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What is this white fluff growing in my basement?
I live in the countryside of Western Europe by the beach with a temperate climate. After a period of unusual humidity at 84%, I noted this white fluff in the basement floor:

The first picture is about 40 cm and the second 10 cm.
The basement is usually closed and keeps humidity. Temperatures average 18-20ºC, and humidity is now 77%. I assume it's a fungus since the floor was clear before and it seems to collapse when I rub my foot on it.
What is this species, and how can I prevent it?
Update: Following @anongoodnurse's suggestions, it's definitely a salt. I scraped the stuff, poured water, and it shriveled instantly. Here are photos before and after:

Here is a close-up of another piece, where the shards look like a crystal:

It did not smell indeed, and I did not taste it. I opened the basement door to ventilate the area, and I understand that it would accelerate the evaporation of the salty water.
I don't know if this growth has happened before, e.g. because of a leak in a pipe, or is a one-off occurrence, e.g. because of the unusual humidity in the last few weeks. I will check if the basement has any pipes.

What is that floor made of?  Looks like square vinyl tiles.  Has it been raining a lot during this period of high humidity?

The crystalline appearance makes me suspect that that is a mineral efflorescence rather than a biological growth.
See for example: https://www.ceramictilefoundation.org/blog/understanding-efflorescence-ugly-white-powder-on-tile

The floor is either ceramic or stone tiles, not vinyl.

@tyersome Efflorescence is intriguing. How would I test if it's a salt, by putting water on it?

@miguelmorin - Yes. Scrape a bit up (it should feel a bit sandy, not mossy) and see what a drop or two of water does. Mold doesn't dissolve in water, it floats. If water seems to dissolve some of it, add more. If it all dissolves, it's probably a salt, and since you live near the beach, it might be mostly salt, i.e. NaCl, with trace minerals thrown in. If it dissolves and you're brave, you can taste a tiny bit then spit  and rinse. Fun!

Salt water is probably entering the basement through the porous grout; as it evaporates, it leaves salt crystals behind. More water = saltier solution = bigger crystals as the water evaporates. If it turns out to be salt, you might ask over on DIY what to do about it. If you have metal pipes under the floor, it can't be good.

@tyersome - Oof, apologies! I just realized your link and mine were identical (an honest mistake.) If you leave an answer, I'll give you all my rep earned plus 10 (my upvote). You basically answered the question with two lines. The rest (of my answer) was fluff.

@anongoodnurse — No problem — I thought this might not be an appropriate question for SE.Biology, so I didn't bother to post as an answer. Your answer is much more complete anyway so I think you earned the reputation, but thank you for the offer!

@tyersome - I know you'll earn it shortly (I've read some of your answers), but it will put you over the rep needed to do magic at 2000K. ;-)

Might as well make this an answer.

...it seems to collapse when I rub my foot on it.

As @tyersome stated, it appears to be salt, not mold. Salt crystals would definitely collapse easily underfoot, and should be mostly quite dry, whereas mold would be... maybe squishy (?) but likely unpleasant in some way. Mold also smells, which you haven't mentioned, whereas salt is odorless.
To test, scrape a bit up (salt crystals should feel a bit sandy, not mossy) and see what a drop or two of water does. Mold doesn't dissolve in water; it floats. If water seems to dissolve some of it, add more. If it all dissolves, it's probably a salt, and since you live near the beach, it might be mostly salt, i.e. NaCl, with trace minerals thrown in.
If it dissolves and you're brave, you can taste a tiny bit then spit and rinse. While salt isn't toxic, I can't vouch for what was in the grout.
My guess is that there may be a low spot or two in your basement where salt water is entering through the porous grout; as it evaporates, it leaves salt crystals behind. More water = saltier solution = bigger crystals as the water evaporates.
If you have a magnifying glass, you should see crystals in the undisturbed deposit. If instead it looks soft and hairy, it is mold. I can't think of a white mold off the top of my head (well, Candida albicans, but that smells yeasty and is definitely not crumbly). Mold/yeast needs a substrate (food) to grow on, and wet grout isn't very nutritious. Mildew, sure, but mot big fluffy mold.
 I don't like this reference because it's not scientific, but it explains efflorescence well.)


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How to extract oxygen from grow chamber
I have been developing LED grow lights for a year or so and one of the things I am trying to do is to build a grow chamber where I can control temperature, humidity, light intensity and quality and levels of $\ce{CO2}$ and $\ce{O2}$.
I don't have any problems with most of the variables except the gases. I can inject $\ce{CO2}$ and monitor the gas, but as the chamber is hermetically sealed, how do I get rid of excess oxygen produced by the plants? Is there something similar to the $\ce{CO2}$ scrubbers used in aquariums? As a matter of fact, plants also need oxygen for their metabolic processes occurring during darkness, but they produce oxygen in excess of this requirement during the day. It is the excess of oxygen the one I want to extract, and not the whole amount of oxygen in the air of the chamber.
The whole idea is that through the chamber, I can adjust light conditions to each crop based on performance. Gas exchange is an important proxy for Chlorophyll fluorescence and has shown a good correlation with performance.
Any ideas?

Hi Jim. Yes, plants also need oxygen, particularly during dark periods of time, but they produce oxygen in excess of their metabolic needs. I will edit the question to reflect this.

Absolutely, this is actually looking more as an engineering problem rather than a biology one.
In any case, I think I have found a satisfactory answer on a paper from the 1997 Proceedings of the Sixth European Symposium on Space Environmental Control Systems. The article is called: Oxygen Scrubbing and Sensing in Plant Growth Chambers using Solid Oxide Electrolyzers.
Basically, a disk of non-porous yttria stabilised zirconia (YSZ) is sandwiched between platinum electrodes and inserted in the chamber half-way, with the other half enclosed in whatever will store the extracted oxygen. The electrodes must be porous to allow gas diffusion. The only problem is, that sort of electrolysis cell needs to be maintained at an elevated temperature (800 to 1000 Celsius) in order to work.
By means of electrocatalysis and thermal dissociation the oxygen molecule dissociates to form two oxygen atoms, these in turn pick up two electrons from the cathode and become ions. The ion is then transported by the electrolyte (YSZ) by means of electron vacancies located in the crystal lattice (basically a similar process to that of a N-doped semiconductor whereby impurities create electron holes).
I think I am satisfied with the above explanation. Doable at home? No way, but it does answer the core question.

It's going to be tricky to strictly regulate CO2 and oxygen in a chamber.
We use a palladium catalyst to maintain an anaerobic environment for microbiology purposes, but this requires a source of hydrogen to work, and it doesn't work well for fine adjustments, but rather for maintaining extremely low oxygen conditions. We also have a hypoxic chamber that regulates O2 concentrations with good precision (0.1%), but it's expensive to maintain, and requires sensors for oxygen, CO2, and nitrogen, and an automatic gas injection system for each component.
A simpler design would probably be to have some gas exchange with the room your chamber is in, using a tyvek membrane to minimize water loss (and HEPA filters if you're worried about pathogen contamination). My friend who farms oyster mushrooms did something similar, and also rigged up a humidity sensor to a humidifier using a RaspberryPi to manage the moisture loss.
However, if you're dead set on having a strictly regulated atmosphere for you grow chamber, you might want to consider consulting with Coy Labs. When we needed a chamber with the ability to tightly regulate oxygen levels for microbiology research, they came to the lab and worked with us on our specific needs and together we develop their first working model nearly from scratch (we modified one of their existing anaerobic chambers). But it worked so well that they now sell hypoxic chambers as part of their standard line of products. As far as I know, they haven't done any work with plant grow chambers, but they're a small company with a lot of experience building contained atmospheric control systems. Pretty much every order is custom built, so they're used to answering a lot of questions and tailoring their products to the specific needs of a customer, and they're very helpful and responsive with maintenance and upkeep. Just know that they're products aren't cheap.
https://coylab.com/

Hi @MikeyC, good stuff on your above answer! There are plenty of clues on what direction to take, even more so after checking the company's site you've recommended. I'll leave it open though as it does not necessarily answers the question of how to extract the extra concentration of O2 from within the chamber.

Fair point. The system I'm describing is additive, not subtractive. Essentially, the gas injectors would add other gasses (either Nitrigen or CO2) to keep the O2 below a set concentration. To avoid over pressurizing the chamber, it would need a vacuum pump to purge some atmosphere after injection, or maybe even a simple water-filled airlock system like beer-brewers might use. It's starting to sound like your problem is one of engineering, rather than biology. Maybe try an engineering forum.

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Issues obtaining Fo in DIY Imaging Fluorometer
I have successfully built an imaging fluorometer at home (see project details here) and so far is working amazingly well.
But I am having serious issues in obtaining Fo to calculate Fv/Fm (Fm-Fo)/Fm. The reason is less technical than theoretical, as after scouting dozens of academic papers all I can find are contradicting accounts as to how to set up the fluorometer to effectively obtain an Fo value.
Without Fo, the Fv/Fm values of all plants I have analysed range around ± 0.90 which is way above the usual 0.83 the literature cites as an unstressed plant. If the number were below 0.83, I would believe the plants are stressed, but a higher number clearly indicates my setup is not correct.
Most literature states that the measuring beam must be of the order of < 1 μmoles m−2 s−1 to avoid eliciting any photosynthetic rate. The reason for the literature to be so scant about this protocol is that 99% of fluorescence research is done with commercial fluorometers and researchers don't need to adjust parameters as they are adjusted by the software. There seems to be a bit of esoteric mistery around these fluorometer parameters, probably due to some commercial sensitiveness.
Under my setup, using a measuring light of < 1 μmoles m−2 s−1 elicits a signal of 0.3 on the camera, while the saturating pulse can be over 100 (0-255 scale or 8 bits) and above depending on intensity. Calculating Fv/Fm using these numbers gives a number above 0.98 which is clearly wrong. Increasing the camera exposure does not help.
Another issue is that we are talking about fluorescence imaging and not the traditional photodiode based fluorometer which is closer to the source and way more sensitive. A camera is far away from the subject and increasing too much exposure leads to noise, etc.
Then again, I do not think this is a technical issue, as I've got the feeling the measuring light of the commercial imaging fluorometers is much stronger than otherwise stated.
Has anybody dealt with this specific issue?

This paper1 gives a definition of all the various parameters. F0 (that's Fzero, not F letter "o" I think) is defined as the dark state fluorescence. There is a second parameter F0' that is the light state fluorescence.
F0 would be your ground-state with minimal induced fluorescence, it seems that this might require "overnight in the dark" for true measurement values. Measure the fluorescence with the measurement (far-red I think) light turned on. You should then apply a saturating pulse of actinic light to measure FM. You should also determine the background from your rig using reads taken with no sample in place and with and without measurement light turned on. This paper2 provides a description:

The calculation of fluorescence parameters is probably best explained by reference to a typical experimental trace (Fig. 1). Under field conditions, an experiment of this type may not always be appropriate, however, most of the parameters can still be calculated. The measurement is initiated by switching on the measuring light, giving a measure of the Fo (minimal) level of fluorescence. A saturating flash of light is then applied, allowing the measurement of Fm in the dark‐adapted state (
Fom
). Following on from this, an actinic light is applied and, at appropriate intervals, further saturating flashes are applied. From each of these, a value for Fm'
, the fluorescence maximum in the light, can be measured. The steady‐state value of fluorescence immediately prior to the flash is termed Ft. After a flash, removal of actinic light (preferably whilst simultaneously giving a far‐red light) allows measurement of Fm'
.

1: Lichtenthaler et al. Photosynthetica volume 43, pages 379–393 (2005)
2: Maxwell and Johnson. Journal of Experimental Botany, Volume 51, Issue 345, April 2000, Pages 659–668

I am well aware of those papers and they don't answer the fundamental question, nor does your answer. In the meantime, I have found the answer to my question but I need to test it before posting my answer here.

@MaykeSantos - I read your question to ask how to set F0, due to this bit "But I am having serious issues in obtaining Fo to calculate Fv/Fm (Fm-Fo)/Fm." I don't see any other questions in your post (other than last sentence). If you could solve F0, then your problem would disappear. Can you calculate F0' as a proxy?  the literature suggests that this is a reasonable substitute. I doubt the measurement light on commercial instruments is strong as calibration is a common part of set-up when purchasing these sorts of instruments.

yes, the question is how to calculate F0 in a Chl imaging fluorometer system, that is different to most common photodiode-fibre fluorometers. There is a long paper about how to calculate F0' (not F0) as a proxy, but that's different and it can be achieved with far red light. Now, to answer the question itself, my problem is light modulation. I need to apply a very strong light pulse but at a much higher frequency (below 300us) in order to avoid eliciting photosynthesis. The answer is in Oxborough 2004

@MaykeSantos - you should edit that into your question, as it isn't clearly stated what you are actually looking for. 300 us is very short, you might be able to do it with a shutter mechanism, but you would need a very fast processor controller. You might be better asking for migration to the electronics SE

I will leave it as it is. Thanks.

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Are there solitary animals communicating with themselves?
I can imagine 3 different kinds of communication between individuals:

Communication between individuals of the same species.
Communication between an individual and another from a different species.
Communication between an individual and the same individual at a different time, i. e. some individual "taking notes" or "marks" for later use.

My question is whether there are animals showing (3) but not (1) or (2).
In order to make sure the absence of (1) I stipulate that the individual animal should be capable to live a completely solitary life, which excludes e. g. all mammals from the list of candidates.
Here, the criteria for "communication" are the following:

The message is created by a defined action of the animal.
The message is an object, separate from the animal's body.
The animal is able to interpret the message at a later time, i. e. removal or modification of the message artifact would result in a different behavior.

This question is motivated by the more general question whether the ability to communicate necessitates a social context.
EDIT: In order to make it clearer what communication could be, as suggested by the comments, here are a few examples:

territory marking: matches the categories (1), as a signal to rivals and probably (3), as a reminder for the territory owner.
alarm call: matches (1) and/or (2)
behaviour of the Honeyguides: a typical example of (2)
creation of trails: may have a communicative function (e. g. for ants), and is also seen with solitary animals. Is there a case, where the communicative function is predominant and all other criteria are met?

Here is why I think that some classes of species can be excluded:

mammals, birds: every individual enjoys parental care, which has a communicative aspect of type (1)
plants: may be able to communicate with other plants or animals, but self-communication seems hard to imagine.

I think this is an interesting thought, but almost certainly bound to lead to an inconclusive result relative to the motivating question. I think your (3) might be bound up too much in "language" and abstractions that are far higher order than communication more generally. If an animal recognizes a burrow as smelling "like home" and part of that scent includes smells originating from the individual animal, does that count as taking notes or marks?

There's also the problem of identifying a truly solitary animal; you've excluded mammals already, but even non-mammal animals that live alone find a mate, for example, and even animals that don't mate with a particular individual, like cnidarians, communicate with each other to coordinate gamete release. Even unicellular organisms communicate with one another, as do plants. Communication seems to be a much more generic feature of life than the premise in this question seems to recognize.

@BryanKrause I think the burrow smelling "like home" would meet the criteria (2) and (3) (if there is the observation), but perhaps not (1) unless the scent is applied by an act like spraying or so.
Please note also, that animals that do mate are not excluded, because that fact says nothing about a particular individual that might well live its life alone (I've tried to clarify this by an edit of the question).

It would be cool to have a brief beside the three common types, like "territory marking" "alarm call", it would make the question more accessible.


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Examples of animals who 'forget' their offspring
Occasionally on the news I read about young children dying in hot cars on a sunny day. Usually the article reports that the parent(s) 'forgot' about their children still being in the car.
Obviously natural selection would select against a trait where parents forget about their dependent offspring or their whereabouts. However, I can imagine that under certain circumstances and on the fringe of the bell curve for offspring-caretaking, this occasionally happens.
Are there documented examples of animal species (preferably mammals or birds) who truly sometimes 'forget' about taking care for their dependent offspring, or forget their whereabouts?
Disclaimer:
I'm aware of possible anthropomorphism in this question. With 'forgetting' I don't mean behavior such as abandoning offspring at the age where they need to become independent, or accidentally being separated from their young.
Here's an example of what I would file under forgetting:
A parent feeds their young every two to three hours. One day, they go out to find food, but get distracted by something interesting (let's say a mate). They spend a day frolicking around with the mate, and eventually return to their young. On return, they find out one of the young has died due to starvation, and they are visibly surprised / startled / upset about this.
Edit:
To respond to Tyersome's comment: I have done plenty of searching and research. I haven't been able to find anything, neither in the scientific literature nor pop-culture websites / books. When you Google 'animal parenting' you'll find plenty of examples of various species who abandon their young (such as harp seals or rabbits) or who don't care for their own young (such as cuckoos), but these are 'deliberate' actions across an entire species, not examples of accidentally forgetting.

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Do you make a distinction between “forget” and “overlook” in responses to this question? The only thing you can observe in animals other than humans in behaviour. The latter is fairly common in birds, e.g in feeding of young.

@fileunderwater: yes, I would exempt the 'deliberate' overlooking of feeding certain young (by birds) from this question, since that seems to stem from some sort of choice for one or two offspring, not randomly forgetting a different one each time.

@YoupT With e.g. birds I think it is hard to make that distinction. Again, what you can see in feeding situations is behaviour. If certain weaker young are not fed because stronger siblings are more active and monopolize the feeding situation, and the parents do not observe this and actively feed the weaker young, you will end up with an forgotten/overlooked offspring which may eventually die. Was this chick forgotten or deliberately ignored? How would you make the distinction? It would certainly not be random, but I find it hard to label it a deliberate decision to choose one offspring.

I'll add a better description of 'forgetting' in animal behavior.

If the action of forgetting the offspring is accidental, and thus with a random frequency, how do you expect us to know if some species are more lenient then others to randomly "forget"?


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How many generations are required for a specific neutral mutation to reach fixation?
In population genetics, the term “time to fixation” is defined as the time it takes for a specific mutation to appear in a population, plus the time required for this mutation to spread throughout this population. My question is, how many generations are required for a specific neutral mutation to reach fixation? I need a general formula for number of generations as a function of mutation rate and population size, valid for all kinds of biological entities. Note that a neutral mutation is not fixed by selection, it is fixed by genetic drift.

The only definition of fixation (in genetics) I've seen involves one allele completely replacing all other variants of that gene. 2) I doubt that there can be a "universal" law for all biological entities. Some examples: many organisms are not sexual, ploidy varies particularly within plants, and dispersal rates within a population are going to be different. All these factors seem likely to affect how long fixation takes.

How many generations are required for a specific neutral mutation to reach fixation?

Kimura and Ohta (1968) showed that the expected time for a neutral allele to reach fixation is
$$\bar t(p_0)=-4N\left(\frac{1-p_0}{p_0}\right)\ln(1-p_0),$$
where $p_0$ is the initial frequency and $N$ is the population size. The model assumes a Wright-Fisher population (panmixia, constant population size, exclusively sexually reproducing hermaphroditic individuals, ...) and negligible mutation rate at the locus of interest.

how do i calculate po in terms of known quantities, such as mutation rate?

You can compute the expected allele frequency at mutation - drift balance (e.g. see here or any decent intro textbook to population genetics). In short, let $\theta = 4N\mu$, where $\mu$ is the mutation rate, the expected heterozygosity is
$$H = \frac{\theta}{\theta + 1}$$
From that you can compute the allele frequencies $p$ and $q=1-p$ by solving $H = 2pq$.
If needed, you can get the entire distribution of allele frequency given $N$ and $\mu$ (and even $s$ and $h$ if needed) in Wright (1937).

I think your answer would be more generally useful if you provided some examples of actual numbers.

Maybe worth noting what assumptions are behind this model? I could easily be wrong, but I would expect that how fast individuals, propagules, and gametes disperse through a population must have some effect. Also, is this true for species that aren't obligately sexual (e.g. many plants can reproduce vegetatively) ...

@tyersome The model assumes a Wright-Fisher population. Information added to the post. Thank you

thanks for the formula. Since neutral mutations are often phenotypically silent, it can be difficult to detect their presence in wild populations, which means it can be difficult to assign an accurate value to po. So, I would be very grateful if you rewrite the formula in terms of the mutation rate, which is known for a broad range of organisms. I apologize that my math skills are too low for the job, otherwise I would do it myself. Actually, I found a paper (Lanfear et al, 2014:36) that gives the rate of neutral evolution as a function of mutation rate, but I can’t see how it reduces to your

Lanfear, R. et al, (2014) Trends in Ecology & Evolution 29:33-42  http://dx.doi.org/10.1016/j.tree.2013.09.009

I found a paper (Lanfear et al, 2014) that gives the rate of neutral evolution as a function of mutation rate, but I can’t see how it reduces to your formula. I would be grateful if you show me how it reduces. Once that is accomplished, the number of generations to fixation is easily obtained as the reciprocal of the rate of neutral evolution. Thank you for your valuable time.

@igorbrznovskaya If you are looking for the time to fixation, then you cannot ignore the allele frequency. If you are looking for the rate of fixation, then of course, it is a different story. In a Wright-Fisher population, the rate of fixation at a neutral locus is simply equal to the mutation rate (see this post)

@Remi.b  In Kimura's equation, how do i calculate po in terms of known quantities, such as mutation rate?

@igorbrznovskaya Please see edited post that attempt to answer this follow-up question

@Remi.b  Thank you very much for the new formula


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Evolution of the unique mating system of the scorpion Androctonus australis
Sperm transfer in the scorpion Androctonus australis involves a sclerotized spermatophore, which is formed in the paraxial organs of the male reproductive system. The right paraxial organ produces the right half of the spermatophore (hemispermatophore), and the left paraxial organ the left hemispermatophore. The hemispermatophores are mirror images of each other, and are always produced one pair at a time.
During mating activities, a sexually mature male locates a receptive female, grasps her pedipalps, and proceeds to drag her along in his search for a suitable substrate onto which the spermatophore will be glued. This search may last for several hours. When the male finds a suitable substrate, the hemispermatophores slide out of their respective paraxial organs, move past the genital atrium (where the hemispermatophores are glued together), and the spermatophore is attached to the substrate.
The spermatophore contains the sperm mass in a concealed vesicle so that sperm aren't dessicated. The male then pulls the female over the spermatophore, guiding her so that her genital opening reaches a position directly above the spermatophore. A brief struggle ensues and the female's rocking motion helps to engage the spermatophore with her genital operculi. Continued rocking by the female triggers spermatophore opening, and the sperm mass is transferred into her genital pore. The transfer requires a pressurized vesicle that forces the sperm into her genital pore.
The spermatophore originated in aquatic organisms, but it has undergone extensive modification for use in terrestrial organisms like scorpions. Which evolutionary developments caused the transition from an aquatic deployment of the spermatophore to a terrestrial deployment involving the various interdependent behavioral and physiological elements described above? Since the behavioral elements are invariant, they must be encoded in the genome just as the physiological elements are. A rigorous answer to this question necessitates the elucidation of a series of intermediate steps, each of which was driven by natural selection, and each of which involved a set of mutations whose overall probability was not prohibitively low. If one or more of the steps was driven by genetic drift, then we must take into account the fact that, although the time for fixation of a neutral mutation is shorter in small populations (such as occurs during a population bottleneck), there is less opportunity for mutations to appear in small populations.

Hi and welcome to Bio.se! I learned something today, thanks! Be careful about asking "why" evolution occurred. Maybe tweak the question to ask for more literature on this. Currently, it sounds like you are asking generally about (i)"is the behaviour genetic", and (ii) "has the genetic evolution been mirrored by the behaviour"? The second point is incredibly subjective.

Is this homework?

Dear James, thanks for your comments. You are right -- more literature on this would be appreciated.

What specific part of the process is problematic we see most of this behavior represented in other species as well. As it stands this is not asking for an answer it is asking for a dissertation.

Dear John, the transition from aquatic deployment to terrestrial deployment necessitated extensive physiological changes acting in concert with behavior changes. I am interested in the details of the process.

Why would it need both a behavioral and physiological change at the same time. plenty of aquatic animals use spermatophores. you seem to be confused about what a transition to a terrestrial environment looks like, from what we know from the fossil record of other animals it is a gradual process that happens is shallow swamps were better osmotic balance, limbs are already valuable and humidity hovers around 100%, it is not a single sudden event. there was likely even an amphibious stage like some crabs.

@John  I can’t think of any functional intermediates between aquatic spermatophores, which are attached to the female’s body as she floats in the water (see Cephalopods), and terrestrial spermatophores, which are glued to the ground, as in scorpions. As soon as the evolutionary transition is made to a spermatophore that is glued to the ground, then there must be the associated searching and dragging behavior to find a suitable spot on the ground to glue it to, as well as all the other behavioral steps listed in my original post.

@john  Moreover, there must be the secretion of glue, which is absent in aquatic spermatophores. Vague scenarios won’t do -- you have to deal with these unique points.

not all scorpions use glue, and plenty of aquatic organisms use glue for spermatophores and egg cases, why look at cephalopods when you have much more closely related crustaceans. You seem to think evolution has to go right from marine crustaceans right to this one modern species, all the steps don't have to evolve at once, heck the variation in reproductive apparatus is so diverse  in scorpions has been proposed as a way to classify them. I think the issue is your not very familiar with scorpions or their relatives.

I will research this and get back to you.


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Small Black Fly Identification
Could anyone help to identify the following small black fly please?

Here is some relevant information which may help:

Location: London, UK
Length: ~5mm
They are slow to react and drift lazily & silently around a room

After my own research, I thought it might be a fungus gnat, but I'm uncertain.
Hopefully, if the species can be reliably identified, I can then look to find out what attracts them and how to deter them.

We need a photo with the wing venation in focus for a reasonable chance at family-level identification; if on getting such a photo the family is Sciaridae (which does seem likely given the animal's color), good luck (species level identification in that group is firmly in the "some disassembly required" camp).


text:
Is genetic equivalence a universal truism or are there exceptions?
Someone who I have been discussing scientific topics for some time came around to the notion that, on a biological level, the seed of a plant is not the same organism as the mature stage of the plant. When I brought up the theory of genetic equivalence he completely shut down and refused to go further. He then told me to pose the question here so here I am. To be concise "is an acorn a tree".

Is an acorn a tree?
It all depends on your definition of identity. What makes two things being the same things to you? There is no "fundamental biological definition of identity". Therefore a sentence like

[..] on a biological level, the seed of a plant is not the same organism as the mature stage of the plant

This sentence has no meaning as it wrongly assume that there is some kind of fundamental biological definition of identity but there is no such thing. Scientists are not dictators stating how things must be defined. Scientists use terms that they define that help them describe the world. Anyone is free to come up with its own definition and work with it.
Let's consider two possible questions that are better defined
Is the genetic material found in a tree cell the same as the one that was found in the acorn before it became a grown-up tree?
Yes for most cells you would consider and yes again but except for somatic mutations and shortening of telomeres.
Is an acorn the same weight as a tree
No!
So, really it all depends upon what your definition of identity is.


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When does the vertebral column finish chondrifying and begin to ossify?
I have read many articles on vertebral column development in embryos on the internet.
Different articles give different time periods for the end of chondrification of the vertebral column and the beginning of ossification.
Some websites and books(like The Developing Human: Clinically Orientd Embryology 10th edition) say that 'the 2 centers in each centrum fuse at the end of the embryonic period to form a cartilaginous centrum', which is rather confusing since they also say that ossification begins in the 7th week. How can ossification in the centrum begin when the chondrification centers in the centrum have not even fused yet? Why does it takes so long(2 weeks) for the chondrification centers to fuse?
When is the chondrification of the vertebral column complete and when does ossification start?

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I've made some edits that I hope clarify your question, but I think it would be helpful if you could elaborate on why you think the quote (BTW: you must add a reference for that quote) conflicts with "ossification begins in the 7th week".


text:
If mutations are random, why do antibiotics 'cause' resistance?
Full disclosure: I am not a biologist and this is more of a general question about understanding antibiotic resistance of bacteria.
We are always told that careless antibiotics use is the cause of new more resistant bacteria, which can obviously devastate huge societies and even have global impact. At the same time from my knowledge it seems that bacteria mutates in a purely random fashion.
So, thinking about this concept probabilistically, the virus mutating and antibiotic consumption seem to be completely disjoint events such as:
$$P(M|A) = \dfrac{P(M \cap A)}{P(A)} =\dfrac{P(M) P(A)}{P(A)} = P(M)$$
Where $M$ is the event that the bacteria mutates and $A$ is the event of taking an antibiotic. I couldn't find any research online as to how $P(M)$ is actually modelled or what probability distribution it even roughly follows, but intuitively it would depend on time as the longer the bacteria spends inside the host the higher the probability of mutation would be. So from this train of thought it would seem that taking antibiotics would actually be a good idea as to eradicate the bacteria quicker and give it less chance to mutate down the line.
I am obviously not trying to discredit hundreds of years of research and understand that there must be a gap in my thinking somewhere. My question is, why are we told that antibiotics cause antibiotic resistance even though the mutations are described as 'random'?
(ELI5 explanations are preferred as I said I don't come from a biology background)

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. In particular, you are ignoring the effects of selection, which suggests to me that you would benefit from this introduction to evolutionary theory from UC Berkeley. ——— We also encourage you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). Thanks!

I have found that when learning about a new area starting with a relatively accessible and reliable source like Khan Academy is very helpful. Wikipedia is also generally a good starting point and you can then check their references. Online platforms called MOOCs offer free (or very low cost) courses on a wide variety of subjects — two I am familiar with are Coursera and edX. Finally, textbooks with a good level of detail are also freely available online e.g. from NCBI.

Presence of antibiotic does not significantly affect mutation, but rather affects selection of variants.  You may find this Khan Academy page helpful.

Mutations are random. Selection of mutants (with use or overuse of antibiotics) is not random.

There are many models for mutation accumulation (Liò and Goldman, 1998). The simplest model (Jukes and Cantor, 1969) assumes mutations to be a Poisson process. With a given mutation rate, the number of mutations accumulated will follow the Poisson distribution.
This basic model has been extended to include non-uniform mutation rate across the genome and different rates for different kinds of mutations. You can check out the link and the works it cites to have a better idea.
However, the answer to your question does not pertain to how mutations happen. Although there is some evidence that some antibiotic treatment can actually increase mutation rate (Long et al, 2016; Meouche and Dunlop, 2017, Windels et al., 2019), the main principle pertains to selection and not actually the mutations. Improper antibiotic treatment can lead to some cells with moderate resistance to survive, which in turn can evolve strong resistance. Here, we assume that the infecting bacterial pool already has enough variation (or develops during infection) some little resistance. Moreover, there is another phenomenon called persistence (ability to survive antibiotic, Brauner et al., 2016). Windels et al (2019) report that persistence can increase resistance.


text:
What brain regions consume the most energy?
It's well known that the human brain consumes roughly 20% of the body's energy, and that grey matter is much more energy-intensive than white matter.
Beyond this basic information, it seems difficult to search for the total energy consumption of the brain broken down by lobe, or ideally further. For instance, how much power is consumed by the typical hippocampus, averaged over a typical human lifespan?

Welcome to Biology.SE! This is well outside my area, but I think you need to clarify and focus your question. For example, it is well known that energy consumption in different regions varies depending on what the brain is doing.

@tyersome I'm not sure what you mean, but I want the time-average values for a typical human.


text:
Can catecholamines degrade back into tyrosine, or, is synthesis irreversible? (in human body)
Catecholamines like dopamine, noradrenaline and adrenaline are broken down with enzymes that catalyze the reaction. Can they degrade back into tyrosine (a conditionally essential amino acid), or is the synthesis of catecholamines like adrenaline irreversible? (in context human body, but, broadest possible phylogenetic or biochemical context welcome in answer.. )

What do you mean by “are broken down with enzymes that catalyse the reaction”? Which reaction?

A glance at the relevant BioCyc entry tells us that each reaction in the catecholamine biosynthesis pathway is irreversible. The standard free energy change of each reaction—again from BioCyc—is given below.
\begin{array} {|r|r|}
\hline
\text{Reaction} & \Delta _r G' ^{\circ} \text{ in kcal mol}^{-1}\\
\hline
\text{Tyrosine hydroxylation} & -93.0 \\
\hline
\text{Decarboxylation of DOPA} & -3.09
\\
\hline
\text{Hydroxylation of dopamine} & -67.9
\\
\hline
\text{Norepinephrine to epinephrine} & -10.5
\\
\hline
\end{array}
Note that all the free energy changes are negative, i.e. all reactions are irreversible under physiologic circumstances. (For the last one, there is a simple explanation: S–adenosylmethionine is a powerful methylator [1].)
Another aspect is worth a mention. Under physiologic conditions, the reversibility of a reaction depends not only on the free energy changes involved, but also on what happens to the reactants and products. A large supply of reactants, or rapid removal of reaction products, can make the reaction physiologically irreversible. Applying this principle to the catecholamine biosynthesis pathway:

A steady supply of oxygen is available from the atmosphere—this drives the tyrosine and dopamine hydroxylation reactions in the forward direction.
The dihydrobiopterin produced by tyrosine hydroxylase is scavenged by reduction to tetrahydrobiopterin, which further takes part in the tyrosine hydroxylase reaction [1].
The carbon dioxide produced by DOPA decarboxylase is exhaled out.

This further adds to irreversibility.
Of course, as mentioned by @user1136 in the comments, it is theoretically possible to have a "reverse" pathway by coupling to ATP hydrolysis. However, I could not find any such pathway in database searches.
Summary: To the best of my knowledge, humans cannot convert catecholamines back to tyrosine.

Reference

Nelson DL, Cox MM. Lehninger principles of biochemistry. 6th ed. New York: WH Freeman and Company; c2013. Chapter 18, Amino acid oxidation and the production of urea; p 695–730.

@user1136 True. But I could not find any such reaction for tyrosine. The only reaction in humans that favours tyrosine biosynthesis is (to the best of my knowledge) hydroxylation of phenylalanine.

@user1136 — The poster asked whether the synthetic pathway was reversible. This answer gives the correct response. Whether there is a pathway for degradation is a completely different matter. I imagine there is, but it is not the reverse of the pathway for synthesis, any more than the reaction of ribonuclease is the reverse of that of RNA polymerase. (No NTPs in the former, in case you hadn’t noticed.

I do believe it's irreversible.  When catecholamines have done their duty, they are degraded by COMT and MAO into products that are excreted in the urine.
I'll make an example out drugs that are MAO inhibitors.  The enzyme MAO participates in the degradation of dopamine, NE, and Epi.  MAO-A inhibitors are non-selective and used for depression/anxiety because their inhibition will increase levels of dopamine and NE (this might help show that there is no reverse reaction, because we don't see an increase in tyrosine).  MAO-B inhibitors are dopamine specific, and therefore used in parkinsons which is a disease of low dopamine.
Hope this helps!


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how can we identify the novel protein amino acid sequence and function?
if there is a novel protein, how would you know the amino acid sequence and  how would you determine the number of subunits and the function of that protein?
Specifically what molecular techniques we can use to identify the novel protein?
Basically, this is a question asked during a biochemistry interview? It will be helpful, if someone just clarify it

What do you know about the protein?

This is very broad and sounds like a homework question. In any case you should show what attempts you have made to find an answer yourself.


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Can Serous inflammation on pleura pulmonalis cause dry cough and runny nouse?
I am interested in the mechanism between the dry cough and runny nose (serous inflammation) here.
I started to think how Acute respiratory viral infection is causing the dry cough.
The serous membrane, pleura pulmonalis, connects diaphragma to pars basalis pulmonalis.
It can be the source of the serous inflammatory response spreading to the nose probably.
There must be some source of inflammatory responses such that reflex arches can use them fast, thinking physically.
Assume medication Montelukast (stop asthmatic symptoms), codeine (to stop irritated dry cough) Flixotide (with Montelukast).
Assume that there is a diaphragm press on pars basalis pulmonalis.
Assume you breath mostly by abdomen 15 minutes in the supine position.
Assume opposite-astonic person in thorax.
You then feel that you exhale too much - the serous membrane pushing on pars basalis pulmonalis - serous inflammatory response in pleura pulmanalis.
The breathing process moves thoracic muscles and thoracic cavity gets shortly extended only little.
Negative tensor on lungs i.e. the volume of the lungs is getting smaller.
Consequently, a cough reflex arch and sympaticus start a deep dry cough to protect lungs.
Characteristics of the pathway against Acute respiratory viral infection

serous inflammation on pleura pulmonalis
serous membrane pleura pulmonalis presses on pars basalis pulmonalis
negative tensor on lungs
cough reflex arch and sympaticus
dry cough
positive gradient on the pleura spreads inflammatory response through the surrounding lymphatic system is sensed as dry in larynx
negative gradient is sensed on the nasal mucosa membranes as serous inflammation (runny nose)

Can the serous inflammation of plera pulmonalis cause a deep dry cough and runny nose?
The cause of this inflammatory response can then be Acute viral respiratory infection in some part of the lungs.

If serous inflammation produces a large amount of serous fluid this leads to lung compression and limitation of respiratory movement. This, as you said produces dry cough by means of reflex arch.
However lung compression leads to alveolar collapse or atelectasis through pleural effusion. After atelectasis, pneumonia can develop quickly as a complication.
And nasal congestion is a symptom of pneumonia. Also if pneumonia develops, the cough, initially dry and reflex, will turn to cough with mucus expectoration.
Cough stimulates nasal congestion when it brings up mucus from the lungs and extends the alveolar inflammation up to the nose by taking and concentrating all the bacteria in the upper airway (pharynx and larynx bacteria gets in the nasal sinuses) - and in case of bacterial pneumonia mucus also contains the etiologic agent of that pneumonia (so not only from the upper airway).

Thank you for your clear and logical answer! I think the atelectasis which I just described above is caused due to lack of movement in the supine position. Change of position seems to be its best way of prevention. That is a logical. Medically inhibited, cough can start again by atelectasis. Atelectasis is a respond to the congestion in the lungs. Atelectasis seems to be tied to the reflex arch because Codeine blocks the cough center.

@Masi Yes, change of position and deep breathing are the best ways to prevent atelectasis (and also treat atelectasis without airway blockage).

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What is the cause of dry cough?
I first thought this question in the case of

the cause of dry throat after 3-day recovery of dry cough?

but then I realised that the cause of dry cough can be a general thing.
Assume the person had three days recovery of dry cough under Montelukast and codeine (tablet).
He visited gym with little cardiotraining just after the catarrhal inflammation ended (no yellow mucose from throat during mornings anymore.
Just after the training, he felt dry throat after very weak coughs (no codeine medication when doing sport).
I am not sure if the dry throat is caused by

atrophy of the membranes in the throat
or dry cough by Acute respiratory viral infection (possibly through reflex arch; cannot be sure this because no codeine medication).

Let's assume that the dry throat is caused by dry cough (although weak) because virus particle can pass easily the scarring of the mucose membrane in the throat.
I think the atrophy of the membranes in the throat are NOT felt as dry.
Dry cough of the infection is felt shortly as dry.
The sympaticus activity clears the mucose membrane from the throat which alleviated the pain and also irritated the scarring.
Acute virus infection stimulates serous inflammation (as described here) which in the scarred tissue is felt once again as catarrhal inflammation.
So I think the cause of dry cough is catarrhal inflammation.
The localisation of the inflammation is essential to determine the type of inflammation, I think.
What is the cause of dry cough?

Cough-variant asthma is a common cause for a non-productive dry cough.  Asthma is not a single condition involving bronchospasm and with associated wheezing - there is a variant that is primarily or only coughing.
There are different inciting factors that bring on symptoms cough-variant asthma.  Most commonly they are exercise-induced, cold-induced, allergy-induced, or quite commonly it happens following a viral respiratory infection (post-viral-URI).  Symptoms can be acute (exercise or cold) lasting minutes, or chronic lasting days-weeks or even indefinitely.
The pathophysiology for each is different.  The latter 2 are inflammatory processes, as you mentioned, each a little different (hypersensitivity versus residual infectious inflammation).  I am a little uncertain about the mechanisms you described, and I am not sure the correct thing to focus on is scarring.  I would focus primarily on the inflammation.  Inflamed mucous membranes are extremely sensitive, reacting to even dry or cold air.
Using a long-term steroid inhaler is a preferred method of handling chronic cough-variant asthma, as it reduces airway inflammation.
There can be other causes of cough such as postnasal drip, chronic rhinitis, sinusitis, or gastroesophageal reflux disease (GERD or heartburn).

How do you differentiate between chronic rhinitis and cough-variant asthma? I think the latter can be a complication of the former. There is no cause such as atrophy of mucose of throat in your list. Assume you use Flixotide. Without washing your mouth after the inhaler, the steroids can cause bleeding from throat. So I think the mucose membrane of throat is vulnerable to atrophy too.

Cough variant asthma has few to no nasal symptoms; chronic rhinitis can have a cough component.  As for atrophy, good point.  I am not certain about that, but it sounds solid.  Inhalers are things like what's listed here: http://www.webmd.com/asthma/guide/asthma-control-with-anti-inflammatory-drugs  (these arebrand names like QVar, not chemical/generic names like beclamethasone btw - look them up.)

UpToDate and AccessMedicine are great resources for human physio/pathophys if you are connected with a university.  If your univ doesn't have it, UTD is IMHO worth its weight in gold for mechanism of action/pathology, differential diagnoses, treatment, and prognoses. Medscape is also excellent too, which is probably cheaper.  WebMD is not supported by a university and is supported by ads; its reliability for accuracy and unbiased info is questionable.

I should add that UTD and Medscape are what many many medical professionals (from med students to residents to practicing physicians, as well as PA and NP and probably RN students as well) use for a source of peer-reviewed best-practice guidelines in addition to journals and digests from one's field (like AAFP etc).

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Why/How do Cyanobacteria Produce Toxins?
I've been doing some research on the versatility of nitrogen-fixing cyanobacteria, particularly of the genus Anabaena, and I often run into safety hazards and have to add extra steps to my procedures because of the toxins produced by the genus. After doing some reading, I've found that most cyanobacteria produce toxins (collectively dubbed "cyanotoxins"). The wide variety of different structures and mechanisms of the toxins across multiple genera is astounding, especially because some of them are carcinogens, which would logically affect the host unless a mechanism to prevent this had evolved. This tells me that a lot of evolutionary "effort" must have been put into the evolution of toxin production in cyanobacteria. Originally, I just thought that the toxins were a natural part of their metabolism that evolved normally because these compounds didn't affect them in the same way as they did us. Now that I see the Huge, variable trend throughout the class, I have begun to think otherwise. My questions are as follows:

What is the evolutionary basis for the production of cyanotoxins by cyanobacteria
Are the cyanotoxins a necessary part of the bacteria's metabolism, or can they be eliminated by way of genetic engineering without directly affecting the success of the organism?
How do cyanobacteria cope with the constant exposure to native carcinogens?

These questions are only the major ones that I have, so any extra information is greatly appreciated

This available paper has some ideas,
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3736421/
Search terms cyanotoxin and evolutionary give at least two more promising papers.
https://www.biorxiv.org/content/10.1101/615542v1.full
says:
i) photoprotection due to absorption of harmful ultra-violet radiation; (ii) facilitating the acquisition or more efficient use of available but limiting resources; (iii) impeding growth or resource use of competitors such as green algae or other cyanobacteria; and (iv) limiting predation by inducing toxicity in organisms predating on cyanobacteria. While the role of cyanobacterial metabolites in photoprotection, resource monopolization, and habitat dominance has been demonstrated experimentally, hypotheses regarding the anti-predation role are not entirely consistent


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Exact average molecular weight of a dsDNA basepair
I am trying to calculate the exact weight of a given dsDNA.
On the Internet and the literature, different values for the av. molecular weight of one basepair are given :

660 g/mol (probably wrong),
other sources say 617.96 g/mol
Thermofisher gives 607.4 g/mol
(https://www.thermofisher.com/de/de/home/references/ambion-tech-support/rna-tools-and-calculators/dna-and-rna-molecular-weights-and-conversions.html)

I tried to calculate the average weight using following molecular weights:

molecule
.
weight

2'-Deoxyadenosin- 5'-monophosphate
dAMP
331,22 g/mol

2'-Deoxycytidin- 5'-monophosphate
dCMP
307,197 g/mol

2'-Deoxyguanosine 5'-monophosphate
dGMP
347.2212 g/mol

2'-Deoxythymidine-5'-monophosphate
dTMP
321.2005 g/mol

water
H2O
18,01528 g/mol

adding the matching nucleoside monophosphates together and subtracting one water for each peptide-bond condensation (one on the sense; one on the antisense side);
I get following formula for the average dsDNA basepair weight:
$$
avg.BP.weight = \frac {(dAMP+dTMP-\ce{2H2O})+(dGMP+dCMP-\ce{2H2O})}  {2}
$$
resulting in :
$$
\frac {(331,22+321.2005-36,03056)+(347.2212+307,197 -36,03056)}  {2} = 617.3892 \frac{g}{mol}
$$
which is very close but still 0.57081 short off the "best" literature value.
What am I missing?; Im trying to get this calculation as exact as possible.
Maybe i didn't consider some hydrogen or protons in bonds?
Thank you in advance!

The different protonations forms are considered in the averaged Mw.
Removing two H2O is the step that makes your average different than the traditional 650Da per base pair. But you must remember that the last base pair in the sequence will have it's OH group so you need to add 17.008 gr/mol * 2 = 34.016 gr/mol.
The effect of this changes with the length of your sequence, here is a graph showing it.

Blue line is your calculation and red line is the one from literature.
Literature one is achieved around 60bp (I calculated Mw(63bps) = 617.93) and yours at 10^6.6 (Mw(10^6.6) = 617.3892085)
Why you need this calculation to be so exact? Knowing the length of you sequence and region can help. Remember that some regions are richer in one type of nucleotides (CpG islands, hairpin coding sites)

Thank you for the precise answer and the great plot! I did this out of pure curiosity - I recognized that there where some inconsistencies (more generalizations) in the literature data so i tried to do my own calculations. I wrote a script to calculate the weight of an input sequence. My next goal would be to try to add the molecular weight of histones, linkerDNA , chaperones and the centromer, to calculate the total theoretical weight of the chromatin during metaphase. However i have now idea how to include variables like methylation. If you have further advice i would be truly thankful. :)

@user12256545 I try to be as doubtful as I can while modeling. If X happens in N stage how do I know it still happens in N+1 or K stage (everything in biology makes sense in retrospect but rarely in advance). Send me a message if you have code you'd like me to look at


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How Do Pressure and Temperature affect arthritis?
Here, in Houston Texas we were hit by a cold front tonight and I remembered the old saying that I'm sure you've all heard "My joints hurt, must be a storm (or change in weather) coming in". It piqued my curiosity as I wasn't sure if it was due to the temperature itself or the atmospheric pressure difference causing the flare up of pain. I looked into it and, as far as I can tell from what I've read, scientists are unable to agree on what exactly causes the flareup of pain as the evidence from the myriad of studies done on the subject are inconclusive and different in each situation. The evidence being that both temperature and atmospheric pressure changes have shown to affect flare ups in joint pain due to arthritis as well as the opposite. It almost seems like all of it can affect arthritis pain, as well as none of it. However, I began to think "What if it has nothing to do with how much the atmospheric pressure or temperature changed, or in which direction they changed? What if it's simply due to change itself?"
My source: https://www.amjmed.com/article/S0002-9343%2806%2901026-6/pdf
The article expresses that temperature drops cause pain. However, it also states that the reasons for why this occurs is unknown. I also believe temperature raises may cause this as well as I myself, along with others I've talked to with arthritis, have felt that arthritic ache in both increases and decreases of temperature. I am posting this question because I have learned that temperature is unrelated to atmospheric pressurization as both high and low temperature air may have either high or low pressures.
I'm no expert in any of the scientific fields that are involved in this question. So, what do you as the community of StackExchange Biology think?
Bonus source from SE Physics for those of you unfamiliar with temperature and atmospheric pressure: https://physics.stackexchange.com/questions/326315/does-hot-air-have-high-pressure-and-does-compreesed-air-have-high-pressure/471775?newreg=ef5c317e3a114a3d8e4bb5fb680c477e

The first two sentences are completely unrelated to my question and only act as an, hopefully interesting, introduction into how I began to ponder my question. However, this was closed as it was deemed a personal medical question when it isn't. I am in no way asking for advice or help in my situation and just want to know how pressure and temperature affect arthritis in general. I believe my question to have been unfairly closed, or even not read fully before being closed.

I edited the question further. I would advise you to add your prior research and additional sources of the connection between arthritis  pain and weather conditions. As a sufferer from it myself, I've noticed cold has a pronounced effect, and my martial ars teacher, quite proficient in the physique of man, affirmed that notion. However, I have no knowledge about the topic whatsoever. Please add sources  and background info and perhaps the question can be re-opened.  I really like this topic btw.

Lastly, feel free to roll back my edits; but I'd advise to not put the personal background information back in, as it may trigger people thinking it's self-help. The Medical Sciences SE site may be helpful as well. We can migrate it for you (please don't cross-post).

I rolled back, but edited the post to be more-so in accordance to your advice on how to pose a question. I returned my internal ponderings as they are the questions of the post and I believe they are integral to the topic itself. Thank you for your time and help.

If you believe that the SE site is a better location for this post, then by all means move it. I'm am a new user (this being my first question) so I was unsure where exactly to post it.

Meant The Medical Scientists SE. Also, I included my source and what I was able to conclude from said source.


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What is the representation for Sulfur in organic matter?
We often represent organic matter with the following equation:
$$
(CH_2O)_x(NH_3)_y(H_3PO_4)_z \tag{0}
$$
For example, the organic matter with the Redfield ratio has the form of $(CH_2O)_{106}(NH_3)_{16}(H_3PO_4)_1$.
But if we want to put inside the element Sulfur ($S$), which form below should we use?
$(CH_2O)_x(NH_3)_y(H_3PO_4)_z(H_2S)_m \tag{1}$
$(CH_2O)_x(NH_3)_y(H_3PO_4)_z(S)_m \tag{2}$
$(CH_2O)_x(NH_3)_y(H_3PO_4)_z(SO_4)_m \tag{3}$.
These different forms assume the different covalency of sulphur (-2, 0, or +6). Which form above should we take to describe the composition of organic matter with S?
I guess maybe Eq.(2) $(CH_2O)_x(NH_3)_y(H_3PO_4)_z(S)_m$? Because in this way, sulfur has the covalency of zero, which is the same as carbon (0).
I asked this question because I found many papers use the Eq.0 to build the mineralization of organic matter (e.g., O2 oxidation, [R1] in Table 2 here. See Fig.1 below). The amount of O2 depends on the assumption that carbon in OM has the covelency of zero (then, 1 mole of C corresponds to 1 mole of O2).
Since I didn't find a paper that put S into the OM compositon to balance the similar equation like [R1] in Fig.1, I am curious about which covalency value is "more common" for such an equation (because Sulfur's covalency can affect the amount of O2 needed).

Welcome to Biology.SE! Please provide a more focused question. Those chemical formulae are gross simplifications of the species that exist in biological compounds. For example, carbon and nitrogen commonly participate in both single and double bonds with themselves and other elements (also in aromatic contexts), and can also form triple bonds in biological molecules. Similarly sulfur can occur in several oxidation states. This makes your question in its current form impossible to answer in any way that I can see as meaningful and so I'm going to vote to close as "Needs details or clarity". ...

(cont) Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. Thanks!

I have found that when learning about a new area starting with a relatively accessible and reliable source like Khan Academy is very helpful. Wikipedia is also generally a good starting point and you can then check their references. Online platforms called MOOCs offer free (or very low cost) courses on a wide variety of subjects — two I am familiar with are Coursera and edX. Finally, textbooks with a good level of detail are also freely available online e.g. from NCBI.

@tyersome Thanks for your advice! I have edited my question to make it more clear. Yes for example carbon in the organic matter has several oxidation states, but when modelling it, we often assume its oxidation state is 0. Under this assumption, we can balance the equation. So I'm curious about if there is a common "assumption" for sulfur.


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Why is muscle force more dependent on cross-sectional area than on fiber length?
I was looking up why smaller animals are proportionally stronger than larger animals. The answer that comes back everytime is that muscle force depends on the number of muscle fibers, which is proportional to the cross-sectional area of the muscle.
However, I don't understand why muscle force wouldn't depend on fiber length.
I'm not a native english speaker, so I'll try my best to articulate my reasoning in the most concise way possible.

Force is exerted by the myosin motors. Force is therefore proportional to the number of myosin motors.
The number of myosin motors is proportional to the fiber length.
The number of myosin filaments is proportional to the cross-sectional area.
Then, muscle force is proportional to muscle volume, and therefore to muscle mass.

What am I missing ? Why is muscle fiber length not that important to muscle force ?
Thank you in advance for your help.

Here is a thought experiment that might help. Consider a single muscle fiber as being like a rope. Granted, a rope won't shorten on its own, but if you think of an isometric muscle contraction, then it's closer to what is happening when a single fiber contracts.
Now think about two situations:

You double the length of the rope. Does the total force that the rope can hold get larger, smaller, or stay basically the same?
You halve the length of the rope by doubling it up (so two ropes instead of one). Does the force that the rope can hold get larger, smaller, or stay basically the same.

So lining up more fibers in series is like making a longer and longer rope. It's still basically as strong (or weak) as a single rope. But when you bundle more ropes, increasing the cross-sectional area, the overall force that they can hold increases.
I'm not sure why a thought experiment needs citations, but here you go:

The canonical source for discussion of muscle fiber architecture is Gans C. 1982. Fiber architecture and muscle function. Exerc Sport Sci Rev 10:160–207.

I see... but I was thinking of the myosin motors kinda like people in a game of tug of war. If you increase the number of people, don't you increase the force ?

To expand on the rope analogy, is it correct to think of the protein strands as ropes which would be glued together in some places (similar to how myosin binds the actin strand) ? If so, then wouldn't it be correct to think that glueing the ropes in several places is more robust than glueing the ropes in only one spot ? I'm sorry If I'm missing something obvious about how muscle works... I feel like my brain isn't wired correctly today

@Gabel Luc, I was a part of game of tug war without a rope as a kid. The kids did hold each other hands as a substitute. They also decided to put the older stronger kids at the ends so they can better pull. Stupid. I was in the middle. It was painful. Imagine seven people puling your one hand and eight puling on your other hand. There was no question of me contributing, I was just holding myself together. My joints felt like giving in any second and I did let go the hand very fast. Ever since I understand that the force the chain of people can exert is only what the weakest link can withstand.

There is a distinction to be made between the tensile strength of the muscle, that is, how much force can be applied to it before it breaks, and the strength the muscle is capable of applying to move something. In an actual game of tug-of-war, the rope is very strong, and what is being contested is the motive strength of the two teams. But the motive strength of a muscle is obviously no greater than its tensile strength, which as a matter of materials science is measured on a per-area basis. There may be more to it than this, but I think this is at least part of the answer.
To extend the tug-of-war example, if you had unlimited staffing to pull stones up the ramp to the pyramid, you would add pullers to each rope until you were afraid to add any more because the rope might break. So the pulling strength would ultimately depend on the number of ropes.


text:
Plant with purple/white/yellow flower
This plant popped up as a volunteer in a flower box in Winnipeg, Manitoba.
It is roughly 6-inches tall by 6-inches wide.
What is it?

The plant is Convolvulus tricolor, the dwarf morning-glory. It belongs to the family Convolvulaceae.Blue, white, red and pink flowering cultivars of this plant are available$^1$. It is a annual/perennial growing to 0.3 m (1ft) by 0.2 m (0ft 8in) at a medium rate$^2$.

Image source
References:

Plantasm

PFAF database


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Is it possible to force Sars-Cov-2 virus to mutate?
The title may definitely be a stupid question since I have no background in biology. I would like to know if the coronaviruses or any other can be manipulated artificially so that they stop spreading among humans and target other animals, for example cats. I like cats but they can spare one of their lives for humanity.
¿Is it possible?
Furthermore, is it possible to create a surface made of articifial cell membranes which is better than human cells for the viruses to stick? As I understand the viruses have no life, which means they are like machines, they have no aim in "life" other than stick. Am I correct?

Have you heard this suggested as a solution? How would you plan to collect all the viruses in all the different people who are infected?

I haven't heard or read anything about this. So your point is each virus is different genetically, correct?

My main point is that you'd have to introduce your mutation in every viral particle, otherwise at best what you've done is create a new virus that infects cats, while not having done anything to the 99.999999999% of virus that you haven't touched.

This idea is conceptually similar to creation of a live attenuated vaccine, where a virus is passaged through some other host (like lab animals or cultured cells). Mutations benefiting infection of the new host accumulate. Hopefully, after enough passages, it's no longer infectious to humans, but still similar enough to help an innoculated human develop immunity to the infectious form. https://en.wikipedia.org/wiki/Attenuated_vaccine


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Upon drinking water for the first time in a long time, why do I sweat?
If I don't drink water for a long period of time (e.g. 10 hours), as during fasting, and then I break the fast by drinking water, I start sweating. Why is this?

During the time when you are not drinking water, you still lose some water to sweating and urine. Especially in hot climates, sweating is an important function of the body to maintain the body temperature in the desired range. If this water is not replaced, the body gets dehydrated. This induces a reaction which reduces the activity of the "body thermostat", in order to tolerate a higher body temperature without excessive sweating. This, in turn, helps to maintain the fluid balance of the body.
When you start drinking again after this the dehydration period, the body starts sweating to regulate the body temperature again, since the loss of water is no longer critical. For a detailed discussion, including further references, please see:

The effect of water temperature and voluntary drinking on the post
rehydration sweating


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Available Protein sequence alignment dataset and HMM model
I am new to biology and I find my algorithm may be used in the Protein sequence alignment, since it is a henced HMM model. I find that people use HMM to generate noisy copies of the consensus sequence of different lengths. There is a figure show the process:

It seems Professor Richard Durbin may release some dataset. But how can I find available datasets? I lost in the bio-vocabulary and fail to find datasets. Also I am wondering whether or not this topic is very minor in this community?
Update:
Since I may abuse the vocabulary, it may be better to post the original word I read.

It may be helpful to post this on bioinformatics.stackexchange.com, which is specifically focused towards bioinformatics questions such as this. Additionally, when you say "dataset", what do you mean? Are you talking about sequence alignments, HMM parameterizations, profile HMMs, or consensus sequences? I would guess sequence alignments, but those are extremely common and fairly trivial to generate so it seems unlikely.

@MaximilianPress Thanks for your comment. Maybe it is a good place to post it. I add more details. When it comes to the dataset, I mean we need some data to train the HMM model and learn the model parameter. I guess the dataset is some real sequence instead of generated artificially.

DNA and protein sequences (both are reasonable to use in HMMs) are available at a variety of sources, such as EMBL, NCBI, and others.
To input them into a model such as an HMM which draws on comparisons between different sequences, you will most likely need to produce a sequence alignment, which is a data format in which the sequences are processed into a matrix (generally not delimited in any way but rather where each column is a single string character) where columns or positions of the matrix are considered to occupy the same position in the sequence. These positions can be "gaps", represented usually by "-". The diagram at the top of the Durbin figure is such an alignment.
There are many many many tools for aligning sequences, both protein and DNA (DNA is a "nucleotide"; RNA is also a "nucleotide" sequence, but DNA is much more common to align in most applications).
Some of the common tools for generating multiple sequence alignments are ClustalO and MAFFT. Notably, you are not as interested (I think) in tools such as BLAST which are mostly about searching single sequences against databases using local alignment, rather than for generating multiple sequence alignments for input to other programs.
I believe that with some searching you can find existing multiple sequence alignment databases. People do not usually save them and put them in databases or repositories because usually which data you use is very specific to the problem that you are interested in, and they are quite simple to generate. Most of the databases are likely to be quite old for this reason; I found one such old database (described here) with a bit of googling.


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Sperm formation - Frequent Ejaculations
I have visited various authenticated websites and other materials and learnt that a complete sperm development takes approximately 64 days.
My doubts :

If sperm truly takes 64 days to develop, how can a man ejaculate multiple times (e.g., 4-5) in a day and still have sperm come out each time? Why don't all the sperm come out at once? And each time he ejaculates, the sperm are complete (i.e., the "head" and "tail" portions are always included), right?
Does frequent ejaculation, then, reduce the sperm count of each subsequent ejaculation? If so, do the sperms remain depleted for extended periods (i.e., 64 days), or are they replaced more regularly? At what rate are they replaced?

Comments are not for extended discussion; this conversation has been moved to chat.

The arithmetic of human sperm
A young, healthy man produces about 1000 sperms every second, which comes to about 90 million per day [1]. These sperms are stored in the epididymis and ductus deferens until ejaculation. With several days of storage, the number can easily become big enough to allow for multiple ejaculations on the same day.
The maturation period of 64 days does not matter here, because sperms form and mature asynchronously [1]. While one spermatogonium is on day 1 of its life, another is on day 2, another on day 3 and so on. Only those sperms that are mature are released from the testes (NOT directly in semen, but into the epididymis for storage).
Does semen normally contain sperm with abnormal morphology?
Yes. Even men in whom 96% of the ejaculated sperms have abnormal morphology can successfully conceive [2].
What happens on ejaculating repeatedly?
This has already been assessed in several studies [3–5]. Overall, the results have been that with repeated ejaculation in quick succession,

Semen volume decreases.
Sperm count decreases (pointing to sperm depletion) but not to zero.
The percentage of sperms with abnormal morphology remains unchanged.

Hope that answers your questions.
References

Mesiano S, Jones EE. The male reproductive system. In: Boron WF, Boulpaep EF, editors. Medical physiology. 3rd ed. Philadelphia: Elsevier; c2017. p 1092–1107.
Cooper TG, Noonan E, von Eckardstein S, et al. World Health Organization reference values for human semen characteristics. Human Reproduction Update. 2010 May–Jun;16(3):231–45. doi: 10.1093/humupd/dmp048
Oldereid NB, Gordeladze JO, Kirkhus B, Purvis K. Human sperm characteristics during frequent ejaculation. J Reprod Fertil. 1984 May;71(1):135–140. doi: 10.1530/jrf.0.0710135
Zvĕrina J, Pondĕlícková J. Changes in seminal parameters of ejaculates after repeated ejaculation. Andrologia. 1988 Jan–Feb;20(1):52–4. doi: 10.1111/j.1439-0272.1988.tb02363.x
Mayorga-Torres JM, Agarwal A, Roychoudhury S, et al. Can a short term of repeated ejaculations affect seminal parameters? J Reprod Infertil. 2016 Jul-Sep;17(3):177-83. http://www.jri.ir/article/674

Thank you for the answer!

Spermatogenesis begins in the seminiferous tubules.  In this process, sperm are formed from the processes of mitosis and meiosis from germline cells called spermatagonia.  Given continuous signaling from Sertoli cells, although the meiosis cycling takes about 64 days, all cell lineages are on their own schedule depending on unique signaling pathways they synergize.  Thus, there is no problem ejaculating 80-300 million sperm per ejaculation, several times per day, if the proper levels of testosterone and temperature are present to regulate the process.
This may seem like a lot of cells, but note one sperm is about 85000 times smaller than an oocyte (cell in an ovary).  A certain fraction of spermatogonium is always reserved no matter how much a healthy male ejaculates, thanks to Sertoli cell signaling.  Leydig cells that regulate spermatogenesis through testosterone production are also critical for spermatid maturation from the seminiferous valves to the epididymis. Further understanding the signaling pathways and genetic traits allowing the spermatogonia to be retained and replenished to form semen could have huge implications for regenerative medicine from a genetic engineering stand-point (aside from reproductive physiology).
Information pertaining to the rate of sperm production is highly dependent on individualized omic data. The 64-day cycle you mention is analogous to the circadian rhythm which repeats every 24 hours.  With a super healthy metabolism because you ejaculate three times in one day does not mean it will be impossible to ejaculate once or twice the next day, like if you run thrice in one day it doesn't mean you can't run twice again the next day.
Thanks for the interesting question!

Thank you for the answer. Could you also help by answering the questions of "fully developed sperm or the incomplete sperm during the ejaculations"


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What is the function of ocreae on a mile-a-minute vine?
There is a plant called the "mile-a-minute" vine.  (See link below)
https://mam.uconn.edu/species-identification/#trait3
I noticed the plant has ocreae surrounding each branch point but I cannot find any description about the function of ocreae online.
Does anyone have any idea what the function of the ocreae are on this vine?  The only thing I could think of is that it helps collect water and distribute it down the vine towards the root assuming that the plants' roots are below the ocreae.

From an article on Wikipedia (linked to from Persicaria perfoliata).

An ochrea (Latin ocrea, greave or protective legging), also spelled ocrea, is a plant structure formed of stipules fused into a sheath surrounding the stem, and is typically found in the Polygonaceae.

There are no citations, but if correct then the name suggests it's for protection.

I'm going to take the unusual route of explaining my down vote because I realize that, as a new user trying to be helpful, it seems unkind not to. It's a mistake to think that taxonomic nomenclature does anything more than label taxonomic groups. At its best, it does explain function, but often it is simply based on the appearance of a thing. The ochrea resembles what was a familiar enough object: a greave, or today, a shinguard. So the person who named this plant basically named it "like a peach with a greave". The heck if I know why it's like a peach (or a red shank, the other possibility)

... As stated, I gave this a DV, and did so because it's wrong. I apologize for not explaining the DV. I hope you see this, and also hope to express that I appreciate your willingness to help (so please, do so again!), and again, I'm sorry. (A well known example of silly nomenclature is Pieza rhea (2002), meant to sound like "pizzaria", Pieza pi, and Pieza kake. See what I mean? Nomenclature explains when it's well done, but it's all over the place.


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Why do earthworms have so little colour?
Earthworms (or at least the ones that I have seen) tend to be pinkish, but with the front dorsal region being a camoflagued brown. Why is this the case, rather than the entire body or back being pigmented. I couldn't find any reference to the reasons behind earthworm colouration

Here is a picture from the wikipedia page on earthworms, showing the concentrated pigmentation

If they spend most of their time under the ground where nothing can see them, then what use is pigmentation?

@jamesqf But when it is raining they move to the surface where they are visible. And rains are not that rare. And besides that, why pink, of course?

@rus9384: Re "rains are not that rare", that depends on where you live, but even in a rainy place, the time spent above ground (and during the day) is a very small fraction of an earthworm's life, thus any color selection pressure would be small. (Besides, a lot of dirt IS more-or-less earthworm color :-))  As for pink, flesh is generally pinkish, especially if your blood contains hemoglobin, as that of earthworms does: https://en.wikipedia.org/wiki/Earthworm#Circulatory_system

@jamesqf But why would the pigment of an earthworm be so concentrated on the back, rather than more spread out?

@Ichthys King: Is it?  I am no expert on earthworms, beyond those I run across while gardening &c, but they seem fairly uniformly colored to me.

@jamesqf I have definitely seen earthworms with completely brown backs and pale pink bellies and rear-ends

When creatures live in caves and darkness, they have negative selection against skin color, so they develop albinism.
Here's a quote:
Epidermis pigmentation normally protects organisms from the harmful effects of UV irradiation, reduces the extent of predation through camouflage and mimicry, and facilitates sexual reproduction by mediating colorful behavioral displays (Protas and Patel 2008).
Healthy soil has easily 100-200 worms per square meter of soil, (as many as 1000 even), and we only see 1% of that, so it suggests they spend nearly all the time underground.
When it rains they migrate some distance.

The reason appears to be the light cells of Hess, which are light-sensitive cells distributed over the back of earthworms, being more concentrated towards the head

This doesn't seem to answer the question which is "Why?" i.e. for what (adaptive) reason. The light cells of Hess are not a reason so much as a small part of a mechanism.


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Are Flippase Recognition Target sites read through during transcription?
I believe it is quite straight forward, but if i have a FRT site following the last exon of a gene (with the stop codon removed), would the transcription factors read through the FRT site and transcribe whatever follows it, or would transcription be halted?

Welcome to SE Biology. One general piece of advice in communication is always to define acronyms and avoid using them in titles of questions unless they are very well known (DNA etc.). This will increase the likelihood of people looking at and understanding your question and answering it. You can edit your question. Perhaps shorten the title removing what comes after "or" (that can go in the body) and putting in the question mark.

@David thank you! And appreciate the advice, made the changes as well!


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Are sizes of potatoes normally distributed?
I'm currently researching the variability of sizes of potatoes when all of the potatoes in question have been harvested from a single field. One question keeps coming up in my statistical analyses: Under normal circumstances, are the sizes of potatoes - within a single field - normally distributed? (Please feel free to define the weasel words "normal circumstances" in the most helpful way you can imagine.)
Human height is often given as one of those classic examples of a normally distributed phenomenon. The little that I know about plant biology suggests that the central limit theorem applies just as much to potatoes as to the human body: the lengths of potato tubers and the lengths of human bones should have similarly-shaped distributions. But is that correct?

A bit of context to my original question: what I'm trying to do is to take the mean and standard deviation of my data and then, using the 68-95-99 rule, construct a series of confidence intervals, which I can then test or refine by looking at other data sets. Obviously, no real data set is going to conform perfectly to a model; I just need to know that, in principle, potato sizes are normally distributed enough that my method for drawing up confidence intervals isn't hopelessly misguided.

There seems to be some misunderstanding of the central limit theorem (CLT). CLT emphatically does NOT say that all variables in nature are normally distributed. Rather, it says that the sample means are normally distributed (approximately) when sample size is large.

The only way to find out whether the sizes of potatoes or human beings are normally distributed is empirical measurement.

@Adhish Forgive me if I didn't express myself as clearly as I might have done. I did not claim that, because of the CLT, all natural phenomena are normally distributed; I merely suggested that, because sizes are normally distributed in humans, it is plausible that they might also be normally distributed in potatoes.

@Adhish 'The only way to find out whether the sizes of potatoes or human beings are normally distributed is empirical measurement.' I was hoping that someone would point me to some empirical research on the topic. That's why I asked the question.

If you have data from your potatoes of one field, can't you answer empirically what the size distribution is from your own data?

@BryanKrause I have to emphasise that I'm not a professional statistician, but the data from the one field I've had a chance to examine properly do seem to be normally distributed: they're clustered symmetrically around the mean. But it's not a classic bell curve, and I'm anxious about seeing only what I want to see. If someone could point me to a paper that said something like, "Potato sizes generally follow X distribution", that would save me a lot of weeping and gnashing of teeth.

@Adhish as far as I know, since height is the average of many QTLs it is normally distributed since it becomes a distribution of the means of these genes. I use this alot so I'd like to be corrected on this if I'm wrong

@Hachiloni That seems to be a valid approach, but I'd still say it depends on the trait in question. What is valid for height may not be valid for other quantitative traits. (See https://www.genetics.org/content/204/3/1281 for a discussion on non-normal quantitative traits.) I guess a lot would also depend on how much of a deviation from normality one is willing to tolerate.

Not an answer, but you might want to reconsider what a normally distributed variable means and why you want to know it, since height seems to deviate significantly https://stats.stackexchange.com/questions/360254/why-does-the-distribution-of-height-follow-normal-distribution. Also https://stats.stackexchange.com/questions/2492/is-normality-testing-essentially-useless

It is important to keep in mind that the normal distribution is a model. George Box had something so say about models. You should also carefully consider why you care about the distribution of potato size. You might be looking at the wrong thing here (e.g., in regression analysis you'd care about the conditional distribution only) or be able to remove this assumption (non-parametric statistics comes to mind).

Thank you to everyone for contributing your brain power to this surprisingly tricky question. I've just added some context to my original post which might simplify things a bit.

If your sample is not too small, you could use bootstrap to derive CIs for the mean, no distribution assumption needed.

Empirical observation (growing potatos in my garden) suggests not.  From any mature plant (that is, when the tops die back) I will get several large ones about the size you'd find in a store, several smaller ones that might go as "baby" potatos, and a bunch that are marble to pea size.  Presumably commercial growers sort out the small ones before sending the rest to market.

@TomHosker if you are only trying to calculate CI for the mean of the potato size in the field AND you have enough samples (usually 30) you can assume the mean size of the potato is distributed normally. There are methods to find the best distribution fitting your sample and than you can calculate CI.

According to Evaluation of the Effect of Density on Potato Yield and Tuber Size Distribution potato tuber size was estimated using a normal distribution but they are not normally distributed
They found that a Weibull distribution with specific parameters estimated better than a normal distribution.
In fact you should not expect a normal distribution because there are no potatoes of negative size  As such you expect a gamma distribution.  The Weibull distribution is in the same family of distributions.
But in many cases the normal distribution is used since the probability of a negative number is negligigble.
Does this mean that potato sizes are still the result of many factors? It would seem so

The link to "this article" for me yields "access denied".  Perhaps a bit more explicit citation would be good.

StackExchange answers should stand on their own; other references are great and are even required in many cases here at Biology.SE, but people need to be able to read your answer and understand it by itself, too.

@BryanKrause could you elaborate? I don't know where to elaborate more. One good article states they are not normally distributed and cites others that say the smae. I edited for the name of the article per mgkrebbs comment

i added more explanatory text with a reference.

I'm on the cusp of accepting this answer. I've just added some context - hopefully helpful - to the end of my question. If you could make a brief comment on that, then I'll give you the green tick.

As a side note: I'm not convinced by your claim that 'you should not expect a normal distribution because there are no potatoes of negative size'. There are plenty of normally distributed phenomena which never take negative values. Am I misunderstanding something here?

If you are looking for the CI of the mean and you sample n >30 you can assume the mean is normally distributed per CLT which is different from the distribution of the potatoes. I added another link explaining why the normal distribution is used for only positive vallues. In short, the probability of a negative is so low that it is ignored