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How much does capillary action contribute to blood flow to the human brain?
The BBC News Universal Wonders short video Why water is one of the weirdest things in the universe says after 01:50:

Water molecules can float upwards against the force of gravity. That’s because they love to stick to each other. They’re so good at it that they can actually pull each other up through tiny channels, such as the tiny blood vessels in your body. That’s how oxygen and nutrients reach the edges of your brain.
The same process, called capillary action, allows plants to move water from deep below the ground to nourish the leaves and branches that grow in the sunshine.

We learn about the importance of capillary action in water transport in plants, but I'd never heard that it was important for blood transport in Humans.
Question: How much does capillary action contribute to maintaining blood flow to the human brain? Is it a small effect compared to the difference between arterial and venous blood pressures, is it a substantial contributor?

None. I have no idea what that video is talking about.
Capillary action of water happens when you have a thin tube and water likes to stick to the "edges." Blood vessels are already full of water, there is nothing for them to capillary up against: there is already water there, so there is no surface tension (there is no surface at all). Blood flow through capillaries is caused by the heart which creates a pressure gradient between the arterial and venous circulation, in the brain and everywhere else.

Cipolla MJ. The Cerebral Circulation. San Rafael (CA): Morgan & Claypool Life Sciences; 2009. Chapter 2, Anatomy and Ultrastructure. Available from: https://www.ncbi.nlm.nih.gov/books/NBK53086/

Capillaries are very fine vessels that exist everywhere blood is distributed to tissues including the brain, and capillary action is a physical phenomenon of fine spaces that absorb liquids allowing anti-gravity pull of water on top of trees.
Same word, but unrelated objects here. Both come from the same Latin origin meaning hair. Capillary action is not the way capillaries work (blood is pushed in because of pressure).

While "Capillary action is not the way capillaries work (blood is pushed in because of pressure)" sounds like a common-sense statement, can you actually support it somehow? Can you exclude any influence of capillary action in addition to the effect of blood pressure? Good Stack Exchange answers need good supporting links or references. Thanks!

You are welcome. Look up capillary action definition and tell me how it could possibly take place in vessels with varying diameter already filled with blood, having no equivalent of evaporation or other depressurization at the other end you find on a tree leaves besides blood lower pressure. And importantly, there is almost no attraction between the walls and blood. Unless you are talking about a non physiological situation where you dry up a piece of brain and then puts it in a water bed to get it wet, I have no idea how you can mix up those two different concepts in the first place.

It's not my place to tell you how something could possibly happen. This is Stack Exchange and an answer should try to support assertions whenever possible. Rather than tell me to look up something for you, it's more appropriate for you to find something suitable and cite it or quote from it. Concepts and phenomenon are not exclusive, two or more can apply simultaneously with different weights. Thus my question begins: "How much..." If you are certain it is zero, then you should state zero, support that, and let people vote on your assertion.


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Don't understand figures in this citizen-science mosquito ID project
The Citizen-based mosquito monitoring system is a Citizen-Science vector tracking project that involves using any of a wide variety of cell phones to capture "sound bites" (sorry!) of mosquitos. These are collected and analyzed in order to gain some insight into the distribution of different species of mosquitos at different times and locations. Attention is paid to ensure the system works with older model phones that are distributed more widely.
While a positive identification of a single insect form a single recording is not likely this way, over time a statistical analysis is expected to give meaningful information. I believe the idea is that similar sounding species are expected to not be in similar places at similar times so often that it muddles the identification too much. This is citizen-science; imperfection is not a deal-breaker.
I was happy to see that there is a BioRvix paper. In fact, I was surprised to see there is such at thing as BioRvix in the first place!
The principle is illustrated in Figure 5, and some of the argument behind species differentiation is illustrated in Figure 7, and screenshots of both are shown below.
I think there is a lot of information densely packed within the figures, and I'd like to understand more of it. In the second figure below, which is Figure 7 in the paper, what does the color scale and color coding represent?
There seems to be some suggestion of time of day as well, but I don't understand exactly how. What about time of year - that should also play a major role.

Some may recognize Manu Prakash as "Foldscope guy".

Thanks for asking about the interesting study. However, you need to clarify your question a little bit. What exactly are you asking? (please update your question with a bolded well-framed, specific question). Right now I htink it's a little too broad. Also, if you could perhaps modify your post a bit so one doesn't need to go to the paper to answer your question (useful for if the link dies later on). This would include better referencing/labeling your photos and perhaps quoting the chunk of statistical text that is most confusing to you). Thanks

@theforestecologist Thanks for your recommendation, and I see what you mean. I will try to dig in and identify what it is that's making it so difficult to understand, and rewrite. This could take as long as 24 hours - should I delete in the mean time, or leave it as is for that long? I'm happy either way.

Thanks @uhoh. You can just leave this post up and update it as soon as you can. Most likely others will see these comments and will wait for you to edit before answering further.

@theforestecologist I've decided to split off the statistics as a separate question - I need more time to read.

In the second figure –
  What does the color scale and color coding represent?

Each color is an individual mosquito species,
arranged the same from top to bottom on all plots.
Here, on the left, all species are gathered on one plot,
with the y-axis now labeled “Species.”

The sounds of many mosquitoes apparently have statistical profiles
similar to each other,
so the individual plots
demonstrate how additional factors help distinguish species
in some such cases.
In the plot for “Time” (C),
the sun and moon merely accompany the species
whose differing circadian habits they illustrate.
It is only a coincidence
that the daytime species is plotted higher.
Just to complete the picture,
here is how these plots mark statistical profiles.

This is a really helpful answer! I'm going to split off the question about the statistical arguments as a separate, new question (it needs considerable effort on my part to define it more narrowly), and edit this question to limit it to the information in the plots. Thanks!

source: Stack Exchange

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

sort: votes


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How to express total eradication of bacteria (inhibition zone) when placed into a table
I am a grade 9 student studying the inhibition zones of several different essential oils by comparison to Tetracycline to prove there is merit to treatment of bacterial infection (investigation is being conducted evaluating efficacy against S. epidermidis). I am analysing it by measuring the efficacy of 100% essential oil, in addition to MIC and 10x MIC.
One of the essential oils totally eradicated the bacteria. How would I express that in a table?

Please specify in which method bacteria were eradicated.

It would probably help if you included a cell-phone picture of what you mean by "totally eradicated," and something that would not fit that description, for comparison.

The real piece of information that you need to supply is what measurement in what units is in the column in your table that you are worried about. If it is "diameter", as I believe is normal in this sort of semi-quantitative assay, what is your problem? Perhaps you are worried that the reader will not realize that 10cm (or whatever) is the diameter of your petri dish, and the limit of your ability to assay high doses. If this the case, perhaps the solution is not to use cm but % of total diameter, so complete eradication is 100%. (You might even use simple geometry to find % eradication.)

And, of course, there is the question whether you should be putting the results in a table or plotting them as a graph. That might make it obvious that you have reached a saturating dose of your magic potion.

Sorry I haven't been able to  respond, I've been super busy all week with World Scholars Cup... sadly, i dont have access to cell phone images as of now, however I can answer some of the other questions. The bacteria was inoculated onto a petri dish with agar. Then, right after the bacteria was introduced, 3 filter paper discs (that had been soaked in the essential oils) were introduced to the petri dish.

In terms of David's question, the problem i face is that there are multiple discs on each petri dish, meaning that i wouldn't be able to work out a percentage eradication? Correct me if i am wrong.

Then what do you mean by "totally eradicated"?  What did you actually see?  Are you saying (I'm guessing here) that all the bacteria in the dish died off, leaving you unable to tell which disc did it?  In that case, I'd say you should re-do your experiment.  If not, what was it?  (I suppose this difficulty in explaining to us what happened is proof that you do need a better way of explaining it in your paper!  Pity you can't send a picture!  I take it you can't send a sketch either?)

Ok, so by totally eradicated, I meant that there was no visible bacteria on the dish, while on my control dish (no antimicrobials) there was evident bacterial growth. Don't worry anymore, however, as I got a chance to consult with my teacher who provided me with a way of expressing this. Thanks for all the help!

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The effect of low pH on HIV virus
I've read a couple of articles that state that HIV is an enveloped Retrovirus that is so sensitive to the acidity of the environment and it cannot survive or will be inactivated at pH below 7. What exactly happens to the virus when exposed to an acidic environment. Does it denature the GP120 AND GP41 proteins on the virus envelope and make them ineffective? If not, how do hydrogen ions in the acid react with the virus?
Thanks for your attention.

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


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Virus variant transmissibility: empirical data or spike protein shape?
Well first I am not in the field of Biology or Medical Sciences. Since these days we are waiting scientists to tell us if the Indian variant of SARS Cov 2 is more transmissible than the original virus, so these two questions come to my mind:

Do scientists confirm increase in transmissibility based on empirical data?
Can scientists know how transmissible the variant is based on how well the spike protein binds to receptors of the cell, for example by doing a simulation of the 3D folded shape of the spike based on its code in the genome?

Generally based on (1). To quote the website:

The variants that are cause for most concern may:

spread more quickly,
evade natural or vaccine-related immunity,
cause more severe disease,
evade detection by available tests, or
are less responsive to treatment.

If you look at the features they say they look for in variants, the one they mention first is "spread more quickly" - the only way to tell that is to look at the genetics and how often the variant is turning up in a relative to a previous time-point. Bullet point 2 can only be seen by testing - do people who have had an infection, get infected again? Bullet point 3 - look at the severity of disease in patients.
I am sure by now that you get the drift; surveillance is the answer - all empirical data.
(2) may or may not help, all that does is tell you the potential affinity for a receptor, which is only one part of the transmissibility. In fact, we generally need to wait for the emergence of a variant (no point chasing each one; every infection will have some form of variant in some of the virions produced - they exist as a quasispecies), before modelling will take place. In addition, modelling is actually a pretty poor method of working out whether the virus will bind to a receptor. Check out this paper and see that many of the Mustelid family have poor binding by modelling, but in reality they actually get infected easily by SARS-CoV-2.
Many other factors come into viral transmission, such as viral titre in the patient, number of viral particles being shed in each droplet/aerosol, survivability of the particles in the air/droplet/aerosol etc.
Here's a nice paper from PNAS that covers the biological features of transmissibility based on a statistical/modeling analysis. While this doesn't specifically address SARS-CoV-2, it does cover a bunch of the features that are looked at for increased transmission in viruses overall.


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Has anyone tried the petri dish experiment with and without mask but at the side?
There are quite a few videos and experiments online that show the benefits of wearing a mask by holding a petri dish in front of their face while talking, singing, coughing etc., once with a mask and once without a mask. However, I have realised that while wearing a mask, despite the mask doing a good job blocking water droplets in the front, a lot of my breath (i.e. water droplets) goes to the sides of the mask.
Given that authorities are saying that the virus is airborne, I would think that the water droplets that come out of the side of the mask matter as well, especially in an enclosed room where many people would be spending their day. Has there been anyone who has put the petri dish at the side and did the same test as mentioned earlier? I can't seem to find any, but then again, my researching skills are not the best.

I’m voting to close this question because it is not about a problem in biology but appears to be an attempt to start a discussion.

@David Where would you suggest I ask this question then? I'm not looking to start a discussion. I'm asking if it had been tried before. I'm curious, in what way is this question attempting to start a discussion?

I have no idea where you should post your question. All I can say is that this is a Question and Answer site about problems in Biology as made very clear in the [Tour] and Help on asking questions. This is the SE model and what makes SE distinct and valuable.

A properly-fitting mask should not have any breath/droplets leaking out the sides of the mask.

@Armand While that is true, what percentage of the population would/is actually wear/wearing a properly fitting mask? (rhetorical qn) A large number of people either wear surgical masks, which have huge gaps at the sides or cloth masks, which don't fit the face exactly.

Properly-sized surgical masks seem to have huge gaps at the sides, but are intended to seal against the cheek inboard of those gaps, not at the side edges of the mask. I added another paper in the comments of Luigi's answer.

While I'm not sure about the petri dish experiment, I will answer the main question I think you're asking: how important is the air that escapes out of the sides/top of the mask?
This question is answered with really cool visuals in this paper: Visualizing the effectiveness of face masks in obstructing respiratory jets. While the main point of the paper aims to test the effectiveness of different masks in blocking coughs, you can see the trajectory of all the air (including the air coming out of the side). This example here shows a labelled diagram of air moving through and around through a folded handkerchief mask:

Fig 3b
Looking at both the homestitched (top) and commercial masks (bottom) below, you can see that there isn't much leakage around the mask, and the leakage that does happen out of the top of the mask appears to stay close to the cougher:

My interpretation is that the leakage around the mask is likely much less of a risk, since it probably is not moving as rapidly as air expelled directly out of the mouth--since the leaking air has already bounced off the mask, it does not get as far away from the person breathing/coughing. So, while stuff may escape out of the side/top, it doesn't get very far (hence the synergy of social distancing plus masking).

Here's another recent article on mask leakage effects: Cappa, C.D., Asadi, S., Barreda, S. et al. Expiratory aerosol particle escape from surgical masks due to imperfect sealing. Sci Rep 11, 12110 (2021). https://doi.org/10.1038/s41598-021-91487-7


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What are these micrographs of?
There are some images floating around the Internet that were supposedly taken with a microscope, built in the 1920s, that was supposed to achieve resolutions that would normally be ludicrous for an optical microscope, then or now, due to being smaller than the wavelength of light (and is caught up in a complicated conspiracy theory).
By the way, there seem to be strong indications in the surviving documents that it was actually an ultraviolet microscope as well as or instead of a visible-light microscope, so that might have some bearing on what's plausible in the way of resolution.
Not sure whether this question belongs here or at Physics.SE, but it seems like here might make more sense since the question is what these micro-organisms are.
There are about twelve or thirteen of these pictures floating around.  Some of them, on investigation, turn out to be magnified only 5000x or so, which, from what I've seen, seems to be considered impressive for a light microscope but not unheard-of.  These are some of the ones that I'm still puzzled by.
(Can put more details/refs of the microscope in the question if you like - wasn't sure whether you'd object to things being discussed on your site that are connected by association with a conspiracy theory  :-D  )
Question - I'm not a microbiologist, what do people here who are more used to microscope images think these images show, and at what magnification?
These three were published in a Smithsonian Institute annual report in 1944, pp. 240-242.

Caption - "Chlorophyl cells (algae)" - doesn't make sense.  From my limited knowledge of these things, it looks like a diatom, which seem to be a very commonplace subject for microscopes.  But one article I read implied that a trained biologist had been very impressed by this photo - maybe the writer had the wrong end of the stick.  Not sure what sort of diatom it is, if it is one.

Supposedly, the head of a tetanus bacterium, showing the spore, which, according to my brief Internet research, is possibly about 5 micrometres wide - so the quoted magnification of 23,000 sounds about true, if it really is a tetanus bacterium.

Supposedly, a typhoid bacterium, which, according to my brief Internet research, is possibly about 1 micrometre wide by 3 long.

Included because it's not labelled and I'm not sure what it is.  Diatoms?  No reference for where this one originally came from.  This copy from https://www.rife.de/images/calibrate1.jpg.

"Magnification" isn't a particularly useful measure; you can magnify anything as far as you want as long as you don't care about resolution.

Top picture is probably a dinoflagellate, possibly Gymnodinium family. Last are almost certainly diatoms of some sort, maybe Actinocyclus. Browse the beauty here

@BryanKrause That's true - and the "typhoid bacterium" does seem to be magnified considerably further than it has the resolution for.  Not sure how to express "resolution" numerically, though, so I just left it at "magnification", meaning "magnification possible without the image being reduced to a smudge".  (Which, in the case of the "typhoid bacterium", might be about half what it has there - but making the image smaller might have made the caption illegible).

Having had a quick read of the report, I have a few comments - first off, this seems to be a second-hand report of something that hasn't actually been observed by the authors.
Second, the light microscopy resolution limit is limited by
$$wavelength/2$$
As defined by Abbe's law, where x,y is the plane of focus, $λ$ is wavelength and NA is the numerical aperture of the lens.
$$Abbe Resolution_x,_y = λ/2NA$$
Practically this means that the shorter the wavelength, the smaller the resolution can be. For visible light the shortest is around 380 nm, so the limit would be 190 nm or 0.19 micrometers. This is about the size of the smallest bacteria and a few viruses reach this size. However, because of the limitations in how we make optical media (lens glass etc) the practical limit is quite a bit higher. Electrons have very short wavelengths (around 4 picometres), so much greater magnifications can be achieved, which is why EM is used for imaging viruses. Based on these physical laws, I would be very surprised if Rife achieved the magnifications he thought he achieved. Indeed, many of his claims of discoveries based on his magnifications (e.g. that cancer is caused by tiny E. coli-like cells that take up to 5 morphologies) are utter nonsense - of course he was the only one capable of seeing these, with his high-power microscope and he wouldn't let anyone else handle or use these...
So, I do have doubts about the magnifications expressed. In the journal Rife's magnifications are based on "diameters" rather than an actual dimensionless magnification (ratio of actual size to apparent size). Diameters was a commonly used method of working out object sizes, but I don't know how to convert between the two. I would say, seeing as there are actual fundamental physical limits to the resolution, that what is being seen here are what is known as empty magnification - increase in size without increase in resolution. The same sort of effect you get with a digital camera when it doesn't have an optical zoom, but instead relies on making the pixels bigger in the field of view. In this case it will simply be bigger projection than the limits of resolution.
Now, on to the actual question. What are these things? Taking on face value that images 1-3 are what the captions say they are on pages 222-224 of OP's linked publication, then we have some candidates.
OPs first image is almost certainly a dinoflagellate, these are a polyphyletic group of single-celled algae that, like diatoms, have beautiful structured cases. They also have flagellae, which enable movement. Which dinoflagellate this is, I don't know, they are diverse and not at all my field. I suspect something in the Gymnodiniaceae.  Dinoflagellates are about 30 micrometers in size, so easily within the limits of a light microscope, and you can see this in the ability to resolve the chloroplasts inside the organism. This image has no better resolution than would be produced by a decent conventional light microscope, only much bigger - camera trickery!
Image 2 could well be the spore end of Clostridium tetani, as the caption suggests. The spore is round and surrounded by a thick walled structure, but to my knowledge should have the rest of the bacterial body coming off to one side - looking rather like a spoon, with the body being the handle and the bowl of the spoon being the spore. I would expect to see the body of the bacterium sticking off to the side here, so I don't know for sure that it is what it is claimed to be, but we could be looking down on one along the longitudinal axis. There is some sponge-like "structure" visible in the middle of the "spore", but to me this looks like what you sometimes get in the middle of air bubbles on the slide.
Image 3 could be a member of the Salmonella group of organisms that cause typhoid, as these are slightly sausage shaped rod bacteria, however, I have seen many a stain blob that looks just like this using a low power objective. Note that Salmonella has flagellae too, and despite the large size and supposed massive magnification, we still can't see them. Hence, magnification and resolution probably not what is noted. So, whether this is actually Salmonella, is hard to say, but it could be.
Image 4 is from a different source - Rife.de, who seem to be an website for promoting Rife and his "cancer treatment". These look a lot like diatoms to me, but there is nothing to suggest that these were taken by Rife, and they look suspiciously like modern photographs using a modern microscope with something like Normarski optics or perhaps dark-field illumination, given that all the rest of Rife's images look much less clear.

Thanks very much for looking at this in so much detail!
According to https://www.britannica.com/technology/magnification "diameters" is the same as "x", so, if so, that's easy at least!

I'm not sure where Rife.de get their images from, other than the caption "Rife Research Group Of Canada" (which isn't them).  They seem to attempt to be a site seriously discussing the topic (there's a forum attached, and a lot of other archive materials), but they do seem to take the "it's basically real" position.  Full set: https://www.rife.de/observations-with-the-rife-microscope.html .

In #3 the flagellae seem reasonably visible at the right, if not well focused.  The internal detail is reasonably impressive - I'm not ready to hail it as a wonder, but it was at least a well-done job of staining and photography.


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By what mechanism do cephalopods regrow limbs?
As far as I can tell, there are two types of limb regeneration: epimorphosis and morphallaxis. Epimorphosis is used by animals such as amphibians and various phyla of worms, while morphallaxis is used by hydras.
I have been trying to find out which of these mechanisms is used by cephalopods, and no reliable source paints a clear picture one way or the other. Can anyone here help?

well gastropod mollusks use Epimorphosis, so it is likely cephalopods use the same mechanisms. Basically all triploblastic organisms use this mechanism so phylogenic bracketing points towards it as well.
morphallaxis is generally restricted to very simple organisms.
Regeneration of the visual system in gastropods (Mollusca)
Oksana Tuchina  Victor Benno Meyer‐Rochow
Neural regeneration in gastropod molluscs
Author links open overlay panelStacia B.Moffett
Regeneration of the visual system in gastropods (Mollusca)
Oksana Tuchina  Victor Benno Meyer‐Rochow (alternative link)


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What is the difference between using an open or a closed configuration for a microfluidic chip?
I am doing a college BioMed project on Lungs-on-a-chip to make disease models and I have seen some authors use open configurations, while others use closed configurations. What advantages and disadvantages do they offer on the making of this device?


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What is the time frame for coagulation of blood cells & the resulting separation of the cells and platelets from the plasma in a dead body?
I have had this subject come up repeatedly in the context of a discussion about death and how it affects the body.
I found this statement, which is typical of the common understanding among non-professionals:
"Blood starts to coagulate within minutes of death and pool into layers (e.g., red blood cells at the bottom, platelets and white cells in the middle, and plasma on the top, much like sand sitting still in a glass of water). The blood pools at the lowest part of the body (e.g., the left side of the body if the body is lying on its left side)."  ~Cited by a seemingly intelligent non-expert who identifies as a "Blood Drive Coordinator, Blood Donor"
I was corrected by an authoritative person years ago, who claimed that this doesn't actually happen for hours in the body. But now I am doubting their credibility. And I am growing embarrassed of having passed-on this commentary.
I would appreciate knowing if it is possible for this to happen within an hour or so of a person's demise?  It appears that there are scant clear answers to this question. I have used a variety of search terms on multiple search engines and research sites.
Thanks.

"I would appreciate knowing if it is possible for this to happen within an hour" - referring to coagulation, layering, or pooling?

I am not an expert on this at all, however I did a quick google search using the terms "timeline forensics death" and one of the top hits was a scientific book on the National Centre for Biotechnology Information bookshelf with the title "Methods Of Estimation Of Time Since Death"
This is a fairly short book and broken up into short sections. One of the sections is "Livor mortis" (best I can translate as "colour after death"). This section states:

The final change in the classical triad is livor mortis, which is the purplish-blue discoloration of the skin in the dependent parts of the body due to the collection of blood in skin vessels caused by gravitational pull. Hypostasis develops as spots of discoloration within half an hour to 2 hours. These spots then coalesce to form larger patches, which further combine to form a uniform discoloration of the body's dependant parts that have not been subject to pressure, which appears from 6 to 12 hours. The discoloration becomes ‘fixed’ after a certain period, owing to the disintegration of blood cells and the seepage of hemoglobin. This fixation is confirmed by applying pressure with thumbs and is traditionally used to denote a PMI greater than 12 hours.[12] This method of estimation of PMI required an objective and modern approach, leading to the development of colorimetric methods to estimate PMI from livor mortis.[13]

So it takes between 30 min and 2 hours for discolouration to show, but for this to cover and stabilize takes >6h.


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Is it even possible to cut just the phloem from the stem of a plant?
I often see questions related to this kind of diagram:

Basically, the diagram shows a that phloem is removed from the stem in the middle of the plant. Thus, the stem swells because food produced by the leaves cannot travel further. However, is it even possible to do this experiment in real life? Is it possible to cut just the phloem from the stem?

Welcome to Biology.SE. Please take the [tour] and then go through the [help] pages starting with [ask] effective questions on this site. In particular, we expect users to demonstrate that they have done the expected prior research — search for 'homework' in the help section for details. I suggest you start with this wikipedia page. After that please either delete or [edit] your question to make it on-topic for this site. Thanks.

The phloem and xylem are tissues with reinforced tubes, they are stronger than the meristematic tissue between them. This sort of splitting happens easily.


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Gene regulation and epigenetics in specialized cells
Gene regulation is aided by epigenetics. Epigenetics determines which genes are turned off and which are switched on, and it varies throughout our lifetimes. Is it feasible that epigenetic modifications switch off the genes that determine whether a muscle cell or a neuron is a muscle cell or a neuron? I have searched this question but I could not find an explanation.

This and this may be of interest to you.

Correct me if I am wrong but it seems you are asking 'do epigenetic mechanisms influence cell fate/determination?'. If this is your question, the answer is yes. Epigenetic modifications play a key role in 'deciding' what type of cell a given stem cell will differentiate into. Here is some more information: https://www.nature.com/articles/pr2006122


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Epigenetic marks
I was lately researching epigenetics and the current research on age reversal. Because epigenetic processes are influenced by the environment and can vary over time, I wanted to know if all epigenetic marks and mechanisms, including those that play a key part in cell differentiation, are reversible?
I am extremely keen to learn about this and any assistance would be greatly appreciated.

Welcome to SE Biology! When you say "reversible", what do you mean exactly? All chemical processes are theoretically reversible. It would help to know more about what specifically you have read, and what does not answer your question from e.g. a google search or wikipedia page. For example, I find multiple resources on this topic by google (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3411986/, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5137275/). Is there something specifically that you don't understand? Otherwise this question will be difficult to answer as it is quite broad.

I second the comments of @MaximilianPress but would ask you whether you know what “epigenetic tags” are in chemical terms. Because if you do not, you need to find out before you are in a position to ask here about their specific reversal because it is unlikely that you will understand an answer. Do you?

@David Sir, yes I studied them  and I understand them

@Maximillian Press Sir, I was curious if the epigenetic processes that drive cell differentiation and aging may be reversed. Can we undo all of the aging-causing epigenetic mechanisms?

@AIA that is good information to have in the question, but it is still very generic. There are many kinds of changes that people call epigenetic that play roles in development/differentiation, and yes they are reversible in some sense at the biochemical level. However, this does not necessarily have any relevance to aging. It would be helpful to know more specifics about what you have read and what specific questions remain unanswered. This is too broad to answer as is.

@Maximilian Press Sorry sir, I am not delivering clear information. Basically, I am making a video for a competition on the topic of slowing down and reversing aging with epigenetics. I read David Sinclair and other scientists' researches about it. So I just want to clarify that if we are reversing aging, so it mean that we are changing our epigenome and reversing some epigenetic marks? so I want to clarify is this right. Sir, if you have references to any research articles that would help me in getting great insight into this topic, i will be thankful if you can share them

To some extent, there are people who believe that we can reverse aging by reversing epigenetic marks. I don't know that I believe this, but there is certainly an academic literature on it. Notably, some of the same epigenetic marks associated with aging are also associated with tumor suppression, so reversing marks is not necessarily always a great idea. Here is a link to an article, that in turn links to a study. I wouldn't necessarily trust it, but it should lead you to more information: https://www.nature.com/articles/d41586-019-02638-w


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Is MPseq more cost effective than FISH when looking for chromosomal abberations?
There are some papers out there that propose to use MPseq in addition to or instead of FISH when looking for chromosomal aberations in the context of cancer
e.g. this one on infiltrating lobular breast cancer refractory to standard therapy or this one even claims that MPseq outperforms FISH...
I do understand that pricing may vary widely given the individual contracts a hospital may have with a certain vendor. But can anyone answer this roughly.
I've never done FISH myself so  I don't know how time intensive it would be. Considering prep and interpreation of the results. I could imagine that it keeps a lab tech busy for some time.
For MPseq, I imagine that several samples can be run a the same time and I would imagine that the output is less prone to operator bias.
I know it is not a simple yes no question and more of a discussion but your thoughts on this would be much appreciated.

There are many high-throughput products that perform roughly this function of finding karyotypic variants. Bionano sells an optical mapping product that claims to do this, I have not directly inspected their viability; their tech is slightly complex.
Hi-C-seq is rather simpler and there are several competing firms that offer products that perform karyotyping:

Arima,
Dovetail Genomics,
Phase Genomics (of which I am a former employee and equity holder).

I am sure that there are other methods including mate pairs and even plain whole-genome shotgun sequencing that could do ok at this task.
The Hi-C companies sell relatively inexpensive kits for library preparation, and some will also sell analysis services at fairly high throughput.
All of those methods should outperform mate-pair sequencing (which I think you call MP-seq) significantly, due to the relatively high rate of chimera formation (on the order of 0.1-1%) and generally the lower signal of mate-pairs, which are restricted by the insert sizes chosen. All of them should find the large karyotypic events found by FISH, ideally with more precision and sensitivity.
Traditional karyotyping services (such as FISH) run ~\$11000 per diagnosis, whereas the high-throughput methods I note (not the ones in that paper) probably are closer to ~\$500-1000/sample for preparation + ~\$500-1000 for sequencing plus maybe ~\$2000 / sample for analysis costs with a vendor (at a guess, for many samples). The companies in question may also do your sample preparation at a significant increase in cost (an extra $2000, perhaps). This would be a total of ~\$4000 / sample, as a high estimate.
Mate-pair costs would be cheaper at the sample level but more expensive at sequencing and analysis, not sure about the exact numbers. I don't think there are providers offering the package as a service, as it may not be economically viable, but I could be wrong about that.
I don't have refs for these prices, the providers themselves are the source of truth for that. Any of the companies above would happily prepare a quote for you.
If my very rough math above is correct, any of the sequencing methods should be cheaper, except possibly for Bionano (which is still probably more precise).
I'll note again my conflict of interest with Phase, though I don't work there anymore and I don't speak for them.


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Are CpG sites always palindromic? If so how?
I'm having a bit of difficulty understanding why CpG sites are said to be palindromes. In what sense are they palindromes? Like they always have this shape CGGC? (for example)

CpG motifs are always palindromic. A palindrome is something which reads the same way forwards as it does backwards. A palindromic sequence is a DNA sequence which gives you the same string of nucleotides regardless if you are looking at it on the forward or the reverse strand, so long as you are reading in the same (5' → 3') direction.
Notice that the nucleotide sequence of a CpG island is just CG. So on the forward strand you might denote the sequence 5' CG 3'. On the reverse strand, the sequence is 3' GC 5'. So long as you read both strands in the 5' → 3' direction, you end up with the same nucleotide string: CG. Therefore, because the nucleotide sequence is the same in both the forward and reverse strands, a CpG motif is a palindromic sequence.
An example of a sequence which is not palindromic might be 5' ATT 3' on the forward strand and 3' TAA 5' on the reverse strand. On the forward strand, the sequence is ATT. Reading 5' → 3' on the reverse strand, the sequence is AAT. Because ATT ≠ AAT, this sequence is not palindromic.

Gotcha! now it make sense :) thanks


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Why is relative change highly correlated but absolute values for phenotype and PGS are not?
I have n "couples" (female-male pairs).
And I compute the correlation for PGS (polygenic risk score) and phenotype:
corr(PGS_female, PGS_male)
corr(phenotype_female, phenotype_male)

None of this gives a high correlation.
However corr(ΔPGS, Δphenotype) where
ΔPGS=PGS_female-PGS_male
Δphenotype=phenotype_female-phenotype_male

is actually quite high. What could this imply? That even though the traits are not strongly correlated among partners, the relationship between PGS and phenotype across couples is?

I would highly recommend plotting your data, such as with a scatterplot.

The problem is that it is difficult to see the actually couples since those are 50k pairs. Any suggestions? Sure I can see correlation of PGS with phenotype among all individuals, but I don't see the relation with the actual couples.

It's not really the individual points but the shape of the data that is useful. You could use a density plot (basically a 2D histogram) if there are too many points to render.

I think what you're probably just discovering, through, is that PGS and phenotype are correlated.

To @BryanKrause's point: try plotting PGS_female against phenotype_female and PGS_male against phenotype_male!


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Do crabs actually "rip the legs off of other crabs" if they try to escape a bucket?
I read this strange remark:

Picture a bucket full of crabs with no lid. The moment a crab tries to get out, the other crabs will literally rip its legs off.

It was said as something that is common knowledge. I had no idea about this. What are they talking about? Huh? Why would crabs behave like that? Is this just nonsense?

No, that's an exaggeration of the "crab bucket" phenomenon.  They just pull the other crabs down: https://en.wikipedia.org/wiki/Crab_mentality  It's also a metaphor for a certain type of human behaviour.  See for instance Terry Pratchett (in Unseen Academicals): https://wiki.lspace.org/mediawiki/Crab_Bucket

@jamesqf Well, I watched numerous videos on YouTube but couldn't find a single one where this actually happened. Very frustrating.

I've no personal experience of live crabs, so I can't say whether it actually happens.  But as a metaphor, it's perfectly understandable.

As lobsters are crustaceans that I am more familiar with, I will say that lobsters are cannibalistic at times, so in addition to aggression, crabs may also exhibit the same predation behaviors when in close contact. I am not sure if that explains this behavior, but it is possible. Both crabs and lobsters do randomly bite each other when trapped together though.

Thank you for your enthusiasm, but please review the criteria for [answer] — in particular we want answers that provide detailed explanations with references to reliable sources (preferably primary literature). Speculation that isn't backed by such sources is indistinguishable from opinion, which is expressly off-topic on this site.


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Which hornet-like insect is this?
This insect flew through my open 10th floor window, around midnight.
Its flying pretty fast for insects, and bumping into the ceiling a lot.

Location: southern Germany.
For me it looks almost like a hornet, except for the eyes, which in my opinion are way to big for hornets.
The wire mesh in the background has a 12mm spacing.
Any guesses?

Not a hornet at all, nor any Hymenoptera but rather a Diptera. As you suggest, the eyes as well as the wing structure give it away.
It looks like a horse fly, possibly Tabanus sudeticus or Tabanus bovinus based on the large size and coloration in the abdomen.


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In the Kok cycle occurring in Photosystem II's Oxygen-evolving Complex, what exactly does P680 do?
I've been reading up on the oxygen-evolving complex using a few sources, but am a non-biology major so my understanding might be somewhat/very flawed. I've been using this source mainly:
https://faculty.missouri.edu/~glaserr/3700s13/PS-Review2.pdf
and have so far gathered that, along phases S0 to S4, the Mn complex holds onto the 2 water molecules while it is "oxidized" by P680 with the help of tyrosine Yz; instead of oxidizing water directly, P680 oxidizes a total of 4 Oxidizing Equivalents, which act as "stand-ins" for the redox reaction involving water. At the final stage, the Mn complex has a total charge of 4+, which then causes the 2 oxygen atoms (from 2 H20) to give up their  electrons and turn into molecular oxygen, something this source also says:
https://www.life.illinois.edu/crofts/bioph354/lect25.html
My preliminary question is, is my understanding correct at a basic level? And if it is, then what is P680 doing?
We've been told that it's one of the strongest organic oxidizing agents, which made me think that it stripped the hydrogen from H20 immediately, but instead it seems like the "splitting" of water occurs in the Mn complex thanks to the 4 oxidizing equivalents.
Is P680's role still essential in this process? As in, is P680's strength the only natural thing that can oxidize the Mn complex at each step so that it eventually splits the water? Or am I misunderstanding the "water-splitting" step entirely?


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Aging from inception until forming of reproductive elements
Aging from inception until forming of reproductive construct.
For example, it takes two months for Spermatogonia to develop.
Why is DNA damage over generations not accumulated?
I have this study.
https://www.biorxiv.org/content/10.1101/2021.03.11.435028v1.full
Is that consensus on the subject?

Somewhat relevant are the answers to these questions: Is each generation getting older?, and How are new people created from the DNA of an aged person, and DNA damage theory of aging and sex.  Also related: Why doesn't mitochondrial DNA accumulate damage over successive generations?.

Excellent ansert/comment. Thanks.

Does this answer your question? How are new people created from the DNA of an aged person. i.e. Why are we young?


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Is atmospheric nitrogen chemically necessary for life?
It is my (very basic) understanding that neither plants nor animals utilize the nitrogen in the atmosphere.  Humans do not make use of atmospheric nitrogen through respiration and plants do not extract nitrogen from the air, but rather from the soil.  First of all, am I correct in this understanding?
If I'm right so far, then what role (if any) does the nitrogen in our atmosphere play, biochemically speaking?
I understand that it plays a significant physical role, contributing to air pressure, allowing light to permeate, allowing liquids to exist on the surface, burning up incoming meteors thus protecting life, and basically being a physical gas that is not oxygen or carbon dioxide thus keeping the concentration of those gasses low.  But I'm interested in the biochemical use of atmospheric nitrogen if any.  So, is nitrogen a necessary atmospheric component for life, in terms of its chemical reactions with living things?  Or is the atmospheric nitrogen essentially unused in the chemistry of life?

Nitrogen is a necessary part of amino acids which are building blocks for proteins. Animals get this nitrogen from eating plants, plants get them from symbiotic microorganisms and those germs get nitrogen from the atmosphere. So we do need atmospheric nitrogen in order to make meat.

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

@slebetman. Nicely put, but there is also the Haber process (industrial N2 fixation) without which agriculture as we know it would be very different. As the quoted wikpedia article puts it: "With average crop yields remaining at the 1900 level the crop harvest in the year 2000 would have required nearly four times more land and the cultivated area would have claimed nearly half of all ice-free continents, rather than under 15% of the total land area that is required today"

To get soil nitrogen in the first place, nitrogen fixation is necessary which takes atmospheric N2 and converts it into biologically useful forms.
Nitrogen fixation is performed by bacteria and archaea. You may occasionally hear about nitrogen fixing plants, especially peas and beans in an agricultural context, but these involve symbiotic relationships with bacteria that do the actual work.

@user253751 I haven't yet found any other planets with life so I'm stuck with this one for observations about how these things work.

@user253751: No, the reduction of nitrates to nitrogen and oxygen is endothermic and does not gain energy by itself. But some lifeforms can use nitrate to oxydise something else and gain a bit of energy this way.

@jk-ReinstateMonica And yet, life does finds a way to burn non-atmospheric nitrogen compounds to get energy and nitrogen gas: anammox. https://en.wikipedia.org/wiki/Anammox
One can, however, imagine an anaerobic, hydrogen-rich world where nitrogen is mostly in the form of ammonia/ammonium, and perhaps there's no energetically favorable reason to transform it to N2. In such a world, you'd be unlikely to come across nitrate, and if an organism did find or generate some, it would be more energetically rewarding to use it to oxidize hydrogen to form water and ammonia.

@BrendanFurneaux: Ammonium Nitrate is a quite unusual compound (even an explosive) consiting of reduced and oxiydised nitrogen in one salt. Of course you can use nitrate to oxydise ammonium and gain energy, this is no contradiction to my previous comment.

I'm surprised: Are you saying that without life, there would not be a substantial amount of nitrates on Earth? (I'm not skeptical but merely ignorant ;-). )

@Peter-ReinstateMonica There are other sources, like lightning, and nitrates for fertilizer are made artificially using Haber–Bosch, but yes my understanding is that most nitrate on Earth has a biological origin, though it's also used by biology, so it's quite possible there'd be as much or more nitrate from other sources if there was no biology - this I'm not sure about.

@BryanKrause Nitrate (dissolved in water, not as concentrated nitric acid of course) is thermodynamically favored compared to a blend of oxygen and nitrogen gases in the atmosphere, so in the absence of life and over geological time, we would expect all of the oxygen in the atmosphere to react with nitrogen to form nitrate.  However, I expect the nitrate itself would further react to oxidize other compounds dissolved in the ocean.  But the elephant in the room is that the free oxygen was generated by life, and most/all nitrate on Earth is generated by a reaction involving free oxygen.

@jk-ReinstateMonica Your statement started with "No", in response to user253751' s question about whether life would "burn" non-atmospheric nitrogen compounds to form nitrogen gas; I provided an example of that actually happening, which is furthermore a major part of the nitrogen cycle on Earth.  You focused specifically on nitrate, rather than ammonium, but that's not what the original comment asked about.  As for ammonium nitrate being an unusual compound -- as a pure salt, sure.  But it's not so strange to find the two ions dissolved in the same water.

@BrendanFurneaux Yes, that's a pretty big elephant. I'm a bit suspicious over whether geological time is really long enough, though. Yes, conversion to nitrates is energetically favorable, but breaking that triple nitrogen bond is not trivial. Biological fixation of nitrogen goes through a reducing pathway even, not oxidation, just like with the Haber process. Without knowing too much more about the detailed chemistry, I'm a bit skeptical that the oxidation pathway you propose would occur fast enough over geological time, even with a high (i.e., modern) oxygen atmosphere.

@user338907: By nitrogen I mean elementary nitrogen N$_2$, indeed.

@BryanKrause I was expecting things like lightning to be part of the mechanism over geological time; but you are probably right that it would be an extremely slow process.  Chances are, in the absence of photosynthesis to replenish it, the atmospheric oxygen would be depleted in many other ways before it had a chance to oxidize much of the nitrogen.

Also, birds poop (en masse) was historically a good source for nitrogen rich fertilizer. Like others say, there was historically a big problem gleaming on the horizon about acquiring it and being able to feed quickly increasing population of people, before Fritz Haber (quite controversial character) made a breakthrough! To dive deeper into the whole story, I very recommend this youtube video by Veritasium: "The Man Who Killed Millions and Saved Billions" https://www.youtube.com/watch?v=EvknN89JoWo

While atmospheric nitrogen is definitely necessary for keeping up the ecosystem of Earth as we know it (as Brian Krause has already pointed out), it is not really a necessity for some life form on earth, especially among the extromophiles species and even complete ecosystems can be found that do not rely on atmospheric nitrogen at all.
Atmospheric nitrogen also helps keeping up the atmospheric pressure, without any nitrogen in the atmosphere, water would boil at about 27°C.

Could you explain how the extremophiles obtain the nitrogen atoms in amino acids etc. if it is not ultimately from molecular nitrogen. At present your answer is just an assertion and for the large number of users who are familiar with extremophiles, the Wikipedia link does not clarify the matter.

They can be taken from nitrate which is readily accessible and the most natural form for nitrogen in the lithosphere.

And how does the nitrate arise?

Well, the nitrogen has to be somewhere, and under oxydising conditions nitrate is its stable form. Under reducing conditions it would be ammoniak. Elementary nitrogen is only metastable under either condition. Without biological activity, it vanishes rather quickly.

You are kindof right, Atmospheric N2 is bound with a triple covalent bond, which is the strongest of all simple diatomic molecules.
If you have a vivarium with helium/argon breathing gas and the soil has a ready supply of dissolved nitrogen for fixation into NH3, then the animals and plants will live just fine for a very long time, but many plants that fix N2 that depend on nitrogen fixation symbiosis may fare worse.
N2 is nearly not soluble in rainwater, so ultimately, all plants and animals that depend on nitrogen in the soil require atmospheric N2.
If there was no airborn N2, the forests would be in trouble because they would yellow and have diminishing reserves of nitrates and nitrites...
Nearly all the biospheres would perish unless you keep on fertilizing the soils, them most plant species would be virtually ok growing hydroponically in an atmosphere without N2.


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Can anyone identify this seed, pit, or nut?
I found this on the recessed top of the intake manifold of my car engine.  It may have been there for weeks.  It was likely brought there by a rat or squirrel who was unable to chew through the outer shell/husk.  The white part seems to be where an animal gnawed on the outer portion.  Note the orange color where it was apparently not chewed on.  It likely was deposited in my engine compartment by a critter somewhere in inland/coastal southern or central California.  The air temperature when I found it (while changing a headlamp) was 106 degrees F (41 degrees C) and the temperature of the engine routinely gets well above that.  It has been well-toasted.
The size-reference coin is a US one cent piece that is about 19 mm in diameter.
I think it had the very faintest citrus aroma when I first found it and I thought it was a small orange (orange outer skin, white pith) that had been dehydrated and then chewed on by a small animal.  Then I shook it and it rattled - clearly not an orange.  When I cracked it open with a large pair of pliers I found the 'nut' that you see in the images.  It smells faintly nutlike and has a slightly waxy/oily finish - something like the appearance of a skinned hazelnut.  Note that the 'nut-meat' has shrunk away from a dark, shiny skin.
I haven't cut or tasted the nut-meat myself on the off chance it is toxic.
Are there any forensic botanists out there?

I'm going to go with California Beaked Hazelnut (Corylus cornuta).
While it is hard to tell from the chewed outer, it has the reddish-brown colour of hazelnut shell, and inside the shell is a dark brown papery layer. The nut (without the papery layer) is smooth and rounded

Certainly looks very similar to hazel nuts I grew in IL

This one is somewhat larger than any hazelnut I have ever seen.  And I don't think I've ever traveled in that particular car as far north as any of the areas noted as its natural growing area.  But that doesn't mean that it wasn't transported to somewhere I had travelled and was picked up by a naïve squirrel who couldn't figure out how to open it.

@OCPatch - people grow them in their gardens too; they are certainly available from nurseries. The nuts get up to about 4 cm/1.5 in long, so that's pretty big for a hazel, but not outside the realms of size for your one. The main argument against is the bumpy shell to my mind - hazels are all smooth AFAIK. Could be a pit from a (large) fruit?

@bob1 - Good point about people maybe having them as a novelty plant.  If it weren't for the orange and white husk I would have guessed it could have been a small avocado pit.  It could have been a small whole avocado but for the red/brown/orange outer skin and the hard, dried husk on the outside.


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Sexual dimorphism of the Amphimachairodus genus of saber-toothed cats
Amphimachairodus is an extinct genus of particularly large saber-toothed cats.
Per Alan Turner and Mauricio Antón's The Big Cats and Their Fossil Relatives: An Illustrated Guide to Their Evolution and Natural History (which I lack a copy of and cannot find an E-copy of), Amphimachairodus was "markedly" sexually dimorphic, "with males being much larger than females".
Before I get into sources, the overall question: does anyone know how sexually dimorphic Amphimachairodus was — specifically in terms of physical size? Was it like modern lions, where males weigh somewhere between 1½ to 2 times the females, or was it more or less pronounced than that? Google search results for this are few and far between.
Now, I found calculated sexual dimorphism indices for Machairodus aphanistus and Promegantereon ogygia (not to mention several modern species, such as the lion, serval, leopard, and jaguar, as well as Smilodon fatalis) in this article; said figures suggest M. aphanistus was between modern tigers and modern lions in terms of sexual dimorphism. But Machairodus is a wastebasket taxon out of which several species have been moved into Amphimachairodus, so I have no idea whether the figures for M. aphanistus are representative of Amphimachairodus as a whole.
This source can be cross-checked against the first source to slightly improve one's understanding of Amphimachairodus's overall size over what a Wikipedia article can tell you (specifically, compare tooth sizes), but has no information on sexual dimorphism. The best it gets:

The three available tali from Las Casiones show strong differences in
size, but comparable to those observed within the sample from
Crevillente-2 (Montoya,1994), supporting the existence of strong
sexual dimorphism in A. giganteus

Indeed, what I assume is mean mesiodistal length ("MDLMean") of the fourth premolar ("P4") of Amphimachairodus giganteus varies from 24.9 mm to 32 mm. However, I doubt comparing one type of tooth across a handful of specimens gives an accurate picture of A. giganteus size, let alone an accurate picture of dimorphism across all of Amphimachairodus. It also means you need to assume that the smallest teeth represent females and the largest ones males, which isn't necessarily true when it comes to big saber-tooths, as Smilodon demonstrates.
Basically: I'm asking for information specifically concerning this, if there is any. It would also be helpful to have more sources on the Amphimachairodus genus which aren't Wikipedia or books I can't get ahold of without buying them.
I believe Biology Stack Exchange is the best Stack Exchange for posting this question, as Earth Science Stack Exchange's "paleontology" tag states that:

Questions about the biological aspect of paleontology (such as
taxonomy and anatomy) are off-topic here and should be asked on
biology.stackexchange.com


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Are the muscles of all animals mechanically similar?
For instance, is the skeletal muscle of an elephant made of the same balance of fibers and cells as the skeletal muscle of a hippopotamus?
I recognize that slow- and fast-twitch muscles are a thing, and that which animals have which vary. I also recognize that different animals might have different numbers of mitochondria per muscle cell, and that there's a difference between skeletal, smooth, and cardiac muscle, but am still conflicted on one thing would it be accurate to claim that the mechanical properties, density, and the like of all types of animal skeletal muscle are the same?
If you happen to have a source for your answer, please supply one - it'll be useful for something I'm trying to write.

I recall Comparative Biomechanics by Vogel stating the power density is roughly similar. Similar enough to group together and make comparisons with groups of man made actuators.

@DKNguyen Thanks.

This doesn't appear to be answerable by anything other than opinion — can you please specify your criteria for "similar".

@tyersome Having similar physical densities, compressive and tensile strengths, Young's moduli, extensibilities, and so on and so forth - essentially, properties of the muscle in regards to materials science.


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Does nacre/mother-of-pearl have a greater compressive strength than human bone?
Exactly what it says on the tin: as measured in mPa, does nacre/mother-of-pearl have a greater compressive strength (i.e. it can take getting squeezed more before breaking) than human bone?
I recognize that it's rather brittle and doesn't do well with shear loading, but that's not the question here.

Yes.
According to this article, the compressive strength of nacre is $300{-}500\;\mathrm{MPa}$, whereas the compressive strength of human bones ranges up to around $200\;\mathrm{MPa}$.


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Monogenic disorders vs multifactorial inheritance disorders
There's a condition called SYNGAP1-related intellectual disability which is caused by mutations to the SYNGAP1 gene.
I believe that this is called a monogenic disorder, while disorders that are caused by multiple genes are called multifactorial inheritance disorders. Other examples of monogenic diseases are apparently cystic fibrosis, sickle-cell anemia, and Huntington's disease. Examples of multifactorial inheritance disorders are heart disease, cancers, Alzheimer's, athritis.
The number of monogenic disorders are limited to the number of genes at $\approx20000$, while the potential number of  multifactorial inheritance disorders is then $20000!$ or about $10^{77000}$. This upper bound is not very helpful since I would assume that most multifactorial disorders aren't going to affect anywhere near all genes.
How common is it that diseases/conditions are caused by the mutation to only a single gene? If I pick a random disease/disorder/condition how likely is it that it's caused by only a single gene?
Is there a list somewhere of all known monogenic disorders? If I search "monogenic" in OMIM there are 185 results, of which many don't appear to actually be monogenic. For example, the second result is obesity which is not monogenic.
If I look at Type 1 Diabetes there is only one gene-phenotype relationship which leads me to believe that it's monogenic, but the phenegene graphics shows three genes linked to type 1 diabetes: 600716, 147620, 142410. So not only are there multiple genes linked to diabetes, those multiple genes are also linked to multiple disorders.
The gene that causes sickle-cell is also connected to other disorders. Is this because different mutations in HBB lead to different phenotype disorders, where sickle-cell is one, but sickle-cell itself if just caused by that single gene mutation? I.e. sickle-cell is monogenic, but the responsible gene can mutate in other ways giving rise to other disorders?
Maybe I'm interpreting things in the graph wrong. But, what I'm looking for are gene, disorder pairs like SYNGAP1 where the one gene is linked to one and only disorder. I think what I'm looking for then is not just monogenic disorders, but also "monodisorder" genes.
Is there a way I can search OMIM for these?

Just a note that since different mutations in a single gene can sometimes cause different disorders, the possible number of disorders is not limited to the number of genes. On the other hand, many gene defects will result in non-viability before birth, so will not be seen in practice. There are also disorders caused by chromosomal abnormalities involving duplication/deletion of multiple genes or a chromosome.  Apropos your final question, our knowledge is nowhere near complete, so genes that are today listed as "monodisorder" could easily have additional disorders recognized down the road.

Re: " Is this because different mutations in HBB lead to different phenotype disorders, where sickle-cell is one, but sickle-cell itself if just caused by that single gene mutation? " In general, yes. There are often groups of related but somewhat different disorders for different mutations in the same part of a gene, for example see the beta thalassemias also caused by certain mutations in HBB.


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"mutant" codon translations?
AFAIK codon->protein translation is pretty much universal (very few exceptions). I've seen people explaining this means every living organism descends from the same ancestral.
That's certainly a possibility, but perhaps any other translation would be extremely unlikely to evolve (chemically) and/or would end up evolving to the current one because it requires less energy (I'm speculating, but the tRNA could be simpler for example).
Are there evidences that it's possible to have a very different translation table? For example, an experiment in which the encoding of a couple of codons is swapped? I'm guessing this wouldn't work if genes are encoding more than one protein - but even if it did work, perhaps it would be too dangerous to have a lab leak of this mutant?

consider that many codons code for the exact same thing.

While the basis of the genetic code are highly conserved there are several variations that can actually be quite frequent. For example the mitochondria in your body use an encoding that is a little different from the cell nucleus.
As you stated, the most likely explanation for these small variations is evolution from an ancestral version.
Other encodings are clearly possible since all 64 possible triplets are used. Swapping the encoding can be achieved by modifying the enzymes that bring together t-RNAs and amino acids (so called t-RNA synthetases). This is quite complex and mainly done to enable the incorporation of new amino acids into proteins.
Not all potential codes would work equally well and might for example slow down translation. One possibility to completely alter the code without major problems would be to swap the first and second positions in each triplet.
And for your last question, an organism with a highly altered genetic encoding would actually be more save. This is because it would be impossible for this organism to exchange genetic information with its environment. Bacteria frequently obtain antibiotics resistances by gene transfer from other bacteria. The modified organism would not be able to make sense of a resistance gene obtained through this way.


text:
How does medicine work?
Take aromatase inhibitors for example. In order for a molecule to stop the enzyme aromatase from converting androgens into estrogens, it must meet 6 criteria:

Not get broken down by the acidity or enzymes in the stomach (or get broken down in a helpful way)

Not get recognized as waste by the body and be absorbed through the small intestine

Not get broken down by the liver (or get broken down in a helpful way)

Get inside the cells that produce aromatase, via diffusion through the cell membrane or through a protein

Stop the production or inhibit the performance of aromatase

Not stop the production or inhibit performance of another enzyme

Despite all these criteria, multiple aromatase inhibitors exist. How did scientist find a molecule that meet all the criteria? What in biology and chemistry are they taking into account?

Pharmaceutical and chemical companies have libraries of millions of compounds that they can test using ultra-high-throughput screening with biochemical and biophysical assays. A lot can also be inferred just using structure alone, as well.


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Function of SMAR in plasmids?
A few years ago, the Thought Emporium published a video (https://www.youtube.com/watch?v=aoczYXJeMY4) in which he refers to a study in which they mix plasmid DNA with Chitosan and feed it to mice to express LacZ gene so the mice's intestines could produce Lactase (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4717060/?fbclid=IwAR0K7C8GounA9DZwkIRm8qSGMSKuo_uHsl8-2qd2fGjnIgn5SkPXddcODsY).
Thought Emporium then shows a plasmid that could do the same for humans. In the plasmid (image below), there is this "SMAR" sequence. He says this acts like an ori but for mammalian cells.
I don't understand how SMAR functions like an ori. When I look up SMAR, it seems to be a protein structure in the nucleus rather than a gene. And the original paper doesn't mention SMAR at all.
What is SMAR? How does it function? Why does it act like an ori?

Sequence for plasmid here says that it is ncRNA. It is added as in the cassette with the Lactase, so will likely be as one RNA, possibly as a nuclear localization signal or something

S/MAR (nuclear scaffold/matrix attachment region) Is a DNA sequence pattern that recruits the nuclear protein hnRNP-U/SAF-A a multifunctional scaffold/matrix specific factor.
Jenke et al. 2002

Immunoprecipitation of the crosslinked DNA–protein complex demonstrates that pEPI-1 is bound to this protein [SAF-A] in vivo. These data provide the first experimental evidence for the binding of an artificial episome to a nuclear matrix protein in vivo and the basis for understanding the mitotic stability of this novel vector class.

Jenke et al. 2004 confirmed their previous finding and shows that a tetramer of a 155 bp region together with upstream transcriptional activity is sufficient for mitotic stability (mediated by SAF-A).
It seems to me that the sequence of SMAR is the binding surface for an adapter protein that elevates foreign DNA to a chromosome-like state. It was also shown that SMAR handles chromosome-associated processes like nuclear localization, S-Phase, etc. (Stehle et al. 2007


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On the Origin of Homo Sapiens
Paleoanthropologists are certain Homo sapiens originate from Africa. However where in Africa is still contested.
Could you give the reasons why it is thought that Homo sapiens evolved in Eastern Africa, Northern Africa and Southern Africa?

This seems like a question that could use some preliminary research. For example, why are paleoanthropologists "certain Homo sapiens originate from Africa"? Do those techniques extend to subregions of Africa?

How is this different from your previous question? And please take the trouble to read the [Tour] to find out how this site works and how to ask questions here. Armand’s remark reflects the requirement to demonstrate the effort you have made to answer a question yourself.

The reason is that the oldest and most primitive proto-human signs of life have been found in Africa. The seminal research was done by Louis Leakey, an anthropologist. It is possible that older forms of life may exist undiscovered in other places, but so far the evidence for that is scant.
Part of the challenge is that many geographic areas feature acidic soils which will eventually dissolve bones, which are composed of calcium carbonate, so it requires a neutral or slightly basic soil to preserve bones over millions of years.


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Where in Africa did Homo sapiens evolve from?
I’m aware that the possible oldest homo sapiens fossil was found in Morocco. The vast majority of our fossils however is found in Eastern Africa. In recent years,a controversial study on mitochondrial DNA seems to suggest an origin from Southern Africa. Where is the majority scientific opinion on this issue at the moment?
You can read this article for my source on the study of mitochondrial DNA

Possibly the currently favoured view is that anatomically modern humans didn't evolve in one location, but evolved in a structure population that spanned Africa (and perhaps the Middle East):

We challenge the view that our species, Homo sapiens, evolved within a
single population and/or region of Africa. The chronology and physical
diversity of Pleistocene human fossils suggest that morphologically
varied populations pertaining to the H. sapiens clade lived throughout
Africa. Similarly, the African archaeological record demonstrates the
polycentric origin and persistence of regionally distinct Pleistocene
material culture in a variety of paleoecological settings. Genetic
studies also indicate that present-day population structure within
Africa extends to deep times, paralleling a paleoenvironmental record
of shifting and fractured habitable zones. We argue that these fields
support an emerging view of a highly structured African prehistory
that should be considered in human evolutionary inferences, prompting
new interpretations, questions, and interdisciplinary research
directions.

Scerri, Eleanor ML, et al. "Did our species evolve in subdivided populations across Africa, and why does it matter?." Trends in ecology & evolution 33.8 (2018): 582-594.
For a criticism of the mtDNA Southern Africa origins paper, see this paper.

This is rather interesting. I have 2 questions. Firstly, does this represent the majority of scientific opinion? Secondly, does this “African Multiregional” approach imply a sort of convergent evolution of multiple groups of archaic humans into modern Homo sapiens?

This view is scientifically so weakly supported that I wouldn't give it much credence at this point. The number of human fossils recovered is tiny, they are poorly dated and by no means a random sample. Similarly, the "material culture" (basically stones that are often hard to identify as intentional human artifacts versus naturally-occurring pieces) is notoriously difficult to link with any fossil or even date to an accuracy finer than a few hundred thousand years.  The identification of many more fossils and genomic sequencing will sort it out in the future.

@Armand So what do you think is the majority opinion then?

@DavidOkogbenin The correct opinion is "insufficient data, likely for at least a number of decades". Majority/minority doesn't matter in science -- data matters.


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Are there any congenital anomalies that cause a lack of epicanthic folds in a child who would normally have them?
Wikipedia lists several medical conditions associated with epicanthic folds. Mount Sinai says that epicanthic folds in a baby who would not be expected to have them is a diagnostic tool that indicates that the baby may have Down syndrome or another genetic disorder and should be examined further. Presumably this means that those disorders are slightly harder to diagnose in populations where epicanthic folds are the norm as it is less visually obvious that there is a congenital abnormality though all the other symptoms would still be present. But are there any congenital anomalies that cause a lack of epicanthic folds and thus would be easier to diagnose in a population where epicanthic folds are ubiquitous?


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Why did the dinosaurs not have gigantic brains and become really smart?
All my life, I've heard that all these gigantic dinosaurs that used to live on Earth had peanut-sized brains. I just accepted this as a fact, and I guess it may be a fact.
But now I wonder: why?! If their bodies were so incredibly huge and everything was so big back then, why did the brains not also follow that rule? How is it possible that such big animals (or elephants/whales today) apparently have such small brains?
Why doesn't the size of the body roughly dictate the dimensions of the brain inside? Or do they mean this in a more metaphorical way, such that "small brain" really means "low-capacity brain" rather than it actually being physically small? I would assume that if a brain is big, it automatically features more "raw power" rather than being full of empty, unused space.

And this was downvoted why exactly?

Why not check on the sizes of brains vs. bodies for various big animals today and for various dinosaurs?

Welcome to the site. Your question seems to be unresearched from your side. I recommend you to read this (https://biology.stackexchange.com/help/how-to-ask) before putting your question on the site.

whales and elephants have very large brains.

It is quite possible that the dinosaurs were very intelligent - we have no way to know it. It is also possible that a few millions years from now, some creature will wonder, how humans, being so intelligent, managed to run down themselves to extinction.

@Z. B.: I would imagine that it was downvoted because there's really no answer to "why" questions about evolution, and even more so about "why didn't" questions.  The most you can say is that there was no evolutionary pressure to develop great intelligence.  When it comes to intelligence, size isn't everything.  Elephants & whales DO have large brains: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4053853/  And some of those dinosaur descendants, the birds, can be quite intelligent despite having small brains.


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Definition of semiquantitative
I'd like to understand differences between how biologists and statisticians deal with uncertainty. As a concrete example, I'd like to understand if "semi-quantitative" can be defined in terms of statistics and probability. As a first step, I'd very much appreciate any definition (either statistical or not) of "semi-quantitative". What is the distinction between a "quantitative" and "semi-quantitative" method?
Google scholar has many papers including "semi-quantitative" in the title. As an example, I'll quote a portion of the abstract from Marone, M., Mozzetti, S., De Ritis, D. et al. Semiquantitative RT-PCR analysis to assess the expression levels of multiple transcripts from the same sample. Biol Proced Online 3, 19–25 (2001). https://doi.org/10.1251/bpo20

As for all quantitative techniques, great care must be taken in all optimization steps: the necessary controls to ensure a rough quantitative (semi-quantitative) analysis are described here, together with an example from a study on the effects of TGF-β1 in TF-1 cells.

Caveat:
This answer differs fundamentally from that given by @acvill. I have not provided authoritative support for it — it is merely my understanding of the use of the terms in biological science.
The use of the terms Quantitative and Semi-quantitative in biology refer to measurements, not to statistics, although if the measurements are accurate meaningful statistics can be performed upon them. Nor is the distinction fundamentally to do with accuracy. Both types of measurements can vary in accuracy, depending on the methods used to obtain them.
In the example given, the problem is to measure the quantity of transcripts — RNAs of a particular kind (generally specific mRNAs) — that are present in only small quantities.
Quantitative measurements of such transcripts would determine one of the following:

Their number or molarity (molarity)

Their weight or concentration (grams per litre)

However doing this is difficult in the case of such small quantities of molecules found in a mixture.
Semi-Quantitative measurements of transcripts attempt to measure something indirectly related to their concentration, which, while not producing a number, concentration or amount, gives some value related to these that can be used for comparison with other mRNA transcripts.
In this case the mRNA is copied many times by PCR to eventually give an amount of product that can be measured. As far as I can see from the paper it was intensity of staining with ethidium bromide after gel electrophoresis. However it might have been incorporation of radioactivity or amount of some radioactive probe hybridized to it. In any case the measurement would have arbitrary units which could be used in comparison.
In my opinion it is the fact that the method does not measure the quantity of the mRNA (or whatever) in standard units that makes it semi-quantitative, although the indirectness of the measurement involving several stages can compromise its accuracy.
Addendum: Definition in relation to Covid antibody tests
I am wary about talking about a definition of ‘semi-quantitative’ because the definition in the reputable Merriam-Webster dictionary, citing the first use in 1927:

constituting or involving less than quantitative precision

does not correspond to current biological usage by implying that it relates to the precision of measurements. (See, for example, the Wikipedia entry on Precision to see why.)
It is of interest that the emergency approval by the US Food and Drug Administration of certain SARS-CoV-2 antibody test in late July 2020 specifies explicitly that they are semi-quantitative, and the pharmaceutical company, Roche, provides the following explanation of the term on its website.

A qualitative test determines the “if;” quantitative and semi-quantitative tests answer the question “how much?” By measuring the level of SARS-CoV-2 antibodies in a patient’s blood sample, quantitative and semi-quantitative tests give a more definitive answer about the body’s immune response to the virus. Quantitative tests are traceable to a specific international standard that ensures the result produced correlates to a numeric quantity of antibodies. Due to the current lack of an international standard, the FDA has not granted EUA to any quantitative tests. Semi-quantitative tests estimate an approximate concentration of SARS-CoV-2 antibodies in a patient’s blood sample, and can be traceable to a specific standard to ensure consistent results.

The italicization is my own to indicate the relationship to my explanation, above.

Thank you for your answer. If you have a chance, I'd appreciate hearing a generally applicable definition that captures the key features of what you wrote. Here is one attempt:
Consider an experiment designed to measure a physical quantity. That measurement is quantitative if it can be expressed in the same units as the target physical quantity. All measurements that are not quantitative are semi-quantitative.
I think most people would agree that my attempt needs some modification.

@rileysg — At present I think your definition is on the lines of my standpoint. However I am wary of definitions. In biology things are always a bit less defined than in the physical sciences. I would like time to look at other examples of usage of the term and its application. One problem with my answer is that you can try to calibrate non-standard units against a standard. Another consideration is that the nature of the assay may be internally consistent and usable for comparison in an individual setup, but the values not transferable to another setup.

@rileysg — I decided not to go in quite the direction I mentioned when I discovered the recent application of the term to covid antibody testing. This seemed to me of more contemporary general interest.

There is no strict statistical definition of semi-quantitative. Generally, a quantitative method yields results that can be compared across different experiments, whereas a qualitative method yields results for which comparisons are only meaningful between samples within a single experiment. Per your quote, we can see that the authors are using the semi- prefix to indicate to readers that the technique has not been fully optimized, and therefore any results obtained by their semi-quantitative method should be interpreted with a grain of salt.
In context of RT-PCR methods, quantitative methods typically undergo rigorous optimization to define necessary controls and a strict parameter set. This should include (1) instrument and reagent specification, (2) constraints on primer / probe design, (3) some measurement of expected experimental error, and, most importantly,  (4) use of a well-defined spike-in or control sample. A control sample or set of samples of known concentration is necessary to back-calculate the nucleic acid copy number for your experimental samples, and any RT-PCR without such a control is necessarily qualitative.
By calling their RT-PCR protocol semi-quantitative, the authors are saying to the reader "Hey, we made this method. We think it's pretty good. We tested some things, but not everything. Caveat emptor."

Thank you! Could you give a reference for your definition? Even if it's simply something you learned by working as a biologist, that would be helpful to know.

The definitions I give are just my understanding. I am a biologist.

I think David's answer fits my understanding better, but my bigger quibble with your answer would be the definition of "qualitative". Something qualitative is something that can't be put into numerical representations. It might include comparisons like "more/less" that get closer to "semiquantitative" but also includes things that can't really get any number, like lists of words or semantic relationships.


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What is the difference between the cheeks and the near parts?
Linguistically, there should be the different property or feature between cheeks and the parts right near them for us to call cheeks “cheeks.” What is the main difference between cheeks and the other parts right near the cheeks? I mean, how do we distinguish cheeks and the other parts?

https://en.wikipedia.org/wiki/Cheek seems to cover it.

@user438383 It says the only difference is position.

"Cheek" isn't really a biology specific word with a specific definition within the field, it's more of an everyday expression. Vis-a-vis Grey's Anatomy 3rd Edition doesn't even use the word at all.
In fish, for example it's mainly defined as the space between important features which have a defined function (eye and front edge of operculum).
Even the Cambridge dictionary defines it by (mostly) what it's in-between:

the soft part of your face that is below your eye and between your
mouth and ear:

So definitions seem to be fairly consistently that the cheek is defined by its spatial relation to other features, rather than a "thing". Loosely speaking, this would be reification (treating something abstract as a physical thing), and it's quite commonplace.


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Why are we more sensitive to green light when 65% of our cone cells are red cone cells?
I read, "human eyes are most sensitive in 555nm which is green. Human eyes are more sensitive to green than to red, and in low-light conditions even more to cyan than to green."
But it doesn't explain: Why are we more sensitive to green light when 65% of our cone cells are red cone cells?


text:
Do plants originate from a single cell
I read the generalization that life originates from a cell, and from my understanding animals, they originate from a single cell, produced as a result of sexual reproduction. And then life begins to develop from there on. But when it comes to botany, I stumble upon this doubt because of plant seed varieties. During any stage of seed production, can the seed be designated as having come from a single cell. Can i use the following generalization and correct me wherever i am wrong.
every life is made of cells, and every life comes from a single cell

Welcome to the site. Please take a [tour] and visit the [help] for how to ask questions and what we expect here. In particular this site values questions that show some attempt at answering themselves. So, what do you know about spermatogenesis and oogenesis in plants and fertilization?

nice of you for helping me with the terms, i will look up and get back. So my question is supposedly looked down upon as being vague, and ill-researched ?

In a nutshell, that's correct. The homework help section states: *What is a homework question?... ... A question that addresses a basic biology concept that may seem trivial to biology professionals" among other things.  You might also want to look into plant cloning and things like coppicing and stolons and compare to sexual reproduction.

Obviously a plant has to come from a single cell, because cells can only multiply by division, so at one point there must have been a single cell. In plants the germ cell is called an "ovule" and it is a single cell.

Or, as Rudolph Virchow famously put it in the 19th century: omnis cellula e cellula (“every cell stems from another cell”).

plant single cell phase is caled plant gametes.

You are actually right by saying that. The embryo of a seed is a single cell that germinates after several cell division and differentiation resulting in to a whole plant.

Welcome to SE Biology. At SE we're looking for answers that provide some explanation and context. Don't just give a two-line answer; explain why your answer is right, ideally with citations. Otherwise how can the poster or anyone else know whether or not you are correct? See the Help for "how do I write a good answer?".

In addition, to what David pointed out your answer is misleading. Most plant embryos consist of many cells and germination is often (if not usually) triggered by environmental factors and has no direct connection to cell division.  ——— NB:From "How do I write a good [answer]?" in the [help], Answer well-asked questions. Not all questions can or should be answered here. Please delete this post as it is both inadequate and encourages the posting of questions that are not appropriate for this site — please see the [tour] and other [help] pages such as [ask] and [answer] for more information.

Bro, most life on earth start drom a single celled condition called the zygote. And it is applicable to most plants also ( I say "most" because biology is full of exceptions and pretty much most of the time, we can generalize ).

Welcome Adithya. Please take our [tour] and refer to the [help] for guidance, you'll find that we need answers. to be supported by references and citations, you can improve your answer by [edit]ing those in.


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Bladder size based on child height/weight
My son is 10 years old, but weighs 24kg, which is quite little for his age.
Is it correct to estimate his bladder volume based on a formula using age? This seems to be a generally accepted way, for example: (age + 1) * 30 = volume in ml.
I would assume that a smaller and thinner child will also have a smaller bladder?

Obviously there are more factors involved than just age. But age is easy to use even if it's wrong. Very much like how BMI ignores a bunch of other stuff about people.

May I ask why you are asking this question? There are studies that answer this, and it's most important in the pediatric population because of kids with urinary tract issues. At which point is it related to height more than weight? Because obviously it's not linear.

Personal medical questions and health advice are off-topic on Biology.SE. We cannot safely answer questions for your specific situation and you should always consult a doctor for medical advice.

@anongoodnurse I'm asking to be able to discuss further with a urologist. I'm not convinced with their judgement by age, because my son is in the lowest 10 percentiles for weight and in the lowest 25 for height his age. Nonetheless, she is convinced this does not matter for his bladder size and required volumes. I'm not looking for a big discussion, but it did make me wonder if there are studies saying otherwise.

Ah, in that case, it's personal medical advice, but it's easy enough to Google, esp. if you use Google Scholar.

Well, I'm not looking for advice actually, just wondering. Because, I'd assume, smaller body, smaller organs, larger body, larger organs. I'm wondering if my assumption is correct. I did come across these studies yesterday, but I don't know enough about the subject to be able to interpret correctly: https://www.academia.edu/resource/work/12317425, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2062747/

So, to clarify further, I'm obviously consulting a doctor for this, and won't use any answers as medical advice. I'm just wondering, as an outsider, if organs are larger in larger children of the same age?


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How does sperm gets oxygen in the female reproductive tract?
At the time of insemination, sperm along with seminal plasma enters in female reproductive tract and the plasma contains fructose for providing the energy to sperm
If the fructose follows just EMP pathway (and not further Krebs cycle). Then what's the need of mitochondria. and if it does enters in Citric acid cycle and further performs oxidative phosphorylation, from where does the oxygen comes?

Do you think it is anaerobic in the reproductive tract? How do you think the cells of the reproductive tract survive?

Do you think, the cells of female reproductive tract provide oxygen to spermatozoa, well what makes you think that? I wonder if you are considering the glandular secretions to contain dissolved oxygen (do share the references of your idea if possible)

No, I was thinking more along the lines of where do the cells get there O2 from and why would the spermatozoon be any different?

Why it wouldn't be different, when a cell is not any association with any tissue fluid, what can be the transporting medium for oxygen from a foreign body of female.

Kindly upvote the question, for a better reach, Purpose is just to get the query solved asap.

Glycolysis and oxidative respiration are the main sources of ATP production in a sperm which causes oxygen regulating inside the sperm and makes it capable to move itself in the reproductive tract. But, the nutrients required for the survival of sperm are limited INSIDE THE SPERM.
But, as it enters the reproductive tract, the female body gives all the nourishment required for the sperm to survive, resulting in increased lifespan of the sperm (4-5 days).
Source: Oxidative phosphorylation versus glycolysis: what fuel do spermatozoa use?

"which causes oxygen regulating inside the sperm" what does it mean? Kindly clarify the source (precise) of oxygen.

I wrote "OXYGEN" to make you easily understand the process going on. Actually the sperm doesn't require any external oxygen. It is ATP (Adenosine Triphosphate) the energy source that provides the energy required by the sperm to travel to the ova (or the egg). This is the process of ATP formation:  ATP can be formed by 2 processes: oxidative respiration and glycolysis, both of which occur in bovine spermatozoa. Oxidative respiration occurs within the mitochondria, located in the midpiece of the spermatozoon, and results, in the case of glucose, in 36 ATPs being formed per molecule.

Full Article Source: https://onlinelibrary.wiley.com/doi/full/10.2164/jandrol.107.003533#:~:text=ATP%20can%20be%20formed%20by,ATPs%20being%20formed%20per%20molecule.

You should first understand the question, before jumping to answer it. Read the question asked.

Wait, What?? "Sperm doesn't require any external oxygen. ATPs are formed by glycolysis and oxidative respiration". Does your theory says oxidative respiration occurs without oxygen?? and the article, it doesn't holds any relevance related to question.

"Does your theory says oxidative respiration occurs without oxygen??" I didn't say that sperms don't require ANY oxygen. I said that sperms don't require EXTERNAL OXYGEN. that means the don't require external respiration mechanism. The oxygen formed from ATP synthesis is enough for them to move and fuse with the ova.

I gave you the source article to make you understand the process of ATP synthesis in Sperms.

I request you to kindly read the question asked.

Thats what I am trying to answer. The oxygen required comes from ATP synthesis.

Does ATP synthesis yields Oxygen?


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Chemiosmotic hypothesis
During the transport of electrons, some H+ are removed from the chloroplast stroma, which causes a proton gradient to build up inside the thylakoid lumen. But what's the source of H+ in stroma at the first place?

Welcome to the site. Please take a [tour] and visit the [help]. The [help] has information on what makes a good question. In particular this site values strongly questions that show some evidence of an attempt to answer it by the person asking. Please edit your question with information that you have found.

I suggest you do some research before posting here. Try reading Lehninger's Biochemistry book. They have explained it very well. If still any confusion, you come back and rewrite your question.


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Can I use the Winkler method as a way to measure the rate of photosynthesis?
I want to make an investigation where I measure how the color of light affects the rate of photosynthesis.
The idea is to put an Elodea plant in a test tube and shine with different color of light during time. I want to measure the dissolved oxygen in the beaker every minute for 5 minutes for different colors. As I have no access to a dissolved oxygen sensor I thought I could take out different samples of water every minute and separate them in bottles to conduct the Winkler method on each one. Hence, calculating the mg/L of dissolved oxygen and make a line of best fit for each color.
Is this a functioning idea? Could I get feedback?