits' from pdb. what are these, just very similar sequences?

Do those hits come with a score?


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What E-value BLAST cut-off is best?
What is the best cut-off for e-value in BLAST?
Some say 0.01 ,others 0.0001?
Even BLAST tutorials don't give a very clear idea about which cutoff suits which purpose?
Could some experts give me a clear idea on this.
Why are we using 0.0001 and not 0.00011?

There's virtually no difference between 0.0001 and 0.00011; cutoffs work in orders of magnitude. Depending on what I'm doing, sometimes I'll use 0.1, sometimes I'll use 1E-30 (0.000000000000000000000000000001).

Honestly, e value means very little and is hard to judge. Its often case dependent

For nucleotide alignment use 1e-05 --> http://pathblast.org/docs/e_value.html

There is no perfect cut-off. It always depends on what you're doing. The e-value is basically a measure of how many such alignments you would expect to find in a database this size by chance. Therefore, e-values greater than 1 mean that you'd expect at least one alignment similar to what you've found by chance alone.
As others have stated, the e-value is not a rigorous measure of significance. It depends on

The length of your alignment.
The alignment's bit-score score (this takes into account amino acid substitution scores based on the matrix being used, BLOSUM65 by default).
The size of the database you are searching in.

I have at different times and for different projects used e-values ranging from 10 to 1e-100 or less. You always need to take into account what you are looking for. For example, to run a tBLASTn looking for distant homologs, you'd use a relatively high e-value, say 1e-10 or even 1 or greater depending on the details. For example, the default e-value for ncbi-tBLASTn is 10.
To find extremely similar sequences in closely related species, you'd use a much smaller one. Say 1e-20 or 1e-50. Normally, you tweak these settings after seeing your results.
After running a few hundred blasts, you get the hang of it and you can have a pretty good estimate of the e-value cutoff you want to use. Until you get that experience, you will have to use trial and error. Just remember that the conclusions you can draw from your data will be heavily influenced by that e-value. Don't try to publish something claiming you've found a homolog if the supporting BLAST hit has an e-value of 45 for example.
Personally, when looking at BLAST out files, I check the e-value, the alignment's length (as a percentage of the query), the alignment's %id score and the bit score itself. Of these, the most reliable is the bit-score but, again, that too changes depending on what question you are attempting to answer.

@OP I would also add this point that the cutoffs, scoring schemes and inferences are dependent on what you really want to find. It is to be first reasoned if BLAST is the right tool for what you are seeking.

The e-value is supposed to be a metric for the chance that an alignment could occur at random, but it is a crude estimate.  As pointed out in other answers, this significantly does not include the length of the query sequence.
It also does not include the conservation of the gene or the frequency of amino acids (in protein blasts).  It does take into account the database of sequences queried, which might be something you know very little about if you didn't make it yourself.
That being said, 1e-5 is a pretty poor score.  Its really awful for nucleotides - maybe a perfect alignment for 10 or 12 bases. So I'm going to assume that you are looking at peptides.
You should also look at the coverage statistic.  That is the length of the alignment divided by the query or the hit sequence.  It should be 70%+ depending on what you want.
If the coverage is good even answers pretty far down the score rankings might be relevant.
Similarity is usually performed with a BLOSUM matrix.  Regardless, the number of exact matches compared to the number of similar matches of amino acids in an alignment poorly approximates what is going on in evolution.
Lastly protein alignments tend to have gaps - lots of gaps.  The penalty to the scores for allowing gaps might low for long evolutionary distances or completely unreasonable for more recently diverged results.  So you have to look at those qualities of the alignment yourself.

"It does take into account the database of sequences queried, which might be something you know very little about if you didn't make it yourself."
This is incorrect. Database size directly affects E-values.

@5heikki.. what are you refuting here? Both the statements mean the same thing...

Sorry but this is really not correct. As explained in the page you link to, the e-value is given by E=Kmne^λS where S is the alignment's score. Since this is a measure of (among other things) the conservation of the two sequences, the e-value includes both "conservation of the gene" and "the frequency of amino acids". Also, to my knowledge, all popular BLAST implementations (and certainly ncbi and wu-blast) use BLOSUM65 matrices, not PAM by default. In fact, I don't know of any program that uses PAM matrices by default and I can't imagine why you would want to.

http://en.wikipedia.org/wiki/Point_accepted_mutation#Use_in_BLAST

CLUSTALW uses PAM and BLOSUM both.. It is preferable to use BLOSUM for local alignments and PAM for global alignments.. Makes intuitive sense, thats it; no hardcore reason..

Thanks for the edit. Note that the wikipedia article you posted cites the same ncbi link you have in your answer which also states that "A number of tests suggest that the "BLOSUM" matrices produced by this method generally are superior to the PAM matrices for detecting biological relationships." Essentially, PAM have been replaced by BLOSUM.

E-value refers to the expected number of random hits for a given alignment score. Smaller it is more reliable is your match. There is no hard and fast rule for e-value cutoff. You can keep whatever you want depending on the level of stringency that you require. But you should note that for smaller sequences (< 30nt) there is always a higher likelihood of random matches. In such cases it is practical to relax the e-value cutoff.

The E-value of 0.0 indicate the number of alignments with scores equivalent to or greater than that are expected to occur in a database by chance therefore the lower the E-value the more significant the score hence a better quality of the alignment blast search.

can you share a reference that others can read for more information on your answer? it would definitely strengthen your answer - thanks for your contribution!

A score of 0.0 zero isn't actually zero it's just lower then 10^-100

The e-value is required to have confidence in the hit, along with hit. Generally, an e-value of e-4 is preferred because, this cutoff is found to be sufficient enough by blast to confirm a hit as homolog. But, for a hit, an e-value greater than e-4 does not mean it is a homolog neither we can say it is not a homolog. We cannot surely infer anything from these hits. Therefore, researchers choose a value

There is no magical threshold that defines homology! It depends completely on the specifics of your situation. There are cases where you can find true homologs and an evalue >10. Everything depends on the length of your sequences, the size of your database, the conservation of your homologs etc.

Sorry if my answer seems confusing. But, is it not that an evalue much closer to zero is considered homolog? Because, i see in some papers and tutorials using e-4 or lesser value to assess homology as a rule of thumb. Those hits, where the evalue > 10 may or may not be a homolog, but i think we cannot definately say they are homolog, without further insights. Would like to hear your comments. Thanks.

No. We can never decide on homology based on the e-value alone and there is no single magical threshold. The threshold you choose will always depend on the particular question you are asking (how diverged are the species? How long is your sequence? How large is the database? Is this nucleotide or protein blast? etc). What is important for deciding homology is the particular regions of a sequence that are conserved (e.g. domains). For example, if you search for a homolog of a very short sequence with repetitive regions, you will never have a small e-value.


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Is there any kind of "unintended consequence" in evolutionary systems?
In the social sciences, unintended consequences is a term used to describe an unexpected positive or negative effect of a particular action. This is obviously the wrong word to use in the context of evolutionary systems but I am looking for something that has a similar concept. It may be related to concepts in dynamical systems theory.
For example, if we look at one trait or a group of traits, we may be able to see how this adaptation benefited a population. However, the mutations that occurred along the way would no doubt alter other systems/properties of the organism. In many cases these effects would be negligible. I am looking for any cases where the effect of one set of adaptation leads to another comparably impactful (either positive or negative) effect for the population.
The following is more theoretical and controversial but I am particularly interested in larger, more complex traits such as behavior (which may be considered the product of many different evolutionary adaptations and molecular changes) and any "unintended consequences" that could occur as a result of such a behavior. For example, empathy may be considered a very complex trait that has an evolutionary advantage (post hoc we might say it evolved because it allows specific kinds of communication in social groups) but it may also cause populations to react incorrectly (with regards to survival) in threatening situations when an empathetic response is not the most optimal response. I realize I am treading in vague territory here and it may be controversial to reduce empathy down to the molecular level as I have done in this example. But if there is any work at least related to this idea on a basic level I would be interested.
In summary, I am looking for either the term that describes this sort of analysis, if it exists, or some major examples that may help me do further research on the topic.

There is a lot of text here. I have tried to answer the question "Where has a seemingly beneficial/detrimental evolutionary change had the seemingly opposite affect?"

You have addressed my question correctly. There is a lot of text because I wanted to make sure I was clearly stating what kind of answer I was looking for. Sorry if this made it more confusing.

I get what you are trying to say, but want to point out that the terminology is poor - there are no intended or unintended evolutionary consequences of mutation, evolution is a random process, not driven by intentions

@rg255 I should have been more clear. In my first paragraph I said it was the wrong word to use in the context of evolutionary systems and that is exactly why - it is an undirected or non-teleological process. I'll make an edit when I get a moment to be more specific about that.

The term "exaptation" might be an interesting one for you to look into.

Slightly more tangentially, you might also enjoy reading about the Baldwin effect in this context. In particular, since you mentioned dynamical systems, you might like Geoffrey Hinton's famous model of it. (That's the same Geoffrey Hinton who's now very famous in the field of deep learning.)

There is also a field of research from the 90s called "adaptive dynamics" which gets pretty directly at the kind of thing you're talking about, where an evolutionary response is not the optimal one. In fact they claim that in particular ecological contexts a species can end up at a fitness minimum instead of a maximum, and that this can lead to speciation. Those papers tend to be quite impenetrably mathematical, but if your background is dynamical systems that might not be a problem for you.

@Nathaniel This is is exactly when I was looking for. I was having difficulty finding the right wording which made it challenging for me to explain myself in my question. If you want to turn your comments into a more complete answer I will accept it. But for now, this is great to get me starting and gives me a direction to search further.

Are you referring to tradeoffs; advantage in something causing disadvantage in some other thing?

Preamble
Evolutionary systems do not have these exact terms as far as I'm aware (although I'm not a behavioral expert) This mainly is because generally speaking we must stop thinking about traits in terms of "advantageous" or "intentional consequences" when discussing evolution. However there are countless examples where a seemingly detrimental evolutionary trait flourishes, or when a seemingly beneficial trait can be exploited by other species. Here I point out two simple, well known examples that might be what you're looking for.
Physiological disease trait emerges
The most well known is sickle cell anemia (SCA); a disease that also reduces susceptibility to malaria. In areas of the world with high instances of malaria, there are also high instances of SCA (Piel et al 2010).
Behavioral altruistic trait exploited
For behavioral studies I think humans would be too vague... (okay, I know very little about sociology) But there is one story that springs to mind from another animal. Birds are ideal models for behavioral studies.
The cuckoo and warbler are an endless evolutionary arms race in terms of camouflage and behavior. The cuckoo parasitises the nest of the warbler with a single egg in a clutch of 3 or so warbler eggs. The warbler parents will watch the newly born cuckoo kick the other eggs out of the nest, and then continue to feed the cuckoo chick thinking it is their own. The reason is thought to be because the warblers respond to the feeding call of their chicks (altruistic, albeit from parent to chick), however the cuckoo chick can mimic this call much more intensely than an entire brood of warbler chicks (altruism is exploited)(Davies et al 1998). By the end, the tired parents are feeding a chick three times their size.


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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