text:
Booger like things growing on my walls
Can someone help me dealing with this? They're constantly growing on my walls whether I clean them or not. They're very solid.

I live in Yerevan, Armenia. The place where these creatures are, is my apartment which was renovated before I moved here. They've been more than just these two, I removed them but they're still growing. The size is similar to booger size, some of them might be bigger, so 3cm+ and as for the photos, it's required to post no more than 2mb and I don't know how to post a better quality as I only have a phone.

Magnifying glass? Also, please [edit] your post to include your additional info. Thanks

@theforestecologist I don't have a magnifying glass. Do you have an email that I can send photos? I'm trying to take better quality photos with more than 2 megabytes that are not allowed here.

No email. You could try cropping them to reduce size.

Do you think these could be mold?

if you crop the pictures before uploading them they will fit,what type of material is in the walls,concrete,wood,stone?

@trondhansen it's mostly concrete covered with wallpapers. They're mostly growing on wallpapers and rarely on fabrics, however one time I saw it on my tv screen. I stripped that off from the tv screen and after 1-2 days I saw it's grown again the same place on screen. I removed that and cleaned the screen with alcohol and it never grew again.


text:
Doubt in Pedigree chart : why can't the attached pic be autosomal recessive?

Why is the attached Pedigree chart can't be called as autosomal recessive also?

Pretty similar to this one: https://biology.stackexchange.com/q/114172/27148

But in there they speak about 2 families, And it's more detailed. My question is simple.

Not really, it's exactly the same. What assumptions need to happen exactly out of the things unknown for this pedigree to result from an autosomal recessive trait? What assumptions are necessary for it to result from an X-linked trait?

The premise of your question is wrong. This pedigree can very well be explained also with the autosomal recessive inheritance, and there is no way of knowing whether it is autosomal recessive or X-linked recessive purely from this pedigree.

Indian English “doubt” does not work in International English, and is not generally understood. Use “question” or “problem”.

@domen can't we decide by writing and seeing out the possibile genotype and finding out the progeny. If I am wrong ,can you correct my ideology?

@david can you say in which part you can't understand the question? I can clarify

I am not interested in the science of your question, I am only trying to help you communicate it in International English. I have suggested words to replace it and suggest you consult an online dictionary such as Merriam-Webster that will give examples of usage of "doubt": https://www.merriam-webster.com/dictionary/doubt.

@SanjayS, try it yourself! Write down the genotypes, and you will find out that the pedigree can be explained by either of the two aforementioned inheritance patterns.

@domen yeah doman I have done that , and let me attach my image in the question

Great, you've find one possible set of genotypes (not the only one though) which is compatible with the hypothesis that the inheritance is autosomal recessive. So you've answered the question yourself :)

According to me this chart applicable for both autosomal recessive and x linked recessive. I just wanna confirm you guys whether this is correct or not?

Yes, but consider what initial unknowns have to be for that to be the case and how reasonable/likely that is. In this case your autosomal recessive chart only works if the two unknowns (numbered 2 and 3) happen to be carriers. If carriers are rare in the population, that might not be reasonable.

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text:
Can someone explain the color-changing unit (CCU) to me?
I've been physically carrying out serial  tenfold dilutions on samples of Ureaplasma to work out the color-changing units (CCU).
As a definition, the CCU is the highest dilution at which there is a color change.
If the highest dilution is 10^3, apparently that means that there are 10^3 cells per ml in the original sample. But this is what I do not understand. How are we sure of this?
I feel like there is a lot that I am missing.
Any help would be greatly appreciated.

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text:
Mitochondrial diseases inheritance
I've read information about mito genes inheritance but some parts are still obscure for me.
Here is the context:
Mother has a son that is affected by some mitochondrial disease and a healthy daughter. So I suppose that mother is carrier of the recessive mutated gene which she passed to him, right? Articles in the internet tell that mito genes are always inherited from a female (link), but some also tell that two carriers are needed in order to child be possibly affected ("How is mitochondrial disease inherited?" section). But this is controversy, isn't it?
My question is:
Can daughter be also a carrier of this mutated gene? If yes, what conditions should be met in order to her to create an affected child?
Can someone please explain me this?

We can't do personal medical advice here for you or your sister. We can, however, help you to understand mitochondrial inheritance. Please refer to the specific sources you're reading (rather than "articles in the internet"), and depersonalize your question a bit to ask about mitochondrial disease inheritance rather than your family so it can be acceptable here.

@BryanKrause I am not asking personal medical advises but about general inheritance mechanism. Here is one of the articles: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3757997/ "Mitochondrial Biology and Genetics" section. However, this specific one as far as I see doesn't tell about two carriers.

Actually you are asking for personal medical advice: whether your mother is a carrier is a personal medical advice question, whether your sister is a carrier and should be worried about possible children is a personal medical advice question.

You write in your question "Articles in the internet tell that mito genes are always inherited from a female" - you should have a specific source for this (rather than "articles in the internet"), and reference that source in your question (not a comment). "two carriers are needed in order to child be possibly affected" - you should have a specific source for this, and reference that source in your question. Referencing these sources will help answerers help you interpret what you're reading.

@BryanKrause I am working on it

Your second link is from a content farm website, effectively a scam for search engine traffic. Do not rely on websites like this for information.

@BryanKrause Ok, thank you. But what about the first one? It tells that mutated mitochondria number must be larger than some threshold in order to individual be affected. Is it easy for a newborn to pass this threshold when their mother already have some of these genes?

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Water consumption of the average housefly
So, I have this question:
How much water does the common fly consume in its lifetime?
I was able to find the following facts:

Born from swine waste under 40% (waste to water ratio)
Lifespan of 15-25 days
They are 40-45% water (the flies)
avereage weight (in mg) 0.005 to 0.01 (the flies)

Also, I'm not sure where, but, I heard that flies defecate whenever they land, but I'm not sure on size or frequency.
Here are my resources:
https://en.m.wikipedia.org/wiki/Housefly
https://www.arrowexterminators.com/learning-center/pest-library/flies/house-flies
https://www.researchgate.net/figure/Average-weight-of-flies-Each-bar-represents-the-mean-and-range-thstandard-deviation-The_fig3_318433682

Welcome to the Biology Stack Exchange. Please take a [tour] and visit the [help] for more information on this stack and what makes a good question and answer. That being said, we need a bit more information in your post (edit these into the question) - What are your units for the values 0.005 and 0.01 in the list. What is under 40% in point 1. Were you able to find anything on how frequently they drank?

Please don’t waste space telling us you have a question. We’re smart enough to work that out as this is a question and answer site. More to the point, explain why you wish to know something that most of us would find completely uninteresting, and why you think modern biologists would clog their minds with such things. Houseflies, bedbugs, moths, dung beetles… What next?


text:
If microwave radiation is dangerous for rats why is not for human?
This study show how cell phone radiation(microwave) cause brain cancer at rats.
If microwave is dangerous for rats why is not for human? What is difference between rat and human cells, so we are protected from DNA damage?
more about this topis;
source 1
source 2

This is not what this summary says. There is some evidence for it in male rats, but this could not be determined in female rats of mice. Sounds fishy to me. Additionally it seems that these animals where exposed to high doses of this radiation and we already know that high doses of microwave radiation can be harmful. The question is how comparable this setup is compared to everyday usage of mobile phones. Also: Brain cancers are relatively rare, if there is a widespread problem with mobile phones usage in this context, we would see it in the population data.

@Chris It is not true that brain cancer not rise..https://www.sciencedirect.com/science/article/abs/pii/S0928468014000649

This is at least debated: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3297541/

The full report is a PDF available here1 and as a webpage at the NCBI. It is quite technical. Much of it is written in fairly plain English, but should be read with an understanding of the scientific method and the biology associated with the study.
In the OP's linked summary, the second and third paragraphs state (my emphasis):

“The exposures used in the studies cannot be compared directly to the exposure that humans experience when using a cell phone,” said John Bucher, Ph.D., NTP senior scientist. “In our studies, rats and mice received radio frequency radiation across their whole bodies. By contrast, people are mostly exposed in specific local tissues close to where they hold the phone. In addition, the exposure levels and durations in our studies were greater than what people experience.”
The lowest exposure level used in the studies was equal to the maximum local tissue exposure currently allowed for cell phone users. This power level rarely occurs with typical cell phone use. The highest exposure level in the studies was four times higher than the maximum power level permitted.

So, in the report they looked at male and female rats and mice and concluded that for male rats alone, there was some evidence of a relationship between some cancers and radio frequency radiation (RFR) exposure for 2G and 3G transmissions. The evidence was unclear for female rats and not seen in mice, and the only clear evidence in male rats was for heart tumours.
The studies were not comparable to human exposure, because they used much higher power and very extended exposures over the whole body to get this data. In humans, most of us hold our phone to our ear only rarely (certainly not the 9 hours per day used in the study), and almost never near our heart or kidney (adrenal gland sits on top of the kidney).
The paragraph on methodology goes into it a bit more:

The animals were housed in chambers specifically designed and built for these studies. Exposure to RFR began in the womb for rats and at 5 to 6 weeks old for mice, and continued for up to two years, or most of their natural lifetime. The RFR exposure was intermittent, 10 minutes on and 10 minutes off, totaling about nine hours each day. RFR levels ranged from 1.5-6 watts per kilogram in rats, and 2.5-10 watts per kilogram in mice.

As stated earlier, the power levels and duration are much higher than a typical cell phone user would ever experience, and even when they might experience such a power level, they are very very unlikely to do so for more than a small portion of the durations studied, and almost certainly not from early embryogenesis as was used for the rats.
As to exactly why these effects are not comparable to those seen in humans. The full report (linked at top of this answer) goes into this in more detail, but a summary can be made - basically it is thought that most of the effects seen and the most biologically plausible mechanism of action is heating of the affected tissues (see page 9 of the full report). Humans, being much bigger than rats experience much more localized heating and as such can absorb and dissipate greater amounts of radiation than a rat, so the effects are less.
A full review of the toxic effects of RFR has been conducted and published by the International Agency for Research on Cancer2, and for further reading see the reference section in reference 1. , Heating does not explain in full some of the effects seen and other mechanisms are being investigated, it's just that we don't currently know all the details of how RFR affects the body or even individual cell types.
Refs:

National Toxicology Program. NTP Technical Report on the Toxicology and Carcinogenesis Studies in Sprague Dawley (Hsd:Sprague Dawley® SD®) Rats Exposed to Whole-body Radio Frequency Radiation at a Frequency (900 Mhz) and Modulations (GSM and CDMA) Used by Cell Phones: Technical Report 595 [Internet]. Research Triangle Park (NC): National Toxicology Program; 2018 Nov. Available from: https://www.ncbi.nlm.nih.gov/books/NBK561730/ doi: 10.22427/NTP-TR-595

IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Non-Ionizing Radiation, Part 2: Radiofrequency Electromagnetic Fields. Lyon (FR): International Agency for Research on Cancer; 2013. (IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, No. 102.) Available from: https://www.ncbi.nlm.nih.gov/books/NBK304630/

So this is wrong? https://www.youtube.com/watch?v=BwyDCHf5iCY

@user628075 As stated in the answer: heating, the way it's done and the capacity to dissipate it. What's that or the question to do with cigarettes? That would need a separate question.

If you've a question relating to something stated in the video, please ask a question (in it's own thread) related to that, ensuring to quote the salient part and reference the time signature of where it occurs in  the video. Remember, comments are not for discussion, and asking people to watch an hour long video without stating which part concerns you isn't  helpful. @user628075


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Does lack of mental activities reduce "function" of human brain?
On internet there is lots of text how the brain "reduces its function" if you dont  use it.
Quote from link:
"In order to build connections between brain cells, and increase the connections between existing brain cells, you need to use the cells to establish the connection, and then keep using the cells, to maintain that connection."
Is this just speculations or it has been scientifically proven?
If this is true how this mechanism works?

Colloquially this is called "forgetting". Yes, forgetting is proven to exist. Everyone has experienced it personally.

Your link is to a very good article; if you look at the end, you'll see supporting literature (i.e. it's not speculation.) You can learn about how this came to be known by reading the supporting literature, or by reading this Wikipedia entry.


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Help reading gene markers
I'm sorry if "gene markers" is not the correct word. An edit could be appreciated but I don't study in an English speaking country unfortunately.
Question overview:
In a family, there is a genetic, dominant disease. The father and a son is sick.
A gene marker analysis is performed with markers close to the assumed mutated gene on chromosome 11.

Marker D11S4088

Marker D11S1344

How do I read these and "What sort of markers are these"? I'm not sure what is going on here and I'm not sure what to search either due to language problems.
Thanks!

From what kind of experiment / machine etc do these graphs come from?

I have no idea. It doesn't say unfortunately. Could be a chromatogram?

@BjarniJóhannsson Those are not chromatograms from what I can see but rather a sort of counts per marker graph. "Genetic markers" is a better word. Do you know about linkage mapping? If not read this wiki and this post, it should help.

I was thinking the same, or some sort of sequencing read coverage. I'm still not sure.

Just googling, they are SSLPs.  You do PCR, and the different alleles make different length amplicons.  Looks like there is some kind of artifact that causes some of the amplicons to have peaks that look 2, or 4, or 6 letters shorter than the true length.
So for the top marker, the 211 bp long allele is linked to the disease, and for the other one, the 118 bp allele is linked to the disease.

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text:
Help me understand my membrane potential assignment
Epithelial with the ability to transport NaCl is bathed in an isotonic salt solution with these values (in mM): 136 Na, 6 K, 140 Cl.
The intracellular concentrations are: 45 Na, 100 K, 13 Cl.
The cell's resting potential is -63 mV and the temperature is 37 Celcius.
Which ions will passively diffuse over the membrane?
My attempt: I calculate the nernst potential of each ion and taking the first ion (Na) as an example I get that it's equilibrium is at 29 mV. So as there are more of these cations outside the cell and the membrane potential is negative, the ions will want to "reach" 29 mV by flowing INSIDE the cell (to increase the membrane potential). I think they will do this by diffusing into the cell? I'm not sure if I am attacking the problem correctly or if it's rather lunging at my abilities in transporters. The NaK transporter is active transport so maybe the do not diffuse at all?? However there are Na channels that can open...Which is passive diffusion..
Calculate the cation permeability Pna/Pk
I have no idea how to do this. I still need more constants in the Goldman equation (Pcl for example) before I could isolate even one of these.
Thanks!

You can find the relative permeabilities here: http://nernstgoldman.physiology.arizona.edu/using/

Btw. if this is a homework you probably don't have to use the Goldman equation to solve it. At least my experience is that they usually give you all the variables you need.

You think I should just use the average P values like on the link? This is not really "homework", it's an assignment for next class where it will be discussed and solved in front of everyone. It's best that I try to solve it before class.

If there is passive transport for each ion, then every ion will diffuse over the membrane until the concentrations will be the same, and the membrane potential will be zero. So there is active transport in the cell, which maintains the resting potential which is -63mV.
So with the current concentrations the membrane potential will differ from this -63mV, and so the cell will change the ion levels to change the current potential to be equal to the resting potential.
I think you should try to simply summarize the Nernst potentials. It won't be so accurate as the Goldman equation, but you don't have the relative permeabilities of this cell type, so the questioner probably does not wait the Goldman equation from you.
I would solve it this way:
Em = RT/zF * ln(out/in)

R = 8,314 J/molK
T = 37 + 273 = 310K
F = 96485 J/molV

RT/F = 26,712mV

ENa = 26,712mV*ln(136/45) = +29,543mV
EK = 26,712mV*ln(6/100) = -75,152mV
ECl = -26,712mV*ln(140/13) = -63,486mV
Em = ENa + EK + ECl = -109,95mV

Emr = -63mV
Emr - Em = -63mV + 110mV = +47mV

So we have to increase the membrane potential. Decreasing intracellular K+, Cl- concentration and increasing intracellular Na+ concentration can do that.
Concentrations: extracellular 136 Na, 6 K, 140 Cl, intracellular 45 Na, 100 K, 13 Cl. So possible passive transports are increase Na+, decrease K+, increase Cl-.
Conclusion the passive transports will be increasing Na+, decreasing K+ the active transport will be decreasing Cl-.
Note that I haven't used these terms for 5 years, so if you can consult with somebody else about this, then ask him/her whether this is correct.


text:
Preservation of human tissue
At my med school we have human samples (body parts, organs, etc.)
They are soaked in some sort of solution for long term storage. I'm quite sure that it's not formaldehyde as that would be really toxic and we're allowed to pick them up from the tubs.
What sort of solution could this be?

I would assume you're using gloves to handle them?

Embalming solutions for cadaver study differ from institution to institution (and are reportedly somewhat different from embalming for funerals, but I'm not sure of those details). Typically embalming solutions for cadavers meant to be stored indefinitely consist mostly of water with lesser but roughly equal amounts alcohol (usually methanol), gylcerin, phenol, and a smaller percentage of formalin/formaldehyde to prevent mold.
A document from Albert Einstein College of Medicine lists:

Methanol: 11.1%
Glycerin: 11.1%
Phenol: 9.3%
Formaldehyde: 1.9%

If you want to know what your institution uses, you should just ask, and they should be willing and able to tell you.

Thank you. That explains why it's okay for us to handle them.


text:
Problems understanding membrane potential
I understand that membrane potential is the difference of the extracellular and intracellular ionic charges, due to their concentrations. We say that the extracellular space has a charge of 0 and then take the membrane potential with respect to the extracellular space. The intracellular space is normally around -60mV due to more negative charges being in the cell than the extracellular space.
This is how I understand membrane potential.
From this understanding, it is hard for me to see why I can't get this right:
We work with a regular cell with potassium 120mM inside and 4.5mM outside.
Say that we increase the intracellular concentration of potassium by 10 mM, a +1 valence ion which contributes to POSITIVE membrane potential.
What I envision is that as we put more positive ions in the cell, the cell is now more positive in regard to the extracellular matrix. However the Nernst equation states that the membrane potential actually gets MORE NEGATIVE!!
http://www.physiologyweb.com/calculators/nernst_potential_calculator.html
What is it that I am misunderstanding? Thank you.

An increase of the intracellular concentration of potassium decreases the membrane potential, i.e. makes it more negative. The Nernst equation provides the potential required 'to keep' the ions from flowing out of the cell, down their gradient. You shouldn't view those positively charged ions within the cell as positively contributing to the membrane potential. It's the contrary, the Nernst equation provides the potential to maintain the electrochemical equilibrium, as if it needs to stop the ions from flowing out of the cell (you need a negative potential to oppose + charged ions).

I think this question has more to do with kinetics / transport phenomenons than biology, but that's okay, everything is connected especially my computer to the internet. ;-)
The basic idea behind transport phenomenons is that there will always be a flux of quantitative properties (e.g. charges, particle number, entropy, volume, etc...) where the qualitative properties like (electrical potential, chemical potential, temperature, pressure, etc...) have a gradient in space (note that kinetics of chemical reactions can be described similarly without the space gradient part).
In this case we are talking about electrochemical potential gradient and ion flux. It is very important to recognize that the electrochemical potential is not the same as the electric potential. It has a chemical component, so the result will depend on both charge and concentration gradients. By a single ion channel system (e.g. Na⁺ channel only) you can count the potential of each side of the membrane using the Nernst equation, by a system with multiple ion channels it is more complicated, so in that case you have to use the Goldman equation. So at the end you can say something like one side has a potential of x[mV] and the other side has a potential of y[mV] and so the difference is:  d[mV] = x[mV] - y[mV]
The sign of d depends on x or y has a greater value. By single ion channel systems this expresses an x → y direction so by positive d the cation flow direction is x → y and by negative d it is y → x. By anion flow it is the opposite.
By cells we use the out → in direction by counting the membrane potential. We can count the potentials using the

Nernst equation:
$$E_m = \frac{RT}{zF} \times ln \left(\frac{c_{out}}{c_{in}}\right)$$ or the
Goldman equation:
$$E_m = \frac{RT}{F} \times ln \left(\frac{p_{K^+}.[K^+]_{out} + p_{Na^+}.[Na^+]_{out} + p_{Cl^-}.[Cl^-]_{in}} {p_{K^+}.[K^+]_{in} + p_{Na^+}.[Na^+]_{in} + p_{Cl^-}.[Cl^-]_{out}}\right)$$
where

$Em$ is the membrane potential
$z$ is the ion charge
$[X]$ is the ion concentration
$p_X$ is the relative membrane permeability for the actual ion

and so on...

So for example by an average human cell in blood plasma, assuming that the inside of the membrane has a small negative charge

the Na⁺ has a positive effect (positive charge, high out → in concentration gradient, low out → in charge gradient),
the K⁺ has a negative effect (positive charge, high in → out concentration gradient, low out → in charge gradient),
the Cl¯ has a negative effect (negative charge, high out → in concentration gradient, low in → out charge gradient)
the Mg⁺⁺ has a small positive effect (positive charge, low out → in concentration gradient, low out → in charge gradient)

on the membrane potential. It is hard to find an ion in this case which flow is charge gradient dominated instead of concentration gradient...

I understand that membrane potential is the difference of the
  extracellular and intracellular ionic charges, due to their
  concentrations.

The (sign and) value of the membrane potential is not determined by the charge gradient because the concentration gradients usually have a much bigger effect on it. The cells maintain these concentration gradients by using up energy.

We work with a regular cell with potassium 120mM inside and 4.5mM
  outside.
Say that we increase the intracellular concentration of potassium by
  10 mM, a +1 valence ion which contributes to POSITIVE membrane
  potential.

In your case K⁺ has a negative effect on the membrane potential, because of the high concentration gradient with reverse direction. So decreasing the concentration gradient will increase the membrane potential.
If you want to learn more about how to count membrane potentials, you should read this and its next section instead of wikipedia...

@WYSIWYG Thanks the edit, I did not know it is possible to use an equation description language.

yeah it is $\TeX$

So basically K has a negative effect because of its gradient. What if I'd put 100mM outside and only 5mM inside? Shouldn't the gradient now change and the effect be opposite?

Yes it will be then positive. ln a/b = - ln b/a

I can't seem to replicate this effect with the tool in the link you posted in another question: http://nernstgoldman.physiology.arizona.edu/using/
If I put 100mM outside and test the slider for inside around 100mM it still just goes one way.

@BjarniJóhannsson Then I am wrong or your counter is wrong, I don't know, I learned it this way... ;-)

I think I was misunderstanding the tool

I think inf3rno's answer is very complete, so I will just be adding some notes that might help OP understanding what's happening.

Say that we increase the intracellular concentration of potassium by
  10 mM, a +1 valence ion which contributes to POSITIVE membrane
  potential.

Let's say we do that, in an in vitro cell model, using a syringe with only K⁺ ions. What would happen?

What I envision is that as we put more positive ions in the cell, the
  cell is now more positive in regard to the extracellular matrix.

And that is true, at least instantly. However, due to the differences in concentration gradients, the K⁺ would quickly flow out until electrochemical balance was restored. This would lead to an increase in K⁺ concentration outside our cell model so, in the end, the net charge would decrease inside the cell.
So you can think of the Nernst equation as a mathematical model to the cell in equilibrium.

"However, due to the differences in concentration gradients, the K⁺ would quickly flow out until electrochemical balance was restored. ... So you can think of the Nernst equation as a mathematical model to the cell in equilibrium. " - Yes that's true.


text:
Are there any studies of epigenetic difference between twins during their lifespan?
Are there any studies of epigenetic difference between twins during their lifespan ? I ask because I wonder if there exist phases during lifespan, when environmental factors plays major role (expecially in early adulthood) - twins study should allow to distinguish between changes in epigenetic  profile caused by external factors and that from "inner dynamics" of organism.

I would think there have to be, though do you mean collecting samples on a regular basis and plotting out the difference at each point? Or do you simply mean the total accumulated change. If it is the latter, the answer is certainly "yes". You have probably seen the Nova documentary "Ghost in Your Genes" (The US, not BBC one). In it they show comparison of accumulated epigenetic change between a pair of identical twin Spanish women. I'm guessing you are more looking at measuring this change on a regular basis and looking for points of rapid divergence.... I don't know if this has been done for individuals, but it appears that it has been done for sample sets (see the same documentary). They discuss accumulated genetic change in younger twins vs older ones...

Great ! I think similar, regular studies are going to come, but can you write more on the latter case, for example about rate of epigenetic changes ?

I have seen "Ghost in Your Genes". Excellent doc, which, in part, got me thinking about this (yes the Spanish twins in particular). I was meaning more systematically through life (testing at regular intervals). In the documentary, the observations seemed a bit less pre-defined. On a related note, could anyone point me to the specific methodologies for assessing whole-genome epigenetic differences?

good question, ask it but not as a comment


text:
Snake with red eyes and black skin found in a plant pot
It was found dead/stiff in an empty plant pot in a kitchen.

Could it be a young Höllenotter (a melanistic vipera berus, photo in Wikimedia Commons)?
Is the reddish/brownish part an injury? And what are the greyish parts (especially at the snout)?
Size (only estimated)
Diameter: 2.2 cm
Length (in this rolled-up state): 10–12 cm
Location
Western Germany.
In the kitchen were three plants pots in a row that were used for culinary herbs, one still had basil, the other two were empty for some time. It’s unknown if the snake was already there when the pot was emptied.

Are there any pictures, which are not out of focus? Or maybe a close-up of the head?

@JulPal: Unfortunately not, this is all what I’ve got (I didn’t make the photos).

For me it looks more like a leech or a worm than a snake. a better pic of the head would be more useful.


text:
Formaldehyde turns plantar region of feet red?
I'm a freshman med student and I've noticed that on all the feet (and hands) of deceased people that I've worked with, the bottom of the feet always turns red and also the inside of the palm? Why is this?
Thank you.

I haven't seen any cadavers, how red are you talking about?

It might be due to livor mortis, also called postmortem lividity, which is the settling of the blood in the lower parts of the body which in your case might have been the limbs. By time the color can be interpreted as either blue or purple, but given, that not much time has passed it can very well be the reddish color you might have asked, as stated here on page 39:

The first manifestation of livor mortis can be expected 20-30 min following the irreversible cardiovascular arrest, initially as bright-red spots that subsequently become confluent and turn bluish-violet.

Which might better describe your case is the fact, that cold conditions can cause bright red color in livor mortis, as it can also be found on page 39:

Cold conditions, such as keeping a body in cold storage, cause ... bright-red livor mortis.

You can read more about it here or here.
EDIT
I have added references thanks to @Kendall, who provided them.

On these sites it says the extremities turn blue/purple with livor mortis: http://noirtek.weebly.com/embalming.html  and http://deemzet.nl/5/3/3/links.htm (dutch site)

After long time it can be seen as blue/purple as pretty dense amount of blood indeed have a color like that, but earlier it might very well be considered red.

A case study in this text on forensic medicine, page 23, makes note livor mortis may be bright red. Then, on page 40, a table notes bright red livor mortis is result of postmortem cold storage, among other causes like CO poisoning.


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Confused with gamete sorting problem
A man has the genotype AaBbCc, in other words he is heterozygous in three uncoupled loci on three different chromosomes. A, B and C are the dominant alleles while a, b and c are the recessive alleles.
1. How many gametes can he form?
The answer is 8 and I can see how you derive that by just manually writing each and every one down but what is the mathematical method to derive this? I tried permutations but none I came up with worked.
2. He has a child with a woman of the same genotype (AaBbCc) how many different genotypes can the offspring have?
Here the answer is 27. I'm not sure how they came to this conclusion either?
3. What is the probability that the offspring has the genotype AaBbCc?
This is about the time I start flipping tables because it seems to me that it's 1 out of 27. There are 27 different genotypes and this is ONE of them?!
But the answer is 1/8 as there's a 50% chance of Aa, Bb and Cc when mixing apparently so it becomes 1/2*1/2*1/2. Why isn't it just 1 of the possible genotypes?

Since there are 2 alleles of each gene and 3 different genes, 2EE3 = 8? Let's test this by making a table, for 1 gene there are two different kinds of gametes, so 2EE1 = 2, for 2 genes there are 4 different kinds of gametes (AB, Ab, aB, ab) so 2EE2 = 4, and you already did the calculation yourself for 3 genes, and 2EE3 =  8.

Why don't you try working it out yourself for 4 genes and see if you come up with 16 different kinds of gametes?

Two words: Punnett Square. In this case for a trihybrid cross:

That is a Bernoulli coin-flipping probability. If you are flipping a true coin three times in a row, how often will you get three heads in a row? 1/8? All the events are independent, right? what about the Punnett square? Does it give the same result somehow?

Here is the answer worked out for you.


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How are ketone bodies used?
While searching for literature on ketone bodies, I can only seem to find how they are synthesized, but not how they are broken down.
I'm looking for the series of events with enzyme names and intermediates. Does anyone have this?

First, there are three ketone bodies: Acetone (top), acetoacetic acid (middle), and beta-hydroxybutyric acid (bottom), see the illustration from the Wikipedia:

The second and the third are taken up by heart and brain cells and then converted into Acetyl-CoA which is fed into the citric acid cycle where it is further metabolized. Acetone is mostly excreted. See here for some more information.
Aceto acetic acid is either converted into acetone and removed from the body or enzymatically converted into beta-hydroxybutyric acid by the beta-hydroxybutyrate dehydrogenase.
The third possibility is that it is converted into Acetyl-CoA. See the figure for the scheme:

For a more detailed explanation of this process (both, the generation and the metabolization of the ketone bodies) see here.

You say the second and third are taken up by heart and brain cells. Aren't they also used by muscle cells during starvation?

During starvation/fasting*

@Paze - muscle cells predominately continue to oxidize fatty acids in the fasting/starvation state


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Advantages and disadvantages of sporulation compared with competence in bacteria?
Why do bacteria have both of these mechanisms to deal with the same environmental stress: nutrient deprivation? In a culture exposed to this condition, often both competent cells and sporulated cells are found.

Sporulation is a process that is very hard reverse. While it is a good as last resort, trying to find a solution (Competence) might be a faster way to resist the stress. Lets say antibiotics were introduced into medium. Part of population might sporulate when detecting malignant conditions but part of population might search for plasmid with resistance genes. In other words, these two mechanisms are independent so we can increase fitness by applying both.


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What is the purpose of two cell divisions in meiosis?
At the moment, my thoughts are that the two cell divisions are necessary for recombination to occur, although I am not sure. I cannot really see why technically, the chromosome from each parent cannot just recombine with the other chromsome when each is a single DNA strand and not in the form of two sister chromatids joined at the centromere. Something tells me that there are several reasons why there are two cell divisions. Perhaps the S phase of interphase triiggers some further stages of cell division such as cytokinesis, and the splitting of the cell will not occur unless some DNA replication has taken place? However in meiosis 2 there is no further DNA replication, so this can't quite be right...

For developing a 2N cell, we need a N cell from each parent. In any division(meiosos or meitosis), chromosomes are doubled at first. In firs meiosis a 2N cell in divided into two N cells and as you know these N chromosomes are doubled( 2N chromatids). In second meiosis a N cell is divided into two N cells but this time chromosomes are not doubled(in fact N chromatid cells)
1.Firs division in meiosis is needed because we need N cells to combine, if they are 2N the result of recombination is a 4N cell.
2.Maybe your question is: why a 2N cell is not directly divided into two N cells without doubling? the reason is same in mitosis and meiosos, it is because of a stage of division as you know it is called anaphase in which a kind of protein, connects centromer to centriol, this stage is needed because we need one chromatid of each chromosome in each cells so if this part is not done there is no guarantee to have all N chromosomes in both cells and in fact a kind of distribution is made.
( I hope that I could understand you, well.)


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Sex linked genes?
I am learning about genetics and sex-linked traits. All of the X-linked traits we have considered (eye colour in Drosophila, Duchene Muscular Dystrophy to name a couple)follow the rule that, a female will only express the phenotype if she has both of the alleles and a male will necessarily express the phenotype if his X chromosome contains the allele.
However this got me thinking, is there a gene that requires two copies to be expressed (and not just due to dominance considerations)? I.e., are there any x-linked genes which, even if the male has this gene, it will not be expressed as there is one copy of it only (despite the fact that this gene is on a non-homologous region of the X chromosome and therefore there is no second allele to this gene present in the male). In that case only the females could express this trait if they are homozygous for the allele, and men would never exhibit the trait.

then why is the other x chromosome gets inactivated?...

@JM97 I'm afraid I didn't understand your question :/

What @JM97 appears to be saying is that in females there is a process called X-chromosome inactivation which shuts down one of the chromosomes to prevent females having a double dose of a particular gene product. This would invalidate your premise that genes that require a double-dose of expression (as it were) could be only expressed in females.

It is not easy for an individual to figure out if it is haploid or diploid at a given sequence. To my knowledge, this is feasible only by searching for specific case of heterozygosity.
The most famous case is mating types in yeasts. In yeasts, haploid cells have mating types. Individuals are either "a" or "$\alpha$". Individuals can only fuse with individuals of a different mating type. As a result all diploid cells contain both the "a" allele on one chromosome and the "$\alpha$" allele on the other chromosome. The "a" sequence codes for proteins that can bind only the proteins coded by the "$\alpha$" sequence. If "a-$\alpha$" dimers are formed, then the cell "knows" it is diploid. Read more about it on wikipedia > mating of yeast.
Following this, a cell could figure out what sexual chromosome it has by searching for heterozygosity. This is typically NOT how gender determination works in mammals. I can't think of a specific example where this would be a thing but I would surprise if it is not.


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Reason for variation in the site of onset of edema
What is the reason for the observed clinical difference in the earliest site of onset of edema in cases of different etiologies?
For example, in Congestive Heart Failure, it appears initially as pedal edema (edema of the dependent portions, in general) but in nephrotic syndrome (or other kidney causes) appears first as periorbital edema?
In both these cases, since the onset of edema is distal to the organ of the original pathology, it must be a systemic hematological effect caused secondary to the pathology that causes this specific pattern (as opposed to a localized portal hypertension in liver disorders initially appearing as ascites). Although all of these may progress to anasarca, what determines the specific pattern observed?

We should first recall how plasma (intravascular) fluids moves to the extravascular space. It can be approximated by Starling equation. Briefly:

The rate at which fluid is filtered across vascular endothelium (transendothelial filtration) is determined by the sum of two outward forces: capillary pressure ($P_c$) and interstitial protein osmotic pressure ($\pi _{i}$), and two absorptive forces: plasma protein osmotic pressure ($\pi _{p}$) and interstitial pressure ($P_i$).

See more: Starling equation
Primary edema localisation depends on the underlying pathophysiological mechanism that disturb the balance between aforementioned forces pushing fluid outside the vessels. Whether the Starling forces are alerted globally or locally, how long the edema develops etc.
Example from Harisson's Principles of Internal Medicine (I recommend the whole section regarding the edema):

Edema due to an increase in capillary pressure may result from an elevation of venous pressure caused by obstruction to venous and/ or lymphatic drainage. An increase in capillary pressure may be generalized, as occurs in heart failure, or it may be localized to one extremity when venous pressure is elevated due to unilateral thrombophlebitis.

In Congestive Heart Failure edema usually appears in places, where intravascular hydrostatic pressure is the highest. When the individual walks it is typically seen as ankle swelling, when the individual lies down, it is lumbar region edema.
While there is a decrease in osmotic pressure (like in nephrotic syndrome), the fluid moves toward extracellular tissues of relatively "loose"  structure (so for example periorbital region).
What is important, in some medical condition (eg. renal failure) different mechanisms may coexists and change the clinical picture.


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Why can't fish extract oxygen from air?
I've read many posts here and elsewhere for example:

Wikipedia where breathing is well described, but does not answer the question (or anything close.)#
Wikipedia Gills, more specific, but still doesn't answer the question
This blog post
Several Quora's blogposts including this one.
Also some Youtube videos like this one

and I do not think that the fact that gills surface / contact area is larger with water wrt to air fully explains the reason why they can not breathe in air.
I wonder if one possibility is that they do not control the bones that open the gills (I don't know the name.) since they seem to use the water pressure to some extent for that matter.
Is there a more detailed explanation that you can offer, or point to?

What about how fish gills collapse in air? And they have no way to pass air over their gills? Or how gills dry out?

@DKNguyen gills have still a lot of surface area, and more oxygen density; for the dry out, that's a second question, but not the main one.

Surface area doesn't mean much if your gills collapse.

Drying out is not a separate question.

The microstructure, too small to see with the human eye absolutely collapses to a small fraction of its surface area. Just to note: 1) Prior research is a requirement when posting, 2) the purpose of comments isn't to be "interesting", or to make derogatory remarks, it is to request clarification from the OP and to provide direction to new contributors those who may lack familiarity with the site's ways and with the topic.

What you've cited is blog-posts and Quora threads, not scientific papers or from scientific journals. I've requested that you show your prior research, please do so - bearing in mind that we accept scientifically credible sources (Wikipedia is a secondary source but a good place to start as they have references you can follow-up on). I've also explained to you what comments are for, they are not for answering the question (with or without references).

They are not considered credible on this site or any scientific site on the network.

There really isn't any discussion to be had, I'm just trying to help you to use the site the way it's intended. You can read the [ask] section of the [help] for clarification, or wait for "someone more knowledgeable" if you wish.

The blog-post is fine, seems credible to me, as far as it goes, but it's very broad and not specific to your question.

added 2 relevant sources that i read completely and you asked for @JiminyCricket.

From the Wikipedia page on gills that you link:

The density of the water prevents the gills from collapsing and lying on top of each other, which is what happens when a fish is taken out of water

Wikipedia's source for this statement is a biology textbook: M. b. v. Roberts; Michael Reiss; Grace Monger (2000). Advanced Biology. London, UK: Nelson. pp. 164–165 though I'm not able to access this source.
You need a lot of surface area for gas exchange. If the gills collapse as they do if not submerged in water, there's not enough surface area for gas exchange. If you did somehow spread them out mechanically, they'd dry out. You might think about how a net can sit expanded in water, but if you pick it up it all bunches up; same as gills.
Other sources:

Gills are very delicate, almost paper-like structures that depend on the buoyancy of water to remain open. The fragile gills will collapse if the fish is taken out of the water because air doesn’t have the same density and buoyancy water has to keep the gills open and functioning. This is why a fish cannot live outside the water.

https://blog.limnology.wisc.edu/2016/09/14/at-home-in-the-water-condemned-to-life-on-land "This essay originally appeared in the Lakeland Times in Minocqua, Wisconsin. Carol is an Aquatic Invasive Species expert and outreach specialist with the CFL and Wisconsin DNR."

A paper on a fish with modified gills that allow it to breathe in air:

The bowfin, Amia calva is a facultative air breathing fish restricted to North America and is reported to estivate. ... The secondary lamellae are fused to form a lattice-work of rectangular pores, a gill arrangement unique among freshwater fishes. This highly modified gill structure imparts considerable rigidity such that these do not collapse upon air exposure.

Daxboeck, C., Barnard, D. K., & Randall, D. J. (1981). Functional morphology of the gills of the bowfin, Amia calva L., with special reference to their significance during air exposure. Respiration Physiology, 43(3), 349-364.

What is being said here, is not how one should reason imho it's at best suggesting that they correlate. Yes, they collapse and the surface area decreases, we all know that, it's even included in the post, so doesn't add anything new. Maybe the source has some extra details. Currently, this isn't at all an answer. Feel free to downvote again, since that's how people reason here apparently.

I will also add, that I do not find that quote, or even an equivalent statement, in the linked article from Wikipedia (not a book as you said, and we should include the source if it is open source): https://evodevojournal.biomedcentral.com/articles/10.1186/2041-9139-3-24

@MahNeh The source is the one that I posted in my answer (ref "#4" on the Wikipedia page), which is a book, not the link you have ("#7") - not sure why you're looking at that one. And no, this is not saying that they merely correlate. Surface area is critical for gas exchange and causal for sufficient gas exchange. Surface area of gills decreases massively in air, to the point of insufficient gas exchange. That's the answer. If you want a different one, that's not likely to work out well.

In any case, you should have include the source of your claim. And for the blog-post you include that's a simple paragraph, not an experiment. I don't just follow possibilities as if they were true. If that's a theory, must be validated, the link you should is not the validation, so it's wrong and not an answer.

@MahNeh I did include the source: Wikipedia, as well as Wikipedia's source. I've now included a couple other corroborating sources. The idea that surface area is important for gas exchange is quite trivial physics, but isn't something you asked about. I'm not sure what experiment you're looking for, this is something that anyone looking at gills can observe: they collapse in air. We know that surface area is critical for gas exchange, so observing the collapse is all you need to do as an 'experiment'.

I am a physicist, and don't need explanation on that (as I said, it was included in the post since the beginning.), because that's not the only variable here, but I don't think this is any good, and won't bother helping more. Bye.

I hadn't downvoted your question before but now I will as I see it has not been asked in good faith. Good luck.

@MahNeh - Please define ignorance, because the user answered your question definitively, with sources. That's generous and informative, not ignorant, unless your definition of ignorance is different from mine. You have repaid the user with insults.

Please, re-read the comments @anongoodnurse

@MahNeh Do you buy the reasoning that human lungs work in air but not underwater because they have do not have enough surface area for lower oxygen levels in the water, but have measures to prevent collapsing when not submerged? I am not sure any answer will be good enough for you since it sounds like you want comparative artificial or mathematical models of what are biological structures and technology just has not enabled those to be as readily available in biology as they are in physics.

@MahNeh Should she re-read the comments where you're confused between reference 4 and reference 7, and what should she conclude from those?

@DKNguyen, sorry I am tired. Thanks though, geniuses, for explaining to a simple man.

@BryanKrause she should read tribe behaviour, then you will understand how you behave, as the monkey with the stick. Take care.

Fish can't exchange gas efficiently in air with their gills.  However, many more fish can breath air than people often think, even those you wouldn't normally think of as "air breathing", but they don't use their gills.  All bony fish have a swim bladder, a sort of internal water wing that fills with air and allows them to remain suspended in the water column at rest.  Fish can change their buoyancy by diffusing gasses into or out of the blood, changing how full the swim bladder is.  So, you actually have something that does almost all the stuff lungs do.  It holds gasses and allows for them to be exchanged between itself and the blood stream.  Give it a way to be filled from the outside and you have a simple air breathing system, and many fish do just that.  They gulp air and have some way of getting that gulped air into their blood, either from the stomach or the swim bladder.  A lot of fish who live in murky water or water likely to be somewhat de-oxygenated not only are able to do this, but need to.  Beta fish will actually drown if they are blocked from surfacing to gulp air.  So yeah, lots of fish, even ones that you don't think of as "air breathing" can breath air, but they don't tend to do so with their gills.  Some gas exchange can still happen through the gills so long as they remain moist, but you need something that won't collapse or dry out to actually be able to breath out of the water.


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Radiocarbon dating tooth from living person
Would it be possible to use radiocarbon dating on a tooth, lost by a person while they were still alive, to determine that person's birth year?
Imagine an adult who loses a tooth for whatever reason at age 40, but lives to age 100.  Would that tooth suffice to approximate their birth year?
Edit to include:
In an effort to not waste people's time reading a long question, I erred on the side of too little information.

Yes, I'm very familiar with the Wikipedia article on radiocarbon dating.
I have read the linked similar question and all of its responses.

Which leads to these specifics:

Is one adult human tooth adequate for radiocarbon dating purposes?
Could such a tooth from a period of 200 to 700 years ago be dated to within a small enough window to make a difference, i.e. the window would be smaller than 500 years.

Delving into that, I found a number of articles.  This one on radiocarbon dating on recent human remains was partially helpful:  https://nij.ojp.gov/topics/articles/applying-carbon-14-dating-recent-human-remains
TL;DR:  For people who acquired adult teeth between roughly 1965 and 2030, the technique will work, thanks to unusual amounts of C14 in the environment as a result of nuclear weapon testing.
This article suggests the ability to date samples of a similar recent vintage, though I did not purchase the article and read the whole thing:  https://www.cambridge.org/core/journals/radiocarbon/article/abs/application-of-radiocarbon-dating-to-forensic-investigation-and-evaluation-of-formaldehyde-influence-on-radiocarbon-age/1B02FEF83B5D1F5E11F8E02D9550A57D
This is sadly not useful for me, with my teeth samples carefully preserved from someone who was born in 1552.
It looks like the answer to my question is "no" -- C14 dating is too imprecise to be useful for such a recent and short time span.  But this is my non-expert reading of the various articles mentioned and linked.

Possible duplicate: https://biology.stackexchange.com/q/24084/5198

@John Make your comment an answer and I'll mark it as the answer I was looking for.


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Why do monoclonal and polyclonal antibodies behave differently as labeled secondary antibodies?
According to the MBL guide to generating antibodies, the differences between monoclonal and polyclonal antibody extend beyond the fact that the latter is heterogeneous, binding to various epitopes for the same antigen. According to the source, monoclonal and polyclonal antibodies behave differently with respect to labeling:

Labeled (secondary) antibodies:
Similarly, only one antibody molecule can bind to a primary antibody molecule if the secondary antibody is a labeled monoclonal antibody. Whereas multiple antibodies can bind to a primary antibody molecule if the secondary antibody is a polyclonal antibody.
Consequently, polyclonal antibodies provide a higher sensitivity of detection (amplification of the signal) and, therefore, are commonly used as a secondary antibody.

What is the mechanism for this difference?

The mechanism for this is (as stated in the first sentence of the quote) that in a monoclonal antibody all antibodies bind the same site (epitope), whereas in a polyclonal antibody you have a mix of antibodies that all recognize different parts of the antigen. Therefore, multiple polyclonal secondary antibodies will bind the primary at different sites, while in a monoclonal secondary there is only one site in the primary antibody that is bound.


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Will diffusible protein aggregates coated in cell-free nucleic acids near a depolarizing neuron's soma diffuse along the axon to synapsing neurons?
Edit in response to feedback in comments requesting specific details, etc.: Will aqueously diffusible protein oligomers and protofibrils coated in cell-free nucleic acids in the aqueous interstitial space near the neural soma of a cluster of long-projecting hippocampal pyramidal neurons diffuse along the length of their axons (i.e., parallel to the velocity of the axon potential) if the neurons depolarize, causing them to migrate from near the cluster of hippocampal pyramidal neurons proximal to the group of neurons their axons are synapsing with in a neocortical association cortex as part of the default-mode network?
To clarify a commment, we already have evidence (most of it already published) that these aqueously soluble and diffusible nucleic acid-coated protein oligomers and protofibrils do accumulate significantly in the cerebral cortices (and probably the hippocampi and entorhinal cortices too) of patients with the disorder we study  compared to those of control individuals who passed away without this disorder. However, we do not know if these particles diffuse stochastically with no net vector, or whether they might migrate in specific directions under some circumstances, which could promote inter-regional seeding of these aggregates. This is not something we intend to build.
I think nucleic acids (and proteins) diffuse in a partially charge-density dependent manner through aqueous spaces in a voltage gradient. For example, Bass and Weintraub found that RNA duplexes migrated further than their constituent RNA monomers did on native 4% polyacrylamide gel electrophoresis (PAGE) (1). RNA duplexes have a higher mass than monomers, but they have approximately twice as much charge density. As they wrote, "RNA was extracted from these oocytes and embryos and analyzed by electrophoresis in a native 4% polyacrylamide gel. This gel system
easily resolves the faster migrating duplex RNA (D) resulting from the hydridization of sense and antisense CAT RNA from nonhybridized
monomer RNA (M) (Figure 1)." Below is their Figure 1 (A) showing the gel in question, with the legend stating it is a native gel.
As far as I understand it, native (i.e., non-denaturing) PAGE is a somewhat ideal model of the aqueous diffusion of small charged particles. Polyacrylamide mixed with water forms a gel with small holes in it. Molecules are free to diffuse in the aqueous phase, but they have to pass through these holes to migrate far. Negatively charged particles are pulled  towards the positively charged electrode (anode). SDS-PAGE is a common variant of PAGE wherein proteins migrate according to their size, because they're denatured and coated evenly with the negatively charged chaotrope SDS, making their charge roughly proportional to their size.
Here is a GIF of a depolarizing neuron to help visualize the question:

As a simplifying assumption, let's say it's improbable that the nucleic acid-coated protein aggregates will cross the plasma membrane. In reality, oligomers of this particular protein, and structurally and functionally analogous virus-like particles, can cross the plasma membrane primarily via heparan sulfate proteoglycan-mediated macropinocytosis, and secondarily via clathrin-mediated endocytosis. Whereas, soluble fibrils of this particularly protein do not get taken up by cells (at least the larger fibrils). I would rather not provide citations to these claims, as it's not necessary to understand or answer the question, and doing so would give away what I'm working on specifically, which I would rather not do publicly yet.

Bass, B. L. & Weintraub, H. A developmentally regulated activity that unwinds RNA duplexes. Cell 48, 607–613 (1987).

Original post: Let's say there's a small, densely negatively charged object just outside the cell body of a neuron. It is freely diffusible in the aqueous interstitial space. Let's say it's improbable that it will cross the plasma membrane to enter the neuron. Then the neuron depolarizes. Is enough of a voltage gradient (and electromagnetic field) created by deplarization that it will cause the negatively charged object to diffuse? If so, in what direction? Will it diffuse down the length of the neural axon as it depolarizes?
What if the object can cross the plasma membrane? Then will it likely do so?
This object diffuses far in a native polyacrylamide gel electrophoresis (PAGE).

Welcome Odin. Please take our [tour] and read-up in the [help] particularly the [ask] section. We require one single clear question per post, and for you to show your research when posting. At the moment you've several vague questions - can you please [edit] to clarify what "object" you might be referring to, what you mean by "diffuse down the length of the neural axon as it depolarizes" and why you think electromagnetism might be a major factor, then add your research.

This is purely hypothetical, ions travel through specialized channels and pumps and typically 'objects' whatever that may be don't travel passively across the membrane. I suggest to focus the post into one specific question (and not a bunch of unrelated ones) and use a relevant, plausible situation instead of talking about hypothetical objects with ill defined characteristics

Hi Jiminy and Alice, thanks for the feedback. I have updated the post accordingly. Please let me know if you have any further feedback.

My short answer would be "no I don't think whatever you are planning will work". The longer answer is, if you want to engineer something new, you have to be prepared to build and test it, and if you don't know what you're doing you have to be prepared to hire people who do, not ask on StackExchange.

@BryanKrause This is naturally occuring, not something I plan to build. We know that these aqueously soluble and diffusible nucleic acid-coated protein oligomers and protofibrils do accumulate to some extent in the cerebral cortices and probably hippocampi and entorhinal cortices of patients with the disease I study. The question is simply, will they diffuse randomly, or in particular overall direction, e.g., when outside a cluster of long-projecting pyramidal hippocampal neurons with axons synapsing with distant neurons in a neortical association cortex as part of the default-mode network?

Okay, do you know that if the neuron in your diagram is a pyramidal cell you've drawn the depolarization along a dendrite?

@BryanKrause That's just a GIF of a depolarizing neuron I found online to help visualize the voltages created by an action potential. It's not of a pyramidal neuron.
We do not know that pyramidal neurons would be involved in this specifically. It just seems somewhat likely since they appear to degenerate especially severely in this disease, and they often synapse relatively long distances. Commenters seemed to want more specific details, so I added that in too in hopes of making it clearer.


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How do you find the template strand for a sequence where start codon is in both strands?
Maybe I'm missing something very obvious but I can't seem to understand how to find the template strand given a sequence and its complementary strand if both strands contain ATG from 5' -> 3'. Consider the following example of a DNA sequence:
5′ TCAATGAGCTGCCTTCATTAA 3′
3′ AGTTACTCGACGGAAGTAATT 5′
I can find ATG in the top strand from 5' -> 3' but also in the bottom strand when reading it 5' -> 3'. I usually try to find the start and then know that it will have to be the coding strand, but I'm lost in this scenario.
The sequence is originally from an exercise where the given sequence has a mismatched A - A mutation. This is the original sequence:
5′ TCAATGAGCTGCCTTCATTAA 3′
3′ AGTTACACGACGGAAGTAATT 5′
If we check what would happen if either the top or bottom Adenine was replaced with a Thymine, we would get different types of mutations. This was just an example sequence I thought would be alright to set the stage for a start codon on both the top and bottom.

Welcome to Biology StackExchange! Can you please explain a bit more what these sequences are? Do you have a DNA sequence or mRNA sequence? Note that the coding/template strand identity is determined by the promotor for each gene separately! Without knowing the location (direction) of the promotor, you cannot determine which of the two strands is the coding one.

I see you edited the question and added "DNA". But still: Where did you get this sequences from? Have you read my comment about the promotor?

Is this some sort of contrived homework problem?

Maybe I'm misunderstanding something or the exercise was a bad example, but just in general, I have trouble identifying the template strand, and all the answers I can find tell me to look at directionality. But my question is: what if both strands have a start codon when reading from 5' -> 3'? Doesn't that mean both have 'correct' directionality? So how would I know which to pick? And in regard to Domen's comment, the location of the promoter is unknown for these problems, but we were told to identify an ORF for which I need to know which is the template or coding strand, right...?

In real life, you can't predict the start of a protein by looking for ATG.  in organisms, the shape of the DNA (which is based in part on sequence) determines where transcription or translations begins, because the shape of the DNA molecule determines where those proteins can bind.  This is not perfectly predictable.  In real life, you'd need to have some kind of verified annotation to know where translation will begin.  You'd have to be empirical.  You can't just look at a DNA sequence and know for sure.


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Why does increased age cause degradation?
(I'm not super familiar with biology just curious, so bear with me!)
My understanding:
As people get older (or are very unhealthy) they have accumulated more "bad habits" than others who are younger. The best way I can describe my understanding of this is with the sun. As people get older they have had more time on the planet to be exposed to the sun and are more likely to get skin cancer (which can be exacerbated by tanning and such).
Older people are also more likely to have strokes. Usually caused by age-related conditions (hypertension, heart conditions, artery build-up, etc).
Question(s):
To get to the gist of it, why do we get more sick/have more conditions as we age? Is the body just breaking down? are the muscles (like the heart) getting tired?
I believe a lot of deterioration is because the cells degrade and don't multiply/do their jobs properly anymore. I've vaguely heard that this can cause damage to DNA and something called "cellular senescence" which I don't fully understand.
Is this DNA damage the reason women over 35 are more likely to have babies with birth defects? Because the baby can't form properly with the damaged "instructions"?
Thanks!
edit - I now know more about senescence. This seems to be that we know this deterioration happens, but I'm still missing the why portions. Why do our cells struggle to multiply correctly and function properly as we age? what concept of aging makes this happen? We often explain something happening (like a cell deteriorating in function/health) as a result of aging. But why does more time, mean worse function? Is it just because statistically more time = more opportunity for mistakes? The question about DNA damage and pregnancy still stands.

Welcome to Biology StackExchange! Generally, it is expected that you do some prior research on the question yourself before posting it here. Ageing and senescence are very complex topics, and there are many different theories trying to explain these phenomena. You can start with a Wiki article on Senescence and familiarize yourself with the basic terms and concepts :)

Thanks for the article! I've tried to do some research, and only really found things about cell division and mutations. I suppose it is hard to research when you don't exactly know what you are searching for haha! Now knowing about Senescence, I'm still left with the same question of why it happens (this just seems to imply we know it happens). I'll be updating the original question accordingly. Thank you!

Perhaps your researches need to include some basic evolutionary ideas. The reproductive years are over by the time senescence sets in. The flip-side argument would be: Why would we have evolved to live longer than we do?

A cell that can divide indeifnetly without end in a body is either a stemm cell or a cancer cell. you want cells to have limited replication in a multicellular organism to prevent the latter.

Let me start by answering your biggest "why". Ultimately, since human beings are fertile from their mid teens and up until their middle age, there was absolutely no reason for us to live any longer than 40 or 50 while we still lived in the wild. The sad thing is that biologically speaking we COULD have evolved to live for hundreds of years but we simply don't. Deterioration associated with ageing happens because there is nothing to stop it.
Now to get more specific. Human genetic material is LINEAR, which means it has an end (like a shoelace). The ends of our chromosomes do not have any genetic information but as cells divide, the ends get shorter and shorter and eventually we start to lose important genetic code. This is just one of  many ways in which our bodies get worse with age. There is no single mechanism behind it. Our immune systems also get weaker for several different reasons. As mutations accumulate you also have and increased risk of cancer.
If you want to learn a bit more on this topic the YouTube channel Kurzgesagt has several different videos on ageing and they specifically touch on senence like you mentioned yourself. If you wanna get really REALLY deep into this then you are going to have to pick up some textbooks on genetics, immunology, and cell biology.
Sources as if any of this is somehow controversial:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5719695/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5291468/#:~:text=Beginning%20with%20the%20sixth%20decade,to%20support%20appropriate%20wound%20healing.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5322748/#:~:text=The%20aging%20process%20is%20driven,their%20efficiency%20declines%20with%20age.
https://pubmed.ncbi.nlm.nih.gov/11327115/#:~:text=The%20regulation%20of%20telomerase%20activity,cellular%20immortalization%20and%20in%20cancers.


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Long-term-potentiation and memory. Where do we stand?
I was reading the answers to the question: How and where, in the human brain, are memories stored? and, as expected, LTP and LTD came out.
Every time I read about LTP/LTD there is always something that bugs me a lot.
When I read papers about LTP/LTD (OK, I should really say "when I browse", as I'm not exactly in that area of neurosciences, and that is probably the reason why I am confused by this) I always see these very neat experiments where stimulating a neuron in a certain way increases/decreases its further responses. Then, I look at the time axes on the graphs, or read the Methods, and I see that the LTP was induced and analysed few minutes after the stimulus.
So my questions are:

Is there clear evidence that LTP is involved in long-term memory (not counting 1 hour as long-term...)?
Has LTP/LTD been shown in vivo after long period of time (e.g. months).
For those who work in the field, is there a strong belief that LTP/LTD are the only phenomena underlying memory?

Is there clear evidence that LTP is involved in long-term memory (not
  counting 1 hour as long-term...)?  Has LTP/LTD been shown in vivo
  after long period of time (e.g. months).

This Journal of Neuroscience paper shows LTP in vivo measured out to one year:  Abraham WC, Logan B, Greenwood JM, Dragunow M. 2002. Induction and experience-dependent consolidation of stable long-term potentiation lasting months in the hippocampus. The Journal of neuroscience : the official journal of the Society for Neuroscience 22: 9626–34.

Thanks, that is what I was looking for. And bizarrely I even know the first author of that paper!

Really good questions. As the guy who brought up LTP/LTD in the question you referenced, I thought I would weigh in.
There is the traditional definition of LTP/LTD as an increased/decreased synaptic efficacy at a single synapse or in a single cell. As you've noted, this is unlikely to be the only phenomena underlying memory and sometimes it's hard to see how some of these mechanisms can result in memory on behavioral timescales.
Let me propose, therefore, that the term long-term plasticity is more relevant these days, as it can refer to a variety of mechanisms that relate to the ability of the nervous system to change in stable ways over time. Physiological mechanisms involving changes in protein expression include traditional LTP/LTD at single synapses, but also homeostatic plasticity and long-term changes in intrinsic excitability where the tendency of the cell to fire changes independent of changes in synaptic weighting. Some structural mechanisms include the growth of new synapses, new spines, and new neurons--synaptogenesis, spinogenesis, and neurogenesis.
In the end, it is all of these mechanisms (and probably more) at play. Note, for instance, that the plasticity may move through structural changes in the system. This means that the lifetime of LTP in one cell or at one synapse does not necessarily have to be the same as the lifetime of the memory itself. All that said, I think all plasticity mechanisms ultimately reduce down to a change in the ability of an input to elicit an action potential somewhere in the brain (known as EPSP-spike coupling). This is likely to be the basic underlying mechanism of memory.

Good questions. I don't think that LTP has been (or will be) shown to be THE mechanism for long term memory. It is one of many mechanisms, all with different time courses, that contribute to the modification of synaptic efficiencies.
One mechanism not mentioned much anymore, but which I feel is absolutely crucial, is dendritic spine growth. Spines are malleable and formation/destruction of spines is probably very related to long term memory. But as always, the full picture is going to be a combination of mechanisms.
Here is a paper to have a look at:  Engert F, Bonhoeffer T. 1999. Dendritic spine changes associated with hippocampal long-term synaptic plasticity. Nature 399: 66–70.

Isn't this called engramming?


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How is the rate of gluconeogenesis controlled in the cell?
As far as I am aware, all steps in glycolysis are readily reversible except the phosphorylation of glucose, the phosphorylation of fructose6 phosphate, and the phosphorylation of phosphoenolpyruvate to pyruvate. I understand how control of the rate of glycolysis can be achieved through allosteric means (for example glucose 6 phosphate inhibiting hexokinase in muscle cells, phosphofructokinase being under allosteric control of the ATP/AMP ratio in muscle or hormonal control via glucagon in liver), however how is the rate of gluconeogenesis controlled compared with glycolysis? When a cell has a high rate of glycolysis, then as the rate of forwards reaction increases the concentration of substrate for each gluconeogenesis reaction also increases. Thus there must be some way to shut off the gluconeogenesis enzymes.
I would be grateful if someone could explain how the relative rates of glycolysis and gluconeogenesis are controlled, and perhaps if this varies according to the cell type (muscle/liver cells etc).
I was also wondering whether every cell is capable of gluconeogenesis. I was considering putting this on a separate post so that there is only one question per post, but I thought that it is quite a short question so it may be better to put it here.

Read the location paragraph of https://en.m.wikipedia.org/wiki/Gluconeogenesis

which cells are you talking about - hepatocytes?

@VanceLAlbaugh having researched the link provided and seeing that gluconeogenesis does not occur in the muscle cells, then yes; my interest is mainly in hepatocytes as this is where most gluconeogenesis takes place.

Regarding "there must be a way to shut off these enzymes". Enzymes are not entities that are pushing molecules through the pathway in one direction, they're facilitating a faster equilibrium. If you put a non-reversible sink at the end of the pathway it will go in that direction.

In mammals gluconeogenesis occurs primarily in the liver (together with the kidney to a much smaller extent). When the blood glucose concentration falls, it is the role of the liver to generate glucose for other tissues that are dependent upon it.
Hormones play a key role in this. If one considers the decrease in blood glucose concentration during starvation, this is signalled by a decrease in the concentration of insulin and an increases in the concentration of glucagon. These have differentials effect on the uptake of glucose by different tissues, depending on whether they have receptors for the hormones and the consequences within the tissues, and mass action effects of metabolites will certainly influence whether glycolysis or gluconeogenesis occurs in liver.
However, you are correct in your concern that there must be a way to prevent the futile cycling of intermediates through the different reactions of the three steps that differ between glycolysis and gluconeogenesis. The short answer to how this is accomplished is that the concentrations of various metabolic intermediates change during starvation/feeding, and that these intermediates are allosteric regulators of the reactions, switching one off and the other on. This is described in the section on Regulation of Gluconeogenesis, in Berg et al. (available on-line), from which I reproduce the  diagram below (Fig. 16.30).

Although this diagram illustrates the principle, a few words of caution about the detail are in order. First, the edition of the book this comes from is 15 years old. Second, it is not clear that all the regulatory molecules are effective in liver — some of the work may relate to bacteria. Third, much of the evidence is from studies with purified enzymes. Although it can be shown that an enzyme can be regulated by a particular effector in these conditions, it is different matter to establish that this occurs in a particular physiological condition. Thus, you will need to consult more recent and specialized sources if you are interested in particular details.


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Question about genetic recombination
I am having some difficulty understanding a few things about genetic recombination, in part because of confusion from different diagrams in books.

First of all, I wanted to verify whether I have understood correctly: It seems to me that when homologous chromosomes (which at this point are as sister chromatids joined at the centromere) join during the zygotene/pachytene stage, only one of the chromatids from each homologous chromosome form synaptonemal complexes with one of the chromatids in the other chromosome. Is this correct? Then only one of each of the chromatids is involved in the DNA recombination...

Leading on from my previous point, I think this would mean that in the final four zygotes that are formed, there are four different chromosome possibilities: the maternal chromosome (call it m) which has not had any recombination events; the maternal chromosome M whih has had recombination events with the paternal chromatid. Then the corresponding paternal chromatid p and chromatic which has undergone recombination event P. Is my understanding correct here?
Also, I have seen in some diagrams there is a single chiasmata forming between the homologous-chromosome chromatids and in other diagrams I have seen more than one chiasmata. I think the one chiasmata picture is a simplification and there can in fact be more than 1 crossing over point between the chromatids of homologous chromosomes.
Finally, if it is so that only one of each pf the sister chromatids is involved in recombination between homologous chromosomes, is there a a preference as to which chromatid this is, or is it random?

I realise that if both of the sister chromatids undergo these recombination events, then many of my questions would be redundant! However from the books I am looking at now, it seems that only one chromatid undergoes these crossings over...

I can't imagine point 1 being correct. I've taught out of many textbooks and have never encountered this. I can't think of a mechanism which would inform one chromatid that synapsis is occuring on the other and then prevent it from occuring on that chromatid.


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Relationship of disease to alternative strand - microRNA-3p or -5p
I am working in a project involving microRNAs in a cohort of patients (controls and cases of coronary artery disease). I got results from sequencing of HDL-lipoprotein involving diferentially expressed genes which could be down or upregulated in cases/controls.
I don't have much experience working with miRNA but I got results involving e.g. hsa-miR-28-3p as a significant molecule and implicated according to miRDB, TargetScan or miRTarBase in several pathways that are related to the disease I am working. The thing is in the search I found that hsa-miR-28-5p is related to my disease as well, as is hsa-let-7e5p and hsa-let-7a5p. I don't have much experience in this topic, DEG microRNAs in -3p, to which extent is related this finding with findings in same microRNA -5p. As far as I know the nomenclature reference in which strand was found to interact the microRNA under observation
Apart from the sources I mentioned before (miRDB, TargetScan or miRTarBase) where is possible to find disease-associted evidence with microRNAs? Or pathways?

Can you include some links or other information? What exactly do you see with differential expression? "Associated with disease" is a pretty generic statement. Why would you expect associations mechanistically?

This is really a request for literature references, but you can find these from an internet search for the microRNAs of interest, perhaps coupled with “disease”.

@MaximilianPress — Association is all one can say. Cause and effect follow, if indeed there is such. As for expectation, this is irrelevant if there is an observation.

I see a differentially expressed genes in a sequencing standard procedures. The results concluded in a set of genes up,or downregulated in cases versus control. What I mean is, the relationship of finding certain x-5p, how is this related with x-3p? If x-5p is widely described in an specific tumor (breast), has it been studied the impact of finding x-3p?

As far as I know, not all the databases are based on experimental evidence, just mirTarBase. If "mechanisitically" involves experimental evidence, it's better than in silico. However my question is pretty generic, afterwards my feeling is I cannot extrapolate the behaviour of x-5p/x-3p for y-5p/y-3p

Is your main concern whether it is valid to expect an effect on a 5’p microRNA to hold true for the 3’p complement? The answer to that is obviously not.

For pathway associations, the generic answer is Gene Ontology, which does appear to annotate microRNAs (see section "Annotating MicroRNA clusters").
One could imagine annotating microRNAs with respect to their targets' functional annotations mechanistically.
However I'd like answers to my questions in comments.


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Portobello looking mushrooms growing in yard
Sorry, I know this is probably kind of a lame question for this forum, but I live in Northeast MA, and it has been a mix of hot, sunny, and wet over the past few weeks. These guys started popping up in my garden in the past few days. I went to remove them, and I noticed they were very familiar-looking—large caps, black undersides, some with big white fleshy stalks some without (ie: photos).
I know very little about mushrooms, aside from the basics and what I cook with. These to me looked like portobello (stalks aside), but I assume that is not the case.
Did some "foraging" on the internet, hard to find what these are.
Either way, they were delicious in my morning omelette (jk).

Probably a fieldcap, wine-cap, or maybe a widow, but I can't narrow it down enough. Could you go out and take closer up photos? Look for small ones, and large ones, get closeups of their undersides and stems, as well as "roots". A good picture of the top is important as well.

Obligatory - don't eat fungi that are not positively identified by a local expert, and certainly not ones ID'd over the internet, even if the person seemingly knows what they are talking about.

too late burp - next question, how do I get my dog to stop talking me?


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Do all species of wasps eat nectar?
There are many species of wasps, some of them are consuming other insects and meat. But do those wasps that eat insects also eat nectar from flowers? Are there known species of wasps that are solely carnivores?
An article about what wasps eat says that

most adult wasps feed primarily on sugary substances like nectar.

However I don't know if they refer to all known species of wasps and if that means there some wasps that do not eat nectar.

Vespid wasps that consume other insects, etc. do so during their larval stage, but feed almost exclusively on sugars as adults. Those sugars primarily come from flower nectar, but they can also come from things like aphid honeydew. They occasionally feed on pollen as well.
https://link.springer.com/chapter/10.1007/978-3-030-29654-4_14


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Is there lysozyme in cooked egg whites?
Egg whites are a phenomenal source of the antibacterial enzyme lysozyme.
I was wondering if eggs are cooked, will they retain there lysozyme count?
And will cooked lysozyme retain its antibacterial properties?

Hi and welcome (apologies if this comment seems unwelcoming.) This site strongly recommends evidence of prior research attempting to answer your question (e.g. a quote and a link). Proteins are all still there on cooking, but most proteins are denatured with sufficient heat. Did you google search Is egg lysosome denatured by cooking? (Most - not all - denatured proteins don't function.) If so, what is confusing about what you found? A quote and a link is helpful to getting an accurate answer. Thanks!

amount depends on how you cooked it (i.e., at what heat). hard boiled eggs vs. scrambled @ medium/low heat

i presume a tiny amount of lysozyme would be present (someone probably found a quantitative answer in a research experiment, i don't know) but the egg would predominantly denature the enzyme, causing it to not be active anymore


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Any selective media for corynebacterium acnes? What about isolation methods?
Looking for a media that is selective for Corynebacterium acnes or any isolation methods. Help is appreciated. Will be isolating from a bacterial consortia.

Welcome to the Biology Stack Exchange. Please take the [tour] and visit the [help] for more information on this site and how it works. Please note the homework policy. I suggest you find a copy of Bergey's manual.


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What is a typical value of the selection coefficient s?
I am trying to gain an understanding of the real world effects of natural selection from the equations, especially comparing it with drift. However I have been unable to find any examples which give an estimated value of the selection coefficient for a population considering a particular trait. Could anyone link me to some studies that give an actual value for a selection coefficient? Thank you in advance!

Try http://scholar.google.se/scholar?q=estimate+%22selection+coefficient%22

This is a very fundamental and important question! But first, be cautious not to confound the Fitness effect of segregating alleles with the mutational effects.
Fitness effect of segregating alleles vs mutational effects
One must not confond the distribution of fitness effect of segregating alleles in a population with the distribution of mutational effects. The distribution of mutational effects will always be narrower in comparison to the distribution of fitness effects of segregating alleles as very deleterious mutations won't stay long in the population and very beneficial mutation will sweep to high frequency very quickly so that it is unlikely to see them.
I am assuming you are interested in the distribution of mutational effects. Below are some papers and generalities that will be of interest to you. Some data come from the quantitative genetics literature and some from classical empirical population genetics. I also talk about mutation rate as these two subjects are highly related typically at determining mutation load.
Short answer
A typical deleterious mutation has a mutational effect of $s=0.1$ or $s=0.05$. In theoretical studies, authors often used a constant value of $s$ as being equal to one of these two numbers.
Longer answer
Distribution of mutational effect
Generally speaking distribution of mutational effects (on both the deleterious and the beneficial side) are thought to approximatively follow a gamma distribution with an extra bump of probability density around lethal mutations. shape might take values around 0.5 or 0.05 while the scale parameters might be of the order 0.1 to 0.001, with typically an average around 0.05. See Halligan and Keightley 2009. I have seen (see Nemo's documentation for example) that the dominance coefficent $h$ is modelled as $h=-log(2 Exp[h])/Exp[s]$.
Mutation rate
Concerning the mutation rate, a reasonable approximation is to consider a deleterious mutation rate per diploid genome of 1. This is known as Drake's law (see this post). Drake's law appears to be an underestimate for humans (Keightley 2012), about right for Drosophila, (Haag-Liautard et al. 2007), C. elegans (Denver et al. 2004) and possibly non-human endothermic vertebrates (Baer et al. 2007), and probably an overestimate for many other organisms (Baer et al. 2007, Halligan and Keightley 2009).
Quantitative traits
If you are uneasy with basic quantitative genetics and the below notation, you should have a look at this post.
For quantitative trait, there is evidence that $\frac{Vs}{Vp}≈5$ on average (Kingsolver et al. 2001, Johnson and Barton 2005). If heritability is $\frac{1}{3}$ (as it rarely significantly different from), then $Vs=7.5$. Empirical estimates of the mutational heritability $Vm$ suggests that $\frac{Vm}{Ve} = 0.001$ (Houle et al. 1996)

@21joanna12 Please let me know if you think I answered your question or if I am off-topic in your opinion.


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Why Rh conflict happen but no ABO conflicts?
I wonder why Rhesus conflict can happen during pregnancy and mother can make antibodies against Rh protein (I think the correct name is D protein), but it doesn't happen if mother has different ABO type than the child?

It happens, but it is very rare.
Anti-A and Anti-B antibodies are IgM type. They do no cross the placenta. Sometimes IgG can be produced and lead to the hemolytic disease of the newborn.
Anti-D antibodies are IgG type and can pass through the placenta.


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Is hunger pushing cognitive ability in humans?
We have a lot of those questions here that base on personal anecdotes and I try to avoid asking any of those. Still, after skipping breakfast and an extremely effective work day so far I started wondering.
I have always felt, that for most cognitive tasks I perform best before breakfast. Of course some of it is sure related to being very awake and supposedly having a biorhythm that favours working in the morning, but I have always related this to not having eaten and also surprisingly not feeling hungry at all until basically deciding to eat "because I really should eat something" around noon.
So today I decided to find out, if this phenomenon is more widely known or just anecdotal for me. Of course there is a lot of information on how digestion makes you feel tired and you should not expect to be very productive directly after eating. That was not what I am looking for.
Finally I found this 2006 NY Times article about "Empty-Stomach Intelligence", where it is stated that at least for mice being "mildly starving" seems to increase cognitive ability based on the hormone ghrelin targeting not only the hippothalamus, but also the hippocampus.
I then tried finding a relevant publication and was only lead to this one, describing the original study about ghrelin influencing food intake, but seemingly not the "sidetrack" of it influencing cognitive abilities during starving.
Now I am lost. Is there any newer publication about this phenomenon that I completely missed, possibly even in relation to how humans can perform cognitive tasks while being mildly starved?

my guess is following: today people have much more food and food has much more nutritious value than in previous times. So average body is generally running in parasympathetic mode, digesting and resting. That takes attention from CNS, including brain functioning. Mild fasting releases that external pressure. I'd suggest search for link between daily glucose level and brain ability/performance

Still it is curious for me because it is so counterintuitive. Most people I know if they have to work hard on a cognitive level they tend to snack nuts, chocolate, anything they are used to to keep their attention up. And this does boost your attention for a short while. The mild fasting on the other hand seems to be a more long-term approach (long-term being around 6 hours).

This question is more suitable for cognitive sciences and I vote to close therefore. I bet it will be well received there.

I'm voting to close this question as off-topic because it is a well targeted question for Cognitive Sciences. +1 for the nice question :)

I think it has a biological answer. I vaguely remember reading somewhere that either leptin or ghrelin (or both) have an effect on cognitive performance. Orexins also regulate wakefulness, so they may be part of it as well, as more wakefulness tends to produce better attention, and lots of cognitive ability depends on focused attention.

@rumtscho I was kind of looking for that biological answer, especially any additional explanation to the ghrelin theory from the newspaper article. I am not at all into cognitive science, so saw this as a biological (endocrinology) question.

@skymningen Moderate hunger can serve as an activating factor for the body to increase its alertness and thus, as a side effect, can mildly push cognitive ability. Another factor which can make you percieve hunger as a more sober state of mind is that endorphines are released in response to satisfaction of hunger. Endorphines are known to be able to cause unconditioned happiness which reduces the need in any activity, even make one sleepy, thus seemingly decreasing cognitive abilities of the person.


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How did Hämmerling manage to transplant nulei in Acetabularia?
In all educational sources, the method of determining the role of the nucleus in a cell by Joachim Hämmerling is clearly described, however, no method is presented which would enable the experiment's reproduction.
A part of the experiment also involves cutting up the elongated part of the cell and swapping it with other species of Acetabularia. How was it done?

I'd recommend searches including "method" like "Acetabularia grafting method". That led me to this book chapter:
Keck, K. (1964). Culturing and experimental manipulation of Acetabularia. In Methods in Cell Biology (Vol. 1, pp. 189-213). Academic Press.
Some quotes:

DeWecker iridectomy scissors with short, pointed blades are recommended for cutting the cell into various segments. During the grafting
operations, the components are held and manipulated with fine forceps
(Watchmaker’s Forceps)

So, to cut up the cells you hold them with a fine tweezer and snip them with scissors.

A cytoplasmic surface exposed by a cut will retain its tendency for
fusion when brought in contact with similarly exposed cytoplasm of
another cell section. In practice, the components are joined by inserting
the cut end of the narrower stalk into the opening of a slightly wider stalk.
...
The joining of two stalk ends can be greatly facilitated by making
the plane of the cut slightly oblique to the long axis of the cell.
...
During the grafting operation the partners
should be gently pushed in place; parts may also be guided by holding
them in the gap above closed tips of forceps. Any hard pinching with
forceps will cause a local fragmentation of the cytoplasm.

To graft them together you physically manipulate the cut ends and push them together. They recommend cutting "on the bias" to make it easier. The process seems a bit finnicky and requires gentle handling. It seems like failure is fairly common, success comes by attempting many grafts and keeping the ones that work.
As you can see, it's conceptually quite simple which is likely why there isn't much of a detailed description in the other sources you've read. The methodology is mostly in the maintenance of cultures of these cells and in fine surgical manipulation skills.

Thank You, that is very imformative, however, by grafting we can only conclude that something in the rhizoid is responsible for the cap's colour and shape. As far as I am aware, one of the experiment's steps involved the removal and transplant of the nucleus, which was the denfinite proof that nuclei are responsible for morphology, not the entire rhizoid.

@Inva7 Nope, just the rhizoid containing the nucleus versus other parts of the cell.