text:
Is DNA from more parents (than two) better for the fitness of the offspring?
I'm designing a system (a computer system actually) and (a whole while ago) I spoke with a friend about it and he had this opinion:

If you combine DNA of more parents (than 2) it's better for the
  offspring.

It's a bit of a theoretical question but is this true?
I'm using genetic algorithms where you can choose the number of parents,
if this were to be true I'd take 4 parents, if not I'd stick to 2.
I saw here a question about the occurrence in nature but it remains unanswered.
(2 parents are easier - in this system - so maybe that's the reason it is not observed in nature)
About the system: it needs to produce 'fit' offspring (as fit as possible and as fast as possible), where fitness is measurable (this part is already covered...) and the most fit individuals in the population are selected to pair.
The only limitation set on this kind of systems is that the offspring has to have a chance to be fitter than the parents (so children are allowed to be less fit than parents (being it 4 or 2).
(Of course this lowers the importance of the question but still: does offspring of more than 2 parents have a higher chance to be fit? (my friend mentioned: the more diversity in the DNA the better...))
If you need more information about this bit I'll try to answer comments (if I do know the answer or can give more information about it).

Ignoring the complications that S Pr mentions in their answer below, this would totally depend on the individuals involved. If you could include the DNA from a distant relative (or no relative at all) to the DNA of two siblings, you could easily eliminate the risk of inbred deleterious homozygous recessive traits. However, if just two parents are distantly related and/or would not develop an embryo with deleterious traits, then it shouldn't matter a whole lot.

Can you create an answer with this? (I'd upvote it), also - if you'd like - we could use you in the chat room: https://chat.stackexchange.com/rooms/93100/offspring-from-more-than-2-parents

There are very many details to address in this question. I will try to keep it brief and keep the scope of your question in mind, which is rather narrow. I also think your friend is over-simplifying and misleading you, assuming he is honest about the explanation he gave you.
We are talking about sexual reproduction, correct? Firstly, with 3+ parents:

it's not obvious that you will have "more diversity" in the DNA, nor that
"more diverse" DNA will be a cause for increased fitness.
Additionally, it would take a whole lot of machinery and evolutionary happenstance at the cellular and molecular levels to recombine DNA from 3 or more parents to make a stable, recombined genome, and this itself may introduce more problems than solutions.
More so, you're implying that a sexual organism that requires mating between 3 or more individuals will be fitter than an organism born of fewer parents. This is subject to whether the gain in fitness of having more genetic parents will outweight the cost of maintaining such a system. This would certainly be dependent on the environment, the population, and all the nasty little details of life, such as how mate choice would work, whether a backup for 2-individual mating would exist, etc.

Remember that fitness is a probability of obtaining a number of offspring rather than the number of offspring. I think it is self-evident that the requirement for more parents, rather than less, lowers the probability (i.e. fitness).
This is quite a hypothetical discussion. In nature, for all its ever-experimenting and ever-diverging forms of life in the last 4 billion years, we find no organisms with more than 2 sexual parents. Take this as a sign that the natural occurrence of this kind of system is probably not favorable to survival and reproduction.
And I realize we could discuss this topic on many fronts (I have a few more ideas that I omit here), it's a rich question to digest.

excellent answer, would you like to digest this here or do you have a place that's better suited for this kind of discussions (I have quite some remarks as well and we seem to diverge on the meaning of 'fitness', so - from my part - further digestion would be most welcome :-D

If it's brief, ask here in the comments, otherwise you could make a chat room for it. I recommend making it public!

I created a room: https://chat.stackexchange.com/rooms/93100/offspring-from-more-than-2-parents let's digest :-D


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Where can I find and download HMMTOP training set?
I would like to perform redundancy reduction for my test set for membrane topology prediction. I checked the 1998 paper and website of the HMMTOP server but haven't found any download links for the dataset that they have used for training.
Links:

paper
server

In the Appendix Section of the paper, there is a table of entries and topologies.  Below, there is a note:

*Entries which are included in the initial parameter and
  pseudocount settings from the 83TMP set.

Please correct me if I'm wrong, I suppose these those 63 protein entry names with an asterisk are the data used for training?

From materials and methods: The first data set was originally collected by Jones et al. (1994), and was also used by Rost et al. (1996) (83TMP set). The second one is an extension of it by Rost et al. (1996) (48TMP set). The third data set contains prokariotic transmembrane proteins collected by Cserző et al. (1997) (prokTMP set).

You might have to look at these papers individually or mail and ask the authors for a properly formatted dataset that they used for training. The last update was 18 years ago; so I'm not sure if the author is still active (alive)!! Perhaps you should try more recent tools based on HMMTOP. Check for citations.

source: Stack Exchange

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

sort: votes


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Emergence of novel protein interactions by mutation of amino acids
Are there any examples of proteins that, without coming from a recent duplication event, underwent a mutation(s) that caused it to have a novel interaction with a new ligand, substrate, other protein or molecule? By novel I imply that it doesn’t revert to an ancestral interaction or develop an interaction that is already performed by a close relative. I imagine that such mutations would be extremely rare, and that duplication is almost always necessary to have them fixed in a lineage.

Just to make sure I understand what you're saying... You're asking for an example of a protein which changed functions throughout generations without leaving a trace of the original protein or a paralog?

I edited your question a little to remove some typos, but also edited your title. "Genuine" isn't required as you explain this in your quesion, and best to keep it short, but avoid abbreviations like aa — need to spell in full for indexing.

Thank you. I meant a protein that acquired new interacting partners (ligands, proteins, etc) without being duplicated. Because I’m already aware of evidence of proteins acquiring new interacting partners by being first duplicated and while one of the copies maintained the original interactions the other acquired the new ones.

@Marlo, I have restructured my answer to address your question more directly and focus specifically on the AB polymorphism which does not involve gene duplication. Does this fit the bill? I don't quite understand the import of "an interaction that is already performed by a close relative". If the protein is distinct and original mutations occur in it independently, what relevence do the interactions performed by other proteins have? Is there some philosophical or other concern underlying your question? (Please include the @ handle in any reply — that way I'll be alerted.)

I must say that I am disappointed that you have not responded to my last comment. You appeared to be keen to have an answer as I understand you also posted to SE Bioinformatics, and you can hardly deny that I took your question very seriously and have supplied an extensive, detailed and fully documented answer. I see that you have been a member of the SE community for over two years, so I would expect you to realize that it would be courteous to let me know whether or not the answer is what you require.

Sorry, the reason is that just after reading your answer i started reading your other answer and from there a chain of articles regarding the topic, some theoretical and some experimental, and i still don't reach a conclusion if it's a satisfying answer or if i can formulate specific counterpoints to your post, i am still very much in the process of this. What i do recognize is that i find your answer more detailed than i expected and for this you have all my gratitude. Sorry that i wasn't courteous enough to provide at least one comment saying this.

The polymorphism in the gene product of the human ABO locus seems
  to provide an example of what the question demands. It does not
  involve a gene duplication or recovery from loss of function; rather it involves changes that cause
  interactions with a different ligand, and the mutations that produce
  these changes have been identified and examined at a molecular level.

I have described the biochemistry of the human blood group system in an answer I gave to a previous question, so the cartoons of the reactions are reproduced from that answer. The diagrams of the molecular interactions and the gene cluster are new.
Human AB polymorphism
The products of the A and B alleles of the human ABO locus are glycosyltransferases:

One of the enzymes recognizes the sugar, galactose (activated by UTP), whereas the other recognizes N-acetylgalactosamine. There is no doubt that they are the products of different alleles of the same gene, even though this is a member of a gene cluster (see below).
The structures of both these enzymes have been determined and the differences of the interaction with their substrates at the active site modelled as shown below:

There are four residues that differ critically between the two enzymes, three of which are shown. Two of these (Met/Leu 266 and Ala/Gly 268) make contact with the UDP-glucosyl substrates. The third (Ser/Gly 235) appears to affect the conformation of the H-antigen co-substrate.
How is a change in function possible without gene duplication?
The poster expresses the opinion (my rewording):

“I imagine that such mutations would be extremely rare, and that
  duplication is almost always necessary to have them fixed in a
  lineage.”

Why, then, is gene duplication not necessary in this case? The reason is that the enzymes involved are not indispensable: the product is an elaborated branched cell-surface polysaccharide, the function of which can be served by a range of variants. Indeed, the polysaccharide is functional without elaboration, as in the case of blood group ‘O’, where the enzyme is inactive. However, as discussed in my answer to the previous question, there may be a ‘hidden’ function that has driven the evolution of the polymorphism in humans. It has been suggested that the blood cell surface antigens were used by parasites such as the malarial parasite to enter the cells, and that variation provide resistance (albeit temporary, i.e. until the parasite evolved in response).
Footnote: Gene Clusters of Glucosylating enzymes
The question specifically asks for examples that do not come from a recent gene duplication. However I feel it important to mention the gene duplications that have produced such changes in the gene cluster to which the ABO locus belongs. This is to make it clear that the polymorphism is distinct from such examples.
Animals have the ability to vary the sugars on their cells by selecting from a large repertoire of genes with the potential to specify different glycosylating enzymes. An example is the GT6 gene family (glycosyltransferase family 6):

There are about seven members of this family, not all of which are present in every species. A paper by Turcot-Dubois et al. gives a detailed comparison of the genes in human, rat, toad and zebrafish. I just reproduce the gene map for the human cluster in which the four members of the family are indicated by solid triangles:

The enzymes specified by some of these gene have been characterized by X-ray crystallography, e.g. in this paper by Gastinel et al..

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


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What species is this grey insect with red antennae and mouthparts?
I’m very curious to know whether this is a type of ant or not, I only see 6 legs. Found in Tampa, Florida near Tarpon Springs.

Definitely not an ant.  Where was it?  I mean, it looks like it's in an old box with a strap...?  Is it rotten wood?  It looks like exterior lighting: was it outside buildings?

Also, how big is it?

See Horned Mohawk looking insect. What is it? for more info.

It was approximately 1 inch long, no bigger than an American 25 cent piece. Located on a farm in Tarpon Springs. Found crawling on the wash racks for the horses.

It's some type of Reduviidae, or assassin bug - possibly a juvenile wheel bug.  Here's a few pictures of Floridan assassin bugs I've found just browsing the net:

Tagged as unidentified Reduviidae from Tallahassee

Tagged as assassin bug

Tagged as a Wheel Bug

Tagged as a wheel bug nymph

Bottom line:
Not an ant, for sure: it's almost certainly in the family of Reduviidae, possibly the subspecies of Arilus cristatus.


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What kind of spider is this? hoping its not poisonious

Found outdoors, after it was killed we found little tiny baby spiders on our ceilings throughout our house. really wanting to know if this spider is venomous or not as we have a baby of our own in the house..
Found in Bligh Park 2756, Sydney NSW Australia.
I would say it’s around 10cm.

Hi Emily. Please review the guidelines for writing a [tag:specied-identification] post. Specifically, we need your location and the size of the specimen. Ideally, if you can provide additional photos of the spider (especially of its abdomen and eyes) that could benefit getting a positive ID, too. Please [edit] your post with this additional information. Thanks. Please also consider taking our [tour] and checking out How do I ask a good question?


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what is this bug ? i found it on bed 2 times
What is this 1mm long bug I found on my bed in Egypt?

Here is its back photo

It's a soft-bodied tick (family Argasidae). See Identification of a small flat bug for an example. Without providing us your location, nobody can give you a definitive ID. Please [edit] your post with more information.

Possible duplicate of Identification of a small flat bug


text:
Are there five common fear responses in animals?
It's been claimed on psy SE that are five common fear responses  Fight, Flight, Freeze, Fawn, and Faint (or maybe fright, flight, fight, freeze, fawn as in a post further linked from there).
To me this classification doesn't seem well supported by animal experiments... (The poster is a certified psychologist, however). Do biologists agree with a 5F classification of fear responses?
And to make this less of a yes/no question: do biologists (commonly) classify fear responses in a more fine-grained manner (than the simple fight v flight paradigm)?
It seems to me that the 3F classification fight-flight-freeze (which seems more widely endorsed even in psychology than the 5F) has a reasonable correspondent in animal behavior. But I haven't found much biological literature discussing it as such... although it presented as such in a news/pospsci video-article in Nature. The actual paper that that video is about, presents a somewhat different 4-way nested classification :

Adaptive behavioural responses to visual
  threats fall into two general categories: those that reduce saliency to
  predators (to avoid detection), such as freezing or hiding, and those
  that enhance saliency (to avoid capture), such as fleeing or retaliatory
  aggression.

N.B., one of the review papers cited by that one does use the 3F though:

Freezing, fleeing or fighting back are general defensive responses in many taxa. These defenses are mutually exclusive, since a prey cannot
  simultaneously flee and fight, or freeze and flee. Each of these defenses by itself is rudimentary and probably cannot provide a completely
  effective means to elude predation. Freezing is efficient only if employed before the prey is spotted by the predator, otherwise the prey
  becomes a stationary, easy to catch target. In fleeing, the prey can move directly away and maximize its distance from the predator, move
  toward the predator to confine it to a single clashing point, or dodge sideways to evade the attack. Prey can also run in a straight path that is
  efficient against slow or distant predators, or in a zigzag path that is efficient when a raptor is close or fast. In all, freezing and fleeing
  constitute together a complex and flexible defensive response, and are probably controlled by different motor systems that are interconnected to allow fast switching between these behaviors, as required for an effective and versatile response.

So is there a commonly agreed classification in biology for fear responses?

After thinking a bit more about this, it's probably reasonable enough to consider "fawning", that is submissive behavior as an alternative response, with the caveat that it doesn't show up much in predator-prey contexts, but mainly in contests between sexes (usually males) of the same species. I don't know if biologists see it this way though... i.e. as related to the other responses.
And if that's not complicated enough, one author suggests "risk assessment" (behavior) as a separate part of the response repertoire (in predator-prey interactions):

In rodents, an extensive repertoire of innate defensive behaviors can be seen in predator-prey interactions in natural and semi-natural (laboratory) situations. To predator threat, rodents of small prey species exhibit a general cessation of ongoing non-defensive activities (e.g., grooming, playing, foraging, feeding and sexual behavior) in both adults (Blanchard and Blanchard, 1989) and preweanling pups (Takahashi, 1992), along with enhancement of avoidance, flight, freezing, risk assessment, defensive threat and defensive attack behaviors (Blanchard and Blanchard, 2008). Rodents will also readily bury novel, aversive, or potentially dangerous objects (Treit et al., 1981). Manifestation of specific behaviors is dependent on a number of factors: (1) context – an animal will typically flee a threat within an environment in which escape is possible, yet when trapped it will freeze; (2) stimulus ambiguity – whereas ambiguous stimuli, such as predator odors, elicit risk assessment behaviors (e.g., stretch attend, stretch approach, olfactory investigation) and are often associated with a state of anxiety, discrete, present threats elicit flight, avoidance, defensive threat and attack, and are associated with a state of fear; (3) defensive distance – the distance between predator and prey shifts defensive coping strategies from avoidance to escape, with short distances to the threat and unavoidable contact culminating in defensive threat and attack postures.

This last quote highlights something else I've been pondering, namely the difficulty in delineating fear from anxiety in animals. Depending where one draws the line between these, more or fewer responses qualify for a classification...

To add to the discussion, there is talk of a 6th response. This is a newspaper article. I will try and find the clinical psychologist's report, but may be next week before I find it

I've never heard "5F" referred to in animal behavior; this seems a bit opinion-based, though, is it not? Sort of a lumpers-vs-splitters argument. As far as fear vs anxiety, that's somewhat of a separate issue, although it is certainly of great interest especially in designing rodent experiments to apply to human psychology. From a neuroscientific perspective, though, I think fear and anxiety in rodents are considered to have the same responses, the fear vs anxiety distinction is more about context and higher order processing.


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How do researchers define the region a lead SNP encompasses?
As I understand it, a lead SNP captures the variance for all unmeasured SNPs in a region due to it's low p-value and high linkage disequilibrium. However, in different papers the region size differs (e.g. from 500kb +/- to 1mb +/-), how are these sizes chosen and why do they differ?
Edit to add examples:
Xia et al. Transl Psychiatry. 2017 Aug
"Genome-wide association analysis identifies common variants influencing infant brain volumes"
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5611727/
-500kb region
Polushina et al. Transl Psychiatry. 2017 Dec
"Analysis of the joint effect of SNPs to identify independent loci and allelic heterogeneity in schizophrenia GWAS data"
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5802566/
-1mb region

It would be great to reference papers which use the different sizes.  Otherwise it's hard to say why they chose the sizes they did.  Thanks!

Thank you for your response, added some papers I have been looking at now, is it likely to depend on the disease being looked at? As in, the more complex and heterogenous the wider the region you might look in? Or does it depend how many SNPs pop up how big you set your boundaries? Do researchers risk a loss of information with however they set these regions?


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In cell division, are daughter cells "newer" than the parent cell?
I learned that cells go through cell division to generate new cells to replace dead or damaged cells.
Are the daughter cells "newer" than the parent cells? For example, the parent cell has an "age" of 9 days and the daughter cells will have an "age" of 2 days.  Because if they are not "newer" than the parent cells and all have an "age" of 9 days, they will all still die  together at the same time in the end.
For a real world example, skin cells only live a few weeks. But not all skin cells on our body die after a few weeks. So the only logical way I can think of to get around this is that daughter cells are "newer" or "younger" than parent cells. Or perhaps my notion about the "age" of cells is wrong.
And if the daughter cells are "newer", why is that possible?

Hi and welcome to Biology@SE! Have you read about telomeres? In general, you have to define "cell age" more precise, i think

I think you need to read about cell ageing and sort out what you mean by new and how the two do or do not relate and then come back with a properly defined question.

There may be an interesting question here. Cell division can be asymmetric (asymmetric partitioning of the biomolecules and orgaqnelles) and the "age" of the two cells can be different. This is at least known in yeast. Are you asking about something similar?


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Is this headlice or bed bug

This is very small. About the size of a grain of rice. I Felt it crawling in my hair.  When I brushed my hair off this fell out in the sink. I was wondering if it's lice. I'm in Mojave county Az

Please add your location and the approximate size of the specimen. Both are needed for an accurate ID. I also advise that you upload any additional pictures you may have of the specimen. Currently, your post is lacking adequate detail and will be closed and unanswered. Please [edit] accordingly. thanks.

That is a Thrips, order Thysanoptera. Not harmful. Not a bedbug or a louse. You can read about them here.
https://en.wikipedia.org/wiki/Thrips
(by the way the singular form of "Thrips" is "Thrips": there is no such thing as a "Thrip")


text:
How does nitrogen gas partial pressure change when ascending during scuba dive?
Scuba divers suffer decompression illness in which during sudden ascension, gas bubbles form in blood vessels and do not get reabsorbed quickly, leading to various problems including a stroke.
The mechanism is as follows. At high pressure, more nitrogen gas in the air can be dissolved in the blood. This is due to Henry's law, which states that with greater partial gas pressure exerted onto the liquid, more gas is dissolved. When the partial pressure of nitrogen gas returns to normal, solubility of the blood decreases, leading to the formation of gas.
From above, it seems that the air that blood is exposed to (the lung's alveoli in most cases) changes in the partial pressure of nitrogen gas. Another study isolated the effect of partial pressure by conducting an experiment in which the subject's breathed air was changed from heliox (combination of helium and oxygen) to nitrox (combination of nitrogen and oxygen) without change in total pressure and this led to bubble formation.
However, it is hard to imagine that the pressure of the air breathed in by a scuba diver would change, due to the fact that air is brought from an oxygen tank that seems to be independent of outside pressure. Thus I ask the question: if the air breathed in by the diver does not change with depth, how does nitrogen partial pressure exerted on the blood change?

What has your research told you?

I do not understand your reason for asking that question. Could you specify because I stated what I know and the assumptions made? I do not have resource on which I can test my assumptions.

The Biology.SE community has agreed that questions that show little or no prior research effort are off-topic on this site unless you have shown your attempt at an answer. Please [edit] your question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Since this is a pretty common textbook-style topic, there is a lot of information available about depressurization from scuba diving in particular.

I have not found any online (as shown by edits), but I would love any specific reference that I could look at.

please delete this question. I will re-ask it. I do not like the fact that I asked the question under the premise that blood pressure does change when even that is not certain to me when reading various sources anymore.

You can simply edit the question, including the title if you so choose. The only time to avoid doing that is once you've already gotten answers if the changes would make the answers invalid. Thanks for doing some more work on your own!

The change has been made. Please feel free to answer (dear community)!

'However, it is hard to imagine that the pressure of the air breathed in by a scuba diver would change, due to the fact that air is brought from an oxygen tank that seems to be independent of outside pressure' You are misinformed about both points. SCUBA tanks usually use ordinary compressed air, and are equipped with a regulator valve that matches the pressure of the gas supplied to the diver to the ambient pressure. The regulator is essential Too much pressure would burst the divers lungs, and too little would keep the lungs from inflating.

Thank you I did not know about the existence of regulator valves. In that scenario, it makes sense because the pressure of air going to the lung is dependent on water pressure. The question can be closed now.


text:
ID bug found in Mojave county, USA

What is this? I found it under a bed sheet. I live In Mojave county, AZ, USA, in the middle of the desert. It was probably 1/8 inch long. And narrow.

Initial guess based on mouthparts, coloration and small size:
Neuropteran larva. Possibly a green lacewing (family Chrysopidae).
See:

 Source: Bugguide.net

 Source: Cedar Creek Ecosystem Science Reserve
According to here, green lacewings are found in Arizona deserts.
I will update in the morning with more detail...


text:
Could certain drugs enable one to consistently eat above TDEE or BMR without fat gains?
I heard anabolic steroids and stuff like DNP and ephedrine and etc. can somewhat enable one to eat more and get away with it without much or any fat gain, despite eating more than the body would normally use.
Is this true? Can hormones, AAS, HGH and other fat burning drugs or stimulants or etc. enable one to consistently eat more than their basal metabolic rate without becoming fat?

Do you remember where you heard this


text:
Classes of Graphs used in Biology
I am a student of Mathematics.Since I found no better place to ask my question I post it here.
I was looking for some classes of graphs which are used in biology.
I came across this particular class of graphs called kite graphs whose link can be found here https://rpubs.com/thoughtfulbloke/kitegraph.
I found it interesting because graphs are mathematical objects and finding them useful in biology is naturally very interesting.
I also find research papers in Mathematics involving kite graphs.
My question is what are some classes of graphs like the kite graphs which are used in biology.
Where can I find them?
In case someone helps,I will be grateful to them.

this question is currently very broad and may be closed for that reason. Please consider narrowing the scope of your question further. Thank you.

joining the question - I am looking also for common categories of graphs used in biology. When I write categories, I mean for instance: tress, unicyclic graphs, bipartite graphs, and so on.
I tried to look for scientific articles that reviewing it, but did not find any related survey.

I don't think there is a single "class of graph" that isn't used in biology.
In biology (just like in any other natural science), we have all kind of data types;

non-ordinal variables
boolean
ordinal categorical
numeric
tree data
other types of network data
pure functions (from statistical or theoretical models)
pictures
sounds
etc..

We make all kind of graphs out of these data;

scater plot
points or lines with eventually error bars
bar graphs with eventually error bars
kites
boxplot
images (colored shaped kind of things; e.g. density maps)
phase diagrams
multidimensional graphs
pie charts
function graphs
Venn diagrams
existential graphs
flow diagrams (incl. alluvial diagrams, spankey diagrams, ...)
trees
matching trees
other types of networks
schematic representations
pictures
spectrograms
videos
interactive graphs
etc...

One can really display any kind of data / information in anyway (s)he wants to.
Kite graphs are just simple graphs to compare frequencies variation along a continuous variable and among a categorical (ordinal or not) variable. It isn't the most common types of graphs but we see them. As a matter of fact, in a paper of mine that is currently under revision the figure 1 is a kite graph (with nested non-ordinal categorical variables).
Just look at random papers to find graphs. Go on google.scholar.com and search for any biology subject and you'll find papers with graphs.

I am asking for graphs which can be described mathematically

A kite graph is a graph with a closed cycle and a path

But can you describe the graphs you have written like that


text:
Plant identification and toxicity
What type of plant this is and is it poisonous (and, if so, in what quantities)?
The pictures were taken at Gullane Bay, Scotland. The plant is widely present in that region.

You should try Google search by image. Its pretty handy when you dunno what you're looking at.

@user79161 I’ve tried but results are not conclusive. I reckon the pictures are not the best and algorithms fail to properly differentiate plant from the background and surroundings.

This is common sea buckthorn, Hippophae rhamnoides. The blueish leaves and the orange berries are unmistakable.
It occurs mainly in coastal regions, but is also cultivated throughout the world. The berries are processed to all kinds of food.
In their natural habitat in Northwestern Europe, the berries serve as a food source for migrating birds that fly from Scandinavia to the UK or the Netherlands. However, because the berries are often rotting and contain alcohol in september, sometimes drunk birds can be observed.

Thank you very much for this comprehensive and informative answer.


text:
How many frames per second do human eyes see?
I observed when a helicopter rotor or fan is spinning the blades blur making it impossible to count the blades, but after a certain speed the blades seem to become visible making it possible to count the blades. Cameras can also do this better.
Do human eyes have a frame rate? What is that called and the most a person can see?
This video in the link shows how these blades seem not to move by timing with the cameras frames rate.
https://www.youtube.com/watch?v=R-IVw8OKjvQ

The term you want is "flicker fusion rate".  For humans, it's about 30 frames per second, though it varies somewhat between individuals: ps://en.wikipedia.org/wiki/Flicker_fusion_threshold

@jamesqf I revised it so your comment can be an answer. Thanks

@BryanKrause TEKKEN?


text:
How is the eye damaged by computer screens?
Eyes are damaged by persistent use of computer screens. On giving it some thought, it felt quite magical that your eyes are damaged simply by looking at something. I googled where there were articles about blue light and stuff and having felt dissatisfied come to the wiser community here for help.
The question is pretty plain, how does the simple action of looking at a computer screen cause damage to the eye? Is it due to focussing the eye continuously at something close-by?
Is the damage caused to the retina, or the cornea or some other part and in what form? Does the light reshape the lens or something?
Edit: I got glasses of power +1 for both eyes about 3 years ago and 4 years ago, my exposure to computer screens increased to about 6 hours a day. Before that, it was hardly an hour or two a week. The ophthalmologist I consulted also credited it to increased exposure to computer screen.
Hope the questions are clear.

You really need to support the claim that eyes are damaged by computer screens in particular - that is, aside from the problems caused by spending extended periods focussing on any close work.

@jamesqf Sorry but, I'm not getting what you are trying to express.

You need to show some credible source that looking at computer screens damage the eyes. Without it, your question is a wild guess.

How old are you? Becoming long-sighted is nothing unusual with age.

I am barely 18 years:)

Re your edit, being rather older than common access to computer screens, I remember that the same thing would be said about people who'd spend a lot of time reading, or doing other close work like sewing.  IOW, it's not something unique to computer screens, but to the muscular effort involved in keeping the eyes focussed on something close.  Eventually they adapt to it.

The light from computers is safe, it can only be the distance and the reading habit which are a problem, so the same applies to books. avoiding excercising your eyes in their near and far ranges is known to be a problem, that's why reading is not recommended to those with growing eyes.

This would be better placed at skeptics.


text:
Is newly produced sperm healthy if there was previous DNA damage?
I read that sperm cannot repair DNA damage. So does this mean that if your sperm has DNA damage, then all of your sperm (whether present or future) has DNA damage? Or does it just mean that the present sperm has DNA damage, but new sperm will be healthy?

Male gametes (aka sperm) is produced by meiosis of numerous germ cells (gametes precursors). It is unlikely that all germ cells have damaged DNA so the newly produced gametes should be healthy. This also implies that if the DNA inside the gametes was damaged after they were produced, then again, the new gametes will be healthy.
As a disclaimer, I am talking exclusively about damages to the DNA, it could very well be that gametes are unviable for other reasons than just spurious DNA (e.g. low mobility). In this case, viable gametes are unlikely to be produced unless the reason underlying the original production of unviable gametes is fixed (e.g. via medication).


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Can you help me identifying an insect I saw?
I'm a student of biology and yesterday we went to the fields to collect some plants for our herbariums.
Suddenly one student of our group said that he saw a very strange bug that he thought that was related to the family of wasps/hornets.
He pointed to some dried bushes and that insect was hidden inside. I could not do a photo but I hope that you could help me identifying this bug since it surprised me a lot (and even scared me a bit).
From what I remember, this insect had an enormous abdomen (around 5-7cm long and 3-4 cm wide) that had a similar shape to the abdomen of wasps and hornets. The rest of its body and head were very small (around 1cm). It had no wings and I think it had no "hair".
It was mostly black with very few red marks/stripes.
I've been "researching" a bit and the most similar insect I found on the web was the Dasymutilla occidentalis but the insect I found had no hair (or rather I believe so), had a much bigger abdomen and was way bigger than the average "Cow Killer". Also, this bug is native to the US and I live in southern Europe, so I think it's very unlikely that this insect lives here as well (I've found no information about Dasymutilla occidentalis living in my country)
The exact location was (in UTM): 30T 0462625 4447661
(East of Madrid, Spain)
I know this description may be vague, but it is all I've got and I'm very curious about that insect I found. It would be great if you could help me

It will be difficult to id the insect based on your description. What surprises me is the relative wide abdomen, compared to the length and the size of it's head. To me a insect with such a wide abdomen would not look like a wasp. Can you explain why it reminded you of a wasp?

@RHA As I said, one student of our group (who is very interested in zoology) said that this insect was probably related to wasps/hornets and also it had the "typical" "triangular" or "conical" shape that wasps abdomens have. Maybe the head was a little bigger (2-3cm) but the entire insect was around 7 cm


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Did Plant Cells Evolve from Animal, Protist, or Fungal Cells?
I know protists and animals preceded plants but I am unaware of when fungi arose in relation to plants. At the moment, I cannot find a resource stating how plants evolved from existing kingdoms, or whether they evolved independently from prokaryotes. Thanks for the help, sorry if this is common knowledge.

cladistically speaking plants, fungi, and animals are all protists.

@John protist is not even a clade, actually. It was a group of all unclassified unicellular eukaryotes.

Plants were almost always considered a separate group from fungi and animals.
As per the latest classification both animals and plants are included in the clade Opisthokonta: animals and related unicellular organisms (holozoa) form a sister clade with holomycota (contains fungi and Cristidiscoidea).
Plants (archaeplastida), aveolates and rhizaria are now grouped under Diaphoretickes (previously they were grouped under Bikonta).
To cut short the plant and animal lineages merge only at the level of the last eukaryotic common ancestor. This means that plants are as unrelated to fungi as they are to animals.
Protista is no longer considered a proper clade. It used to be a group where all unclassified unicellular eukaryotes were dumped. Now these organisms have been reclassified; some are closer to animals (for e.g. Amoeba), some are closer to plants (e.g. Plasmodium) whereas some are part of a group that is distantly related to both plants and animals (for e.g. Euglena).
Have a look at this WikiSpecies site for a detailed classification (latest and historical). It also cites proper references.


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Is it impossible to increase skeletal bone mass, as opposed to just bone density?
I've heard exercise and resistance/strength training increases the density, but doesn't increase mass. So basically, experimentally or theoretically possible at least, can modern science do this/is it feasible?
Density is just how "packed" the current bone is on the micro-level -- i.e., doesn't affect total mass potential. Filling or adding "density" is just like putting water in a fixed-size bucket until it fills. By "adding mass" I want the bone's bucket to be able to hold more density, i.e., a larger potential of density along with an overall greater weight to the bones themselves. I can't find any evidence that this is possible with long and flat bones alike, AKA the spine, leg and arm bones, clavicles and etc. -- or any bone.
I've heard facial bones are more malleable, but their bone mass cannot change with diet/training either.
So to make this as easy to understand as possible: Can bone mass in an adult be significantly changed somehow? Can I make my whole skeletal set heavier somehow, rather than just dense? Like for example, say I am considered "small framed." Rather than just density, could I make my frame bigger? Could I make my entire frame base more robust through some possible bio/drugs/etc. means?
And since I know someone will come along and claim this is a "medical/personal question," explain to me how this would be possible to ask in a non-medical/personal way then to enlighten me. Go ahead.

Bone mass probably does vary with bone density, and it's the volume of the space that the bone occupies that doesn't change much due to exercise and resistance/strength training, at least in the short run. But I could be wrong...

Density = mass/volume. If volume stays the same and density increases, mass would also increase.

@MelaGo My assumption would be that it's a limitation on volume in which density can take place. You can't "out-volume" the potential of the bone, which is my argument the whole "density vs. mass" simplification -- i.e., you can add as much density to the given volume/genetic/epigenetic/adult size/etc., but cannot really make the bones bigger in any significant way such as a smaller frame to a medium/large one.

@WasteOfTime, your entire question can be clear enough if you just ask if exercise can make someone's bones bigger in the sense of a bigger frame. There's a lot of unnecessary confusion by mentioning mass and density.

If you search for
 - bone growth training
 - bone hypertrophy athletics,
 - bone diameter increase,
 - bone strengh hunter gatherer,
on google, you will find more articles than I could possibly summarise:
stimulation of longitudinal bone growth and widening of the joint space (cartilage hypertrophy) occur. The possibility of bony hypertrophy as a result of athletic training, especially with regard to increases in of bone density and bone diameter, should lead to incorporation of sports medical considerations into the prophylaxis and therapy of osteoporosis.
https://www.ncbi.nlm.nih.gov/pubmed/7856798
https://www.ncbi.nlm.nih.gov/pubmed/7478507
I have slender bones and it was the gain of muscle which helped me to balance my physique.

Gaining muscle != making any significant difference of skeletal bone mass/shape/volume/etc. If anything, muscle can at best hide some smaller frame along with fat if you have the natural genetic potential for decent musculature (unlikely with a small skeletal frame).

When you are 15-18 your bones grow a lot faster than what your musculature can adapt for. I found myself with hands and arms which were 30 percent longer in the space of a few years, so they would basically flap about and I didn't know why they had lost their agility. In that sense, you get used to your physique as it adapts.

I've found the opposite -- good muscle strength, but frame not good enough (on my body/my experience). A smaller skeletal frame overall is a death sentence when it comes to your ability to play brutal contact sports, as you're more susceptible and injury prone, along with generally having less physical potential due to bone shape/etc. There is a reason why most pro athletes don't have very frail/narrow/small bones/etc.

I mean nobody will believe this guy plays in the NFL just by virtue of his body frame alone: https://discourse-cdn-sjc1.com/tnation/uploads/default/optimized/3X/f/8/f83761f1b6276c54d664c7e07eef63bdb2fdbb16_2_405x500.jpeg And no amount of muscle building will improve such a small body/skeleton shape/etc. that's always vulnerable. This is what I mean when I talk about skeletal mass, as it's the overall structure that can't be changed in any significant way vs. just merely adding some density/etc. that won't really do much if the guy in the photo above wanted to play organized contact sports.

In short, yes, you can increase your bone mass by increasing both the bone density and thickness, but the increase may not be as great as you expect.
The body frame consists of the length and thickness of your bones, and is mainly genetically determined. After age about 20, you cannot increase your bone length further, but you can increase the bone thickness by few millimeters by regular heavy exercise. In this study in tennis players, the bones in their main arms were thicker by 2 mm at most compared to the weaker arms.
The bone mass also increases with bone density, which means more collagen fiber in your bones or, as you compared, more water in a glass. Bone density is 95% determined at the age about 20, when your bones stop to grow. Your bone mass probably reaches the peak between age 25 and 30 (OrthoInfo).
Until your bones still grow, you can somewhat increase your bone density by consuming enough calcium and vitamin D and by being regularly physically active (PubMed, 2015). Please note, that consuming excessive amounts of calcium or vitamin D will note further increase your bone density.
After your bones stop to grow, you can maintain your bone density, again, by sufficient calcium intake and regular physical activity (PubMed, 2008).

Wouldn't the thickness be attributed to just the most density built possible? They use the arms a lot so it's obvious the bones would be a little more dense there in their dominant arm/etc. This doesn't really mean an overall change in bone mass, other than just the same bone structure becoming more ossified/calcified/etc. I mean the actual bone didn't really "grow" or change in any significant way. The same bone shape/size/etc. that was/were genetically determined for the most part just became more dense by a super-tiny bit (2mm isn't even noticeable without like a DEXA scan or etc. maybe).

I mean it's obvious sports and exercise make anyone's bones more dense, but this doesn't really make a real change in the overall bone mass/volume that is comparing, say, a small-framed man's skeleton to a large-framed man's. The bones may get stronger and as dense as possible, but do not really gain mass/noticeable thickness/size in any way that one could compare like an untrained individual's muscle mass to that of a multi-year weightlifter (on average). So no, this seems more like repeated use adds (very insignificant) density to bones, which is known -- but no real change in frame/size.

They DID observe an increased diameter (thickness) of the arm bones but this was relatively small, so I said you may be disappointed. This bone growth doesn't really change your look and it certainly doesn't make your frame larger. It's not even nearly comparable with muscle mass increase. Looking only at bones you would barely notice the increase. You asked for a scientific evidence and that's it.

I'm not discrediting your post or the source you gave -- both are valid/"okay" as far as info and sourcing/answering goes. What I am just adding on to is the fact that this doesn't and cannot make any significance in overall skeletal base/mass/frame by adding density itself. So it's meaningless in that regard, but still valid in general. Basically this confirms that it is indeed impossible to make any significant change to your overall skeletal frame from exercise at least, as evidence shows negligible results over long durations.


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Mysterious spherical mass of feathers (Reddit)
Original posting from Reddit
I am posting this here in the hopes that an ornithologist might be able to shed some light on this unusual finding.  Locality is Boise, Idaho.
This appears to be a roughly spherical mass approximately 6 cm diameter, most of which comprises tightly packed feathers with a central core of dermal tissue.  The mass has been parasitized by maggots.
I speculate that this is some kind of tumor, which detached from the afflicted organism, and the decaying tissue attracted flies after detachment.  But that's just a guess.  If anyone has seen such a phenomenon before, please feel free to enlighten me!
Note, I am not the individual who found this object.  I am merely relaying the question to this forum.

This is a flap of feathered skin from a Mallard, birds do not shed their skin. The bird in question is likely dead or at the very least, severely injured.
The skin and curved feathers has curled up around itself into a "ball". As it's flattened/separated you can see there is reddish skin with some tissue on it the maggots have gathered on. The feathers here are relatively small and curved and the pattern is SPOT ON for the breast/belly feathers of a Mallard.
While it's not really obvious in the photo of the Mallard below, it is very common for them to have that little bit of pale edging on the dark reddish-brown feathers, as seen in the first photo.

Photo by Jo Garbutt (Flickr: https://flic.kr/p/jVbHwP )


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In marine DNA viral diversity studies, what would "paradigm of rampant mosaicism" refer to?
The recent paper in Cell Marine DNA Viral Macro- and Microdiversity from Pole to Pole describes the (huge) new Global Ocean Viromes 2.0 (GOV 2.0) dataset.
In the Results and Discussion section, the subsection Validating Viral “Population” Boundaries begins with the paragraph:

Defining species is controversial for eukaryotes and prokaryotes (Kunz, 2013, Cohan, 2002, Fraser et al., 2009) and even more so for viruses (Bobay and Ochman, 2018), largely because of the paradigm of rampant mosaicism stemming from rapidly evolving ssDNA and RNA viruses, whose evolutionary rates are much higher than dsDNA viruses (for review, see Duffy et al., 2008). The biological species concept, often referred to as the gold standard for defining species, defines species as interbreeding individuals that remain reproductively isolated from other such groups. To adapt this to prokaryotes and viruses, studies have explored patterns of gene flow to determine whether they might maintain discrete lineages as reproductive isolation does in eukaryotes. Indeed, gene flow and selection define clear boundaries between groups of bacteria, archaea, and viruses, although the required scale of data are only available for cyanophages and mycophages among viruses (Shapiro et al., 2012, Cadillo-Quiroz et al., 2012, Gregory et al., 2016, Bobay and Ochman, 2018).

I know what "rampant" means in the colloquial sense, and the colloquial form of "paradigm" is familliar as well. Mosaicism usually relates to genetic differences between groups of cells within an individual multicellular organism. I am not sure how it applies to virus populations.
Is it possible to explain the meaning of "paradigm of rampant mosaicism" in this particular context, and give it some background?

If you check definitions of the words you arrive a the logical meaning: "... the standard model of uncontrolled, widespread, pervasive mosaicism ... "

@com.prehensible consider writing that up as an answer and letting people vote on it then?

It could possibly be related to packaging of different viral genomes in the same capsid. Not sure about it. I'll read the paper and get back.

As I understand it from skimming the Cell paper and that by Bobay and Ochman, 2018, which it cites, the concern is the validity of the established method of defining viral species. Quoting from this latter paper:

Members of a biological species are defined by their ability to exchange genetic material…

The problem would appear to be that ssDNA and RNA viruses evolve rapidly (rampant is probably meant to convey this idea), but most importantly, not just by acquiring point mutations or deletions, but by horizontal gene transfer from other viruses (and from bacteria).
The net result of this is that such viruses are made up of segments from different sources, some evolved by conventional mutation and others ‘hijacked wholesale’ (my own hyperbole) from other organisms. Another way of putting this is that their genome is a mosaic of genes from different organisms. An example of this is in the diagram below, taken from a paper by Juhala et al. entitled “Genomic Sequences of Bacteriophages HK97 and HK022: Pervasive Genetic Mosaicism in the Lambdoid Bacteriophages”.

For anyone unfamiliar with the word ‘mosaic’ (or its applicability in relation to genomes) I reproduce below a Roman mosaic from Pompeii. The idea is that what appears as an integrated organism is composed of disparate pieces with distinct boundaries.

(The protagonists in the mosaic are about to exchange blows, rather than genes. There are also mosaics at Pompeii depicting the latter type of exchange, but these are a little too ‘rampant’ to present here.)
The implications of ‘mosaicism’ for defining viral species is — I imagine — that viruses which could be regarded as distinct species from examining the sequences of the majority of their genes might still be able to exchange genetic material by crossing-over at genes they have acquired by horizontal transfer.
Oh, and what about paradigm? It would clearly be unfair of me to suggest that this is a fancy word that the authors have used to sound important. The Oxford Dictionary online defines it as:

A typical example or pattern of something; a pattern or model.

I think that the authors mean that the viruses provide a good example of horizontal gene transfer.

Okay, this is really helpful. I've absorbed as much as I can; it's too unsettling to try to really imagine the extent of gene flow in these huge systems, though I'm sure it's quite exciting to the molecular geneticists. I'm going to keep it simple and just remember the anecdote that Sputnik was found in a Paris water-cooling tower in 2008.

I don't think this is an answer, but I have been told to write it as an answer by a mod:
it means
" ...the standard model of uncontrolled, widespread, pervasive mosaicism..."
Mosaicism mechanisms are probably for another topic, Wiki states that:
Genetic mosaicism can result from many different mechanisms including endoreplication, anaphase lag, and chromosome nondisjunction.


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Phenotypes caused by mutations in mitochondrial DNA?
Will mutations in mitochondrial DNA necessarily affect phenotypes?
I have some cursory knowledge of serial endosymbiotic cell theory, and find it difficult to consider that the DNA of the former cell — now organelle — would affect anything outside of the mitochondrion itself, although I can imagine the alteration of mitochondrial processes having an indirect effect on non-mitochondrial processes associated with certain phenotypes.

I have edited your question slightly. It's best to make titles short and punchy and ensure that the body is self-contained (i.e. comprehensible without reference to the title). One thing I had difficulty with was your phrase "mitochondrial process as a catalyst for certain phenotypes". Catalyst means one thing in biochemistry, and this is not it. I have replaced it by "having an indirect effect". Is this what you meant? If not, try to phrase precisely what you do mean.

Assuming that I have understood (and reworded) the question correctly, I find the logic strange. It is the disruption of or change in process that produces phenotypic changes following a mutation in the gene, so if the process is critical for life — like those occurring in the mitochondrion are — what difference does it make where it is encoded?
Perhaps the problem is the endosymbiotic theory of mitochondrial origin. Yes, most of us believe that, but, whatever it was millions of years ago, the mitochondrion is an integral part of modern eukaryotes. Extensive changes have occurred, the most relevant to clearing up this way of thinking is the fact that most human mitochondrial genes are now encoded in the nucleus. Would you these genes would be any more or less likely to produce phenotypes on mutation? Hardly.
Now to the facts. There are certainly mutations in mitochondrial genes that are associated with disease in man and hence produce phenotypes. Some are listed in the table below, taken from a review by Taylor and Turnbull in 2004.

An account of Mitochondrial DNA and Mitochondrial Diseases written for less advanced audiences is this Scitable article.

No, it will not necessarily affect phenotype. Of course silent or inconsequential mutations are possible in mtDNA just as they are in genomic DNA.
But, for example: In some cases, inherited changes in mitochondrial DNA can cause problems with growth, development, and function of the body’s systems. These mutations disrupt the mitochondria’s ability to generate energy efficiently for the cell.
(https://ghr.nlm.nih.gov/primer/mutationsanddisorders/mitochondrialconditions)


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Growth on raspberry cane: What is it?
I have raspberries growing in my garden.
One of the raspberry canes has some sort of growth on it.

Size: Approximately 2 inches long
Location: Zone 5; east of Toronto, Ontario, Canada
Date: April 4, 2019.

What is the growth? Is it insects, fungus, bacteria, a defect, or something else?

Not sure, but possibly the raspberry cane midge, Resselialla theobaldi? Or some other cane midge?

A botanist at a local university says it is most definitely Crown Gall.

He didn't provide any other information than that, so all I can do is quote Wikipedia:

Agrobacterium tumefaciens (updated scientific name Rhizobium radiobacter, synonym Agrobacterium radiobacter) is the causal
  agent of crown gall disease (the formation of tumours) in over 140
  species of eudicots.

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


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What is the scientific name of this plant that is possibly called ogre ears?
I already did a reverse image search and came up with "ogre ears" as a name for this plant. However, this name is associated with other plants: Crassula argentea and Crassula ovata. What is the scientific name of this plant?
Thanks

plant identification I believe falls under gardening.

This (lovely) succulent is Crassula ovata variety "Gollum", known also as "gollum jade" or "finger jade".  Search for the name and you'll find lots of commercial sources.  One informative source is here.

Okay thanks. Looks like Wikipedia has pictures of other varieties mixed in with this one.

You are welcome.  Any plant of horticultural interest can be tough to track down if there are lots of varieties.


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How do animals learns seductional behaviour?
I was curious how the gender behaviour, the male role or female role, is known in mammals. Do mammals instinctively know how to do seduce the opposed sex or do the animals learn it from their parents/companion of the same sex (e.g. by imprinting)?

some do some don't, "animals" is pretty broad category, there are plenty of animals that don't even have sexes. you may want to narrow it down a bit. Some birds for instance have to learn their mating songs, and won't be able to mate is raised in captivity and never learn them when they are young, other know them from birth.

Thats a very cool question but its difficult to answer because insects birds fish and mammals can have very complex courtship even in their first year, and spend most of their energy on reproducing. A lot of it must be innate and instinctive behaviour.

Some behavior can be traced to the genome. In Drosophila there are many interesting studies that show how genes and courtship behavior are related Example.
In mammals, the environmental component in determining courtship behavior is for sure, much more relevant than in Drosophila.


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My understanding of chromosomes and the processes related to them is lacking
I'm sorry for the incredibly simple question, I just can't seem to find any answers elsewhere online.
I am a high school student currently studying for the upcoming AP biology exam, and recently I have realised that I do not quite understand chromosomes. To be specific, I understand what they are (the condensed form of chromatin that one sees when viewing a dividing cell), but my understanding is still lacking when it comes to:

Ploidy, specifically when it changes.
Alleles and how they move/interact during meiosis.
How homologous chromosomes work: When do they occur? Is each chromatid pair identical, or is one chromatid in each pair from each parent?

I made a diagram that details my current understanding, because it can be a bit difficult to describe what I don't understand, but I can try to elaborate more if necessary.

If this is the wrong sort of place to ask this question, some advice on a better place to ask would be greatly appreciated.
Thanks.


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When do the first neurons appear in humans?
According to this
Neural Plate
The neural plate appears in day 18 in humans (very specific).
and according to this
Neural Plate (wiki)

The progenitor cells that make up the precursors to neural tissues in
  the neural plate are called neuroepithelial cells.

And according to this
Neuroepithelial cells

Neuroepithelial cells are the stem cells of the central nervous
  system, known as neural stem cells, and generate the intermediate
  progenitor cells known as radial glial cells, that differentiate into
  neurons and glia in the process of neurogenesis

So, if it's known when the cells which are precursors of neurons appear, I suppose it should be known when the first neurons appear, but I can't find information about it.
When do the first neurons appear in humans?

define a neuron

Apparently, olfactory axons and GnRH producing neurons are among the first neurons that migrate from neural crest at around 39th day of gestation in humans (Cassoni et al., 2016).

In rodents, early GnRH neurons migrate together with a heterogeneous
  coalescence of placode-derived and neural crest-derived migratory
  cells (Forni et al., 2011) and olfactory axons, collectively called
  the ‘migratory mass’ (MM) (Miller et al., 2010; Valverde et al.,
  1992). This cell migration precedes the targeting of olfactory sensory
  axons to the developing olfactory bulb (OB). The existence of a
  similar MM in the human embryo has not yet been described. We thus
  immunolabeled consecutive sagittal sections of a CS 16 embryo† for GnRH
  and doublecortin (DCX) (Fig. 1D,E,G), a marker of immature migratory
  neurons (Gleeson et al., 1999). We identified a very small number (50
  in total) of immature GnRH-expressing cells in the nasal mesenchyme,
  in the medial portion of the olfactory placode (Fig. 1C-E), adjacent
  to the basal lamina of the VNO, showing that the acquisition of cell
  identity occurs outside the VNO between GW 5 and 6. At this stage, we
  observed a mixed mass of immature GnRH neurons expressing DCX (Fig.
  1F,G) or βIII-tubulin (Fig. 1H-J), migrating across the nasal
  mesenchyme towards the telencephalon. As in rodents (Miller et al.,
  2010), GnRH neurons in humans only represented a small proportion of
  the MM (Fig. 1G). Furthermore, these pioneer neurons of the MM
  expressed the delta/notch-like EGF repeat containing (DNER) (Fig.
  1H-J), a transmembrane protein specifically localized in the dendrites
  and cell bodies of postmitotic neurons.

†Carnegie stage (CS) 16 = ∼39th day of gestation


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How do apiarists cultivate homeycomb without nicotine or a smoker?
I don't see a better stack site for this so I'll just post it here. I remember an apiarist I met saying they cultivated honeycomb without a smoker or anything like that, but I never asked them how. Figured it would be interesting to ask if there is any consensus on how one could do that without bees swarming or anything like that.

for the rest of us, "Apiarist is a fancy word for a beekeeper." Phys.org: Nicotine enhances bees' activity CBSNews: Are bees getting addicted to nicotine? fyi the nicotine comes from neonicotinoid pesticides in places the bees visit, not from the bee-keepers' use of smokers.

Ok, well is there a consensus on how to do it without a smoker?

It'a a good question! If you would like to ask about beekeeping without a smoker, then it's better if you click "edit" and adjust the wording of your question along the lines of your comment. I don't think you want to ask about neonicotinoid pesticides, and the smokers can use various kinds of smoke. You might consider asking a second question also, as a new post, something like "How do beekeeper's smokers have a calming effect on Bees?"


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If fish gills do not split H2O into H2 and O, and just take the dissolved oxygen what is left leaving the gills?
Could you please explain to me the exact left overs after a fish takes oxygen out of H2O?


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What is a myotube?
If I understand correctly, the following images show the main components in a human skeletal muscle:
From Life: The Science of Biology:

From Human Physiology/The Muscular System in wikibooks:

However, both resources don't mention the word "myotube" even once.
Wikipedia's Myogenesis page says:

Muscle fibers generally form the fusion of myoblasts into
  multi-nucleated fibers called myotubes.

But I don't know how to parse this sentence.
To Add to my confusion, searching for "myotube" in Wikipedia redirects me to Wikipedia's Muscle page.

So my question is:
What exactly is a myotube?
Could you point it out in one of the images above?

Wikipedia now redirects "myotube" to the Myogenesis page, which seems appropriate according to mgkrebbs' answer :)

A myotube is a type of cell which will develop into a muscle fiber.  It is formed by the fusion of multiple myoblasts, and thereby acquires multiple cell nuclei.  The nuclei are in the middle of the myotube cell, unlike the mature muscle fiber where the nuclei are at the periphery of the cell.  A myotube has a tubular form instead of the more typical rounded cell form of the myoblast.  The myotube starts with few or no myofibrils, and goes through a long, gradual development which assembles filaments, myofibrils and other structures of a muscle fiber.  The transition into a mature muscle fiber is not distinct, but might be defined as the point where all nuclei have migrated to the periphery of the cell.
More concisely, the Dictionary of Cell and Molecular Biology entry for myotube says:

(biology) Elongated multinucleate cells (three or more nuclei) that contain some peripherally located myofibrils.
They are formed in vivo or in vitro by the fusion of myoblasts and eventually develop into mature muscle fibres that have peripherally located nuclei and most of their cytoplasm filled with myofibrils. In fact, there is no very clear distinction between myotubes and muscle fibres proper.

Since the diagrams given in the question are for mature muscle, they do not show myotubes but instead show their result: muscle fibers.

Myotube is A skeletal muscle fiber formed by the fusion of myoblasts during a developmental stage;
a few myofibrils occur at the periphery, and the central core is occupied by nuclei and sarcoplasm so that the fiber has a tubular appearance
and u have the diagrams.


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What is the difference between "hamstring tendon" and "common hamstring tendon"?
What is the difference between "hamstring tendon" and "common hamstring tendon"?  I have seen both terms being used but I don't know whether they referred to the same tendon.
For example,
Johnson, Anthony E., Robert R. Granville, and Thomas M. DeBerardino. "Avulsion of the common hamstring tendon origin in an active duty airman." Military medicine 168, no. 1 (2003): 40-42. (https://doi.org/10.1093/milmed/168.1.40) uses the term "common hamstring tendon" but I don't see any difference with the "hamstring tendon" when reading the article.
Since there are more than one hamstring tendons, I would have guessed that  "common hamstring tendon" specifies which hamstring tendon is being referred to, but I haven't seen the term of any anatomy diagram yet.

The hamstring tendons that I am aware of are:

Lateral hamstring tendon of the biceps femoris (long head) (2 tendons: distal+proximal)
Lateral hamstring tendon of the biceps femoris (short head) (2 tendons: distal+proximal)
Medial hamstring tendon of the semitendinosus (2 tendons: distal+proximal)
Medial hamstring tendon of the semimembranosus (2 tendons: distal+proximal)

(image source)

(image source)

In the paper you cite, they are talking about the tendon on the other side from the ones you've listed, at the "origin from the ischial tuberosity" (quoted from the abstract).
In this case, the word "common" is used in the dictionary sense of "same" rather than "ordinary": it's "common" because it's the same origin for the different muscles that make up the hamstrings. This terminology is used elsewhere in anatomy, too, for example the common carotid artery splits into the internal carotid and external carotid; the "common" portion is the larger proximal vessel.

Thanks very much for the information, makes sense! It seems that the semimembranosus tendon has its own attachment though, separate from the conjoined [semitendinosus tendon + long head of the biceps femoris tendon]. I've posted some details as another answer as I didn't have enough space in the comment. If you look at my answer, please let me know if it is incorrect, I'd  appreciate any feedback.

Expanding on Bryan Krause's answer:
From {1}:

The semitendinosus (ST), long head of the biceps femoris (long head, lhBF) and semimembranosus (SM) muscles
  originate from the ischial tuberosity (Fig. 1a, b). The ST and
  lhBF have a common origin on the posteromedial aspect of
  the ischial tuberosity, over its top. Tendons of the ST and
  lhBF are conjoined at a distance of 9.1–10 cm [35, 37, 58,
  81]. The SM origin is separate from the previous one and
  it is located anterolaterally from the ST/lhBF attachment.
  Fibres of the proximal SM attachment are twisted before
  forming a proper tendon (Figs. 2a, b, 3a, b, 4).
A majority of authors agree with the presence of a conjoined tendon of the ST/lhBF, but the precise description of
  its attachment area varies amongst authors. Most of authors
  observed the attachment on the posteromedial aspect of the
  ischial tuberosity as in our dissection [61, 68, 82], whereas
  others indicated it to be directly medial [10, 58] or lateral on
  the ischial tuberosity [35, 60]. Consequently, the SM attachment is also described in different ways: on the anterolateral
  aspect of the ischial tuberosity as in our dissection [61, 68,
  82, 84], but also anteriorly [35] or purely lateral [58]

Subsequently the "common hamstring tendon" = the conjoined ST tendon + lhBF tendon, but doesn't include the semimembranosus tendon as its attachment is distinct from the attachment of the conjoined ST tendon + lhBF tendon.

To visualize the attachments of the conjoined ST tendon + lhBF tendon, and the semimembranosus tendon to the ischial tuberosity:

Fig. 2 a, b Posterolateral view of the area of the proximal attachment
  of the hamstring muscles (right lower extremity). (1) Area of
  the attachment of the conjoined tendon of the semitendinosus and the
  long head of the biceps femoris; (2) the proximal attachment area of
  the conjoined tendon; (3) conjoined tendon of the semitendinosus and
  the long head of the biceps femoris—cut and rotated 180°; (4) proximal
  tendon of the semimembranosus muscle; (5) area of the attachment
  of the semimembranosus muscle; arrowheads—shape of the
  semimembranosus attachment

(image source: {1})

References:

{1} Stępień, Karolina, Robert Śmigielski, Caroline Mouton, Bogdan Ciszek, Martin Engelhardt, and Romain Seil. "Anatomy of proximal attachment, course, and innervation of hamstring muscles: a pictorial essay." Knee Surgery, Sports Traumatology, Arthroscopy (2018): 1-12. (https://doi.org/10.1007/s00167-018-5265-z)


text:
Photosynthesis: Can light directly excite the reaction center instead of going through the antenna complex?
The reaction centers that I am interested in are P680(photosystem II) and P700 (photosystem I)
Here is what I think:
If pigments such as chlorophyll a and b capture light in the antenna complex, and
if the reaction center contains chlorophyll a,
then the reaction center should be able to directly capture photons and transfer their electron to an electron acceptor.
Or do reaction centers use energy from both the sun and antenna complex?
Also, a side question, I thought chlorophyll a were also efficient at absorbing light in the 400nm to 400nm range, but then why are reaction centers called based on their absorption of 680nm and 700nm light?
Thanks!


text:
Is there a way tell apart dinosaurs from similar extinct reptiles?
When I was a child, I thought I knew what a dinosaur was. But, as I grew older, I was told that many of the extinct species that I thought were dinosaurs (dimetrodons, pterosaurs, plesiosaurs, etc.) were not in fact dinosaurs. Is there a reasonably quick way for a lay person to tell apart true dinosaurs from non-dinosaurs without taking up an in-depth, species-by-species study of paleontology?

There are several defining morphological characteristics of dinosaurs. Including their ankle structure and perforated acetabulum, Aka the hole in their hip goes all the way through, as well as a few other minor features. These combined makes it literally impossibly for a dinosaur to take on a sprawling pose without breaking hind leg in many places, this is why you will often see an erect posture given as the reason, but that is a product of these feature not the defining feature itself, there are many ways to achieve upright posture.
Now of course we are moving away from purely morphological definitions, cladistically dinosaurs are defined as The last (most recent) common ancestor of Triceratops horridus and Passer domesticus (common pigeon), and sometimes Diplodocus carnegii as a third, and all of its(the ancestor's) descendants.
A more superficial quick and dirty method is if it is a pterosaur or lives in the ocean it is not a dinosaur, If its limbs sprawl it is also not a dinosaur. I should also include this guys work, since he attempted to create a complete cladogram of every dinosaur, so you can visualize the group.

Could you explain how dinosaurs could possibly be defined as "the last common ancestor...", since birds diverged from the dinosaurs tens of millions of years before the K-T extinction?

Sorry that should say the "most recent" common ancestor,  which is probably closely related to Nyasasaurus. It is worded that way because it is assumed we will never find the exact ancestral species this way any new discoveries can be assessed. If the common ancestor thig is giving you trouble try this, https://evolution.berkeley.edu/evolibrary/article/0_0_0/evotrees_primer_04

I understand the common ancestor bit, what I don't understand is the choice of species.  IIRC Triceratops was a late Cretaceous (group of) species, while birds diverged from theropods sometime in the Jurassic.  But there are dinosaurs going back to the Triassic (e.g.  Nyasasaurus).  So how can "dinosaurs" be defined as the descendants of something that existed tens of millions of later?  Wouldn't there be many dinosaur lineages that coexisted with that ancestor, but diverged earlier and followed different evolutionary paths?

@jamesqf You misunderstand, all the descendants of the common ancestor, not those two (although their descendants would be included). Since those two are from each of the major dinosaur lineages respectively that means the descendants of their common ancestor will include all dinosaurs. Triceratops and birds are about as distantly related as you can get within dinosaurs.

But aren't the ancestors (or at least some of them) of that last common ancestor also dinosaurs?  At least back to the point where they could be confused with reptiles?  Also lineages that branched from the ancestors of that last common ancestor?

@jamesqf No they are not, this how clades are defined. Every organisms on earth shares a common ancestor with every other organisms, the only thing that varies is how far back you have to go. You may want to familiarize yourself with something called cladistics, which is about the only way of defining biological groups that makes even a lick of sense. Wherever we draw the lines is always going to be arbitrary but cladistics is at least consistent in its rules.

Yes, the legs of dinosaurs are directly beneath their bodies. This is more efficient that the sprawling stance of lizards, crocodilians, pelycosaurs, and other mammal-like reptiles. It is likely no coincidence that another successful group, mammals, also have their legs directly beneath them. Also, as far as I know there were no fully marine dinosaurs.

Please provide support for the various claims you make in your answer. Thanks, Karl.

This would hardly seem to apply to pterosaurs and plesiosaurs.

Points of fact do not need to be supported by citation. Also, it does apply to both pterosaurs and plesiosaurs, whose limbs come out from the sides.

There are many examples of "upright" postures among animals you list as having sprawling posture.


text:
Tiny dark-colored bug ID in Amman-Jordan
I live in Amman-Jordan and I keep finding this bug species on my walls. I saw four till now on the walls of another room. A little bit bigger than the first one.
Click on all photos to open full-sized image:

With cm ruler:

I also have a video, but don't know how to post it.

Hi Rashah. Please provide an approximate size of this insect. If you can, also provide a clearer picture. Your photo quality makes this insect difficult to ID accurately. Could be a bedbug, but might also be a beetle (perhaps a grain beetle). A better photo will help us ID this accurately for you, so please [edit]. Thanks.

I don't know if that will help but the walls I keep finding it on has some mildew on them. Though I sprayed the wall with vineger. Nothing on my bed. No bites on any of my family members. And it's brownish red with naked eye

Regarding your video. Try uploading it to ezgif.com, convert it to a gif file (optimizing to get it below 2mb) and then you can post it directly into your post. You could upload the whole video to youtube and link to it as well.

These are very likely flour beetles (Tribolium spp) of some kind. These small (~3mm) reddish-brown beetles are some of the most widespread and common pests of stored food products worldwide [source].

 Left: red flour beetle; Right: confused flour beetle. Photo credits: Rebecca Baldwin (left); James Castner (right)
The photo is too blurry to be able to differentiate between the most likely candidates: red flour beetle (T. castaneum) and confused flour beetle (T. confusum).

You can learn more about differentiating these insects here and here, and you can find more general information about them via UF/IFAS.

Distribution: Both species are essentially found worldwide; This UF/IFAS page provides a bit more nuanced explanation of their distribution:

The red flour beetle is of Indo-Australian origin (Smith and Whitman) and is found in temperate areas, but will survive the winter in protected places, especially where there is central heat (Tripathi et al. 2001). In the United States, it is found primarily in the southern states. The confused flour beetle, originally of African origin, has a different distribution in that it occurs worldwide in cooler climates. In the United States it is more abundant in the northern states (Smith and Whitman).

Extermination tips are available via epetsupply.com:

Prevention is key!
Keeps your home clean and free of food/crumbs
Sticky traps and pheromone traps

If I had to guess, I'd guess from your poor images that you have red flour beetles, but honestly it doesn't much matter from a pest-control standpoint.

The red and confused flour beetles live in the same environment and compete for resources (Ryan et al. 1970, Willis and Roth 1950). The red flour beetle may fly, especially before a storm, but the confused flour beetle does not fly. [source: UF/IFAS]

UPDATE:
Alternatively, now that I've looked at your picture with such a small specimen, it could be possible this is another "grain beetle": Ahasverus advena, the foreign grain beetle. From Wikipedia:

 Source: Wikipedia

Description:
The foreign grain beetle is approximately 2 mm (1⁄12 in) in length. It can be distinguished chiefly by slight projections or knobs on each front corner of the pronotum, and its club-shaped antennae. The larvae are worm-like, cream-colored and often reach a length of 3 mm before pupating into darker adults. Males and females are identical in appearance both as larvae and adults. The adult is usually reddish brown, or sometimes black.

Distribution
The foreign grain beetle is found in tropical and temperate regions [and is distributed all throughout the world -- see Spanish translation of Wikipedia page].

@Rashah, your updated pictures in your question post make it pretty clear that this is not a bedbug. See Insect identification - Is this a bedbug? for some images of bed bugs.


text:
Are the Fastq files content is truly random
I'm building a system to generate fastq files as they are being output from HiSeq 3000 and HiSeq 4000. This will serve us to test our internal systems with some gold standards.
As we are working with microbiome a standard sample may contain around 1500 different species, is there a a bias in the output regarding how 'close' each assembly record appear next to each other or is it truly random?
If record 1,1 is from assembly 2913, what are the odds that record 1,2 is of that assembly as well (assuming 1500 species with the same strain length) ?
I couldn't find any paper on that so any help from experience would be great.
Thank,
Eden

I'm a bit confused what you mean by 'close' - is it the order of the entries in the fastq file? I'm pretty sure that is completely random (it should be more or less dependent on the cluster order on the flowcell). Also note that the primary output of the HiSeq (or any Illumina Sequencer) are not fastq files, but bcl files. Most sequencing facilities do the demultiplexing which generates fastq files for you, so you never see the 'raw' sequencing data.

@Nicolai By close I mean records in the fastq file one after another. But by now I think it totally random
I didn't know about the bcl file. I'll check it out. Thanks.

In my experience, the distribution of reads on the flow-cell is pretty much random, but the sequencing errors are not necessarily randomly distributed.  In all Illumina instruments I have seen, it is common to see edge-effects, or other localities on the flow cell where the error profile differs from the rest of the cell, and QC pipelines generally test for this problem.
A particular issue with the HiSeq3000/4000 patterned flow-cells is that, in situations of under-clustered runs, it would be typical to find the same sequence repeated multiple times in nearby 'clusters' - in other words, a clustering of clusters all containing replicates of the same underlying molecule.  Even for runs where there is no severe under-clustering, it might be expected that duplicates would be found in adjacent cells.  qcfail.com has an outline of this phenomenon: https://sequencing.qcfail.com/technologies/hiseq/


text:
Tiny white very hard cell bug! Please help to identify!
I found these bugs walking on the floor/ wall and on my laptop.  And unfortunately I think they could be in my bed, too, since I bring my laptop to bed sometimes.
I live in a big city in the Netherlands without pets. My house has humidity issues.
I have noticed that the bugs are very tough to exterminate; meaning that when trying to squeeze them it really needs a lot of effort for their size. Their size is about 1 - 2 mm and their color is whitish.

Please note that my lightbulb is having a yellow color.so it makes it look darker than normal. It's more white than looks in the picture

This is a pic of it walking on my screen...

Very likely a tick, though b/c of poor picture quality, I'm not certain if it's Ixodidae or Argasidae. Can you upload additional pictures (preferably of better quality)? A gif of it moving would be helpful to.

Do you have a nearby bird population? Perhaps living outside the window of your room?

Do you work with wildlife or do outdoor work?

@theforestecologist thank you for your reply. I will make sure to reply/ edit my comments. I do have some birds at my window but not that often. I have an office job and I rarely go to a forest or similar.

I found this great mite ID key tool at idtools.org.

Definitely an arachnid and mite (subclass Acari), and very likely a member of the order Parasitiformes, of which there are more than 100,000 species!!
The body plan is not all too different from a tick (order Ixodida), but the movement of your specimen in the video doesn't seem to match that of typical tick. As such, I next began examining species in the related order Mesostigmata.

Unfortunately, according to here, a clear detailed shot is needed to ID this specimen confidently:

In most cases identification of Mesostigmata to family or lower can be accomplished only if the specimen is an adult female. The easiest way to determine the stage and sex of your specimen is to look at the intercoxal region.  Adult females have a genital opening that is almost invariably in the intercoxal region (species of Metagynella are exceptions) and covered by a sclerotized shield which may be truncate posteriorly or continue onto the ventral region.

However....
Mites just always seem to be associated with birds in urban homes, so I thought I'd do some google sleuthing....and voilà! I've found a near and reasonable match!
Specifically, your specimen looks quite similar to mites in the genus Ornithonyssus of the parasitic family Macronyssidae -- these are bird mites (or possibly rat mites). According to here,

The tropical rat mite, Ornithonyssus bacoti, is one of the most common house invading species. The tropical fowl mite, Ornithonyssus bursa, and northern fowl mite, Ornithonyssus sylviarum, are also frequently encountered in homes. The latter two species are found principally on domestic or wild birds. The house mouse mite, Liponyssoides sanguineus, may also be found in structures with house mouse infestations. The tropical rat mite is a parasite on rats. Although none of these species are truly parasitic on humans, they bite people readily, often producing dermatitis and itching.

As for knowing the specific species, citybugs.tamu.edu suggests:

Distinguishing between different species of Ornithonyssus mites to determine whether birds or rodents are the likely source is difficult and requires special expertise.

You can read more about Ornithonyssus bacoti, Ornithonyssus bursa, and Ornithonyssus sylviarum on Wikipedia, and you can see videos of these mites crawling on people here and here.

According to here, Ornithonyssus bacoti can be found as far North as Iceland.

 See below for images:

 Rat mite (Ornithonyssus bacoti). <1 mm;  © Erling Ólafsson; Source: www.ni.is

 Ornithonyssus spp.; Copyright 2014 Tom Murray; Source: bugguide.net
Note: I do not know this group of organisms well, so my answer serves as an (educated) guess to get you on the path toward proper identification...

Thank you very much for taking the time to do all this research. I have further researched with a local organisation and their educated guess was as well that this is most probably a bird mite. To add more on the whole story; I have cleaned all around my house and washed my clothes, bed sheets etc with very hot water. And in general I havent seen any more of these bugs in my room! So I think it was somehow a one time incident.

@Panos thanks for the confirmation. Glad I could help! Just out of curiosity, do you have a mouse problem in your building?

I can't tell much else due to the photo quality, but it could very likely be a tick. Find them all and get rid of them if you suspect there are more. Ticks are sources of some very nasty diseases. If you have pets, check them thoroughly, the ticks will be embedded in their fur.
Please address the Wikipedia link above for more information. The tells here are: it's (1) small, (2) an arachnid based on the number of legs, and (3) lacks a segmented abdomen. The rest of the features are blurry, and so I wouldn't comment on anything I couldn't discern clearly enough. Much of my ID here is coming from personal exposure to ticks in the wild. The nymphs tend to be somewhat translucent like that.

Please provide support/evidence for your answer. thanks!

@theforestecologist Added the rationale I thought made a solid ID. As for sources, I wouldn't recommend much else than the linked Wikipedia article. My ID is largely based on personal experience.

Netherlands has ticks, yes. Here are some distribution maps of tick spp.. There are also quite a few Google hits for "ticks in the Netherlands". Apparently Dutch spring is quite a season for ticks.

@CKM I look at the pictures of the ticks and they look nothing like the ones that I saw in my house. But still could be wrong. I will try to upload a video too; so to make it easier for people to help. Thanks once more for the help!

Actually, now that I've seen the OP's now-added video, the movement of the OP's specimen looks much more like a non-tick mite. So I'm going with subclass Acari: yes, but order Ixodida: no.

@theforestecologist I would have guessed a tick, but your post has convinced me that a rat mite could very well be a good candidate in the 1-2mm range.


text:
Identify this frog from Bangladesh
Description: About 5-6 in long
Time: March,2019 (summer)
Location: (Alutila Cave) Khagrachari, Bangladesh

Pleae provide approximate size of the specimen and time of year (month and season if possible). Thanks.

Thanks for the updates. +1 for the post. Hope you get an answer! :)


text:
Is there a vertical measure of appearance of a genotype over generations?
Is there some kind of a vertical measure of appearance of a genotype $g$ throughout ancestry, i.e. a measure of how many ancestors of $g$ had genotype $g$. Like for example in saying that on average each member of a population $P$ have 60% of its ancestors having genotype $g$ over 20 prior generations.
A clarifying example, lets take some genetic trait like color, suppose we have a population $P$, and suppose we know all of the ancestry of each individual $x$ in that population up to say six generations, i.e. we know specifically the color of each mother and father of $x$, the grandmothers and grandfathers of $x$, the first great grandmothers and the first great grandfathers of $x$, up to .. the fourth great grandparents, call the set of all those as $Ancestry^6(x)$, lets denote the set of all individuals of $Ancestry^6(x)$ that are $a$ colored as $Ancestry^6_a$, let's denote the total number of members of any set $y$ by $|y|$,
Now what I'm looking at is the proportion $p^6_a(x)$ of all $a$ colored members of the 6 generations ancestry of $x$, from that ancestry.
$$p^6_a(x)=|Ancestry^6_a(x)|/|Ancestry^6(x)|=|Ancestry^6_a(x)|/(2+2^2+..+2^6)$$
Now for population $P$ we'll look for average $p^6_a(x)$: $x \in P$, symbolized as $\mu^P(p^6_a)$ which is $$\mu^P(p^6_a) = \big{(}\sum^P p^6_a(x)\big{)}/|P| $$
In general the measure is $\mu^P(p^m_a)$, where $P$ is the population, $m$ the total number of generations in the ancestry of each member of $P$, $a$ is the genotype, and $\mu$ signify average, and $p$ for proportion. So $\mu^P(p^m_a)$ is: the average proportion of genotype $a$ in ancestry of each member of $P$ up to $m$ generations.

Question: is that measure directly proportional to fitness?

The idea is that if genotype $a$ is more fit than others, then it would appear more frequently in the ancestry of each member in the population.

I don't really understand the statistic that you are trying to describe but it sounds like you might want to read about "coalescent theory" (the usage of branching patterns to describe patterns of ancestry among individuals) and the "folder/unfolded site frequency spectrum" (SFS; frequency distribution of allele frequency in a population). The SFS is one of the many statistics for which we can get theoretical expectation from coalescent theory (see Watterson's estimator function maybe).

Remi.b, OK I've added a clarifying example, that defines it exactly.


text:
Force applied to the human body
This is the basic premise of a physics question I have been attempting to solve over on the Physics SE. (I'm working on solving the actual science behind an old movie myth).

How hard a punch hits is determined by your
  hand's momentum, or the combination between mass and velocity. . . . What acceleration would Super Man need to achieve during
  his attack in order to impart enough force to punch his fist
  into/mostly through a human body?

Unfortunately, in order to solve this problem, I somehow need to figure out the amount of force needed for an object to enter/pass through the human body (by either passing through the sternum or directly below it). Since I have so far been unable to find anything helpful in online searches, and naturally I'm not about to test fire an object through human beings until I find the right amount of force, I'm asking for a little help from the experts on human biology... Does anyone know where I can find or how I can figure out this number?

this may be a helpful place to start https://biomechanics.stanford.edu/me338/me338_project02.pdf

As this is homework related I won't help with the math but I can help point you in the right direction.
Basically, you need to find the density of a human chest and then calculate the force required to "break" it. Looking into the average depth of the human chest we can see from this website, It comes out to be about 250 mm for British man.
The density of human muscle tissue  is about 1.06 kg/liter. Average bone density is 1600 kg/m^3.
For now lets just assume that the heart and lungs also have 1.06 kg/liter as the density. This means we can calculate the overall density of the chest and the required force it can withstand.
The average surface area of a mans fist is .043 sq m.
Knowing the size of the fist and how much force the chest can take, we can from here calculate the penetration force needed to pass through the chest.
Granted this is gross approximations and doesn't account for surface area of the fist. You would need to find a better equation to be more accurate.

This actually isn't homework, just a personal project related to a book I'm writing. (I have a superhuman character who was going to perform this feat, and I began to wonder about its plausibility/the related science.) Thank you for these numbers, it's a start, and more than I found on my own. In order to determine the overall density of the chest, do I need to figure out the ratio of bone to muscle and organs in the chest as well?

To be more accurate yes but there are a lot of variables to account for. For instance one assumption being made is that the objects do not compress. Skin and muscles can compress a bit which would increase the amount of force needed to pierce. Ballistics and penetration are rather large topics. Here is a [paper released in 2012 discussing simulations of depth] penetration(https://www.ias.ac.in/article/fulltext/sadh/037/02/0261-0279).

Oh, And in general, the larger the surface area the less likey to pierce. This is becuase more area spread out requires more force to penetrate. One reason why characters in Grapler Biki or Fist of the North star Tended to attack with straight finders for stabbing.

For a very rough upper bound you could assume that the punch force is translated into 100% pressure on the bone, 100% traction on tendons/ligaments (and generally all tissues which contain collagene type 1 and aren't bone) and so on (which is obviously not true in reality where a punch from the side will generate a torque moment rather than a pressure).
The second step would then be finding the numbers for maximal pressure bone can take per mm^2 , maximal traction a tendon can take per mm^2 as well as the numbers for mass and volume of each in the human body.
These number exist so you can find them with enough effort.
The last step would be to decide which ratio you use for each (i.e. in the given area how much does each layer constitute) , this number (in reality) too exists most likely you can find it in some MRI studies.
So while you won't be able to get exact estimates (because they depend on the geometry of the person, constitution and infinite amount of other variables), you can get a very good upper bound by assuming that the force is translated into exactly the type of stress each tissue is supposed to work with!
Note also that you do not need to know the size/area of the attackers hands or the size of the impact area  if you choose this method!