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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.


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How can I download histological slide from Cancer Digital Slide Archive
Could you tell me if it possible and how to download images data from http://cancer.digitalslidearchive.net ?
Thank you.

source: Stack Exchange

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

sort: votes


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What do halophytes do with the salt?
The answer to "How do some plants grow in salt water, while others die?" offers some hints as to how salt-tolerant plants store salt by shifting it out of cells, and also can deal with higher salt concentrations in cells, but what happens after that?  Do the plants somehow excrete the salt? Store ever-increasing amounts in more and bigger vacuoles? Convert it into something more useful by chemical reactions? Reach equilibrium concentrations with the water in which they grow and rely on osmosis?
It seems to this layman that plants growing in salt-water in the tropics will transpire quite a lot of water, and if that's replaced with salt water, they'll take up quite a lot of salt.

There are a couple of strategies that salt-tolerant plants can use to survive in high-salt conditions.
Plants can increase the concentration of compatible solutes in their cell to the point where the intracellular concentration of solute approaches the concentration of the water in the environment. By doing this, the plants are able to minimize water loss through osmosis, while ensuring that the cells do not reach harmful levels of salinity.
However, compatible solutes are often not enough to completely combat the effects of salt stress. Salt stress creates higher concentrations of oxygen free radicals, which can cause harm to DNA and other cell components. Mangrove trees have been found to have heightened expression of repair proteins and anti-oxidants when exposed to salt stress.
Additionally, mangroves have been found to be able to excrete salt from their root cells and their leaves. They have ion-transporters which actively pump sodium ions out of their cells into the extracellular space. They have salt-filtering mechanisms that allow them to uptake the water from salt-water without up-taking the salt in the water.
So in conclusion, salt-tolerant plants sequester some salt within their cells, but also use ion-pumps and compatible solutes to limit the concentrations of salt within their cells. They can selectively uptake water from salt water, and use repair mechanisms to limit the damage of high salt concentrations in their cells.
Kao, C.H. 2015. Mechanisms of salt tolerance in rice plants: compatible solutes and aquaporins. Crop, Environment & Bioinformatics 12:73-82.
Wang, L., Pan, D., Lv, X., Cheng, C.L., Li, J. Liang, W., Xing, J, and W. Chen. 2016. A multilevel investigation to discover why Kandelia candel thrives in high salinity. Plant, Cell & Environment 39:2486-2497.
Srikanth, S., Kaihekulani, Lum, Y., and Z. Cheng. 2016. Mangrove root: adaptations and ecological importance. Trees 30:451-465

I'll have to follow the references when I'm back on a network with journal access but already I'm greatly enlightened.

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Is the basic reproduction number unique?
Given any epidemic model of an infectious disease, there are various ways of computing a basic reproduction number($R_0$) such as;  the next-generation method, survival function, largest eigenvalue of the Jacobian matrix and so on.
My question is,

Do we get the same $R_0$ for the same model but using different methods of computing $R_0$?

If we don't(if $R_0$  is unique) what is the explanation?
Are we allowed to use "this" different $R_0$ in writing a paper?

Generally, as with all statistical model fitting, you need to separate between the actual (unknown) value of R0 and the estimate of R0, based on model fitting from empirical data. If you consider this, different estimates of R0 are rather unproblematic (and expected). However, large deviations between estimates using different methods is worth digging into, since it could indicate problems with some of the data.

It should be noted that many of the methods you talk about aren't necessarily for getting a number but rather a formula for $R_0$, all of which should be equivalent.
However, when those methods step into the realm of getting a number by fitting parameters, they may give different results as they handle certain aspects of the data differently.
You are certainly "allowed" to use any formulation of $R_0$ you want - just document what you did.


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What is the Attributable Risk of birth defects in Zika infected pregnancies?
Vital Signs: Update on Zika Virus–Associated Birth Defects and Evaluation of All U.S. Infants with Congenital Zika Virus Exposure — U.S. Zika Pregnancy Registry, 2016
A recent CDC report shows that 10% of laboratory confirmed Zika pregnancies in the US had "birth defect reported."  However, I cannot seem to find an attempt to compare this to a base rate in the US of a similar population.  Is there existing information or a way to determine the Attributable Risk (difference in rate of a condition between an exposed population and an unexposed population).
10% sounds scary, but without a base rate, it's not very meaningful in the context of determining how dangerous the Zika virus is.
EDIT (for clarification):
I'm primarily concerned with the method in which birth defects were collected. 'Clinical experts reviewed reported information to ensure that each fetus or infant with birth defects met the criteria of the USZPR case definition.', but this seems to have been done only with the Zika-positive groups and not with a Zika-negative group. They compare it to a pre-Zika baseline, in which inclusion to the surveillance was different and determination/clinical review of each case was different. Did they (or another research group) perform clinical evaluation of birth defects during the surveillance period on Zika-nagative pregnancies using the same methodology?

The article cited in the question (Vital Signs: Update on Zika Virus–Associated Birth Defects and Evaluation of All U.S. Infants with Congenital Zika Virus Exposure — U.S. Zika Pregnancy Registry, 2016) gives the base rate for the definition of "birth defect" that they use:

The baseline prevalence of defects consistent with those that have been observed with congenital Zika virus infection was approximately 2.9 per 1,000 live births in the pre-Zika years (4). The initial findings from the USZPR represent an approximate twentyfold increase in Zika virus–associated birth defects among pregnant women with laboratory evidence of possible recent Zika virus infection, with an approximate thirtyfold increase in brain abnormalities and/or microcephaly.

The reference for that background is Baseline Prevalence of Birth Defects Associated with Congenital Zika Virus Infection - Massachusetts, North Carolina, and Atlanta, Georgia, 2013-2014.:

These data, from Massachusetts (2013), North Carolina (2013), and Atlanta, Georgia (2013–2014), included 747 infants and fetuses with one or more of the birth defects meeting the case definition (pre-Zika prevalence = 2.86 per 1,000 live births). Brain abnormalities or microcephaly were the most frequently recorded (1.50 per 1,000), followed by neural tube defects and other early brain malformations† (0.88), eye abnormalities without mention of a brain abnormality (0.31), and other consequences of central nervous system (CNS) dysfunction without mention of brain or eye abnormalities (0.17). During January 15–September 22, 2016, the U.S. Zika Pregnancy Registry (USZPR) reported 26 infants and fetuses with these same defects among 442 completed pregnancies (58.8 per 1,000) born to mothers with laboratory evidence of possible Zika virus infection during pregnancy (2). Although the ascertainment methods differed, this finding was approximately 20 times higher than the proportion of one or more of the same birth defects among pregnancies during the pre-Zika years.

According to Estimating the Number of Pregnant Women Infected With Zika Virus and Expected Infants With Microcephaly Following the Zika Virus Outbreak in Puerto Rico, 2016. the background of microcephaly in Puerto Rico was around 12 cases per year, while they estimated 180 cases would occur in the presence of Zika.

We estimated an IQR of 5900 to 10 300 pregnant women (median, 7800) might be infected during the initial ZIKV outbreak in Puerto Rico. Of these, an IQR of 100 to 270 infants (median, 180) may be born with microcephaly due to congenital ZIKV infection from mid-2016 to mid-2017. In the absence of a ZIKV outbreak, an IQR of 9 to 16 cases (median, 12) of congenital microcephaly are expected in Puerto Rico per year.

This is modeling, not pure observation, but was based on observed risk. The paper is online full-text (I think) so you can follow through the assumptions if you want.

thank you for the information.  Unfortunately, the answer I'm looking for is slightly different.  I just want the rate of "birth defects" in the US in a way similarly defined by the CDC.  The rate of microcephaly alone is far to narrow when considering all "birth defects", and I would be hesitant to use Puerto Rico rates, because of obvious differences when compared to the continental US.

That answer seems to be in the first paragraph of the article you cited, so I'm not sure exactly what you are looking for. I updated my answer anyway

I'm primarily concerned with the method in which birth defects were collected. 'Clinical experts reviewed reported information to ensure that each fetus or infant with birth defects met the criteria of the USZPR case definition.' but this was done only with the Zika-positive groups and not with a Zika-negative group.  They compare it to a pre-Zika baseline, in which inclusion to the surveillance was different and determination/clinical review of each case was different.  Did they not perform similar tests during the surveillance period on Zika-nagative pregnancies?

With the moving goalposts and the changing demands, it seems like you have some weird axe to grind, and comments are not the place for it, so you're on your own.

your information is helpful.  Typically, attributable risk is done by tracking the exposed and unexposed population in the same way.  I'm interested if this has been done by the CDC or some other group.


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Are left-handed people more likely to be colorblind?
My friend, uncle, and I are left handed and also suffer from Protan colorblindness. Is it more likely for left-handed people to be colorblind?
Disclaimer: I was originally Right handed and due to a physical handicap I developed left-handedness.
EDIT: We also suffer from either ADD or ADHD.

I myself am left handed and also suffer from Protanomaly colourblindness. What gets me the most is that I’m also diagnosed with ADHD. Rarely do I ever come across someone who shares the same as I do.

In research literature, colorblindness and handedness appear to be correlated through male-ness.
Genetic causes of colorblindness are on the X chromosome, which explains why males are much more likely to suffer from colorblindness than females, as high as 16x more likely for red-green colorblindness.
Handedness is a complex polygenic trait governed by dozens of genes. A recent paper, Brandler et al., PLOS Genetics 2013, studying handedness implicated genes in chromosome 10.
However, males appear to be 25% more likely to be left-handed than females.
I wasn't able to find any studies directly addressing whether or not handedness is correlated with colorblindness, but it appears that if the only thing you tell me is that you are left-handed, then I can guess that you are more likely to be male than female, which means you are more likely to be colorblind than a person picked at random. So yes, a correlation appears to exist through maleness.
However, it's possible that being left-handed is conditionally independent of being colorblind given that you are male. In which case, for males, there may not be a correlation between left-handedness and colorblindness - there haven't been any studies addressing this question that I have seen.
To put this another way: if you tell me that you're male and left-handed, then insufficient scientific studies exist for me to guess whether or not you're more likely to be colorblind or not.

To answer you,  I am Male.

Are there any other aspects of your question you feel like weren't adequately addressed? Otherwise, it would be useful if you accepted this answer.


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How would circular dominance of alleles be determined on the genetic level?
The distinction between dominant and recessive alleles seems to be due to loss or gain of function in the proteins they code for. Alleles have been observed exhibiting incomplete and hierarchical dominance.
Another type is "circular dominance," which is modeled in some computer programs but it isn't clear whether this occurs in nature. In this case, the dominance of alleles works similarly to rock-paper-scissors.
Would circular dominance exist in nature? How would alleles determine circular dominance?

Thomas Lenormand did some work on the subject if I am not mistaken. If I am not mistaken empirical evidence of such type of dominance suggest specific sequence of the expressed protein that will directly bind to the other allele causing reduction of its expression. It is therefore easy to imagine such circular dominance.

@Remi.b: So the proteins interact like a literal game of rock-paper-scissors? Do I understand that right?

Yes, exactly. I did not post my comment as an answer because I don't know much and failed to provide a reference for my claim. So you should wait for a good referenced answer and not just take my word for granted.


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What does "local folding" means in secondary structure?
I'm new to biology field, so I'm learning all kinds of biochemistry knowledge for a bioinformatics project. I've found a few definitions of secondary structure online. For example, I found this brief definition here:

A structure of a biological molecule characterized by the local
  folding within the biopolymer as a result of hydrogen bonding (within
  the biopolymer).

What does "local folding" mean here? More specifically, what does "local" in this context refer to? Thanks in advanced.

Please provide a link to your quote. We need to be able to see it in context.

The most common examples of secondary structure in proteins are alpha helices and beta sheets, and the most important distinction between secondary and tertiary structure is that a single protein can have multiple "local structures", alpha helices and beta sheets, within its complete global structure. In contrast, a protein cannot have multiple "global structures" by definition.
In other words, a local structure can occur multiple times within a protein, while a global structure by definition can only occur once, and describes the complete shape of the protein.

Ok, so it means a local segment of the global structure? And because secondary structure do not specify the exact position of an atom, it is just a general template to represent what it is? And therefore, secondary structure do not specify the function of that segment?

Secondary structures don't have specified positions in a protein, they can occur almost anywhere depending on the protein. However, secondary structures often do have important functions. For example, alpha helices are useful for proteins binding to DNA and for proteins crossing cell membranes.

It's interesting to know that the secondary structure has such a generic function. Could you also briefly explain why the secondary structures can occur almost anywhere?

There are likely a few structural constraints for where secondary structures can occur, to allow for energetically stable folding and bending, but I'm not too familiar with them. Secondary structures are very common though - why? probably no better answer than simply evolution found them useful. It's fairly straightforward to construct secondary structures, you just need to ensure that your linear sequence of amino acids has certain bioechmical properties, like a lot of MALEK: https://en.wikipedia.org/wiki/Alpha_helix#Amino-acid_propensities

This is very helpful for me to understand what's going on because I've been reading some papers using these parameters to predict the secondary structure.

No problem! Glad to help.


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In genomic DNA extraction, is it possible that too much CTAB hinders subsequent DNA precipitation with isopropanol?
I'm trying a genomic DNA extraction protocol that uses 4% CTAB, 3M NaCl, 2.5% PVP-40, 20mM EDTA (pH 8), 100mM Tris-HCl (pH 8) and 3% beta-mercaptoethanol as lysis buffer. I incubate at 65oC for 60 - 80 min. Then, precipitate complexed cell debris with chloroform:isoamylalcohol (24:1). Collect the upper fase and precipitate DNA with isopropanol.
I tried this procedure in 51 samples of cotton leaves. In most samples I obtain a nice DNA precipitate after adding isopropanol. However, in 12 of them, I obtain 2-phases, with no DNA precipitate at all. The lower phase looks yellowish and sometimes a bit dark. Why would this happen? Any thoughts?
Thanks!

I'm sorry to hear you had this issue, but relieved that I'm not alone in the unexpected seemingly random results. Did you ever figure it out? I'd love to know!


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If you suspended your DNA like a rope in its 6ft full length, could you feel it if you waved your hand through it?
Maybe a silly question but I was wondering about this.  Trying to understand how small things are.
I have read that the DNA in a single cell if stretched out, would be about 6 feet long.
If you actually stretched it out and had something hold it - so that it was n a vertical line from about 6 ft to the floor, and then

would it cast a visible shadow?
if you waved your hand through it, would you be able to feel it?

Welcome to Biology.SE: I'm voting to close this question as off-topic because this is a question of physics and the strength of chemical bounds but not so much of biology.

@Remi.b I think we might be a bit overzealous in voting to close/migrate questions that could be appropriate here. I'd recommend we keep it open, I don't think it is any more relevant at physics or chemistry.se than it is here.

You should post this at http://physics.stackexchange.com Briefly, you should consider the fact that the width of the strand is an order of magnitude smaller than the wavelength of light, so even at very close range you won't get a shadow. Even much wider obstacles won't cast a shadow some distance away, and even if a small but much larger object than the DNA strand geometrically covers a light source, you may not get a shadow due to diffraction. If the angle subtended by the strand is smaller than the wavelength of light divided by the diameter, you'll see light diffracting around it.

The energy needed to break chemical bonds is of the order of a few eV, so, you won't feel any resistance as your hand moves through a DNA strand.

@BryanKrause Ok, I retracted my close vote.

I don't see why people are retracting close votes. This question has nothing whatever to do with biology. At the least it should be migrated to Chemistry or Physics or somewhere where it would receive the scorn it deserves. Trying to understand how small things are indeed! Yes it is a silly question.

I found this question interesting and I thought this question earlier. Agree, a search for such unique physical property may look silly apparently; but it gives a sense of scale. (Like "is it narrower than spider's web?"). And it would be really interesting to know the "appearance" of the molecular thread to us. As well the physics and chemistry community will need  biological informations about human tactile detection limits.

What on earth do you mean by "wave your hand through it"? Through what? the two strands of the double helix? I think you must be on the wrong site. Try SE Science Fiction and Fantasy: http://scifi.stackexchange.com.

Research on tactile detection has found humans can detect wrinkles in a surface on a nanoscale. One could argue that we may be able to feel a strand of DNA.
However, this research found only wrinkles of 10 nm were detectable. Therefore it is unlikely we would detect a DNA strand by simply touching it, considering DNA has a radius of one nanometer radius (10 ångströms).
We still may feel a pull of the strand depending on the tensile strength and bond strength but I'm not sure how those values relate to human perception.

I originally thought it might be likely that the covalent phosphodiester bonds holding together the DNA backbone may not be able to support the weight of the polymer chain. I did a few napkin calculations to investigate the issue. Here is my analysis:
The nucleotide at the bottom of the chain has a certain very small weight, and will probably not break the bond to the nucleotide above it. The two bottom nucleotides weigh twice as much as the single bottom one, but that also probably won't break the bond above them. If you keep going up with this logic, you might reach a point where some number of nucleotides has enough weight to break the covalent bond above them, and that chain of nucleotides would fall to the floor (making a very tiny puddle).
The bonds in the sugar-phosphate backbone are: $...O-P-O-C-C-C-O-P-O...$ (just a random bit of the chain, where the carbons are 5', 4', 3' of a deoxyribose sugar). The lowest bond energy, thus the most easily broken, is $P-O$ at 335 kJ/mol (Ref). I'm taking this as this how much energy is required to break the DNA sugar-phosphate backbone (in a single place).
An experimentally derived estimate of the linear density of double stranded DNA is $2.1\cdot10^{12} \frac{g/mol}{m}$. So every meter of DNA weighs about a trillion g/mol. Does this sound like a lot? It's because that is the meter-weight of one mole of DNA helices. The linear density of one molecule of DNA helix can be found by dividing by avagadro's number: one molecule of DNA has a mass of $3.5\cdot10^{-12} g$ per meter.
Let's take our vertical strip of DNA and imagine it is divided into two segments: an upper segment held by some vise, and a lower segment which dangles freely. The two segments are connected by a covalent bond of the sugar-phosphate backbone, specifically a $P-O$ bond. The lower segment has some mass $m$, and its weight $mg$ exerts a force against the bond ($F=mg$).
The bond requires energy $E=335 kJ/mol$ to break. This energy can be provided by the lower segment doing work to break the bond. Technically this work would be done by the force of gravity on the lower segment, which releases energy if the segment is moved closer the center of the earth. But the segment will only fall toward the earth of the energy released by that process overcomes the energy barrier $E$ of the bond holding the segments together.
Work is force times distance (roughly speaking), so what distance will the lower segment move in the process of breaking the bond? I think 1 angstrom (about a bond length) may be a reasonable approximation. That is, if we stretch the $P-O$ bond (which is already around 1.5 angstroms long) by 1 angstrom, it should be reasonable to say it is broken and the atoms will not re-attract each other (see Bond Dissociation graphs for details).
So! Our energy $E = 335 kJ/mol$ to break the bond will be supplied by work $W=Fd$, performed by the force of gravity $F=mg$, which acts for a relevant distance of $d=1$ angstroms $= 10^{-10} m$:
$$E=W=Fd=(mg)d$$
The mass of the lower segment is $m=\rho l$, where $\rho=2.1\cdot10^{12} g/mol/m$ is the linear density of the DNA segment and $l$ is the length of the segment. The question we should ask is "how long must the lower segment be for it to have enough weight to break the bond?" Well...
$$E=mgd=(\rho l)gd$$
$$l=\frac{E}{\rho gd} \\
= \frac{335\cdot10^3 J\cdot mol^{-1}}{(2.1\cdot10^{12} g\cdot mol^{-1} m^{-1})(9.8 m\cdot s^{-2})(10^{-10} m)} \cdot \frac{kg \cdot m^2 s^{-2}}{1 J} \cdot \frac{10^3 g}{1 kg} \\
= 1.6 \cdot 10^5 m$$
So, according to my admittedly crude approach, a segment of DNA would have to be on the order of 100,000 meters long to weigh enough to break the covalent bond holding it to the rest of the chain above it. I suppose this is a testament to the powerful strength of covalent bonds (or I've made some grave error somewhere in my physics). So my calculations suggest a 6-ft segment of DNA (magically extracted and assembled from trillions of humans cell) should have no problems holding together when you grip it in a tiny vise and hold it vertically.
I realize this was not exactly your question, but it was a practical consideration that I found myself investigating, and I figured I'd share my results.

I have a sincere question. Did you consider the resonance effect of the phosphodiester linkage when you told the P--O bond energy was 335kJ? There would definitely be some resonance by the negatively charged oxygen. I'm sure that this would increase the bond dissociation energy, but not sure by how much though.

I did not consider it, but I'm not certain it is relevant. Here is a diagram for reference: (http://s3.amazonaws.com/chegg.media.images/board/681/68166991-56d8-47ef-8ccb-7a36b44d9e97-original.png) On a given phosphate, the two oxygen atoms involved in the sugar-phosphate backbone are neutral, and participating in resonance would require them to become positive. The negative oxygen is much more likely (indeed, guaranteed) to participate in the resonance with the doubly-bonded oxygen, but neither of those last two oxygen sensor are involved in the bonding arrangement of the backbone.

Nice! I think the calculations are reasonable.  I did something similar for a polyphosphate chain and found that its P-O bond should support an even longer polymer, about 1000km. And DNA should have higher linear density than polyphosphates, so your numbers make sense. I guess this is the reason for all the hoopla about nanomaterials --- pure molecules have incredible tensile strengths. (Yes, it's not really biology but it is kinda fun :)


text:
How is energy acquired from ATP?
How is energy acquired from ATP (i.e. What is the energy-releasing equation involving ATP plus water)?
I Would be grateful for the answer.

The basic reaction is ATP + H2O --> ADP + Pi + energy
It is the common hydrolysis of ATP, in which the nucleophilic oxygen of water attacks the electrophilic central phosphorus of the last phosphate group, resulting on its separation from the rest of the molecule (which becomes ADP).

In this image: LINK you can see more clearly the steps of the reaction. Keep in mind that the arrow 3 should be pointing to the P and not the O.
To know more about the energy and thermodynamics check this page: http://www.life.illinois.edu/crofts/bioph354/atp_hydrolysis.html
The trick here is the cells being able to utilize that freed energy to their benefit, instead of letting it disperse. This can be done, for example, by adding a phosphate group to a protein, altering its shape and consequentially its function, or by the nucleophilic attack of the first or second phosphate in the ATP molecule of a susceptible electrophilic centre, starting a reaction that could otherwise be energetically unfavourable. If the hydrolysis happens spontaneously in water without coupling it with another reaction, the freed energy will be "wasted" as heat.

very clear and easy to understand now. thank you very much indeed.

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


text:
Are there functional examples of parallel DNA double helices?
The anti-parallel structure of the DNA double helix is well studied, but I am curious if there are any examples of parallel DNA double helices. There are reports of synthetic such structures; see this paper, for example. However, my question is: are there functional examples of parallel DNA double helices? Here are some implicit/additional/guiding criteria:

It should be double stranded. This excludes structures such as G-quadraplexes, which do have some parallel strands.
It does not have to be an extended helix. I don't have any specific length restrictions, but don't assume it needs to be hundreds or even tens of base pairs long.
The structure need not be solely composed of DNA. If a parallel helix is induced by, say, protein or small molecule binding, so be it.
By "functional examples", I mean that the parallel structure should have some effect on cellular processes. The structure can be studied in vitro, even using synthetic constructs, but it should have some functional significance in vivo (or, at least a proposed significance).

Note that although I only mention DNA above, papers discussing parallel RNA double helices in the same spirit would also be welcome.
Related question: why is DNA antiparallel? Can it be parallel?

I hope this question is interesting to others. Please let me know (or edit) if it can be improved.

At first sight I thought the question was crazy, but having checked the NAR paper in the answer you quote (it might be worth providing a direct link) I changed my mind. I suspect you may have to end up answering your own question though. Have you checked for more recent papers that cite the NAR paper? That might be fruitful.

@David Ha! I made the suggested edit. I only skimmed through the NAR paper. I also came across another which showed an intercalating drug promoting a parallel helix. I will post an answer when I have some time to read through the literature.

Surprisingly, a parallel DNA duplex has been reported! In a paper, Tchurikov et al have reported the presence of parallel complementary DNA in the non-coding region of alcohol dehydrogenase gene as well as between two Drosophila DNA sequences. The region, which is ~40 bp long, has 76% bases in same polarity along with complementarity. However, its presence in vivo and its significance are not known (they observed its existwnce in vitro).
Tchurikov et al, in another paper, have reported that parallel complementary RNA in E. coli plays some role in RNA interference and is indeed more effective than antisense RNA in silencing mRNA for gene expression regulation. They also propose the presence of such a system in vivo in E. coli cells. (Seemingly, this paper alone is enough to answer your question since it fulfills all your criteria).
In another paper, Szabat et al have shown that DNA, 2'-O-MeRNA and RNA oligonucleotides can adopt parallel duplex configuration at pH 5 and lower. Also, presence of LNA stabilizes parallel duplex configuration. This might seem helpful in processes such as RNA interference, though this study too was in vitro (obviously, in vivo LNA is not known).
Many such papers, like Westhof et al, Mohammadi et al, etc. have reported the presence of parallel duplex DNA.
References:
 1. Tchurikov NA, Chernov BK, Golova YB, Nechipurenko YD. Parallel DNA: generation of a duplex between two Drosophila sequences in vitro. FEBS letters. 1989;257(2):415–8. pmid:2479581
 2. Tchurikov, N. A., L. G. Chistyakova, G. B. Zavilgelsky, I. V. Manukhov, B. K. Chernov, and Y. B. Golova. 2000. Gene-specific silencing by expression of parallel complementary RNA in Escherichia coli. J. Biol. Chem. 275:26523–26529
 3. Szabat M, Pedzinski T, Czapik T, Kierzek E, Kierzek R (2015) Structural Aspects of the Antiparallel and Parallel Duplexes Formed by DNA, 2’-O-Methyl RNA and RNA Oligonucleotides. PLoS ONE 10(11): e0143354. doi:10.1371/journal.pone.0143354
 4. Westhof, E., and M. Sundaralingam. 1980. X-ray structure of a cytidylyl-3′,5′-adenosine-proflavine complex: a self-paired parallel-chain double helical dimer with an intercalated acridine dye. Proc. Natl. Acad. Sci. USA. 77:1852–1856.
 5. Mohammadi, S., R. Klement, A. K. Shchyolkina, J. Liquier, T. M. Jovin, and E. Taillandier. 1998. FTIR and UV spectroscopy of parallel-stranded DNAs with mixed A-T/G-C sequences and their A-T/I-C analogues. Biochemistry. 37:16529–16537.

Nice finds! I look forward to reading the papers.

All articles I found discussing parallel helices are purely speculative with regards to biological significance; but, they are still interesting. Here are some that I found, in addition to the other answer.

Safaee N, Noronha AM, Rodionov D, Kozlov G, Wilds CJ, Sheldrick GM, Gehring K. 2013. Structure of the Parallel Duplex of Poly(A) RNA: Evaluation of a 50 Year-Old Prediction. Angew Chem Into Ed 52:10370-10373.
This paper presents the solved crystal structure of parallel poly(A) RNA and shows that Poly(A) Binding Protein (PABP) promotes parallel duplex formation. A biological role is hypothesized:

As the great majority of eukaryotic messenger RNAs (mRNA) are tagged with 100 to 250 adenines at their 3′ end, the polymorphism of poly(rA) is also relevant for present day cellular processes involving mRNA translation, storage, and decay. Under conditions of cell stress, cellular mRNAs are transported into RNA granules, increasing the local concentration of poly(rA). It is possible that nature evolved proteins such as PABP in part to regulate the occurrence of poly(rA) duplexes in cells.

There are several reviews that discuss the possible role of parallel RNA in the RNA world which revolve around the problem of replication using complementary, anti-parallel strands:
Taylor WR. 2005. Stirring the primordial soup. Nature 434:705.

Some mechanisms for replication in the RNA world have been put forward, and following the current systems of protein polynucleotide synthesis, all involve the creation of a complementary daughter strand using Watson–Crick base-pairing. But from a mechanistic viewpoint, such a model contains a fundamental problem: if a ribopolymerase were to make a complementary copy of itself, it would need to recopy this to obtain a new functional ribopolymerase. This implies that both the ribopolymerase sequence and its complement would have to coexist. But if these two copies came together, the result would be a double stranded Watson–Crick helix (as found in some RNA viruses) — not a new ribopolymerase. Even if both sequences had well determined secondary structures, the perfect complementarity of the Watson–Crick pairing would act as a sink, leading to a sterile population of double-stranded molecules.

The proposed solution is that early RNA polymerases may have created parallel complements to prevent such inhibition:
Taylor WR. 2006. Transcription and translation in an RNA world. Phil Trans R Soc B 361:1751-1760.

Replication strategies. (a) Replication via a reverse complementary strand leads to (b) a stable double-stranded duplex if the two copies meet. (c) Replication via a parallel complementary strand leads to (d) a relatively unstable double-stranded duplex if the two copies meet.

The propagation of information in a nucleic acid strand from one ‘generation’ to the next using Watson–Crick base pairing logically does not have to involve a reverse complementary strand. Providing that there is complementary base pairing, a parallel complement would also propagate the same information...
...all that need change from the viewpoint of replicase is the direction of its progression along the template. The resulting transcript could only be expected to base pair with the template over a short region before parting, but, faced with the problem of irreversible hybridization, this would be a desirable feature of the model.

This paper mentions some proposed functions of parallel stranded (ps) DNA, with accompanying references, but I can only access one of them:

Other functions have been proposed for ps-DNA in gene expression, recombination, RNA processing (14,18,20), the packing of single-stranded and dimeric viral genomes and the function of reverse gyrase (12).

This is the one reference that I could find from the above paper:
Ramsing NB, Jovin TM. Parallel stranded duplex DNA. Nucleic Acids Res 16:6659-6676.

The possibility that ps-RNA might exist is intriguing in view of the rich
  structural and functional repertoire of RNA species in general. Three canonical situations in which ps helices could arise by interactions of wholly or partially homologous strands or looping of single stranded nucleic acid of appropriate sequence are shown in Fig. 12. The topological implications of such structures are of great interest, particularly in relation to the potential roles of ps-DNA and ps-RNA in (nonhomologous) recombination, RNA splicing, stabilization of ribosomal RNA, and other cellular processes. In addition, it can be anticipated that specific ligands, particularly proteins, could intervene in order to stabilize and exploit the parallel stranded conformation.


text:
Why do palpitations happen when someone is nearing something rewarding?
When you are nearing something rewarding (IE: winning a prize, or winning a game), why do you experience tachycardia?
For example, if someone entered a raffle with the number 9284938, and the announcer was starting to announce 9..2..8..4, the closer the announcer gets when palpations would start to occur.
My guess this is something to do with dopamine since dopamine is a rewarding hormone and it gets metabolized directly into epinephrine, but I don't think I'm right.

Palpitations (irregular, extra heart beats) are different from tachycardia (an increased heart rate often accompanying excitement/fear, etc. It's cause is norepinephrine (also known as adrenaline in some countries.) There may also be dopamine in there somewhere, but the major effect is the rush you get from adrenal release of nor-epi.

@anongoodnurse Thanks! I edited the question.


text:
Sodium potassium balance in a cell
In a resting cell at steady state, is sodium influx or potassium efflux higher according to the concentration gradients and permeability, and given that the sodium potassium ATPase is active?

If potassium ions were alone inside and outside of the cell, they would be tended to diffuse along out of the cell due to high gradient inside. Because of potassium ions have positive charge, potassium lose would cause negativity inside. Within a few seconds, potential loss would rise enough to be able to stop potassium exit out of the cell. Because against decreasing concentration gradient, there would be reverse direction electrical gradient increase so these forces have to be balanced somewhere. For a large mammal nerve cell , needed potential gradient is about-94 millivolts.
We can assume similar concepts for sodium ions also. This time direction will be outer to inner side of cell. And this makes a positive potential (about +61 millivolts) due to gaining positive ions .
When we calculate total diffusion potential for only one ion, Nernst equation is used. For ions more than one we have to use Goldman equation, which is more complicated , instead.
Goldman equation consists of three factors:

Electrical charge for each ions.
Permeability for each ions.
Concentrations inside and outside of the cell for each ions.

Major factor on this resting potential is membrane permeability. For potassium ions, membrane permeability is about 100 times more than sodium ions. Because potassium leakage channels makes potassium leakage more easier than sodium. When we put this factor on Golman equation, we find resting potential about-86 millivoltes which is closer to potassium diffusion potential.
(source:Wikipedia)
(source:KhanAcademy)


text:
How to calculate the Position Weight Matrix score?
Can anyone explain me how to calculate the Position Weight Matrix score?
I know the formula, but I don't understand it. I have a table with the frequences of nucleotides, and a table with the PWM scores:
Frequences of nucleotides:
Position:            1       2        3        4        5

A                    0       0.9      0.1      0.6      0.2
C                    0       0        0.2      0.1      0.2
G                    0       0        0.1      0        0.1
T                    1       0.1      0.6      0.3      0.5

And I have the corresponding PWM scores:
Position:            1       2        3        4         5

A                            1.848   -1.322    1.263    -0.322
C                                    -0.322   -1.322    -0.322
G                                    -1.322             -1.322
T                    1      -1.322    1.263    0.263     1

But, I have no idea how this scores are calculated.
The formula is:

But I don't understand this.
Can anyone explain me step by step how I can calculate this scores?
I especially don't understand how to calculate p(b,i).
Thanks! :)

p(b,i) comes from the frequency of the nucleotide b at position i divided by the number of sequences you have taken for considering the score. This wiki page explains all need to know.


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Why is a mosquito feeding on human blood not a parasite?
I recently read in my Ecology course notes that a mosquito feeding on human blood is not considered as a parasite. However, since it sucks blood from the human body, shouldn't it be regarded as a parasite, just like lice and ticks?

What research have you done before asking it here?

@another'Homosapien' While its understandable that OP should do some research before posting a question, I still feel we should encourage new and interesting questions as our Biology SE needs much more questions (given how vast Life Sciences are!)

@talhairfan I have no problem with the question as well as your point. But we must also not forget the website policy. The same question, with some prior research, would be a nice hit...

How is the mosquito feeding on blood different from the lion that kills its prey?

not killing prey/reducing its fitness to zero (see my comment on the accepted answer)

female mosquito , indeed is considered as a parasite and it comes under the category of temporary parasite.

Its not considered a parasite

@JM97: reference please?

@BenBolker http://learning.uonbi.ac.ke/courses/SZL310/scormPackages/path_2/lecture_5__categories_of_parasites_and_hosts.html

OK, thanks. FWIW "Temporary parasites are often referred to as micropredators" (which links with Lafferty and Kuris).  Obviously there is a variety of terminology circulating, depending on sub-field ...

A mosquito is a biological parasite, it is not a medical parasite.
There are two definitions of parasite. A biological/ecological definition and a medical/physiological interaction definition.

A parasite in biological terms is an organism that benefits from a parasitic relationship; a parasitic relationship being a non-mutual relationship between species, in which one species benefits at the expense of the other. Generally the host is not killed by a small number of parasites. When the host is killed the organism is usually called predator or parasitoid.
A parasite in medical terms is an organism that lives on or in a host and gets food from or at the expense of its host.

The difference is small but important; only the medical definition requires the parasite to live in or on the host for prolonged periods. It is a much narrower definition.
Biologically, a female mosquito is an indirect ectoparasite, it can be facultative or obligate depending on the species. It harms its host to benefit itself, that is all that is needed to be a parasite by the biological/ecological definition. And just like a leech or vampire bat it is hemophagic and leaves the host as soon as it is done feeding. Brood parasites are another great example of a biological parasite that does not live on or in the host. So a cuckoo would be a biological parasite but not a medical parasite. When you consider the function and practice of medical science the more narrow definition makes sense, they are not concerned with parasites that are not going to stick around or not affect the host organism's physiology directly. By the narrower medical definition, none of these organisms are parasites even though by the biological/ecological definition they are.
Consider the wiki or a paper on parasite evolution vs say the CDC to see the difference.

I've read in several books which considered mosquito as parasite. (but don't know why... because mosquito does not live on/in human body). If I find the sources or some similar sources, I'll mention.

So, to clarify, you are saying that a mosquito is a parasite and consequently that the OPs "Ecology course notes" are incorrect? @AlwaysConfused John's answer would appear to state that a mosquito is a parasite "in biological terms".

Correct, which is not surprising the quality of textbooks vary widely, especially with things that have two or more discipline based definitions like this. Plus one thing you learn about biology as you advance is that there is a lot of gray area since living things dont care about our attempts to categorize them or the imprecise language we have to use to do so. JayCkat points one our very nicely, what constitutes "harm".

@AlwaysConfused Biological definitions of behavior are more like blurry venn diagrams than exclusive boxes.

Short answer
Female* mosquitoes are generally not to be considered ectoparasites because they spend so little time with the host. Instead, they are sometimes classified as micro-predators.
*Male mozzies don't practice hematophagy at all
Background
According to some sources, the term parasite hinges on the time the parasite spends on, or in its host and hence it is a gray area whether a mosquito is considered a parasite or not.
The CDC, a renowned center on disease control & prevention, states the following:

Although the term ectoparasites can broadly include blood-sucking arthropods such as [female] mosquitoes (because they are dependent on a blood meal from a human host for their survival), this term is generally used more narrowly to refer to organisms such as ticks, fleas, lice, and mites that attach or burrow into the skin and remain there for relatively long periods of time (e.g., weeks to months).

In contrast, female mosquitoes need only about 4 minutes to finish their drink.
Wikipedia, being explicitly not my favorite source of information, says on their Mosquito page:

Females of most species are ectoparasites...

But then, when clicking through to the Ectoparasite Wiki page no mention of mozzies are made and the more accepted parasitic arthropods are discussed, namely the ones stated above by the CDC (lice, ticks and fleas).
However, as mentioned in the comments below, with credits to Fileunderwater, other sources like this veterinary work on Ectoparasites also discusses mosquitoes.
Hence it seems to be a gray area whether mozzies are classified as (ecto)parasites. Personally, I would stick to the careful definitions provided by credible sources like the CDC - mozzies are not considered ectoparasites, because they spend just a few minutes siphoning blood before they are off again.
But then, as rightfully probed in the comments, what are they then if not parasites?
One classification I've found for insects practicing hematophagy for short periods at a time is

Micro-predator: a temporary parasite (source: English Encyclopedia);

or

Micro-predator: e.g., the mosquito, that derives elements essential for its existence
  from other species of organisms, larger than itself, without causing
  their destruction (source: Medical Dictionary).

Then what is the relationship between mosquito and the animals it sucks blokd from called? There's gotta be a name for something with that much significance (eg. spreading of diseases).

@hyde,very good question and I looked for it too, but to no avail. Above the term 'grazer" is brought up. I couldn't verify it's use, but it sounds quite apt :-)

in this context (disease transmission) a mosquito is called a vector and the animal sucked from is called a host

@BenBolker afaik, a mozzie is only a vector when talking about the transmission of diseases carried by them such as the malaria parasite. Outside of disease transmission they are not a vector

I agree, it depends which aspect of the relationship you're talking about. In the ecological/evolutionary context "grazer" is indeed the most common term, e.g. see http://bit.ly/2oPhlRa . Lafferty and Kuris use "micropredator", but in my experience that's less common.

I is quite easy to find other examples from "credible sources" where mosquitos are called ectoparasites, outside of Wikipedia; see e.g. "Veterinary Ectoparasites: Biology, Pathology and Control"

@fileunderwater - thanks for that. I might have to rephrase my answer and stress the grayness of the matter. Thanks.

For the record, I find the CDC criteria for determining parasitism (time period used) quite silly, as a way to define ecological interactions.

@fileunderwater - you may be right and thanks for your comments here. I mentioned your source in my answer now. It is definitely a gray area. However, when I think of ectoparasites I think more of lice, fleas and ticks but that may indeed be a personal bias. I think John's answer matches your view better.

The CDC don't seem very consistent to me re: being used as a reliable source for definitions; they still define bedbugs as parasites on their own webpage, even though their own definition shouldn't agree with this. To me, mosquitoes and bedbugs are obvious parallels - they both rely on bloodmeals, but only stay in proximity to their hosts for occational access and do not live on the host(s).

Mozzie means mosquito? how funny slang :P

@AlwaysConfused - It's Ozzie slang for mosquito, yes :)

Micro -predator and parasitoid are both areas where parasite and predator overlap.

To be a parasite, an organism needs to fulfill two criteria
1) It needs to have a non-mutual relationship between itself and its host.
The organism derives benefit and the host suffers harm.
2)The organism also needs to live in or on their host for an extended period.
Often, a parasite will also have biological specialization to mediate the relationship between itself and its host.
However in reality, there is a spectrum of relationship. So a parasitism is not always very clear cut. How much "harm" is needed to be harmful enough? How long does a relationship need to be?
In your example the first criterion is fulfilled, but the second is not. The mosquito benefits from the blood meal and the host mammal does not. However, only female mosquitoes feed on blood and only when they are about to lay eggs. A mosquito does not spend most of its life in or around its host.
So by definition a mosquito is not a parasite.
https://en.wikipedia.org/wiki/Parasitism

Your own source does not agree with your definition.

another ref: https://parasiteecology.wordpress.com/2014/02/05/predator-vs-parasite-vs-parasitoid/ Lafferty and Kuris would call mosquitos "micropredators", another commonly used term is "grazer"

The reference to the wiki page is indeed off as it explicitly counter argues your answer..

I also disagree with this answer -1

Additionally, not benefiting from something does not imply harming per se.

Where does Wikipedia disagree? "Unlike predators, parasites typically do not kill their host, are generally much smaller than their host, and will often live in or on their host for an extended period."

@BenBolker “will often” is very distinct from “always do by definition”

Don't know is it a "wrong" answer. Actually in our school-level biology we've been taught strictly as the condition to count as parasite is to simultaneously 1. dependence for food and 2. dependence for habitat . At college level I've seen some sources quite unclearly wrote mosquito as a parasite.

A flea would be an ectoparacite because both male and female fleas feed and spends their entire life cycle on its host. As for a mosquito.. only the female has blood meals and only when they are laying eggs. It is a very specific part of its life cycle, and only one sex. A vampire bat in contrast... both genders feeds on bloods and it does so as a normal part of its diet.

@BenBolker Looks like I was beaten to it but I would agree Lafferty and Kuris is the key source here - why don't you write their explanation up as an answer? I would myself but apparently my laptop battery is about to die :(


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What is GST RhoA fusion protein?
Would you please explain to me what GST RhoA fusion protein means and how it differs from RhoA protein? I am a kind of doing an experiment using this protein.

GST is glutathione-S-transferase, an enzyme that binds reasonably tightly to glutathione. It is often used as a tag to purify proteins of interest. In your case, GST has been fused to RhoA most likely so that you have some means to purify it by applying it to a glutathione conjugated column. See here for more information.


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Does the speed of muscle contraction within a single sarcomere differ between people?
Of course the number of muscle cells can be different person to person. But within a single sarcomere, are we all the same?
Would the frequency of the protein motor binding and release cycle different for each person? And if that is a constant, then do we all attain the same speed of muscle contraction?
If not, what causes the different speed?

In consideration of the fact that protein structure is encoded by your DNA, I would assume that it could be possible to have different muscle-contraction speeds that are dictated by the exact amino acid composition of a sarcomere. I don't know if the effects would be measurable or not. But I suppose it could be possible to have sarcomeres that are able to make stronger bonds than the sarcomeres of other people, thus having an increased reaction rate. And, as you said, release cycles might not be the same for each person which could also contribute.

@user1589188 if you talk about potential then initially yes, but considering the fact that muscle contraction is regulated chemically by the nervous system they would be different in different people even of the same age. Unless the portion of the  muscle fibre under consideration is damaged then they would show same frequency for requiring Ca+2 and ATP level. (Mutation in the DNA most likely lead to failure of proper binding)

Muscle contraction speed is also situation dependent-- varies with force and length even within an individual, even just by virtue of the sliding filament model... I'm not sure that the initial assumption that an individual sarcomere has a fixed speed is correct.


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Majority rule definition
In this book, they talk about the majority rule.

Majority rule, which retain s the edges present in more than 50% of the trees.

They used that rule also in this article (Grant, P. R., and B. R. Grant. 2010. Conspecific versus heterospecific gene exchange between populations of Darwin's finches. Philosophical transactions of the Royal Society of London. Series B, Biological sciences 365:1065–1076.)

We applied the majority rule (p . 0.500) to assign individuals to
  groups.

This was when using the software STRUCTURE.
I haven't found a convincing definition of the "majority rule" except definition in politics.
So what is the "majority rule" and how is it applied?

Majority rule is a binary decision rule that attributes an individual a category or rank based on the majority. I think you would get a fairly comprehensive answer if you asked this on stats.stackexchange.com

There's also an interesting example of judges voting for skaters here, but again it doesn't provide a clear definition (pg 288)


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I read that the average cell will divide between 50-70 times before cell death. How, then, can human cells be constantly dividing?
Aren't those 2 statements contradicting each other?
See https://en.wikipedia.org/wiki/Hayflick_limit and e.g. http://book.bionumbers.org/how-quickly-do-different-cells-in-the-body-replace-themselves/.
Take stomach cells. If they divide every 2-9 days, doesn't that mean the stomach cells will all die in about a year (5 days x 70 division)?

What brings you to the idea that human cells are constantly dividing? And why should this contradict the Hayflick limit?

Clarified question.

Has something to do with progenitors I think? I don't exactly know how stomach cells divide, but I would imagine that there is a lining of undifferentiated cells that consistently differentiate towards the inner lining of the stomach. It's differentiated cells that are constricted to the hayflick limit.

I think your problem might be with a misunderstanding of the meaning of "average".  That doesn't mean that every cell type divides that many times, e.g. neurons seldom if ever divide.

The answer may simply be yes, as the parent cells are dead, but no since the daughter cells are still alive and kicking.

You have to consider telomere length, rate of proliferation and the presence of stem cells.

@Bob that makes sense. Can you write the answer? This brings another question: why is hayflick limit associated with ageing if it doesn't apply to stem/progenitor cells and thus body repair?

@jamesqf I'm not convinced. Average means average - in case of stomach cells, if I randomly pick one stomach cell, on average it will divide in 2-9 days. Some cells (neurons like you mentioned) might be different but most cells do.

@AliceD Are you saying that if I have a cell that can divide 50 times, after 1 division the daughter cell can still divide 50 times, but the parent can only divide 49 times now? That doesn't make sense.

YuZhou, I do not think that I know enough about the subject to formulate a proper answer. But, I think doing some research on what I have commented, and on what @CMosychuk has commented, you will be able to find a reasonable answer to both your first question, and your new question. Maybe afterwards you could share your findings in the form of an answer for anyone else who ever asks a similar question?


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Does the term "Biophysics" have two different meanings?
1.
Some sources (including  the current Tag-info at biology SE)  state; biophysics is the adoption of techniques / methodologies from physics to study biological systems.

The use of methods from the physical sciences to aid in the study of biological systems…

Bio-SE- Tag biophysics.

Biophysics or biological physics is an interdisciplinary science that applies the approaches and methods of physics to study biological systems…

Wikipedia (permalink).

Biophysics — the branch of biology that applies the methods of physics to the study of biological structures and processes…

Dictionary.com

2.
According to other sources, biophysics is the subject concerned with how the laws or phenomena of physics work in living systems.

“The subject of biophysics are the physical principles underlying all process of living systems.”

Google Book: Biophysics, An introduction, By Ronald Glaser (permalink).

Biophysics is a bridge between biology and physics. ... Biophysics looks for principles that describe patterns. If the principles are powerful, they make detailed predictions that can be tested. ---

Biophysical society

These two, although apparently quite similar (and I agree, have overlapping areas) basically indicate completely different things.
The first group of definitions refer to techniques and methodologies; such as “how does an electron microscope work?”, or “what could be the best strategy to separate membrane-lipids?”, or “how could you identify cells with the expression of certain RNA”; etc.
The second group refers to the physical principles applicable to living systems. Such as “why do phospholipids form a bilayer?” or “how do brain waves reach the scalp?” or “how does a humming bird move its wings when it hovers in a stationary manner?” or “what are the mechanisms working in the path of transport through phloem?”.
Now my question is: Is there a dual and different meaning, or use of the term ‘biophysics’?

You may be thinking of "techniques and methodologies" too narrowly. It doesn't mean just the experimental techniques and methods but the mathematical techniques and theoretical frameworks as well. For example applying the theoretical framework of statistical mechanics to understanding molecular models. When you expand your notion of "technique and methodologies" to include those as well, the two definitions seem more in-synch.

In brief, you are correct. Although there may be a spectrum of uses, the sources that you quote illustrate two distinct meanings for the term, ‘biophysics’. Your interpretation of the first class is a little off-target (see comment by Charles E. Grant) but, in essence, you have answered your own question.
What is there to add? Perhaps, “Don’t judge a book by its cover”.
You may not be aware of the factors leading to the naming of new ‘disciplines’. Although they arise as the result of genuine developments in existing disciplines, the need for a name to be distinctive and attractive (for a new chair, society, journal or course) may outweigh considerations of accuracy. And once the name is coined, anyone can confer it on their own newborn, or discover that they were a systems biologist or a practitioner of translational medicine all along. And nobody will sue you for saying you are a molecular geneticist, even if you have no idea what a backcross is.
So what about biophysics?
In fact it would seem that the main usage is in the first sense defined in your question. Although the physicist, Max Delbrück, made a major contribution to ‘biology’ his initial motivation — that processes in living organisms might require new physical insights to explain them (biophysics in the second sense of the question) — was not borne out by his subsequent studies. It is ironic in this context that the institute he established at the University of Cologne did not bear the name ‘biophysics’, but ‘molecular genetics’, and the institute named after him in Berlin bears the name ‘molecular medicine’ (Max-Delbrück-Centrum für Molekulare Medizin) — whatever that may mean.
It is worth looking inside the covers of the Biophysical Journal to see what biophysics is in practice. The contents of the first and subsequent issues indicate a focus on electrophysiology, photosynthesis and the use of different types of electromagnetic radiation and spectroscopic techniques to study biological systems. A more recent issue is much wider in scope, but is subdivided mainly on the basis of the biological system being examined. As mentioned, the fit is more with the first sense of the use of ‘biophysics’ in the question.
Finally, I note that one of the first university departments to bear the moniker ‘biophysics’ — ‘The Astbury Department of Biophysics’ at the University of Leeds (1962) — was named after William Thomas Astbury, who studied X-ray diffraction of fibres, notably wool. However, it has since been renamed ‘The Astbury Centre for Structural Molecular Biology’. How fickle is taste!

Short answer
Biophysics encompasses the study of biological systems in physical terms and the methods involved to achieve that goal.
Background
I'll approach this question first from the area of research I'm actively involved in at the time of this writing -
Psychophysics is

[...] the scientific study of the relationship between stimuli
  (specified in physical terms) and the sensations and perceptions
  evoked by these stimuli. The term psychophysics is used to denote both
  the substantive study of stimulus-response relationships and the
  methodologies used for this study.

source: (RIT)
In short this would translate as

The study of the sensation and perception of physical stimuli and the methods involved to accomplish this.

To illustrate I will cite the titles of two well-read articles in this area highlighting the dual use (study & methods):

Issues in psychophysical measurement
Spatial hearing: the psychophysics of human sound localization

And to illustrate a compelling example that merges both uses in one:

Psychophysics: Method and theory

Now to  your question; I've done electrophysiology which might, arguably, be considered biophysics, but I'm less comfortable in the arena of biophysics. But given my reasoning above, you can safely replace Psycho with Bio and say that Biophysics is

The study of biological systems in physical terms and the methods involved to accomplish this.

For example, the University of Wisconsin describes it as:

[B]iophysics combines state-of-the-art physical measurements with computational models to understand the detailed physical mechanisms underlying the behavior of complex biological systems.


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Does posture matter while drinking water?
I have heard a lot of people (where I am from, India) say that one must drink water sitting, not standing. Recently, I also came across a video that said the same thing (link). The reason given is that when you drink water standing, it goes to the colon too quickly, whereas while sitting, the water is better absorbed by the organs. Is this true? Is there a biological basis for why I should drink water sitting?
I tried to find literature on this matter, but apparently there isn't a whole lot. I found this paper where they tried to see the water passage rate in the GI tract of rabbits, mentioning how the water goes from stomach to cecum to proximal large colon, but obviously did not study posture.
Note: I think this question belongs here better than Skeptics.SE as I am looking for a biological explanation

Nothing you drink goes straight to the colon; the small intestine - between the stomach and the colon - is 20 feet of twisted tubing. So this is a colorful myth. If you do a bit of helpful research and add it (no videos please; I don't want to spend that amount of time), I'll be happy to answer what happens to fluids when drunk in any position, even upside down.

@user1993 it would be cardiac sphincter of oesophagus which is affected by drinking water while standing not colon. As it in not a true Valve the force of impact of water which goes straight down the oesophagus while drinking water fast and standing would damage it's activity upto some extent so that regurgitation may happen.

I'd imagine that literally billions of people have drunk water (or other beverages) while standing, but I've yet to hear of any adverse health effects from the practice.  While I'm no anatomist, I'd think anything you drink or eat, sitting, standing, or laying down, would spend some significant time in the stomach before entering even the small intestine.  Indeed, practical experience suggests that the greater part of any liquid consumed gets absorbed into the bloodstream before reaching the colon, and eventually excreted via kidney & bladder.

@user30561 - That's pretty much a less colorful myth.

@anongoodnurse, i tried to research a bit, you can have a look

Related question:http://skeptics.stackexchange.com/questions/27338/is-drinking-while-standing-unhealthy

@Mesentery, great find! but sadly the study mentioned there did not compare sitting and standing :(

The stomach is equipped with the pyloric valve to regulate transpyloric flow to the duodenum.
Both cold and warm drinks stimulate a pattern of motility associated with retardation of transpyloric flow.

The pyloric valve is responsible for acidifying water that you drink, and if the body's guard against amoeba's and dysentery depended on body position, it would be low survival performance, given that sedentary posture is associated with poorer health outcomes, including an increased risk of type 2 diabetes. You will benefit from minimizing time spent sitting each day, and from breaking up periods of time spent being sedentary, as often as possible. It's aperture at rest is 3mm, so it's of minimal difficulty for the stomach to hold water as required for optimal health. It's highly likely that water is kept for enough time to expose it to stomach acids, regardless of body position, and then it's transmitted.
Water doesn't flow straight through the stomach like a straight tube when it's empty.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1382811/pdf/gut00528-0043.pdf

First off: pure, reverse osmosis treated, bottled water HAS NO NUTRIENTS. Secondly, of everything you swallow, nothing goes too fast on it's way to the colon. The small intestine is a network of twisted tubing, around 20 feet long. Nothing is going through there "Too fast".
Sources: https://carta.anthropogeny.org/moca/topics/smalllarge-intestine-length-ratio

could you comment on the difference when a person is sitting vs standing while drinking water?

There is no observable difference. It does not matter whether the drinker is standing or sitting, the small intestine is the same length, and is still folded accordingly.

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


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Why do we have bacteria in our alimentary canal?
Our alimentary canal contains lots of bacteria. Most of these are found in the small intestine and large intestine.
Can you a give a few reasons why is it a good thing to have bacteria in our digestive system.
Thank you.

Is this a homework question? If yes - homework questions are warmly welcomed, barred OP shows prior efforts to answer them. Have a look at our homework policy in the help center. If not, we generally still expect users to give a question at least a shot on their own. For example, What are your thoughts on the subject? Which reasons can you think of?


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ID Fish from Florida?

This fish was caught in St. Augustine, Florida. What species is it?

Looks like a Goosefish (aka. monkfish) to me.

Could be a species of flathead

Does it have spines?

Did you catch it in fresh water? saltwater? brackish water? And at what depth did you catch it?

Was the fish caught at the location of the photo? Approximately how deep was the water?

Looks most likely to be a Gulf Toadfish, Opsanus beta, judging from its size, location caught, and other similar identifying features.

More detailed species information at:
Opsanus beta on FishBase.org

I live in Florida and I've neither caught nor seen one of these. I was kind of taken aback!

It can depend on the environment, with this species common in bays. You would not likely catch it far off from shore.

I am not familiar with fish from Florida. However, that one belongs to the family Lophiidae. Most probably it is Lophiodes reticulatus.
Need better resolution photos for identification.
http://www.fishbase.org/summary/3082

It seems to me to only appear like a member of Lophiidae. There are other families that are similar in appearance because they are also benthic dwellers. According to FishBase, L. reticulatus is found at depths of 64-820 meters. From the photo provided you can see what appears to be an embankment along the shore. If the fish was caught at the same location, it is unlikely that the environment was of the correct depth for the fish to be L. reticulatus. There are physical features that do not match, for instance, the pectoral fins in the photo are not barbed like L. reticulatus.


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Roughly at least, how many types of cells comprise human blood?
A long time ago there were only three kinds - red, white, and rose platelets. Advances in cell sorters and more recently in genetic techniques and differentiation studies have led to the identification of a wide variety and complex lineage of cells that comprise human blood.
Roughly at least, how many types of cells are currently identified?
I understand that "types" is a non-technical term, and I'll try to better define what I mean. For example, I do not mean to enumerate each antigen specificity separately because that would make the number fairly large and probably dependent on the individual's history.
One possible definition of a "type" would be that it has been given a name.
I don't mean to include cells that are present due to injury, clean-up, trash collection, or foreign cells including bacteria, viruses, parasites etc.
Just for an example, here is an overview of types of hematopoietic stem cells. There may be further recognized subdivisions, I don't know how far it goes. There are certainly other cells that comprise human blood. (From here.)

The short answer is that there are still three "kinds" of blood cells: red (RBCs), white (WBCs) and platelets. The graph above names pretty much all of them.

@anongoodnurse I always liked the sound of T-helper cell - are they not a well-defined type?

Maybe discussing an application or disease could help.
Let's take WBCs as an example. The journal of immunology, which is dedicated to WBCs and immune response, prefers to make sections as innate immunology, allergy, antigen recognition, immune regulation, immune system development, etc.
Same story can happen for thrombocytes and erythrocytes.
The point is discussing an application can help to answer about each cell "kind/type" more precise.

@uhoh Helper T cells are quite well defined but are constantly undergoing subsetting due to advances in phenotyping. CD4 is the classical marker denoting a Th, but on cytokines or receptors you may be Th2, Th2, Th9, Th17, some sort of Treg, or a newer one is Th3. Th cells have also been shown to be cytolytic where they're known to simply "help". If you count lineage plasticity, they can be whatever they want depending on the microenvironment they're in..

@CMosychuk OK great! Cells that have distinct, generally recognized and accepted names among biologists can all be included. I have a hunch the answer will be roughly a few hundred total, but don't know. However if there is so much plasticity in vivo (blood still in a person) that it is impossible to give even an approximate number, that could be the answer. Thanks!

@uhoh I think being less specific here is more informative, since regardless of CD4 or CD8 both are still T cells. Exceptions aside, your circulating subsets will define your blood composition. So RBC, WBC and platelets most broadly, and then probably at a finer level: RBC, platelets, monocytes, granulocytes, and lymphocytes so about 9 cells types just based on your chart. Everything else tends to hang in the bone marrow or tissues and so you wont often or in significant numbers find them in blood.

@CMosychuk Thanks. I'm wondering — do you think this question might be unanswerable? If specifying "human blood" makes an answer difficult because there are so many types with such a wide range in frequency that it is too hard to establish a lower cut-off, then I think that would be a really informative and insightful answer, to me at least. However, if the answer is "about a hundred types of distinctly named cells are usually found in the blood of a healthy human individual" then that would be an informative answer as well.

@uhoh Here's a chart I cited in a different question. I think that's among the better estimations of what you might find, and in what quantity, ignoring unlimited subsetting.

@CMosychuk please consider posting this an answer! You have a great way of explaining/summarizing the big picture in short comments, and I think future readers can benefit better from this as an accepted answer than as a comment. Thanks!

I think any answer will be subjective, depending on what you consider to be distinct cell types --- how detailed should the classification be. As you already mentioned, if you consider all cell populations that can be separated by surface antigens, that's already a pretty large number. Also, what previously was thought to be terminally differentiated cell types are increasingly found to be more like cell "states" that can change over time, so-called "plasticity" (see for example http://www.nature.com/ni/journal/v11/n8/abs/ni.1899.html). This makes it hard to even uniquely define a cell type.

@Roland can you consider expanding that explanation into an answer? I would be happy accepting a thoughtful answer that explains why the concept of "number of cell types" is simply problematic, and I'd be interested to find out if it's problematic particularly in blood cells, or for many categories of human cells. There are a number of thoughtful comments here but so far nobody's chosen to pen an answer. I'm here to learn!

I think any answer to this question will be subjective, depending on what you consider to be distinct cell types --- how detailed the classification should be.
As you mentioned, if you consider all immune cell populations that can be separated by surface antigens, that's already a pretty large number. In 2013, the Immunological Genome (Immgen) project reported characterization of 249 immune cell types, and I think they are still working on expanding their catalogue (see immgen.org). One can argue about which of these are really different enough to be called "cell types", but I think it gives a pretty good ballpark number.
At some level of resolution though, the notion of "cell type" itself becomes slippery. While previously it was thought that many cell types were terminally differentiated (unable to change back to more primitive forms), we now increasingly find that these "cell types" are more like temporary "cell states", or phenotypes, that can change over time. For immune cells, this phenomenon is often called "plasticity"; for more information, see for example this paper. The advent of single-cell genomics has further strengthened this view, demonstrating that individual cells can dynamically change their gene expression pattens. These issues makes it hard to uniquely define and count cell types, and it might be more useful to reason quantitatively in terms of the phenotypes and behavior we can measure --- expression patterns, signalling molecules, metabolism and so on.

Nice answer!...

When I started to write this question, I chose blood instead of a solid organ (e.g. liver, heart, kidney) because its natural state is individual cells in fluid and so it lends itself more naturally to some types of cell characterization. I'd thought that a 3D organ would have to be sectioned or destructively disturbed before individual cells could be separated and "typed" and that would still be difficult to do without bias. Now I'm wondering if I should ask a new, similar question using one of those solid organs where the "slippery slope" is not so steep.

The abstract of your linked Genome Research paper Trapnell 2015 is really well written and works hard to explain the "landscape" well. It turns out "how many kinds of cells are there" in the human body is a 60 year old question, and the historical answer used to be "210". I wonder if a block quote or two from that paper in your answer might be informative to future readers. I certainly found it helpful. Thank you very much for taking the time to post a well-written answer my question and to use the space to teach some important points!