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Reference to hypothesis about breast sexual attractiveness?
Some time ago there was a hypothesis published,suggesting evolution made breasts mimic buttocks for either primitive men being attracted to women when they started to walk on two legs, or to discourage sexual intercourse from behind for other reasons I can’t remember. I can find many posts about this online, but I can’t find any reference to the original idea. Can anyone provide information about this?

Do breast ressemble buttocks so much?! You can use google scholar for example to search for papers. Among the first results I got there are Furnham and Viren 2007 and Anderson 1988. Note by the way that you are confounding the term theory with hypothesis.

What is the difference between theory and hypothesis? arent they both unconfirmed?

@Remi.b those researchs you linked are interesting, but they arent the one I'm looking for. The one I'm looking for states the opposite to the second one.

In science, a theory is a set of hypotheses that are highly supported by many evidences (e.g. theory of gravity, theory of evolution, ...). The definitions of these terms are up the the field of philosophy of science but we have one post on Biology.SE that explain them brielfy (here).

I know it is not exactly what you were looking for that's why I posted it as a comment rather than an answer.

We use a different meaning for theory in my country. In the universities I attend, in subjects like research methodology or philosophy of science, theories are unconfirmed or unvalidated statements, which might have support, but not conclusive evidence. I dont think we are the only ones who uses the term this way, because I've seen the term being used in this way amongst american  Psychologists for example. What is different to a hypothesis or a theory is a scientific law. I didnt mean theory as a synonymous of scientific law, if that's what you understood from what I wrote

I have modified your question, improving the English and scientific statement. If I have changed your meaning please say. I am still not sure this is on-topic. It is not really a question about science — you just want a reference. However I will leave others to decide on that.

A scientific law differs from a scientific theory. A law does not attempt to explain a natural phenomena, they just posits a causality relationship (e.g. law of thermodynamic) while a theory attempts to explain a natural phenomena (e.g. theory of gravity). A hypothesis is a guess about nature (e.g. the hygiene hypothesis). Anyway, it is not the place to discuss this. Just have a look at any intro course to philosophy of science or philosophy of knowledge (or even just wikipedia) or ask questions on Philosophy.SE. Note that the term theory is often misused in the popular culture.

and what do big and red lips look like? why do men and women have equally large big lips? your theories are only components of a larger image, and in a concensus of all theories on breast shape, that theory is only one dimension of it.

Eventually, I found it, here it is:

In considering the human animal, zoologists proposed that the human
  female is the only primate that possesses permanent, full-form breasts
  when not pregnant. Other mammal females develop full breasts only when
  pregnant. The zoologist Desmond Morris proposed that the rounded shape
  of a woman's breasts evolved as frontal, secondary sex characteristic
  that is a sexual-attraction counterpart to the buttocks, and so
  encouraged frontal copulation, the reason being that while other
  primates mate by means of the rear-entry position, the upright,
  bipedal human being was likelier to successfully copulate face to face
  in the missionary position.

https://www.reddit.com/r/askscience/comments/uflgy/why_are_breasts_so_attractive_after_all_theyre/

Pan paniscus (bonobo) also copulates face-to-face.

I said I was looking for a hypothesis which refered to that. That's the hypothesis I was looking for, I didnt say the hypothesis was confirmed or denied as being "right" or "wrong".


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Is Sda a protein, or is it a protein domain of DnaA?
I initially thought that a domain was a specific part of a protein, with it given tertiary structure, to which a given molecule is able to bind. (I think I recall phrases such as "the haem binding domain of protein X..." being used in lectures?)
Having consulted Wikipedia on protein domains, I see the definition is a bit more subtle:

A protein domain is a conserved part of a given protein sequence and (tertiary) structure that can evolve, function, and exist independently of the rest of the protein chain. Each domain forms a compact three-dimensional structure and often can be independently stable and folded.

I can understand this, however the reason why I started questioning what a 'domain' actually refers to was because if it's use in reference to Sda in control of endosporulation of bacteria. In my lecture notes, it is stated that "KinA is bound and destabilised by Sda, a DnaA target,"
From this I was under the impression that Sda is a protein (although to the best of my knowledge DnaA only binds DNA, so I do not know why Sda would be target of DnaA. Anyhow,) on the other hand Wikipedia states "the protein domain Sda is short for suppressor of dnaA or otherwise known as sporulation inhibitor A.", which seems to me to suggest that Sda is a part of DnaA whose modifications allow DnaA suppression?
Also, on Wikipedia, it is later written "Sda protein domain is a checkpoint which prevents the formation of spores." How can a protein, if Sda is one, be a checkpoint?
On the other hand my lecture notes later talk about the regulation of Sda levels, so it again is referred to as a separate protein!
I would very much appreciate if someone could explain what 'domain' means in this context.

There is nothing in the idea of a domain that requires it to bind a particular molecule. The definition in Wikipedia sounds reasonable enough — domain doesn't mean anything else in a protein context. So I am unclear what your question is. Are you asking us to clarify the use of this word in a text to which you don't give a reference and may be poorly written and use words loosely? Surely not. Or are you asking us to explain a scientific description of a DNA-binding system in sporulation? If so you need to present it more clearly with references and do a little more research yourself.

Short answer
Wikipedia has unnecessarily made an already confusing situation much worse. Sda is its own protein, it is regulated by DnaA, and it prevents sporulation.
Full answer
I don't think your misunderstanding is based on the meaning of 'domain' - the definition you give sounds quite reasonable - but rather the use of the term domain with respect to Sda and the naming of Sda itself, which I agree is quite confusing and made much worse by Wikipedia in this case.
Sda is a protein that inhibits KinA activity (Burkholder et al., 2001) and is a completely separate protein from DnaA. I don't see where you jumped from your notes to the idea that Sda is a domain of DnaA except for from Wikipedia: I don't know why Wikipedia thinks Sda is a protein domain, it is a protein. It is a very small protein, so perhaps it would be appropriate to think of it all as one domain, but there is not a single result for "Sda protein domain" on Google Scholar - no one else is using this terminology. A full Google search only returns a few (~150) results, most of which are direct copies/translations from Wikipedia, or Wikipedia is a direct copy of them. Wikipedia can be useful, but if it starts to cause you confusion, don't assume it is correct.
The phrasing "KinA is bound and destabilised by Sda, a DnaA target" means that Sda binds KinA and destabilizes it, and notes that Sda is a target of DnaA; since DnaA is a transcription factor, you can infer that this means that DnaA controls expression of Sda in some way.
In biology a checkpoint just refers to a place that a process can be halted/arrested, often in reference to the cell cycle. Sda is considered a checkpoint because when Sda is expressed, it prevents cells from sporulating by indirectly preventing activation of Spo0A (Burkholder et al., 2001).
Another source of confusion is that the name "suppressor of dnaA" on Wikipedia is WRONG, but further, molecular biologists sometimes have an impenetrable way of naming things, owing to the complexity of control of gene expression and the circuitous way that new proteins are identified and understood.
The correct name for sda is "suppressor of dnaA1". dnaA1 is NOT DnaA - dnaA1 is a MUTANT ALLELE of DnaA that results in cells that are completely unable to sporulate. But! sda is also NOT Sda: sda is a MUTANT ALLELE that produces non-functional Sda (the protein).
I'll quote from the title of the table in Burkholder et al:

sda Mutations Suppress the Sporulation Defect of dnaA1 Mutants

Or, stated again, in dnaA1 mutants, there is a defect in DnaA which prevents sporulation. The researchers searched for mutations that would reverse this effect. They found one, and named it sda, because it reverses (suppresses) the effect of the mutation they were studying. The dnaA1 mutant's effects on sporulation seem to be caused by an increased expression of Sda, which is why the sda mutant reverses the effect.
References

Burkholder, W. F., Kurtser, I., & Grossman, A. D. (2001). Replication initiation proteins regulate a developmental checkpoint in Bacillus subtilis. Cell, 104(2), 269-279.

+1 at least for this: molecular biologists sometimes have an impenetrable way of naming things, though the whole answer was great.

@canadianer Seriously, I mean come on.

Ha! That was the exact example I was thinking of as I typed that comment.

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Could a 3D Printed Plant Seed be Possible with Existing Technology?
The first genetically cloned animal was Dolly the sheep. As I understand it, this was possible because all that was needed was an embryo containing the cloned genetic material and a womb for that embryo to grow in. Would the same process also work to clone a plant?
I assume that the problem with embryonic cloning techniques and plants stems (forgive the pun) from the need to implant it into a host seed without destroying its ability to germinate. I haven't found a reference that claims this has been attempted... If anyone knows of a study related to this, I would love to read it.
Given my assumption I tried to imagine another way to achieve this goal which lead me here, to pose my question to the brilliant minds of this community:

Is it possible to implant a cloned plant embryo into a synthetic 3d printed seed that would germinate with existing technology.

I know we have successfully 3D printed living tissue using state of the are equipment like the 3d Bioplotter. If you guys don't think it is currently possible then what technological advances would need to be made to achieve this goal.
Note: The answer to my question is relevant to a number of possible applications. A hypothetical "Seed Printer" could be used in a future manned mission to Mars. Due to the logistics of shipping supplies to mars, it could be more practical (cost effective) to ship the raw material needed for printing seeds than it would to send actual seeds.
Edit*: Thanks for the comments, I feel a little foolish for not knowing about artificial seed coats prior to posting this question. In light of new information, I would like to additionally ask:

What are the current limitations of creating artificial seed coats that could possibly be enhanced with the application of 3d printing technology.

Welcome to Biology.SE! As long as you have a cloned plant embryo, an artificial seed coat would certainly work (this is quite common, but not in 3D printing). Yet, the question is very likely to get opinion-based answers.

Thank you! The hardest part of learning about a new subject is knowing what to research. I had seen the phrase "Artificial Seed Coat" but it was never used in a context that indicated that it was exactly what I was looking for.

Hint: look for plant tissue culture and you'll most likely get what you want ;)

Also note that the chances of all the raw materials, plus power supply and assorted hardware for the printer being easier to carry than <1g seeds seem very low.

You make an excellent point! I am more concerned with the effects of ionizing radiation on the seeds and the weight of the technology and materials needed to properly protect them during shipment. You may be right however and it would be more feasible simply to ship the seeds.

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Advantages and disadvantages of sporulation compared with competence in bacteria?
Why do bacteria have both of these mechanisms to deal with the same environmental stress: nutrient deprivation? In a culture exposed to this condition, often both competent cells and sporulated cells are found.

Sporulation is a process that is very hard reverse. While it is a good as last resort, trying to find a solution (Competence) might be a faster way to resist the stress. Lets say antibiotics were introduced into medium. Part of population might sporulate when detecting malignant conditions but part of population might search for plasmid with resistance genes. In other words, these two mechanisms are independent so we can increase fitness by applying both.


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How are viruses in vaccines weakened in a laboratory
I would like to know how viruses in vaccines are weakened or attenuated in a laboratory

Welcome to Bio.SE! Can You share what efforts you have done in finding the answer. Low-research effort questions are likely to be closed.

Short answer: You take viruses from humans and grow them in a different organism until it no longer elicits pathogenicity to human, through generations adapting to a different organism. Typically chicken embryos.

You can remove either the genetic material of the virus, or its functional proteins and then inject it.


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Which kind of caterpillar is this?
Which caterpillar is this? It was found in mid Europe during this time (April). Size about 2cm in length.

That ain't a caterpillar buddy. Thats a millipede.

Caterpillars have six true legs, and only six. That thing looks like it has two pairs of legs per segment, so... like @PrittBalagopal said.

I see. Any idea which kind of millipede it is? I know that there are more than one kind -- but maybe some "popular" one.

"in mid Europe" seems a big vague for me, some more details like country, city and natural habitat would be a bit more helpful.

Actually it's Germany

Based on the body structure and double pair of legs per body segment, this is a millipede.
Based on the small size and spacing between body segments, it could possibly be in the Paradoxosomatidae family. You could check by examining the specimen more closely:

Most species possess a groove or furrow ("sulcus") on the dorsal surface between the keels (paranota) on each segment.

Although the color is wrong, this millipede reminds me of the somewhat-cosmopolitan invasive, the Green house millipede (Oxidus gracilis), which is about 1.8 to 2.3 mm long.

 Source: NCSU Plant Disease and Insect Clinic; Credit: Matt Bertone
Due to the color difference, I cannot tell definitively whether this is your species or not. Your poor picture quality makes this more difficult. However, I thought I'd provide this post for you as a jumping off point. good luck!

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Are there examples of animals that live in groups, where all have the same role?
For animals that live in groups, are there examples where all of them have the same role? For example, in animals we know there are bee queens or alpha, beta and omega mammals. But are there groups of animals where all the members have the same role? My question is aimed at 2 different groups actually, first animals in general (which includes reptiles, insects, etc.) and second to mammals only.

Since you mention alpha/beta/omega, it's worth noting that with wolves, that organization only shows up in captivity.  In the wild, a wolf pack is simply a breeding pair and their offspring.

Yes, there are many examples. Those species are said to be gregarious. See below for examples.
Level of sociality
When it comes to social behaviour, it is common to categorize species into one of four categories: Solitary, gregarious, presocial, and eusocial.
Note that definitions may vary among authors and that there are limit cases that make the question of categorizing much richer than the simple definitions I am using below.
Solitary
Solitary species are species where individuals mainly live alone and are independent of each other (They may still meet to mate, though).
Examples: fox, polar bear
Gregarious
Gregarious species are species that gather into a group but do not share any labour. Each individual is selfish. Such gregarious behaviour can be driven by safety (typically during migration), to taxis toward a resource, or any other reason that may cause these individuals to gather!
Note, when you say "have the same role," it is clear that different individuals may use different life strategies (like typically territorial males vs. sneaker males in birds).
Examples: wildbeest (during migration), many insects attracted to a given lightsource.
Presocial
Presocial species are species that are gregarious and have a separation of labour but no separation of the the reproductive labour.
Examples: Humans, many hymenopterans, vampire bats
Eusocial
Eusocial species are species that have a separation of labour including separation of the reproductive labour.
Examples: Termites, ants, naked mole-rat

Does Gregarious include species who gather in groups and share the same labours ? That's what I'm more interested to know. Like for example, all hunt for the group, all gather for the group, or all dig for the group, etc.

Gregarious species do not share labours. It means that they all do the same thing (that is doing their best to survive and reproduce) although they may use different strategy (like being territorial vs a sneaker in birds).

Creatures that 'flock' or 'school' ['shoal'] benefit from shared awareness and their movements can confuse predators.

Insects attracted to a light source is rather an awkward example, as this is no social behaviour they benefit from. On the contrary, many die.

What about migrating birds (e.g. geese, crane that fly in groups) or wintering groups such as Starling or Tits.

@RHA that's the point of gregarious animals. As long as they father, whatever the reason is, they are called gregarious. At least it is my understanding. The example was given to me a number of years ago by a prof. during my bachelor  degree but his definition might differ from what is being used in the literature.


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What is the name of this plant I found in a park?
I found this on Garret Mountain in Paterson, New Jersey, USA. Does anybody know the name of this plant?

@Always_Confused For a good botanist, most species can be identified even without flowers. If this would have been a North-European species, I'd probably be able to tell you what it was.

Today i saw them also in dover, nj usa. The enviroment is swamp area. Same in paterson park. Their sizes are around 30 cm, 40cm. Actually i see them all over the new jersey. I did not realize any flower.

related: this answer containing the image

I think this is Lysichiton americanus,  skunk cabbage. It has these large, rolled-up leaves and grows in wet habitats as you describe. In Europe, it is an invasive species, but in America it is native. I am not 100% sure, because I don't know if there are any similar species in the US.
EDIT
As Anongoodnurse pointed out, I was right to be unsure. This is Eastern skunk cabbage, Symplocarpus foetides. This species occurs in the Eastern parts of the USA.

I found that also they call skunk cabbage.

@RHA wow a command for strikeout.


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Recycling and storage of nitrogen from breakdown of macromolecules?
If nitrogen is so important (it's a constituent of both proteins and nucleic acids), why are animals still throwing them out, and needing to eat it again? Is it true that in almost a billion years of evolution, life still haven't found a way to recycle nitrogen inside the cells or inside the body of multi-cellular organisms? Why does this seem so hard to achieve? Or are there animals that don't need to excrete nitrogen compounds (like ammonia, urea and uric acid), and instead reuse them?

Ammonia, urea, and uric acid are toxic to the body; why would we want to keep them around? Asking why didn't "x" evolve to happen when what actually has happened is working fairly to extremely well is fairly pointless.

Also the necessary nitrogen-containing compounds seem to be in more than adequate supply in the diet, so that eating enough calories, proteins, &c provides more than enough nitrogen.  What to do with the excess, except excrete it?

@anongoodnurse yes they are toxic, but they are created as a by-product. Why not recycle them back into protein and nucleic acids? Then there would be no toxic residuals asking to be excreted.

@jamesqf we store fat and glycogen for energy, but we must eat nitrogen to replace what was excreted. I guess we could pass more time without eating if we were able to recycle nitrogen. This could be an advantage in lots of animal groups, but as far as I know, all animal groups have nitrogen excretion mechanisms. This makes me think nitrogen recycling is somehow very hard for animals to do. The question is: why?

@tomd - Yes, and in nature (before all this population) we used to return that fixed nitrogen to plants which could use them (whereas we can't). Benefits all around. I have two dogs who have not yet learned to use the toilet. You should see my back yard...

@tomd - Chill, man...

@Rodrigo: I admit I'm no expert, but what I do know about physiology suggests that you are utterly wrong.  First, because we don't use nitrogen, we use nitrogen-containing compounds, mostly proteins.  (Simplistically) in digestion these are broken down into amino acids, which are either used to build/repair tissue, or are further broken down for energy.  End products of this process are fats & glycogen, which are stored, and various nitrogen-containing waste products, which are excreted.  Bottom line is that there's an excess of nitrogen in the diet.

I have reworded the title to remove any implication of volition in evolution. I think it important always to say an organism or a pathway has evoved or not.

It would be helpful if you could mention the biochemical pathway — absent from multicellular organisms — by which unicellular organisms recycle nitrogen (as implied in your title).

@jamesqf By nitrogen I mean any molecule containing it, which we convert in the forms useful to us (or any other organism, by the way). And I tend to agree with you, the answer probably lies in that there's an excess of nitrogen in any animal diet.

@David Thanks for the edit. The title is much better now. About unicellular organisms, I was actually thinking about the nitrogen assimilation process that happens mostly (only?) in plants. Confused it with the nitrogen fixation process...

Possible duplicate of Why do some bad traits evolve, and good ones don't?

@BryanKrause I edit the title of the question, because it's more specific than that.

The premise of the question is incorrect. Mammalian organisms do recycle nitrogen. They only excrete excess nitrogen.
Ammonia from deamination of amino acids can be incorporated into glutamate and glutamine:

Transamination can then transfer the amino group from glutamate, for example, to other ketoacids for the synthesis of other amino acids.

The capacity for recycling nitrogen is presumably determined by requirement. If there is excess to requirement, then there is no evolutionary advantage in retaining the excess and instead a mechanism has evolved to neutralize it and then excrete it.
Addendum: Recycling, yes, but why not also storage?
Although nitrogen from the degradation of amino acids is recycled, the excess is excreted, rather than stored in some form. Why has no storage form (analogous to glycogen or triglyceride) evolved? I will consider this from two inter-related  viewpoints.

Yes, nitrogen is important for the proteins required for growth and maintenance of organisms, but the effects of depravation are only seen in the long-term. Carbon is of more immediate importance, i.e. the supply of carbohydrates to provide energy. Indeed, in extreme starvation of mammals metabolism treats muscle protein as expendable, breaking it down for the carbon skeleton of the amino acids. Thus, the selective advantage the evolution of a nitrogen storage system might give to an organism is not so clear.
If there were a nitrogen storage system one needs to consider what form it might take. Obviously not as ammonia, because of its toxicity, but it could be condensed into a neutral form. However a small metabolite, such as glutamate (above), would disrupt the metabolic balance, and a dedicated small molecule such as urea would be excluded because of the effect on osmosis and general water balance. So we are thinking of a macromolecule — a conventional  protein like ovalbumin (which may, in fact, be a storage protein), or some special ‘new’ branched protein. The trouble with this method of storing nitrogen is that involves tying up large amounts of carbon — a price, as I argued in 1, that the organism cannot afford to pay.

I wonder who downvoted that and why?

@Rodrigo — Don't worry. I don't any more.  I actually plan to add some ideas on why the excess nitrogen is excreted rather than stored, which I hope will improve the answer further.

Well, it will be great if you do that, because it's really interesting.

You might want to add that this process does not offer a way of long-term storage of nitrogen and is only for immediate usage of released ammonia due to side effects of its products and requirement of substrates in other metabolic activities. See my answer.

@another'Homosapien' — I didn’t wish to get into a discussion about your answer, but "ammonia is too toxic to be stored" seems to me a red herring. The toxicity of ammonia is only relevant if it is not recycled because it is surplus. Then, if it cannot be released into the environment (as in fish) it has to be converted to a neutral form until it is excreted in the urine. Your reproduction of the urea cycle deflects the reader such as me from the valid points in your answer.

@another'Homosapien' — Not that I can think of at the moment. Busy week ahead and am away at the weekend, so low profile until next week.

Short answer: This is because the most common form of nitrogen found in multicellular organisms (not incorporated into any other compound) i.e. ammonia is too toxic to be stored or recycled.
Background: Ammonia, the product of deamination of amino acids, is basic in nature ($NH_3~+~H_2O \rightarrow NH_4OH \rightleftharpoons NH_4^+ + OH^-$) and thus disturbs intracellular pH (Ohmori et al, 1986). Though the mechanisms through which ammonia exerts its toxic effects are not known, hyperammonemia is known to alter several amino acid pathways and neurotransmitter systems, cerebral energy metabolism, nitric oxide synthesis, oxidative stress and signal transduction pathways, leading to irreversible damage to the developing central nervous system: cortical atrophy, ventricular enlargement and demyelination; causing cognitive impairment, seizures and cerebral palsy (Braissant et al, 2013).
Talking about how it is produced (just for information, skip this part if you are aware of urea cycle): Amino acids are deaminated for storage since the carbon skeleton of these amino acids can be easily converted to glucose or fatty acids for storage. This reaction yields ammonia which, in liver, is converted to urea (via urea cycle) which is not only less toxic, but also requires lesser water for excretion. See this page for more information and the diagram below.

Talking about why it is not recycled, there has always been a constant supply of amino acids to organisms (through nitrogen fixation or food). Indeed, amino acids are deaminated for storage i.e. we already have more than enough of it. Also, storing urea is also not easy since it is toxic too (it is just less toxic than ammonia). And since these products are so much harmful, it seems difficult for an organism to evolve itself so that it can store toxins rather than just throwing it away so that it can later be ingested in a useful form (amino acids from plants or herbivores). Finally, evolution works as decent with modification, meaning if something is a better alternative of current situation, it is not necessary that organisms will evolve towards that (unless there is strong selection pressure for it). In short, evolving to recycle nitrogen is (most likely) just not worth it.
P.S. you might be interested in this question to know more about evolution. Another answer here talks about storing excess nitrogen by adding ammonia into amino acids, yielding glutamate and glutamine. However, this process can be used only to a limited extent due to limited amount of substrate ($\alpha$-keto glutaric acid and glutamate) in the body. Also, excess glutamine in the body can have many major and minor side effects like skin rash, vomiting, etc. (see here for full list). Also, excess glutamate has much more pronounced effects. Since glutamate is a neurotransmitter, its excess causes cellular damage. This is what makes it an excitotoxin (see this for more details). Apart from this, the substrate ($\alpha$-keto glutaric acid) is an intermediate of Krebs cycle and is important in many other cellular activities (see here for details). So, its deficiency (caused due to conversion into glutamate) can easily affect many crucial metabolic activities. Thus, though this process seems an effective way of recycling nitrogen, it has many side-effects and is not much reliable i.e. can only be seen as an immediate solution. This is why when glutamate and glutamine build up in body, they are converted back to $\alpha$-keto glutaric acid and glutamate and the ammonia released via urea cycle.

Thank you! I know how evolution works, just thought that, in the huge variability of animal kingdom, there might be some animal able to recycle nitrogen. I disagree that it seems difficult for an organism to evolve itself so that it can store toxins. What about all the venom stored in snakes, wasps, scorpions, spiders, rays...?

@rodrigo venoms are specific to some special proteins (see this), and their effect can thus be prevented by storing them in structures lacking those proteins. Since ammonia disrupts as basic cellular properties as pH, it doesn't seem easy to store it inside a cell/tissue/organ. Yet, there might be organisms who can do so, about whom we don't know yet...

@Rodrigo: But for animals, the problem is not storing nitrogen, but getting rid of the excess.  It's rather like asking why we haven't evolved to store carbon dioxide :-)

@another'Homosapien' Right. But we can convert ammonia into urea and store urea (or uric acid, for the animals who use that). Maybe we could convert urea (or uric acid) back into a form of nitrogen that we could use to build more proteins, instead of throwing it out. But it seems there's really an excess of nitrogen in animal diets.

@Rodrigo, if you want to go in that direction, you might ask why we don't just store it in the form of protein (the same way we store fat). I guess you could argue that muscles are in fact big stores of protein :)

@VictorChubukov Very nice. But muscles require one to eat more to keep them (since they use lots of energy), so this is kind of problematic, isn't it?

@Rodrigo Converting urea and nitrogen back into protein or storing it would take calories, quite a bit since they are in low energy states.  More calories than just digesting more nitrogen in an available form which is happening anyway to get calories for everything else. Most biological process come down to a cost/benefit question, there is a solid cost and no substantial benefit since organisms are taking in protein whenever they eat anything.


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Does the cactus wren use a call to elicit insect prey movement and detection?
I will be referring primarily to a 2013 paper, If a bird flies in the forest, does an insect hear it?, and my own investigation. Bird flight sound frequencies overlap with the hearing range of most tympanate insects. There are several insects that possess hearing for which the function is not known and it is hypothesized that this capacity is used to avoid predation. For example, silent butterflies and grasshoppers have broadband audio sensitivity and some calling insects appear to have hearing tuned outside of the call frequency.
I have observed cactus wrens (Campylorhynchus brunneicapillus) foraging for insects on the ground outside my window (southwest desert, USA) and have noted that they invariably emit a characteristic odd periodic call while they are so engaged. You can hear my recording of one such hunting wren made April 18, 2017 here. Cactus wren foraging call
I used the open source audio processing application, Audacity, to analyze the wren call I recorded. Here is a spectrogram of the call:
.
You will note that the call is periodic at about 7 Hz. For comparison, typical pulsed bird wing sounds (the sound of bird wings as they are hovering or approaching prey) are around 18 Hz frequency. Those wing sounds are broadband bursts though, approximately 49 kHz +/- 18 kHz. I mention this because the cited paper and many others looking at bird sounds and insect hearing have explored primarily the hypothesis that it is the flight sound the insects are detecting. My own idea is that some bird species actually generate sounds within such a range in order to provoke prey insects into fleeing from hiding or a stationary position.
Typical moth and butterfly audio frequency response is given here:

(reproduced from the work cited earlier).
The cactus wren call may be seen to exhibit energy in the 1.6kHz - 2.20kHz range primarily, peaking at 1954 Hz (spectrographic analysis of exactly that portion not shown). This seems interesting given that Cyphoderris crickets call at 12 kHz, but their ears are most sensitive to 2 kHz (almost exactly the wren burst frequency peak).
I could not find research examining my hypothesis and thought I would ask the question here, i.e., is there research examining the possibility that certain bird species use calls to enhance detection of prey insects (and the related question, does this seem likely given what others may know about the subject of insect hearing, its range and uses, bird predation behavior, etc.)?


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Is DNA replication a serial or parallel process?
This video entertainingly supplements this 3d animation of DNA strand replication. Does this process happen serially from the beginning to the end of a DNA strand (like having to unzip a six foot long zipper - example A below) or does the strand get chopped up into chunks, unzipped individually, replicated then brought back together (example B)?

I suspect the answer is case A. If so, is any phase of replication done in a parallel fashion? I would think something has to be (since it happens so fast and serial anything is typically very slow in comparison).

The DNA isn't cleaved, but replication can be initiated at multiple points on a chromosome and proceed in both directions. I'll elaborate on this later and post an answer in the future if no one else has. This paper estimates that there are 10,000 to 100,000 replication origins in a human cell. This means that the average leading strand would be approximately 60,000 to 600,000 bp long.

It's like having a zipper with multiple "pulls" along its length.

My personal opinion is that videos of this type and 3D animations are scientific poison. OK, for popularising science, but not a useful source of serious information. Rather than speculation, however intelligent, I suggest you consult text books that have been carefully written by experts, professionally illustrated, and edited by other experts. You can get access to older editions of some of these on NCBI Bookshelf: https://www.ncbi.nlm.nih.gov/books/. If you search there for DNA replication you will find clear and comprehensive accounts to answer your question.

@canadianer, you're picture is perfect! That's the answer!

@David, thank you for the link. I'd like to add that popularizing science is good for science (which is antithetical to poison). Science without much interest or support doesn't get very far

Short hint: Yes while cell cycle in eukaryotic cell (many pieces of nuclear-DNA, each with many origin-of-replications) there are signaling/regulation mechanisms that ensures within a certain time period all-the nuclear DNA copies multiplied only upto certain times (ideally doubled) and chromatid numbers doesn't show anomaly. However exceptions are there... such as prokaryotes' plasmid DNA replication does not necessarily conforms with that of their nucleoid DNA... that is why plasmids replication called as semi-autonomous.

Your zipper-model in incomplete; because it shows a situation where origin of replication is at one terminus of linear DNA. That is atypical. Usually origins are found at inner portion(s), that cause replication bubble (containing 2 replication fork face to face). It is like a zipper track with 2-zipper opening from the same point. However this misinterpretation is very common among school-students.

@David Agree; ultramodern teaching-aids like powerpoints, animations, e-readers etc. are being mishandled too-much. They becomes useful only after I get the concept through 'backdated' slow method of boardwork, printed textbooks, notebook, paper and pencil. However the website tells it is "advanced" level; so it is not the basics lesson.

@canadianer Your link can't be accessed. Browser warns "the page is not working".

@AlwaysConfused Which one? They both work for me.

I think I made a mistake with my math. Should be 30,000 to 300,000?

@canadianer http://www.biomedicinaonline.com.br/2015/09/replicacao-do-dna.html

@AlwaysConfused I didn't post that… and I can access it fine.

@canadianer eh sorry it was pinged to you by zelusp. Maybe mistake due to i slept less for last few nights. Thanks however the link is not working from here (screenshot) ; may be the site works within definite countries.


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What is the name of this tiny creature?
Place: South India,
Metropolitan, Year: 2017; Night Time.
Size: 1-2 cm (Very Tiny)

Looks like a moth.

It's 'Indian skipper'. Family :Hesperiidae.
Source: http://abeautiful-butterflys.blogspot.in/2010/04/hesperiidae-butterflies-of-india.html

This is not a skipper. Skippers are bigger, have a different shaped body and a different wing pattern, as can be seen from your picture.

From the posture, it looks like it can belong to Geometridae (Larentiinae). But I haven't been able to find a species that has that particular color.

Definitely a moth; possible families are Pyralidae, Crambidae, or Thyrididae (Window-Winged Moths); the first two listed (Snout Moths) are less likely and would be eliminated if a photograph showing the front of the head were available and it turned out that the palps were not elongate and projecting.

Arthur, I've noticed you've provided a handful of species ID answers lately. All of your answers are short, lack references/support, lack photos, and typically don't try to identify beyond the family level. These answers will all likely get downvoted as they do not represent the effort or specificity that are typically expected on this site (and desired by the asker). Please start expanding upon your answers or simply providing your posts as comments instead. See here for a guide to writing good answers on this site. Thanks!


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What is the name of this green plant with fat leaves with green color fruits?
Location: South India,Metropolitan
Year: 2017

It look like Almond tree, but small doubt not sure.

Looks like Terminalia catappa. Could you provide close-up of its fruits? Also; does the plant shed red leaves at late-autumn to winter?


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How much current various kind of body tissues can tolerate without any serious damage?
Human body can tolerate some amount of current. How much current (and duration) various kind of body tissues can tolerate without any serious damage?

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

@another 'Homo sapien' I hope you're not asking him to electrocute someone are you?

@PrittBalagopal haha of course I don't mean a practical ;)

Regarding this, if the O.P has access to organs from a hospital or any source (preferably a rejected one for grafts), the O.P could do an experiment to find out. I invite @wgc to answer his own question after doing some research. It would be great for us to learn new stuff (not for electrocuting people of course).


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In the process of oogenesis, when the egg completes meiosis 2, what actually happens?
oogenesis is the process of egg formation in females.
The process of formation of the ovum is as follows

oogonium
primary oocyte
secondary oocyte
ovum

The meaning of question is not clear to me. "oogenesis is the process of egg formation in femalesformation of the ovum The process is as follows". If you are asking "formation of the ovum The process is as follows" then none of your options is a "process". All the options are either a structure or a stage.

Welcome to biology SE. Please take helps from tour, help centre, ask, don't ask and formatting. Before asking homework questions, visit the homework policy

Inside oogenesis it wouldn't be sperm. It would be ovum.

Though the original question is terribly unclear;  seemingly the question wanted to  mean "what should be the correct time-order of the following structures in the process of oogenesis in human?".

Fig-Human oogenesis.  Source: *
Oogonium(in zoology), is a diploid cell (female gametogonium), that gradually gives rise to primary oocyte
In case of human oogenesis, this primary oocyte (diploid) get divided into 2 cells through meiosis-1 ... a (1) secondary oocyte and a (2) first-polar-body.
(In human) After that, meiosis-2 take place; where the secondary oocyte give rise to 2 haploid cell: an (1) Ovum and a (2) secondary polar body. In other hand; the first polar body also due to meiosis-2 division, gives 2 haploid cells (both are secondary polar body).
So the order would be
Oogonium(1)-->Primary oocyte (2)--> secondary oocyte (3)--> ovum (4) if they meant the temporal order of these structures.
Reference:

1: * Advanced BIOLOGY: Principles and Application; by C.J. Clegg and D.G. MacKean; John Murray publishing; copyright 1994.


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Probabilities of mutations in telomeres?
Frankly I am a programmer, I've been looking at sites like NCBI and others, but couldn't find what I was looking for so if someone can help:
Can you give me the probabilities of

mutations in Saccharomyces Cerevisiae's telomeres.
Probability of having an insertion
Probability of having a deletion.
Probability of having a substitution.

The reason I need this is that I want to generate true-telomeric data based on, the telomere structure consensus.


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Consensus sequence for selection of initiation codon in eukaryotes
In bacteria the AUG (or other) codon at which translation of mRNA is initiated is preceded at a precise distance by a sequence known as the Shine and Dalgarno sequence, to which the 30S subunit initiation complex binds through base pairing of the 16S rRNA.
In eukaryotes, in contrast, the 40S initiation complex normally binds to the 5′-cap of the mRNA and scans until it reaches the appropriate AUG codon — usually the first. Marilyn Kozak, who originally proposed this model in 1978, updated it later to try to account for the approximately 10% of eukaryotic initiations that do not occur at the first AUG. She identified a consensus sequence surrounding initiating AUGs and suggested that this was important in their selection. (see Wikipedia article entitled Kozak Consensus Sequence).
What is the current status of this consensus sequence now that so much more sequence and transcript data are available? Is there any evidence as to how it might function, e.g. by interaction with 18S rRNA in a similar manner to the Shine and Dalgarno sequence?

What research have you done into this topic? You mention a Kozak sequence, but this is not a meaningful term or one in general use. Try searching for Kozak Model and you should find the answer to your own question. If not, repost explaining your problem.

@David, thanks for you comment. I was referring to Kozak consensus sequence, is this term still ambiguous? I saw many publications, characterising the Kozak consensus or highlighting its significance, but none providing a mechanism for its action. If you could refer me to any such paper, that would be very helpful.

I don't want to answer your question in a comment, and I suspect that this question may actually be a duplicate of another on this general topic, so I have rewritten it to illustrate how to formulate a question providing basic evidence of research. This is required, not only to prevent laziness on the part of posters, but to allow others interested to check the basis of the question. (In this case, for example, I might take issue with the second Wikipedia article.) I will withdraw my close vote and leave others to decide whether it is a duplicate of another question.


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Please identify this moth from Bangladesh
Sorry for bad resolution of the picture. This picture is taken from JU campus, Savar.

I think I have found the identification. It is a planthopper from ricaniidae family. Most likely Ricanula stigmatica.

Image source: https://en.m.wikipedia.org/wiki/Ricanula_stigmatica


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Protein in fruits
Why do fruits have such a low protein content (with a few exceptions) ? Don't seeds need protein while growing up? In comparison, the egg of a hen contains lots of protein, used to make a chick.

Do plants need proteins in high quantity like animals?

I think this premise of this question may be wrong.  As @jamesq points out in his answer, the sugar in fruits are generally not used by the seed, but consumed by animals.  The relevant comparison is between seeds and animal eggs, and I don't think it's true that eggs generally contain more protein than seeds.  A sesame seed for example has more protein (per weight) than a chicken egg (see https://ndb.nal.usda.gov/ndb/search/list ).

@Roland, You should make this an answer, the question is based on a misunderstanding so correcting is a good answer.

It is don't have time to document this enough to make it a good answer but it's too long for a comment so I'll post it anyway.
A big difference between plants and animals is how they get their food, that implies they have different elements to work with. Proteins are made of amino acids, which contain nitrogen, meaning to make proteins you need lots of nitrogen. Plants get their energy from converting CO2 to carbohydrates; this is a plentiful source of carbon, but they can't get nitrogen that way. There are two ways of getting nitrogen: from the ground, and from converting atmospheric nitrogen to organic nitrogen, a process so energy-intensive that only bacteria evolved the ability to do it and only some plants use those bacteria (basically feeding them some of their hard-won carbohydrates "in exchange for" the organic nitrogen compounds).
Animals on the other hand get their food from plants, which contain all the carbon they might need and contain much higher concentrations of nitrogen than you find in the ground (the plant basically went to a lot of trouble to get all that nitrogen from a large volume of ground into its comparatively small body, or to convert atmospheric nitrogen into organic, useable nitrogen), or from animals which contain even higher concentrations of nitrogen. Note by the way that some herbivorous animals are limited by lack of nitrogen as well; I'm thinking of pollinating insects which can struggle to live off of sugary nectar alone and also need to eat some of the protein-rich pollen even though that's much less advantageous from the point of view of the plant (sugar being very easy to make for the plant but proteins much less so).
Obviously animals who eat other animals don't need to worry about nitrogen intake much at all, other than making sure they get food in general, because the animals they're eating will contain pretty much the same carbon:nitrogen ratio they themselves contain.
tl;dr: the egg contains more proteins than the seed because the chicken that made the egg ate a whole lot of seeds, and all the protein in those seeds ended up concentrated in that one egg.
EDIT: running into this much later I realized I missed a pretty vital half of the question, because there is a difference between fruits and seeds. The difference is the following: nitrogen is precious for plants so they'll try and use it for very important things. Seeds are very important to the plant, so while a seed has less protein than an egg it will still have lots of protein by plant standards. Fruits now, that's another story. Like the sugary nectar, fruits are a bribe for animals, a bit of food offered to them so that they'll spread the plant's seeds. And like with the sugary nectar, the plant has every incentive to pack that bribe full of cheap carbohydrates and as few precious proteins as it can manage.

many seeds contain more protein by weight than an egg, eggs are just bigger than most seeds.

Oh dear. I might need to actually document this answer, at this point I can't exactly pretend "I don't have time" do I

If we look at just the fruits people generally eat, the fruit part is seldom (if ever) needed for the seed(s) contained within the fruit to sprout.  Rather than the fruit being nutrition for the seed, it seems to be more of a lure.  Fruit-eating creatures  eat the tasty fruit and so disperse the seeds, perhaps contributing a packet of nitrogen-rich fertilizer.  The plant thus has an evolutionary incentive to make the fruits inexpensive to produce yet tasty, so lots of sugars, few proteins.
You can compare this with flowers that produce nectar to attract pollinators.

In brief the lower protein content of a seed compared to an egg is caused by two reasons.
(1) The structural components of a plant versus that of an animal.
The structural components of plant is made by cellulose which is made of glucose subunits. Animal in contrast are have large amount of muscle tissue to allow movement and much of animal is held together by collagen and keritine. All these components are different types of protein which are build from amino acid sub-units.
Hence to build a seedling you need glucose. To build a chick you need amino acids.
(2) Metabolism. A plant can build all amino acids that it needs from glucose and fixed nitrogen source. Animals in contrast are not as self sufficient. Some amino acids cannot be synthesized and must be obtained from an external source.
Hence a seed need not carry much or as varied quantity of amino acids. In fact this metabolic completeness has been used as an anti herbivore defense mechanism. Many seeds are severally deficient in one or more amino acids. Any animal that feeds solely on just one type of a seed would experience malnutrition.
An egg however has to carry more amino acids, especially the essential amino acids that it cannot synthesis from other amino acids.


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Can human perception differentiate between monochromatic and polychromatic light?
Maybe monochromatic is not the right word, what I mean is light consisting of a single wavelength (i.e. a spectral color) versus light composed of photons of multiple wavelengths (intermediate color).
For example, suppose we had a single, violet "laser" and a set of "lasers" combining into a purple color.*
Is it possible to combine the latter light sources such that their composite would perfectly match the violet one such that both look the same to a human eye (assuming perfect alignment)?
And would they look the same to all human eyes?
My guess is a no, because people might have different susceptibility to red and blue hues, and their aggregation functions may differ as well.
* Apparently, there are alternative definitions to distinguish the two colors (purple is reddish, violet bluish), but I am referring to the ones found in Wikipedia: Purple being an intermediate color and violet being a pure spectral color.
Interesting article on color perception in the animal kingdom:
https://arstechnica.com/science/2020/06/experiments-show-hummingbirds-see-colors-youve-never-dreamed-of/

The short answer is no. Because of metamerism, the human vision system cannot distinguish monochromatic light from the infinitely many metameric equivalents that elicit an identical tristimulus response as that of the monochromic light.

There might be nonlinearities in the photoreceptor, and chromatic aberrations of the lens (optics) that might allow a well trained eye to discriminate using tricks...(just a guess, hence not an answer)

Err... You're presumably reading this on a computer display, no?  Which produces colors by combining essentially monochromatic red, green, and blue pixels.  So can you see differences?

@jamesqf well, people can perceive flickering on computer displays, even on LCDs with temporal dithering, as I do, and there may be reasons why people distinguish between purple and violet, even leading to different names for the "same" perceived color. And if you look closely at an RGB display, you can see red, green and blue dots. Also, some people are tetrachromats and can see differences in skin tones where trichromats cannot. Some can even see polarization. Certain purple and violet hues might look the same to some people but different to other people, unless proven otherwise.

@jamesqf also, I don't have proper, comparable monochrome light sources to compare them in any scientifically significant manner, much less people to experiment on.

@Archimedix:  Those red, blue, and green dots are monochromatic, or nearly so, yet combining them produces a multitude of perceived colors.  What I'm suggesting is that you experiment on yourself, and see whether those computer-generated colors look different than "natural" ones.  As for the flicker that some people can see (I'm one, at least on older displays), that's a function of scan lines & refresh rates, nothing to do with color.

@jamesqf I have no polychromatic light sources I could compare to those RGB dots, and I have no monochromatic light that is comparable to a mic of those RGB dots. Regarding flicker, temporal dithering uses different colors one after another to create an "average" color, so yes, in theory, most people should have similar perception (maybe along a Gaussian distribution). However, a prism would be able to make a monochromatic ray of light distinguishable from a ray of polychromatic light, and lenses do have prismatic effects.

@Archimedix: Why not create an image that is say all red - RGB = (255,0,0)?  That should be a pretty good approximation to a monochromatic source, no?  (You could test it with a prism.)  Then compare it to something that is naturally red,

@jamesqf say I compare a red patch on the screen with a piece of red paper of the same size: Both look different to me, of course, but this is because of their different surfaces/textures/hues/brightness/reflection/viewing angle and one consists of pixels where maybe one third is black while the paper is all red. Using a red LED will yield different properties, but the verdict is the same. Too many factors. Does something that looks the same to me look the same to everyone else? Is it because my two test objects are not equal enough, or do different eyes/brains render them differently?

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


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Identification of a caterpillar
My daughter has become one with nature somehow and came across an odd looking caterpillar. The odds of finding one never found before is great,  however I'm unable to find what kind it is. It's head is bright red.
From Eastern North Carolina, USA.

Would anyone be able to point me in the right direction?
Thanks!!!

From eastern North Carolina

This is a tussock moth caterpillar in the Lymantriidae family.
The image is not clear enough for a definitive ID, but it appears you have some species in the genus Orgyia.

Likely, this is a white-marked tussock moth caterpillar (Orgyia leucostigma).

From Auburn University:

The full-grown larva (Photo 2) is around 35 mm long. The head and shield on the segment behind the head are red. There are two long black pencils of hairs on the first segment of the thorax that project forward. A single black hair “pencil” arises from the eighth abdominal segment and projects upward and rearward. The back is mostly black and the sides yellow, cream, or grayish. There is an erect brushlike tuft of white or yellowish hairs on each of the first four abdominal segments, and a conspicuous red dot on segments six and seven.

Range: Entire eastern U.S. and west to Minnesota and Texas. [source].

@Brittany glad i could help :). If you're satisfied with the answer, please "accept it" by clicking the checkmark next to my answer. And don't forget to upvote if you like the answer ;)


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Insect that has evolved to recognize carnivorous plants
Obviously in a biome consisting of high density of carnivorous plants any insect that can recognize these plants or at least recognize organs associated with carnivory will get fitness advantage. So it seems a very natural thing to evolve from insects point of view. Has it happenned? If yes, what are some of the examples? If not, why it hasn't happened?


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What are the consequences of inbreeding?
Inbreeding increases the risk of getting two identical recessive genes, alleles, that cause a disease which wouldn't have been activated with mixed genes. That's how I understand it anyway. But I sometimes read and hear that inbreeding among humans also causes decreased intelligence, especially emotional and social intelligence. Is there any support for such claims, and if so how does that work?

There is indeed evidence that inbreeding in humans lowers intelligence of offspring.

In summary, our comprehensive assessment revealed that parental consanguinity and degree of inbreeding was significantly associated with depression in intellectual behaviors among children. Factors other than inbreeding showed little influence, suggesting that genetic component (i.e., inbreeding) was more influential over these parameters under study. Moreover, the depression in cognitive abilities seems to be more prominent due to increase in the degree of inbreeding (F).

Estimating the Inbreeding Depression on Cognitive Behavior: A Population Based Study of Child Cohort

A thorough literature search resulted in 95 studies. There were 15 studies that provided sufficient data for a meta-analysis. The studies were divided into four categories of inbreeding, showing values of an inbreeding coefficient (f) of .046, .063 (first cousin marriage), .125 (double first cousin marriage), and .25 (incest). The study’s hypothesis of a linear relationship was strongly confirmed. Over four categories, degree of inbreeding correlated highly with average IQ depression, r = .91. The current meta-analysis shows that the most common type of consanguinity, first cousin marriage (f = .063), may lead to a depression of about six IQ points, whereas incest (f = .25), the most severe type of consanguinity may cause a depression of about 28 IQ points.

Is there a linear relationship between inbreeding and mental ability?: A meta-analysis
Another study reaches a similar conclusion:

This result is interpreted in light of cultural feedback theory, whereby it is suggested that consanguinity could subtly influence IQ at larger scales as a result of small IQ handicaps bought about through inbreeding being amplified into much larger differences through their effect on factors that maximize IQ such as access to education and adequate nutrition.

About the mechanism behind the IQ decline caused by inbreeding:

The study of Morton (1978) study revealed that the offspring of
  first-cousins had over a five times higher risk of mental retardation when compared to controls. The study concluded that declines in IQ and the increase of mental retardation are consistent with rare recessive alleles associated
  with around 325 loci, whose likelihood of being transmitted into offspring increases with the relatedness of the parents.

Inbreeding depression and IQ in a study of 72 countries

Do you have any clue as to how such a complicated or subtle effect can be caused genetically, microbiologically?

If you want more information about the genetic effects behind iq depression caused by inbreeding read the answer by @AlexDeLarge below. He describes the mechanisms very well.

You are right. Inbreeding strongly increases overall homozygosity which subjects inbred individuals to diseases caused by rare recessive alleles. In non-inbred individuals the chance is quite low to receive those because many deleterious variants (and in fact, most segregating alleles we can observe) are recessive. Most often, but depending on the dominance coefficient, these 'hide' in healthy heterozygous carriers and when very closely related individuals breed (with a lot of variants that are identical by descent) there is a high chance that some of the 'hidden' deleterious variants are passed to the offspring.
You have to be aware that there are in fact two conceptually different processes that can be both be referred to as inbreeding but are also somewhat continuously linked (see below):

Mating systems that allow offspring between actually related individuals (measured by the degree of relatedness), what in humans often is referred to as incest or consanguinity.
Populations with very low effective population size $N_e$ generally exhibit higher relatedness due to lack of genetic diversity (excess of homozygous sites). Therefore, populations with low $N_e$ are referred to as inbred even if no actually related individuals are mating.

There is some evidence that inbreeding in the first sense is linked to cognitive abilities in humans:

Bashi (1977) investigated the effect of offspring having first-cousin (i.e. between children of siblings) and double first-cousin (i.e. between children of siblings and unrelated siblings, sharing as much variants as half-siblings but with more recombination events) parents while (at least somewhat) correcting for socioeconomic effects. He found an inbreeding depression with respect to cognition that could

result either from the general increase in homozygosity [...] or from decrease in performance resulting from homozygosity for specific recessive alleles (highlighted by me). The higher variance of the double cousin group in some of the tests favours the second interpretation.

Woodley (2012) presents evidence for slightly lower IQs caused by inbreeding, however, he also mentions that the effect is way smaller than socioeconomic effects:

Consanguinity could subtly influence IQ at larger scales as a result of small IQ handicaps bought about through inbreeding being amplified into much larger differences through their effect on factors that maximize IQ such as access to education and adequate nutrition.

Fareed and Afzal (2014) investigated verbal IQ, performance IQ, and full-scale IQ and found that all of these IQ parameters are significantly lower in inbred children compared to non-inbred children - actually the difference increases significantly with the degree of relatedness. They conclude that there is

evidence for inbreeding depression on cognitive abilities among children.

Please keep in mind that, for for sociological/ethical reasons, this is highly controversial, especially when the two concepts above are intermixed - human populations underwent differential and variably strong periods of low $N_e$, i.e. were subject to stronger or weaker inbreeding in the second sense. When reading the citation of Bashi (1977) above carefully, you will notice that he takes good care not to intermix those. Inbreeding in the first sense leaves large runs of homozygosity (ROH, blocks without heterozygous sites, i.e. a clustered and local lack of variation) whereas inbreeding in the second sense increases homozygosity in the genome less selectively. Therefore, the distribution of homozygous sites can be used to infer whether inbreeding is recent (first sense) or old (second sense) (see for example McQuillan et al. (2008) - here you see that both concepts form a continuum: where do you set the cutoff between recent and old? what is an appropriate threshold size for ROH? ...). Regardless, Bashi's findings indicate that effects of inbreeding are caused by recent inbreeding as he presents evidence that his results are rather driven by specific deleterious recessive variants than overall excess homozygosity. Finally, even though the study by Fareed and Afzal (2014) shows rather large effects of recent inbreeding in IQ measures, the results from Woodley (2012) show that one needs to be really careful to separate genetic from environmental components as his study suggests that the latter contribute more to the observed decrease in IQ.

Does the depression in cognitive abilities, or the effects of inbreeding in general, cease when having children with a non-related partner, or are there effects that last for generations after inbreeding stops?

@LocalFluff: That's not easy to answer. Usually, intelligence is pretty heritable but also strongly influenced by the environment. On the other hand, outbreeding is also very powerful, so I would expect (and this is based on intuition) that mean intelligence of individuals with recent inbreeding would increase rapidly in the subsequent generations but might still be sightly lower than average for some time, especially if socioeconomic factors (that tend to go along with consanguinity and could have a stronger impact on intelligence than the actual inbreeding) also have a negative effect.

Inbreeding, in nature at large, has one primary effect, as you said. It increases the chances of two copies of harmful, recessive alleles. Consequently, offspring are much more likely to suffer from genetic and/or degenerative diseases.
As for intelligence, some studies have indeed concluded that inbreeding can lead to a lower IQ (see this answer for the exact quotations), it is possible that there are other factors at play. For instance, those from a lower socio-economic background tend to be of lower intelligence, although as with everything there are exceptions. Whilst I have struggled to find a source for this, it is statistically more likely that those of a lower socio-economic background will exhibit poor mental health and/or partake in the act of inbreeding.
Consequently, due to the fact that intelligence is largely heriditary, the offspring of inbreeding will tend to be less intelligent. As a result, it is difficult to determine that there is a causal relationship between these correlating factors.

I would think that poverty and oppression are consequences of low intelligence rather than its cause. Instead of adjusting data for how poverty and oppression affects intelligence, one should maybe check how inbreeding causes poverty and oppression. An economy only consists of specialized humans interacting with each other, so social competence is the most important factor for wealth creation.

In addition to everything mentioned above, it should be noted that inbreeding leads to an increased chance at schizophrenia and bipolar disorder. According to one of the studies called Inbreeding and serious mental illness in the first Spanish Bourbons states that inbreeding leads to a point where a person "accumulates pathogenic alleles", which is what leads to an increase risk of suffering from these particular mental disorders.

"accumulating pathogenic alleles" seems like very loose wording (as explained by other answers, inbreeding doesn't inherently lead to higher mutation rate, fixation rate, or drift - it primarily exposes the phenotypic effect of existing deleterious recessive alleles) - can you provide the link to the study you're referring to?

(article is in Spanish so it's hard for me to follow it .. .Royuela-Rico, A. “[Inbreeding and serious mental illness in the first Spanish Bourbons].” Revista de neurologia 71, no. 2 (July 1, 2020): 61–68. https://doi.org/10.33588/rn.7102.2019508.
)

@BenBolker I can provide another study in English and I am not saying inbreeding inherently causes higher mutation rate in all patients, but the study seems to say that inbreeding may increase the chance of accumulating alleles that could lead to genetic changes in the subjects that raises the chance of developing schizophrenia and bipolar disorder: none of this is absolute, but it seems to boost the probability of something like this happening.

All I was suggesting was (1) it would be good to include the citation information in your answer (e.g. in the format I gave in my comment, and (2) that last statement seems a bit muddled to me (it may be muddled by the original authors, or it may be a translation problem/might make sense in context).  The rest of your answer seems fine to me.

My understanding, NOT based on any study, it purifies the gene 'pool' since mutation derived alleles variation will be lost thru' generations just like we don't have much of our grand grand's 'unique' allele.
This is bad as it happens in farms, when an decease that infects one, could eliminates all the populations, to be exact, barring a few left.
In the ever changing environment as in evolutions, singular gene pool will be hit with extinction even thought it might prosper if and only if the same good old 'environment' persists.  Environment here includes everything in the ecosystems.

Welcome. We ask answers to be backed up by credible sources, and preferably journal papers. Unsubstantiated claims face downvotes and deletion.


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What's so special about Chassaignac tubercle?
1-How does massaging of carotid artery at chassaignac tubercle( anterior tubercle of transverse process of C6 vertebra ) can relieve the symptoms of Supraventricular Tachycardia?
My attempt: I think by massaging carotid artery we are somehow stimulating the satellate ganglion present at level of c7. Or, I think, by massaging the carotid artery we are increasing BP, thereby affecting the baroreceptors and somehow this relieves the symptoms of supraventricular tachycardia.

2-Why can't the same massage be done at level of other cervical vertebrae?

It's not the vertebra that is important, but the carotid artery, and where it is most likely influenced by massage. There are too many interfering structures at C1/2; I believe C3-5 is ~ normal. Some guidelines indicate midpoint between the angle of mandible and the superior border of thyroid cartilage (so about C4-5), others just below the angle of the mandible (C3). C6 seems to be well below the carotid sinus to me. If you can refocus your question (not where and why) and show some research, I'd be happy to answer your question.

@anongoodnurse Unfortunately  I could not find any reason by doing research. All the websites I saw only state the fact but didn't explain and my textbook too.

OK, then I won't post an answer. Sorry I could not help you, but I really prefer to help those who post according to our guidelines when possible.. :(

Is it related to stellate ganglion ? Or it's just because massaging increases BP thereby affecting the baroreceptors??

Please edit your question to reflect the new information. Thanks!

Ok, I'm busy at the moment, but I will answer today. :)

The reason massaging the carotid artery can relieve symptoms of supraventricular tachycardia is because by massaging the artery, as you point our yourself, you artificially increase BP within the carotid artery, this activates a reflex (via the glossopharyngeal nerve) that lowers bloodpressure by reducing the heart rate via the vagus nerve, by increasing the refractory period of the AV-node, so the heart rate drops.
It should be noted though, that it can be a bit dangerous to play with these reflexes in some patients, especially because massaging the carotid arteries can lead to an embolism in older individuals with atherosclerosis, or in some patients, it can lead to asystole or ventricular fibrillation (i.e. cardiac arrest).
It's not really about which vertebra is at the level you are massaging, rather it's about being near the carotid sinus, which is where the baroreceptors are located, and that might vary between individuals and how you position the head etc.

Welcome to Biology.SE! This looks like it could be a good answer, but non-experts have no way of verifying your post. Consequently, answers are much more likely to receive a favorable response if you include supporting references (primary literature is best). Without that support, your answer is indistinguishable from opinion. This is a good example of how to format references. ——— You may also want to take the [tour] and then consult the [help] pages for additional advice on [Answer] effectively on this site. Thank you!


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Ear ossicles a part of Skull?
Is there anything special about not considering ear ossicles as a part of skull?
I could not understand the reasoning behind such  classification.

The justification is simple.
The bones of the ear [ear ossicles] do not articulate with any other bone of the skull hence it is not considered as a part of the skull, similar is the case with the hyoid which is attached to the tongue.These bones have been placed under the group of associated bones.


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Identification of an insect from Bangladesh
This is a video of the insect. Sorry, I don't have any still photograph.
Location: Savar, Bangladesh.
I've been suggested by an insect photographer that it is a caddisfly.
EDIT: Here are two images from the video


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Possible to get Furniture carpet beetle specimen for collection?
I was wondering if anyone knows how it'd be possible to get a Anthrenus flavipes (or furniture carpet beetle) specimen for my collection?
I can't find a source anywhere online, only the dermestid beetles used to clean skulls and such. Any help would be appreciated!
Bump

You might try calling up a local exterminator (ideally not a franchise) and asking them to save you a specimen the next time they are called out to deal with such insects. Donate some beer/weed/customer referrals by way of thanks and they'll help you out with future specimen hunts.


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Why are sutural bones more common in lambdoid suture?
Why are sutural bones (Wormian bones) are more commonly present at lambdoid suture? Is the tortuous nature of lambdoid suture a reason for that?

Evidences for my claim:

They(sutural bones) occur most frequently in the course of the lambdoid suture, which is more tortuous than other sutures. They are also occasionally seen within the sagittal and coronal sutures. (1)

They are commonly found in the lambdoid suture and fontanelles but are occasionally seen in other sutures especially the coronal, squamosal, and sagittal sutures. We examined 25 dried human skulls with the aim to find out the occurrence and variations of Wormian bones, and surprisingly we found Wormian bones in the coronal, squamosal, and sagittal sutures in 6 skulls. These are uncommon sites of occurrence of sutural bones as reported in the literature. These findings prompted us to report these cases as their presence can lead to confusion in diagnosis in cases of skull fractures.(2)

Sources:
1- https://en.wikipedia.org/wiki/Wormian_bones
2- https://www.ncbi.nlm.nih.gov/pubmed/22117248

Is the question now more clear?


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A fully understood living organism
I have no background in biology but in the context of other research I am wondering if there is an organism, however simple it is, whose functions and structure is fully understood by biology or biochemistry. This would mean that all the functions and roles of all its genes are documented and all its internal procceses also. In other words is there an organism that can be fully analyzed in terms of its chemical processes and its RNA/DNA?

Welcome to Biology.SE! It depends on what you mean by fully. We don't know function of every gene present in any organism (we don't even know how many genes we have!). However, if you exclude some processes from your list, most probably E. coli or C. elegans might fit in.

No, there is not. Biological organisms are complex and have substances/interactions which have yet to be discovered. We are discovering new things about relatively simple organisms every day. However, the closest you will come is a "simple" bacteria like a ssp. of E.coli. Better yet, a virus, if one could classify it as an organism.

I was asking this question because I was trying to come up with examples of "strong emergence". The idea that there can be properties of very complex systems that are irreducible to the properties or even the interactions of its constituent parts. The property of conciusness is an example of strong emergence and I guess the emotional effects of music is another one. From your answers I can see that there are examples of strong emergence even in single cell organisms.


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Why is only one primer used for DNA sequencing instead of two?
I understand that PCR uses two primers that anneal to the two ssDNA's in order to exponentially amplify a DNA and that Sanger sequencing uses only one primer because a sequence can be determined with only using one primer and one single-strand with ddNTPs. However I've read this:
"Sequencing uses one primer, while PCR utilizes two. If we try to sequence with two primers present, you'll get the two sequences back, superimposed on each other and completely unreadable."
I'm struggling to visualize why using two would be an issue though, how will that make the DNA unreadable?
Thanks in advance!

The reaction for the Sanger sequencing reacting contains beneath the normal dNTP (which are needed to make most of the DNA) the dideoxynucleotides, which lack the 3'-OH-Group and which are labelled with a fluorescent dye. Once one of this nucleotides is incorporated, the chain reaction stops here, leading to a product with a specific length and a known (by the fluorescent dye) end base.
In theory this leads to products of a length primer + 1 ddNTP base, primer + 1 base + 1 ddNTP base, primer + 2 bases + 1 ddNTP base and so on. The sequencer seperates these bases by sizes and the sequentially reads out the fluorescent dye and translates this into a sequence of bases. See the image from the Wikipedia for illustration:

If you now add two primers (and of course have a double stranded DNA), this reaction will start from both ends of the DNA (always in 5'--> 3' direction) leading to two sets of marked DNA of the same size (so again the base + 1 ddNTP, base + 1 base + 1 ddNTP and so on). Since these are equal in size, you will always read out two bases at the same time and you will not be able to tell, which signal belongs to which strand. This looks like this (from here):


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Is it wrong to consider an allosteric inhibitor a non-competitive inhibitor?
Supose Caspase-1 is allosterically inhibited. Since the inhibitor is not binding in the active site but instead in the allosteric binding site, can I conclude it is a non-competitive inhibitor?

Could you give me examples, please? The link you have provided is too technical, and these concepts are still somewhat confusing.

The concepts are clearer now. I'll definitely read your links. Thank you very much.

Why are you asking this question? Why do you want to use another name for an allosteric inhibitor? In any introductory text book you will see the kinetics of what are called non-competitive inhibitors described as being quite different from allosteric inhibitors.

@tomd — perhaps you could formulate your comments into an answer. At the moment we seem to have an accepted answer that is at variance with them.

Actually, this was about distinguishing concepts which were confusing, and applying them.

No, you cannot assume that an allosteric inhibitor is non-competitive. "Allosteric" refers to the location of binding, whereas terms like competitive, non-competitive, uncompetitive, or mixed inhibition refer to how (or if) the binding of the inhibitor affects binding with the substrate.
The Wikipedia page on competitive inhibition is a reasonable source for this question.
A competitive inhibitor is one that prevents binding of the normal substrate(s) at the active site. It is possible to achieve this either by literally getting in the way by binding in the active site or by binding elsewhere, causing a conformational change that prevents binding the active site. Both cases are considered competitive inhibition because of how they influence substrate binding.

I am puzzled by your answer. The question is about non-competitive inhibition, but you quote a link to competitive to an article on competitive inhibition. Are you concluding that if an inhibitor is not a competitive inhibitor then it must be a non-competitive inhibitor? I am no enzyme kineticist, but I thought the usage of the term in enzyme kinetics was much more restricted. I cannot see the utility of calling an allosteric inhibitor a non-competitive inhibitor. I would just say it is not a competitive inhibitor. Surely it is better to use definitions related to the kinetics of inhibitors.

@David I think the title of the OP's question might be a little unclear, I read it to be "If an inhibitor is allosteric, does that mean it is non-competitive?" I answered that no, that is not always true, and used the definition for competitive inhibition as an example proving that you can have allosteric inhibition that is competitive, rather than non-competitive. I could have also gone into mixed or uncompetitive inhibition but I thought one example was sufficient.

The question was formulated this way because I didn't know an allosteric inhibitor could be competitive or even mixed.

It may be technically correct to say that an allosteric inhibitor can be (or is) a “competitive inhibitor”, but, in terms of communication and education, I would advise a more measured approach. Most students encounter the terms “competitive inhibitor” and “non-competitive inhibitor” in the context of reactions exhibiting Michaelis–Menten kinetics. Their mental image of such an inhibitor will therefore be of the type:

In discussing allosteric inhibitors I would therefore focus on the different mental model, below, in which substrate (or positive effector) and negative effector (use of this different term being deliberate) have opposing effects on the equilibrium between tense and relaxed states:

I would then go on to say something to the effect that because the relative concentrations of substrate and negative effector determine the rate of the reaction “the negative effector indirectly competes with the substrate”.

First of all, I take your point about the previous post being too technical.  On this occasion, there will be no equations and no diagrams.
When dealing with reversible enzyme inhibition, we are mainly concerned with the meaning of four terms: competitive, uncompetitive, non-competitive and mixed. As I said above, the literature is very confusing to the point of making relatively simple concepts appear very complex, and the confusion often arises from the meaning of the term 'non-competitive'.
First things first: reversible inhibitors are best classified by their effects on two kinetic constants rather than by the mechanism that gives rise to a particular inhibition pattern.  The two kinetic constants are kcat and kcat/ Km. (So why not kcat and Km? This is discussed in a previous post, but the short answer is that it is simpler:  Km is often a very complex kinetic constant). We can distinguish two 'limiting' cases. (i) A competitive inhibitor effects kcat/ Km but not kcat and (ii) an uncompetitive inhibitor effects kcat but not kcat / Km. (iii) We can also now distinguish a third case where both kinetic constants  are affected. Let's call this one non-competitive inhibition.
The confusion in the literature arises because some authorities call non-competitive inhibition as defined above mixed inhibition, and (to really screw things up), they consider non-competitive inhibition  a special case of mixed inhibition where both kinetic constants are changed to the same extent!  For the purposes of this answer, I am not going there as I think what you mean by non-competitive is as defined in (iii) above. In any event, this is how Cleland, the leading authority in this field, defines non-competitive inhibition.  In other words, 'mixed' inhibition is banished from this answer from this point on.
We could be a little bit more adventurous here and say that a competitive inhibitor only effects binding of the substrate to the enzyme and that an uncompetitive inhibitor effects only the catalytic step. Or, we could say that a competitive inhibitor effects only the apparent second order rate constant for the combination of enzyme with substrate (which the enzymologists call kcat/ Km) and that an uncompetitive inhibitor effects only the apparent first order rate constant (which the enzymologists term kcat).  But that is becoming too abstract. But perhaps you can see where I am going? There are only two limiting cases,  one affecting substrate binding and one affecting catalysis, and a combination of both.  It really is as simple as that.
Having got the nomenclature mess out of the way, I will now attempt to answer your question: if an inhibitor does not bind to the active site can we conclude it is a non-competitive inhibitor?
IMO, the answer is an emphatic no. An allosteric inhibitor (one which binds to a site other than the active site) may be competitive, uncompetitive or non-competitive.
As Bryan Krause put it , a  competitive inhibitor  prevents binding of the normal substrate(s) at the active site, but there is no requirement that the inhibitor bind to the active site. Binding of the inhibitor at the allosteric site may cause a conformational change that prevents substrate binding, for example.
The same argument applies to uncompetitive inhibition.  A simple mechanism that gives rise to uncompetitive inibition is where the inhibitor cannot bind to the 'free' enzyme but binds to the enzyme-substrate complex.  And of course binding to the allosteric site might not be possible unless substrate is bound.

The confusion had arisen from the unawareness of those constants. I didn't know an allosteric inhibitor could be competitive or even mixed. Thanks a lot.


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Sephadex column for alpha-amylase
I want to purify crude alpha-amylase with column chromatography. I am using a spehadex 75, But for some reason I can't find any information on how to make the slurry.
I can quickly find tons of information on how to pack and store a column, but what i really want to know is how much powder and buffer do I mix together?

The '75' of Sephadex G-75 refers to the water regain value, which is defined as the grams of water absorbed upon hydration of 1g dry powder, multiplied by 10 (see Reiland). Thus the water-regain value of Sephadex G-75 is about 7.5ml. This value refers only to the water contained
within the gel particles and not to the water trapped outside of the particles in a packed gel (Reiland). As a rule-of-thumb, the latter figure can be estimated to 50%.
So ... 1g of dry Sephadex will give about 15 ml of packed gel
From here: 1 g swells to 12-15 mL gel
Just a thought ...
Does alpha-amylase interact with Sephadex?  Maybe 'thinking' it resembles a substrate, and (reversibly) binding to it or otherwise interacting to cause effects in addition to gel-filtration ?


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Why were wisdom teeth not eliminated by evolution?
Supposedly evolution was very efficient and evolved many human proteins over a few thousand generations. Yet obvious detrimental traits like wisdom teeth remained. Why?

You're asking about one specific case, but I think the more general question here has good answers for you.

Not everyone has problems with impacted wisdom teeth, and removing them is a profitable enterprise, so please use caution before you say we should evolve to 'x'. We have always had wisdom teeth, but removing them is a relatively recent affair.

Please explain why wisdom teeth are "obviously" detrimental, because it's certainly not obvious to me :-)

I dunno who would describe evolution as "very efficient", it can result in amazing solutions that would be incredibly hard to arrive at by design but making random changes and throwing away the bad ones is not exactly quick or waste-free.

I would also point out that evolution does not have a will! It just happens. The fact that some traits change faster or slower over time is a matter of chance.

I am changing the title by removing "yet it evolved several proteins". "Evolution evolved" is like saying "change changed" — redundant. And the idea that only several proteins evolved is quite wrong. All proteins evolved.

@Liu Considering the answer to the question this is supposed to be a duplicate of gives a long lost many possible factors, you could make this a valid question just by asking which point or points on the list are responsible in this case. including the list or a link to it would a good idea if you do this.

In addition to other points, Google says that wisdom teeth usually come in in the late teens or early 20s.  In prior ages, many people would have had at least one offspring by then, perhaps more, reducing the space for evolution to act against any detrimental effect.

Reductions in the size of our lower jaw that result in wisdom teeth sometimes becoming impacted result from changes in our diet, and are not the direct result of the evolution of a smaller jaw. This means that natural selection has had at most 8000 years to act on the phenomenon, which occurs in people in their mid to late 20s (who, historically, probably would have already reproduced if they were going to), and so the selective advantage of lacking wisdom teeth has not had enough time or been strong enough to cause the no-wisdom-teeth phenotype to spread throughout the human population.
Global human mandibular variation reflects differences in agricultural and hunter-gatherer subsistence strategies - Cramon-Taubadel, PNAS (2011)
Before Agriculture, Human Jaws Were a Perfect Fit for Human Teeth - Smithsonian.com (2015)
Incongruity between Affinity Patterns Based on Mandibular and Lower Dental Dimensions following the Transition to Agriculture in the Near East, Anatolia and Europe - PLOS One (2015)

the real risk with wisdom teeth is splitting the jaw, but as you said that only became a problem after the invention of soft processed food.

I would wager that removal of impacted wisdom teeth has resulted in more deaths than infection from said teeth. There is not a single randomized trial proving - or even attempting to prove - that removal of wisdom teeth has a beneficial effect on quality/duration of life. The UK's NHS stopped paying for the standard procedure, and the Cochrane Report advises against it. I have my wisdom teeth; my dentist was peeved because one of them had a small cavity. When I asked why he was upset, he answered that they were hard to fill way back there. He advised me to have it removed. Um, nope.

Furthermore, neither of your your citations (one depends on the other) does not deal with wisdom teeth, but with malocclusion. You need better sources. -1 for misinterpretation/misinterpretation of support sources.

@John - Whaaaaaat???

@anongoodnurse It's possible that wisdom teeth cause problems and also removing wisdom teeth causes problems. I wasn't arguing in favour of surgery, or against it, modern surgery is irrelevant to the discussion.
The PLOS One paper discusses jaw size changes as a result of change in lifestyle, I've found another paper that discusses it more explicitly. I've made the assumption that this would be the cause dental crowding and impaction of wisdom teeth problems, I suppose this assumption could be wrong.

Your assumption ignores the much more common malocclusions which create "problems". Modern surgery is not irrelevant to the discussion. The death rate from impacted wisdom teeth is not known (contrary to your statement that infections from impaction kill), nor has it ever been known. In other words, the "problem" of wisdom teeth is largely a recently manufactured problem. Malocclusion is not. Yet we have lived with it for 10 millenia or more.

It seems a fairly safe bet that before antibiotics all infections carried a risk of serious repercussions, but I don't actually know that, so fair enough.

@anongoodnurse, problem=/= death. The fact that our change in diet is responsible for smaller jaws in industrial societies and this is responsible for the majority the problems associated with wisdom teeth is what matters for question. The cost/benefit of surgery was not mentioned becasue it is irrelevant.

@John - I'm not sure what you're talking about. My comment to you was about wisdom teeth splitting jaws. In almost 40 years of treating patients, I have never heard that one! If you could cite a source, I need to read it, please. Otherwise I will continue to believe it's a whopper, that one; it is indeed! We're scientists here.

@anongoodnurse http://www.sciencedirect.com/science/article/pii/S1079210405802999 You should not rely on anacdotal evidence, esspecially when refering to something that became a problem prior to the development of modern medical technology. And I was referring to several of your above post, I would not normally rely to "Whaaat?" or anything like it.

@John - Thanks for the link. Please note that there is no control group; everyone in that study had a fractured mandible. What percent of people with M3s have mandibular fractures? Is it significant? And, please note: people make a great deal of money by pushing for the removal of M3s. Whenever someone who does this for a living publishes a study which supposes to support it, you should always ask, is there a conflict of interest? In other words, quis bono? Too many third parties have found differently. Again, quis bono?

control groups for injury causes tend to be prohibitively expensive to create becasue you must have a much much larger sample size usually combined with an extremely long study length, it doesn't bother me in the slightest they don't have one.  We already know wisdom teeth are more likely to develop impaction, the cost/benefit of surgery is largely individualistic and irrelevant to the discussion. If you have links to any of these third party studies showing no connection that would be helpful to your case.

It is not irrelevant that the researchers have a vested interest in promoting the agenda that impacted wisdom teeth should be removed.

@John: http://onlinelibrary.wiley.com/doi/10.1002/14651858.CD003879.pub2/full "There is some reliable evidence that suggests that the prophylactic removal of asymptomatic impacted wisdom teeth in adolescents neither reduces nor prevents late incisor crowding."

@anongoodnurse you do realize that does not show no connection,  just no connection between a very narrow subset of wisdom teeth and another narrow set of complications. If you want to continue this I suggest creating a chat.

Wisdom teeth do have a function. If you are missing a molar before the age of 20, a wisdom tooth can easily move in to fill in the gap, by filling in the space or by pushing the molar ahead of it.
This trick has been used by dentist to "fix" the teeth of teenagers who have  molars with large cavities but still have wisdom teeth that have not erupted. So rather than go to extremes to save a bad molar, it is just yanked out and the wisdom tooth slips in. Problem solve. ( of course it depend on the actual wisdom tooth as some wisdom teeth are improperly positioned or appears unlikely to erupt to enable this  trick to be used) example
Modern dental hygiene is good (but not good enough). So people tend to have all their molars in their early 20s (but not in their mid 30s). The the wisdom comes in too early to be useful to modern people. But i am guessing it had more use in earlier times.
That said... the trait for (third molars) wisdom teeth does not appear to be under positive selection in the human population as not everyone has it. Numbers vary depending on population.  10 to 25 percent of Americans of European ancestry are missing at least one third molar. For African Americans it is 11% and Asian Americans, the figure is 40 percent. The Inuit, a group of people who live in the Arctic regions of Canada, Greenland and Alaska, have the fewest wisdom teeth; about 45 percent of them lack one or more third molar.
percentage

You need a source for your statement that wisdom teeth are being selected against. That is not a credible claim.


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Open access datasets for QTL analysis?
I'm just getting started out learning how to use the QTL package in R studio, and I'm trying to find additional datasets to practice with. I've already worked through the datasets here on the Rqtl website. Is there anywhere I can find similar datasets to work with? I'm specifically looking to work with autosomal data.