text:
Identifying a thin, black, worm-like creature with a hammer-shaped head
I came across the creature shown in the photo below yesterday evening while walking the dogs. At first, I thought it was an earthworm, but a flashlight revealed it to be something I had never seen before.

It is approximately 12 inches (300 mm) in length and about 1/3 of an inch (10 mm) in diameter at its maximum. It is pitch black and very shiny—like piano black. It moves very slowly, using a snake-like motion. It had a very strange head, like a hammerhead shark.
I live in Durban, South Africa, if that helps to narrow down the possibilities.
Can anyone help in identifying this creature?

Was it moving (like most animals, including earthworm) do? Also, is it climbing up the wall? or it is floor?

Sorry, the picture is of concrete paving and yes it was moving, but very slowly, not as slow as a slug, more like a very lazy snake movement

Why sorry? Both the photograph and descriptions are good enough to your effort. It was just a suggestion to improve the description. You could add this details, that would make the creature less-weird when I'll try to imagine it from the photograph.

Hi Always confused, Your suggestions are most welcome, it is the first time I am using this forum and if I came across to strongly, please excuse me, it was not intended. Using your suggestions as to what it could be, I googled "hammerhead worm" and there is an identical picture and it is called a hammerhead slug. Very interesting animal / creature. Regards,..Graham

Careful, they might be deadly :) . https://www.youtube.com/watch?v=XW8F1boWgv0

@GrahamMattsson "about 3 inches (10 mm) ". heh?? :)

@bic:  I would guess that is 0.3 inches, 10 mm, from the photo and the quoted length.

Hmm, I don't believe I have ever seen that before, but it looks  like a Hammerhead Worm (Bipalium kewense).

Fascinating. Once of your links documents this creature as being an invasive species in Texas, although I have never come across it. It's particularly interesting that it produces tetrodotoxin, probably as an aid to killing its earthworm prey.

Fascinating indeed. Here is a very interesting read about Platydemus manokwari, an invasive flatworm from new Guinea.

Sorry I meant to say that on your link to Bipalium kewense, the hammerhead worm looks very similar to the one I saw in my garden crossing the paving, but was totally shiny black and round in girth, I meant to say 3/8" and not 3 inches in diameter (10mm).

I am not sure if I should destroy it the next time I see it or should I seek advice locally, maybe capture it in a bottle.

I think this still fits your description. It can't be shown in the linked pictures, but it is shiny black

If this completely answers your question consider accepting it. It  marks the question as resolved. @GrahamMattsson

"Slug" feels like a misleading term, since that is normally a common name for some molluscs (snails), while this is  Platyhelminth (flatworm)

@fileunderwater You are right, my bad...

Thank you for your interesting comments, another misleading term is flatworm as it is actually round.

That looks like a predatory land flatworm.  They eat snails and worms.  I think they are native to New Zealand, but have been introduced to many parts of the US through ornamental plants.
https://en.wikipedia.org/wiki/Geoplanidae

The OP pretty clearly states the photograph was taken in Durban, South Africa. Additionally, none of the images in your Wikipedia link are similar to the one provided.

Missed the location.  I see that now.  In the Wikipedia article if you scroll down and look at the "variety" picture there is one that is pretty close except for it has a stripe down the back.  Incidentally, I've seen black ones that look exactly like the one pictured in OP's original question several times in Southern California.  I used to see the striped one like in the wikipedia picture frequently in Central Texas.

Hi Cowan, There is a similar picture on the subject of Hammerhead worm shown in Google images. I was very fascinated as I have never seen this before.


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Why do we feel cold in the lower part when we lie down?
This question is based on my personal experience. But I believe that this common for many of us.
Let us say that I am sitting on a chair in normal indoor dress. Then, if I lie down on bed, I will feel the need to cover the lower portion of my body.
As I have seen at home, I am working sitting on a chair. Then I lie down in the same dress, and i feel the need to cover my lower part. When traveling in some sleeper train, people ask for blankets when they lie down, not while they are sitting. It is not that they change their dresses when they lie down, they are in the same dress.
Why does this happen? Why do we feel colder, specially in the lower portion, when we lie down?

Could you clarify whether it's just sensation of cold or does the feet actually get cold? Please touch the feet whether when you are feeling cold, if they are warm to touch them it may be peripheral neuropathy.  Atlast welcome to biology.se

@JM97 It's just sensation of cold. My feet are perfectly warm.

Then it may be due to peripheral neuropathy? It's my opinion , please consult a doctor.

@AlwaysConfused please don't use the term "everyone". A), you don't know that, and B), it's not true.

@MattDMo Thanks for your correction. so, the corrected comment would be, it is a widespread phenomenon, many people do this (including me, Doraemon and Nobita for say :P ), but for me it seems to be not exactly "feeling extra cold" but a complicated psychological need ("wish" to to get covered).

source: Stack Exchange

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sort: votes


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What is meant by increase in information embodied in the system?
From Ecosystem Ecology
edited by Sven Erik Jørgensen

After the initial capture of energy across a boundary, ecosystem growth and development is possible by

an increae of the physical structure(biomass),
an increase of the network (more cycling)
an increase in the information embodied in the system.

What is meant by increase in information embodied in the system?
Does it mean increase in diversity of the genes (genetic information)?

Doesn't the book explain it? We could speculate on this, but I think it will be difficult if not impossible to give a final answer.

@RHA No, it doesn't.

Table 1 on the next page (p. 36) lists a number of properties for each of the three "growth forms".
For information, properties include:

Life history types
Diversity (taxonomic & ecological)
Body size
Stability

I have to admit that some of these properties doesn't really make sense to me under these headings (at least from the common use of these terms). However, I suspect that they are used in a very specific sense that might make sense if you read the entire book. And systems ecology isn't really my thing.
Note also that exergy (which is used in relation to these three growth forms in the book) is a term borrowed from thermodynamics (ie physics), and it describes potential/available work. Exergy is also negatively related to entropy, so when exergy decreases, entropy increases. Since higher entropy is related to disorder, the opposite goes for exergy, so high exergy means a higher amount of order (within the system), which can be translated into "structural information". I suspect that this is the form of information that the book is referring to, as one of the "growth forms".

I'd also add that "information" can be closely related to "complexity" in many contexts outside of contexts where "information" has its usual colloquial meaning (e.g., application of Shannon information/Shannon entropy outside of communication systems). I suspect that's what this author is referring to, the complexity of the ecosystem, such as the number of hierarchical levels that the energy passes through.

@BryanKrause I agree, and the "structural information" that I mention is clearly a way of expressing system/structual complexity. To me, one slightly confusing aspect of how information is used here (in the book/question) is that high entropy (so low exergy) is equivalent to high information (see Shannon entropy), which is kind of the opposite of the  complex, ordered system that the question describes. Random or chaotic systems have high information but are disordered.

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Does cell phone radiation promote longevity?
This preprint presents results from a 2-year National Toxicology Program study on the effects of cell-phone radiation in rats. On page 8 of the PDF, survival results are presented. The presentation of the results is complicated by the fact that some treatment groups experienced significantly different effects when compared to the control group, while in other groups the effect was small but not significant. However, the gist is that rats treated with phone radiation lived longer, and that the effect is stronger in male rats.
I was confused by the fact that this result is presented in the "Results" section on page 8, while the seemingly less significant finding - that treated rats had higher rates of cancer or tumors - was presented in the "Summary" section on page 4. Obviously the study was funded to address concerns we have about observed relationships between cell-phone use and cancer, but when an effect on longevity was discovered, shouldn't this have become the primary result?
The plots on page 11 (Figure 3) and 12 (Figure 4) show some more interesting relationships between the survival of the various groups. Figure 4A shows the high-dose (6W/kg) CDMA male group overtaking the control males only towards the end of the study. With the GSM males (Figure 3A), as well as the low-dose CDMA males, the control group does worse almost from the beginning.
I'm curious to know why more people haven't commented on this result in news outlets. My opinion is that controlled experiments in animals aren't perfect, but they're much better than cheap "longitudinal" studies in humans. As far as I can tell, this is the best evidence we have to date, and it says that cell phone radiation promotes longevity. So why aren't we being required to sleep with phones next to our heads?

I don't think it is useful or relevant to discuss preprints. Wait until they have appeared in peer-reviewed journals.

@David There are actually a bunch of reviews at the end of that document. Most take (quite negative) issue with the study design and power.

"I'm curious to know why more people haven't commented on this result
  in news outlets"

Because for once the news outlets appear to be behaving responsibly, and waiting until the results are published in a peer-reviewed journal. You could do worse than follow their example.

@AliceD — I am sorry but it answers the part of the question I quoted. It is not a request for clarification nor a critique (in the correct or incorrect usage of the word), and it is in no sense suitable for a comment. In any case this is an old question that has only resurfaced because someone has dug it up. Not worth a flame war now.

If you read the discussion, and also the full contents of the PDF which include some reviewer comments, there is concern about the control group:

The survival of the control group of male rats in the current study (28%) was relatively low
  compared to other recent NTP studies in Hsd:Sprague Dawley® SD® (Harlan) rats (average 47%, range 24-72%).

Specifically, the control group had an abnormally high mortality rate for that strain of rat. There is no increase in longevity if you compare to historical data.

Yes, I read that. Is your argument that we should (a) do away with control groups and just compare with non-randomized controls from historical rat populations used in different studies in other parts of the world? Or that we should (b) use control groups but ignore the results when we disagree with them, falling back on historical statistics?

Because a randomized trial gives us a p-value, which, although not reported by the authors of this study, tells us that the in case of the null hypothesis, where the treatment is not doing anything, the observed differences between groups must indicate that a e.g. 1 in 20, or a 1 in 1000, event happened. And I thought the point of statistical analysis was not to fall back on explaining our results as due to extreme randomness.

@Metamorphic No, a control group should still definitely be used. p-values don't prove truth, they tell you when your results are more different than you would expect if there is no real effect, with some reasonable margin for error built in. You always have to use other sources of information at hand to interpret your results. It would already be a little extreme to change behavior based on just one study, and even more extreme to change behavior based on a study where there seems to be a significant problem with the control group.

@Metamorphic Not to mention the study also showed more tumors in the test groups than the control group, though that is also suspect because of the short lifespan of the controls. Truthfully, it seems like whether by randomness or some unknown factor not accounted for in the study, this work will have to be repeated with a new set of subjects to provide a result that can inspire more confidence.

I admit that the idea of changing behavior was a bit tongue-in-cheek - although for many people this would not be a change of behavior. But I'm not sure we're on the same page with the results - why do you say there is a "significant problem with the control group"? What would make it different from the other groups? They were all treated identically, except for radiation levels. Further, your quote indicates that the control group survival was not outside of the range of normal survival rates, so your use of the adjective "significant" seems misleading given the context.

Well, they gave a full range, not an interquartile range, and I am assuming they are basing that on many studies. It could be that only 1 study out of 1000 had lower survival than this one. It was sufficiently significant for both the authors and the reviewers to comment on it being an issue with the study. As far as the control group, we don't know precisely how the control group was treated. The researchers no doubt tried to treat the control group equally, but maybe they did not. Maybe control animal cages were in a row and disease spread between them when they were handled.

...the point is, we don't really know, but the control group is enough of an outlier from other studies that we should think more carefully about the results. You are much more likely to make a type 1 error if the control group itself is in the lower end of normal, and in fact this sort of thing happens all the time, especially if you consider a p-value of 0.05 to be significant. Part of your question was asking why this study isn't getting more play and why the authors didn't focus on this point: I think it's because they are not confident it is a real result, and they expressed that concern.

Thank you for thinking about this. I think that what it boils down to is, the authors don't give us enough data to make sense of their results. This is somewhat frustrating and makes me wonder what is being covered up - whether it is experimenter incompetence, as if the control group rats were all "in a row" as you say; or, alternatively, if it is a result which might threaten their National Toxicology Program funding, such as "X is not toxic".

@Metamorphic don't look for conspiracy where there likely is none. I personally applaud the researchers for publishing mixed results - that's not done often enough, and skews the literature (and our understanding) to a potentially large degree. Not every study will give perfect, absolutely clear-cut results. We don't know a lot of things, but that doesn't mean they're being covered up intentionally. Maybe it was a poorly-trained grad student. Maybe it was disease, or the animal facility staff, or the facility itself, or the supplier, or a million other possibilities. Don't be paranoid.

@MattDMo: "Don't look for a conspiracy"? "Don't be paranoid?" I don't appreciate your patronizing generalizations. Everyone has bias and you know very well that we can discuss that here. If you're so interested to distinguish between bias and incompetence, don't write to me. Write to the authors and ask for their p-values. Maybe you'll have better luck than I did.
I don't even know why you would bring up conspiracies in this case. The bigger "conspiracy" would be if they had bias in the other direction.

@Metamorphic I don't think MattDMo meant any harm. You are coming here and saying "Why aren't people taking this study more seriously?" and we are giving you a very good reason: because the data are suspect. That doesn't mean you throw out the results. I don't think the researchers are incompetent, as you suggest, I think they are pragmatic and reasonable: something in their results looks funny, so they aren't putting much stock in it until it gets confirmed. That's responsible research. I also wouldn't say the NTP's funding is dependent on finding particular things toxic.

@MattDMo makes a great point as well about the skew in the literature: that many studies go unpublished when the results are suspect or borderline. That's actually a big problem. It's much better to publish the results, with the appropriate caveats noted, so that future studies can take it into consideration. If you zap two more studies worth of rodents with cell phone radiation and their control groups suffer again, we can start to conclude that the radiation is making telekinetic rats that suck the life force out of their kin to prolong their lives. Until then, let's be cautious.

@Bryan: If you or Matt write asking for p-values and quantiles, that would be great. They exist, and at this point getting them should be easier than theorizing about our beliefs about other people's beliefs. ... Until then, I like your last hypothesis :)

@Metamorphic The paper hasn't even completed the peer-review process; the reviews included in the pdf you linked have already asked for some additional statistical presentation of the results, including p-values. I suspect all of these will be in the final publication.

@Bryan: I think that the pre-print phase is a great time to correspond with the authors of a paper. If you want to wait, that's fine. Just remember that the purpose of getting those numbers is primarily to validate the assumption in your answer, that certain deviations were significant. My question is based on significances already validated by the reviewers (e.g. p. 53). You could also replicate what the authors did by tracking down recent NTP SD-rat studies. Then collate the control group survival rates, and run a t-test. If you get say p < 0.05 then I would accept your answer.

@Metamorphic Did you read the entirety of the PDF you linked in your original question? NIH reviewers have already raised these issues, and uniformly show concern about the survival rates. Page 53 and similar was simply checking that the statistical calculations were performed correctly, and says nothing about the reviewers opinions of the data themselves, which they clearly feel are suspect.

@Bryan: I'm not interested in counting the number of reviewers that expressed concern, what's more interesting, for your argument, is counting the number of rats that survived and relating it to other studies. Is the relationship statistically significant?

Let us continue this discussion in chat.

I'm curious to know why more people haven't commented on this result
  in news outlets.

This is an easy point: nobody is interested in publishing this. A quick scan of my (not that bad) local newspaper shows stories in a few categories:

Photogenic stuff. About the moon, Antarctica, animals etc.
Male/female stuff, why we are not the same, or why women are better at something
Everything about food, medicine and vitamins
Climate change

Besides that, the story has to be news. It has to have some actuality, fit in with previous/further stories people are talking about, and people have to want to read it.
This story has none of that. Nobody is talking about cell phone radiation, and people are already convinced that it's not dangerous. 15 years ago this would definitely be on science pages everywhere.
Then there's also the science. Apart from what people are saying in the comments, you just cherry picked a single data point from a single study. The study was not designed and powered to show that cell phones increase survival, the authors don't focus on it (rightfully so), and there's also no plausible mechanism how this should work.
You can have a theoretical discussion about whether or not this fact is a reliable fact, and about whether or not the authors did everything right. However, I would put all my money on future research showing no enhanced survival, because circumstantial evidence is pointing in that direction and there's no mechanism.

Good first half, but... "you just cherry picked a single data point from a single study" - What are the other studies? I mean, other studies that would provide evidence about survival effects. "The study was not designed and powered to show that cell phones increase survival" - not designed in what way? "circumstantial evidence is pointing in that direction" - good if true, but can you elaborate? Thanks

It's highly likely there are other studies where animals are exposed to cell phone radiation. Probably there this effect is absent or not significant. Not designed / powered: if there is an effect it's likely that it's (extremely) small. By doing the study with low power, you're very likely to get either nothing (expected) or, if you get a statistically significant effect, the effect size will be overestimated. The circumstantial evidence is that similar mice in identical control groups that usually live longer.

See #3 in my question. If you think another study is relevant, I need you to track down the citation. Otherwise you're asking anyone who disagrees with you to cite every study ever published and show that it doesn't meet your advertised criteria. Some estimate that a total of 50 million journal articles have been published to date. It's much easier if you just tell us where to look.

You were interested enough to look this up in the first place, why would you stop looking when you find one number that fits what you want to think?

I don't appreciate your condescension. I made a simple request. Please back up your claims, or don't participate here.

@Metamorphic VonBeche is not condescending you. Every single person who has answered or commented here has roughly the same opinion. You are here asking for our help - no one is being paid here to do work for you. Sometimes it's helpful to teach by giving the answers, but more often its best to give someone the tools to do their own work on the subject.

I don't have time to play your games @Bryan. This page is for people who want to answer my question. If you think it would be a waste of your time to do that, or if you think that you would be hindering me from "getting tools", then either way you don't belong here. It's a Q&A site.

Your question wasn't about the dangers cell phone radiation, it was about why nobody was talking about this research and why the WHO doesn't advice us to sleep with our phones. The answer to that is just that it's not interesting and that the result is probably wrong. If you want to know more about this field of research I can recommend you to read some more literature and look up some reviews. To refer to the guidelines: "some thorough searching for the answer is expected". You came here with one cherry picked data point.


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Topic in bioinformatics
I am looking for a presentation topic in bioinformatics. I haven't occupied with this field yet, but I find it really interesting.
It would be nice if the topic would include an algorithm. What source do you suggest to me?

as Joe Haeley suggested you can take a look at alignment algorithms, another algorithm which is quite a lot used is BLAST (https://en.wikipedia.org/wiki/BLAST )

This is not a question about biology.

This question is open-ended, allowing for many possible answers. This is not an appropriate question for SE.

A fairly easy to get to grips with topic, but that digs down to the meat of bioinformatics algorithms, is sequence alignment. Read around Needleman-Wunsch and Smith-Waterman alignment algorithms.
Wikipedia will be a perfectly adequate starting place :) - steal all the references at the bottom of the page!
I don't know how strong you maths ability is, but you'll find quite a few equations while you dig around in the bases of bioinformatics algorithms!

It depends on what you define as introduction. For a start you could always do what Joe Healy suggested and read around to see if it is a field that suits you.
If you want a textbook I found An Introduction to Bioinformatics by Jones and Pevzner to be indeed a great introduction to bioinformatics. It treats you like an absolute beginner and I think you will be able to follow no matter your programming or math abilities.
Now, if you want to get your hands dirty I can't recommend Project Rosalind enough. It introduces you to a variety of (mainly) programming problems while simultaneously teaching you the corresponding biologic concepts.
Phillip Compeau (co-founder of Rosalind) along with Pavel Pevzner have released a textbook of their own: Bioinformatics Algorithms: An Active-Learning Approach, which I admit I haven't read, but it is generally well recieved.
But before all that, I suggest to take a small introduction to Python (if you haven't already) and get familiar with the basic libraries (mainly BioPython). Perl is also a language you would like to consider, but far less beginner-friendly.

Cool I'd heard of Project Euler, but not Project Rosalind


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What spider is this?
I found this spider in my flat in Berlin, Germany. It looks like a Cheiracanthium, but which species? Mildei? Or is it a different spider?
The body is approx. 8-9mm long and it lost 4 legs when I tried to catch it unfortunately.

I'm not an expert.It seems to be a male Cheiracanthium mildei.

ghost spider,miturgidae ?? Spiders are really a pain to identify


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Is this lizard protected or endangered?
We think that it's a type of alligator lizard. It was found in the open space area near my home in Moss Beach California (about 10 miles south of San Francisco). Thank you!

It appears to be a California Alligator Lizard - Elgaria multicarinata (subspecies multicarinata), although another photo from the side would be helpful for a positive ID. This species seems to fit the range for the observation as well.
According to CaliforniaHerps.com, there are no associated conservation concerns for this particular species.
Elgaria multicarinata multicarinata conservation status


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Homologous structures under Lamarck
I've read that Lamarck's theory doesn't explain homologous structures.
But, what about the following hypothetical under Lamarck's theories:

A population develops an adaptation to its environment
Part of the adapted population moves away
The adaptation is passed onto the population's offspring
All offspring of the original population have the adaptation, regardless of whether or not their ancestors moved away

Isn't this adaptation a homologous structure?

I agree with you that I can't see why Lamarck's hypothesis could not explain the presence of homologous structures.
The link you offer also claim that Larmarck's hypothesis would fail to explain "Biogeographical diversity patterns". While this expression is a little vague, I would fail to understand why Lamarck's hypothesis would fail to explain patterns of biogeographical diversity.
The phrasing of your scenarios (absence of the term allopatric speciation, usage of the term "develops" instead of "evolves" of just "adapts") suggests that you may take advantage of an intro course to evolutionary biology such as the short and good course by UC Berkeley called Understanding Evolution


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Why does this karyotype start numbering at 11?
Here is some image I found for karyotyping a chromosome:

Why does the band numbering start at 11? When I count other things I usually start with the number one, and in some cases zero. Eleven seems random.

What research have you done before asking it here?

I read the Wikipedia pages on the topics, which are very limited. And I studied a few graphics I'd chromosome bands. I have no background in biology and I did not check any textbooks yet.

@FullDecent It is not exactly my field but I don't quite understand what these numbers and band colours are supposed to mean? Can you please add a link to where you found the picture. It may help me out. I don't really understand the expression "karyotyping a chromosome". Does it mean 'to recognize a chromosome while performing a karyotype' or does it mean 'Figuring out past chromosomal translocation events' or something else?

Why does the band numbering start at 11? When I count other things I usually start with the number one.

It does start with the number one!
What is happening here is clearly a small confusion. Looking at the centromere in this idiogram of chromosome 12 you can see two number 11, as you stated in your question, one above and one below the centromere:

An idiogram of a Giemsa-stained chromosome 12. © 1994 David Adler, University of Washington. All rights reserved.
However, those two 11 below and above the centromere are not, in fact, an 11 (eleven): they are just two number 1 together, 1-1 or one-one.
According to Nature (2017):

This particular idiogram depicts the pattern of Giemsa staining at a fairly low resolution (i.e., it produces about 400 total bands in a karyotype, which is just above the threshold that is clinically useful). At this resolution, the long q arm of chromosome 12 can be subdivided into two main regions, which are designated 12q1 and 12q2. Region 12q1 can be further subdivided into five subregions, designated 12q11 through 12q15, each of which corresponds to a band detected by Giemsa staining. Orally, these subdivisions are referred to as "12q one-one" through "12q one-five" (not as "12q eleven" through "12q fifteen"). The more distal 12q2 region can be subdivided into subregions 12q21 through 12q24. In addition, subregion 12q24 can be further subdivided into regions 12q24.1 through 12q24.3, even at this relatively low resolution.. (emphasis mine)

Thus, those two 11 you see above and below the centromere are (or should be), respectively, 12p1-1 and 12q1-1 (remember that this is the chromosome 12).
The confusion here, therefore, is due to:

The omission of a 12p or a 12q before all those numbers.
The omission of some separator, like an hyphen or a comma, between those numbers.

A detailed PDF from the International System for Cytogenetic Nomenclature (ISCN) can be found here.
Bonus: In case you want to know, that number 850 in the top of the idiogram refers to the number of bands:

At this higher level of resolution, approximately 850 bands can be distinguished in a karyotype

Source: Nature.com. (2017). Chromosome Mapping: Idiograms | Learn Science at Scitable. [online] Available at: https://www.nature.com/scitable/topicpage/chromosome-mapping-idiograms-302 [Accessed 23 May 2017].


text:
What is the counter-reponse to a sound stimulus?
I am slightly confused on finding out what is the counter-response because of a stimulus.
For example, if we hear a sound, I believe the sound waves are the stimuli? So is the counter-response the vibration of our eardrum or the sensation of hearing the sound?

A tittle should be intelligible on its own. "In this case" is obviously not. Next time put in the effort to make it so.

Is this question one based on clarification of terminology, or rather one on the physiology of hearing? Either way, the question is unclear and needs clarification. E.g., what else than sound waves would be the stimulus for audition? Photons? EM waves? And what is a counter-response? This terminology is akin to Newtonian physics. What is your question?

All stimuli do not generate reactions. It is the CNS that decides if a reaction has to be generated on receiving the information about a stimulus.

External stimuli are capable of producing systemic responses throughout the body, as in the fight-or-flight response. In order for a stimulus to be detected with high probability, its level must exceed the absolute threshold; if a signal does reach threshold, the information is transmitted to the central nervous system (CNS), where it is integrated and a decision on how to react is made. Although stimuli commonly cause the body to respond, it is the CNS that finally determines whether a signal causes a reaction or not.

From Wikipedia
The changes that occur inside ear,vibration of tympanum, movement of ear ossicles and all are responses to the stimulus (the mentioned two are mechanical responses) to transmit the information about the stimulus(sound) to the brain.
If the brain finds out that the sound is actually a noise then it would instruct the body (limbs for example) to move away from the source of the sound. This is then called the reaction.
If the sound is not that loud, i.e. not potentially damaging to the ears then the CNS does not instruct to retreat.


text:
Sister chromatids during meiosis

Sister chromatids
$A)$ Cross over during prophase I of meiosis
$B)$ separate during the first mitotic division
$C)$ are produced during $S$ phase between cell divisions
$D)$ cross over during prophase II of meiosis
$E)$ are also called homologous chromosomes

My thoughts:

$A$ is incorrect because it's nonsister chromatids that cross over
$B$ is incorrect because they separate during the second mitotic division
Don't know about choice $C$
$D$ is incorrect because there is no crossing over during Meiosis II
$E$ is incorrect because well...it's just not true

So is the answer $C$?

It is C. During S-phase the DNA of each chromosome duplicate and the two sister chromatids formed get attached by cohesin proteins. These sister chromatids separate at Anaphase-II of Meiosis.
From wikipedia:

A sister chromatid refers to either of the two identical copies (chromatids) formed by the replication of a single chromosome, with both copies joined together by a common centromere. In other words, a sister chromatid may also be said as 'one-half' of the duplicated chromosome. A full set of sister chromatids is created during the synthesis (S) phase of interphase, when all the chromosomes in a cell are replicated.


text:
Does the brain always think of an appropriate response when reacting to a stimulus?
Does the brain always think of an appropriate response when reacting to a stimulus?
For example, when seeing things, does the brain have to think of an appropriate response to the eyes?

From the two answers seems this really unclear question.

This question seems sort of oddly upvoted and answered - it is pretty low-quality and unclear what you are asking compared to the normal standards for Biology.SE. What does "appropriate" mean?

This is the most vague question I've ever come across. What are you on, exactly? And why was this upvoted?

@Servaes It was in Hot Network Questions

Well, not always but most of the time; reacting to stimuli is what defines the nervous system and the part of the nervous system that includes the brain is called the 'central nervous system' or CNS. Reactions to stimuli (nerve impulses) don't always have to pass through the brain as the CNS consists of the brain and the spinal cord. This means that in the case of thinking, if what you see (or sense) is something harmful (a man with a knife, feel extreme heat) then you will react without the nerve impulse having to pass through your brain (instead it will simply pass through your spinal cord). This is because the body does not need nor want to waste time thinking about an obvious and protective response. This reaction that requires no conscious thinking is called a 'reflex reaction' or an 'automatic reaction'. If you want to know more about this you should probably look into the nervous system.

If you take the stimuli as light entering the eye, then this answer is a bit misleading, since even basic object recognition (e.g. to identify dangerous objects) is going to be performed by visual cortex in the brain. Yes other parts of the response may not be in the brain, and even if in the brain, it is not too clear what the OP means by "think".

@NeilSlater: The contraction of the iris when the stimulus is bright light entering the eye is an interesting one. It does involve the midbrain, so it's not like the knee-jerk reflex that involves only the spinal cord. But it might serve as an example which the question doesn't consider under the heading "the brain thinking of a response", if "thinking" is intended to refer to activity of the cerebral cortex (including image-recognition). I do agree with you though: this answer says that the reaction to seeing a man with a knife involves only the spinal cord, not the brain, which is false.

... in fact I think arguably the retinae could be considered part of the brain. In any case they connect to the brain via the optic nerves, and the spinal cord isn't in that path at all.

@Steve Jessop: Not only is it false, there's still the whole question of whether the response the brain comes up with is actually appropriate.  Present the same "man with knife" stimulus to a random sample of people, and I think you're likely to get a wide range of responses.

@jamesqf of course it goes without saying that each individual's reaction will vary due to several factors: situation, environment raised in, personality, self-confidence, etc. However, it I no question that every single person WILL react and upon impulse too; since not a single person will do nothing at all (obviously)

@Lucas Dyson-Diaz: I don't know about that.  Seems like the reaction of many people to that sort of situation is simply to freeze, or "run in circles, scream and shout".

@jamesqf or fight back or call for help or team up on him or throw stuff at him from a safe distance or call the police or don't call the police or accept your death or try to reason with the man. There are more responses to any situation than just stand there or don't (I just named 8).

@jamesqf: I don't put too much weight on the word "appropriate" in the question: surely the question here is not intended to be, "are humans always right about everything?". If so it belongs on Philosophy. If you see someone with a knife and shoot them, then I think for the purpose of this question that was the "appropriate" response, that is to say the response the organism makes to a particular stimulus, regardless of whether the jury eventually decides it was "appropriate" or "inappropriate".

@Steve Jessop: But the OP is specifically asking about "appropriate response", no?  Certainly we could go into philosophical/legal discussions about what reaction is appropriate to any given circumstance, but I think it's pretty obvious that there are some reactions that are inappropriate by any reasonable standard.

@jamesqf . Whether it is appropriate is not a decision for any one or two people to decide. Especially in such a desperate and life-threatening situation, there is little you could call inappropriate (other than killing the man, possibly, however that could philosophically be argued as appropriate too).

@jamesqf: I would say "no", the questioner is not intentionally asking specifically about the "appropriate" response in the wider sense that you refer to when you describe "scream" as an inappropriate response. I think they just mean "appriopriate response" in a sense something like, "the neural response necessary to make the organism do whatever it is that it does in response to the stimulus". So if the organism screams in response to knife-wielders, then the "appropriate response" is to signal the lungs, throat, face, etc. Even if screaming is a dumb idea by any reasonable standard.

No:

Optical illusions trick your brain and elicit an inappropriate response. Of course optical illusions don’t need to be engineered, they abound in reality (remember The Dress that went viral two years ago)?
In addition to optical illusions, other senses can be tricked. There are auditory illusions, an illusory sense of touch, etc.

I can barely look at that. What's actually going on in it? It's like it's moving. Wow! It's weird. Now it's sliding. It's worse if you focus your eyes, if you unfocus your eyes it's easier to look at. I still can't figure it out. What's it doing?

@DanielCann It’s really just straight, equidistant, parallel lines with black/white coloured square boxes between them. The sequences of boxes in each row are offset at different distances from the left side. That’s all there is to it.

How do you know? We're both human, and it's an optical illusion which is designed to deceive humans.

@DanielCann Well I mean you can simply check with a straightedge and a set square/triangle/compass …

@DanielCann: or assuming you trust your PC not to conspire with Konrad to trick you, zoom in on the image in any image-editing program. The illusion doesn't work on a small enough section. Then you'll see that nothing's moving and everything in any given small section of the image is straight and square. Pan around the image until you're convinced it's true everywhere.

The answer to the question is if thinking is always a response to some external stimuli depends if we consider the memory. Thinking about the event in the past is surely possible many years after the stimuli is long gone. Continuous stimuli from the environment may not be required for the thinking process itself as spontaneous brain activity exists as well.


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Liebig's law of minimum
I was reading from Odum about Liebig's law of minimum.
It said that

the law is appicable in steady state condition i.e. when the inflow of energy and material balances out the outflow.

I got two questions:
1.Here what is actually in steady state? Photosynthesis? or Plant community? or Biotic community?
2. Inflow of energy and material balances out the outflow.
What is the net material/energy that is flowing in an out of a system? Could it be amount of light absorbed and amount of glucose and O2 produced respectively? He used the word balances which means they are not equal actually but proportionate I suppose.

Your second question isn't a question. Please reformulate as a question.

The question is beneath the statement that is numbered 2.

Your question is not directly related to Liebig's Law of the Minimum. Instead you ask about a conditions under which the Law holds according to your quote.
From the quote it is clear what is in steady state: it is the total amount of energy and material. If the the amount of energy and material flowing into a system equals ("balances out") the amount of energy and material leaving the system, the total amount in the system does not change, that is, it is in steady state.
This does not mean that other quantities in the system are necessarily in steady state. For instance, the species composition of a bacterial community may fluctuate or evolution may cause the community to change.
An example of the sort of systems we are talking about here is the chemostat. A chemostat is a device for culturing microorganisms. It consists of a culture vessel connected to a feed bottle. A solution of nutrients (the growth medium) literally flows from the feed into the chemostat. Microorganisms in the chemostat will grow and reproduce (if the concentration of nutrients is sufficient). A mixture of microorganisms, unused nutrients, and byproducts of growth leaves the chemostat in the effluent flowing out of the outflow of the vessel. The rate at which this happens is the same as the rate at which medium flows into the vessel. Typically, after a while the concentration of microorganisms and the concentration of nutrients in the chemostat and effluent do not change anymore (if the inflow is constant, that is). The chemical conditions in the chemostat have then become static (hence "chemostat"). The concentration of nutrients and microorganisms are then at steady state.
In the case that the microorganisms are phototrophic, the nutrients may be inorganic and energy is added to the system through light. The light absorbed may then be considered as the energy flowing in, and the energy flowing out is then the chemical bond energy in the organic material that make up the microorganisms and the byproducts, and heat.
Chemostats are culturing devices, but are also models of natural systems such as lakes or ecosystems.
Liebig's Law of the Minimum says whichever resource (nutrient of light) is in short supply determines the growth rate of an organism. For instance, if nutrient concentrations are in ample supply but light levels are low, changing the nutrient concentrations will not change the growth rate of the organisms, however, changing the light levels will. The quote of Odum suggests the Law only holds under steady state conditions, but I do not understand very well why this would be so.

Thanks for the answer. I don't have time to read it now. I'll let you know if I have follow up questions in a few days.


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Interpreting ChIP-qPCR or ChIP-seq
I have a really basic question. Studying ChIP coupled with q-PCR or sequencing, I see different levels of a certain protein among a genomic region. I cannot really understand how can we have different protein levels. I thought that the binding of a protein in a region is bivalent-it occurs or not. But, as I can understand, we can have different concentration/quantity of protein bound to a region? And if this is the case, how in ChIP-qPCR we get finally DNA fragments, so how can we measure this binding from the quantity of fragments?

Could you explain more what "I see different levels of a certain protein among a genomic region" means, and how you determined that? Also, your last sentence is not very clear.

Protein binding to DNA is not bivalent. ChIP is enriching for DNA to which your protein of interest is bound, but that protein may bind certain sites throughout the genome more strongly and frequently than others. Stochiometric effects play a role, as do the strength of the binding motifs.
Some proteins bind very specifically to a given sequence, but most allow for some degeneracy in their binding sites. A strong site will be bound more frequently (and thus more highly enriched during ChIP) than a weaker site. Not just the presence, but the frequency of binding is what ChIP really measures.


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Organism-specific Kegg Pathway: Must all boxes be high-lighted/present for a reaction to occur?
I'm new to using Kegg and not sure how to interpret the position of the pathway enzymes in the pathway that I'm looking at. More specifically: If all boxes (of KOs) must be present/colored green or not for a reaction to occur.
I'm looking at this pathway: http://www.kegg.jp/kegg-bin/show_pathway?ooe00010
Looking at the 'help' for Kegg indicates that the KOs represent a protein complex, because the boxes are 'stacked' against each other. Is this correct?
Specific reactions that I've been looking at: alpha-D-glucose-6P to beta-D-glucose-6P (One box is there, the other is missing).
Or the route from Glyceraldehyde-3P to pyruvate. I'm thinking that these pathways must be present, but in the very first reaction only 1 of 2 boxes are colored. I suppose it's also a possibility that Kegg's database is simply incomplete?

Also note that green boxes indicate that the enzyme was found present in the organism you are looking at, however White boxes do not mean that the enzyme is not present, it only means that there is no evidence (or not yet) found that the enzyme is present in the organism. (Probably in some cases it's found that the enzyme is not present, but in general it means that there is simply no evidence)

Your interpretation of the pathway map is incorrect.
The boxes do not represent KOs (Kegg Orthologues) and they do not represent a protein complex. They are Enzyme Commission (EC) numbers and where there is more than one box this means that there is more than one enzyme that can catalyse the reaction.
In the case you cite the two enzymes are EC 5.3.1.9, glucose-6-phosphate isomerase, as you can see by clicking the box, and EC 5.1.3.15, glucose-6-phosphate 1-epimerase. Only one is needed to catalyse the reaction.


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Are polyploidal organisms parasatized by selfish genes? And if not, why not?
Certain prokaryotes are polyploids. For example, Thermus thermophilus has about five copies of its genome (http://jb.asm.org/content/192/20/5499.full). One extreme polyploid, Epulopiscium fishelsoni, has tens of thousands of copies of its genome (http://www.pnas.org/content/105/18/6730.full). (Some eukaryotes are polyploid as well.)
As each copy replicates separately it would seem likely that spontaneous mutations would arise and over time, and such an organism would become a hybrid of many distinct genomes coexisting in a single cell.  This seems like an ideal place for selfish copies to arise (though perhaps no more so than any other organism - I think I've read that even prokaryotes are prone to plasmid parasites).
So, does this happen?  If not, why not? Is there some copy-checking mechanism (some extremeophiles seem to have a DNA-repair mechanism) or some mechanism that inhibits reproduction by genomes that are (somehow) determined to not be contributing to the overall metabolism of the cell?

Do you have some basis for supposing that they don't? I agree with your premise, and every genome I've ever looked at is absolutely riddled with selfish elements (and thats just haploid organisms).
You only have to look at most replicons (plasmids etc) and they usually harbor a greater than average density of these types of element. Thus me agreeing with you that polyploidy likely invites it even further!
Also, what makes you think there is no copy checking mechanism nor DNA repair mechanisms 'supervising' the process?

Is there any reason you are talking about polyploidy in bacteria only? I don't know much about bacteria polyploidy. I typically doubt they recombine unlike most eukaryote polyploids.

Joe Healy: Edited question, thanks.  Remi B: bacteria/archea have the most extreme polyploidy, but one could generalize the question

In short, being haploid or polyploid should not protect you from Selfish Genetic Elements (SGES).
Almost all eukaryotes are polyploid. Plants are the oft-cited example. Wheat, I believe, is hexaploid for example. Polyploid bacteria are the exceptions typically (if we consider ploidy to be of the whole genome). However, even in truly haploid bacteria, the genome in any given cell is usually actively being replicated, so some of the genes are actually present more than once.
Regardless, replication and repair is an enormously well controlled and regulated process: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1479556/

SGEs can take many forms depending on your definition and are ubiquitous in nature as far as we can tell. Plasmids which harbour addiction factors, insertion elements, transposons, prophages etc are all technically SGEs. See here for a review:
https://www.ncbi.nlm.nih.gov/pubmed/21227262
I can't find any literature on SGEs in polyploidy directly, but it is well documented that bacteria harbour a considerable amount of selfish DNA - it seems likely that this will be the same if not worse in polyploidy. Plasmid detection is a difficult computational and experimental process (http://bioinformatics.oxfordjournals.org/content/early/2016/11/18/bioinformatics.btw651.full) but one of the hallmarks of plasmid sequences are typically addiction factors (a gene that the host cell must maintain in order to survive - usually an anti-toxin to neutralise a toxin present on a different DNA molecule) as well as phage genes.

To address a couple of things specifically:

As each copy replicates separately it would seem likely that spontaneous mutations would arise and over time

This is somewhat true, there is always minor variation in a population (else evolution wouldnt work!). Sometimes you'll find this is also the case in a single cell - but less often. All cells we have found so far have DNA replication and repair mechanisms - https://en.wikipedia.org/wiki/DNA_repair. The frequency of mutation in the genome is not directly linked to the amount of selfish elements though, making your second point contentious:

This seems like an ideal place for selfish copies to arise

I agree with the premise of polyploidy probably inviting more SGEs (thinking specifically of IS elements and transposons here really), but not because of mutation - rather, just because there are more DNA molecules and sites present for those elements to incorporate into.


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Explanation of universal model of energy flow
I am trying to understand the Universal model of energy flow by Odum.

In this linked diagram I is the input energy(the amount of energy present in the food consumed by this tropic level, say its, the 2nd tropic level, the herbivores), part of this food is excreted as undigested food (the NU) , the rest is digested, absorbed and assimilated reaching the cells and then the energy accumulated at cellular level is called the assimilated energy (A). Now part of A is utilised to make ATPs that are being used to fuel the metabolisms occurring in the organisms which is represented by R and the rest is available to the next tropic level(?) as P ?
Then what makes the standing biomass? The organisms the are not eaten up?
Besides I don't understand the Energy Storage part. What physiological process corresponds to this?

If you were to take a snapshot of the biomass present for a species at an instant of time, that would be its standing biomass. So, in a way you are correct with "the organisms not eaten up". But this can be quite misleading when used to attempt to explain pyramids of production up trophic levels. For example, in some aquatic ecosystems the standing biomass of primary consumers is greater than that of primary producers. On study in the English Channel showed 21 g/m3 of zooplankton but only 4 g/m3 of phytoplankton. This is due to the rapid proliferation of the phytoplankton and the rapid consumption by the zooplankton.
Typically it is preferable to describe the energy flow through ecosystems in terms of energy units, Joules for example. However, you could do this with biomass if you summed the biomass produced over time. When done like this, the English Channel example would look like a proper pyramid with the producers out-massing the consumers over a meaningful period of time.
Energy storage is simply the energy stored in the chemical bonds of the molecules created during growth that add to biomass.
My example, and context, is from Biology, Campbell & Reece, 7th edition.


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Can assimilated energy be simply lost from a trophic level?
I was reading Environmental Studies By B. S. Chauhan and there a diagram of a model of transfer of energy.

NU = Not used energy has been shown, energy that was neither stored or exported to the next level.
I wonder what physiological process causes this loss of energy at all trophic levels?

In this diagram, since this is the only loss between trophic levels (along with  respiration and NA within each trophic level), NU represents dead organic matter, that is not transferred along the food chain. In other words, this represents dead leaves that are not eaten by herbivores, hares that die of old age and not predation, and foxes that are killed by falling rocks. So NU is the amount of energy that goes directly into the  decomposer community (another flow to decomposers is coming from matter that is excreted by herbivores and predators), since this diagram only includes primary producers, herbivores and predators.
NA, on the other hand, represents energy that is consumed by the next trophic level but not assimilated (Not Aassimilated). So this represents faeces etc.

fileunderwater I just had some thoughts I wanted to know what you have to say, I couldn't ping you in Biosphere so I would just address you here.
I was wondering do food chain end with a trophic level where the energy content is 0?  I think it is possibly never happening (because if an organism feeds on some food it is sure to consume some sugar/fat/protein if the food is not entirely minerals and vitamins) so it is never zero. Besides though food chain theoretically ends with a greater carnivore but there's no terminal organism at the end to eat-to-be-eaten cycle (the food web). .cont..

So in an aquatic ecosystem where a hawk is supposed to have a very low A it is actually supported by different other food chains, raising its energy content to a sustainable level?


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How many Laws does Mendelian inheritance have?
I know of 3 laws of Mendelian inheritance :
1.law of segregation
2.law of dominance
3.law of independent assortment
But, I've also come across a couple other "rules" of Mendelian inheritance such as principle of unit character/factor and principle of paired factor. I cannot understand what these other rules actually mean and whether they are a part of the Mendel's law of inheritance.
Further is there a distinction between the words Law,Principle and Rule or they mean the same thing.

Welcome to Biology.SE. The last question Further is there a distinction between the words Law,Principle and Rule [..] is a question of philosophy, not of biology (have a look at philosophy.SE).

We commonly tell about main 2 findings of mendel... (1) Phenomenon of segregation, and (2) phenomenon of independent assortment (second one later came out as as an incomplete-truth)... however normally there were more principles behind these findings. okay I'll write an answer when I'll get time.

Principle of unit character/factor
To understand this concept, it is good to fall back into the era in which Mendel lived, an era where we knew so little about the nature of genetic information. Consider a famous (and highly racist) argument by Jenkins against the hypothesis of natural selection as formulated by Darwin.

Jenkins supposed that a white man was wrecked on a desert island inhabited by Africans. The shipwrecked European would kill many black men in struggle for existence. He would have many wives and children. Many of his subjects would live and die as bachelors. In the F1, there will be some intelligent young men who are mulattoes (mixed race) more intelligent than negroes. Eventually instead of the beneficial white characteristic rising in frequency through natural selection acting on intermediates, Jenkins said that the European alleles and genes will be diluted out.

Putting aside the obviously racist and false assumption that whites are superior to blacks, the argument is not silly. Why would not the beneficial characteristic of an individual just dilute into the majority unadapted population? The answer is in the long forgotten Mendel's work. Individual characteristics are not 'fluid'. Characteristic of parent don't just average to give the characteristic of the offspring. There are actually particular unit of heredity (a gene) which has some seemingly atomic property in the sense that its effect will be diluted by crossing individuals carrying a given allele (an allele is a variant of a gene) with individuals carrying different alleles.
Principle of paired factor
Here is the underlying discovery of diploidy. Of course, by far not all living beings are diploids (or diplontic) unlike Mendel may have thought but he still discovered that diploidy is a thing.
Mendel discovered that it is the combination of two 'alleles' (the terms 'gene' and 'allele' did not exist at that time yet) that would determine the 'phenotype' (this term did not exist yet either) of an individual.

thank you for clearing things a bit , but going back to my basic question do these principles hold as the principles of inheritance or not ? Moreover do you perceive that there maybe a difference in what Mendel's law and principles ? also is the principle of unit character a repetition of the principle of paired factor or are they separate for they all seem to be overlapping to me

Answering your 3 questions in order. 1) Sure, they relate to inheritence. It is a human decision to call them one way or the other then. 2) The difference between principle and law is a question of philosophy, not biology. 3) No, they are different. Maybe try rereading my answer and if it does not help, you can try to specify what is unclear to you.


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How do humans know what goes on in optical illusions?
Optical illusions are designed to deceive humans, I think.

That thing is moving! It really is! It's moving!
However, user Konrad Rudolph just told me what went on in a different optical illusions through a comment on a separate answer. I believe he is a human, as stack exchange has a box you have to tick to prove you're not a robot. Considering Konrad Rudolph is a human, how did he know what was happening?
Loads of people have told me 'what's happening in the illusion' but I just can't see it. How does everyone know?

How can people know what is going on in an optical illusion?

Or maybe... You're all robots?

We know what's going on in optical illusions because we have a great deal of knowledge about how sight and visual perception work. That should be pretty obvious. I really don't understand what your question is.

Furthermore, if you look at the actual pixels in that image or just a small segment it is clear that it isn't actually moving. And a person created that image, and it is a still image.

Of course it's not moving. It's merely a bunch of pixels. Please refine the question and get rid of the robot fluff.

"Optical Illusions" or sometimes referred to as "Geometrical Illusions" aren't illusions in the sense that we are seeing something that isn't there. It's an illusion in the sense that the interpretation of what is there is wrong.
Typically this involves seeing movement where there is none as in the picture you provided. A scientific way of describing them could be:

When subjects are instructed to carry out a task to which the visual system is not adapted.[1]

Which in layman's terms means our brains cannot handle the way the information is being presented to us. It is presented in such a way that our brains force us to interpret something that is not happening physically, even though what we see is actually present.
Interestingly this doesn't just happen with optics but audio as well. [2] This gives credence to us being able to detect what is actually going on versus what is being interpreted as going on by our brains. As noted in the study:

Listeners were presented with a sequence of sinusoidal tones, each tone 250 msec in duration and with no gap between adjacent tones. All tones were either 400 or 800 Hz, and these frequencies were presented in strict alternation. This sequence of alternating tones presented at equal amplitude to both ears simultaneously for 20 sec. However, when one ear received 800 Hz, the other received 400 Hz and vice versa.

It's important to note that this study found that no listeners interpreted the stimulus properly. We know this because the researchers only used 400Hz & 800Hz frequencies and controlled exactly which ear was receiving it. People either heard something that was not there or something contradictory to what was being played. This shows we can measure what actually happened in the illusions since we created it and are able to quantify it.
This can similarly be done with your image.
1) A human created that image thus we can create a similar image and know exactly if we created a moving image or not, then compare to what people interpret to see if illusions occur.
2) You can track any pixel on that image using software to see if it moves and compare to what subjects interpret.
There are also other interesting studies such as the optical illusion of a baseball being in motion. [3] This is particularly useful as this can be described with physics which can tell us what is actually going on versus what we are thinking is going on.
Another interesting study is that autism may change the way the brain interprets optical illusions. [4] Leading more to the idea that our brains are flat out wrong about what is happening because even though the information has not changed it has been interpreted differently. Sometimes resulting it people being less susceptible to an illusion.
The answer to "How does everyone know?" is that people can know because we can use tested methods of interpreting data correctly and observe the difference between that and what our brains alone interpret. Our brains are evolved for specific types of environments and sensory illusions are things that are often too unfamiliar to our brains to deal with properly.


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What are the floating translucent little objects called in the field of view?
Sometimes we see these small translucent shapes moving by when the eyes are open. When the eyes are moved they seem to follow that movement, but with a certain delay, as if they are floating in a thick viscous liquid. What is this phenomenon called?

First of all microorganisms are not visible to naked eyes. Secondly it is not clear what you mean by 'organism like structure'? The question is very likely to get closed as unclear. Please add some more information.

BTW, floaters as mentioned below are typically more prevalent for the nearsighted. The floaters are sometimes indicators of problems, sometimes not. You should consult an eye doctor.

This was never disclosed to me.  I didn't know this would happen as I grew older.  I want my money or my years back!

"Oh squiggly line in my eye..."

I think you are talking about floaters (a.k.a. eye floaters or flying flies). You may want to have a look at this english.SE post in case you were not talking about floaters.

Floaters are deposits of various size, shape, consistency, refractive index, and motility within the eye's vitreous humour, which is normally transparent.

You can read the wikipedia article to better understand the causes. These floaters are typically not microorganisms unlike you seem to think. Their scientific name is 'Muscae volitantes' and they are mostly caused due to degenerative changes in vitreous humour due to aging.

Are you referring to the "worms or strings/dots swimming on the eye/vision"-phenomenon?
These are also called "eye floaters" and quite common. According to IFLscience: http://www.iflscience.com/health-and-medicine/what-those-strange-things-you-see-floating-your-eye/ they are usually harmless, but may of course cause visual annoyance.
I was unable to quickly find a scientific source, but hope this helps.
If this was not what you were talking about, I misunderstood.
Regards

What you might be referring to are white blood cells in your retina as described here: https://en.wikipedia.org/wiki/Blue_field_entoptic_phenomenon

The blue field entoptic phenomenon [...] is the appearance of tiny bright dots [...] moving quickly along squiggly lines in the visual field, especially when looking into bright blue light such as the sky. The dots are short-lived, visible for a second or less, and traveling short distances along seemingly random, curvy paths.

The rapid, random movement does not match the description in the question.

What you are likely seeing are tiny shadows cast upon the retina from strands of protein (and other debris) in the vitreous humor. They are indeed harmless and do correlate with age.
However, any which obscures your vision should be investigated as blood may have leaked into the eye.
Reference Floaters

Please add some references to your answer.


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Designing primers with restriction sites
I want to design a forward and reverse primer that include overhangs with restriction sites, with the dna used for restriction enzyme cloning.
If I want to send my dna to a synthesis company should I include the attached overhang with the restriction sites to the dna? Does it matter if the primers have the overhang of the dna within their sequence ?
From the sequence right at the end what bp sequence would be recommended I use for my primers if I want approx. 20-25bp for the primer?
See below for cDNA sequence:
Nde1 cut site: 5' ... CA|TATG ... '3'
Xho1 cut site: 3'...GAGCT|C...5'
cDNA with overhangs that have restriction sites, Ndel1 (5'->3') and Xho1 (3'->5')
5' catatg - ATGGGTTCAAACACTTCCAAAGTGGGTGCTGGTGCAGAAAAACAACAAGTCTATACTCCG
CTAACACAGATCGATTTTTCACAGTCTTTGGTTTCTCAATTGGATTCATCGAAGGAATCA
GACTATGTCACCAAGCAAAATGCAGAAAAGTTCATTGAGAAGAAGGTTTCACAAAGGCTA
TCTAACCTAGAAGTTGAAACGTTAAAGAAGTTTGAAGATACTTTGAACAATTCACTATTA
TCAGACGACGACAAGGATGCCGTTGATGGAATATCATCAAGTTCATTGAATAATCAAATC
GAGTCGTTGAACAAGAAACTAACATTATTTGATCAATTAGAGTTACAAAAGTTGGAGAAA
TATGGGGGTGCCAAAGGTAAATCTGATAAAAAAACCGACAACGGCAGCATTTCTATAAAG
GCAAAATTGACTGAGTGTCTTTTGGCCAATAAGGGCAAGCCATTGAATTGTTACGAAGAG
ATGGAAGAATTCAAGAAGCTCGTTATGGGTTGA - gagctc 3'

I've added an answer, but I don't fully understand what you mean when you say: >"From the sequence right at the end what bp sequence would be recommended I use for my primers if I want approx. 20-25bp for the primer?"
Are you asking us what sequence you should use for the reverse primer?

Yes I was just wanting to get an idea for the primer sequence, or essentially if I could just start (i.e including entire overhang) the primer right at the start of the overhang

Your priming sequence should be the reverse complement of the last ~20bp of the coding sequence. Add the restriction site at the 5' end of this, then your overhang after that. All in all your primer will be 20+6+3= 29 bp

Yes.
If you intend to subclone the fragment via classical restriction enzyme cloning you need the overhang.
Different restriction enzymes require different lengths of overhang to allow them to sit fully on the strand and then cleave the sequence.
NEB has a great page detailing how many bases are needed for the enzymes they sell:
https://www.neb.com/tools-and-resources/usage-guidelines/cleavage-close-to-the-end-of-dna-fragments

No, it doesnt matter if the overhang appears elsewhere in the DNA, just so long as your restriction sites don't (obviously).
Here are some considerations I use when designing primers for PCR (though not wholly applicable if you're just having it synthesised):

Use the 3+ basepairs present the given number of nucleotides in your restriction site away in the sequence you're PCRing from as your overhang sequence to allow a few more bases to bind. I.e
With the following primer:
Overhang - Restriction Site - Priming sequence
AAA-GGATCC-ATGACATGCAGTAGC     PRIMER
|||        |||||||||||||||
TTT--------TACTGTACGTCATCG     TARGET SEQUENCE
Alternatively, I use those 3 or so basepairs to add or remove GC content and manipulate the Tm if the annealing temperatures of the 2 primers aren't ideally matches

Thanks that makes sense, but if the restriction enzymes I am using cut the overhangs they are also going to leave a few base pairs upstream and downstream of the actual gene, will this cause framing issues or doesn't it matter where the GOI is inserted in a plasmid MCS?

To fix framing you should / could add bases in between the restriction site and the fragment of interest. But as your NdeI ATG is in frame with the start-ATG I don't expect any problems. You could even remove one of those ATGs if you want.

Ok so should I delete TATG from 5' ... CA|TATG ... '3' (Nde1) and C from 3'...GAGCT|C...5' (Xho1)? If I add bases wont that just create blunt ends?

The only concern I have is the space the leftover base pairs creates upstream, not really sure if this will affect translation

The overhang will disappear when you digest with the restriction enzymes. the only sequence that will persist is the restriction sites that allow seamless incorporation in to your vector.
The extra bases of the restriction sites can't be translated as they will be before your start codon, and after the stop codon.
If this doesn't make sense to you I'd suggest reading up on the basics of cloning in Sambrook et al or another good textbook.

The bases will make a difference if you want to clone something in-frame with a tag / fusion protein or something like that. Also changing the space between the RBS and the start codon might alter expression a bit.


text:
What is the name of classification of water, air and soil?
The definition of living organisms is all types of organisms are capable of some degree of response to stimuli, reproduction, growth, development and homeostasis.
Non-living organisms are inanimate and have stopped displaying capabilities for growth, reproduction, respiration, metabolism and movement. So what do you call air, water, and soil.
plus I am writing an assignment about environment protection. So  I am talking about how certain chemical affects the air, water(sea, and river) and soil.
So how do I classify this three thing, making them be very specific, other than non-living things, as this group is too broad.

Air, water, and the non-living components of soil, along with rock, sand, etc. are all part of the environment. They don't have a specific class or name. Of course, living organisms are part of the environment or ecosystem as well. I don't understand what your question is asking.

In ecology, non-living components can be grouped under the term abiotic factors or abiotic components. This includes water, air, light, soil, temperature, and many other qualities that describe the organism's surroundings. These are in contrast to biotic factors, which can include predators, prey, and competitors.
Abiotic Component- Wikipedia

Gas, liquid & solid are three classes in to which the majority of the matter - as generally understood - in air, water & soil would be included in.
Gases, liquids, and solids are only 3 of a multitude of possible states of matter. They are the 3 states that we are most familiar with in normal life. Air, water and soil are not broad categories of non-living matter, but is each just a mixture of matter (unless you mean pure water).
If by air you mean the gas mixture of our environment then it is a particular mixture of gases including nitrogen, oxygen, carbon dioxide, and others - or if you mean "the air outside" then it would include solids like small particles of, say, leaf debris or car-tyre rubber.
The matter that makes up living and non-living things is exactly the same and is categorised by chemists and particle physicists.
Living things are unique in the way that matter is caught up in a self-reproducing and entropy-offsetting complex system, which have evolved in to the elaborate systems of the living cell.
If by non-living organisms you mean "dead organisms" which once lived, then these can be thought of as the matter which was left when the dynamic process of life that animated the matter ceased or moved on. Simplistically, life is analogous to an eddy (or 'whirlpool') in a stream of water. Water molecules enter and exit the eddy, just like atoms enter and exit our bodies. If the currents change and the eddy disappears, the water where the eddy was still remains.
Of course the stream carries the water away quickly, rather than it sitting there as a dead organism for some time as the ecosystem recycles its matter.


text:
changing DNA of an organism
is it possible at least theoretically to change the DNA of an organism ?
so we take for example an organism with multiple cells then we change its DNA without killing this organism
to correct genetic defects or to improve it

See this.

Yes, it is possible, but you have to engineer the totipotent stem cell that forms all the other cells in the organism's body. There is no way to alter the DNA of every single cell in a human or mouse, for example, after they have begun developing.

Erm. Sort of. Kind of depends on your definition. It hasn't been done for multicellular organisms though.
Craig Venter et al did this exact experiment a few years ago with a completely synthetic Mycoplasma genome.
http://www.jcvi.org/cms/press/press-releases/full-text/article/first-minimal-synthetic-bacterial-cell-designed-and-constructed-by-scientists-at-venter-institute-an/
If you just want to change small segments of DNA that's where cloning and gene therapy come in, and we do that A LOT.


text:
Minor Allele Frequency (MAF) higher than 0.5?
I have a set of data in PLINK format (*.bed, *.bim and *.fam files).  There are around 2000 individuals in my dataset.
I used PLINK to calculate allele frequencies in the population:
p-link --bfile data --freq

However, in the produced results file, many SNPs have a MAF over 0.5 (up to 0.82).  Would that not then make that the major allele frequency, as the other allele would have a frequency of 0.18?

can you add some more info about PLINK format and background info for the question so other users not as familiar can follow?

You should post an example section from your data file that reports MAF>0.5.

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text:
Confusion regarding Lindeman's law
I came across Lindeman's 10% law at school. It states that 10% of the total energy entering a trophic level is available for transfer to the next trophic level.
I was reading Ecology: Principles and Applications
By J. L. Chapman, M. J. Reiss and they mentioned two contradictory statements:

The 10% law, i.e. the trophic efficiency is always 10%
The trophic efficiency increases with trophic level (which was substantiated by data).

This is the statistics:

What is right? Is Lindeman's 10% law actually valid?

Lindeman's "law" is not a true "law" like the laws of thermodynamics, it's more of a catchphrase for a concept.
The true, valid concept from Lindeman is that "lots of energy is typically lost as you go to the next trophic level, especially at early stages...but there might be exceptions." This is characteristic of most of the "laws" of biology: there is always a lot of flexibility and leeway in biology.
The data in the chart you provide support this generalized version of the law: namely, most of the energy is lost at each trophic level, and a rough average or rule-of-thumb is that it's about 10%.
The usefulness of the 10% number is that it presents a nice benchmark: when you look at these data, you should notice and remark on the relatively high 22.3% level for secondary consumers on the Cedar Bog Lake: you should wonder "what features of this ecosystem or these consumers mark the relatively high energy transfer here?" Without the "10% law" you wouldn't know which numbers should stand out and which are unremarkable.


text:
What is the most-stable gene identifier?
I've struggled in the past with designing data(bases) around gene-identifiers that evolve over time.  For example, UniProt and Ensembl change their identifiers for certain proteins/genes and the IDs go stale after a while (years).  HGNC seems possibly better for this?  What I'd like is to have a single unique identifier for each human gene that will remain stable for many years.  I know genes get re-classified occasionally, but you shouldn't end-up with a new identifier for the same locus.
Suggestions?
Thanks

We use HGNC. But there's certainly no guarantee the symbol will stay the same for years.

Maintaining IDs consistency is a common problem. I've never seen any reasonable solutions for it and don't believe that there are any. However, there are a few shortcuts.

You can create an extra table with aliases for later renamings and refer them to original ids. Pros - it is flexible. Cons - maintaining is exhausting and you need to figure a way to explain to users why they input one id and receive other.
The solution is pretty obvious - if you'd like to have "a single unique identifier for each human gene that will remain stable for many years" you can just take a snapshot of current state of any database you like and don't touch it for many years. You can release version-specific releases of your database and specify versions of reference database you use. E.g. "Glioblastoma_drug_perturbation_2016_(GRCh38_ENS87)".


text:
How do chameleons signal cells to change color?
I have read about how they can change color, but is there literature about the chemical signaling process they use to do so?  I read that it could be some combination of hormones and neurotransmitters, but I couldn't find specific information on the receptors or chemical mechanisms.

As said by @dblyons, there has not been a lot of research (biochemical) on chameleons. So, the exact part of mechanism that you're looking for is still not understood. However, we have recently caught the broad end of the stick. Chameleons don't have special cells for color, their complete skin has a layer of pigments (dermal iridophores) which helps them in changing color. See this (or this) article:

Chameleon skin has a superficial layer which contains pigments, and under the layer are cells with guanine crystals. Chameleons change color by changing the space between the guanine crystals, which changes the wavelength of light reflected off the crystals which changes the color of the skin.

These guanine crystals are actually like colorless mirrors, but by changing the distance between these crystals, wavelength of light absorbed (and reflected) can be changed. It is quite similar to how the color of ozone changes from pale blue in gas to violet-black in solid form. However, how chameleons trigger this change in distance of crystals, is not yet known.
This is how these crystal lattice works:
sourcesource
This is what a guanine crystal looks like ((a) is guanine):

You can also see a nice real-time video of guanine crystals changing color of chameleon here.
The color changing portion of skin has 3 main layers:

superficial s-iridophores which help in changing color in visible region rapdily.
deep d-iridophores which reflect light in infrared refion and are thought to provide thermal protection to chameleon.
layer of melanin which is actually yellow in color, making chameleons naturally yellow(!) in color. When the guanine crystals come closer, they reflect the blue portion of visible spectrum. This blue light, along with the natural yellow color of melanin, becomes green which gives green color to chameleon. So, the actual color visible to us is a combination of color reflected by guanine crystal and yellow color of melanin.

As I said already, the exact biochemical signalling process behind this process is not known yet. It could be complex hormonal or neurotransmitter signals. However, hormones are considered as the main triggers because chameleons have been shown to change color due to changes in mood instead of environmental protection.

Cephalopods such as the octopus have complex chromatophore organs controlled by muscles to achieve this, whereas vertebrates such as chameleons generate a similar effect by cell signalling. Such signals can be hormones or neurotransmitters and may be initiated by changes in mood, temperature, stress or visible changes in the local environment.

the thing i didn't like about the chameleon wiki was that they cited a national geographic article... no primary source

@dblyons I have added another citation in the first paragraph which has (quite) plenty of references. Please let me know if it helps.

it doesn't.  the original citation is this paper: http://www.nature.com/articles/ncomms7368

@dblyons This nature article has also been cited in the reference I added. Along with it are many other citations including some books too.

This is a good question and... kind of remarkable because I don't think there is a specific body of literature regarding chameleons.
Generally though, vertebrate skin cells responsible for color (these cells are called chromatophores and arise from the neural crest during development) are responsive to the hormones melatonin, MSH, and others.  These hormones, which are released from the pineal (melatonin) or pituitary (MSH), bind GPCRs on the surface of the chromatophores which elicit intracellular activation of PKA, for instance.  This activity can cause mobilization of pigment within the cells.  This article about fish coloration may help guide you somewhat in your studies, but chameleons in particular seem like an understudied clade of color-changing animals!


text:
What is this raptor on a building in California?
So I took this picture of a bird that was sitting just outside my workplace a few weeks ago:

At first I searched the internet for raptors in California and found the Cooper's hawk. It looked so much like this bird so I thought that must be it and left it at that. However I just recently came across this bird and also this recent hawk identification question and they both look very similar to my bird as well. So I realized I don't know what to look for when trying to identify this bird.
Does anyone know what this raptor could be?
If it helps, the specific location was the city of Tustin in Orange County, California (Southern California). It is about 10 miles from the coast.

where in California?

@VanceLAlbaugh Southern California. Near the coast and part of the Greater Los Angeles Area.

It is a Red-shouldered Hawk (Buteo lineatus).

Its breeding range spans eastern North America and along the coast of California and northern to northeastern-central Mexico.

Identifying features:

Presence of dark wings with white spots.
Presence of dark-brownish head, orangish-brown chest.


text:
Chimera in bacteria
Would you please define me the chimera in bacteria? Some sequences are clustered as a chimera table in metagenomics analysis, I know OTU table is used for clustering bacteria based on 16S rRNA, but I cannot find out the chimera? What is the difference between chimera and OTU table exactly?


text:
Are there neuron mediated reactions faster than reflexes?
I'm interested in how fast the human body can respond to a stimulus.  I know the fastest reflex, the blink reflex, operates around 100ms from stimulus to reaction.  I also know that the blink reflex is known as the fastest reflex in the human body.  My interest is in the fastest responses to stimuli I can find in the body.
Are there any faster responses to stimuli within the human body which use neurons but are not categorized as a reflex (due to some technicality), meaning they could be faster than the fastest reflex?  To the best of my understanding a reflex is defined by the use of neurons to convey the information, I'm just wondering if there are any grey areas which don't qualify as a reflex but may be faster.  I don't want to potentially write off an entire class of neurological behavior in my research simply because I stopped at the blink reflex.

I think the vestibulo-ocular reflex is the fastest. It typically operates in 7-15 milliseconds.

A reflex as fast as the blink in a neural circuit:
I would consider suppression of outer hair cells in the cochlea to be a reflex; the faster component of this reflex is about the same as the blink reflex, around 100 ms. The hair cells themselves aren't considered neurons, but the pathway that suppresses their motility certainly is.
A much much faster non-neuronal "reflex":
That said, the outer hair cells themselves also dance along quite fast in response to sensory input, even faster than the typical hearing range for humans, faster than 20kHz! In some ways, this is a reflex because you are taking sensory (specifically, auditory) information and turning it into a motor response, but all the "action" is taking place within one cell, and it isn't a neuron.
A more classical reflex that is substantially faster than 100 ms
Reflexes in the periphery can be much faster than 100 ms. The myotatic reflex, or stretch reflex, can be as fast as 30 ms in the knee - this is the reflex that is tested when a physician smacks you on the knee with a hammer (used as a test of spinal and peripheral nerve function, not as a punishment). It's likely there are other stretch reflexes that are faster just because distances to the spinal cord are shorter, but these might be more difficult to test (in this paper they report latencies as fast as 20 ms).
Eyeblink reflexes can also be faster than 100 ms!
For example, see this paper: strong auditory stimuli evoked blinks within about 20ms!
tl;dr: I'd check your source that 100 ms is the fastest reflex! I stuck with mostly human examples here (some of the hair cell work is in other mammals), but you will find even faster reflexes if you look at smaller organisms, such as insects.

I was thinking of human reflexes when I wrote the question, so your examples are spot on!  I've edited the question to add "human" to the wording, but that shouldn't invalidate anything in your answer.  Thanks for the answer!

@CortAmmon No worries, you did indeed have "human" elsewhere in the body of your question, but I certainly prefer it from biological, evolutionary, and philosophical perspectives when people refer to "the human body" rather than "the body" - as if all bodies are human or that the human is the archetype or exemplar animal, so thank you for the edit!

In a paper studying Rhesus macaques, Huterer and Cullen showed that latency of the vestibulo-ocular reflex (measured from head movement to eye muscle contraction) can be as little as 5 milliseconds1.
Reference:
1: Huterer, M., & Cullen, K. E. (2002). Vestibuloocular reflex dynamics during high-frequency and high-acceleration rotations of the head on body in rhesus monkey. Journal of neurophysiology, 88(1), 13-28.

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text:
How is the rate of gluconeogenesis controlled in the cell?
As far as I am aware, all steps in glycolysis are readily reversible except the phosphorylation of glucose, the phosphorylation of fructose6 phosphate, and the phosphorylation of phosphoenolpyruvate to pyruvate. I understand how control of the rate of glycolysis can be achieved through allosteric means (for example glucose 6 phosphate inhibiting hexokinase in muscle cells, phosphofructokinase being under allosteric control of the ATP/AMP ratio in muscle or hormonal control via glucagon in liver), however how is the rate of gluconeogenesis controlled compared with glycolysis? When a cell has a high rate of glycolysis, then as the rate of forwards reaction increases the concentration of substrate for each gluconeogenesis reaction also increases. Thus there must be some way to shut off the gluconeogenesis enzymes.
I would be grateful if someone could explain how the relative rates of glycolysis and gluconeogenesis are controlled, and perhaps if this varies according to the cell type (muscle/liver cells etc).
I was also wondering whether every cell is capable of gluconeogenesis. I was considering putting this on a separate post so that there is only one question per post, but I thought that it is quite a short question so it may be better to put it here.

Read the location paragraph of https://en.m.wikipedia.org/wiki/Gluconeogenesis

which cells are you talking about - hepatocytes?

@VanceLAlbaugh having researched the link provided and seeing that gluconeogenesis does not occur in the muscle cells, then yes; my interest is mainly in hepatocytes as this is where most gluconeogenesis takes place.

Regarding "there must be a way to shut off these enzymes". Enzymes are not entities that are pushing molecules through the pathway in one direction, they're facilitating a faster equilibrium. If you put a non-reversible sink at the end of the pathway it will go in that direction.

In mammals gluconeogenesis occurs primarily in the liver (together with the kidney to a much smaller extent). When the blood glucose concentration falls, it is the role of the liver to generate glucose for other tissues that are dependent upon it.
Hormones play a key role in this. If one considers the decrease in blood glucose concentration during starvation, this is signalled by a decrease in the concentration of insulin and an increases in the concentration of glucagon. These have differentials effect on the uptake of glucose by different tissues, depending on whether they have receptors for the hormones and the consequences within the tissues, and mass action effects of metabolites will certainly influence whether glycolysis or gluconeogenesis occurs in liver.
However, you are correct in your concern that there must be a way to prevent the futile cycling of intermediates through the different reactions of the three steps that differ between glycolysis and gluconeogenesis. The short answer to how this is accomplished is that the concentrations of various metabolic intermediates change during starvation/feeding, and that these intermediates are allosteric regulators of the reactions, switching one off and the other on. This is described in the section on Regulation of Gluconeogenesis, in Berg et al. (available on-line), from which I reproduce the  diagram below (Fig. 16.30).

Although this diagram illustrates the principle, a few words of caution about the detail are in order. First, the edition of the book this comes from is 15 years old. Second, it is not clear that all the regulatory molecules are effective in liver — some of the work may relate to bacteria. Third, much of the evidence is from studies with purified enzymes. Although it can be shown that an enzyme can be regulated by a particular effector in these conditions, it is different matter to establish that this occurs in a particular physiological condition. Thus, you will need to consult more recent and specialized sources if you are interested in particular details.


text:
Excluding the Exon, What Does the Rest of the Genome Do?
The exon is the portion of the genome that encodes protein synthesis, if I understand correctly.
But, this exon is apparently less than 5% of the genome.
So, what does the rest of the genome do?

that's the trillion-dollar question

The exome represents about 1.5% of the human genome, not 5%

A few percent codes for RNA, like microRNA, long non coding RNA, shRNA ect. These RNA while not translated into protein do have a function.
Some RNA are ribozymes, catalytically active in their own right, but they do work with proteins. An example of such complex is the ribosome, where the catalytic peptidyl transferase activity that links amino acids together is performed by the ribosomal RNA
https://en.wikipedia.org/wiki/Ribosome
Then there are miRNA, that control gene expression by RNA mediated silencing.
https://en.wikipedia.org/wiki/RNA_silencing
Then there lncRNA... these long RNA can regulate gene activity by binding to transcription factors. So a cell can maintain a high concentration of transcription factor in an inactive state that can rapidly go into use once a signal is received. This is rather recent discovery.
About 45% of the human genome is composed of what is essentially viral parasites. While some of these viral genomes are full functional and encode endogenous viruses (this is why there is come concern about xeno tissue transplant). Most of these viral parasites have degraded somewhat, having accumulated mutations that either render unable to leave the cell, but still able to replicate and multiple in the genome (we call them transposable elements), or are completely inactive (repeat elements).
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4124830/
Examples are
Alu element make up 10.7% of the human genome. It is rather old parasite... youngest expansion is about 30 million years old. Mostly inactive, although some Alu elements are still active.
https://en.wikipedia.org/wiki/Alu_element
Line repeats. ~17% of the human genome.
Some DNA is structural. The centromeric repeat array which may be several Mb long per chromosome (exact length is unknown due to variation between people and difficulty to clone and maintain for analysis). Here the DNA serves as a pad over which the kinetochore forms. This DNA tend to be transcriptionally quiet, few if any genes.
And there are pseudo genes... genes that are no longer active due to mutations.


text:
Besides X. morgani praedicta, are there any species whose existence was predicted before they were discovered?
The orchid A. sesquipedale has a spur so long that at the time of its discovery, no insect was known that could pollinate it.
This led Charles Darwin to predict the existence of an undiscovered moth based on the idea that the moth and the orchid had co-evolved. That moth, X. morgani praedicta, was subsequently discovered in 1903 – a triumph for early evolutionary biology.
Has it ever happened again that a species was predicted to exist before being discovered?

I'd imagine there would be numerous examples of this. One species I can think of is Monocercomonoides sp., before the discovery of which we didn't know any examples of eukaryotes that had completely lost their mitochondria, or the derived forms of these organelles, such as hydrogenosomes and mitosomes. A prediction wasn't necessarily coined by any particular person like in your example, although there might be some papers somewhere that make such a prediction, I'm sure many people hypothesised that it was probably possible for eukaryotes to completely lose mitochondria if their iron-sulfur cluster biogenesis pathway was replaced by a cytosolic system that could fulfil the same role but we didn't know of any that had.

See paper: http://dx.doi.org/10.1016/j.cub.2016.03.053


text:
How migration creates Linkage Disquilibrium
I want to know how admixture and migration creates linkage disequilibrium? I am reading about it but I really don't quite get it.

Imagine one population is fixed for A1 at locus A and for B1 at locus B. Here is a representation
--- A1 --- B1 ---

Another population is fixed for A2 at locus A and for B2 at locus B. Here is a representation
--- A2 --- B2 ---

Further imagine that the recombination rate between loci A and B is 0 $(r=0)$. Any migration rate will cause some individuals --- A1 --- B1 --- to be present in a --- A2 --- B2 --- population (and/or vice-versa). So linkage disequilibrium is complete.
If the recombination rate is in between 0 and 0.5, then there will be some level of linkage disequilibrium at equilibrium that can be calculated for a specific demography (incl. migration rate).

Thank you :) I just have one more question. When you say that A1 is fixed at locus A and B1 at locus B, does that mean that A1 and B1 are in linkage disequilibrium too?

Linkage disequilibrium is defined for a pair of loci, not for a pair of alleles. It is defined as $D=p_{ab} - p_ap_b$ (see wiki). I think the misunderstanding you may have has more to do with the definition of linkage disequilibrium than about the effect of migration and recombination on linkage disequilibrium.  Without migration, each population in the above example is at linkage equilibrium (because there is no variance), while the overall metapopulation is at complete linkage disequilibrium.