text:
What exactly does adaptive mean?
This is a quote from Dey et al 2014:

Hatching asynchrony is thought to be adaptive because...

What exactly does adaptive mean here? Does it mean hatching asynchrony has fitness benefits? Or does it mean hatching asynchrony is likely to be selected for?

A trait is said to be adaptive when it causes fitness to increase. Fitness is generally understood as the (relative) contribution to future generations in terms of offspring or genes. The trait is selected for by the environment and hence increases fitness.
In the paper of Dey et al. this is the fitness of the parent birds. Hatching asynchrony causes size differences between chicks which may (1) "facilitate brood reduction in unfavourable environmental conditions", (2) "provide insurance against the failure of core offspring" and (3) "reduce competition among nestlings". Dey et al. also cite a reason why hatching asynchrony may be sustained in a population despite being maladaptive: initiating incubation before the clutch is completely laid is selected for and causes asynchronous hatching as a by-product. In this case, hatching asynchrony merely correlates with fitness, but does not cause fitness to increase and is thus not adaptive.

Can you add a link to the paper you cite?

@Chris, the link to the journal's webpage in luciano's question has links to the full text of the paper, however, you need a subscription to access them.

Thanks. The subscription is not so much a problem for me :-)

The question is probably more complicated than it seems because, if I am not wrong, the word adaptation here is understood at the group level.
Definitions of adaptation
Unfortunately, there is not such thing as a single, standard definition of adaptation. But for most cases the accurate definition the author is using is not of much importance as all of the usual definitions totally fit in the sentence without changing the meaning of the concept they want to express. In you case however, the concept of adaptation seems to be a bit more complicated (and interesting) because it refers to a group-level adaptation.
Note that most people does not really care about the exact definition they're using and this might yield to some confusion. It will probably be a bit hard to know exactly what the authors  (Dey et al.) of your article had in mind.
Definition of Group-level adaptation
I am here going to talk about how the term adaptation can be understood for a (social) group. This is important as I suspect the authors to use the term adaptation on a group phenotypic trait (emergent trait if you want).
Pareto optimality
To my experience, the concept of group-level adaptation is defined in relation to the concept of Pareto optimality which is a concept used in evolutionary game theory. Shortly speaking, in a system that is at Pareto optimality no individual can by any change of the trait under consideration increase its fitness without decreasing the fitness of another individual. In other words, a population that is at Pareto optimality has the greatest achievable population mean fitness. Therefore, it makes sense to consider a group to be (perfectly) adapted when it is at Pareto optimality.
Nash equilibrium
Depending on the underlying evolutionary game, the Pareto optimality may or may not be a Nash equilibrium. Shortly speaking, a population is at Nash equilibrium if no individual can increase its fitness by changing the trait under consideration. Therefore, group-level adaptation can only be stable if the Nash equilibrium is Pareto optimal. An example of game where the Nash equilibrium is the free-market game.
In your case
At first sight, because asynchrony is a group level trait, it seems to me that the sentence "Hatching asynchrony is thought to be adaptive [..]" means that hatching asynchrony is thought to be at Pareto optimality. In other words, it means that hatching asynchrony is thought to be the state of the system where the mean fitness of the group is maximized, that is no individual can increase its fitness without decreasing the fitness of another individual by being synchronous.

Your questions mean basically the same. Birdcare.com says:

The situation in which all the eggs in a clutch do not hatch at (more or less) the same time, as is more usual among birds, but have their hatching spread over several days. It is well seen in the various types of raptor, and is an adaptation to a type of food supply which may fluctuate. During seasons when food is short the later hatched young will probably starve as the earlier hatched young, being larger and stronger, deprive them of food, and so the size of the brood is reduced to a level in balance with the available food supply. In years of plenty all the young may be able to survive. In 'synchronous hatching' all the eggs hatch at more or less the same time.

The fitness benefit of hatching asynchrony on the species level is due to increased range of individual fitness among the young birds. The available resources do not need to be distributed equally among the offspring during unfavorable seasons such that fewer, but at least some of the hatchlings (the 'strongest') can survive. You see that this is the same as beeing selected for because on average the number of agents passing their genes to the next generation is higher with asynchronous hatching than with synchronous hatching. Of course, the success of this strategy is strongly dependent on environmental factors. In very stable habitats it might turn out to be disadvantageous on the long run.


text:
Speciation by polyploidy
Speciation can occur by polyploidy. My understanding of the process is as follows:
'polyploidy is when the number of chromosomes in an organism's cell doubles. This means that the organism has more chromosomes than other individuals of the same species, meaning it cannot mate with other individuals. The polyploidy organism then evolves, eventually leading to it becoming a separate species'.
I realise this may not be exactly correct. Is someone able to provide a better description of speciation by polyploidy?

By definition, polyploidy just means that a cell or organism contains more than 2 pairs of homologous chromosomes (or is more than 2n). This is more common in plants than it is in animals. The plant, as shown below, undergoes failed meiosis, which means that the diploid (2n) cells never become haploid (n). As a result, a plant ends up with more than 2n when it self-polinates. The shown result is tetraploidy (4n), but there are other possible results (3n, 5n, etc).

Multiple plants within a population can end up with the same polyploidy number. They can then reproduce with each other but not with the original plants or any other plants. As a result, they become biologically isolated from the original group of plants and are considered a different species. It is a type of sympatric speciation, which means that it occurs without geographic isolation.

In the genus Rhododendron polyploid species are common especially in deciduous azaleas and lepidotes. Yet complete reproductive isolation of the poylpoid species from the closely related diploid species is the exception rather than the rule.
Closely related diploid and tetraploid species interact in natural contact zones to create triploids and some triploids are able to reproduce with both populations.
Hybrid triploid lepidotes seem to freely set small amounts of viable open pollinated seed.
Tetraploid and hexaploid species and hybrids appear to interact even more freely than diploids and tetraploids. Pentaploids are often semi-fertile.
For Rhododendron, ploidy level creates a barrier to sexual interaction but that barrier is not absolute and is sometimes surprising porous. In fact the triploids may act as a pathway in the transition from diploid to tetraploid in that 2x (reduced) X 2x (unreduced) can create 3x and 2x (reduced) X 3x (unreduced) can create 4x. Moreover, C D Darlington established that triploids can throw 1x and 2x gametes so 3x (reduced to 2x) X 3x (reduced to 2x) can produce 4x or 3x (reduced to 1x) X 3x (unreduced) can produce 4x. Darlington documents the historical development of garden hyacinths from diploid species to triploid and then to tetraploids using a triploid pathway.
The development of tetraploid hybrid elepidote Rhododendron 'Countess of Derby' also illustrates a triploid pathway.
One cannot rule out the possibility that the ability of the diploid species to interact with newly created polyploids actually contributes to the creation of the tetraploid species.
The diagram below illustrates how the triploid 'Pink Pearl' has produced diploid, triploid, and tetraploid offspring when interacting with diploids and has produced a tetraploid offspring by interacting with another triploid.

The flow cytometry for this research on the genus Rhododendon was performed by Dr. João Loureiro, Dr. Silvia Castro, José Cerca, and Mariana Castro Plant Ecology and Evolution Group, Centre for Functional Ecology, Department of Life Sciences, Faculty of Science and Technology, University of Coimbra, Portugal.
References
Meiosis in Polyploids
by W. C. F. Newton and C. D. Darlington
in Journal of Genetics 1929
The history of the garden hyacinths
by C D Darlington, J B Hair and R Hurcombe
in Heredity 1951
Ploidy level estimations in deciduous and elepidote hybrids of Rhododendron
by José Cerca de Oliveira, Mariana Castro, Francisco J. do Nascimento, Sílvia Castro, John Perkins,Sally Perkins, João Loureiro in Jornadas Portuguesas de Genética, Coimbra, Portugal; 05/2011
Weighing in: Discovering the ploidy of hybrid elepidote rhododendrons
by Sally Perkins, John Perkins, José Monteiro de Oliveira, Mariana Castro, Sílvia Castro,  João Loureiro in Rhododendrons, Camellias and Magnolias, Royal Horticultural Society, Editors: Simon Maughan, pp.34-48 2012
Untersuchung des Ploidiegrades elepidoter Rhododendron-Hybriden by Sally Perkins, John Perkins, Mariana Castro, José Cerca De Oliveira, Silvia Castro, João Loureiro in Rhododendron und Immergrüne , Deutsche Rhododendron-Gesellschaft e.V. , Seite 21: pages 21-42; 11/2013

Can you add the reference (at least) for this figure?

source: Stack Exchange

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

sort: votes


text:
What is neutral genetic differentiation?
What is neutral genetic differentiation? Presumably it's a measure of the distance between organisms in terms of their genetics, but what does 'neutral' refer to?

Seems to be discussed here, looks complicated.

Neutral genetic variation is variation that has no effect on fitness. I suggest reading more about neutral theory on wikipedia.
Neutral genetic differentiation is a way of talking about neutral genetic variation that follows some historical pattern, for example two populations isolated from each other for a long time will show neutral genetic differentiation even if they are individually in Hardy-Weinberg equilibrium. In other words, the two populations will have somewhat different allele frequencies from each other for no reason related to natural selection but rather because of random sampling and genetic drift over time.
It is generally thought that most genetic variation is neutral or nearly neutral. For example, most of the human genome is useless DNA or genomic parasites such as transposons. Almost all of the genetic variation that happens in those regions is not important to human fitness, in other words it is "neutral".

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

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


text:
Can you identify this dead bug?
I found this bug in the kitchen and already killed it. It's in austria area. Can someone tell me if it's dangerous?

Welcome. Could you give us some idea of scale, tell us what you found it on or near, was it eating anything?

Photos of the other side?

Looks like an Ectobius_vittiventris, a so called 'Bernstein Waldschabe' which is recently invading Austria. I might be extending this comment to an answer once I have sufficient time on my hands to provide sources and proove.. Greetings from Vienna, we have lots of them too in the surounding suburbs. It feeds on decomposing plant material, so don't worry it's not dangerous to humans - rather the other way around ;)

Looks like an Ectobius_vittiventris, a so called 'Bernstein Waldschabe' or 'amber wood cockroach' in English, which is 'recently' invading Austria and Southern Germany, especially in hot and dry summers.

Image info: Author: Amada44, Licensed: https://en.wikipedia.org/wiki/en:GNU_Free_Documentation_License
In size, shape and color, the amber forest cockroach is very similar to the German cockroach Blattella germanica, which is feared as a hygiene pest and is usually controlled. The most striking difference is the uniform brown pronotum in the amber forest cockroach, which in the German cockroach has two dark longitudinal stripes.
Source
From Wikipedia:

It is a species of wood cockroach originally from southern Europe . It is completely harmless to humans and does not appear as a storage pest, as it only feeds on decomposing plant material and perishes within a few days in human dwellings due to a lack of food. Its original range is south of the Alps, but this species seems to have established itself permanently north of the Alps and in southern Germany.

From Wikipedia:

The natural habitat of the amber forest cockroach is outdoors in low bushes and in gardens under pots. It feeds on decomposing plant material. Warm, dry summers can encourage mass reproduction. Then the probability is high that the animals can also be found in apartments.

Since it feeds on decomposing plants it's not dangerous to humans - rather the other way around ;)

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


text:
Why Sexual Reproduction instead of Gene Transfer?
So, as I understand it, the prominent theories for the evolution of sex are that it increased variation allowing for faster adaptation in evolutionary arms races, and that it gets rid of deleterious mutations by introducing unmutated alleles in descendants. But why sex specifically for this task? Surely the same benefits could be conferred through horizontal gene transfer. We could even conceive of a kind of non-sexual diploidy.

Why not questions about evolution are usually impossible to answer. Evolution is random and requires precursors from which to evolve. If no sexual beings had the ability to transfer genes any other way, it could not evolve. See Why do some bad traits evolve, and good ones don't?

@anongoodnurse: if you assume that there are no precursors, please provide references for that claim. Horizontal gene transfer  in eucaryotes is being discussed, while the molecular machinery for tunneling nanotubes is present in eucaryotes. Apart from that, this question is very much answerable even without knowing about a precursor, since comparing strategies for increasing genetic variation is absolutely valid and should be encouraged on this site. Referring to that thread is a lazy way of avoiding actual answers.

Bacterial conjugation does provide genetic variation, but wikipedia mentions a vast array of different mechanisms how sexual reproduction recombines genes, which seems to beat horizontal gene transfer in terms of fitness gain. Also: keep in mind that eucaryotes have a different genome architecture (enhancers, histones, genes are bigger and harder to transport), and that DNA outside the nucleus is often interpreted by the cell as a viral infection, which could make horizontal gene transfer difficult without risking immunity.

@markur - Commenters are not obligated to provide references. OPs are required to show research, and answers are required to cite sources. You are welcome to provide an answer about asexual eucaryotic reproduction, or the evolution of sexual reproduction, or whatever your heart desires (with sources.) (Also, I don't get my information from Wikipedia when it comes to science. May seem elitist, but there are just too many errors for my taste.)

@anongoodnurse - yes, the lack of sources is the main problem here (not evolution). I like to cite wikipedia in comments to encourage OPs to start their own research with simple tools. One shouldn’t be afraid of Wikipedia, it is definitely better than providing nothing and would improve the quality of many questions. Wikipedia is neither good or bad, it is what it is. Elitism won‘t attract professionals to this page but rather repel them.

@markur - Wikipedia is a fine starting point; I just don't rely on it for science. As to what attracts professionals to this 'page', why not make a proposal in meta with your insights? I'm sure more professionals (at least those with decent analytical, communication and self-appraisal skills) would be a boon to this site. You can also answer the question yourself, instead of (or in addition to) accusing others of laziness.

Let us continue this discussion in chat.


text:
Terminology for Transgenes
I'm designing an in vivo delivery vector for therapeutic transgenes.
I have two different potential versions of the transgenes. If they were innate, they'd be referred to as "alleles." Does the terminology change if they're transgenes?

I think that "variant" would be pretty generally understandable. It might help to know what you mean by "versions". E.g. they homologous? How different are they?

Please clarify your specific problem or provide additional details to highlight exactly what you need. As it's currently written, it's hard to tell exactly what you're asking.

Yes, I would change to a different terminology. I would not apply the word 'allele', which would be confusing/misleading at best. Even if the transgene is an allele taken from an organism, I would only note such in a writing when needed and still refer to the transgenes themselves by something else.


text:
What is the technical term for a combination-mouth-anus?
Some organisms have a single hole that is used both for food intake and for waste excretion. Does the scientific community have a name for that hole? What is it called? Or is it simply called the mouth-anus?

The mouth.
This is sometimes referred to as the hypostome (most sources, though Wikipedia disagrees). It is usually muscular.
The Pharynx.
This is the muscular part of the tube leading to the gut which contracts in waves (the familiar peristalsis), pushing the meal into the gut. Sometimes undifferentiated from the mouth such as in the hydra where the mouth leads straight to the hollow interior.
Proboscis pore.
Some sources have it that Planaria have just a pharynx, in others the structure the food enters before the pharynx is also referred to as the proboscis within a proboscis sheath, the "mouth" being referred to as the proboscis pore.

The intestine to cap it off.
This is referred to variously as the gut, the gastrovascular cavity, the digestive cavity and, of course the intestine.

Eh? No. I've some sort of virus, just slept 14 hours straight if you're wondering why I disappeared.  I'm very pleased with the answer, not to say astounded by the whole idea of what the spider gets up to. On my main haunt worldbuilding, we always wait 24-48 hours to award a bounty - but your answer'd have gotten one straight away had I not been in the arms of Morpheus.

I'm sorry to hear that, and again, I wasn't trying to pressure you to accept my answer. I just wanted to know if my answer was off track. I hope you're feeling much better soon!

Oh, thanks. I'd not meant to disappear for ages, just the way tiredness caught me. I'd not have needed pressuring anyhow, it's a fine answer and a whole new area for me to get lost in fascination with ;)

If an organism has a single pore for both ingestion and excretion then it is known as incomplete digestive system. Primitive organisms like  Platyhelminthes (flatworms), Ctenophora (comb jellies), and Cnidaria (coral, jelly fish, and sea anemones) has this type of digestive system. It contains only one opening, the "mouth" which also serves as "anus". Ingested material enters the mouth and passes through a hollow, tubular cavity called gastrovascular cavity. Cells within the cavity secrete digestive enzymes that break down the food. The food particles are engulfed by the cells lining the gastrovascular cavity.

(image source)
There is no specific term for this orifice although there is this statement from the Wikipedia article of GI tract:

A through-gut (one with both mouth and anus) is thought to have evolved within the nephrozoan clade of Bilateria, after their ancestral ventral orifice (single, as in cnidarians and acoels; re-evolved in nephrozoans like flatworms) stretched antero-posteriorly, before the middle part of the stretch would get narrower and closed fully, leaving an anterior orifice (mouth) and a posterior orifice (anus plus genital opening) ...

Technically, digestive system of Sponges is also primitive, having pores all over the body called ostia where food is entered but excretion happens at a dorsal pore called osculum. (See image here)
Related: Why porifera is classified to have an incomplete digestive system although it has no organs?


text:
Data on number of viral replication cycles and their duration doesn't seem to agree with observed duration of infection
I'm trying to model SARS-CoV-2 disease progression in individuals (and have very little background in biology).
At first glance, data from the literature on the duration and number of replication cycles that the virus undergoes over the course of a characteristic infection and the observed real world data on duration of an infection seem contradictory.
In The total number and mass of SARS-CoV-2 virions it was estimated that the virus undergoes 3-7 replication cycles over the course of a typical infection, and in SARS-CoV-2 by the numbers the duration of a replication cycle was taken to be 10hrs.
From this I would expect an infection to last 30-70 hrs (plus the time for the last virions to die out) which roughly is at most 4 days.
However, the median time from onset to clinical recovery for mild cases is around 2 weeks. In more severe cases it can take the patient up to 6 weeks to recover.
What causes this discrepancy?
Is it that symptoms are (partly) caused by our immune system's response to the infection, not directly by the virus itself?
In severe cases lasting up to 6 weeks, would one still expect only 3-7 replication cycles?

The estimates you refer to seem to be of the "Fermi problem" variety - that is, these are "order of magnitude"-style estimates.
There's also the issue that they are talking about "typical" cases, whereas it seems you are talking about more extreme cases. I'm not sure where your estimate of "median time from onset to clinical recovery for mild cases is around 2 weeks" comes from but I suspect you may be referring to something based on hospitalized cases or something similar; the vast majority of COVID-19 cases do not involve hospitalization. There's also no reason to expect that time course of symptoms, which primarily involve activation of the immune system, need relate closely to the time course of viral presence.
In summary, though, when you are doing Fermi estimation, at the very most precise you might expect your estimate to be off by an order of magnitude. That means that, for this type of approach, 4 days and 40 days are the same number. In the first paper you link, note the precision of some of the numbers they are using to estimate:

~10–100 infectious units per cell

3×105–3×108 infectious units produced

You can't expect to get more precise when you're starting with estimates that vary over 1-3 orders of magnitude.

very helpful, thank you for your answer!

This is a great answer, and I think this point is key: There's also no reason to expect that time course of symptoms, which primarily involve activation of the immune system, need relate closely to the time course of viral presence. The period of immune activation does not necessarily stop when the offending pathogen is cleared.

@acvill This is so interesting - so you can be really sick despite your viral load being virtually nonexistent? What exactly is going on in the body? One guess would be that it has to recover from the lung tissue scarring caused by the virus


text:
Can organisms grow on acetic acid?
Can organisms grow on acetic acid and water (with <1%, all inorganic, impurities), i.e. using acetic acid as a carbon / energy source?
If so which concentration of water would it start at? (assuming it doesn't happen without water)

Welcome Hans. We're expected to show our own research into a topic when asking. Please [edit] to tell us what you searched, found and where you got stuck. Also, please take our [tour] and refer to the [help] for guidance. Acetic acid (ethanol oxide) is already pretty stable as it's the metabolic product of several processes, would you perhaps be referring to an extreme environment, perhaps a fictional one? Then [worldbuilding.se] might help there.


text:
Sex in diploid cones in gymnosperms
Gymnosperms have male and female cones. If the cones are diploid, how can individual cones be male or female?

Welcome to Biology.SE. The Biology.SE community has agreed that questions that show little or no prior research effort are off-topic on this site as are "homework" questions unless you have shown your attempt at an answer. Please [edit] your question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Under researched questions may be subject to down-voting and closure. Please take the [tour] and consult the [help] starting with [ask] for details.

In addition, can you answer this if you replace gymnosperms with animals and cones with genitalia? If so, then do you really have a question?

Thanks. Yeah, you're right, I didn't think of it that way. I did many searches and thought about it a couple of days. But guess what -- no one explains patently obviously things. I was being silly, as you noted. I mean I still had a question and I'm glad I asked and your rude response makes me glad I also didn't make an account.

I'm sorry you found this rude, but perhaps you are being oversensitive? This site has standards that your question did not meet. You did not bother to take the (very short) tour to familiarize yourself with those standards and yet I took the time to let you know how you could do better and to give you (an apparently) useful hint as too where your thinking had gone wrong. If this level of feedback bothers you I suspect you will not be happy using Stack Exchange sites ...

Being diploid or haploid isn't really related to which sex organs are produced by a plant. As you say, many gymnosperms (and angiosperms) produce both male and female cones on a single plant.
Development of these cones would be caused by genes carried in all of the plant's cells, but expressed differently in different locations.
Some gymnosperms (and angiosperms) are dioecious, meaning they have different sex organs on different individuals (i.e., male and female individuals).

Here, still, the sex determination is not related to ploidy. The sex determination could be caused by several mechanisms, depending on the species, including a single gene, or a variety of sex chromosome combinations.


text:
What are these white, fuzzy dome-shaped contaminants growing on my LB agar plate?
We are attempting to extract bacteriophages from environmental samples. We recently had an issue with an unknown contaminant when trying to grow a lawn of M abscessus for a bacteriophage isolation spot test.
Briefly, we mixed molten top agar with a saturated M.abscessus culture and poured it over a prefilled LB plate. Then we split the plate into nine squares and placed a single drop of environmental sample filtrate in the square—the environmental samples were filtrated by a .22um PES filter.
The result looked like this:

As you can see, a lawn of what appears to be M.abscessus is forming (the yellow-white smaller colonies). But there are also eight circular white colonies of unknown origin.
Here is what we know:

The unknown contaminants are dome-shaped and look fuzzy in structure. They are roughly 5mm across.
They seem randomly distributed across multiple squares, which likely means the contaminant did not come from the environmental sample filtrate drops.
The contaminant could have been in the M.abscessus culture. But we did add Carbenicillin (100ug/ml final concentration) and Cycloheximide (1ug/ml final concentration) to the culture to inhibit bacteria and fungi.
The contaminant could have come from the top agar, which was stored in a 55°C water bath.
We created four of these plates at the same time, and they all had the same contaminant.

What species could these dome-shaped white colonies belong to?

Did you pour control plates without M. abscessus and without filtrate? That would tell you exactly where the contamination is coming from. As for identification, it's going to be pretty difficult without microscopic images of the colonies and without biochemical tests or sequencing.

From a practical laboratory standpoint, it seems like performing the sorts of controls that MattDMo suggests is going to be far more useful to you than identifying the specific contaminant. Assuming all you want to do is grow your organism free of others, it doesn't matter what is contaminating but rather what step in your process introduced contamination.

@MattDMo  that makes sense. We will definitely use more negative controls on the future. We discovered that our final Cycloheximide concentration was accidentally too low, so our best guess is that this is because of that.

Did you use a spreader and sterilise it? If you cold sterilise in pure ethanol you can pickup bugs from the alcohol.; which won’t occur with 70% ethanol. The contaminant I saw for this was Staphylococcus.

If you want to identify this bacterium or any other contaminant, you need a PCR of the 16S rRNA gene, sequence it using Sanger and then blast the results against a database. This is the easiest, cheapest, and most reliable way to know exactly what you are dealing with.


text:
Autoreceptor control of phasic and postsynaptic control of tonic signalling
I have read the following paragraph : "Whereas tonic DA signaling is affected by postsynaptic stimulation/blockade, phasic (transient) release of DA during dopaminergic cell bursting is modulated by presynaptic drug action (Grace, 1991)" in a paper by Frank & O'Reilly, 2006. Whereas I do find evidence that phasic release of DA is negativeley modulated by presynaptic drug action, I don`t understand why postsynaptic would mainly influence tonic DA signalling (and not phasic?). Can anyone help me out here or point me towards relevant literature?
Thank you

Can you provide some surrounding context? What is the book/paper about, what drugs are we talking about, etc.


text:
What is an apple?
Reader : please consider that I don't know anything about biology, which is the case by the way.
Context :  I am currently preparing a presentation for a research grant application, which I will submit to a jury of mathematicians for their decision. My first slide aims to highlight the fact that human beings have a natural reflex to classify the objects around them, and to do this I consider the case of two objects that are a priori distinct, but which are equivalent by convention: they are just two apples (image). To be clear, I need to say why they are equivalent.
Question : Biologically speaking, what justifies that these two a priori distinct objects are indeed two apples, and therefore biologically equivalent? As a biologist, what is the justification you would give to say these two things are quite the same?

Well, personally I wouldn't. The distinctions made in biology go down to the molecular level, we differentiate between the colour red and the colour green on a macro and micro levels. Also on the differing effect the colour has on a species that likes apples - not just humans, that is we'd be looking at the item in context of the environment too. Then there's the evolution of how the differences came about .... it goes on. Doesn't this more come down to a [philosophy.se] question than a biology one?

I’m voting to close this question because it is about ontology and the philosophy of classification. Replace the apples with any two similar-but-distinct objects and the question remains the same. Perhaps there is an on-topic interpretation of this question regarding taxonomy, but it's not clear to me.

On reflection, you might want to take a look at our [psychology.se] stack. If asking there, you'd need to be sure to frame your question in existing models of perception and language.

I agree this is off topic. However, you got some answers anyway before being closed that you seem to indicate appreciating and wanting to employ in your presentation. Just a reminder, then, that I think you should plan to be citing these users as your original source(s) for these ideas (especially since the answers you got are less biological fact and more ontological discussion).

How do you know they are not snapples?

@user338907 proving yet again that there is a relevant XKCD for just about every question on Stack Exchange.

Biologists aren't the people who decided what an "apple" is, the general population of users of language are.
You could try back-create a definition that is biologically relevant based on descent, for example "fruit of plants in the genus Malus", but that would include a lot of apples that aren't really apples the way English speakers in general use the word.
You could limit it to just fruits of Malus domestica, but that probably wouldn't work great, either, because there are several fruits outside that species that a typical English speaker would still call "apple".
A relevant botanical definition is that an apple is a pome:

A pome is an accessory fruit composed of one or more carpels surrounded by accessory tissue. The accessory tissue is interpreted by some specialists as an extension of the receptacle and is then referred to as "fruit cortex",[2] and by others as a fused hypanthium (floral cup).[2]

...but many botanical fruits of this type are not "apples" in the English use of the word, such as pears or hawthorn.
It happens a lot in language that biology and culinary or other language issues conflict, for example the "is a tomato a fruit?" debate. There are also other popular language classification quirks that people debate on the internet like "is a hotdog a sandwich?". These are all questions about language and how language is used, not about any biological or other scientific essence of things.
Biologically speaking, your brain learning these things is a lot like how an artificial neural network is trained to, say, identify road signs. Just like when you complete "Captcha" tasks to "prove" you are a human when acting online like "select all images with a stop sign in them", and this training data is sent to an AI algorithm, as a developing human the adults around you will hand you things and say "apple". You then assign a little slice of all the features you perceive and associate those with the concept "apple" in your brain. They're also correct you and say "no, that's an orange" if you expand your definition beyond "apple", and you'll learn to break associations between those orange-specific perceptions. In this way, the things you call "apple" are just the things that other people call apple, and that's how we can use language to communicate with each other: as long as we all mean roughly the same thing when we say "apple", it's a useful concept, even if it doesn't make sense biologically.

Thanks a lot for your answer. I accepted this one because it answers my question perfectly !

I think one thing you are overlooking is that humans employ hierarchies of classification. We group things at multiple levels depending on the degree and types of similarities. In the picture you've provided the two images are the same in the sense that they are both examples of the genus Malus:

The fruit is a globose pome, varying in size from 1–4 cm (1⁄2–1+1⁄2
in) in diameter in most of the wild species, to 6 cm (2+1⁄4 in) in M.
sylvestris sieversii, 8 cm (3 in) in M. domestica, and even larger in
certain cultivated orchard apples. The centre of the fruit contains
five carpels arranged star-like, each containing one or two seeds.

They are different in that one is perhaps an example of the variety Delicious, and the other is perhaps of the variety Granny Smith. The two varieties differ in skin color and taste among other attributes, but share many of the attributes associated with the broader category of genus Malus.
They are also different in the most abstract sense because they are two different objects.
Which classification is relevant depends on context. If I'm making a grocery list the variety is the most significant classification. If I'm writing a fairy story the genus may be all that's relevant.

Your answer is very clear and helped me to think about what I should say to introduce this topic. Thanks :)

My answer: based on DNA similarities I can confidently tell you whether two "things" are so similar they merit similar names.
Other points to mention: We might call two things similarly without necessarily implying that they are the same thing (e.g., a giant panda and a red panda). Both of those pictures are apples because they look, taste, and feel like an average apple and we decided on that before we could check their DNA. There's a Stanford lecture on Human Behavioral Biology that discusses how we humans tend to categorize objects into groups to ease information processing that you might want to check out.

That lecture seems really interesting !  Do you have a link ? I didn't found it ...

You can find it here https://www.youtube.com/watch?v=NNnIGh9g6fA&t=3s


text:
Is there a standard protocol for isolating bacteriophages from biofilm?
We are planning to screen soil, water, and biofilm for mycobacteriophages, particularly the environments where the bacteria have been found in the past.
We have already isolated phages from soil but have had trouble finding a good protocol for isolating them from biofilm. Nelson et al. isolated Mycobacteria by swabbing the biofilm of rocks. A Google Scholar search for isolate bacteriophage from biofilm gives us results about the phages' ability to penetrate biofilm but not much about isolation.
We found this paper, which described a protocol for extracting phages from skin swabs, which we could try to extrapolate to biofilm swabs.
Is there a paper that describes phage isolation from biofilms on hard surfaces such as rocks and human-built environments?

A 2019 paper in Viruses used sonication to monitor the phage titer of P. aeruginosa biofilms associated with "stainless steel coupons".

In order to better understand the repartition of phages after the treatments, samples were taken to determine the quantity of planktonic viruses in the mineral minimum medium around stainless steel coupons, but also to estimate the amount that was biofilm-associated. In the first case, samples were collected directly on the liquid medium of the jar after 14 h of phage activity and titered by following the previously detailed protocol. In the second case, at the end of treatment, the liquid medium around the coupons was discarded and replaced by the same volume of medium. The biofilm was then resuspended by sonication (Figure 1), allowing the sampling and titering of biofilm-associated phages.
Sonication of controls was assessed by adding the same phage titers in each jar (3 × 1010 PFU/jar). The titer was then evaluated by the spot test method when jars had not been sonicated and after 1, 3, and 5 min of sonication.

Unfortunately, their methods include neither the frequency of sonication nor the specific sonicator used.
A 2016 paper in Frontiers in Microbiology investigating phage mitigation of catheter-associated biofilms found that sonication reduces the viability of phage particles. Anecdotally, vigorous vortexing is sufficient to break the tails off of Myoviridae and Siphoviridae phages when making TEM preps, so it's not surprising that sonication has an effect on phage infectivity. However, if your goal is phage discovery and not phage titer determination, I wouldn't worry too much about viability -- some phage will survive the sonication process.
Riffing on the insights from these papers, here's a simple protocol on which you can build:

Scrape biofilms from hard surfaces using a sterilized razor blade and (carefully!) transfer the biofilm to a conical tube using a sterile toothpick or pipette tip.
Wash the biofilm in phage buffer or similar medium by repeated centrifugation. This will help to remove phage that aren't strongly associated with / contained within the biofilm.
Add the appropriate volume of fresh buffer for sonication. Note that buffer volume is an important parameter in efficiency of sonication (see Figure 1 of this paper).
Sonicate! If you don't have access to an ultrasonic probe homogenizer, water-bath sonicators are relatively affordable and will probably work for your purposes.
Use the sonicated sample as input for your favorite phage enrichment protocol.

Happy hunting!


text:
What are the W and DSM codes for the following bacteria referring to?
In this paper the following bacteria are listed:

Bifidobacterium bifidum W23 (DSM 26331)
Lactobacillus salivarius W24 (DSM 26403)
Lactobacillus acidophilus W37 (DSM 26412)
Lactobacillus casei W56 (DSM 26388)
Lactococcus lactis W58 (DSM 26390)
Lactobacillus plantarum W21 (DSM 26401)
Lactobacillus rhamnosus W71 (DSM 26396)

However, I can't find anything under the NCBI's taxonomy browser or the German DSM system for either the Wxx or DSMxxxxx codes.
Where are the identifying central definitions of these strains?
Thanks in advance.

I only took a look into the DSM numbers and obviously these are not correct. Have you tried contacting the corresponding author?

No, I'll try though. Thanks for the second look.

Update: I've asked the authors.
However, in the paper they say they identifed the strains by matching 16S data in this database:
http://rdp.cme.msu.edu/hierarchy/hb_intro.jsp
But I can't find the referenced Wxx or DSMxxxxx codes in that database under the stated species (you have to open up all the filters to the max and use the ORG:searchterm to search for named organisms).

*they identified the closest species by matching 16S data

After speaking to someone at Winclove Probiotics, who developed these strains (hence the Wxx code), I've found out that they are registered with DSMZ but they're "private" (hence why looking for the DSM codes doesn't work).
The names of the species listed are based on nearest matches of 16S data to species in the RDP database.


text:
How does one prove that a particular bacterium causes a disease if we've found it in the blood of all infected people?
Let's say we have a new disease and are trying to identify the cause. We isolate, though culture, a new microbe from the blood of all infected people. Is it enough to say that it isn't present in healthy people, but in all our infected people, to come to the conclusion that this microbe is the cause of the disease? Why, or why not?
I feel intuitively that using Koch's way of introducing these microbes into a healthy individual to see if they cause the same disease, is a fool-proof way of proving that it causes this disease.
However, some of my students have said that they would like to test the blood of healthy individuals to see if they can find that microbe in it. If not, then the microbe can be said to cause that disease. This seems all right too, except that it only proves correlation, not causation. Does it suffice?

As you're new to this site, you might not be aware that some research is required on your part in order not to get a close vote or a down vote. Providing evidence of a search (not typing that you've searched but found nothing) and editing what you've found into your question is much more likely to get you an answer.

https://pdfs.semanticscholar.org/0361/58a9ea43125e9802bb5e2b5db2118f51d81a.pdf


text:
EDTA in DNA extraction
I thought the EDTA solution binds to metal ions and deactivates the (metal-dependent) nuclease present in the cytoplasm which protects DNA from degradation. But I wondered how that would be the case because if the DNA and nuclease are both found in the cytoplasm, the DNA would just be degraded. (Eukaryotes have a membrane-bound nucleus which prevents the nuclease from degrading DNA, but as prokaryotes do not have one, DNA is just loose in the cytoplasm along with the nuclease) And after some research, I found out that bacteria protect their DNA from autodegradation by modifying their DNA bases.
If that is the case, then why is EDTA used in bacterial DNA extraction?? Wouldn’t the DNA be safe from the nuclease regardless of the metals in the first place?

Why does bacterial DNA not get degraded when it's not protected by a nuclear envelope from endogeneous nucleases in the bacterium? Why ever use EDTA to block nucleases if DNA seems safe in its presence?

Prokaryotic genomes are composed of DNA which is indeed not enclosed in nuclei, but it is regardless compacted into a nucleoid. Thus one major way bacteria protect their genomes is through supercoiling of their DNA, to compact it and render it less easily accessible. Another major way, as you mention, is by modifying their bases, most commonly through methylating nucleotides. Methyl groups are added specifically onto bases in recognition sequences which nucleases otherwise act on, thereby protecting this target from being cleaved by hydrolysis. As with supercoiling, this allows the strand to be nuclease-inaccessible. There are also other ways that bacteria control the activity of their enzymes; their expression is controlled, they may be inactivated or purged, etc.
Also consider that nucleases are usually specific in some way, which means that protecting DNA becomes a lesser task: some target DNA ends only (exonucleases) which can be shielded. Some nucleases target within strands (endonucleases), these can have specific recognition activity, and other (rarer) kinds don't and hydrolyze DNA non-specifically. When you extract DNA you want to make sure that for the entire process - from lysis to isolation to storage - the DNA is free of contaminants and conditions which could potentially degrade DNA.
This means we must consider controlling biological, chemical and physical aspects which may contribute to DNA damage. One instance of each:

We don't want other microorganisms there which may secrete nucleases or digest DNA; thus, we sterilize.

We don't want enzymatic activity which may compromise DNA stability; thus, we chelate ions which otherwise are required for nuclease activity using EDTA.

Last, we don't want the DNA to get lost in isolation, so we control things like temperature and pH and salinity to solubilize, denature, precipitate things differentially, such as DNA, RNA, short strands, long strands, etc. For instance, if you want to isolate plasmids (rather than nucleoid DNA), one quick and dirty way of doing it is to add an alkaline (high pH) reagent after lysis. This is called "alkaline denaturation". The broken cells release their contents, the DNA inside separates into its component strands, or denatures. When you lower the pH once more, the plasmids reanneal easily but the very large, bulky nucleoid DNA can't and you separate them on this basis. In this case you'd also add EDTA out of abundance of caution to protect the nucleoid DNA from fragmenting into smaller bits that would be co-isolated along with the small plasmids. EDTA would also prevent the nuclease digestion of plasmids too, since they are composed of DNA too. EDTA is a well-motivated, preventative measure to upkeep the quality of the DNA during artificial isolation procedures wherein cells and compartments get homogenized and all sorts of things occur which normally don't in nature.

Last note, in the spirit of science and good lab practice: try skipping the addition of EDTA and compare your DNA yields. You may notice it doesn't make much difference, which would suggest that cytosolic nucleases may not have much activity for the bacterium's own DNA!


text:
What is the earliest known animal that could run?
By "running" I mean a land gait that at one point has all propulsion limbs off the ground. Jumping, like a flea or a frog, is not running.
The earliest land vertebrates could not run, I assume. The ability to run would be an advantage when pursuing prey or evading predators.
Our data from the period where running would first evolve is limited to bones and footprints. Is that enough to tell what an extinct animal's gait would be?

Things like sea scorpions walked on the ocean bed so shouldn't be discounted, especially when buoyancy makes it a lot easier to satisfy for your running criteria.

Welcome to the site. Interesting question - but you could improve it by telling us what you have found already, and what criteria you measure running by. Note that the [help] has a page on "homework" questions and what you can do to avoid getting closed for this reason.


text:
Is there any bloodstream chemical composition software simulator?
Let's say I'd like to know how certain substance affects bloodstream levels of certain drug during a period of time. Is there any simulation software available publicly to run such kind of simulation?

Pretty much any spreadsheet can be used for this, you just need the requisite data (and to know how to program equations). Can you be more specific about the drugs and the context in which you're needing the data?

@Jiminy Cricket it's necessary to know what to drink/eat in order to increase suction rate  (into bloodstream) of a certain drug. Where to get data for a spreadsheet?

@Jiminy Cricket or some substance instead of a drug.

This is all very vague at present, also the question you ask doesn't seem to be the question you need an answer to. Please take our [tour] and read up in the [help], paying particular attention to the [ask] section - then [edit] your question to ask what you intend and include the details which are missing such as your prior researches and the substances in question.

Usually you give someone (or a rodent) the drug, and take measurements of their blood regularly after that. How you actually detect the drug in the blood depends on the drug.

In addition, the drug taken isn't the active one sometimes, it's the breakdown products that are the active ones. You'd need to be specific about the substances in question.

@Jiminy Cricket two things: benzimidazole type of substances and caffeine.

Could you please do as suggested - take our [tour] and read the [ask] section of the [help] then [edit] your question into shape. Comments don't last and the question itself should contain all the requisite information necessary to answer.

Welcome to the site Ya Y! I would love to see this question be edited to add some of your clarifying details that you've brought up in the comments.


text:
Intelligence without natural selection?
Natural selection is not the only driving force of evolution. There are other mechanisms such as genetic drift, mutations, gene flow, etc... To what extent can these different mechanisms (which don't influence adaptation to new environments as much as natural selection) evolve a more 'complex' species than when there is no natural selection?
Using a very utopian example... imagine that the first living beings that appeared in the world had access to an infinite amount of resources and space. Thus, the mechanism of natural selection would not make sense because it wouldn't be necessary. However, there could be other mechanisms that allow evolution such as genetic drift.
In a world like that, would it be possible (even if it took a long time) to emerge certain 'complex' species with, for example, traits like intelligence (like human beings)? Or in this case, as there is no natural selection, species would evolve with just 'simple' variations like, for example, bacteria that reproduce faster than others?

"imagine that the first living beings that appeared in the world had access to an infinite amount of resources and space. Thus, the mechanism of natural selection would not make sense because it wouldn't be necessary" - That's not how natural selection works. Even with infinite resources and space, selection would increase the frequency of genes that improved reproductive success.

@BryanKrause Yes, you're right. I was imagining a scenario where species have the same reproductive success. I mean... I know it is not really possible with the laws of physics in our universe, but... if there was no selection/selective pressures... Could a species become intelligente given enough time? Or is it something impossible?

I mean, if you want to go for a thought experiment then you can make almost anything possible, that doesn't mean it's interesting or useful to state for understanding the actual universe we live in or understanding how evolution actually works.

@BryanKrause I've already heard about that thought experiment. With this post I was trying to understand how important is natural selection. In other words...  when complex traits (like intelligence) occur in a species, it means that they were always the result of natural selection? Maybe, given enough time, intelligence could arise in a species randomly, without selective pressures. I don't know... I appreciate your help!

Welcome to SE Biology. Please read the Help on What types of questions should I avoid asking? You will see that "You should only ask practical, answerable questions based on actual problems that you face", and that you are asked to avoid asking subjective questions where "you are asking an open-ended, hypothetical question: “What if ______ happened?”". That is why I do not think your question is on-topic here and have voted to close it.

a lively conversation - its a good question!

The answer is yes, but really no.
It’s probably true that things were kind of laid back at first for life. But selection was still going on. A strong wave might break the membrane, a strong wind or storm. A long cold winter. These were all selective. Selection comes with any sort of challenge, not just from other living things.
Natural Selection sounds like Big Science but it has many simpler humbler forms. A good way of defining it here is that any different traits between two living things can be passed down to their progeny. If a trait conveys even a very small advantage to producing progeny that survive to reproduce themselves then it is selected.
What you are saying is that if a fantastical being appeared that were infinitely superior then it would not be part of natural selection. In fact 'genetic drift' 'mutations' and are the source of nearly all these advantages. An infinitely superior being as you describe would disappear without progeny that maintained the advantage you are right - no natural selection. If that being had progeny and they produced the same advantage it would be preserved by natural selection and part of natural selection as we all know it.
That being said it’s very hard for a large advantage to show up. Even let’s say naturally green hair hasn't shown up on many millennia of human selection. If such a mutation or 'genetic drift' showed up I’d bet that gene would be pretty popular and there would be a good number of green haired people around in about 100 years. But none have shown up. Why? Because it requires too many very unlikely events to happen at once.
It’s difficult to overturn a theory like Natural Selection. It’s really very simple at its base. "If you can print copies of a book, more people will read it." is a similar theory. It’s possible all the books would just show up on peoples' doorsteps sure. It could happen but in all human history it has not become a common experience. People do give books away but they almost always print them. People could give away books that were written at random or by throwing a die. It’s possible to even write a best seller that way. But it’s so improbable that you might wait until the end of the universe before you see it happen. Look at Borges' 'The Library of Babel' which dramatizes the odds you are talking about.

Thanks for your answer. It is a very detailed answer. Our universe wouldn't be like it is if there wasn't natural selection. I was trying to understand that if genetic drift alone could give rise to a human being even with infinite time. I was thinking that, in some way, due to some biological or physical laws, if there are any selective pressures, complex traits can't occur in a species. Maybe they can, but we have to wait a very long long time. Althought, in a universe where species have infinite resources...

every species could reproduce without stop (infinite food and water, for instance)... there would be infinite species, infinite traits, so... given some time... the odds of something identical to humans appear become greater and greater. So it might be possible in a universe like that. I really appreciate your answer. And I'm going to read that short story. Thanks!

its another level up to explain that without eating and drinking that there would be no advantages for competition.  mutation and variation are going to make come offspring more or less advantageous Id think.. anyway its becoming very fantastic a scenario at this point... i dont think were done yet either. Kudos for asking this question!

No
Large multicellular animals only have an advantage in resource conservation monopolization.
So with infinite resources and infinite space you won't have anything that could even have a brain.
In your situation reproductive speed is the only competition, which means a race to the simplest. You can't even get significant predators because prey is a limited resource.
When you throw around words like "infinite" most common sense starts to break down. Of course infinite can't exist in this context in a universe like ours, so it is just a thought experiment anyway.


text:
Can these things be done at home on a hobbyist budget?
I've toyed with getting into microscopy as a hobby for fun and potentially practical reasons. Can anyone tell me whether or not these are doable at home in 2023 with a \$500 to \$1000 budget?

Identifying random molds (on surfaces, on foods)
Seeing what's in dust? (mites, mold?)
Looking for and identifying parasites in animals or soil samples (worms in feces, fleas or fungi on skin or hooves)
Looking for metal shavings in engine oils (maybe not appropriate for this forum, worth a shot anyway)

Quick googling led me to something like the swift sw380t with a camera for around \$500 + some equipment for slides. Being able record is particularly attractive. Is that reasonable? Is it overkill? Underkill? Should I just grab something used off fb marketplace for a fraction of the cost?

With a middle-price optical microscope (I would consider the sw380t to be mid-price), you can get up to about 1000x useful magnification. Look for a microscope with a 100x oil immersion objective. 1000x will allow you to resolve objects down to a few microns - this would include almost all fungi and animals, but not bacteria. A lower end microscope will be able to see almost all fungi and animals as well, but thinner fungi and fungi spores will be harder to see.

I'd definitely recommend getting a microscope off of craigslist or marketplace. It probably won't be as good as the same microscope new, but it will be much better than a new microscope for the same price.

@Eonema 1000x is certainly enough to see bacteria - they are typically 1-5 microns in diameter, which is well within the optical resolution of a microscope.

@bob1 Thanks for the correction, I guess my microscope is just in poor condition.

Yes, and no as to bacterial and fungal samples. For these you need a conventional light microscope that transmits the light through the sample. These are the common ones when people consider microscopes. You can also get reflected light microscopes (and even hybrid versions for hobbyists), that are needed if you are looking at solid objects such as fleas. These are sometimes called dissection microscopes and generally have lower magnifications (10-200x) only. I don't see why you wouldn't be able to see metal shavings in engine oil, with a conventional microscope, though getting enough light through the sample might be a problem there. Don't get oil on the lenses though and be wary of scratching your lens with any metal shavings if you do.
The key with microscopes is quality of the lenses (not surprisingly) - the better the lens, the fewer aberrations you get in the image, both in colour distortion and spherical (shape) aberration. Mid-range microscopes, price-wise, tend not to be the greatest at lens productions, but are certainly suitable for general use - and you may also be able to buy better lenses and swap them on. In this group I would include manufacturers such as Swift and Celestron. The top-end microscope makers such as Olympus and Zeiss are typically much more expensive, but worth it, if you can find a good one second-hand.
For bacteria you need 1000x (100x objective with 10x eyepiece) to see any details, but they are visible at 400x, if you know what you are doing. However, you need a lot of bacteria to do this, as I explain below.
Generally for ID purposes and even just to visualize bacteria, you would need to stain the sample. This involves a bunch of chemicals (iodine, potassium hydroxide etc.) and stains (Giemsa, Saffronin, Toludine blue, Malachite green etc.) that won't be available to the home hobbyist, though there might be alternatives to these that home hobbyists have worked out and/or are available (e.g. crystal violet, part of the Gram stain, is gentian violet used to treat skin infections sometimes, so chemists/pharmacies have it). Food dyes work in some situations.
You also generally need a pure isolate to look at, though you can do mixed floral growths off medium that might work. Just taking something like skin and looking for bacteria or fungi won't work as they aren't abundant enough to see easily. In a proper lab, bacteria and fungi are grown on a solid medium (agar plate - you can think of this as a jelly with nutrients) and scraped off. Generally not done straight from a sample as this is difficult and has lots of other things in there that interfere with the microscopy. That's not to say you can't do it, just it is more difficult!
Having said that, you can look at all sorts of things under a light microscope that don't require high magnifications or any expertise to look at - pond water being the classic. This will be full of small protozoa (amoeba, paramecium, rotifers etc) and algae that look great and are really fun to ID at 100-400x magnifications.
Cheek cells (use the round end of a toothpick to gently scrape the inside of your cheek, fix gently over a flame, stain with crystal violet) look great, and you can see a bunch of internal structures with 400x magnification.
Cross sections of leaves (hold between two thin pieces of polystyrene or cork and slice gently with a new single-edge razor blade or craft knife). . These will show the internal structure of the leaves - veins (xylem, phloem), cells etc. You can also use clear nailpolish to paint on the surface of a leaf (try the underside), then peel off and look at under the microscope - this should let you see the pores (called stomata) in detail, they look like pairs of lips usually. The fine tissue skin (not the brown bit, it's a very thin wet translucent bit) of an onion also looks pretty nice. Moss leaves also are fun to look at.
Along with mosses - take some dry moss, let it sit in water for 30 min or so and then squeeze out - you'll hopefully find tardigrades
Edited to add:
With respect to parasites in faeces; this requires a bit of expertise to get good at. There is a lot of matter in faeces and parasites are generally low abundance. Unless you know a host is infected and are willing to mix faeces with water, filter and do a bunch of screening, you might not find any actual parasites, though you might see things that look, to the untrained eye, like parasites but are really just debris. You also run a significant chance of infecting yourself with something, be it parasitic, bacterial or viral.

Thanks for the detailed response! It sounds like a lot of fun. I wasn't sure if there might be some infection/contamination risks around looking for parasites. I had assumed that preparing slides would involve mixing and processing, but I am completely ignorant to the logistics of doing that safely. How likely is it that a reasonably motivated hobbyist could learn how to do this safely? or is that something best left to the pros?

@Shaun I would leave the parasites to the pros, though it seems that you only need a couple of milligrams of faeces with water on a slide to see something. So long as you wore gloves, face mask and eye-protection. I think you would be fine. For the fungi - scrape some off bread or jam and have a look. These are generally harmless to humans.


text:
How can the most genetically similar populations to Ashkenazi Jews from an admixture standpoint be Italians, Greeks, Turks, and Armenians?
In this study from 2016, Ashkenazi Jews are shown to be the most similar from an admixture analysis test to populations not traditionally associated with being geographically near Ashkenazi Jews. This study was controversial for essentially stating that Ashkenazi Jews aren't native to the Levant, but that isn't really that related to the question. The abstract to the study states that the analysis of Ashkenazi Jewish genomes "demonstrated that Greeks, Romans, Iranians, and Turks exhibit the highest genetic similarity with AJs". In addition, of the twenty-five populations in the reference population (Greeks and Italians were excluded from said reference population), Ashkenazi Jews are shown to be genetically closest to Turks, followed by Armenians. This data is indeed supported by the admixture graphs shown in the study. What I am essentially wondering is how this is possible. The first is because this study demonstrates that Ashkenazi Jews weren't endogamous at all, contrary to popular opinion, meaning they must have had lots of admixture with Central European and Eastern European populations. The second reason is less scientific, but still a reason nonetheless. While there are indeed many individuals among the populations Ashkenazi Jews are said to be similar to in the study who have a light phenotype, from personal experience (I am Ashkenazi Jewish myself) pretty much all Ashkenazi Jews have a light phenotype, while amongst the populations mentioned in the study as being genetically closest to Ashkenazi Jews, a truly light phenotype is far rarer than amongst Ashkenazi Jews themselves. I feel personally that most Ashkenazi Jews, including myself, look far more like Germans and Poles than like Greeks and Turks. The third reason is that outside of small endogamous ethnic groups, a given ethnic group tends to resemble the peoples surrounding it, which in this case for Ashkenazi Jews would include peoples like Germans and Poles. Ashkenazi Jews are a massive ethnic group with a population estimated at ten million or more people, and as shown above, they were not endogamous. I am not doubting this study's results, but I simply wondering how, given the other information I mentioned, said facts are possible?

Maybe a better fit with History.SE?

@anongoodnurse Maybe this user is just trying to stir up shit given that they made two attempts at sneaking the same incoherent ramble into skeptics.se


text:
How to make a negative control
In USP <61> (United States Pharmacopeia), it mentions that we would need a negative control when we are testing products for any microbial growth. It doesn't necessarily explain how to make negative control. So how would I make a negative control? Is it just from any of the diluent buffers such as Phosphate Buffered Saline or is it just simply water? or something else?

This is spelled out under the section of USP<61> on growth promotion and system suitability.

To verify testing conditions, a negative control is performed using the chosen diluent in place the teste preparation There must be no growth of microorganisms. A negative control is also performed when testing the products as described under Testing of Products. A failed negative control requires an investigation

During product testing the purpose of the negative control is to demonstrate what negative/no growth test result looks like, but if done right it can also help demonstrate that any growth observed in your testing actually came from the test article, rather than being introduced during the testing procedure by some non-sterile equipment or reagent. This just entails treating your negative control as if it were an actual test article by preparing them side-by-side follow all of the same procedures.
During system suitability testing, I think you want two negative controls. One that is just the diluent and one that is the diluent with the product in it. Or whatever setup you're using to demonstrate that your protocol can detect the specified test organisms in the presence of your product.

It depends entirely on what and how you are testing.
In general it is a control that is used to show what no growth looks like under your system. Often this means adding a known sterile version of your drug/compound to medium and incubating in some manner. Adding the sterile version accounts for substances that might change a characteristic such as absorbance or turbidity of the medium you are using for your testing.
It could also be that you just retain a vial/plate of medium without anything added to it.

ok cool that is very helpful. Thank you very much!


text:
Estimation of evolutionary time to form DNA
It is often said that life formed on Earth randomly. Hence, the appearance of DNA molecule was the result of a random process. Can scientist estimate the time needed to form DNA molecule from just basic organic molecules, assuming conditions that were available at the born of life? Is there such an estimate? The age of the Earth is 4.5 billion years. How does that number compare to the time needed to form DNA?

Welcome wawa. It is often said that the Earth is flat, but that doesn't represent scientific models. Please take our [tour] and refer to the [help] particularly the [ask] section. You should then do some background reading around the topic and ask a biology question relating to how the science of biology views these things (based on available evidence). We also ask that you show your prior research into the topic, including references to credible source material (i.e. scientific journals, textbooks or at a bare minimum Wikipedia).

Please edit the question to limit it to a specific problem with enough detail to identify an adequate answer.

Right, this is a hot topic in general, but not in the context of the question, i.e. time. The origin of life can be estimated using molecular clocks but the error range makes the calculation unworkable (in my opinion). The second problem is you've got to know the mechanism and when that occurred in the geology of earth.The mechanism, particularly in terms of respiration biochemistry is currently thought to be around hydrothermal vents and respiration via H2S, i.e  anaerobic respiration.

The term "life formed randomly" might be controversial, because even at the earliest stage of life selection would have kicked in; ultimately that random bit of DNA had to code for itself.


text:
Cynobacteria vs. BGA
I am really confused. On google and other places(though very old) it is mentioned that Cynobacteria are the same as BGA(Blue-Green Algae) and are technically bacteria and are places under the kingdom monera. However, in some places is it mentioned that they are not the same and so does my teacher. It is mentioned that Cynobacteria, being a unicellular prokaryote is placed under Monera.
So, I have 3 Questions -

Are Cynobacteria and BGA the same?
Is Cynobacteria a monera or protista ? is it a prokaryote or euakryote ?
Is BGA a monera or protista ? is it a prokaryote or eukaryote ?

Is it true that later it was believed that Cynobacteria and BGA were the same, and now it has been discovered that they are different?
What is the true fact?
I believe this community has experienced biologists, hence I have reached out here.
Please understand that I am a student and this question might sound amateur, so please ignore that and please help clear my confusion.
Any help would be appreciated !

Cyanobacteria are oxygenic photosynthic prokariotes, historically known as "blue-green algae" until their prokariotic nature was unambiguously confirmed. (So, yes, Cyanobacteria and blue-green algae are the same, but they are not algae.)

Since their prokaryotic nature has unambiguously been proven, the term “cyanobacteria” (or occasionally “cyanoprokaryotes”) has been adopted in the scientific literature. ... the taxon Oxyphotobacteria is proposed for cyanobacteria in a strict sense.

Taxonomy has been a big problem for this/these organism(s); there are entire papers arguing the case for various taxonomic classifications.
It cannot be in the kingdom Protista as it is not a eukaryote. (So, they are in the kingdom Monera.)

Is BGA a monera or protista ? is it a prokaryote or eukaryote ?

Blue-green algae is a historical term and incorrectly describes what is now called Cyanobacteria. The question is not answerable as written, but if it has to have an answer, I'd go with "monera" and "prokaryote".
Chorus, I, Welker M; eds. 2021. Toxic Cyanobacteria in Water, 2nd edition. CRC Press, Boca Raton(FL), on behalf of the World Health Organization, Geneva, CH.


text:
Calculating basal area per acre from variable radius plots
I have a variable-radius forest inventory that contains diameter at breast height (DBH) and basal area factor (BAF) data for each tree. I'd like to calculate the basal area per acre, but since the plots were collected with a variable radius, I don't have an area estimate. I know multiplying the "in" trees from a prism by the BAF can produce an estimate of the basal area per acre, but I don't know if the number of trees in each plot of the data corresponds to an actual count of "in" trees when they were measured in the field. That is, using this method, is the convention to record the DBH of all "in" trees, in which case I could simply count the trees and multiply by the BAF? Or, is there an alternative way to calculate basal area per acre using the DBH in combination with the BAF?

According to resources like the Alabama A&M Extension, the convention is to measure the DBH of all the "in" trees, so you could just multiply the count by the BAF to get an estimate of basal area. However, I'd recommend making sure that your data was collected following convention. Do you have access to a metadata file or to the methods used to inventory these plots? If so, refer to those.
Edit: Why can we just multiply the number of "in" trees by the BAF, and not worry about the DBH?
This is because the DBH of the trees is already implicitly considered when using a basal area prism to determine which trees are "in." The DBH of the trees in the basal area plot is just collected for getting additional estimates, like standing volume.
Why does the number of "in" trees give us an estimate of basal area? And how is DBH implicitly included in this estimate? It's not really intuitive, but I'll try to paraphrase an explanation from this technical bulletin:
Imagine you randomly choose a point in a forest. This point has a chance of being inside of a tree. Your chance of being inside of a tree is equal to the basal area of the forest in units of acres/acres. For example, if you are in a forest with a basal area of 80 ft^2/ac, the basal area is equal to 0.00184 ac/ac, so you have a 0.184% chance of choosing a point in a tree. If you count the number of trees you are inside (either 1 or 0), on average, you will count 0.00184 trees. If you multiply the number of trees you are inside (either 1 or 0) by a BAF of 43,560 (the number of square feet in one acre), on average, you'll get the basal area of the forest. Of course, this would be a horrible way to estimate the basal area of the forest, because even though on average you'd get the right number, you'd actually get either 0 or 43,560 ft^2/ac each time you measured.
Instead, suppose you draw imaginary circles around each tree that are 10 times as wide as the tree, and therefore have 100 times the basal area of the tree. Now choose a random point and count the number of circles you're in. Just like how, in the last example, the number of trees your point is inside is an estimate of the basal area of the forest, the number of imaginary circles your point is inside is an estimate of 100 times the basal area of the forest (in ac/ac). Divide the number of circles you are inside by 100 and multiply by 43,560 (i.e., multiply by a BAF of 435.6) to get the basal area in ft^2/ac. This gives a much more precise estimate now, since randomness won't have as much of an effect. And it takes into account the DBH of the trees, since the diameters of the imaginary circles are proportional to the diameters of the trees.
This is how basal area prisms work. They let you know whether you're inside the imaginary circle for each tree, geometrically taking into account the DBH and your distance from the tree.

Imaginary circles around trees. From the Wisconsin Conservation Department Technical Bulletin no. 23.

I guess what confuses me about this is why the DBH wouldn't be used

@brlockwood Great point. I edited my answer to try to explain why.


text:
Why is Archosauria a subclass and not a class?
What is the logic behind Archosauria being a subclass when they have such major differences between Lizards, Snakes, and Turtles. The Amphibians appeared before the Diapsids, which then split into Synapsids and Sauropsids, so classes aren't just based on time of origin. Archosauria have many skeletal and morphological features that separate them from Lepidosaurs as much as Lepidosaurs were separated from synapsids.
Maybe I am just missing something but I can't find the reasoning behind Archosauria not being classified unique from Lepidosauria in the same way. The more I learn the more it seems like the Tetrapod classes should be Synapsids, Amphibians, Lepidosauria and Archosauria.
P.S. Please help me clarify this question. I have spent a long time on this but I don't think I'm being very clear. I can't think of the correct way to word this at all. It feels garbled and all over the place.

The phylogenetic labels like class, order, family, etc are fairly outdated and not meaningful. All that is important is the hierarchy, the specific level and number of levels is arbitrary and highly biased to the humans that labeled them.

See Bryan Krause's comment, but I'll add that the reason is historical. Linnaeus identified three classes of tetrapods (mammals, birds, and reptiles/amphibians), and reptiles and amphibians were later split into their own classes. This was all before Darwin, so classes were defined based on morphological similarity, and not evolutionary relationships. When taxonomists started defining groups based on phylogeny, they tried to preserve Linnaeus's ranks of kingdom, phylum, class, order, family, and genus, even though they're arbitrary. So the classes you suggest would probably make more sense, but we keep the old ones for historical reasons. In fact, the clade Aves is usually considered a class, even though it lies within Archosauria, within the class Reptilia! This is one of the few exceptions to the rule that you can't have a class inside a class (or order inside an order, etc.). No, it doesn't make sense, but try telling an ornithologist that Aves is now a "superorder".

Thank you, I thought it was just me. It makes me wonder if the entire classifications system will be reworked the same way planet classification was back with pluto.


text:
Is inner membrane of mitochondria less permeable than outer membrane?
Given below are two statements:
Statement I: Mitochondria and chloroplasts both double membranes bound organelles.
Statement II: Inner membrane of mitochondria is relatively less permeable, as compared chloroplast.
In the light of the above statements, choose the mis appropriate answer from the options given below:
(1) Both Statement I and Statement II are incorrect.
(2) Statement I is correct but Statement Il is incorrect.
(3) Statement I is incorrect but Statement Il is correct.
(4) Both Statement I and Statement II are correct.
One more thing to note is that answer will be based on this statement from textbook which itself is vague-
"Like mitochondria, the chloroplasts are also double membrane bound. Of the two, the inner chloroplast membrane is relatively less permeable."
Plz answer me based on facts and also based on the statement I have copy pasted from textbook.

Welcome to SE Biology. Please do us the courtesy of finishing the [Tour] and learning about how this site works. In particular you should note that "Homework questions are off-topic on Biology unless you have shown your attempt at an answer. For more information see our homework policy."


text:
Do veinlets of leaves always originate from the midrib?
When studying venation in leaves, I came upon a few diagrams of parallel venation where veinlets originated from midrib, and converged toward the midrib such that they all lay parallel to it...
But I have also seen some monocots (a palm and some grasses) whose veinlets don't look like they're emerging from the midrib at all.
So do they just emerge from the base of the lamina?
If yes, then how are they connected to the transporting vessels which are present in midrib?


text:
Is Protista a kingdom just for unicellular eukaryotes that couldn't be classified under any other kingdom?
Is Kingdom Protista merely a "catch-all" classification for unicellular eukaryotes that do not belong to the kingdoms of Animalia, Plantae, or Fungi? Or does it possess specific criteria that organisms must meet to be classified within it? Furthermore, what are the distinguishing characteristics that unify this kingdom despite its apparent diversity, except being unicellular & eukaryotes?

Welcome to SE Bio! Please take the tour and look at the criteria for asking questions that are likely to get a helpful answer. Among these are doing some initial background research like googling your question. In this case, the wikipedia page for protists has the answer to your question as its second sentence.


text:
Why is a Na-K pump necessary if the neural membrane is impermeable to Na+ ions during the resting phase?
If the neural membrane is impermeable to Na+ ions during the resting phase, why does it require a Na-K pump to expel sodium ions? What causes the accumulation of Na+ ions inside the membrane if it is supposed to be impermeable to them?
Understanding this could shed light on the fundamental workings of neural cell physiology and ion regulation.


text:
What makes dopaminergic neurons fire when maintaining base dopamine levels?
Are they signaled by other action potentials? Other neurotransmitters? Do they just fire on their own? If not triggered by an external stimulus, why does depolarization make them fire more frequently?

It would be helpful to provide some context for your question. What are you reading and where to trigger this question?

I am working on a pharmacology project that provides estimations for the physiological effects of different drugs based on their mechanism of action. I am aware that depolarization of dopaminergic neurons through means such as GABA inhibiton or nAChR agonism makes them fire more frequently, I just don't understand why.

Why would GABA inhibition depolarize a neuron or make it fire more frequently?

Is that not what GABA does? As far as I know, GABA makes the membrane potential of a neuron more negative, so that it does not reach its action potential threshold as easily, and inhibition of GABA makes affected neurons less negative and increases the frequency of action potentials.

I see. When someone says "GABA inhibition" I would assume they mean "inhibition mediated by the neurotransmitter GABA". If you mean inhibition of GABAergic neurons, you should be explicit about that or talk about "disinhibition". If you mean blocking GABA at the neurotransmitter receptor level this is not "inhibition" but "antagonism".

That's true, but disinhibition of dopaminergic neurons could be mediated by GABA receptor antagonism or inhibition of GABA release in the first place (which is what I intended to say and should have specified earlier).

Do you want to [edit] the question to add that and any research you've looked at in trying to find an answer to this as comments are intended to be temporary only.

The brain is very "noisy". Neurons in an actual brain don't just sit around waiting for an external stimulus. The "resting potential" of a neuron in a dish is not very representative of the membrane potential of a neuron in vivo.
There is a lot of debate about what "noise" really is, though. Is it actually "noise" in an intrinsic sense? How much of it is ongoing active brain activity? Given that it isn't as if a person sitting in a chair staring at a black screen has nothing going on in their minds, why should we expect there is nothing going on in their brain?
Practically, from an experimenter's perspective, noise is just "The part I didn't do." Baseline is just "in the absence of some intervention I might do later". We don't shut down the brain to measure a baseline.
Here are some reviews about noise in the brain, this list is not at all comprehensive:
Stein, R. B., Gossen, E. R., & Jones, K. E. (2005). Neuronal variability: noise or part of the signal?. Nature Reviews Neuroscience, 6(5), 389-397.
Faisal, A. A., Selen, L. P., & Wolpert, D. M. (2008). Noise in the nervous system. Nature reviews neuroscience, 9(4), 292-303.
Destexhe, A., & Rudolph-Lilith, M. (2012). Neuronal noise (Vol. 8). Springer Science & Business Media.
Uddin, L. Q. (2020). Bring the noise: reconceptualizing spontaneous neural activity. Trends in Cognitive Sciences, 24(9), 734-746.

If not triggered by an external stimulus, why does depolarization make them fire more frequently?

Imagine you had the membrane potential of any neuron, dopaminergic or not, where the membrane potential reflects the sum of all inputs to that cell, with some spikes occurring at baseline. There are also going to be a lot of times (most of the time) where there is no spike at all. If you were to depolarize the cell, it will fire at some of those other times as well. That's an increase in firing rate.


text:
Help identifying insect, possibly a carpet beetle larva?
I found this bug on my kids mattress when changing the bedding this morning, sorry I didn't include a scale, I would say it is probably about 1 - 1.5mm in length. It seems to have 6 legs and what looks like 12 "segments" for lack of a better word. Underneath it is soft and a little hairy, it has no hairs on the top of its body but you can see from the photo it has them on its rear and front. It doesn't move very fast.
From what I can tell it is a carpet beetle larva, am I correct? If so, is this is an issue regarding destruction of fabrics? I've not seen another one so would assume probably not, but worth asking. Cheers!

Whilst I don't have an answer for you, there's a related post which may inform you. The comments have a number of interesting links. (Carpet beetle larva would seem probable here).

It does seem likely that this is indeed a carpet beetle larva.
Similar to carpet moths, they cause damage by feeding on organic matter (especially keratin, with wool being one of the key targets) during their larval stage (but not in adult forms). They like darker undisturbed areas and particularly enjoy fabrics that have been worn (as they contain extra seasonings of other organic deposits from human wear).
One swallow does not make a summer and you might not necessarily have an infestation. However, seeing one of these should prompt a very careful inspection of your belongings (especially any precious items composed of wool, silk, feathers or leather) and careful vacuuming of the house, focusing on easily neglected inaccessible corners, crevices etc.
If you have any particularly valuable items (and suspect they might have been infested), freezing the suspected item can be effective. Otherwise, the most robust method of preventing damage is ensuring all clothing is washed soon after wear and stored in air-tight containers (e.g. vacuum packs).
Depending on the scale of the problem, you might want to employ these simple measures, use some simple anti-beetle items (although I do not know enough about their efficacy, beetle traps can also be helpful for monitoring the situation) or even consult a local pest control company...
Good luck!


text:
Health risks concerning use of furniture exposed to mould
I am about to buy a piece of second hand furniture. The wardrobe was stored in a room which recently was affected by water damage (it is a showroom not a basement room).
Water damage occured in the ceiling of the room. Since onset of water damage four weeks have passed. A specialist inspected the water damage and detected mould growth, further testing is required to identify the specie.
The wardrobe did not have direct contact with the affected area on the ceiling (e.g. 1.5 m distance).
Now I am asking myself if there are health risks when using the wardrobe in a bedroom.
Specifically my questions are:

Is it possible for fungus material, eg. spores to transfer to the
wardrobe and cause further mould growth even if the condition of
elevated humidity no longer is met?
Could fungus material, e.g. spores transferred to the surface of the object pose a health risk (regarding concentration)?

Remember that we have a one question per post policy and the one about showing your own research.  The biology part would seem to be about mold growth in reduced-humidity conditions and dry rot should give you place to where to start. Health risks of mold would be on-topic on our [medicalsciences.se] site - and are very relative, Some people are sensitive, some not. Remember to show your researches there too.


text:
What free app or program (website) is best for building an interactive food web?
I'm trying to create an interactive food web to give a clear overview of Seal population dynamics based on diet. As food webs have a tendency to quickly become to comprehensive to be easily readable, I'm looking for a free app or program (website) that I can used to build my food web, whilst mitigating some of these issues. I would like to use the following tools:

Adding a picture of the target species.
Turning a picture into a hyperlink which brings you to a PDF-file with information on the targeted species.
Adding symbols, and arrows that are capable of linking-up between two photo's.
A list of the species with a checkbox next to them, that when checked only shows the checked species and their direct connections.
Or, The targeted species and their direct connections light up when you hover over it with the mouse.

If no such app or program exists with all these possibilities, what would you advice to do in order to decrease the issue of comprehensibility?

Welcome Bastiaan. We have a [softwarerecs.se] site that this might be more suited to - that being said, others may come up with some suggestions here. Please take our [tour] and refer to the [ask] section of the [help] before posting there to ensure that your question is in shape.


text:
Understanding STR to SNP imputation methods
I am struggling to find the exact step-by-step algorithm of STR to SNP imputation, but failing so far. I figured there's Beagle software, but I can't find out how it works (math behind it). My actual interest is how to get SNP data for cattle when I have STR data, and vice versa

If I understand correctly, you have STR data, and you want to rely on LD to infer linked SNP genotypes? That sounds hard, for a couple of reasons:

LD decays very quickly between STRs and SNPs (shown variously: here, here, and here). This is due to high mutation rates. That makes any process of imputation difficult.
Relatedly, parallel mutation towards the same allele is common in STRs, meaning that even if you do have matching genotypes, identity-by-state is not a good basis for inferring relationships. This can lead to long-distance apparent LD.

The Beagle docs make no mention of the terms "microsatellite" or "STR". I am not sure that the software can use multiallelic loci. It says:

Each genotype must have two phased, non-missing alleles.

If you do want to try using Beagle, perhaps by collapsing your microsatellites to biallelic populations using a mixture model or something (which I wouldn't recommend but you could do), you can readily find the math in the papers. Specifically Appendices A and B at that link has a description of the HMM approach.
I would suggest instead looking at the Payseur paper, which seems to have some recommendations for attempting this approach. That paper is now pretty old though, so take it with a grain of salt.

Thank you a lot for answering! I got it that it is pretty hard to infer SNP from given STR, and how about vice versa? What if I had SNP data and wanted to restore STR? From your explanation it sounds like is must be same difficult task?
Also, can it be that the precision of such inference would be good enough for cattle examination? My problem is connected with cows breeding, and perhaps such imputation  would work in this field?..
Thanks for the links to the papers, too!

@Helen yes, I think that is true that the converse problem is as hard if not actually harder. Note, people have done stuff like what you want to do I'm pretty sure, but you are going to suffer from significant imprecision. Maybe that's ok from your perspective! If you had really well characterized haplotypes in your pedigree (STR+SNP), which might be possible for breeding cattle stock, you could decide to just map those together after transforming STRs to biallelic, or something similar. I'd repeat that the Payseur paper probably has suggestions for what you're trying to do, old as it is.

the Payseur paper, as I understand it, seems to be more about measuring some correlation between given STR and SNP... Probably the other one (with HMM) is more suitable in my case, I'm currently trying to figure that out for myself.

As for transormation of STRs to biallelic, - could you please give me a hint of how it is done? I tried to google myself but didn't manage to find anything on this topic so far

PS I think I got it, thank you again!

@Helen The correlation in question is linkage disequilibrium, aka how much information knowing a SNP genotype gives you about nearby STR genotypes (or vice versa). Clustering of STRs to biallelic: I have never done this but I have heard it suggested. I am not sure that it's a good idea. What you could do is fit a 2-component mixture model to the distribution of STR allele lengths using R or similar. I'm not aware of any packaged tools that do this.

@Helen In any case: if you have found the answer helpful, traditionally you upvote. If it has solved your problem, traditionally you accept the answer. I am not clear whether this has been helpful or has solved your problem, though.