text:
How do we call a "burst of evolution"?
I have in mind that evolution is not a constant / continuous process and that there are bursts of evolution.
Are there terms to refer to the concepts of fast vs slow evolution rates?

FYI, I was motivated to ask this question to address this question by @HarryWeasley in a comment.

Thanks a lot! It was indeed  'punctuated equilibrium' which I was referring to when I said 'bursts of evolution'! Thanks again, it's rare for someone to post a new question based on just a comment of mine!+1 for both your question and answer! :)

They talk about a cambrian explosion, but that's more an explosion of life. it's a form of genesis in unscientific terms, genesis, so it's an apex/ peak/ of species genesis.

There are indeed periods of fast evolution and period of evolutionary stasis. The term "burst of evolution" is never used in the literature but below are three common terms when discussing these concepts.
First we have to realize that the term 'speed of evolution' does not mean much. We can be talking about change in phenotype through time (See Punctuated Equilibrium and Evolution and Ecology time scales) or speciation rate (See Adaptive Radiation and Mass Extinction). Also, we have to realize that we can talk about such speed of evolution on a given taxon or for the entire life on earth.
Punctuated Equilibrium
We often refer to the fact that there are periods of evolutionary stasis and periods of rapid evolution as punctuated equilibrium

Punctuated equilibrium (also called punctuated equilibria) is a theory in evolutionary biology which proposes that once species appear in the fossil record they will become stable, showing little evolutionary change for most of their geological history. This state is called stasis.

Here is a representation (from the above wikipedia link) of phenotypic divergence following an extremely gradual view of evolution and an extremely "punctuated" view of evolution

Evolution and Ecology time scales
Since the 2000s, there has been increased recognition that evolutionary processes even matter on a ecological/demographics scale. That is ecological/demographics processes and evolutionary dynamics influence each other dynamically and the old view that evolutionary processes are much slower than ecological/demographics processes is sometimes wrong.
See the post History: Do evolutionary and ecological processes occur at the same timescales?
Adaptive Radiation / rapid diversification
The speciation rate also varies through time. There are "burst in speciation rate" if you like the term. A sudden burst in speciation rate is called an adaptive radiation

In evolutionary biology, adaptive radiation is a process in which organisms diversify rapidly from an ancestral species into a multitude of new forms, particularly when a change in the environment makes new resources available, creates new challenges, or opens new environmental niches. Starting with a recent single ancestor, this process results in the speciation and phenotypic adaptation of an array of species exhibiting different morphological and physiological traits. An example of adaptive radiation would be the avian species of the Hawaiian honeycreepers. Via natural selection, these birds adapted rapidly and converged based on the different environments of the Hawaiian islands

You can find a list of classical examples of adaptive radiation on the above wikipedia link or at the post Is there a taxa that radiates faster?. If you don't want to be too extreme, you can as well just use the expression rapid diversification.
Mass Extinction
There are essentially two differences between an adaptive radiation and a mass extinction. 1) one is about an increase in speciation rate while the other is an increase in extinction rate. One is about a single taxon, the other one concern most of life on earth.
Because, a mass extinction sounds quite apocalyptic and because we seem to be at the start of a new mass extinction, most people are familiar with this term.

An extinction event (also known as a mass extinction or biotic crisis) is a widespread and rapid decrease in the biodiversity on Earth. Such an event is identified by a sharp change in the diversity and abundance of multicellular organisms. It occurs when the rate of extinction increases with respect to the rate of speciation. Because most diversity and biomass on Earth is microbial, and thus difficult to measure, recorded extinction events affect the easily observed, biologically complex component of the biosphere rather than the total diversity and abundance of life.

I want to highlight that when thinking of a mass extinction, many people think of a single event clearing up the surface of the earth in a day but the reality is very different. In fact, a mass extinction can well last thousands of years.

Great answer! Almost accepted it before I realized I hadn't posted the question! (+1)!

well to start evolution is continuous but not a constant rate. The rate is controlled by population size and the extremity of the selective pressure. Strong pressures in small populations tends to result in more rapid changes than weak pressures in large populations.
As for what to call rapid evolution it depends on what form of evolution is being seen.

For instance a single large change in a single generation (often becoming a speciation event) is called saltation and is extremely rare, especially in animals, requiring a perfect storm of conditions.
A founder effect induced rapid change is called a Genetic Revolution, although you will see it referred to as just a founder effect more often, and is caused by drastically decreasing the population which causes changes to spread much faster.
Technically extinction might also qualify as a rapid evolutionary change.
Quantum evolution is a hypothetical change in which new higher taxa arrise, but it is both poorly defined and there is absolutely no evidence it has ever occurred, indeed it appears to be mostly an artifact of how classification is determined, so I would hesitate to use it.
Macromutation is the term for large single mutational changes, things like  cold shock gene duplication would fall under this category. Tissue morphogenesis would be related to this, as it is a large developmental change which may or may not be the result of a large genetic change. A frame shift mutation could result in this.
A rapid change in multiple species in the same place and/or time are referred to as adaptive radiation events, rapid diversification, if it is large and  sudden enough it may even be referred to as explosive radiation.

Part of the issue is saying something is "fast" is a more qualitative assessment so it does not have a term in and of itself, the closest you see is things referred to as "rapid" so you might see rapid speciation or rapid extinction, rapid X or Y.

I think the OP is referring to geological periods where lots of different lineages arose suddenly, like the Cambrian explosion. If so, I think “rapid diversification” is exactly right.

A few comments. 1) Strong pressures in small populations result in more rapid changes than weak pressures in large populations is true or false depending on the details of the model and what statistic you are considering to measure speed of evolution. I would advice against using this kind of general statement. 2) I think the term 'genetic revolution' is very rarely used in the evolution literature (see e.g. this google scholar search).

An adaptive radiation is not just [a] rapid change in multiple species. It is a sudden very high rate of speciation. 4)  a single large change in a single generation (often becoming a speciation event) is called saltation and is extremely rate. It depends what you mean by rare. Typically ploidy change mediated speciation and hybrid species are sudden events leading to speciation and not so uncommon in some lineages (Rieseberg et al. 2003). Otherwise, I think the answer is good.

Sudden is a fine qualifier I will add it. Yeah speciation kinda weird in plants to begin with, In runs back to the problems in defining species. And by rare I mean rare compared to other forms of speciation across all of life, for a general question I was trying to keep myself to a general answer.

@remi I'll clean it up and add some qualifiers, tell me what you think.


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Origin of holes at 800 m depth in the Mediterranean
From 8 to 12 small 2-3 cm holes in the bottom mud are forming rounds with a diameter of 20-40 cm. No tentacles or other body parts have been observed. Mediterranean sea, 600-1000 m.
What are they?

Where's the picture from? What makes you think you're looking at biology?

-The picture is from subsea remote operated vehicle. It doesn't look like an occasional structure in mud. There are many of them with the same pattern.

Is it your picture, or someone else's?

I've made it, yes

I take it the 20-40 cm is the diameter between the green lines and the 2-3 cm holes are each of the 9 shapes?, or is it that the 9 shapes are 20-40 cm across each? I'd suspect a moving mollusc or something similar, or perhaps a fish hunting for sub-surface feed.

50 cm between the lines

Can you comment on when these formed (that is, did you observe this ground without the holes last year, but this year they appear? Or is this the first time you see them and they could have formed many years ago?) Can you comment on how solid or soft this ground is (does it leave footprints like sand, or is it harder like dirt?) Have you seen several of these rings, or just this one?

1)Have no idea wether it's appeared this year, but I think it should be something usual. Something, that should be known by zoologists. That's the first time I see such structures. 2) Ground is very soft. It's a mud or dust. It's lifting up with ROV propellers. 3) There are many of rings. Sometimes there are two of them (like 8) or even three. –

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text:
Is Chemiosmosis a hypothesis or a theory?
I was trying to find out whether chemiosmosis is a hypothesis or a theory. Naturally, I first searched on Wikipedia, but the article on chemiosmosis uses both the words, which is confusing.

The chemiosmotic theory
Peter D. Mitchell proposed the chemiosmotic hypothesis in 1961. The theory suggests essentially...

...the weight of evidence began to favor the chemiosmotic hypothesis, and in 1978 Peter Mitchell was awarded...

In chemiosmotic theory transmembrane ATP synthases are...

Then I found several papers; some of them use the word hypothesis like this one, this one and several others, but few others use the word theory like this one, and this one.
To my knowledge, a hypothesis is an educated guess based on certain data that acts as a foundation for further investigation while a theory explains a natural phenomenon that is validated through observation and experimentation but I am not aware of any experiments conducted by scientists to test this?
In summary:
Is Chemiosmosis a hypothesis or a theory, and what experiment has been performed to test it?

Edited your question so that now it's not obvious that it's actually two ;-)

I have now edited the Wikipedia page, changing theory to hypothesis. We'll see how long it lasts before someone tries to revert it, and what the eventual outcome may be. In part I did this to demonstrate that Wikipedia entries can be edited by anyone (unless they are politically controversial etc.) and that they are a communal effort with no single formal editor. You cannot assume that they are correct, only that they are correctable.

Preamble
Although there is a case for closing this question (it is two questions, the first of which is more linguistics, logic or philosophy of science, and the second well-covered in text books) I have chosen to answer it, mainly because neither of the terms hypothesis or theory describe the current status of the proposal (the neutral description I shall employ initially). I have restructured my original answer putting the science first, and providing more information on this.
Mitchell’s Proposal
As the title of his original 1961 Nature paper makes clear (“Coupling of phosphorylation to electron and hydrogen transfer by a chemi-osmotic type of mechanism”) Mitchell was addressing the following question: How is the free energy released from the electron transport chain — involved in the oxidation of NADH and FADH2 by oxygen — used to phosphorylate ADP to ATP.
At that time it was assumed that this was by a mechanism in which the energy was used to generate a chemical compound, X~P, containing a phosphate bond with a high free energy of hydrolysis, which could be used to phosphorylate ADP to ATP. (This was influenced by the ‘substrate-level’ phosphorylation occurring in glycolysis.) In brief, Mitchell proposed that the phosphorylation did not involve any compound, X~P, but was catalysed by an ATP synthase enzyme powered by an electrical gradient, established across the membrane in which the electron transport chain resided.
Mitchell proposed a possible mechanism for oxidative phosphorylation in terms of conventional physics and chemistry. Just as the postulated X~P, had not been identified, neither had the components of his proposed chemi-osmotic mechanism. The paper focused on its quantitative feasibility (making it challenging reading for many biological scientists), although it did also argue that the idea was consistent with a series of experimental observations that were difficult to explain in terms of substrate-level phosphorylation.
It was a hypothesis
Regardless of the interpretation of dictionary definitions, considered below, it was a hypothesis because that was the word Mitchell used in the original paper, cited above, a paper in which the word theory does not occur.
As well as misquoting history, it would seem presumptuous to use different terms to refer to the proposal of the original author, a proposal which resulted in his award of the Nobel Prize.
It is a fact
The mechanism of oxidative phosphorylation has now been explored in great detail and the general features of Mitchell’s hypothesis have been generally validated. It can be considered as much a fact as any other in our general conception of cellular biochemistry.
The famous experiment that resulted in widespread acceptance of the hypothesis was the so-called acid-bath experiment of Uribe and Jagendorf. In this experiment ATP was generated in the dark and without electron transport by loading the inner space of the grana disk membranes of spinach chloroplasts with protons.
More recently the structures of all the proteins involved in the chemiosmotic mechanism have now been determined, including that of the ATP synthase, the molecular machine which uses the electrochemical gradient to phosphorylate ADP to ATP. and the components of the electron transport chain.
Dictionaries
Merriam–Webster, on-line, is quite dogmatic about the difference between the words hypothesis and theory:

A hypothesis is an assumption made before any research has been done.
It is formed so that it can be tested to see if it might be true. A
theory is a principle formed to explain the things already shown in
data. Because of the rigors of experiment and control, it is much more
likely that a theory will be true than a hypothesis.

But is this dogmatism justified, and how does it apply to the current problem? Mitchell’s proposal was made to be tested (as in a hypothesis) but it was intended to explain the observed phenomenon (as in a theory) of oxidative phosphorylation.
An extensive article in Wikipedia begins with a more modest statement:

A hypothesis (plural hypotheses) is a proposed explanation for a
phenomenon.

And chemi-osmosis is a proposed explanation for the phenomenon of ATP synthesis in double-membrane systems; so by this token Mitchell’s choice of words seems justified.
Major dictionaries record how words are or were used in practice. In some contexts there are sharp distinctions in usage of particular words, where in others the same words are used interchangeably. In modern biological science, unlike philosophy, logic or the numerical sciences, laws, theories and hypotheses are generally of no great concern, and the writers quoted may merely feel that the word ‘theory’ (‘Einstein’s’ theory, ‘Darwin’s theory’) has more gravitas than ‘hypothesis’, a word they perhaps use to describe ideas about relatively humble scientific problems of their own.
…or they may just find it easier to spell.

Understood, I don't think I possibly know how to merge my two questions now, but I'll sure keep that point in mind for my future questions. Again, thanks!

also reg the textbook i'll try to get my hands on one

Revised my answer. Principle the same, but more information on theory and evidence for it.

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On the origin and evolution of vaccinia virus
I was browsing Wikipedia and learned that vaccinia virus, the basis of the smallpox (variola virus) vaccine, was originally thought to be derived from cowpox but was later discovered to be a separate species in its own right. Genome sequencing shows that it is most closely related to the distinct horsepox virus†.
My question is whether vaccinia virus was already a separate species when it was first taken and propagated for smallpox vaccines or if was originally a strain of horsepox (or some other unknown pox virus) that only became a separate species after passaging over many years.
† I have consulted the article in Wikipedia and the ICTV 9th Report's section on Poxviridae for background information to this question, but they do not provide a definitive answer.

Thank you for providing a background to this, but could you please clarify your question. Are you asking 1. Does vaccinia exist in the wild as a pox virus infecting a species that has not been identified? or 2. Did vaccinia once exist in the wild infecting such an unknown species but the species or virus has died out? or 3. Is vaccinia derived from an extant pox virus such as cowpox, but has changed so much (e.g. like dog breeds) that its source is not clear? Or something else. But please edit your question so that this is clear and avoid the unhelpful terms, "artificial" and natural.

A quite different question of clarification. Your statement about infectious strains of vaccinia puzzles me. I followed up your reference but cannot find anything about vaccinia strains. Can you give a page reference. There is a phylogenetic map at https://talk.ictvonline.org/ictv-reports/ictv_9th_report/dsdna-viruses-2011/w/dsdna_viruses/75/poxviridae-figures which shows vaccinia most closely related to cowpox strain GRI-90. Also note that horsepox etc. are poxviruses in their own right, not strains of vaccinia.

@David
I'm trying to ask if vaccinia would have existed without humanity. I suppose another way of phrasing it would be "did the vaccinia virus exist before the 1790s when the strains for vaccines were first isolated".

As for the use of the use of natural and artificial I'm using natural to mean "would still have happened even without human actions" and artificial to mean "only happened due to human actions". If that's unhelpful I'd be fine replacing them but unfortunately you haven't given me any terms to replace them with. I can't replace them without any examples of what words would be better yet still communicate what I'm trying to say.

For the  about infectious variants I was trying to preempt any answers which cited those as examples of natural strains as we have no proof they are natural as opposed to strain which escaped from the lab. Wikipedia lists six member viruses for vaccinia three of which are infectious, two of them have pages, buffalopox and rabbitpox, while the third, the Cantagalo virus, has no page and requires googling.

As for the phylogenetic map, could it be that the map just doesn't show enough detail for any strains closer than GRI-90? Wikipeida says that the closest relative is horsepox with a 99.7% genetic similarity and has two citations supporting it.

For the last sentence, yes I know that, that's why I'm asking the question. I want to know if the mutations that made them distinct enough to be separate species evolved naturally or if it only happened due to generations of selective breeding by researchers developing smallpox vaccines.

As you probably know from other SE lists you are on, the aim of SE is to get good questions and answers, and therefore users are encouraged to improve both. As @bob1 had produced an answer that addresses the general question of the origin of vaccinia, I thought it most useful to edit your question in concert.

The answer is that we don't know for sure. All we know is that at some point in the process of developing the vaccine, what was thought to be cowpox, was not in fact cowpox, but was rather what we now know as Vaccinia virus.
Part of the problem here is that the vaccine process was not entirely scientific in its development, there were multiple sources from multiple locations around the world developed more or less independently using an inoculation process (by Jenner's method, just copied). In many cases, before the development of heat-stable vaccines the method of carrying the vaccine to other parts of the world was to transport a live animal infected with a pox virus (I don't have evidence for this, but it is mentioned in "The greatest killer: smallpox in history" by D Hopkins 2002.
The history, as I mentioned is murky. As Baxby wrote in 1977:

Smallpox vaccination was established long before the nature of viruses was known and therefore very little is known about the number of poxviruses circulating in the 18th and 19th centuries.

and as Razzell 1999 also noted:

The main English vaccine (the Lister strain) was sent from Cologne some time after 1871 and is reported to have been taken from a Prussian soldier suffering from smallpox... ... Many of the English vaccines in the 1850s were derived from the inoculation of cows with smallpox and as Baxby has pointed out the most recent evidence suggests it is not possible to produce vaccinia through the variolation of cows.

In addition, Schrick et al (2017) sequenced a 1902 vial of vaccinia vaccine, finding that it clustered with horsepox, noting that Jenner also suspected as much in his 1800 publication, several sections being devoted to the similarity between horsepox and cowpox and the transmissibility between the two such as the below:

In the month of November 1797 my horse had diseased heels which was certainly what is termed the grease and at a short subsequent period my cow was also affected with what a neighbouring farmer who was conversant with the camplaints... ... No other person milked the cow but the lad above mentioned I am firmly of opinion that the disease in the heels of the horse which was a virulent grease was the origin of the servants and the cow's malady

In conclusion: we don't know, but it seems likely that somewhere along the way a horsepox was used and with repeated passaging either in animals or in people, the virus developed into vaccinia as we know it now.

This is a useful answer to the general question of the origin and evolution of vaccinia virus. The question as posed seems concerned with semantics and does not do your answer justice. I shall attempt to edit it. Another questions that comes to mind is that what makes cowpox cowpox and horsepox horsepox is that they infect cows and horses, respectively. So, is it known whether vaccinia will infect cows and horses?

@David - Thanks for the edit, I read the question as being more or less along the lines of you edit. I don't know off the top of my head as to whether they cross species. I suspect so, as most PoxV are capable of it, albeit with limited infectivity.

@David - I'll edit in more information into my answer when I have time - there's quite a bit to this.

It is often good to just take the genbank sequences and do your own tree. Here I just chose a random region of vaccinia reference genome (50000-55000), blasting to get the 500 closely related strains, mafft, iqtree. Result: the vaccinia virus clade is very diversified and contains a few horsepox, buffalopox, rabbitpox strains, and it falls into the diversity of some cowpox clade.
So the main thing to elucidate is the reason for this wide diversity of vaccinia, ie. first selecting a few sequences representative of the early strains, before all the lab/passage work.
The most basal sequence seems to be AY313848 (Acambis clone 3, named CL3 in this paper).
This paper is probably a better start.
There are good chances that it depends on the chosen genomic region, so that the question of vaccinia's origin is more complicated than it seems.


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Best way to estimate wolf density through camera traps
I would like to know the most suitable sampling strategies and analytical methods (possibly, with relative bibliographical references) to estimate the populational density of wolves through camera traps, without single individual recognition.
So far, I've  only consulted this publication (https://besjournals.onlinelibrary.wiley.com/doi/10.1111/j.1365-2664.2008.01473.x), but I'm a beginner in the field, and I would like further advice.

Without being able to identify and count specific individuals, I would think any methods you find would be suspect. Are you able to identify differentiating characteristics between individuals?

@theforestecologist, nope, no differentiating characteristics available.

I can think of ways you might be able to do it with cameras placed in a grid over area and analyzed with time-stamped co-ordination of when counts take place, but I have no idea whether that would be something feasible or not and even if it would be considered statistically reliable.

Wolves are pretty lean animals, so I'd guess their density is in the range of 0.95 - 1.05 kg/L ;-)

Density estimation can be reliable without identifying individuals. Check out the resources  from St. Andrews Centre for Research into Ecological and Environmental Modeling.  https://www.creem.st-andrews.ac.uk/ They regularly offer workshops and are friendly, helpful, top-notch scientists.

Population estimation of wolf is a decade long challenge. Since wolves are wide ranging species, detection rate is very low in the camera traps. As they are difficult to identify at individual level it increase the chance of bias. However, with modern technologies we can estimate the wolf abundance using camera traps. I found two studies relevant to your question, 1. Estimation of pack density in grey wolf (Canis lupus) by applying spatially explicit capture-recapture models to camera trap data supported by genetic monitoring- here they have identified packs and estimated the pack density. This method can be applicable over larger areas where atleast 10 packs exists.
2. Estimating wolf abundance from cameras- here they have used motion triggered cameras and used Space Time Model (STE) to estimate the abundance of wolf.
Both the method have catch in it. Wolf packs are very dynamic and chances of avoiding camera traps (trap happy/trap shy) can cause possible bias. The main challenge is to extrapolate the data at landscape level.

Mattioli, L., Canu, A., Passilongo, D. et al. Estimation of pack density in grey wolf (Canis lupus) by applying spatially explicit capture-recapture models to camera trap data supported by genetic monitoring. Front Zool 15, 38 (2018). https://doi.org/10.1186/s12983-018-0281-x
Ausband, David E., Lukacs, Paul M., Hurley, Mark, Roberts, Shane, Strickfaden, Kaitlyn, and Moeller, Anna K.. 2022. “ Estimating Wolf Abundance from Cameras.” Ecosphere 13( 2): e3933. https://doi.org/10.1002/ecs2.3933

You could look into using a version of point - sampling distance sampling [1]
Also, [2] might help a bit to be more flexible than using a grid (even if it is on spatial capture recapture).
[1] Howe, E.J., Buckland, S.T., Després-Einspenner, M.-L. and Kühl, H.S. (2017), Distance sampling with camera traps. Methods Ecol Evol, 8: 1558-1565. https://doi.org/10.1111/2041-210X.12790
https://besjournals.onlinelibrary.wiley.com/doi/full/10.1111/2041-210X.12790
[2] Durbach, I, Borchers, D, Sutherland, C, Sharma, K. Fast, flexible alternatives to regular grid designs for spatial capture–recapture. Methods Ecol Evol. 2021; 12: 298– 310. https://doi.org/10.1111/2041-210X.13517
https://besjournals.onlinelibrary.wiley.com/doi/10.1111/2041-210X.13517

I edited your post to add full citations (in case those links ever get changed/break)


text:
Is bacterial respiration a continuous process?
Respiration in micro-organisms is the process of releasing energy from food. There are two ways of doing so: Aerobic respiration occurs in the presence of oxygen and produces ATP from the complete oxidation of carbohydrates or fatty acids. Anaerobic respiration involves incomplete oxidation in the absence of oxygen. No matter the method, bacterial respiration is thought of as a continuous process that releases energy continuously. However, the word "continuous" is ambiguous.
My question is:

Is the respiration continuous without rest (e.g. DC signal) where the bacteria are releasing energy at every stage of the respiration process.

or

Is it alternating (Like human breathing (inhale & exhale)) where the bacterial cell produces energy during one stage of the respiration stages and takes a rest in a periodic rhythm (e.g. AC signal) before releasing energy again?

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.

The question is still lacking enough context to form a coherent answer. Like, in what setting are you interested in this problem? And on what scale? I suppose any reaction could be divided into discrete steps at atomic or molecular scales. Like, a single enzyme may only catalyze one reaction at a time, and then it has to release the product, change conformation, and bind a new substrate, which takes a non-zero amount of time. But in a cell each reaction might be happening millions or billions of times each second, asynchronously, such that the metabolic process is effectively continuous.

Please respond to comments from other users by [edit]ing your posts — we are trying to help you craft better questions. Not doing so is likely to be perceived as rude and generate down and close votes. This can result in you losing the privilege of posting further questions.

"Respiration" in this context has nothing to do with breathing, it refers to cellular respiration. These are the chemical reactions that make ATP to be used in energy-requiring processes in the cell. Human cells do cellular respiration, too, and while we require breathing to replenish oxygen (and carry away carbon dioxide), this is not part of cellular respiration. Don't confuse them just because they have the same word in the name.
These processes occur more or less continuously in all cells; the rates can vary with conditions (for example, your muscle cells are going to do more cellular respiration when you run than when you sleep), but cellular respiration isn't breathing so don't expect it to be rhythmic the same way breathing is.


text:
Is lysozyme present in the lysosome?
Is lysozyme present in the lysosome? I cannot find anything about this in the literature.

@infinite if you have got your answer, feel free to self answer it. Self answer are always appreciated and it also help future readers.

lysozyme is not a lysosomal protease and the pH optima is too basic for the function in the lysosome we can conclude that lysozyme is not present in lysosome.

This is not the type of answer required on this site. Lysozyme is either present in or absent from lysosomes. An acceptable answer would refer to papers in which the enzyme was assayed in different cell compartments. Statements that it is not a protease (we know that) and that it has a basic pH optimum ( what, precisely?) do not allow us to conclude anything about its subcellular location.


text:
Why is DNA replication so much faster in prokaryotes than eukaryotes?
There are many statements to be found on the internet of the sort:

“DNA replication occurs at elongation rates of about 500 nucleotides
per second in bacteria and about 50 nucleotides per second in
vertebrates.”

However none that I have read attempt to explain this order-of-magnitude difference. Is it known why?

What research have you done on your own to answer this question? The Biology.SE community has agreed that questions that show little or no prior research effort are off-topic on this site unless you have shown your attempt at an answer. Please [edit] your question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Our goal is not to simply be an answer site, but rather a site that promotes self-learning with some expert help along the way.

I am not sure why this question has been marked as needing detail or clarity. It seems quite clear to me. And as far as research effort, it would help if the poster had given a source and said he had searched the Internet, but if he had done so he would have found that this statement comes up repeatedly but providing reasons is avoided. The observation has been around for years — it's in the 1992 edition of the Biochemistry of the Nucleic Acids.

I have now rewritten to provide clarification and focus. I have deleted the remark "Intuitively, I assume it's just the base rate for growth." As I find this meaningless in molecular terms. I think it is a worthwhile question but I doubt if the answer is known. All I have found is vague statements about histones and greater complexity. However, if someone has anything concrete...

hah, I just saw your new comment. I hope my answer is not too vague.

Note that this is misleading in a way because the eukaryotes divide the replication process among numerous forks starting at multiple initiation sites "Drosophila, alias the
fruit fly, has ~ 5,000 such sites while mammalian cells have ~20,000. [...] Our typical animal cell has between 20,000 and 60,000
molecules of pol α whereas our regular bacterium, E. coli has 10 to 20 molecules of
DNA pol III."

The difference in DNA replication rate between prokaryotes and eukaryotes is still under current research, but the basics are understood. It is very much a matter of complexity, as eukaryotes are more complex in many different ways. I found a very useful reference for this and other kinds of related questions. Briefly, some possible reasons:

[...] in eukaryotes, the DNA template is compacted by the way it winds
around proteins called histones. [...]

The DNA-sequence is not as easily accessible in eukaryotes, the unwrapping and re-wrapping of the DNA takes some time.

[...] The coordination of the protein complexes required for the steps of
replication and the speed at which replication must occur in order for
cells to divide are impressive, especially considering that enzymes
are also proofreading, which leaves very few errors behind. [...]

This underlines another rather important factor. The speed of the polymerases replicating DNA is very much related to their accuracy.

[...] This proofreading capability comes with some trade-offs: using an
error-correcting/more accurate polymerase requires time (the trade-off
is speed of replication) [...]

And just for completeness, here is a compete overview of DNA replication in the three big systems.

Thanks for pointing out my mistake. Have corrected it. Yes, I’ve heard those arguments before, but I’d like to see some hard data.


text:
Understanding Contig NG50
My goal is to do a de novo assembly of a jellyfish. At the moment I'm busy checking papers that did de novo assemblies but I also got some jellyfish papers
Then I stumbled accross this:

Contig NG50 is defined as the length at which half of the predicted genome size is contained in contigs longer than this length.

I can’t understand this and googling returned papers of similar complexity e.g.:

NG50 refers to the length of the smallest contig added to cover 50% of all nt estimated in the
genome; (25)...

Can someone provide a simpler explanation?

Please do not direct users of this site elsewhere for the meaning of specialist abbreviations central to your question. Questions here should be self-contained, and if you request clear answers, I suggest you do as you would be done by.

The Wiki entry "N50, L50, and related statistics" would be a good research resource. https://en.wikipedia.org/wiki/N50,_L50,_and_related_statistics

This stack is for professional/student biologists, not 5 year olds, so I'm unsure why you seem so insistent on on dumbing down the title.

@user438383 Because my professors always told me only truly understand something if you can explain it to your 5 year old brother :) And also because I thought this is a positive and supportive place where people are encouraged to ask questions that other people are encouraged to answer (collecting votes I assume). Have you ever read a paper that was not in your native language? It can get very tough, but I hope that I understand a little bit more every day, with the kind help of smart and motivated people like you and other members of this community, but maybe I'm just a naive dreamer :)

A title SE should indicate the biological content of a question. It should be totally impersonal. Casting it as a challenge to users is against the ethos of this site, and your particular example is made worse for the reasons in the comment made by   @user438383. We welcome new users to this site, but we expect them to follow the norms set out in the Help. Please do so.

I have edited your question to provide a partial model of good practice. (The first sentence is too chatty.) If your aim is to communicate the results of your (genome?) assembly you would do well to study it.

If you arrange your contigs from longest to shortest, what is the shortest contig in the smallest subset of contigs that covers at least half the expected genome length?
An example with arbitrary units...
You have a set of contigs of lengths 30, 20, 20, 10, 5, 5, 1, 1, 1, and many contigs < 1.  Your expected genome length is 150. The smallest subset of contigs that covers at least half the genome length is [30, 20, 20, 10]. The smallest contig in that set has length 10, so NG50 = 10.
Note that the sum of the lengths of the contig subset is 80, not 75. But if you take away the smallest contig in that subset (10), then the sum is 70, which is less than half the genome length. So the sum of the lengths of the contig subset need not be exactly half the expected genome size, but at least half.


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How deep under water can humans open their naked eyes without damaging them?
Humans can tolerate a maximum pressure of 100atm, but it becomes uncomfortable above 30 atms. Deep divers usually wear protective equipment like goggles among other things and our eyes seem to be more fragile than the rest of our body.
So, without using goggles how deep can a human open their eyes under water before suffering from an injury?
The injury, I believe, would be the eye getting crushed by external pressure.

I could be wrong but I can imagine that it doesn't matter much whether you have your eyes open or closed in terms of protecting your eyes against pressure, so it's merely a question of how deep can you go without wearing goggles/mask.

A mask doesn't protect a scuba diver from water pressure, the surface air in a mask will shrink to a 1mm bubble at 300m, and scuba divers often fill their mask with water at any depth to get rid of condensation, to adjust the straps, to fix the red lines and have a scratch. So mask or no mask it doesn't matte. A mask doesnt provide any pressure protection whatsoever. https://youtu.be/PuVXxj70s1w?t=38

@Ivo My eyelids do nothing!

I wonder: What makes you think the heart or ears are not crushed by the pressure? Also "naked eyes": What effect do you think goggles have? Obviously the pressure is the same.

@U.Windl Yes, the pressure would also affect the heart or ears, but my question was directed at the eyes in this case. By goggles, I was referring to protective equipment used by divers. Although now I have realised wearing goggles/masks will not have any effect.

Crushing damage from pressure occurs due to pressure differences. Imagine you have a rigid container. If you have equal gas pressure inside and outside, the pressure acts on just the walls and the container will survive unless the pressure is high enough to heat/melt the walls to failure. However, if you have high pressure outside and low pressure inside, you can expect the vessel to at some point violently collapse due to the pressure difference.
When diving with a mask, it's important to equalize the pressure inside and outside the mask. E.g. from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4943308/

Diving can affect the IOP [intraocular pressure] in a number of ways; firstly from the change in the internal mask air pressure at different underwater depths, secondly from the inhaling or exhaling from the nose, and thirdly through the diving mask itself. The first and second factors can be controlled by the diver by exhaling from the nose during descent, also known as equalizing the mask pressure. Senn et al. [5] found that diving mask pressure spikes were less common in experienced divers compared to beginners. Failing to equalize the diving mask pressure can lead to ocular barotrauma, which ranges from lid edema, ecchymosis and subconjunctival hemorrhage to more serious injuries such as hyphema and subperiosteal orbital hemorrhage [6, 7]. The diving mask itself may also affect the IOP. Swimming goggles are known to increase the IOP, with larger-frame goggles having less effect than smaller-frame ones [8,9,10].

Or from https://www.ncbi.nlm.nih.gov/books/NBK545224/

Mask squeeze is a type of facial barotrauma injury that occurs most commonly while self-contained underwater breathing apparatus (SCUBA) diving or freediving. This condition occurs when divers fail to equalize pressure in the face mask to the surrounding water pressure as they descend. The result is a negative pressure (relative to the surrounding water pressure). The difference in pressure inside and outside the mask can lead to injury of blood vessels and tissue of the eyes and tissue covered by the mask, including forehead, nasal areas, and periorbital regions. The main risk factor for a mask squeeze is the inexperience of the diver. Masks with high internal volume or the use of snorkeling masks or swim masks that do not cover the nose can also increase the risk of this type of injury.

Or, in simpler phrasing, if you have low pressure inside a mask and high pressure inside the rest of the body, the pressure difference is going to push/suck the eyes outward and crush the blood vessels or damage the eye itself. You want to have the same pressure pushing on the eyes from the outside and inside. It's really no different if you 1) have high pressure outside the mask and 'normal' pressure inside the mask, or 2) have low pressure (vacuum) inside the mask and 'normal' pressure outside: both situations have a pressure difference, and it's the difference that does the damage.
So, to answer your title question, a mask is more likely to increase pressure risks to the eyes rather than to decrease it.

I remember one of the record seeking deep divers (those that must use their own custom-made equipment) say "there is essentially no limit to the pressure the human body can sustain". I was not able to find that statement again and it may not be entirely correct (especially the gases solved in the blood can be damaging) but the body can certainly sustain much more pressure than one would perhaps naively think. When in hydrostatic equilibrium, pressure as such is mostly unnoticeable.

@Peter-ReinstateMonica - A sphere is the shape best suited to resisting external pressure; a cylindrical object is next. If there are depths to which cylindrical objects cannot descend (submarines) without imploding, I would imagine there are depths to which humans cannot descend. It's not about "hydrostatic equilibrium" or gasses; it's about the weight of water the further down you go.

@anongoodnurse The difference between a submarine and a diving human is the difference -- in pressure: There is no pressure difference between the "inside" and the outside in the case of the diving human, so there are no forces (or, if you want, there are huge forces, but they cancel each other out). By contrast, the submarine (typically) retains its internal pressure of one atmosphere when diving and thus has to withstand a huge pressure difference resulting in huge forces that try to compress it.

@anongoodnurse To elaborate: Because the body is mostly water and solids it is largely incompressible. It's essentially like submerging a water balloon with a few bones in it: No forces whatsoever. The exception are the gas-filled lungs and the changed solubility of gases in fluids (blood) under these pressures. The lungs need to be filled with equally pressurized oxygen mixtures (I'm sure the bottles with the required mix and pressure are an example of the custom-fitted equipment). High partial oxygen pressures are toxic, nitrogen is a no-no etc.

@Peter-ReinstateMonica - That all makes sense in a way (and I see that the submarine comparison was not well thought out.) But I can't imagine being able to expand the chest against 500 atmospheres. And you're right about dissolved gasses (I just did a bit of quick reading), but I'm stuck at being unable to breathe.

@anongoodnurse, if you're filling your chest with gasses that are at the same pressure as the water outside, there's no differential to fight.

@Peter-ReinstateMonica I have always wondered about pressures in the body that are not able to or which have impediments towards normalizing the pressure differential.  For instance, it is possible for gasses to form along the entire digestive tract, how would it be possible to equalize pressure without essentially "swallowing" air at a higher pressure?  It seems like you couldn't (e.g.) burp to get rid of such gasses if the air pressure outside was larger than inside.

And if the pressures equalize by compression, then it seems like there would be an upper limit due to the fact that you now have extra pressure compressing an internal space in your body through your body.

@Michael Gases in cavities within the body are really only a problem during decompression. As you increase pressure, any existing gas bubbles will get smaller. Bubbles getting smaller don't do any damage. However, if you have a bubble under pressure (dissolved or not) and then decrease the pressure, the bubble gets bigger, and if it gets bigger than the cavity holding it, you're going to have problems. The main problem is with dissolved gases coming out of solution in the bloodstream and occluding vessels, because the surface tension at the blood-gas interface is stronger than blood pressure.

@anongoodnurse One cannot even breathe under 2 feet of water under one's own power because the pressure is already to high (here is a page that has a good description). When scuba diving, the air in the bottle is pressurized and "forced" into the lung, equaling out the pressure. That is very much like we are breathing at sea level, under quite some pressure: The pressurized air around us enables us to breathe at all.

@anongoodnurse: A SCUBA regulator is a key part of the setup: its input is high-pressure air from the tank, its output is air at about the same pressure as the water, so you can breathe from it without needing to fight the water pressure or having your lungs over-pressurized and pop.  https://en.wikipedia.org/wiki/Diving_regulator - they have some mechanical valves that are controlled by ambient pressure (of the water).

@PeterCordes Ah, I wondered about that, thanks.

@Peter-ReinstateMonica - I understand now and believe you. Thanks for sticking it out with me. TIL!

@PeterCordes - Hard to wrap my head around such a sophisticated system, but I understand and thank you, too.

Goggles do not, cannot, protect eyes from pressure. The pressure on both sides of goggles should be nominally the same. In fact, divers tend to use a mask, which communicates with the nose, to be able to equalise the internal pressure with ambient easily, rather than goggles which can damage the eyes if a descent is made without awkardly adding air by exhaling bubbles while lifting the lower edge of the goggles. The only thing that can isolate you from pressure at depth is a rigid suit, or a diving bell.
So why do people wear goggles/mask underwater?
The main reason professionals wear them is to keep a layer of air in front of the eyes, so that the eye lens is working between the correct refractive indexes and giving you normal vision. Replace that air with water and everything becomes very blurred. Basically the front face of the eye lens stops bending light, so you become extremely long-sighted.
The main reason amateurs wear them is to avoid the yuk factor of opening eyes under water, or irritation from biocides in the swimming pool.
There are multiple things that limit the depths divers can reach, but none involve the eyes.
Oxygen toxicity and nitrogen narcosis limit compressed air or nitrox sport dives to a few 10s of metres. To go deeper one needs extensive decompression time and/or expensive helium, and deeper still an addition of hydrogen. Regular commercial dives rarely exceed 300 m, with only the military accessing anything approaching 500 m. Studies (usually in pressure chambers on land) have pushed lower, but seem to run out of human tolerance for the effect of high pressure gases on the central nervous system in the 650 to 700 m range.
I did a short diving course, and the exam started with them throwing all the gear into the pool, mask included. The idea is that you need to be able to recover from an accident where everything is knocked off your face, and then some. So, open your eyes, swim to the bottom, locate blurry tank and take a breath, grab your blurry weight belt, locate blurry mask and put it on, breathe air into mask so now you can see properly, and it gets easier from there.

So the air inside the googles / mask is effectively another lens element between the eyes and the water. Importantly the rear of the air is shaped with a curve that conforms to the eye, and the front of the air is shaped with a flat or near-flat surface that conforms to the plastic surface.

@bdsl The air inside the mask is the dielectric constant that the eye has evolved to work with. Well, approximately at least. I'd imagine the refractive index of the gas increases slightly with pressure, but not to the extent that increases by replacing it with water.

@bdsl Yup, mask/goggles are basically corrective eyewear that since everyone needs the same prescription for and thus are stock rather than from an optometrist.

Currently the record for the deepest dive wearing scuba equipment is 332.35m. The descent took only 15 minutes while the ascent lasted 13 hours 35 minutes.
Liquids do not compress, so the sinuses, inner ear, lungs and circulation are in far more danger from pressure than the eyeballs.
The main danger is not the pressure at depth, it is the readjustment to the expanding gases as the diver rises, decompression sickness, which rarely affects the eyes.

This doesn't answer the question at all.

The question explicitly states "without using goggles". Goggles/masks are included in scuba equipment.

Yes, it does answer the question. Face and mask of the diver could never withstand such a pressure difference, meaning that the diver needed to equalize the pressure, which is normally done by taking of the mask and blowing (high-pressure) air inside. Descending so quickly, there is a chance that you can't get the mask off your face if you wait too long, meaning that pressure would build up until implosion, which would pose an enormous health risk. For this reason, such records are generally done without wearing a mask, while descending. The answer is that eyes are not the bottleneck.

@Ivo He said how deep and why, I said 325m is still ok, no evidence beyond that and some reasons.

@GoalaSestant that's with scuba equipment

@Mast There is no evidence beyond 325m but that's a good start for a general idea. Swimmers use goggles, goggles can't equalize pressure, divers use masks where they equalize the water pressure, it's easy to take the mask off at any depth. Opening the eyes underwater at 325 meters is fine.

@Ivo did you know that scuba equipment doesn't protect the eyes from water and water pressure, and scuba divers regularly take off the mask underwater and fill it with water to get rid of condensation and other reasons? https://youtu.be/PuVXxj70s1w?t=38

@GoalaSestant I'm guessing a lot of people are not aware, which is probably why you should amend your answer. I don't have a great understanding of what scuba gear protects, or when that protection is removed.

@GoalaSestant I didn't know. Thanks for telling me

The answer is incomplete, because at a depth of 100m the partial pressure of oxygen and nitrogen will probably kill your nerves (specifically the brain) (or at least make them inoperative). So there are special gas mixtures used then. For normal air the nitrogen-induced limit is around 56m.


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Rigorous definition of the kinship coefficient and proof of a recursion thereof
I am reading Section 5.2, Kinship and Inbreeding Coefficients, of Kenneth Lange, Mathematical and Statistical Methods for Genetic Analysis. There the kinship coefficient $\Phi_{i,j}$ is defined for two relatives $i$ and $j$ as the probability that a gene selected randomly from $i$ and a gene selected randomly from the same autosomal locus of j are identical by descent. Then the book states that suppose $k$ and $l$ are the parents of $i$,
$$\Phi_{i,j}=\frac12(\Phi_{k,j}+\Phi_{l,j}) \tag1$$
with some exceptions.

Equation (1) seems intuitive. Yet it is slippery for a proof especially considering the exceptions. The root cause is that the definition of $\Phi_{i,j}$ is vague albeit seemingly plausible. I am seeking a mathematically rigorous definition of $\Phi_{i,j}$ and a proof for Equation (1) together with the condition under which it applies.

The definition as set by Kenneth Lange's book is indeed quite vague and thus unrigorous. It is a probability not conditioned on observing an allele $a$ at a locus of $i$ but conditioned on the following where we focus on one particular locus. It is rigorously defined as follows. Then we will give the correct formulation of the correct recursive equation akin to Equation $(1)$ which is in general wrong.

A graph of lineage contains nodes, which we call persons, of a particular locus. Each node, or person, contains exactly two genes. We draw one and only one directed edge (parental relationship) from a gene of a parent person to the gene of a child person if the latter is inherited from the former.  This is a directed acyclic graph (DAG). Each gene can be connected by no more than $1$ edge directed to (as opposed to away from) it. The two genes in one person cannot be connected by edges. Two persons are said to be connected if there is an edge pointing from a gene of one node to a gene of the other node. Two persons cannot be connected by more than one edge. For a pair of connected persons and their directed edge between them, the edge is equally probable to connect to one gene as the other gene of a person, i.e. the probability is $\frac12$. A pair of genes (persons) are said to be connected if there exists a undirected (simple) path from one gene (person) to the other. Two connected genes are called identical by descent.
In this setting, the DAG with respect to the persons is given and deterministic whilst any directed edge in the DAG assigned to two persons are random with independent probability $\frac12$ with respect to the genes within each person.
For a pair of persons on a lineage DAG that is connected, the probability of one gene equally probably chosen amongst the two genes of one person being connected, or identical by descent, to one gene equally probably chosen amongst the two genes of the other person is the coefficient of kinship.
As an additional assumption, the genes that are connected have to be the same and thus assume the same allele.
Definition: Suppose a lineage DAG is given. Let the kinship coefficient between person labeled $1$ and person labeled $2$ be $\Phi(1,2)$.  Denote the set of parents and children of person $1$ each of which is on an undirected (simple) path between $1$ and $2$ as $S_2(1)$.
Lamma: Denote the set of paths through an ordered persons $p$ in that order as $P(p)$. $\{P((1,i,2))|i\in S_2(1)\}$ partitions $P((1,2))$.
Proposition: $$\Phi(1,2)=\frac12\sum_{i\in S_2(1)}\Phi(i,2).$$
Note: The summation in the Proposition is over $S_2(1)$ rather than the set of all parents and children of person $1$. That fixes the condition under which Equation $(1)$ is valid.
Corollary: $$\Phi(1,2)=\sum_{p\in P((1,2))} \frac1{2^{n(p)}}$$
where $n(p)$ is the number of persons on path $p$. $n(p)=|p|+1$.


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At how low a temperature can a snake like a copperhead survive in winter /
Copperheads were very common here, less so now that more people have moved into the subdivision. My yard is sort of an oasis for them . E. TX is expecting record cold in spite of climate change so I was covering a few things; damn ground orchids are already blooming. I let the camellias take care of themselves; there are too many to cover. I lifted a large plastic tub that was inverted on the ground , a smallish ,dormant copperhead fell out on the leaf covered ground. He did not move so I built a well insulated enclosure over him ( with an exit). Temp is now 40 F but 30 is expected tonight and mid 20's the next two nights. I am wondering at his chances of survival ; I estimate his body temperature will get to mid 30's F. I had thought they went deep into animal boroughs; we have many voles and some moles ( because there are not enough copperheads left to keep them under control). I have a well insulated garden shed that will probably not go below 50 F but I don't want to move him unless it is an emergency.

I will try to write a more detailed answer when I get back to my office, but just quickly, you might find this paper useful: Sanders, J.S. and Jacob, J.S., 1981. Thermal ecology of the copperhead (Agkistrodon contortrix). Herpetologica, pp.264-270.

Generally as long as their tissue does not freeze they are OK, brumation makes snakes pretty cold tolerant, it is more likely to die of dehydration than cold. Moving it to a warm area is not a great idea as it may cause it to come out of brumation early. Some decent cover is all they need, your enclosure should be more than enough as long as it is made of something insulating like wood or plastic, (just don't put it in a metal enclosure. Don't worry if it does not move, in very cold temperatures it may not move for days.

Thanks, helpful. I did not know the name but moving him to a warm location where he could wake seemed like a problem . Actually your comment is an answer.


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How is trangender female different from normal female biologically?
I have read in many places that transgender people are usually people who are born with typical male or female anatomies but feel as though they've been born into the “wrong bodies.” The thing that I am confused about is that how someone can not be considered as normal just because he thinks he should not be what he is? I met a female who looked exactly like a normal female and she was very beautiful. She didn't know that she was a transgender till her mom told her that she was transgender when she became adult. What is biological difference between a transgender and a normal male/female?

Remi gives a good introduction to the various terms and definitions you should know when learning about gender identity. However, he didn't really address your basic question:

What is biological difference between transgender and a normal male/female[?]

Except for some likely genetic differences, which we aren't even close to beginning to understand, there is no biological difference between two persons born with $XX$ sex chromosomes, one of whom identifies as female (cis-gender) and one of whom identifies as male, or somewhere on the spectrum between female and male (trans-gender). There is no difference physically - both have the same organs, including sex organs, and both have the same secondary sex characteristics. One cannot tell the difference upon gross physical examination, X-ray, blood test, etc. Gender is a social construction, and while the majority of people in the West have a gender identity that matches their biological sex, some do not, for reasons that are not yet clear.

Let's first consider the difference between the concepts of sex and gender.

The distinction between sex and gender differentiates sex (the anatomy of an individual's reproductive system, and secondary sex characteristics) from gender, which can refer to either social roles based on the sex of the person (gender role) or personal identification of one's own gender based on an internal awareness (gender identity).

Below are some definitions of the term you used (transgender) and of terms that some people confuse.

A transgender person is someone who have a gender identity that differs from its sex. For example, a man (with standard male organs) who identifies as a woman.
A transsexual is a former transgender who seeked for medical assistance to modify its sexual organs to match its gender identity (and unmatch the assigned sex at birth).

Because (1) sexual and romantic attraction are often important driver of gender identity and because (2) many people confuse the terms relating to sexual attraction with the previous ones, I wanted to add the definitions of

A heterosexual is someone who is attracted to people of the opposite gender.
A homosexual is someone who is attracted to people of the same gender.
A bisexual is someone who is attracted to people of both genders.

While all of the above definitions were referring to social gender identity (transgender), sexual and romantic attraction (homosexuality, heterosexuality, bisexuality) and medical intervention (transexual), in my list of terms, only the term intersex actually refers to a 'biological' difference.

An intersex (previously called hermaphrodite) is someone who has variation of both sex.

You should read the linked wikipedia articles who will teach you much more about the definitions and slight variations behind these terms than I could do in the such short definitions I used. There other other concepts you might want to investigate the definition such as gender non-conformity, genderqueer, third gender and pangender for example.

You will note that as only one term was referring to 'biological' variation, the question could be answered in much more depth by a specialist of gender studies (which I am not) rather than by a biologist (which I am).
Finally, note that this post is closely related.

While this is basically correct (+1), I’d say “a transgender” is a bit awkward at best, and should probably be “a transgender individual.” Also, you don’t seem to have addressed this part of the question: “I met a female who looked exactly like a normal female and she was very beautiful. She didn’t know that she was a transgender till her mom told her that she was transgender when she became adult.” I’m not totally sure what the OP is talking about here (people don’t find out their gender as adults, from their parents!), but if you can figure it out it would be worth addressing.

Indeed, transgender is an adjective and not a noun (unlike bisexual, intersex and other terms which are both nouns and adjectives....aahhh english!). I corrected it. Thank you! I don't know what the OP meant and at this point I am too lazy to ask him/her :)

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


text:
How is it known that there are only three macronutrients: proteins carbohydrates and lipids?
It is stated here that in human nutrition, micronutrients are nutrients required generally in less than 100 mg daily quantities whereas macronutrients are required in gram quantities. It is widely stated that our macronutrients are carbohydrates, lipids, and proteins. How was it shown that these are the human macronutrients and that we don't have other macronutrients?
One answer to this similar question on Quora suggests that ethanol or ketones could be considered macronutrients. Ethanol is mentioned in this article, though ketones are not. Other sources I saw didn't clarify.

there aren't, there are four, carbohydrates, lipids, proteins, and water.  Also ethanol and ketones are not even essential nutrients much less macronutrients. you are getting downvoted for not reading your own source.

What about nucleic acids?

i read the sources john, but thanks for the input

if nobody knows, does anyone know a resource where i could hunt this down?

Summary
The question is based on the misconception that the term “macronutrient” originated as a scientific definition, to which entities satisfying this definition were assigned. In fact it was a default term used as a distinction from compounds falling into the earlier category, “micronutrient”, and was used initially to encompass the three specific classes of food that had been established to be sources of energy through decades of nutritional research. Hence there was no question of whether there “should” be more macronutrients. The term is not a scientific definition, and today is used in different ways so that anyone using the term needs to clarify what it should be taken to mean in that particular context.
Food Energy and the history of Nutrition
Scientific studies of nutrition, dating the late 18th century, were initially concerned with chemical structure, metabolic fate and energy produced by different foods, and this is described in a short readable article by Ned Stafford in Nature (2010) 468, S16–17.
By the end of the 19th century protein, fat and carbohydrate had been established as the chemical fuels that supplied energy from the diet, and the energy values (in terms of the, now obsolete, calorie) had been established by Atwood, using his respiration calorimeter.
Micronutrients
The next phase of nutritional research was concerned with constituents of the diet that did not supply energy, but were nevertheless essential for health. The first of these were the vitamins,  organic molecules that in many cases turned out to be cofactors for enzymic reactions. The term, vitamin, introduced in about 1912, was a contraction of “vital amine”, although the chemical description “amine” does not apply to some of the essential organic molecules later assigned to this class.
Later still came the discovery that certain non-organic molecules were essential dietary components, especially metal ions such as copper or selenium, sometimes known as ‘trace elements’ or ‘mineral nutrients’. These were not termed vitamins because of their non-organic nature, but the need to refer to all non-energy supplying dietary requirements together led to the employment of the portmanteau term, ‘micronutrient’. The first mention I can find of this in relation to human nutrition was in a US Senate report of 1954, although it had been employed extensively in relation to plants from 1940, and the word is most frequently used in a botanical context.
The introduction of the word ‘Macronutrient’
The first recorded use of the word ‘macronutrient’, in relation to human nutrition, was in a 1968 article in the Archives of General Psychiatry. The term only appears in the title of the article (“Comparison of macronutrients in the diets of psychotic and normal children”), although it is clear from the tables therein that it refers to carbohydrate, protein and fat. It seems likely that it was (or had already been) coined by analogy with — and in contrast to — micronutrient, as it was shorter and appeared more elegant than ‘energy-producing food’. Indeed the Oxford English Dictionary entry includes this contrast:

1968– Physiology. A nutrient belonging to one of the three major food
groups (carbohydrates, proteins, and lipids) required by animals, esp.
as opposed to a vitamin or mineral.

It should also be mentioned that the term had been in agricultural/botanical use since 1942, but embracing a quite different set of compounds (nitrogen, phosphorus, potassium etc.).
Distinguishing scientific definitions from descriptions
In my opinion the root problem in the original post is confusion between terms that are scientific definitions from those that are merely descriptions. For example, a chemical term like amine is rigorously defined and indicates a class of chemicals to which any with a structure satisfying its definition (‘contain a basic nitrogen atom with a lone pair’) will be assigned. Hence any list of amines will be expanded by inclusion of newly discovered compounds. In contrast, scientific descriptions (at least in this context) start with a collection of known entities and assign a name to encompass them. This, I submit, is the case with ‘macronutrient’. It not a definition, but a term assigned to carbohydrates, proteins and fats, as a group.

Thus, one answer to the question:
“How is it know that there are only
three macronutrients…?” is
“Because that is what the word was
introduced to describe”

But…
…context is all. As already stated, in plant science the term has a quite different meaning, and those who feel that they should regard the term as a definition, redefine it to exclude ethanol, for example, on the basis that it is not essential. In practice, all that is necessary is to make it clear how one is going to use the term. The FAO food and nutrition paper 77 — Chapter 2, for example, merely states “Analytical methods for alcohol, which can be a significant source of energy in some diets, polyols and organic acids were not discussed, and hence no recommendations for methods are made.”

So an alternative answer to the question:
“How is it know that there
are only three macronutrients…?” is “Because that is how macronutrient
has been defined in this context.”

or, as Humpty Dumpty said:

“When I use a word it means just what I choose it to mean….”
Lewis Carroll — Alice in Wonderland

Thank you! This historical context is elucidating, and I did not realize macronutrient is a non-technical descriptor of molecules where we usually get our food energy. This led me to this page (https://en.wikipedia.org/wiki/Food_energy) which states, "However, the direct calorimetric method generally overestimates the actual energy that the body can obtain from the food, because it also counts the energy contents of dietary fiber and other indigestible components..." It also discusses polyols and organic acids, and I have this follow-up question: What gives me food energy?

@imrobert — Your concerns about simple bomb calorimetry are understandable, and were the subject of another question on this list, which I recently addressed in this answer.

Thanks, this is also helpful. If I take away "The amount of energy a food molecule gives me is the amount of energy it contributes to my TCA cycle" is that ok with you?

@imrobert — A few changes to that: "The amount of energy a food molecule gives me is the net amount of energy it produces from the TCA cycle, fatty acid breakdown and glycolysis." 1. "Net amount", because it may use some energy (as in the elimination of N from amino acids), 2. "Produces from" as your present formultion makes it sound as if the TCA cycle needs energy, that food produces. In fact the TCA cycle is a way of breaking down 3C molecules in a way that converts their energy (ultimately) to a useful form, rather than heat. 3. To cover carbohydrates and lipids.

@imrobert — But I would say, more technically “The amount of energy a food molecule gives me is the net amount of energy, in the form of ATP, that can be produced from oxidation reactions in the body.” Just as the heat energy from burning wood is produced by  its oxidation, the energy for movement, growth etc is produced from oxidation of foodstuffs. Although a little is generated directly in particular reactions, most is generated in two-step process. First the reactions use an oxidizing agent NAD, which is reduced to NADH in the process. cont...

...cont Then there is a complex system in the mitochondrion, where the energy in NADH is used to form ATP from ADP through reoxidizing it to NAD. Not so simple. Explaining that is what put bread on my table for many years.

Can I know in advance how much energy a given molecule will give me via oxidation?

@imrobert — I imagine it will depend on your personal characteristics. Exercise physiologists and nutritionists are the people that are involved in this sort of thing. I really don't know — It's certainly not my field.


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Basis of the taxonomic classification of viruses
The Wikipedia entry on Virus Classification contains the following statement:

“Viruses are classified by phenotypic characteristics, such as
morphology, nucleic acid type, mode of replication, host organisms,
and the type of disease they cause.”

The use of such phenotypic characteristics for classification of plants, animals, and fungi ended with the discovery of DNA as the carrier of genetic information. At that time it began to be replaced by classification by genotype, so as to include evolutionary history.
Why would it appear that a similar approach has not been adopted towards viruses? Is it because there are no fossilized viruses?

Thanks for providing your suspicion David, feel free to google it

since some viruses do not have DNA that might be one reason.

Unless you are trolling, I think you will find that people such as @David (with nearly 24,000 reputation on here) will have a strong understanding of such basic concepts as phenotype and genotype.

Thank you for responding to my request for information. In order to attempt to rescue the question I have rewritten it in a less strident manner that reduces the (I am sure unintended) impression of superiority that it conveyed to me, at least. I have tried to improve the presentation of the quotation and made its attribution specific. I have also avoided the use of "we", which suggests a personalization which I, for one, find irritating. If you are willing to accept this modification I can proceed to address some of the points relating to classification of viruses.

I think you will find that you are entirely incorrect in your statement that we classify "higher" organisms by genotype. Yes, that may be a part of it, but until the advent of high-throughput genetic sequencing in the last 20 years or so, we couldn't do this much. Before the development of these technologies, genetic analysis was largely limited to fragments sequenced by Sanger sequencing and various PCR or similar based analyses.
Almost all of botany, zoology, and microbiology is phenotypic in nature. For instance, you might have heard of Eukaryotes and Prokaryotes, two of the highest divisions in nature - these are split on the presence or absence of a nucleus in the cell, not on genetic content. Flowering plants are split into the presence or one or two cotyledons in their seeds. Animals can be split based on the presence if a backbone or not The list goes on through almost all of systematics...
Likewise, we do similarly for viruses. For instance, the type of nuclear material is a major phenotypic feature that is easy to split them apart on; you won't find DNA viruses and RNA viruses in the same family of viruses, because they don't produce the same morphologies and have little genetic similarity.  So you can classify them by genetic sequencing and you would likely come up with similar phylogenies as the current system of phenotypic features. Indeed, so powerful are the higher groupings done by morphology, that we can now find small fragments of virus genome and identify which species they belong to or work out if they are novel through such things as metagenomic analysis

Is it not true that vertebrata, invertebrata, eukaryota and prokaryota are monophyletic, thus grouped by genotype? And for this reason monocotyledon/dicotyledon is no longer an official Plantae classification due to them not being monophyletic? Thanks for the info on viruses, I didn’t realize that

@imrobert No - eukaryota covers everything from plants to animals to fungi. Prokaryota covers bacteria and archaea.


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Toxicity of phaeomelanin
I have been reading an article discussing a study by Tiffany Slater and Maria McNamara in which they identified molecular  evidence of phaeomelanin in the fossil record. Slater is quoted as saying "scientists still don’t know how – or why – phaeomelanin evolved because it is toxic to animals".
I am curious what toxicity is being referred to here, since looking into it has only turned up the fact that phaeomelanin is responsible for red haired pigments in humans as well as reddish coloration in other animals, and the only mentions I've seen of toxicity are either phototoxicity that might occur when exposed to certain kinds of light, or increased susceptibility to skin damage from sunlight.
I did find a few studies in the search results whose titles were completely impenetrable to a layman such as myself, so maybe there is more information there that I wasn't able to dig out.
Is there a little more context around this statement that phaeomelanin is toxic that I am missing? I'm especially interested in information in layman's terms as I am not deeply familiar with the field of biology, but I am always curious!

They were probably misquoted in the press release. That is, the person writing the PR heard "toxicity" when they said "phototoxicity", or thought "phototoxicity" was too "jargony" for a press release and figured just "toxicity" would do fine. Unless you find the authors referring to toxicity in their own writing somewhere.

@David given that you have referenced the actual paper I would be happy to accept that as an answer. Seems like just a bad quote then.

Done that now. I could quote more papers, but the only way to get at what the authors actually meant is probably to write to them. Generally people respond.

The paper in which Slater et al. reported preservation of phaeomelanin does not include the word or root ‘toxic’, so it is difficult to know whether the quotation is correct and, if so, what was actually meant.
The Wikipedia entry for melanin states that as well as being responsible for the ‘red hair’ in certain people (who seem to survive this), phaeomelanins are concentrated in the lips, nipples, glans penis and vagina (depending on sex) of the rest of us. This suggests that phaeomelanins cannot be toxic, per se. The article does go on to say:
“Exposure of the skin to ultraviolet light increases pheomelanin content, as it does for eumelanin; but rather than absorbing light, phaeomelanin within the hair and skin reflect yellow to red light, which may increase damage from UV radiation exposure.”
However this is not the same as saying that phaeomelanin is toxic. Furthermore, the work reported was not concerned with human skin, but the colouration of feathers in the fossils of birds and feathered dinosaurs — presumably an advantageous trait, that outweighed any deleterious effects of UV radiation. This all suggests to me that a complex system for producing different variants of melanins arose in animals long before the appearance of mammals, and that there was differentiation in relation to which cells migrated to or were present in which tissues.


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Why can't a third acetyl-CoA condense with acetoacetyl-CoA in the same way, as two acetyl-CoAs condense in the thiolase reaction?
In the biochemical ketogenesis pathway, acetoacetyl-CoA reacts with  acetyl-CoA to form HMG-CoA (3-hydroxy-3-methylglutaryl-CoA), in a reaction catalysed by HMG-CoA synthase.
But why can't acetoacetyl-CoA simply condense with another acetyl-CoA, just like two acetyl-CoAs condensed to form acetoacetyl-CoA in the thiolase reaction?

Welcome to SE Biology. It is unclear to me what you mean by your question,  so I have edited it to make clear what I think it is likely to mean. I assume you are concerned with ketogenesis and are wondering why a separate enzyme is needed rather than thiolase. If this is NOT  what you meant, please explain and ammend the question. The answer, is likely to be obvious. Are the two reactions chemically the same? If not, will the same enzyme be able to catalyse them?

If you wish an informed answer to your question, please confirm or rebut my interpretation of your intent.


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Why it is rare for person to get infected with two Pathogens?
Why is it rare for a person to have 2 (or more) infectious diseases (for example: Flu & Cold together at the same time)?
Although it's rare, it happens when the immune system is weak (e.g when patient has both AIDS and Kaposi's sarcoma).

This needs a reference - I'd imagine it to be quite the opposite, probably we are often infected with many pathogens (even when not sick) and multiple pathogens would cause more stress on the immune system

This happens more often than thought. Classic examples are secondary infections which get a problem, when the body is already battling one pathogen. This would be for example pneumonia or otitis after other infections like the flu.

Your example is actually quite bad because the “common cold” is often an infection by several strains of viruses (and even bacteria) simultaneously.

There are multiple issues here. 1) Is it really rare to be infected by multiple pathogens? 2) If it is rare, is it rarer than would be expected from the independent probabilities of getting infected by that organism within a given time period? 3) If both the above are true, I would speculate that could be because the body's non-specific immune mechanisms have already been activated by the first pathogen, making it harder for a new infection to take hold.

Because the product of two small probabilities is much smaller than either probability by itself?

OP should consider revising the Q or making a new one..the concept of Interference (interferon) between viral infections is pretty clear, if thats the main thrust.  But per other comments/answers bacterial infections frequently super-infect during other illnesses.

What makes you consider it is rare? It is not at all uncommon to be affected by two infections. Typically I agree we aren't as the number of infectious organisms that we are exposed to which cause a clinical manifestation (i.e. aren't controlled by the immune system) are low. Nevertheless, any chronic infections such as herpes viruses may often manifest when we are under stress with another infection, many bacterial pneumonias are more likely to occur when a viral infection is also present and of course the many immunosuppressed people. Arguably a lot of infections are by two or more causative agents as often if one is able to enter where it shouldn't, another may, but one is likely to be more dominant. Furthermore even our infections can get infections with bacteriophages infecting the bacteria we are infected with.

I like the "infections all the way down" comment.  Can you add refs to bacteriophage infecting bacteria that colonize humans?

Secondary infection is not rare at all. I mean consider babies. When they get the cold their immune system is weak and focused on the cold virus and they can get viral pneumonia from the flu very easily for example.
TB is another good example of a disease often weakening the immune system and raising the probability of a secondary infection and HIV is a viral one with the same weakening and higher probability of secondary infection.

Another example where coinfections are common is with tick-borne illnesses.
One 2006 review suggests that in some regions of North America the prevalence of Ixodes ticks carrying two pathogens may be up to 28% and that from 4-45% of humans with Lyme disease also appear to have ehrlichiosis or babesiosis(Coinfections Acquired from Ixodes Ticks).

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


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Why do some animals and fungi prefer asexual reproduction?
Animals like Sponges and Hydra and fungi like Yeast and Mushroom can reproduce both asexually and sexually. However, they only reproduce sexually if the 'circumstances' are 'bad'. Is there a specific reason for that?

Here is a quite intuitive and straight forward possible explanation:
The key is to rephrase "if the conditions are bad" into "if the focal individual don't fit its environment" or "if the genome of the focal individual is not fit" or "if the focal individual is not fit".
If an individual has a high fitness, it has better to create clones which will be fit as well.
If an individual is not fit, it has better to take the risk to reproduce sexually hoping that some of the offsprings will be fit thanks random recombinations and mutations (there are usually much more mutations during meiosis than during mitosis).

Note:
Sex allocation and evolution of sex is a very broad subject. Your question is linked with discussion on sex allocation. You might be interested by these books:

Eric Charnov
Stuart West
Perrin and Beukeboom

But you might simply have a first look through wikipedia sex allocation, Muller's ratchet or have a look to the diversity of reproduction. You could also have a look to specialized literature, the work of S. Otto for example. Usually introductory books on evolutionary biology contain a chapter on the evolution and diversity of sexual reproduction.

On the long term creating clones will be not advantageous, because the species misses the chance to rearrange and exchange genes. Especially the later can be advantageous for developing further.

Well, yes under the consideration of group (or species) selection, cloning is not advantageous (because of Muller's ratchet for example). But it is not an argument against my answer. I just meant that in orgnaism that can reproduce both sexually and clonally (note: I did not want to make the discussion more complex by talking about various "intermediate" mode of reproduction), sexual reproduction is performed in order to explore the possibility space of genome hoping to fall on a good combination!

It wasn't meant as a counterargument, more to supplement it.


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Is there any danger in putting a magnet in your ear (next to your brain)
I recently bought some wireless earbuds that fit right in my ear, so they're very small.
But the method it uses for charging is magnetic, so it has magnets built into the earbud.
I was wondering if there's any danger in keeping a magnet in your ear for many hours every day? I'm not sure if it would affect things in your skull/brain.

All speakers, all headphones, and all earbuds contain magnets. That's how the speaker diaphragm is driven. Furthermore you are walking around in the earth's magnetic field all day long. There might be an issue with exposure to a superconducting high field magnet, but you wouldn't be able to fit that in your year.

@rasen58 As your question comes from a belief popularized by alternative medicines, your question would be a good fit on skeptics.SE. You might also want to have a look at the posts Do magnets have verifiable effects on humans? and Do magnetic insoles or bracelets increase muscular strength and flexibility? on skeptics.SE

@Remi.b I didn't even know that was a belief popularized by alternative medicine. It was just a question that would seem to make sense from a scientific viewpoint since putting powerful things like magnetic fields close to you seems like it could somehow be dangerous. But thanks for the links!

Every pair of earbuds/headphones have magnets in them, as of now there's no solid evidence that proves that they are harmful or harmless to humans. Keep in mind that, what may be harmful to lab rats may not be harmful to humans as we are more resilient to radiation, etc. (In reference to a study done on truly wireless earbuds.)

You wrote that you a referencing to a certain study, could you please provide a link to that study?


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Opposite results between Blomberg's K and phylogenetic signal in Phylocom (AOT)
I've been trying to test for significant phylogenetic conservatism in some plant traits. So far I used R-package picante (Blomberg's K) and AOT in Phylocom. So far these two methods yield completely opposite results for the same traits, and I'm confused. Is it possible to get such very contrasting outputs from these two methods?
For example, one trait shows Blomberg's K = 0.2892 (P = 0.001), suggesting that the evolution of this trait overall has not been greatly constrained by phylogenetic relatedness. In contrast, for the same trait AOT yields variance of standardized contrasts across tree = 0.006, significance of contrast variance relative to null model (low rank) = 1, and significance of contrast variance relative to null model (high rank) = 1000 (i.e., P = 0.002), suggesting that treewise phylogenetic conservatism is significantly greater than the expectations of random tip swapping.
I've just started looking at these phylogenetic signals, so I may be overlooking something critical. I will greatly appreciate if you could kindly give me directions, thank you very much!

I think I figured. Someone told me that the above results are the same. The absolute value of K = 0.29 indicates the magnitude of the signal is less than expected under a Brownian motion process, but it’s still more than random expectation (according to the P-value,P = 0.001). So both methods suggest that treewise phylogenetic conservatism is significantly greater than random expectations.
Actually the meanings of K statistic and P-value were clearly stated in the original paper (Blomberg et al. 2003). I should have looked at it first... but anyway, I think it is solved now.


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Two different Leucochloridium infected snails - different species?
In the last three days, I have found two snails infected by some species of Leucochloridium. I found them in my garden in the south-west of Sweden. Now I'm wondering if they are the same species or not.
One has broodsacs with green stripes and looks like a typical Leucochloridium paradoxum, and the other has brown stripes, which makes me think it's a Leucochloridium variae, but I've seen it mentioned that their appearance can vary.
Update: I have learned that there is only one (documented) species of Leucochloridium in Sweden, so maybe I should close this question, but I would still like to know if there is a way to tell the difference just by appearance.

And here they are in animated form in case that is helpful:

Those pics and animations are so cool. Just to satisfy my curiosity: How does time scale with your gifs? +1

Thanks! Hmm... I'd say that the gifs might be a little bit faster than real life, but the green one looks pretty close to how I remember it. (More here if you feel a need for it: http://reanimateobjects.tumblr.com/)

This is fascinating! Very very little will creep me out but snails parasitized by these flatworms have since I first learned of them years ago. Great photos and gifts!

I wouldn't close the question yet.  It's possible that there is more than a single species of Leucochloridium in Sweden even if there's only a single documented species. Take a look at https://www.fugleognatur.dk/gallery.asp?mode=ShowLarge&ID=388472 that's from Denmark. I don't have any more info than that to share

@Jude Oh, thanks for that link! Searching for the species L. perturbatum (instead of the synonym L. variae) led me to this article saying you can tell brood sacs apart from colour and banding: https://www.ncbi.nlm.nih.gov/pubmed/23659278 So now I just need to find out exactly how to do that.

An intriguing question. Because I have not conducted any formal research into the parasitic family of Leucochloriidae, I shall hazard two options which would not require genomic sequencing.
Principally, as you suggested, observing the banding of the broodsacs is one critical means to distinguish members of this genus. The study entitled 'A
REVISION OF THE FAMILY LEUCOCHLORIDIIDAE POCHE (DIGENEA) AND STUDIES ON THE MORPHOLOGY OF LEUCOCHLORIDIUM PARADOXUM CARUS' describes its broodsacs 'typically' to have green banding with dark brown and black spots. On the grounds that this indicator is liable to being variable, the next procedure may yield greater accuracy.
The secondary host of most Leucochloridium species, including paradoxicum, is an adult bird ranging from crows to finches in which the larval mircidia enter the bird's tract and develop into distomes through consuming the snail's infested tentacle. Moreover, if possible, determining the secondary host of the parasite may assist your taxonomic identification: the Leucochloridium often gives its host's left tentacle the resemblance of a maggot, attracting the American Robin, for example.
Ultimately, analysis of the distomes produced in the secondary host phase could allow you to discriminate at the specific level.
Information regarding Leucochloridium variae, available from: http://eol.org/pages/849160/details
The cruel world of parasites


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Diffusion coefficient of cells in blood?
What's the diffusion coefficient of white cells in blood?
Is it well defined, or are cells too large and few as to be treated as particles in this context?
P.S. I have tried to look this up, but what I find inevitably is about diffusion coefficients of molecules inside cells, which is not what I want.

Cells in blood flow will in the first approximation follow the flow. Of course blood flow is very complex and includes many interactions, so there'll be some kind of 'effective diffusion' arising from this, which will depend on many parameters (such as the flow velocity, pulsatility, hematocrit...)

Cells absolutely can be considered as diffusing objects.  However, the origin of the "diffusion" can be very different than for, say, a bead in water.  The reason is that the thermal motion that creates the diffusion of a micron-sized bead can be much less important for a (large) cell.  For instance, the diffusion coefficient due to thermal forces of a sphere in a fluid with viscosity $\eta$ is
$$D_{therm} = \frac{k_B T}{6 \pi \eta R}$$
where $R$ is the cell radius (this is the "Stokes-Einstein" result).  For a white blood cell (say 10 microns in radius), this would - assuming blood is at least as viscous as water - lead to thermal diffusion coefficients around 1 microns$^2$/hour- i.e. we would need many many hours for a cell to travel its own diameter.  This result neglects a bunch of complexities - blood is not perfectly viscous, there is a really high density of red blood cells in blood, etc... but the basic result is that the thermal buffeting that drives the diffusion of a colloidal bead is not enough to drive a cell.
However, cells are not passive beads!  They crawl, both randomly, and (as cancerconnector notes), in response to signals like chemical gradients.  If a cell crawls with a speed $v$ and maintains its orientation over a time $\tau$, it's reasonable to describe its motion (over times much longer than $\tau$ as being diffusive with an effective diffusion coefficient
$$D_{motility} = \frac{1}{2} v^2 \tau$$
which you can get mostly from dimensional analysis, or more rigorous models.  For white blood cells, $v$ is on the order of microns/minute - at least when measured on slides - it might be different in the body.  $\tau$ is a few minutes, so $D_{motility}$ is on the order of many microns$^2$/minute - orders of magnitude faster than mere thermal diffusion.
A good introduction to modeling of this question is probably chapters 9-11 of Leah Edelstein Keshet's "Mathematical Models in Biology" and she cites some classic Lauffenberger papers on macrophage response, etc.  You may have access to this online: http://dx.doi.org/10.1137/1.9780898719147
Also, note that everything I've said so far neglects blood flow - if this is important in your problem (which will depend on the context), things can get more complex (have to include flow in your diffusion equation).  But using diffusion equations to model the spread of randomly motile cells is a very common approach, and there is a lot of literature on it!

This is a difficult question because white blood cells do exhibit chemo and haptotactic responses, and also because of their large size - though cells are often modeled as moving by diffusion (cancer cells in particular, see: "Modelling biological invasions: Individual to population scales at interfaces" as one of MANY examples). One could model their movement in a dish, and come up with a diffusion coefficient, but I'm not sure what the utility of this would be. Why do you want to know?  Is there another underlying question?

No underlying question. I am developing a mathematical model of cells in plasma. Just need some order of magnitude estimate.