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Definitions and examples of some math-releated ecology branches
I would like to have an example of application and a brief description/definition (two or three lines) of the following fields. I would like to understand the exact differences between them. Other related informations are also extremely appreciated e.g. if these are fields in growth, the name of the best researcher in that field, best institution etc.

Computational Ecology;
Mathematical Ecology;
Numerical Ecology;
Statistical Ecology;
Ecoinformatics.

I will think more about the Q, but generally these are fairly vague descriptions and I think that different researchers use them in different ways. Also common that researchers working on the same topic/field use different labels on their activities.

Although work in those areas is definitely all related, there are some kind of general differences in how those labels tend to be used, and I'll take a stab at defining them:
Mathematical ecology - this is typically the creation of theoretical models composed purely from math (i.e. not stochastic computer models). Examples include a lot of classics from ecological theory, such as Lotka-Volterra models of predation and competition, but there are also people who still do this kind of research, such as Peter Chesson in his research on the storage effect.
Numerical ecology - this is not a term that I've heard used very frequently, but I think it tends to cluster pretty closely with mathematical ecology, perhaps with more of an emphasis on also including and analyzing empirical data. I hear it used more to refer to techniques than actual ongoing areas of research.
Statistical ecology - I think this term gets used more loosely because obviously statistics are important to most ecology research. It can either refer to research that makes heavy use of advanced statistics because the questions that its getting at are hard to untangle from other effects, or research that uses a statistical model to make its point (note that statistical models are generally different from the mathematical models mentioned above in that their goal is generally to determine how likely something is to happen rather than to untangle some fundamental principle of ecology). A lot of studies on neutral vs. niche-based community assembly would probably fall into the category of statistical ecology. Here is one of many examples.
Ecoinformatics - maybe this is just because I study ecoinformatics, but I tend to think that this is the most distinct of the fields that you mentioned, although it certainly still has a great deal of overlap with the others, especially since it's a pretty diverse subfield. In general, ecoinformatics focuses on making use of large datasets in ecology. This involves both research on developing methods for doing this (for example, I study ways to efficiently collect information from ecological wireless sensor networks. Another good example is the development of GIS tools) and research that uses these methods (e.g. a study that uses GIS to synthesize sensor data and observations of a given organism to determine what that organism's range will be as climate change progresses, or that otherwise seeks to pull ecological concepts out of the data).
Computational ecology - I left this until last, because I think it's the vaguest of the labels you listed. It definitely includes ecoinformatics, but it probably also includes a lot of statistical ecology (and perhaps numerical and mathematical ecology too). I think that the main reason that it's a useful label is that it can catch areas of research that don't really fit in to the other labels. For instance, I once saw a study on quantifying niche space using support vector machines. It was really interesting, and maybe it could be classified as ecoinformatics or statistical ecology, but it didn't really quite fit into either of those. So I guess I tend to see computational ecology as a catch-all term.
These are just the impressions that I have gotten - if others chime in too we can probably build a better consensus definition of these labels.

"Numerical Ecology" is the title of a classic text by Legendre and Legendre, with a recent variation applied to R; but it is not clear how the field is different

Well, this goes to show how differently they are perceived. I find Comp ecol, Stat ecol and Math ecol most common. Don't remember seing Numerical ecol, but can imagine that it can be used for e.g. simulation studies of theoretical models. For me Ecoinformatics is fairly vague (but overlapping with Comp ecol), but often dealing with Big data, next-gen sequencing and remote sensing.

I agree that those are the most common labels - just perhaps not the most descriptive. And I also agree about Ecoinformatics involve big data and remote sensing. My one disagreement would be on next-gen sequencing being part of ecoinformatics. I would definitely classify it as bioinformatics, or else systems biology if it's done in a more ecological context.


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Lystrosaurus was the largest creature on land in the early Triassic, why did they need burrows?
Lystrosaurus was the largest creature on land in the early Triassic, why did they need burrows? What were they hiding from?
(less seriously, why were they so ugly?)

Maybe they were hiding from the weather?  E.g. bears are pretty big, but they find places to hibernate in the winter.  Or perhaps they inherited the burrowing habit from a smaller ancestor?  As for their looks, it's in the eye of the beholder.  I think they're kinda cute :-)

source: Stack Exchange

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Inexpensive way to determine mass of tiny seeds?
My niece is doing a science project and she wants to weigh various seeds, determine their volume and density. She tried using my kitchen scale, but it is not sensitive enough.
I've suggested weighing 100 seeds then dividing to get an average weight, but she (she's 11) wants to weigh each one. I don't want to get in the way too much. I don't mind buying a scale, or other simple equipment as long as it isn't expensive.  Is there any way to do this inexpensively?

A pharmacy is a public business, and they should have a scale sensitive enough to weigh seeds.  They will have to let you in back to use it of course.  If you show up with her and she has the seeds and she asks the manager nicely, they might let you back and help you use it.  I would show up rather than call; if you show up you will see the manager / pharmacist but if you call you will not talk to the manager.
If this works she needs to be sure to credit the pharmacy in her project!
I recommend she weigh several seeds of each type - they might vary.
Your 100 seed idea is a better one, I think.  I understand your sentiment.

You did not ask about volume but this could be done with a graduated cylinder.  Put some water in it up to, say, 5 ml.  Then drop in a seed.  How much farther does the water level rise?  That is the volume of the seed.

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What is the name of this species of bird?
I've enjoyed watching this pair of birds build a nest in my patio light.  One bird now appears to be in residence, and the red bird seems to come and go.  I think they might be mates?  These photos are taken in Mesa, AZ, in the USA.

And here's the red bird:

The birds are pretty small.  I'd say maybe 4-5 inches from beak to tail.  As I said, this nesting behavior started about a week ago.
Can anyone help me identify these birds so I can learn more about them?

Check out the Cornell Lab of Ornithology app Merlin (https://merlin.allaboutbirds.org/) it has a super easy to use and intuitive way to help you ID birds in your yard. You put in the approx size, colors, location, and it gives suggestions with pics and info. Very fun!

Thank you @selene, that app looks fantastic.  I wasn't sure what to put for what the bird was doing so I selected "On a fence or wire" as closest and it listed the house finch as the second search result.  I'll definitely be keeping this in my back pocket.

great! It's pretty forgiving on the location I think so I'm glad it still gave you what you needed :D

Also check out the iNaturalist app. It is for any recent evidence of life, including observing birds.

House Finches Haemorhous mexicanus (pair).

These birds are mainly permanent residents throughout their range;
some northern and eastern birds migrate south. Their breeding habitat
is urban and suburban areas across North America, as well as various
semi-open areas in the west from southern Canada to the Mexican state
of Oaxaca; the population in central Chiapas may be descended from
escaped cage birds.
They primarily eat grains, seeds and berries, being voracious
consumers of weed seeds such as nettle and dandelion; included are
incidental small insects such as aphids. They are frequent visitors to
bird feeders throughout the year, particularly if stocked with
sunflower or nyjer seed.

Copyright unknown, via eu.gosanangelo.com 2022, fair usage
The female is the least colourful of the pair, here seen less fluffed-up:

Paul Lauenstein (mis-named in this case), via Sharonfoc.org, 2022 fair usage.

Looks like a match to me, thank you!  The birds in your first photo seem a bit portlier than mine.  :)   I'll wait a bit before accepting as per convention.

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Interpretation of faint band for Linear Array HPV Genotyping Test
After having used the test for research it would appear as if it is very specific. What is one to make of bands that are there but faint? Or what if there are two bands and one is big and bold and the other is faint? Intuitively, I would believe that the starting concentration of the type represented by the bold band is way higher than the type represented by the faint band. Is my intuition correct? Any insights into what that means? Are both HPV types driving the disease process (eg papillomas) or is it just the bold one? Any data? Any intuitions? Any references?

Could you add some example images of bands of the type you are describing?

I received this answer privately and was given permission (in fact asked) to share it without attribution.
The package insert for the Linear Array assay defines any visible band as a positive band, so a faint band counts as a positive.
The difference in band intensity could be related to viral type abundance but really depends on which bands are being compared.  Because this is an end-point assay, it's possible that some virus types amplify with better efficiency than others when found in a mixed infection and it is also likely that overall sensitivity or detection limits may be different for each type.  Additionally the probe for HPV52 is cross-reactive with types 33, 35, 58 and in the presence of any of those additional types, it may increase its intensity.
The driver of the disease process is the virus with the most oncogenic potential (but I assume that is only when we are talking about cancer or dysplasia, perhaps not when referring to recurrent respiratory papillomatosis or genital warts), which does not change in the presence or absence of other viruses (and regardless of the band intensity).  Additionally, it's important to remember that the resulting disease is clonally derived, originating with a single-type infection (ie. each lesion will be linked to only one HPV type).  When multiple viral types are found within an exfoliated sample it signifies multiple different infection sites (and not multiple virus types within single cells).  Not all of these will progress to high-grade disease, but rather, the lesions caused by genotypes with the highest associated risk are the most likely.


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Can Leptospirosis be spread through human urine
I am wondering if Leptospirosis can be spread via the urine of an infected human individual. All of the sources I have been able to find on the web have stated that the disease is primarily spread through infected animal urine, however, none of them mention human urine.
However, Wikipedia states:

After 7 to 10 days the microorganism can be found in fresh urine

Which would imply that it could be spread via the urine of an infected individual?

It can be spread from human to human through urine but it is very rare seeing as we are relatively clean creatures (most of the time) and our excrement hardly ever comes into contact with other individuals without first being purified.
Sources:

Leptospirosis
CDC: Leptospirosis infection


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Do other animals suffer from myopia or hypermetropia?
Mammals have eyes similar to humas and many other animals like octopuses have a lens in the eye. So do they have such eye defects? If yes, how do they overcome it? Do they feel selection pressure against them in such cases?

This article in Washington Post https://www.washingtonpost.com/national/health-science/animals-eyesight-has-evolved-to-suit-the-differing-needs-of-different-species/2013/03/18/4aaae76c-8b15-11e2-9838-d62f083ba93f_story.html?utm_term=.fb5b97c12f17 addresses your questions

do they have such eye defects?

Yes, eye defect is not specific to humans of course. Cases of eye defect are very common in animals. It is most often witnessed in domestic animals and they are the ones we observe the most (see The physiology of domestic animals)
Eye defects have typically been observed in tree shrews, monkeys (incl. macaques), cats, dogs, horses, rats, elephant and a Cape buffalo.
You should have a look at the wikipedia article Myopia in animals

howw do they overcome it?

They don't wear glasses obviously!
Humans uses the sense of vision a lot. Many animals uses smell (and taste), hearing or touch much more than humans do. For such non-visual animal, having a slight eye defect is not too big of a deal.

Do they feel selection pressure against them in such cases?

That is a bit of an awkward question. Nobody can feel a selection pressure on themselves. A selection pressure is a fitness differential associated with genotypes. A selection pressure is therefore defined at the population level. There is no such thing as a fitness pressure against a single individual.
Let me rephrase this last question to something that makes more sense. I am not sure I will address the specific question that was of interest to you though.

Are non-humans animals that have an eye defect aware that they have an eye defect?

It is unlikely that any animal would have the cognitive abilities to notice that they see more poorly than another animal of the same species. Doing so, would at least require having the ToM and only few species do.

To add on to your point about awareness of eye defects - I'd argue that even theory of mind isn't really sufficient - plenty of humans think they see just fine until someone puts glasses on them for the first time.

I agree. This is why I wrote "would already require" in the sense of "would at least require". I now edited the post now


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Why do some medicines induce sleep?
I have seen lot of people sleep or say that they are feeling sleepy after taking some medicines. Why? I mean, if a medicine acts on some cell of the body because that cell has got its receptors and other cells have receptor for another part of that molecule, then too why do a large range of medicine induce sleep?
This also points to a doubt that there are only one kind of receptors for sleep inducing medicines (the real ones not the ones which have sleep as side effect) or many? If many are there, then it can be possible that a large range of medicines induce sleep.
Is it due to induction of sleep gives relaxation and thus give time for action of other medicines? Or is it just a natural process? If latter, why only some?
I don't want metabolism, just a reason.

Potentially too broad here - many medicines induce drowsiness/sleep but they may (and probably are, particularly comparing sleep medication and those that induce drowsiness as a side effect) by different mechanisms. I think you may need to narrow this down a little.

I'm torn between flagging this as way too broad and thinking that it is a good opportunity to clear up basic misconceptions about drugs in an answer. In any case, I recently noticed that a standard book on pharmacology has three separate chapters entitled "how drugs act", this should give you a hint why the question is hard to answer in this state. Note that these were basic overview chapters, before delving into what specific classes of drugs do.

@rg255 can you suggest what specificity should be added?

You can answer three-four methods. Please give me the common ones.

@InfiniteLight I don't see how reducing it to three-four mechanisms will help. "Why are there many medicines which are H1 receptor antagonists" is not a good question, there is no good reason why there are several of them. Also, I wouldn't say that some mechanisms are more "common" than others, common by what count?

Common meaning here that many medicines exibit them

agree with @rg255 - too broad a question... but could easily just give a broad answer - drugs/medicines are not as specific are they are made out to be - any side effect, not just drowsiness, is an off-target effect

I don't understand the question? Is it why various parts of the same molecule can act on different receptors (atomic level), why a molecule can bind various receptors (molecular level), or why activation of different classes of neurons activate the same brain area (cellular and tissue level). Voted to close because it's unclear. Feel free to edit though. There's enough comments to make this question a cracker.

Hi - I agree with some previous comments that this is too broad because (and this is an assumption) the mechanisms will probably differ between medicines - if you have a few in mind then list them in the question and this will hopefully be answered (I am very interested to see an answer - particularly for antihistimines I take around this time of year... makes me very groggy some days)

Your edits do not fix the problems with this question

I just mean to ask that what can be the advantage of induction of sleep? Is it just as a side effect (like @VanceAlbaugh sujjested) or is it some part of a metabolism?

Is there any general relation which all pathways follow?

@InfiniteLight - within the body naturally occurring compounds as well as medications (i.e. legal and prescription) target a variety of receptors (even if drug companies or other people say they specifically target one single receptor in the body). Almost ALL drugs we prescribe to patients have side effects that are off-target effects. Anti-histamines are probably the most common class that cause people to be sleepy. Even though those drugs "act" through one type of histamine receptor, another type of brain histamine receptor is also targeted unintentionally - causing sleepiness.

@InfiniteLight - you are trying to ask why so many medications cause drowsiness in people. This is a common side effect of many drugs. There are a number of receptors that can cause drowsiness or sedating effects - there are too many drugs to name that act on these numerous receptors. These effects are off-target effects - which we call "side effects" in clinical medicine.

@VanceAlbaugh So, they are always side effects as drowsiness?

I mean drowsiness is always a side effect? I know others are there, I mean to ask if drowsiness is common to all or not

@InfiniteLight - drowsiness isn't always a side effect - it's just a common side effect for a lot of medications. Anticholinergic side effects (i.e. dry eyes, dry mouth) is another very common side effect we see. Those are mediated through cholinergic receptors. I will try and answer this question and give some citations for this stuff.

Give the answer in the answer column now. Don't just comment

Voting to reopen this question. I disagree that it should have been closed for being too broad, because I think this question can be answered with a relatively concise answer that clears up the misconceptions present in the original question.

Me too! @BryanKrause me too!


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When do fireflies glow in their lifetime?
Does a firefly glow only when adult or larva? Or does it glow during its whole life. By glowing, I mean that they glow only when they require, not all the time.
Is there a reason (evolutionary reasoning) why they glow? Also, if the answer is all the time, then why, or if the answer is specific period in life then why?

Is this a homework question? And why would they be required to glow? And what does the last sentence mean?

@AliceD It is not a homework question. Is there a reason (evolutionary reasoning) why they glow? Last sentence means that if the answer is all the time, then why, or if the answer is specific period in life then why?

Gotcha. The way the question is posed it just tastes like homework. In fact, two of the close votes are based on homework suspicion. I would edit the question to remove the demanding undertone and improve its clarity.

A reason is a reason. Keep it simple. Ask whether it performs a function and keep evolution out of it unless your question is specifically about evolution (which it isn't).

@David I think AliceD suggested corrections the way that the meaning of my question won't change. It is clear enough. Maybe you should make the edits. (If you feel so.) :)

Fireflies 'glow' in larval and adult stages but for very different reasons. It is thought that glowing behaviour first evolved in larvae to deter predators(Branham and Wenzel (2003)). This is an example of an aposematic warning, which uses bright colours, smells, sounds, or in this case light, to tell predators they are undesirable as prey. Sometimes a prey animal will use an aposematic warning to tell predators they are poisonous, or simply to mimic a prey that is poisonous. In the case of firefly larvae, they don't taste good to predators because of a steroid compound in their bodies (Branham (2005)).
Adults also glow, but do so in a synchronized pattern of flashes to communicate with mates (Carlson and Copeland (1985)). Mates will time their flashing with physiological fluctuations and even respond directly to another individual's flashing pattern with appropriate delays and timing of responses.
So to answer your first question, fireflies are not continuously glowing, but flash at night as larvae to deter predators, and during active mating as adults.
Your second question can get into a long-winded explanation of how certain traits evolve in response to a pressure, but to simplify, it's likely that fireflies evolved glowing because it relieved predation pressure. This ability then evolved further to communicate the quality of mates more efficiently than phermone signalling.


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Following mRNA vaccination, do proteins mostly exit "naked" from transfected cells or by some more indirect route (EVs etc.)?
Related to someone's elses disbeliefs in how proteins produced from a mRNA vaccine end up in B cells; in theory the process could be more complicated than "naked" egress (which arguably does have simplicity in its favor). There's at least one paper that discussed spike proteins observed egressing in extracellular vesicles (following mRNA vaccination) but it doesn't really say whether this is the common route. And from the general gist of that paper, EVs seem to interfere with detection, so I'm guessing that's not the usual route. For yet another alternative, I could imagine that transfected cells first get killed by CD8 T cells and it's mostly this debris that gets picked up by B cells.
Interestingly, on the last angle, one review mentioned that

Comparative studies performed by
our research group and others demonstrated that nucleoside-modified mRNA LNPs
outperformed unmodified mRNA LNPs in translation capacity, but failed to elicit successful
CTL [cytotoxic T cell] responses due to the drastically reduced production of type I IFNs [119, 157].

So it seems that the mRNA vaccines currently in clinical use for infectious diseases like Covid-19 (which do use nucleoside-modified mRNA) are pretty unsuccessful at killing cells, which makes the 3rd pathway I was considering above somewhat unlikely as a major contributor. (The research group which wrote that review seems focused on cancer immunotherapeutics, and the two cited studies definitely are about that. The lack of CTL activation is a big deal for cancer therapy.)
So, what direct evidence is there for how proteins most often come out cells following mRNA vaccination, particularly in nucleoside-modified vaccines?

During (mRNA) vaccination the spikes mostly don't exit the cells, they get anchored onto the surface membrane. It means that -something nobody talks about- they are likely taken by (dendritic) cells after the cell dies, because the cell is detected by the immune system as "infected". Klling (+phatocytize+presenting on MHC-II the non-self parts) the infected cells is something else almost nobody talks about, whereas it is a very important part of the immune system.

At the 2nd dose things are obvious: the spikes on the surface of the cell are detected by the antibodies produced after the 1st dose which triggers antibody-dependent cell cytotoxicity (NK,..) and phagocytosis (macrophage,dendritic cells,..)

This paper did a serious study of the trafficking of the spike, adding a "HA-tag" (in S1) to detect the spike with labeled antibodies.

@reuns: Thanks for the link. Somewhat inconclusive though. Regarding your other comments, I doubt cell death is the major pathway because the vaccine is administered IM and muscle cells don't regenerate if they completely die (they have complex repair procedures if they're only damaged), but there have been no reports of people losing deltoid muscle strength following vaccination. If killer T-cells persistently target muscle cells it results in major pathologies like IBM (Inclusion Body Myositis), which is very hard to treat.

S.Seneff, G.Nigh suggested that B cells are activated in spleen, not in the muscle. "... the migration of immune cells carrying a cargo of mRNA nanoparticles via the lymph system into the spleen. These immune cells would produce spike protein... and the spike protein would induce B cell generation of IgG antibodies... neutrophils in the marginal zone of the spleen... interact with B cells, inducing antibody production (Puga et al., 2011). This is likely crucial for successful vaccination outcome." https://dpbh.nv.gov/uploadedFiles/dpbhnvgov/content/Boards/BOH/Meetings/2021/SENEFF~1.PDF

I linked to this this paper in a comment on the other question. They detect spike protein on the cell surface using labelled ACE2 or an anti-spike antibody.  They don’t talk about it at all in the paper; just the method and results in supplementary information.

" are pretty unsuccessful at killing cells" - are those vaccines successful  at inducing  B cell production?

@Fizz "but failed to elicit successful CTL [...] responses due to the drastically reduced production of type I IFNs" - This is of high interest. Thanks. I miss some follow up text explaining your  inference that comes next: ("So it seems...): What is the effect of Inteferon block on dendritic and regular host cells? If there is no interferon dendritic cells do not survive their uptake of virus (interesting!!), and, inversely, presenting regular host cells (muscle etc.)  are not apoptotically killed by T cells (not induced) but collapse to "debris"? B cells not induces in lack of T4 induction?

@Roman Riabenko Please set up an anwer based on that reference and the like.

@reuns "... something nobody talks about- they are likely taken by (dendritic) cells after the cell dies, because the cell is detected by the immune system as "infected"... That idiom "Nobody talks about" should wake up the dogs... If anything isn't explicitely mentioned in textbook it should be evident. I do not believe what you say is the following: if infection of target body cell (muscle, epithelium) happens faster than uptake by APC, dendritic cells - "sth. no one thinks of as a possibility" - there should be no apoptotic killing, and that should give a mess - for uptake by PAMP etc./APCs

@reun Your "first comment" seems more and more valuable.  Please set up a question  if it's right or wrong what you are "trying to say". You mention MHC1 and 2 - if dendritic or macrophages clean up debris by non-apoptotically passed away cells  that would be no uptake of "live virus". Similar to  m-RNA-nano-vaccines  debris may contain  some intact mRNA that is still "workable, presentabl" on MHC1. Even more surprising: Not necessary! Regular dendritic MHC1 uptake just has  to catch up, interconnection to B by T4-Helpers. Then, there is both MHC1 and 2 presentation. Textbook doesn't say so!

@PeterBernhard Thank you for challenging me to post an answer. I found the article that I referenced relevant, but I do not know the answer. I just tried to make a hopefully useful comment.

re "picking up debris", Buchrieser et al. e.g., Syncytia formation by SARS-CoV-2-infected cells might be of interest. CoV-infected host cells seem to express spike protein outside the MHC, thus not attracting t-cytotoxic cells -  maybe just falling apart to "debris".

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Primer design for introduction of restriction sites flanking a gene of interest
I am wondering what the correct method for primer design to introduce restriction sites. Specifically between two methods.
1) Primer first partially hybridises to the gene, has a mis-match where the restriction site and extra bases are on the primer, then has a hybridised site following the restriction site, to DNA upstream of the gene.
or
2) Primer first partially hybridises to the gene, then completely dangling and non-hybridising has the restriction site and extra bases.

The option #2 is most common. Do not forget to add 3 or more additional terminal base pairs for optimal restriction enzyme cutting (source: BioTechniques 1998, 24:582-584)

I think the best way is option #2:
Suppose that your gene of interest is AAAAAAAAAAAAAAAAAAAAAAAGGGGGGGGGGGGGGGGGGGGGGGG
and you want to insert EcoRI restriction site GAATCC
Then your Fwd primer will be  GAATCC AAAAAAAAAAAAAAAA
and your Rev primer will be GGATTC CCCCCCCCCCCCCCCC
But in general, it shouldn't matter which option you choose, as long as you calculate the Tm of only the part of the primer that hybridizes to your template.


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Does anyone have any TOPO directional cloning tips?
I'm just about to start working on a TOPO cloning after I couldn't get it to work with standard restriction/ligation. Does anyone have any tips for TOPO cloning?

Ah sorry I should clarify, I first tried the traditional approach to cloning by inserting restriction sites either side of my gene via PCR then double digesting the PCR product and target vector. Following double digestion I then attempted a ligation but I nor my colleagues could get any positive transformants. So I am moving to a different method of cloning using the TOPO kit and I am wondering if anyone has any pointers before I begin using it. It is the pET101/D-TOPO kit.

This may fall under the category of a discussion. I will say that you should make sure that you have the right polymerase if you're doing TA TOPO cloning.

And if you're troubleshooting, I would check the activity of your ligase. If your digestions are working then your doubly-digested PCR insert will ligate with each other. If not, you may have some issues with your restriction enzymes.

thanks @bobthejoe. I suppose you are correct it is more of a point of discussion, apologies for that. The original cloning underwent trouble shooting and the problem could could still not be solved.
This question can be closed.

I think the best way would be to include the details that you've mentioned into the question prompt. If we know what you've tried for troubleshooting, that would be the cherry on top! Essentially, everything that @leonardo asked and we'll go from there.

From what I read, @Ben seems to be saying that he is not looking to troubleshoot the original (traditional) method which failed and is only looking for tips on using the TOPO kit as a first-timer..

See this meta question on the closure of this question


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Life after decapitation?
I saw a video where an ant lost its head and was still walking for some time.
If this is possible for an arthropod, what keeps it from working with a vertebrate? (Humans, especially)

Cockroach bodies can survive without a head for up to two weeks. You cannot really physiologically compare an arthropod to a mammal, for many reasons.

Why? I just want to learn why this happens. I dont care if it is mammal, artopod, fish etc.

Arthropods. Segmented bodies, hemolymph, very simple nervous system. Mammals, unified body, blood, Central Nervous that is removed with head that controls many of the organ systems, endocrine system with hormones originating in the head and throat, organ failure from loss of blood....

So, you say that arthropod because they have different nervous system they can survive without head? Then why they have their brain??

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

@Orphee You probably want to replace your title by walking after decapitation or can a human walk after decapitation or motor activity after decapitation. The concept of life is very different from the concept of  walking.

If someone walks, then he is alive (eg if u see a walking animal you will automaticaly understand that it is alive).


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Cancer cells and their ability to avoid the immune system
Since cancer cell retain their ability to trigger the immune system from their pre-cancerous state and any condition that causes an auto-immune reaction in a specific area of the body will attack any cells in that area then could an auto-immune reaction actually attack any cancer cells in that area also?
Noting that regular human cells are not able to avoid 'attacks' by an auto-immune response so the normal cells can not pass on any 'strategies' for avoiding an auto-immune disease attack to any cancerous cells they 'turn into'.. Is all this possible?

There are several types of cancer immune evasion.
Such as releasing immunesupressive cytokines, downregulation of MCH and comprising mutiations which are not immunogenic.
If the cancer at a tissue is evading immune system by immunosupressive cytokines it may not be affected from auto-immune attack.
However if the cancer is not attacked by the immune system just because it is not "different" enough from the nearby healthy tissues, then at this time auto-immune attack to the tissue may technnically attack the cancer also.

Has there been instances where an auto-immune reaction has attacked tumour cells?

I haven't read about such case.  But it is more like  "Has there been a car  accident which treated cancer by removing the cancerous tissue (skin) "? Even if there is not known case, it does not make such "treatment" impossible.  If normal immune system doesn't attack cancer just because it recognize cancer as "self" then when auto-immune disorder starts it will attack to "self" so to the cancer which is same as that "self".  However if immune system already recognized  and poised to attack the, but inhibited by inhibitory receptors and ligands, then  autoimmune may fail to attack the cancer

PS: could not edit the previous comment for grammar correction.  the last sentence should be "However if immune system already recognized and poised to attack the cancer, but inhibited by inhibitory receptors and ligands, then autoimmune may fail to attack the cancer"

Mostly wrong, yet not a bad notion.
Most* (*all? Been too long.) forms of cancers turn off the natural identification scheme (self-MHC or major histocompatibility complex) as well as the limits on replication. This is because there is a self-kill switch attached to that system.
A cancer would need to release the stand-down signal in a timely fashion, which it cannot do if it is spending its resources on rapid growth.
This means most* cancers are already valid targets without needing an auto immune disorder.
At least one targeted anti-cancer treatment operates by turning MHC back on, causing them to die.
There may be some sorts where the ability to target native cells would help. Doubt it, but could be.

Could a benign virus cause an auto-immune reaction in a persons right knee say and therefore cause all the cells in the knee to be attacked by the immune system including any cancer cell that are there ( even though they can avoid the 'regular' immune system attack??

By normal definitions of "benign", no. You describe an infection that causes indiscriminate damage to the body.

That said, histamine causes a localized region where the body goes killing, taking out native cells as collateral damage. (That's not terribly exotic stuff, but that also makes it that much more believable.) A parasite is more likely to trigger the effect you want than a virus.

So could a mild histamine or a parasite ( that doesn't cause 'unrecoverable' damage) cause all cells in a certain area to be attacked? What causes an auto-immune reaction anyway , is it genetic?

Histamine triggers all sorts of nasty cell reactions. It is quite destructive, so it's fairly localized. It does real harm. A parasite would work by triggering that reaction and, potentially, by eating the cancer cells. Whether or or not that damage is recoverable is contingent on extent, much as with surgery.

Auto immune reactions are often genetic, but that doesn't always mean heritable. Some forms can be triggered by expression errors like in MHC. There are chemical agents that can wreck the body's ability to trigger an immune response. Not totally sure how selective immunity restores itself, but there is some form of coordination between cells and immune system when the self MHC codes are set, so there is likely something that can hack that and change what's read. (This is a really involved topic, though, and better asked over on biology, methinks.)

I mean the questions about immunology with that last bit, there.

Can expression errors in MHC be caused artificially?

Theoretically, since transcription errors can naturally cause this, it should be possible via some form of DNA manipulating enzymes. (a retrovirus, say.) I assume it's possible other ways, too.

So could something like a retrovirus cause an auto-immune reaction in the area where the retrovirus is injected?

Yes, that's theoretically possible. It would need to encode the changes directly or indirectly. (The enzymes to alter that gene expression region or the control signals to create those enzymes or force a situation that otherwise causes this.) I've no idea if that's a phenomenon actually found in nature.


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Single flowers and double flowers on the same plant?
A friend of mine found a strange plant of begonia that at first had regular flowers. After a while it started producing double flowers and has now a mixed inflorescence:

The double flowers look like a result of a homeotic mutant that are also known for begonia, but in this case it is as if such a mutation was somatically "unstable". What might be the mechanism of this abnormality?

I’m unsure of the mechanism, but there are a number of common flowers that change like this. Often it is “age” related:  the young plant gives single flowers, and as it matures, it starts giving double (or more). Some doubles if undernourished will only produce singles. On cosmos, seeing singles and doubles on the same plant is common on plants that are hybridized to be doubles, but not vs. versa. Some sunflowers give doubles on the early buds, but drop to singles on later axillary buds. Your begonia, if healthy, should start producing more doubles.

@anongoodnurse Thanks for the insight. I feel like we might mean different phenomena though. I'm referring to the homeotic mutation that causes stamens to be replaced with petals. Do you mean the same thing for your Asteraceae examples?

I did say that I didn’t know the mechanism, so could not have meant that. Maybe you should clarify your post?

I've updated the question


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How isolated are different areas of the brain?
I'm interested in understanding how isolated different parts of the brain are from each-other. I'm trying to understand the way that different sections of the brain work together.
More specifically, I'm interested in whether or not the different sections are all intertwined together into a wild mass, or work in a more isolated way:
Do different specialized areas of the brain have specific, consolidated connection areas where they exchange information (sort of like they do their job and pass on the necessary information to the other modules)?
Or do they instead mesh very thoroughly, connecting freely to other parts of the brain sort of like tangled string, with no obvious points of consolidated interaction?

Well, to answer your question, both your hypothesis are true, at least partially true.
The brain has several known specialized connections called neural pathways that connect specific areas of the brain and are responsible for determined functions.
For instance, when you move your leg, the stimulus starts at the motor cortex and travels through the pyramidal tract to your leg and then back.
However, one can argue that the stimulus didn't start at the motor cortex. Why? you thought about moving, then made the decision and only then perform the real action of moving your leg.
And here's a more complex (and maybe humorous) example:

You see a dog running ferociously at you.
The stimulus travels through your visual pathway to your visual cortex.
The image of a dog forms in your brain.
It then travels to your Hippocampus.
You realise that's a dog and also remember a traumatic childhood experience with a dog.
The stimulus travels to your amigdala.
You feel fear
The stimulus activates the sympathetic system.
You're now prepared to fight or flight
The frontal lobe is activated
You decide to kick the dog
The stimulus goes from your motor cortex to your cerebellum
Your cerebellum "remembers" the karate classes you had as a kid
The stimulus goes to your leg
You kick the poor dog. He runs.
Nucleus accumbens is activated
You feel good with yourself

So, in short, the brain has pathways that connect specific areas of the brain but, in a sense, all parts of the brain are connected either directly or indirectly. Like the saying "all roads lead to rome!"

DISCLAIMER: I do not endorse animal cruelty.

Poor dog... ;-(


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What roles do circular connection structures play in the brain?
Most neural network simulations are strictly linear, one reason being they don't want to deal with circular connections (and infinite feedback loops if you dont have the right mechanisms). You can deal with them at the cost of some efficiency, but I'm curious about whether in the real brain, circular connections play an important role, or are they really not necessary?
To be clear, I mean any structure where you have a Neuron A, Neuron B, and Neuron C (or a thousand more) and the structure is similar to A > B > C > A or generally at some point Neuron A ends up having a path where its own output can lead back to itself.
What roles do circular connections play in the brain? Or more simply: Are they useful and what are a few reasons why?

'Circular connections', as you refer to them, are super common in the nervous system. This motif usually referred to as feedback connections, and serves a variety of roles.
Connectivity studies can be broadly grouped in to those that look at brain areas, and those that look at individual neurons (usually within a single brain area).
My background is more the latter, so that's what I'll focus on.
Firstly, your question misses an important distinction: inhibitory neurons. So if neuron C was inhibitory, we would have a negative feedback loop, a classical circuit that can be used to produce a homeostatic like signal, keeping a system within certain bounds; a delayed feedback loop can also act as a 'signal terminator', allowing an action to be stopped once it reaches a certain threshold. Lastly, under some circumstance, feedback loops can produce oscillations, which are applicable to a number of tasks.
But more generally, recurrent connectivity is hugely important in the cortex. The majority of inputs to neurons come from neighbouring excitatory neurons (see https://www.ncbi.nlm.nih.gov/pubmed/7638624), and if A connects to B then B is more likely to connect to A than by chance (see http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1054880&tool=pmcentrez&rendertype=abstract for a really nice study on this).
So why? For a variety of reasons. Networks with feedback mechanisms can do more, is the basic answer; from negative feedback for homeostasis, to persistent network states. My personal feeling is that too much of computational neuroscience models a network as an operator - it takes an image, say, and outputs what it thinks the image is. And whilst that is important, it's not what the brain is. We need to maintain a constant internal model of the world around us, rather than going 'that thing is a cat. That thing is a burger'. Perhaps recurrent activity maintains the cortex in a certain state - knowing that the cat is there - and inputs serve to move the state so that we can update our internal models when the sensory environment changes.


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How does the body really react to exposure to the vacuum of space?
I've seen sci-fi movies where the effects the body being unprotected in outer space are wildly different. In one movie, a guy radios for someone who's been ejected into space to breath all the air from his lungs immediately. In some movies, eyes are pulled from sockets. In others, ice crystals form, and the eyes begin to look a bit red... Sometimes the exposed person is a goner right away, sometimes they're shown to last for a minute or more. The Hollywood portrayals of space exposure just vary tremendously.
So I'm curious, what really happens to the human body in the vacuum of outer space?

With regard to the vacuum - Apparently nothing happens as long as you don't hold your breath, just like you shouldn't hold your breath when ascending after scuba diving and the pressure drops. See NASA's answer to the same question. Of course there's the radiation that does other funny things in space, see the NASA link.

And by "nothing happens" he means you pass out in 10-15 seconds from the lack of air and soon die. And btw there are many other reasons why you would die besides the lack of oxygen and radiation..

@zoran404 lol I guess he means "nothing spectacular happens" - no eyes bleeding or instant death.

If a person was in space without her spacesuit/helmet, she would feel a suffocation feeling, likely making breathing motions even though there is no air to breathe. She would also feel her sweat, saliva, tears, mucous, and any other water on her body boil off, though her body would maintain blood pressure, at least until her heart stopped. She would be unconscious within 15-20 seconds and dead within 90-120 seconds.
https://m.youtube.com/watch?v=ZrILTVRcW6A

Please add some reliable references to back up your statements here. And note that the person doesn't have to be teleported, their suit or airlock only needs to fail.


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When the mind is highly active, roughly how many neurons become excited in one second?
I'm curios to know how many times neurons send signals in one second when the brain is highly active (Highly active meaning during difficult problem solving, or any task that might bring the brain to it's higher volume of activity).
When the mind is highly active, roughly how many neurons become excited in one second? The question might also be posed as: "How many action potentials might "occur" in the brain over the course of one second during any form of complex mental process?"

Answers accurate to whatever accuracy we're currently capable of would suit my interests.

What do you mean by "happen"?  Synapses can be strengthened by ongoing activity (or weakened by a lack of it), but they don't really appear out of nowhere on that timecourse.

@jonsca It was my understanding that an action potential sent over the axon to connected neuron dendrites had a chance to either synapse or not depending on the strength of that ongoing activity.

I understand my blunder after some research. I'm still curious about what I intended to ask, so I've fixed my question.

Great question. My first assumption is "nobody knows", but a) I'm no expert, and b) you might be able to get somewhere by using 2-photon microscopy data (or something else that measures neural activity in vivo) and making some inferences. See, eg http://cshprotocols.cshlp.org/content/2014/7/pdb.top081810.abstract

Depends on what you mean by active mind. High resolution FMRI can enable you to approximate how many or which (bunch of) neurons are getting activated.

@WYSIWYG I simply mean, any active mind. Someone solving a puzzle, playing a game, etc. Just looking for a maximum-ish measurement.


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Are neural connections one-way?
I'm trying to think about how two neurons communicate, typically shown in pictures as an electric pulse traveling along a long, thin connective tissue.
Is this depiction somewhat accurate, and if so, what happens if both neurons fire at the same time on that connection?
Perhaps the connections are one-way, or they can facilitate pulses going in opposite directions at the same time, or perhaps it's something different all-together. It'd be interesting to have this explained, at least vaguely.

Are neural connections one-way?

Yes. Action potentials travel only from dendrites towards axon.

typically shown in pictures as an electric pulse traveling along a long, thin connective tissue.

What connective tissue? That thin "wire" which carries the action potential is a part of the neural cell body called axon.
Depending on what the axon connects to, there are 6 types of synapses:
"Blausen 0843 SynapseTypes" by BruceBlaus. When using this image in external sources it can be cited as:
Blausen.com staff. "Blausen gallery 2014". Wikiversity Journal of Medicine. DOI:10.15347/wjm/2014.010. ISSN 20018762. - Own work. Licensed under CC BY 3.0 via Wikimedia Commons.
A synapse is the connection between two structures: the axon of a neuron which "outputs" a signal (chemical or electrical) and the other structure ("input") that can be:

a dendrite or any other specific receptor from a cell
a neural body (can receive both electrical and chemical stimuli)

what happens if both neurons fire at the same time on that connection?

In the situation of an axoaxonic synapse (example 2 and even 5 and 6 from the above illustration), the presynaptic neuron can have inhibitory action (nicely explained on michaeldmann.net at Presynaptic inhibition) from where I quote:

Activity at the axoaxonic synapse partially hypopolarizes the terminal so that, when an action potential comes down the [...] afferent fiber into that terminal, its amplitude is reduced. Because the amount of transmitter substance released by a bouton is proportional to the amplitude of the action potential in it, less transmitter substance is released, resulting in a smaller EPSP and less excitation of the postsynaptic cell [...]

Links:

http://en.wikipedia.org/wiki/Synapse
http://www.getbodysmart.com/ap/nervoussystem/neurophysiology/synapses/introduction/synaptic_contacts/tutorial.html
http://michaeldmann.net/mann13.html

Dendrites don't transduce action potentials. They convert various inputs into membrane potential changes which propagate along them by diffusion towards the cell body. All incoming signals ultimately influence the potential gradient across the membrane of the axon hillock, where an action potential will begin if the depolarisation is large enough. https://en.wikipedia.org/wiki/Neuron#Anatomy_and_histology

First of all, let me clear up a small confusion: a connective tissue is a histological term and isn't relevant to this question :) Check https://en.wikipedia.org/wiki/Connective_tissue on that
That already suggests that the depiction you describe isn't accurate. I would hope that you have seen something like this, which shows a neuron's structure in a very simplified version:

Summarised and simplified, various kinds of impulses (chemical, mechanical or electrical for example) are received at the dendrites, where they generate electrical potential changes. These spread by diffusion across the cell body. At the axon hillock, the point where the axon starts, all of these changes collect and sum up to a net change. If this crosses a certain threshold, the axon hillock generates a so-called action potential, i.e. an electrical impulse. This impulse then travels down the axon until it reaches the terminals. Terminals attach to other neurons (or e.g. muscle cells) via synapses. When an action potential reaches a terminal, the impulse will be carried across the synapse and cause a specific effect on the next cell.
As you can see, there is a clear single-direction signal transfer here: Input -> Cell body -> Axon -> Output. The cell that receives the output can't "fire back" in any way because it receives that signal as an input itself.
A diagram of a pathway including several neurons might thus look like this (neurons are drawn as yellow cell bodies and arrows to indicate where their axons reach):

(Taken from Hubel, D: Eye, Brain and Vision, http://hubel.med.harvard.edu/book/b6.htm)
This does get a bit more complicated when you consider nerves rather than individual neurons. Nerves are bundles of several axons and contain no cell bodies. This means that in effect, nerves are a lot like electrical cables, and like cables it is actually possible to force electrical current running either way along the cable, or to override a signal running in one direction by sending a signal in the opposite direction. This is relevant for example in pain perception where some theories suggest that pain signals might actually be interrupted on their way up a nerve by direct inhibition on the axon bundle (caused by other neurons), see the first diagram here under 8.2: http://neuroscience.uth.tmc.edu/s2/chapter08.html

The connection is one way, the input comes in the dendrites, while the output goes on the single axon in the neuron.

Figure 1 - wikipedia - neuron

The axon of the presynaptic neuron can connect e.g. to the dendrite of a postsynaptic neuron, and so they can form synapses in which they use neurotransmitters to transmit the signal.

Figure 2 - synapse between two neurons

Figure 3 - neurotransmission

There can be different targets to an axon, not just dendrites, e.g. another axon, muscle cells, etc...

Neural axonal connections are physiologically one-way, in that an action potential would never back propagate. Since the signal is physiologically initiated near the cell body (dendritic input region) the normal flow of information therefore is dendritic-to-axonal. However, when axons are electrically activated (through neural implants such as auditory or sensory prosthetics etc), the signal will propagate both ways, i.e., to the axon terminal, but also to the cell body. It is by means of the ion channel opening-and-closing kinetics that action potentials travel only one way, namely away from the point of initiation. The axon itself is not gated in any way- it has no sense of directionality and sustains both directions.


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How much energy is required to blind someone?
As I understand the ravages of sunlight upon the (human) eye; the cause of ocular damage and blindness is too much energy delivered to the cones and rods that ultimately make up our eyes; so the questions arise:
How much light can a (human) rod take?
How much light can a (human) cone take?

there are different kinds of damage.. high energy/high intensity

Light can affect retina in many ways [1]:

photothermal mechanisms - exposure to intense flashes of less than 20 microseconds that cause a rise in temperature of at least 10 degrees Celsius [5];
photomechanical mechanisms - exposure to flashes shorter than 5 nanoseconds [5];
photochemical mechanisms - light is absorbed by a chromophore and leads to the formation of an electronically excited state of it, resulting in chemical transformations [5].

The retina is more susceptible to light induced degeneration at lower wavelengths [2, 8]. The damage degree also depends on intensity and exposure duration. 12 hours a day of more than 500 lux light, more than three consecutive days can affect rat retina [3]. 2 hours  exposure to white light of 3000 lux has lead to apoptosis in rats retina [4].
Sunlight irradiance is about 11 W/cm2 (ranges between 1.5 and 122 W/cm2) and causes damage when exposure time is tens of minutes or even less [5].
Light induces apoptosis by different mechanisms:

Intense light triggers cell death in cones and rods by two distinct mechanisms: rapid, necrosis-like cell death occurs in cones; prolonged, apoptotic death is displayed by rods. However, the areas of cone and rod loss coincide, suggesting some interrelationship [6].

Cones and rods have different vulnerability [7].

References:

Youssef PN, Sheibani N, Albert DM. Retinal light toxicity. Eye (Lond). 2011 Jan;25(1):1-14. doi: 10.1038/eye.2010.149. PubMed PMID: 21178995.
Rozanowska, M. B. (2012), Light-Induced Damage to the Retina: Current Understanding of the Mechanisms and Unresolved Questions: A Symposium-in-Print. Photochemistry and Photobiology, 88: 1303–1308. doi: 10.1111/j.1751-1097.2012.01240.x
Jin X, Wu L, Zheng H, Mishima S. [Retinal light damage: I. The influences of light intensity and exposure duration at moderate and low intensities of cyclic light]. Yan Ke Xue Bao. 1998 Dec;14(4):215-9. PubMed PMID: 12579740.
Remé CE, Weller M, Szczyesny P, Munz K, Hafezi F, et al. Light-induced apoptosis in the rat retina in-vivo. In: Anderson RE, LaVail MM, Hollyfield JG, editors. Degenerative Diseases of the Retina. Plenum Press; New York: 1995. Via http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2831109/
Malgorzata Rozanowska, Bartosz Rozanowski, Michael Boulton. LIGHT-INDUCED DAMAGE to the RETINA (2009). Available from http://www.photobiology.info/Rozanowska.html (accessed 20.07.2014).
Cortina MS, Gordon WC, Lukiw WJ, Bazan NG. Light-induced photoreceptor damage triggers DNA repair: differential fate of rods and cones. Adv. Exp. Med. Biol. 2004;533:229-40. PubMed PMID: 15180269.
Okano K, Maeda A, Chen Y, Chauhan V, Tang J, Palczewska G, Sakai T, Tsuneoka H, Palczewski K, Maeda T. Retinal cone and rod photoreceptor cells exhibit differential susceptibility to light-induced damage. J. Neurochem. 2012 Apr;121(1):146-56. doi: 10.1111/j.1471-4159.2012.07647.x. PubMed PMID: 22220722.
Kuse Y, Ogawa K, Tsuruma K, Shimazawa M, Hara H. Damage of photoreceptor-derived cells in culture induced by light emitting diode-derived blue light. Sci Rep. 2014 Jun 9;4:5223. doi: 10.1038/srep05223. PubMed PMID: 24909301.


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Variation of length of circadian rhythm in humans in absense of time reference
Are there any studies which show the range of the length of circadian rhythms for people that are removed from actual time, (Eg no sunset/ sunrise, no clocks or other reference of time)?
For example, what proportion of people tend to have a natural 30 hour rhythm or greater?
I ask because I would like to know if it is a possible cause of insomnia, how likely insomnia is caused by this, and if this knowledge might in some way lead to solutions for insomnia

This might be the study to which you refer in your answer, the people tested averaged a daily cycle of 24 hours and 11 minutes with a surprisingly small variation in their rhythms:

The variation between our subjects, with a 95 percent level of confidence, was no more than plus or minus 16 minutes, a remarkably small range.

Worth noting they were all healthy and so it doesn't tell us much about insomnia.
This study about insomnia in adults with ADHD shows that circadian rhythms of insomnia sufferers aren't so much longer as delayed (for sleep-onset insomnia anyway). Figure 2 might be of interest, showing that insomnia sufferers have significantly delayed melatonin production.

Apparently, in one(?) study, it was shown that the natural period for humans is actually a bit greater than 24 hours.
I only know this by what Jessa Gamble said in her TED talk:
http://www.ted.com/talks/jessa_gamble_how_to_sleep?
She goes into a lot more detail, and apparently we wouldn't just have one continuous sleep each day, so that makes answering the part of the question relating to length of sleep more complicated.
But interestingly, she gets to the core of how sense of reference disturbs sleep. To quote:

The people in these studies report feeling so awake during the daytime that they realise they're experiencing true wakefulness for the first time in their lives.

Unfortunately it is sparse of detail, short, and lacks any references!


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Pressure produced by blowing with mouth
I need some figures on the pressure humans are capable blowing with their mouth with zero flow. I only need very approximate figures. I'm guessing around 500mm of water? I haven't got a tube handy to try it out.
I've heard that it can also cause damage, eg playing wind instruments has been show to increase health risks due to inter-occular pressure. Any figures on what an acceptable level would be for someone repeatedly blowing for a profession?

Can you add references to "playing wind instruments has been show to increase health risks due to inter-occular pressure"?


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I have a fruit fly problem
I've add fruit flies raising a garden every year I am very familiar with them and how to kill them. But twice now I have killed one by smashing it and upon doing so two little tiny bugs or crawling on me after I smashed the fruit fly and wiped it off of my hand. I am curious of what these little tiny bugs are that are living on the fruit fly. Can you help me identify them[![

Unfortunately the picture is too blurry, so I can only talk from experience : They might be parasitic mites. Insects often carry parasitic mites around.
Look at this article for example :
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10317784/
It seems like Drosophila is no exception.
Moreover in this article :
https://www.jneurosci.org/content/36/44/11275
you can see that Drosophila has evolved a defense mechanism against such mites.
Parasitic mites of insects breach the cuticle and suck the hemolymph (equivalent of the blood + lymph of insects) out of their host.


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Help identifying insect
I live in Milan, Italy in the city center.
I started seeing this insect in August after a long vacation. In this periods the temperature inside the house went up to 36°C (temperatures here range from -1°C to +35°C in average).
I find it mostly in my kitchen in particular in a cabinet where i store food.
The size is about 3mm in length and less than 1mm in width.
What is its name so I can research more about it (i.e., does it pose any risk to my health or to my belongings in the house?)?
I have tried to use a common bug spray to get rid of it (i.e., emptied the cupboard, got rid of food that was not sealed and sprayed the cabinet profusely). It was unsuccessful as after 10-15 days it came back.
Is there a more appropriate bug spray to get rid of this insect?
Should I be looking for nests or eggs?

EDIT
Additional close-up pictures with a cheap microscope.

Welcome back to the Biology Stack. Unfortunately that photo is too low quality to say anything about the insect, we would at least need to see photos of the back of the insect and they would need to have higher resolution to properly identify it. Your best bet is to contact a local pest control company and have them come out and do an assessment.

Thank you for the comment. I have added some pictures, I don’t know if they are very helpful.

Much better. Something in the beetle family I think, but there are a few experts on here, who I will leave it to.

Can't give a species but my first thought would be a grain/flour beetle; you might check your food again, especially any grain, flour, cereal, etc. They may be able to enter through packaging, depending on the packaging type. I wouldn't think you need any pesticides, just to identify the infested food and wipe up any remaining beetles/eggs/larvae, but if the problem persists you could consult a local expert.

Would you know what kind of bug spray should I try before I call pest control?

I don't think a spray is going to help. If I'm right, they're in your food. Spraying outside the food doesn't get the ones that are in your food. Spraying your food directly is not wise because you don't want to be eating the stuff you're spraying. You'll need to find what is infested before you continue. If there are beetles to wipe up, I'd think just a soapy rag is going to be better than any insecticide spray.


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What do the variants on the PolyT sequence mean?
My son has been diagnosed with Cystic Fibrosis.  I am not looking for medical advice regarding his condition, but I am very interested in understanding the genetic causes of his condition.
In addition to the common CF mutation Delta F508, my son's genetic testing revealed both 6T and 9T variants of the PolyT sequence.
If I understand it correctly, it seems that the variants (I have found repeated reference to 5T, 7T, and 9T variants, but almost nothing on 6T) are tied to errors in the RNA transcription of the CFTR protein, but I don't understand how, or what the difference between these variants are.
What does "variant of the PolyT sequence" mean in this context, what are the difference between 5T, 6T, 7T, and 9T, and how do they impact the production of the CFTR protein?

A search in both PubMed and OMIM databases did not yield any result for the 6T polymorphism. It might be not yet described. If you are really interested in the molecular details, you'll have a compendium of mostly all what is known here: http://omim.org/entry/602421

I haven't read too far into this, but from what I understand the variant PolyT sequence is the number of thymine bases in a short sequence within one of the introns of the CFTR gene. Introns and exons are both parts of a gene structure, but introns are spliced out of the final transcript before its converted to protein (for more information see this article on RNA splicing).   Studies have shown that the presence of a 5T sequence in this region may increasethe skipping of exon 9 in the CFTR gene (there is a nice picture showing what I mean here).  This exon skipping will alter the final protein product translated from the spliced RNA species.
I could not find a lot of information about the 6T allele that your son has, however, I found one short article about a patient with 6T and F508 in the European Journal of Genetics. It references another paper that talks about the length of an additional repeat sequence of GT bases and its affect on individuals the the 5T variant.

I can't begin to tell you how helpful this has been to me, both in understanding what the genetic diagnosis means, and what the likely impact for my son will be.  I also found this paper with help from search terms I picked up from the paper you linked. While I'm not taking this as actual medical advice, it does seem like our son is more likely to suffer from CBAVD than symptomatic CF, which is supported by his complete lack of symptoms so far. I can't express how this will help in terms of hope and optimism.  Thank you!


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How are chemical reactions organized in prokaryotic and eukaryotic cells?
I realized I only have a vague understanding based on what remember from high school and I don't know if they ever really broke it down for us but:
In general how do both prokaryotic and eukaryotic cells organize their chemical reactions? In prokaryotic cells I thought there were no organelles so does that mean that every reaction depends on the diffusion of the reactants throughout the cell and that any reaction could happen anywhere in the cell? And in eukaryotic cells, are organelles always used to compartmentalize stages in chemical synthesis?
What I'm getting at is that if everything is just floating around freely within a cell, wouldn't a lot of reactions interfere with each other? I'm wondering how these two types of cells approach this problem.

Okay, this is my first post on this site so please bear with me when it comes to the format of my response!
To begin with I'm going to try and answer your question by clarifying some things.

In prokaryotic cells I thought there were no
  organelles so does that mean that every reaction depends on the
  diffusion of the reactants throughout the cell and that any reaction
  could happen anywhere in the cell?

Yes and no, the fact that there are no membrane bound organelles in prokaryotic cells means a majority of the reactions occur in the cell's cytoplasm via diffusion but something to keep in mind is the selectiveness of the cell's membrane will regulate the substances entering the cell in turn controlling that reactions that occur within it.

What I'm getting at is that if everything is just floating around
  freely within a cell, wouldn't a lot of reactions interfere with each
  other?

When it comes to  eukaryotic cells structures do not float around freely like soup, there is cytoskeleton composed tubules and filaments that is used for  intracellular transport, this skeleton acts like a road system to move substances between static organelles. Prokaryotic cells do not require this since they do not have membrane bound organelles and the diffusion of substances into the cell is controlled by the cellular membrane.

in eukaryotic cells, are organelles always used to compartmentalize
  stages in chemical synthesis?

Not always, you can look at things like cellular respiration to see glycolysis occurring in the cytoplasm.
I hope this helped out some!

Please add references to your post for the sake of those who might want to read further  :-)

One more point to make that wasn't covered in the other answers - in some cases, free diffusion of reactants is desired in order to regulate cellular processes. For example, take amino acid synthesis. At least one of the enzymes in the synthesis pathways of the various amino acids is reversibly inhibited by the presence of the AA itself. Therefore, if AA levels in the cell are high (above a certain threshold concentration) then the pathway is inhibited, and no more of that particular AA is made. However, later on the cell could be in a starved state, AA levels would drop, and the enzyme machinery would start up again to make up the shortfall.
This is a very general example, of course, but there are specific instances of it all over the place - generation of ATP, glucose metabolism, fatty acid synthesis, etc.

Organization of reactions occurs in both prokaryotic and eukaryotic cells. A very basic example of this would be that of multiprotein complexes such as fatty acid synthases and polyketide synthases. Organization of such complexes allows the substrate to be passed from one module to the other; in other words free diffusion of substrate is prevented. This kind of organization can also be seen in case of cell signalling receptors; there are scaffolding proteins that bind different components of signalling cascade together (for example the Grb2 protein).
Regarding organelles:
Prokaryotes do have organelles (in a way); they don't have the membrane bound organelles like ER, mitochondria etc. However, if you consider organelle to be a subcellular structural complex that is dedicated towards a certain function, then prokaryotes do have ribosomes, thylakoids, vacuoles (in some species) etc. All these structures have an organized structure that allows reactions to happen at a faster rate compared to a free-diffusion situation.
In eukaryotic cells, the organelles perform different kinds of function. Organization is one of the molecular aspects; they also can have different chemical (such as redox and ionic) environments which facilitate certain reaction. So their role they play in different metabolic reactions is a composite of all those molecular properties.


text:
What generates variation in a species?
What is the biological mechanism behind the variation within sexually reproducing species? Obviously, the children are combinations, to differing degrees, of their parents. But how does the variation originate in the parents to begin with?
I'm not referring to evolution or mutations rather I have in mind things like facial structure and personality in humans, or fur coloring in dogs. I just thought I vaguely remembered there was some kind of driver of variation... For example, does the parent produce a variety of germ cells that purposely differ from the parent's geneome?
I just think I'm missing something here.
(I'm familiar with DNA and genetics having taken a biology class in college and remembering much of it, I just can't seem to put my finger on this point...)

After mutations, which probably is the source of most variation.  The classic biological model of variation comes from accidents of history and environment.
Many mutations disappear over time because they aren't helpful (advantageous).  The reasons variations persist for more than a few generations is that our differences have helped us to live successful lives and (in biological terms of success) have offspring.  In europe the lactate dehydrogenase gene and others like it that help people digest milk is active through adult life as the result of domestication of milk producing animals,  in asia, this trait is rarer or non existent as agriculture does not produce milk there (in most cases).
This is a broad difference, but its true in smaller ways for all of our individual traits, or so the theory goes.  Individual family traits are helpful to create stronger family bonds, so even something like distinctive dimples or foreheads have claim to being an advantageous trait.  Its possible that blonde hair is the product of such an advantage - its a strong signal to paternity if the father is blonde for instance.
Another answer to your question I think, is that there are probably mechanisms in the cell or in mate selection that increase or decrease variation in the community at given times of stress.  For instance, snakes are among the animals who have a particular ability to select gender depending upon the conditions the female is experiencing.  more males may increase variation in the community - fewer males and more females will decrease it.  (not by a lot mind you, but a bit).
Additional response added as requested:
I see what you are getting at - why do children seem like such individual and unique things sometimes?
In sexual reproduction, the offspring are the product of the shuffling of the parent's genomes through meiosis, where the pairs of chromosomes we have are combined to make a single chromosome that will be half of the children genome.
This process can result in completely novel combinations of genes while conveying many likenesses from the parent.  I would guesstimate that this is the major cause of the uniqueness of offspring/children.
Also in mammals there are some cell lines which splice families of genes which will cause offspring to be potentially quite different from either parent.  Immune genes for instance are created from scratch from a bunch of genes that the parents give.  Making each offspring unique but also the product of the parent's genetic repertoire.  This can be significant as it affects health and also to some extent attraction - studies have shown that people who smell attractive to us are immunologically distinct from us.
@David mentions epigenetic variation, which is a more recent significant development.  During our life, the germline (sperm/egg) DNA may be chemically labelled depending upon environmental conditions we experience.  A famous example is experiencing famine conditions, which caused the children to be born on the small side amongst other effects.   More recent studies have shown that this is a widespread mechanism to control cells in our body during our lifetime as well as communicate to our offspring how life is.  It is expected that this labeling does not affect us forever - the epigenetic labels change over the course of a generation quite often (we believe).

Yeah, but from where does the variety originate in the first place? Given pair of dogs, each pup is different. Is this just due to Mendelian shuffling of the parents' genomes or do the parents have the ability to produce additional variation without mutations? (I just thought I had remembered something like this in the back of my mind). I'm not referring to mutation.

@John yes, there is also epigenetics

Edited to answer more specifically

It wasn't specifically mentioned in your update on meiosis, but just to be clear for John: kids just don't get one of mom's chromosome and one of dad's chromosome for each, but the chromosomes the parents pass on go through homologous recombination. This "single" chromosome (say chr1) the parent gives is built from a "random combination" of the two chr1's the parent has.

@Steve - thanks for clarifying - indeed that's the main effect that causes offspring diversity.


text:
What happens when we know that there is something that we forgot but we can't remember what it was?
I think it happens for everyone that sometimes we go to a room and forget why we went there. Is there any research or article on this?

It is a phenomenon known as room amnesia, some research has shown that your brain may use physical barriers like the room and doorways as a way to compartmentalize thoughts.
One article summarizes it here:

The researchers say that when you pass through a doorway, your mind
  compartmentalizes your actions into separate episodes. Having moved
  into a new episode, the brain archives the previous one, making it
  less available for access. It’s as if you slam a mental door between
  what you knew and…what was I saying?

This is the research.

Nice! I wonder if this works with transparent walls. Perhaps Japanese style semi-transparent paper walls?

Try it! Go to your local garden centre, stand in a display greenhouse, think of something to go and buy, then walk out of the greenhouse and see if you remember!

Thanks for the concise yet comprehensive answer.


text:
Effect of opposing electric charges on cells
Is the affect on a cell between two negatively charged plates theoretically similar to between a positively and negatively charged plate?  In other words, would it induce charges on the inside and outside like in the other case:

But it would induce negative charges on the left and right outer sides of the membrane and positive charges on the inner sides:

Is there a context for asking this question?

Affect or effect? Sounds like the electricity has an effect. It follows the path of least resistance and most cells are generally insulative, blood and nerves probably look a bit like your illustrations.

Sorry about the title.  Just asking out of curiosity.

@Tom From the help: "You should only ask practical, answerable questions based on actual problems that you face". This seems like a toy physics problem rather than a biology one. I can ask at physics and see if they want it.

@ Bryan Krause: I see your point.  My apologies.


text:
What's the probability of a non-pathogenic strain becoming pathogenic from plasmids transmitted through the air?
So the thing is, I was getting a bacterial CRISPR kit for biology class, which is overall pretty simple and I'm just doing this for practice, and my dad was saying he was concerned it would accidentally make the non-pathogenic bacteria I was using pathogenic.  I told him that it was basically impossible for me to accidentally genetically engineer bacteria to be pathogenic because infectious bacteria need a bunch of adhesins to infect the human body.  However, that did make me think, what chances would there be of non-pathogenic bacteria (e coli hme63) becoming pathogenic because of some bacteria in the air getting in the culture and transferring plasmids to become infectious?   Again, I don't think this is likely at all, but I would like to ask those with more knowledge than me.
Edit: it would appear to me that if it was that easy for bacteria to get what they need to be infectious people would be getting sick a lot more than they are.

You have found the reason why genetical work is usually done in confined spaces with defined security measures to avoid even unlikely risks. The CrispR system is safe in this respect, since you need to have some fitting DNA present. The exchange of plasmids however, is a risk which happens in the wild.

But even so, what would have to happen is infectious bacteria would have to be in the air and get into the container with the non-infectious bacteria while it was getting resistance plasmids and give the non-infectious bacteria all the DNA needed to be able to get into and infect the body.  Also, aren't bacteria that grow outside the body not as good growing inside?  Like if some bacteria had extra plasmids they would need more nutrients to grow and they would be outcompeted while growing?  I'm just saying that under normal circumstances, is it almost impossible?


text:
Are there insects who can or try to avoid colliding with raindrops?
Some insects are very fast. Does this mean that they are capable of finding a way through falling raindrops without getting wet?
Probably they don't do that at all, because riding on a bike or in a car they don't avoid colliding eather?!

In the case of mosquitoes, raindrop collisions aren't that serious, apparently: http://www.pnas.org/content/109/25/9822 (and related commentary at http://www.nature.com/news/mosquitoes-don-t-let-the-rain-get-them-down-1.10775)
It's out of my field somewhat but I'd suggest looking at dragonflies as they're big enough to be affected by a 'hit' and they're very agile.

@arboviral almost all dragonflies seek shelter when it rains. I think i read about one exception in the neotropics once.


text:
If our eye lens and cornea were flat would we still receive the world upside down?
Usually the effect of a pinhole (or camera obscura) and the lens of our eyes are creating the world upside down on our retina.
Now imagine the lens and cornea would be flat is the pinhole effect still capable of creating a reversed image or would our vision be total blurred because (parts of) objects  shining straight in the middle into our eye would not be reversed while parts above or beneath the middle would be reversed?

Is this question about visual-cognitive orientation or the physics of a lens focusing light? If it's the former, see this CogSci answer about how visual orientation is perceived relatively- https://cogsci.stackexchange.com/a/339

Cross-posted at Physics: https://physics.stackexchange.com/q/337807/44126

The question is definitely more on-topic on Physics.SE


text:
Does a human body age at any place at the same rate or can there be big differences?
Aging can be caused by bad working mitochondrion, stacking of protein, shortening of telomers etc.
Now all our organs and materials have their own kind of cells, but are they equal vulnerable for aging by eating (which is the main cause of aging).
Probably there are some differences. For example the liver would get much more aged when drinking a lot of alcohol then one would get grey hair, because it is the task of the liver to break down toxic proteins etc.
But can in general be said that the aging of the body goes equal throughout the whole body, or are there more/many special patterns for each organ which are dependent on the kind of food is taken?
So for example a person can have very 'young' intestines but a very old milt or can a person get grey hair but all other organs are very young?

how do you measurably define aging? also you should have googled this first, there seems to be a bit of info on interwebz http://io9.gizmodo.com/scientists-discover-parts-of-our-bodies-age-at-differen-1449085569

So besides the causes I mentioned in my question also DNA methylation (epigenitic cause) is a cause of aging. But in general can be said : 'For the most part, the chronological age of our body parts matches its biological age. But there are some exceptions, including female breast tissue.'?

i suggest editing your question so it has two parts: this is what you know, this is what you don't or dont understand


text:
Is Active Transport Required For Life?
Is active transport required for all living cells to function?
I was under the impression that if a cell doesn't have active transport, it either would lose molecules through the membrane and not be able to maintain a proper gradient, or molecules would be trapped inside the membrane (waste) or outside the membrane (food).

For an organism (think single-celled) living in just the right kind of environment, it might just be possible to survive using only facilitated diffusion, at least as far as small molecules are concerned. This kind of organism would have to maintain exactly the right concentration of the molecules it wants to keep or get rid of, based on the external concentration of those molecules.
For example, if an organism was living in a glucose-rich environment, it might be able to fulfill its glucose requirements by (1) making the membrane itself tightly impermeable to glucose and (2) tightly controlling the number of passive glucose transporters.
It would be nigh-impossible to achieve this for every solute in the environment, especially those that are able to permeate the membrane.
If there were such a thing, it might be found in organisms that live in very low energy aquatic regimes such as anaerobic methane oxidizers, where the solute concentration in the environment doesn't really change in small time scales.
Even in such environments, the number of small ions in the environment is likely to be high enough that some active transport would be required to maintain the osmotic balance within the cell.

So, as far as you know, active transport is universal characteristic of cellular life?

As far as I know, yes. However, as I said, theoretically, life without active transport might not be a total impossibility under exactly the right circumstances.


text:
What is the creature with the lowest neuron count that demonstrates cognition beyond reflexes?
I'm under the impression that nematode worms just perform the same scripted actions over and over again in response to specific stimuli. They have 302 neurons. Chimpanzees display problem solving capabilities, as do other mammals with smaller brains (cats, for instance with ~ 1 billion neurons). You might say that bees demonstrate something more than reflexes when they communicate the location of nectar sources to the hive (~ 960,000 neurons).
What's the creature with the lowest number of neurons to demonstrate something more than mere scripted actions? I would imagine its somewhere between a bee and a nematode worm...

How would you demonstrate that human cognition cannot be boiled down to scripted actions? Your question seems to assume its answer.

Depending what you mean by cognition, it could be zero.

Indeed, C. elegans nematodes (which are the ones you are talking about) do not show cognitive responses. AFAIK, Drosophila melanogaster is also able to learn and display some quite complex behaviors, but no cognitive functions. I believe the "simplest" organism known to display what could be called "cognitive" functions is the honeybee (see for example this article).
But as to your question:

to demonstrate something more than mere scripted actions

I would also ask "what is a scripted action?" and to what extend a complex, cognitive response from a monkey or a human isn't also scripted (though through many different interacting pathways)?

Ahh I guess I'm looking for learning or extremely basic problem solving. So, honeybees definitely learn. If two creatures are fighting and trying to anticipate each others moves, this would also fall under my definition of cognition, as this is not hard-coded genetically.

I wouldn't say learning is the criterion. In fact, nematodes can learn (see http://learnmem.cshlp.org/content/17/4/191.long).
The ability to "anticipate each others moves" seems a bit hard to quantify in real life. I think the criterion would rather be "abstract learning". While drosophila can learn (by appetitive and aversive conditioning), honeybee can learn patterns, "concepts" to take the word of the article. They can then transfer what they have learned in one situation to a new situation they have never seen.
Also, their "waggle dance" is flexible, and they can have a cognitive map.

What's a cognitive map?

You can find definitions in several articles [1,2], and a more general one on Wikipedia [3]. To summarize, it's a mental representation (e.g. from their spatial environment), which allows them to make plans and find novel solutions to a problem (e.g. find a new path to reach a goal). So it's not just "if the odor comes from the left, I go left", the bees "understand" where they want to go, and manage to find a way to go there. −−−−−−−−− [1] http://www.pnas.org/content/102/8/3040.full [2] colinallen.dnsalias.org/Secure/TCA/gould-final.pdf [3] https://en.wikipedia.org/wiki/Cognitive_map

So why do you say that Bees demonstrate a cognitive map, but Flies do not? Is it just that we haven't researched it yet, or do we know for sure?


text:
How are non identical cattle twins capable of transplanting each others organs?
Non identical cattle twins have different genes and by this their immunesystem works differently so initially it was suspected that eg tissue transplantation from one to the other would be rejected by the immunesystem.
Now it appears that it is possible to succeed in a organtransplantion because there body's lived in the same placenta. But how does their immunesystems get compatible with the cells of the other just through the placenta?

Can you give a source for this? Most commonly, nonidentical twins each have their own placentas, not shared placentas.

It is about cattle see: http://onlinelibrary.wiley.com/doi/10.1111/exd.12227/full

If your question is about cattle, please specify. Humans don't share placentas.


text:
How many isomeres of sucrose can we use?
It appears that of sucrose (C12H22O11) there are about 512 possible structures (nine carbon atoms are asymmetric= 2^9). And only one of this 512 forms taste sweet. Now it is known that human can't use all isomeres of amino acids but how many forms of sucrose can we digest or use in the glycolysis for our energy?

How did you come up with the number 512?  To my knowledge, the variants of glucose are (1) D and L stereoisomers (2) the pyranose and furanose forms, and (3) alpha and beta stereoisomers at carbon 1.  Any combination of these can occur, so there are 222 = 8 cyclic forms. Plus the linear form, caused by the ring opening.  But then the pyranose/furanose and alpha/beta isomers interconvert spontaneously in water solution via the linear form (ring opening/closing), so the only biochemically distinct forms are D and L. I think.

This question is totally confused. Assuming the questioner means hexoses, there are 16 isomers of aldohexose. I have no idea what the sentence about "human can't use all isomers of proteins" means — possibly amino acids? And glucose is not used in the citric acid cycle. Perhaps the questioner means glycolysis. Unless the question is revised I shall vote to close it as unclear.


text:
How to combine gene set enrichment analysis with hierarchical clustering?
I would like to find out how to combine gene set enrichment analysis with hierarchical clustering. The motivation for this combination is that potentially
too many gene-set symbols for leukemia may pass the p-value significance threshold. We are using an R-package for fast preranked gene set enrichment analysis (GSEA) with the URL, https://github.com/ctlab/fgsea.
Subsequent to the fast gene set enrichment analysis on a ranked list of gene symbols with different expression t-statistics, we specifically need to identify gene-set symbols belonging to a common functional group using the R language hclust function intended for supervised hierarchical clustering with a Euclidean distance between features in a timely manner, for example 15 or fewer minutes.
Quoting from Alan Moses 2017 book, "Statistical Modeling and Machine Learning for Molecular Biology" , "Clustering is meant for exploratory data analysis and therefore doesn't really have a strong framework for hypothesis testing".A new R package ClusterProfiler provides enrichment analysis of gene clusters as reported in this URL,  http://guangchuangyu.github.io/2015/05/use-clusterprofiler-as-an-universal-enrichment-analysis-tool/
The fact that most quality measures found in the literature have been conceived to evaluate non-overlapping clusterings, even when most real-life problems are better modeled using overlapping clustering algorithms is analyzed
in detail in the following paper and University of Texas Ph.D thesis
Academic paper: CICE-BCubed: A New Evaluation Measure for Overlapping Clustering Algorithms. Available from: https://www.researchgate.net/publication/260421976_CICE-BCubed_A_New_Evaluation_Measure_for_Overlapping_Clustering_Algorithms [accessed Apr 16, 2017].
and
https://repositories.lib.utexas.edu/bitstream/handle/2152/ETD-UT-2010-08-2022/KRUMPELMAN-DISSERTATION.pdf?sequence=1&isAllowed=y
As I am a novice to this type of bioinformatics research, please correct any inaccuracies in my problem statement.

The article, What to Do When K-Means Clustering Fails: A Simple yet Principled Alternative Algorithm with the URL, http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0162259 discusses MAP-DP which is a more flexible clustering technique using a probabilistic model.

You can try Enrichr for enrichment analysis. On 'Results' page you can use Clustergram view.
Or you can upload your results to Clustergrammer itself.

Thank you for your nice answer. Is it possible to measure and refine the quality of hierarchical clustering results generated by the R language function hclust() using Euclidean distance by automatically computing p-values for all clusters contained in the clustering of original data. Could we use the paper "Multiscale mutation clustering algorithm identifies pan-cancer mutational clusters associated with pathway-level changes in gene expression", http://journals.plos.org/ploscompbiol/article?id=10.1371/journal.pcbi.1005347 to refine clustering analysis? Thank you.

Is it mathematically correct to use the R function for combining gene set enrichment analysis p-values from  https://github.com/ctlab/fgsea. in this URL, https://www.biostars.org/p/211307, to calculate the quality of a hclust() clustering result tree? Thank you. I am awarding reputation points to your nice answer.

How does your answer address overlapping clustering? Thank you.

A rising young M.I.T professor told me just now that the volcano plot with 1og(p value) vertical axis can in many cases differentially visualize overlapping clusters where p values come from gene set enrichment analysis,