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Where can I find large datasets of protein-interaction networks?
Where do I find large datasets of protein interaction networks for cancer or alzheimer diseases?  So far, I found String but it is does not have enough proteins for my purposes. Are there such databases with more entries?
I'm still open to any proposition of the disease to choose from .
the most important part is the volume of data .
And how can I get the annotation of each protein  of the extracted network from Uniprot ?

Welcome to Biology.SE. I edited your question to make it more clear. Please feel free to further edit. Thanks!

The String database is one of the best available, how many proteins do you need? (consider that the human genome is predicted to have around 25k protein-coding genes)

@alec_djinn I need for about 5k or 6k proteins for alzheimer or cancer  but i don't know how to retreive that quantity at once

@AM I can't find the exact number of entries for the human proteins, maybe you should contact them, 5k sounds reasonable, I would expect them to have it. If not, maybe you can integrate with other mammalian proteins. As far I know, STRING is the most complete you can find now.

@alec_djinn Okay. Thank you, I will contact them

@AM What makes you think you can find 5k proteins for Alzheimer? Do you hypothesise that 1/5 of the human genome is involved in Alzheimer?
Nevertheless, you could take the genes in the KEGG pathway for Alzheimer disease, or take the genes known to be genetically causative for or associated with AD and include all their interactors. I think the network will get quite big as such.

@alec_djinn ehm, the STRING database is one of the largest available but absolutely not one of the best. Probably the worst, actually, in that it has a lot of crappy data in there. Unless you are knowledgeable enough to parse out the bad stuff, do not recommend it.

@AM please [edit] your question and clarify your needs. Do you want to limit the results to binary interactions only? Are you also interested in non-direct interactions like forming part of the same complex? Do you want only experimentally verified interactions or also those inferred by electronic annotations? Do you have a list of proteins of interest? Please add more details.

@WouterDeCoster would you suggest me an application where i can get such huge dataset ?  I'm not really limited to Azheimer it was just a proposition . I'm open to any disease which will get me this proportion of data

@terdon if it is not then what database would you recommend ? I do not have a protein of interest, I only want a huge dataset of protein protein interaction  for a disease , that's all I'm open to any suggestions .

@AM yes, but what do you mean by "protein-protein interactions for a disease"? How would you define the list of proteins you care about? You normally start with a small list of "bait" proteins and then collect their interactors, moving as many steps down the network as you need.

@terdon  I do not care about the list pf proteins I need , more than the idea of a specific network for a disease , having 4k to 5k of proteins that's all

I don't know how you could even define that. Whether you include a protein in the list of proteins involved in a disease depends very much on how you define disease association. Is it only proteins with a function affecting this disease? Is it also the proteins that interact with them? How many steps removed? How about proteins controlling the expression of related genes? Or proteins that interact with those? Or should it only be protein interactions whose disruptions affect the disease? And should that include ubiquitous proteins that are involved in almost everything?

There is a bunch of decent protein-protein interaction databases: Biocarta, BioGrid, DIP, InnateDB, IntAct, MINT, PPID.
Some of them aren't available now, but you can download datasets from the Expression2Kinases download page because they are integrated into X2K pipeline as part of Genes2Networks analysis. If you need more proteins, you can submit your list of proteins to X2K and use G2N analysis to connect enriched transcription factors through known protein-protein interactions.
Also, the new dataset called hu.MAP was published recently. It is a dataset of human protein-protein interactions determined by over 9,000 mass spectrometry experiments performed by the Marcotte Lab from UT Austin. A paper that describes the hu.MAP project is available on Biorxiv.
BioPlex (biophysical interactions of ORFeome-based complexes) is another database with experimental verification. Authors describe it as a network that is

the result of creating thousands of cell lines with each expressing a
  tagged version of a protein from the ORFeome collection.
  Immunopurification of the tagged protein and detection of associated
  proteins by mass spectrometry are the building blocks of the network.
  The overarching project goal is to determine protein interactions for
  every member of the collection.

I have checked IntAct, and it kind of offers what I've been looking for , I'm wondering If there is a way to  extract all the associated proteins' annotations from uniprot  . because I need to get all the annotations of every protein contained in the dataset


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Get protein annotation from Uniprot out of protein mappings
Having a file of for about 10k mapping identifiers how can I get the annotations of the proteins from Uniprot  ? As it is not possible to do It manually
My mappings are contained in a .csv file
They are from STRING database Example 9606.ENSP00000387699

Can you please expand on this. What format are your ID's in (csv, excel, etc.)? And what is a mapping identifier, a uniprot accession, some other id? Lastly, Uniprot has a batch download system here, which may suit your needs.

@emilliman5 I edited the question , they are contained in csv file , and they are  stringdb external identifier

This problem is discussed here. Apparently STRING IDs are in KEGG format but these can be mapped on to Uniprot IDs using information downloadable from here. I guess that it is either the protein.aliases data or the mapping_files data that you would need. The first link provides a Python script to extract useful info from the downloaded data. These are big downloads so I haven't actually tried this out myself.
Presumably once you have the STRING→Uniprot conversion done you can query Uniprot with the output as a batch request.
Good luck!

@AM please comment again when you know if it worked out. Or even write your own answer.

UniProt's batch download system, suggested by Alan Boyd above, also allows you to directly map identifiers, e.g. STRING to UniProtKB, or Ensembl to UniProtKB:
http://www.uniprot.org/uploadlists
Once you have your UniProtKB results, you can add or remove columns by clicking on "Columns", and once you are happy, you can download the results in tab-separated format (http://www.uniprot.org/help/customize).

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Predicting DNA nucleotide bases sequence from fully formed protein
I know there are many algorithms (and a lot of different implementations) that allow predicting the outcome of protein synthesis given a set of nucleotide bases present in the DNA. In other words, given a sequence of such bases, produce a final protein (going through a simulation of the various processes that end up in a protein). However, are there any algorithms that allow to predict the opposite, i.e. the sequence of nucleotide bases that were the basis for the synthesis into a given protein?

It's trivial in principle, but remember that there are multiple codons that can produce a single amino acid, so reverse-translating a protein will either give you the most commonly-used codons for the protein, or will give you a large number of possible sequences.
Here and here are online programs that will give a single consensus, and here is one that considers ambiguities.

This is a standard method used in bioinformatics.
First step is to convert the amino acid sequence to a degenerate nucleotide sequence using the relevant codon table.
Once you have the degenerate nucleotide sequence, you can blast it against all known nucleotide sequences, including whole genomes.
Since the degenerate nucleotide sequence essentially is a degenerate cDNA sequence, you can then simply identify any genes with exons capable of producing the necesary cDNA through splicing events.
This method is called tblastn and is available here: https://blast.ncbi.nlm.nih.gov/Blast.cgi

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Determine the chances of blood group type and rhesus factor of unknown parent?
First of all, I'm not a biologist so my jargon might not exactly be common on this site. I'm a programmer and as a hobby project I try to make an algorithm that does two things:

Determine the possible blood group and rhesus factor of a child based on the blood groups and rhesus factors of both parents.
Determine the possible blood group and rhesus factor of an "unknown parent" based on the blood group and rhesus factors of the child and the known parent.

I found two great examples online, the "Child Blood Type Calculator" and the "Parent Blood Type Calculator" calculator on endmemo.com.
The first calculator shows some percentages of the chances. But the second calculator does only show a static answer when it comes to the blood group type and rhesus factor. According to the calculator that indicates that the rhesus factor of the "unknown parent" can only be negative when both the child and the known parent have a negative rhesus factor too.
In case the known parent and child have both RH+ the calculator shows that the unknown parent must have had RH+ as well. But isn't the statistical chance  6.25% that the unknown parent still have had RH- instead?
Secondly, how can I calculate the likelihood/chance that the unknown parent has a certain rhesus factor or blood group type? Now the calculator shows 'A/B/O' and 'RH+' when the child has 'O+' and the known parent has 'O+' but what are the chances the unknown parent has A, B or O or RH- anyway?
Side-note: I'm not related to endmemo.com.


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Can a new plant grow from half a Succulent leaf?
Succulents like Crassula ovata can be propagated by simply tearing a leaf from the stem and putting it into soil. The leaf will usually grow roots and additional leaves from the calloused wound, and eventually become a full Crassula plant itself.
Now I only have half of a leaf left, the other half got rotten, and dried out. In particular, the part of the leaf that was attached to the mother plant is missing. The remainder is about 3/4" long.

Is it still possible to grow a new plant from just this part of a leaf? Or is it at least necessary that the part of the leaf that was attached to the stem is still present?

Added wiki link to your post. Adding links to content improves readability for curious and/or competent users, experts and those reviewing your posts.

Can you add some detail to the "from my own experiments" bit? I'd like to hear more anyway, but I'm not sure if you mean you successfully propagated from just the calloused part.

Also, while we're waiting for an answer is there any chance you fancy attempting the necessary experiment yourself? There's nothing wrong with answering your own questions and it sounds like you have access to the plant in question :)

After waiting for a while, I am finally able to answer this question myself:
A part of a Crassula leaf is still able to grow roots and new leaves, even if the part that attached the leaf to the mother plant is missing.
I have tried this out myself. I left the half-leaf depicted in the question on top of soil, watered it occasionally, just to keep the soil humid, but not wet. After roughly 5 weeks the leaf grew a first root from the calloused end. For the photo I have flipped the leaf around, to better show the first root.

In the following month, it grew more roots, and after about a month, the first new leaves started to appear.

At this point there is little doubt that a full plant can grow from this, given the right treatment. It is not different any more from full leaves growing new plants.
Update (June 2018): The plant is now 2 inches tall, and doing well.

So nice to see a story with a happy ending!

I was going to ask you to try it yourself, but you beat me to it by telling yourself to do it and actually did it.. Big bravo to your question and your answer. It's posted on the Stack Bio twitter

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Why do people look different after a long sleep?
What happens during a long sleep that makes people look odd when they have just woken up?  Why doesn't the same phenomenon occur in the case of a person who lies down for an extended period of time, but stays awake?  I've noticed that some nights seem to make a bigger difference than others in the appearance of the sleeper, but haven't noticed a pattern.

Can you elaborate on what the characteristics of "looking odd" are?  I think everyone has some sense of (or experience with!) what you're talking about, but in order to address things scientifically the specific characteristics (e.g., dark circles under the eyes) would be helpful.

Not dark circles (that sounds more like long term lack of sleep); I'm referring to the sort of "puffiness" around the eyes and mouth.  It's hard to describe without a picture.

Puffy eyes are caused by fluid build up in tear ducts from extended periods of lying down. Gravity from sitting or standing slowly drains them during the day. The crusty 'sleep' that accumulates in the corner of your eyes is the residue from basal tear liquid that has seeped out of the eye and evaporated during the night.


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How can you improve solubility of colloidally dispersed substances?
If you solve collidally dispersed substances then the particles can form large colloids. This may block narrow passages and diffusion into dense structures may become completely impossible.
What can you do to improve the solubility of such substances?

This sounds pretty inorganic chemistry-ish. Any way to phrase it more towards biochemistry (i.e. relationship to proteins, biological systems, etc...)?

In my case, three-four rounds of sonication greatly helps in having smaller and more homogeneous hydrophobic particles dispersed in water.


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If insulin secretion is ATP-induced, why don't fatty acids trigger insulin secretion?
I learned in my university physiology course that insulin is released by pancreatic beta-cells  in response to glucose that is metabolized and thus increase cellular ATP levels, which in turn close ATP-sensitive K+ channels. This leads to the depolarization of the cell membrane that opens voltage-dependent calcium channels, increasing intracellular calcium levels, finally inducing exocytosis of vesicule containing insulin.
So I was wondering why doesn't fat that is an energetic source and can be metabolize to give ATP doesn't trigger insulin secretion ? Is it because of the kinetics (carbohydrate metabolism may be faster and thus leading to greater ATP concentrations) ? Or are beta-cells not reliant on fat metabolism for ATP production ? Or another reason I missed ?
Thank you

Well it's also the mechanism described in Wikipedia and the first studies I could find on it. After meals, the blood sugar goes up and so does it in the pancreatic beta cells (glucose transported by GLUT2) and it's oxidized (by glycolysis and cellular respiration) and leads to increase in intracellular ATP levels. Sorry if I wasn't clear, I wasn't talking about ATP in blood. I suppose pancreatic cells can take up a bit of fatty acid and metabolize them but I don't know for sure and I don't see, if it raises cellular ATP levels enough, why it wouldn't induce insulin secretion by that mechanism.

OK. Your account of glucose stimulation of insulin release seems to be standard. The question is valid. I suspect it is to do with lack of fat metabolism in beta cells, but that needs to be checked, detailed and formulated into an answer.

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In a leaf, how does the water get out of the xylem?
In every textbooks, one can read that the xylem transports water and nutriments up to the leaves while the phloem transports the sap down to each parts of the tree, and that both the xylem and phloem are structurally different. The mental image being two different sets of pipes. My question is about their structure at both end, in the roots and in the leaves?
From what I see on leaf cross section pictures, unlike the arteries and veins in the lungs, the xylem and phloem remain separate structures in leaves.

And the vessels seem to form closed loops:

The mental model I have for the xylem is (the same for the phloem with a down arrow):

Question 1

How and where does the water get out of the xylem? Are the walls of the xylem becoming leaky in the leaves?

Question 2

If the sugar rich sap flows down the phloem, it needs to exit somewhere. What happens to the sap once it has reached the roots? Transpiration is the process that generates the outflow of water in the leaves, but what is the equivalent process in the roots for the sap?

Okay, for your second question, consider the force that creates the potential difference as follows: The sugar sap that runs along the phloem contains far more sucrose than the root cell. Although sucrose molecules are supplied to root cells, and one may expect the root cells to have a higher concentration of sucrose over time, they are instead transformed into starch, therefore the concentration of sucrose in root cells stays low in comparison to the phloem. This could lead to a difference in the net transfer of sucrose from leaves to roots, just like transpiration in leaves, which is responsible for water transit from root to leaf. The low sucrose concentration in root cells and the high number of sucrose in leaves cause sucrose to be transferred from leaf to root. The sucrose that has arrived is transported to the root cells via facilitated diffusion and converted to starch.
To summarize: starch is insoluble and therefore it's osmotic effect in roots is small. In that case sucrose from high concentration(from leaves) to low concentration(root cells) is feasible.
https://bio.libretexts.org/Courses/Saint_Mary's_College_Notre_Dame_IN/Foundations_of_Form_and_Function/07%3A_Transport_and_Gas_Exchange/7.05%3A_Phloem_Transport

The xylem is composed of hydrophilic fibers like cellulose and lignin, so it is "water-conductive".
To understand water movement in plants, it's important to differentiate between apoplastic and symplastic pathways. Apoplastic water moves through the cell walls and intercellular spaces, providing a source of extracellular water. Symplastic water, on the other hand, is transported directly from cell to cell through plasmodesmata.
In short, there's no hydrophobic separation between xylem and phloem other than the cell membrane.

If the xylem is water conductive, then how does water manage to get to the leaves without being lost between the roots and the canopy?

It may be worth noting in the answer that the pores are able to be dilated and constricted. The mechanism of that might be the subject of another question.

Cork and wax prevent evaporation from leaves and steams. @Jiminy The pores you referring to are the stomata? If so I didn't mentioned because they are more related to gas exchange and water loss to the environment, and not to symplastic-apopplastic water movements.

No, I meant the plasmodesmata. I suspected Shaktyai's concern was that the leakage due to gravity and "first in  the queue" of the lower tissues might prevent the canopy getting any water. It's regulated by the formation of (temporary) carbohydrate plaques that accrete around the openings, narrowing  and attenuating the flow. @heracho


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Why are heavy metals toxic? Lead and Carbon are in the same group. One is toxic, the other is not
I have read the different answers on the toxicity of heavy metals but I am still confused about the topic. Why does the mass of the nuclei matter when chemical reactions only involve the electrons. Carbon and lead are in the same chemical group and thus have the same chemical properties.

You're right to say that chemical reactions primarily involve the valence electrons of an atom. However, there are other factors that are key to understanding the difference in toxicity between lead and carbon. Mass isn’t really the explanation — correlation isn’t causation. Li and Be may be toxic in certain scenarios.

Some heavy metals share chemical similarities with essential elements our body uses. Lead, for example, can mimic calcium and sneak into important biological processes (e.g., disrupting neurotransmitter release by activating protein kinases).
Oxidative Stress: Some heavy metals can generate free radicals or reactive oxygen species, due to their flexible oxidation states and redox potential, which damage cells. (https://www.intechopen.com/chapters/71913)
Heavy metals tend to bioaccumulate and remain in organisms over time, specifically in the kidneys and liver. Because lead has no known biological role, there are no efficient excretion pathways for it. Carbon is continuously cycled through metabolic processes.

Now, carbon's small atomic size and stable quadrivalent electron configuration allow it to form strong bonds with itself and other elements, creating the vast diversity of organic molecules crucial for life (like DNA, proteins, and carbohydrates). The inability to easily lose electrons prevents it from exhibiting these toxic behaviors in biological systems. Its chemistry is perfectly tailored for the organic molecular backbone.
***It's important to note that not all heavy metals are inherently toxic. Some, like iron and copper, are essential for our body in small amounts.
Good review article to read: https://www.frontiersin.org/journals/pharmacology/articles/10.3389/fphar.2021.643972/full

It's not really the mass of the nucleus, it's the charge that affects the "behaviour" of electrons.

@Domen realised I made a bit of a contradiction. Edited.

This site requires citing (and linking to) sources which support answers. Users should not need to search for evidence supporting your answer. If you are familiar with the material covered in your answer, providing a source should be relatively easy. Lead toxicity is much worse than your answer indicates; "There is almost no function in the human body which is not affected by lead toxicity.". This answer, while correct, almost glances over the issue.

@anongoodnurse fair point about citations — will do. But the question is more about the reasoning behind why heavy metals are toxic and not the effect of lead toxicity on the human body.

Anyone can give an answer based on "reasoning"; reasoning can be faulty. Sites striving for accuracy need answers based on evidence. Otherwise, it's opinion. //Your source has a lot of information on lead, but not what you've written. Where did you get your specific info? Again, not disagreeing with facts. The quality of your answer is affected.

The part about accumulation is funny: Carbon accumulates as well, wouldn't you say? ;-)

That it affects so very many metabolic pathways is not a tangent. It's the essence of its toxicity. It does much, much more than what you've stated.

@Peter-ReinstateMonica You make a fair point. Carbon does accumulate in the body, primarily in the form of biomolecules like proteins, lipids, and carbohydrates, which are essential for life. However, the key difference is that heavy metals like lead can accumulate in an unbound, toxic form and disrupt crucial biological processes, while carbon accumulation occurs in a controlled, non-toxic manner as part of the body's normal metabolism.

These explanations feel very proximal to me. While you technically answer the question, you fail to get to the interesting chemical reasons for leads toxicity. For example: lead can mimic calcium, but what about lead makes it able to mimic calcium? Some heavy metals can generate free radicals, but what about them makes them able to do this? Lead tends to bioaccumulate, but what about it makes it so? And for all of these, why don't carbon?

Iron is also toxic. There's a reason why adult female vitamin tablet bottles have child proof lids but adult male vitamin tablet bottles don't.

@Joshua point I was making was that mass isn’t the explanation. Li is toxic, while being lighter. Obviously over dosage of Fe is toxic. Heck, even oxygen is toxic at high amounts (https://myhealth.ucsd.edu/RelatedItems/3,90904). But as you stated, the fact that there’s even an Iron tablet in the first place suggests that not all heavy metals are potent to health. No such thing as a lead supplement.

@AnshTandon I have heard a lack of aresnic is is also fatal but I'm having trouble finding a source right now.

Lack of a biological role isn't an adequate explanation for why there aren't excretion paths for heavy metals.  The body has excretion paths for many things with no biological role specifically to keep them from bioaccumulating.

I am a bit doubtful that the multivalency of thallium and lead plays any role in their toxicity. The inert pair effect is very strong which makes Tl(III) and Pb(IV) compounds strongly oxidative and unlikely to be created in the mild condition in our body. The ability to induce ROS may be due to the disruption of enzymes (which contain sulfur or selenium) that break them down.

It's not the "heavy" that makes a metal toxic. Lithium and Beryllium are considerably lighter but still toxic to humans. If the metals interact negatively within the human body, it is considered toxic. For e.g. Lead disrupts the functions of the digestive system, nervous system, respiratory system, reproductive system. In addition, it prevents enzymes from performing their normal activities. Lead even disrupts the normal DNA transcription process and causes disability in bones. Lead as such has no physiological role in the body and even smaller levels of lead can cause toxicity.
You can refer to below studies for more information:

Mahdi Balali-Mood,Kobra Naseri, Zoya Tahergorabi, Mohammad Reza Khazdair, Mahmood Sadeghi, Toxic Mechanisms of Five Heavy Metals: Mercury, Lead, Chromium, Cadmium, and Arsenic, . Pharmacol., 2021 DOI: 10.3389/fphar.2021.643972
Jaishankar M, Tseten T, Anbalagan N, Mathew BB, Beeregowda KN. Toxicity, mechanism and health effects of some heavy metals. Interdiscip Toxicol. 2014; 7(2):60-72. doi: 10.2478/intox-2014-0009
Tchounwou PB, Yedjou CG, Patlolla AK, Sutton DJ. Heavy metal toxicity and the environment. Exp Suppl. 2012;101:133-64. doi: 10.1007/978-3-7643-8340-4_6

I should add more on what "actually" makes lead toxic to humans. Please see this simplified diagram:

(Image source)
I'll go by each routes:

Route 1: Lead is known to have a strong affinity towards sulfur. In human body, sulfur exists in the form of thiols.  So, lead tries to bind with thiol group1 leading to major implications.

Route 2: Lead is able to produce free radical and reactive oxygen species (ROS) via Fenton-Haver-Weiss pathway2 possible by stimulating NADPH oxidases or by competing for the metal binding site of an enzyme/protein (Route 3) or by attacking the thiols moiety of protein (Route 1). The mechanism is below:

It causes a destructive behavior known as oxidative stress. One of the major implication of oxidative stress is lead-induced hypertension and cardiovascular diseases3

Route 3: Lead is known to mimic calcium because they share similar properties (In its +2 cationic form, lead has a radius of 132 pm while the calcium cation has a radius of 106 pm. In their elemental forms, lead has a radius of 175 pm and calcium has a radius of 197 pm). And that is the reason, lead compete with calcium and substitutes calcium from cells, tissues and enzymatic sites. One of the major effect is on calmodulin which is a calcium binding protein and lead will try to replace calcium inhibiting phosphorylation of brain membranes4.

There are other diagrams which which shows the mechanistical and pathological effect of lead in human body like this and this (the latter one shows the effect in DNA, RNA and lipids)
References:

Magyar JS, Weng TC, Stern CM, Dye DF, Rous BW, Payne JC, Bridgewater BM, Mijovilovich A, Parkin G, Zaleski JM, Penner-Hahn JE, Godwin HA. Reexamination of lead(II) coordination preferences in sulfur-rich sites: implications for a critical mechanism of lead poisoning. J Am Chem Soc. 2005 127(26):9495-505. doi: 10.1021/ja0424530
Kehrer JP. The Haber-Weiss reaction and mechanisms of toxicity. Toxicology. 2000 Aug 14;149(1):43-50. doi: 10.1016/s0300-483x(00)00231-6
Mechanisms of lead-induced hypertension and cardiovascular disease, Nosratola D. Vaziri, American Journal of Physiology-Heart and Circulatory Physiology 2008 295:2, H454-H465, DOI: 10.1152/ajpheart.00158.2008
Habermann E, Crowell K, Janicki P. Lead and other metals can substitute for Ca2+ in calmodulin. Arch Toxicol. 1983 Sep;54(1):61-70. doi: 10.1007/BF00277816
https://sites.tufts.edu/leadpoisoning/pathways/lead-and-calcium/
FHW pathway mechanism image source: Trace Metals in the Environment by Daisy Joseph, 2023

All you say may be true but why does carbon not "negatively interact" with so many body functions?

@Peter-ReinstateMonica Because it positively interacts with them. At a chemical level, it's just interactions: we're ones applying arbitrary value judgements like "makes the organism not die" to that. (If you want a causal explanation: prevalence in the ancestral environment, and evolutionary selection pressure.)

(+1) Although lithium is toxic at high concentrations, it is used therapeutically, for example in manic depression, where (24-hr) serum lithium concentration may reach high mM levels in patients using this form of medication

Also, for lead toxicity see Lead poisoning, haem synthesis and
5-aminolaevulinic acid dehydratase where it is very convincingly argued that substitution of Zn with Pb in
5-aminolaevulinic acid dehydratase is a major contribution to lead poisoning

I would answer this question in a different way. As others have pointed out above, elements behave differently than one another even when they have the same number of valence electrons. This makes it possible for some elements to be more toxic than others, even when they're in the same row of the periodic table. But (again, as others have pointed out) it doesn't explain why there's a tendency for the heavier elements to be more toxic. And then there's the curious fact that not all of the heavier elements are toxic, and not all of the lighter ones are non-toxic. On top of that, the mechanisms of toxicity are very different for different toxic elements.
I would argue that the general rule is this: organisms haven't evolved to deal with unusually high concentrations of elements. Heavy elements, because they're rare, are hardly ever encountered at high concentrations. Does this mean that they are necessarily toxic? No - organisms might be able to deal with high concentrations of them, just by chance. For this reason, some rare elements happen to be non-toxic. But others mess with biomolecular functions in ways that organisms haven't evolved to counteract.
In contrast, organisms must be able to deal with common elements at significant concentrations - in other words, those elements must be non-toxic, even if they're chemically reactive. For example, oxygen isn't toxic even in high concentrations because most organisms that couldn't tolerate oxygen went extinct eons ago, when the oxygen concentration in the atmosphere first rose to significant levels.
Hypotheses like this run the risk of being circular or meaningless. ("X isn't harmful to organisms because they've evolved to be resistant to X. The proof is that X doesn't harm organisms!") However, we can put this hypothesis to the test, at least to some degree, by looking at organisms that encounter different elements. Organisms should show specific adaptations to deal with reactive chemicals that are common in their particular environment; they should lack adaptations specific to dealing with rare chemicals. For instance, aerobic bacteria should generate antioxidants, and the genes coding for these defenses should show signs of conservative selection; this shouldn't be the case for anaerobic microbes that rarely encounter oxygen.
I apologize for not supplying more specifics (or citations). I'm in a bit of a rush. But I hope this way of re-framing the question is useful!

I apologize for not being very scientific in this, I will explain how I understand this, based on my experience as a chemist, my whole life trying to understand how these groupings of atoms behave.
Chemistry is the science of how electrons fit together. I could say "the orbitals" of electrons, but we all know that there are no balls orbiting in atoms. Electrons are this phenomenon that occupies space in what we call an orbital. Sometimes orbitals are unstable and electrons are accommodated in other ways between nuclei.
Well then. From the moment the number of electrons reaches that of Gold, a very strange thing appears. The orbitals no longer behave according to the Schrodinger equation.
In heavy atoms like gold, relativistic effects become significant because the inner electrons move at speeds close to the speed of light. This increases their relativistic mass and contracts the s orbitals while expanding the d orbitals.
The unique color of gold is due to these relativistic effects. The contraction of the 6s orbital and expansion of the 5d orbital reduce the energy gap between these orbitals. This shifts the absorption of light to the blue end of the spectrum, making the reflected light appear yellow to human eyes.
Relativistic effects also influence gold’s chemical behavior, making it more inert compared to other metals like silver. This is because the contracted 6s electrons are less available for bonding, contributing to gold’s resistance to oxidation and its ability to form unique compounds.
intuitively (it's all we chemists can do to understand these quantum phenomena), this causes a bubble. Extremely stable, causing a gold that does not react with almost anything. This little ball is the nucleus of everything that comes after in the periodic table.
But biochemistry (for me, at least and we are a product of biochemistry for me) is a way for atoms to organize themselves so that electrons can create gradients of thermodynamic properties suitable for creating the minimum entropy outputs we call life. Now, these little balls get in the way, they don't enter the game. They become insensitive to the entropic flows that cause life.
This, my colleague, is how I understand that these heavy metals cannot be eliminated from the body. Biochemistry based on non-equilibrium thermodynamics has no way of dealing with them.
The toxicity of metalloids, on the other hand, appears to have other factors. Biochemistry is a game between complex structures of non-metallic atoms with occasional and specific roles of metals, as in hemoglobin and chlorophyll. Precisely because of the distinct roles that metals are said to be "chelated" when assimilated into biochemical structures.
The periodic table, however, includes a few intermediate elements between metals and non-metals, these metalloids. When they have lower atomic numbers, they have eccentric effects in biochemistry, a widely used property of B, Si, and Se. They may offer an exquisite effect on the molecule, but of course, it's use is limited. Although there is so much Si on Earth, life can't use more than a little quantity.
In contrast, As, Sb, Te, and Ge are highly toxic and exposure can cause various physiological dysfunctions, growth defects, and human diseases.
The toxicity of metalloids, on the other hand, appears to have other factors. Biochemistry is a game between complex structures of non-metallic atoms with occasional and specific roles of metals, as in hemoglobin and chlorophyll. Precisely because of the distinct roles that metals are said to be "chelated" when assimilated into biochemical structures.
Despite being heavier than Si, all four of these metalloids are lighter than gold, so this toxicity comes from other properties.
In fact, the biochemistry of the toxicity has been an object of research (Front. Cell Dev. Biol., 28 August 2018, Sec. Cellular Biochemistry, Volume 6 - 2018 | https://doi.org/10.3389/fcell.2018.00099).
We have to take into account that life developed in the crust of a planet that contains much more phosphorus (1,050 mg/kg or 0.105%) than arsenic (1.8 mg/kg or 0.00018%) and much more selenium  (0.05 mg/kg or 50 parts per billion, ppb) than (tellurium 0.001 mg/kg or 1 part per billion, ppb) and these two pairs of elements have very similar properties.
Phosphorus (P) and arsenic (As) are both group 15 elements in the periodic table, sharing many chemical properties due to their similar electronic configurations. Here are some key comparisons:
Chemical Properties (P/Ar)
Oxidation States: Both elements exhibit common oxidation states of -3, +3, and +5.
Hydrides: Both form hydrides, such as phosphine (PH₃) and arsine (AsH₃). These are similar in structure but differ in stability and reactivity; arsine is generally more toxic and less stable.
Oxoacids: Phosphorus forms several oxoacids like phosphoric acid (H₃PO₄), while arsenic forms analogous compounds like arsenic acid (H₃AsO₄). These compounds have similar structures but differ in toxicity and some chemical properties.
Similar Molecules
Phosphates and Arsenates: Both elements form compounds such as phosphates (PO₄³⁻) and arsenates (AsO₄³⁻). These ions are structurally similar and often substitute for each other in minerals.
Organic Compounds: Phosphorus and arsenic both form organophosphorus and organoarsenic compounds. These compounds are used in pesticides, herbicides, and other chemicals. However, organoarsenic compounds are often more toxic.
Selenium (Se) and tellurium (Te) are both chalcogens (group 16 elements) and share many similar chemical properties, but they also have distinct differences due to their positions in the periodic table.
Chemical Properties (Se/Te)
Oxidation States: Both elements commonly exhibit oxidation states of -2, +4, and +6.
Hydrides: Selenium forms hydrogen selenide (H₂Se), and tellurium forms hydrogen telluride (H₂Te). These hydrides are analogous in structure but differ significantly in stability and toxicity, with H₂Te being more unstable and toxic.
Oxoacids: Selenium forms selenous acid (H₂SeO₃) and selenic acid (H₂SeO₄), while tellurium forms tellurous acid (H₂TeO₃) and telluric acid (H₂TeO₄). These oxoacids are structurally similar but have different chemical behaviors and reactivities.
Allotropes: Selenium has several allotropes, including red, gray, and black forms, with different properties. Tellurium has fewer allotropes, mainly existing in a metallic form.
Similar Molecules
Compounds with Oxygen: Both form dioxides (SeO₂ and TeO₂) and trioxides (SeO₃ and TeO₃). These compounds are used in various chemical processes and have similar structures.
Organometallic Compounds: Selenium and tellurium form organometallic compounds used in organic synthesis and materials science.
The fact that arsenic is confused with phosphorus is a true tragedy, as phosphorus is crucial in the most fundamental of biochemical reactions, the storage and release of energy. Arsenic spreads throughout the body and ends up being treated not as a foreign element, but as an essential part of metabolism.
(see, for instance, Environ Toxicol Pharmacol. 2015 Mar;39(2):668-76. doi: 10.1016/j.etap.2015.01.012. Epub 2015 Feb 3. The arsenic accumulation and its effect on oxidative stress responses in juvenile rockfish, Sebastes schlegelii, exposed to waterborne arsenic (As₃+) Jun-Hwan Kim, Ju-Chan Kang)
Selenium isn't so useful indeed, although there are some crucial enzymes containing Selenium, like glutathione peroxidase.  I'll reproduce what Bienert and Tamas say about tellurium toxicity (Front. Cell Dev. Biol., 28 August 2018 Sec. Cellular Biochemistry, Volume 6 - 2018 | https://doi.org/10.3389/fcell.2018.00099):
Certain chemical Te species, such as the tellurite oxyanion (TeO₂)³⁻, are highly toxic for most organisms (Lemire et al., 2013). The molecular mechanisms of tellurite toxicity and resistance remain to be fully understood. Turner and colleagues (Vrionis et al.) investigated the effect of selenite on tellurite toxicity in the bacterium Escherichia coli. The authors found that co-exposure to selenite strongly increased bacterial resistance to tellurite. Potential mechanisms of this protective effect of selenite are discussed.
I hope it covers the toxicity of the main elements.

Interesting idea but it doesn't explain why things like arsenic are toxic, yet potassium and calcium aren't (in moderation), nor why these smaller (than Au) elements are toxic.


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Spider identification?
enter image description here

Can someone help me identify this spider? I've never seen one like this. I have brown widows and brown recluses in my yard, along with different types of orb weavers, but I have never seen this one before. There are also a lot of different house spiders and jumping spiders of all kinds. This one was huge though. This is the underside of the belly, I couldn't get a shot of the top. I'm in Southern California.

Looks like the underside of a female silver argiope, a.k.a. silver garden spider (Argiope argentata).


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What is the biology behind human population dynamics?
A paradox: Human population growth looks a lot like a simple logistic growth pattern. But the simplest interpretation of logistic growth doesn't seem to fit. Is this peculiar to humans, or does it have a biological explanation?

Ecologically, advances in agriculture over the last ~200 years have increased the Earth's carrying capacity for human population, and the human population appears to have grown and started flattening out as we approach the new carrying capacity -- this basically looks like logistic growth (following a change in the carrying-capacity parameter).

The simplest biological interpretation of logistic growth is that birth rates remain constant (driven by constant biological factors), but as the population approaches the carrying capacity, there are not enough resources to go around, so death rates rise to match the birth rate. In human populations, this rise in death rates would presumably manifest itself in the form of widespread famine and resource wars.

But that is not at all what we see in the human population! In fact, we have seen falling death rates due to advances in medicine. For some reason, birth rates have actually fallen to levels roughly commensurate with the death rates (and in most developed countries, the drop in birth rates has actually overcompensated for the drop in death rates, leading to an ageing population). So although the net population dynamics seem relatively simple, the simplest explanation for these dynamics fails spectacularly. This leads to several

Questions:

Is there an underlying biological mechanism linking our approach toward the environment's carrying capacity to a resulting drop in birth rates?

There are compelling sociological explanations -- education and empowerment of women, urbanization, decreased child mortality, access to contraception, etc. all point individuals toward a reproductive strategy of investing more into a smaller number of children. But from a sociological perspective, it appears to be a mere accident that all of these forces are converging at once to save us from a scenario of high birth rates and high death rates. One suspects there might be something more fundamental going on here.

Are there examples of other species which do the same thing -- throttle down their birth rates as they approach the environment's carrying capacity?

Maybe there's an evolutionary advantage to this. A population which generates lots of individuals destined to fight one another or die of hunger before reproducing seems to be wasting a lot of energy, especially if individuals care for their young. An overcrowded, underfed population may be more vulnerable to catastrophic disease (especially in a social species), and reduced individual fitness may actually reduce the total amount of resources the population is able to extract from the environment. If a species relies on cooperation within social groups, then perhaps excess births lead to intragroup competition that undermines group fitness. The basic principle of group fitness -- that sometimes it is more advantageous to help others in one's social group than to act directly for one's own benefit -- may be magnified when populations are stable with little room for growth (just as in a mature marketplace, it may be easiest to cooperate with an established business, whereas in a new sector it may make more sense to grow a new business from the ground up).
So I would look for this phenomenon among species that form cooperative social groups and care for their young -- colony-forming insects and large social mammals spring to mind. From my amateur reading, it sounds like lions might be a non-example, regulating their population by pushing excess or unfit individuals out of the pride to their likely death (or at least, this suggests that the population is not regulated solely via birth rates). But it seems like this could be addressed experimentally: for example, if individuals from a stable population of species $X$ are introduced into a new environment that can easily support a larger population of $X$, then does their birth rate go up?

If the answer to (2) is "yes", then what biological mechanisms are behind this?

Such a mechanism must be interpreted in the context of individuals' reproductive behavior more generally. There will be (a) factors affecting the advantageousness of reproducing, with (b) environmental cues indicative of these factors, (c) factors influencing individuals' actual reproductive behavior, and (d) biological mechanisms by which (b) influences (c).
Among the (a)-type factors we're particularly interested in might be abundance of food, space, disease, social stability,... Candidates for (b) might include crowdedness, air quality, presence of greenery and wildlife, stress levels,... For (c), one might look at libido, fertility, desire for a mate or for children,... For (d), ideally one could get down to the level of things like hormone regulation.

Can we use the answer to (3) to inform an answer to (1)?

Here are a few crazy theories that might be supported.
In urban areas, the smell of other humans and lack of greenery are cues that the population is overcrowded and food is scarce, which via some dedicated hormone-regulation system common to all mammals suppresses the desire to mate or raise offspring (but in the United States, these factors are mitigated slightly by our constant showering and our sparser settlement patterns, leading to a birthrate higher than in much of the developed world.)
The gradual process of political integration and tolerance has led us to identify larger and larger subpopulations of humans as "us", and a sense of being part of a large group with a stable population both upregulates pro-social behavior and somewhat suppresses the desire to have children of one's own.
The elevated stress levels of modern life are a cue that one can ill-afford the investment required to reproduce, suppressing the desire for children.

Wow... this is one long post! I personally don't feel like reading such a long post. You might get more attention if your post is shorten.

Note that if you google your question you'l get tons of information such as this quora post for example.

I think most of the stuff I could find addressed mostly sociological aspects. I tried to organize the question to be skimmable, maybe I'll make a few modficiations to improve this. The stackexchange sites I'm useful have slightly different-looking interfaces.

The edit already make the post much more attractive :) Side note: sociological phenomenon do affect our environment and they are not to be disregarded as irrelevant when talking about human population growth just because a sociologist said it and not a biologist.

Oh good! That's a great point about the sociology -- I'm hoping that the biology of the situation can help to contextualize the sociological situation.

Animals typically have as many broods and babies as they can physically nourish themselves for, given a basic local territory and fair conditions for breeding. So AFAIK, food and weather throttles parents nourishment and broods in a simple biological-economic way. Human hunter gatherers females have an average of 5 babies or something. Todays dynamics are lab/technological biology.

@aliential A relevant fact which I believe I've read is that the adoption of farming actually led to decreased level of health among humans by several metrics, such as lifespan. I believe I've also read that the adoption of farming also led to an increase in family sizes. If this is accurate, it would be a great confirmation that humans can change their reproductive strategy in response to the environment (whether this happens at a species or individual level is unclear). So human history has not been a linear evolution along this axis, which is actually great evidence for adaptability.

Consider that genes doing what you propose would be immediately outcompeted by selfish organisms who try to dominate resources instead, It can only work as group selection which should be a red flag

I think the key point is that humans cannot be modeled as a wild population.

Its actually much simpler than you are making it out to be, carrying capacity is not an issue, humans long since surpassed the planets carrying capacity without advanced technology. The real factor is infant mortality.
consider both K and r strategies
Say you have two sets of parents each starting with the same amount of resources. In r strategy the approach is to invest little in each individual offspring and have a lot of them, K strategy involves investing a lot of resources in each offspring and having only a few. The same amount of resources are consumed by each set of parents. It seems like r should always win, but as long as offspring mortality is low K usually wins. Why because high investment offspring can usually easily outcompete low investment offspring for finding mates as long as they survive.
Who has an easier time finding a mate the man who was half starved as child and has chronic health issues and missing teeth becasue of it or the man who had top of the line nutrition and medical care and is physically fit, with good teeth. these are the extremes but it holds true all long the spectrum, better health, better education, better environment (moving costs a lot of resources), all correlate with more mating success.
For each individual having fewer high investment children is better as long as there is a high likelihood said children will survive. Which has only become true with modern medicine and sanitation. So by each parent doing what is best for their genes and offspring society as a whole has fewer and fewer children, again as long an child mortality is very low.
But for most of human history child mortality was highs so having few offspring did not work, because there was a decent chance all of them would die. Thus having lots of children was the only way to guarantee having any children who live to mate. As child mortality drops the number of offspring who survive skyrockets (thus population also explodes) so mating success becomes a much bigger factor than chance of survival, because the chance of death is so low.  Modern medicine and sanitation has changed the selective pressures on our mating strategies. More K leaning strategy is now evolutionarily favored in humans, so the number of total offspring declines, so the population growth also declines. This is called the demographic transition model.
The correlation is surprisingly tight, as infant mortality drops population growth drops add in things like access to education and it gets even tighter.

I feel obligated to point out the r and K strategy are not binary but ways of describing a spectrum of reproductive approaches.

Thanks, that's very informative! You make the argument that falling infant mortality evolutionarily favors $K$ strategy reproducers. This would explain the correlation between infant mortality  and population growth IF genetic factors largely determine whether an individual human pursues a more r-type versus a more K-type reproductive strategy. If this is really the case, then because the phenotypic swing from r to K has been so dramatic over the last century or so, the genes responsible should stick out like a sore thumb in studies of human genetic change over that timespan.

But absent such compelling evidence, I'm inclined to doubt the hypothesis that genetic factors strongly influence whether an individual human pursues a more r-type or a more K-type reproductive strategy. That's part of why I suspect there may be some more "meta-level" biological mechanism at play. I suspect that humans (and other species) may have various adaptations which enable an individual to toggle between r-type and K-type reproduction based on subtle environmental cues, rather than it simply being a case of individuals with the appropriate genes for the environment outcompeting others

In my hypothesis, I might incorporate your observations by positing that among these "subtle environmental cues", perceptions of infant mortality rates may have very high (or even overwhelming) importance. Of course, I have equally little evidence to support this hypothesis.

@TimCampion very flew behaviors are hard coded in the way you think,  many if not most of instinctually behavior is trigger based, and it is fairly easy for an social organisms to determine child mortality. we know children instinctually keep track of siblings and gender ratios in there community. Plenty of organisms individually  change reproductive strategy depending on environmental triggers.

@TimCampion the biggest problem with carrying capacity is an organism have few ways to assess carrying capacity. more importantly if they were tracking carrying capacity we should see lower population growth in less abundant environments but we don't instead we see it in technological advanced ones, which are the places were carrying capacity is increasing.

I just read about John B. Calhoun's mouse utopia experiments in an interesting history stackexchange post.
The basic result is that when mice are given unlimited resources but constrained by space, their population does initially explode but this leads to a loss of social cohesion and thence to plummeting population levels.
While far from conclusive, this suggests to me that there are indeed some kind of biological fundamentals going on here which control overpopulation by means other than widespread starvation.
I'm sure there's lots more to say!


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Compare cell types human iPCS lines and human prefrontal cortex
I'm a bioinformatician with less knowledge in biology.
I'm working with human brain cells. I have 2 different sequencing datasets. One was derived from human iPCS lines, and another was obtained from postmortem human prefrontal cortex cells.
These two datasets were provided with their own cell type annotations and they are two different from each other.
What I'm doing is try to integrate the two dataset first. But the result displays that these two datasets are too seperated and I cannot find any common group of cells between the two.
May I ask, if anything of their properties or the cell types of human iPCS lines and postmortem human prefrontal cortex cells are in common? Or are they too different?
Sorry if my question is not correct, because I don't really understand what makes them different. I saw so many papers have been working on iPCS to study brain diseases, so I supposed there must be common things between them.
Thanks in advance for any explanation.

"the result displays that these two datasets are too seperated" - The "result" doesn't display anything, it sounds like you're using some software package that you haven't described to us. It seems like it's not just the biology you're not familiar with, but you don't know how your software works, either. That's a dangerous place to be in. Overall, it's dangerous to try to study biology questions without knowledge of biology, and you're not going to be able to patch the gap with SE Q&A. Plus I assume you're talking about "iPSC" cells and keep writing "iPCS".

Your deceased-samples weren't from some peculiar circumstance involving unbuffered formaldehyde, were they?

Trivial explanation: you have a batch effect that makes comparing the two datasets possibly non-informative (Jiminy's question is one case of this). More generally, iPSCs are pluripotent cells, whereas cortex cells are (I'd assume) fully and fairly dramatically differentiated cells. You'd expect them to behave quite differently!


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Bioavailability of plant food?
The kcal count of food is evaluated by either bomb calorimetry or mostly by determining macronutrient concentration and multiplying with their atwater factors.
I am interested in the bioavailable kcalories of plant food assuming that we cannot extract nutrients as efficiently from plant matrices.
We see in every plant based diet study that participants loose weight even if it is a calorie matched protocol.
Do you have a comparison or estimation between theoretical and real energy value of plants? Its not easy as it will vary significantly between individuals considering differences in microbiome and metabolizing enzymes.
.

you probably want to look up the effects of fiber on digestion, that will be the biggest effect.


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Small jumping bugs inside Swiss flat
Saw these bugs inside the flat I'm renting (Switzerland), but I really can't figure what kind they are. What I can say about them:

They can do small jumps (up to 5cm I would say). It doesn't seem to be for locomotion, but as a means of escape when I try to catch one.
Size: about 1.5mm for the "big" ones. There are of various sizes down to 0.25mm for the really tiny ones (approximately; never managed to get one without crushing it). They behave much the same as the big ones (including the jumps) and are whiter in color.
They don't seem to live as a colony or in a nest (or I simply didn't find it), but sparsely on the wood floor, often near the baseboards. Found some on the walls, but those were the exceptions. They don't seem to like the bathroom.
Rather delicate; can easily be crushed.
Seem more active in the evening and at night, but don't mind going out during the day.
I live alone, without pets, but I don't remember having been bitten. I guess they don't feed on blood.
Seem to have long antennas (about half their body size) and small wings.

Side note: the flat is on the 3rd floor of a recent building (finished 14 months ago). I'm the first tenant.
An exterminator came and quickly classified them as some kind of flea. He put some pesticide on the baseboards, and their number is now quickly decreasing. But I'm still curious.
My first thought was "fleas" (because of the jumps), but I deemed them too squishy and not "vampire" enough for that. Also, I don't think that (what I assume to be) the young ones should be able to jump.
Then I thought "springtails", but I didn't see any furcula (granted, I don't have a good eyesight) and I don't think they are supposed to have wings.
One of them was nice enough to jump on some tape.
Top (on a ruler):

Front/Side:

Also, blowing on it (to open the wings):

Youtube video of one of them

They're definitely not fleas despite what the exterminator said. Fleas can REALLY jump, don't have wings and aren't easily squished. But I've no idea what sort of insects are found in Switzerland, especially in homes.

You must be mistaken. The Swiss are very, very clean.

I've resized the images to reduce the amount of scrolling. You can still click on them for the large version, but feel free to rollback if you want.

I believe these are some sort of Psocoptera, "booklice", even though they don't really jump much. Could it be that they ran or flew a little bit instead? I won't try an identification of the species, but in general booklice like damp places and most of them aren't considered serous pests.
Example of a booklouse:

Slender legs and antennae, wings, and general appearence close to your specimens.
(Image from Wikipedia)

Yep, this is the one! That would be a Dorypteryx (domestica or longipennis) then, I guess? I can't tell if they are jumping or flying, I will try to record and upload a video next time I corner one of them.

See this question, this question and this question for other posts about psocids...

@theforestecologist Yeah, this seems like a recurring thing. I guess this sort of question could be closed as a duplicate? But species identification is pretty hard to find answers to by searching if you don't know what to search for, so they'll probably keep coming.


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Why it is important to vaccinate a human newborn within 24 hours since birth?
In Poland a newborn has to be vaccinated within 24 hours against hepatitis B and tuberculosis.
As I understand it is good to be vaccinated against both, I do not see the need to hurry so much.
Hepatitis B is transmitted sexually or by blood. The former vector is definitively unsuitable for a newborn, and the latter... Well, I do hope so far all Polish hospital adapted to Ignaz Sammelweis advice on antiseptics.
In case of BCG vaccine against tuberculosis (containing alive bacteria) there would be an additional risk if the newborn's immune system were in any way impaired which is unknown within first 24h. It is not that tuberculosis is common disease in Poland - is endemic (probably due to the obligatory vaccination indeed).
What possible biological benefits are there to vaccinate a newborn so early? Especially which of them prevail over possible risks of BCG vaccination?

What is the route for maternal to child hepatitis b transmission?

@GrahamChiu possibly, but if the mother is positive, then child shall be rather given antiglobulin as it takes time to build active immunity

Well, in the Netherlands we don't vaccinate so early and AFAIK we don't vaccinate children against heb. B and tuberculosis at all. So it is not that important. I can only guess that they do it because they are afraid the mother might carry hepatitis B.

And how long is hbig effective for?

@BenBolker agreed

@GrahamChiu I guess no longer than transplacentally transmitted IgGs, which I estimate to be at least several months ($T_{\frac{1}{2}}$ is about 1.5 month). The problem is that AFAIK children of HepB+ mothers are not given antiglobulin as there is no HepB screening at all.

Since another posted answer addresses HepB vaccination at least as effectively as I would have, I'll say something about first-day scheduling for BCG, which is consistent with WHO guidelines (emphasis added):

In countries with a high burden of TB, a single dose of
  BCG vaccine should be given to all infants as soon as
  possible  after  birth.  Since  severe  adverse  effects  of
  BCG vaccination are extremely rare even in asymptomatic,  HIV-positive  infants,  all  healthy  neonates
  should be BCG-vaccinated, even in areas endemic for
  HIV ...

(it goes on to discuss recommendations for symptomatic HIV-positive infants. I didn't look at the details of the Polish vaccine policies, but I'd be extremely surprised if there weren't an exception/variation for newborns who are known to be immunocompromised. We can argue about the frequency of newborns who are immunocompromised based on factors that are unknown before birth [i.e. not based on known factors such as genetics, mother's condition, etc.] ...)
I'm admittedly speculating a bit here, but based on what I've read it seems that the main reasons for "as soon as possible after birth" are (1) to allow for development of immunity and (2) logistics, i.e. increasing the actual coverage achieved.
Development of immunity: it takes time for immunity to develop, so the issue is not that babies will be exposed to Tb in the hospital, but that they may be exposed before the vaccine has taken effect. Gaisford and Griffith 1951 quote Wallgren (1950) as saying that effective immunity may be delayed by 10-12 weeks. More recently, Saroha et al 2015 say

BCG vaccine induces delayed type of hypersensitivity reaction and cell mediated immunity (CMI) in the host 4–8 weeks after immunization.

Logistics: Oberoi et al. 2017 report on changing scheduling of BCG vaccination in Indian clinics:

Rescheduling of BCG dose, from twice weekly to daily, the coverage of BCG and OPV zero dose increased from 54% (in 2014) to 78% (in 2015), and a marked increase from 8.2% to 42.9% was noted for the birth dose of hepatitis B.

Is Poland a high-incidence Tb country?

Tb incidence in Poland in 2016 was about 18 per 100,000: based on this map, that's about twice the level of most Western European countries (and more than triple the rate of Canada, which is what's referenced in the link you give above about dangers to immunocompromised people), but half to a third of levels in the former Soviet Union ...
The World BCG Atlas shows that vaccine policies follow a similar geographic pattern - BCG is used in Eastern but not in most of Western Europe

the rate of adverse advents following BCG vaccination in Poland is low and hasn't changed much after changes in timing of vaccination:

It is generally estimated that local adverse reactions usually occur at the rate of 0.1 to 0.5 per 1000 vaccinations, and serious disseminated complications occur at rate of less than 1 in a million vaccinations

Some research studies suggest that delaying vaccination for a few weeks may have different (better or worse) effects (e.g. here, here).

There has been a long standing shortage of bcg which is diverted for bladder cancer use rather than vaccination here in NZ.

In the US, infants are vaccinated against Hep B at birth and again a month or two later as well, because of the risk of maternal transmission. If the mother is known to be HepB positive, HBIG will also be administered.

Perinatal HBV transmission can be prevented by identifying HBV-infected (i.e., hepatitis B surface antigen [HBsAg]-positive) pregnant women and providing hepatitis B immune globulin and hepatitis B vaccine to their infants within 12 hours of birth.

The reason for the HBIG is obvious, but it doesn't last for life. Therefore, the vaccine and its booster.

Hepatitis B virus (HBV) infection in a pregnant woman poses a serious risk to her infant at birth. Without postexposure immunoprophylaxis, approximately 40% of infants born to HBV-infected mothers in the United States will develop chronic HBV infection, approximately one-fourth of whom will eventually die from chronic liver disease.

In countries where HepB is not prevalent, there is little cause to immunize at birth. However, it is too common in the US.

Preventing perinatal HBV transmission is an integral part of the national strategy to eliminate hepatitis B in the United States. National guidelines call for the following:
  - Universal screening of pregnant women for HBsAg during each pregnancy
  - Case management of HBsAg-positive mothers and their infants
  - Provision of immunoprophylaxis for infants born to infected mothers,   including hepatitis B vaccine and hepatitis B immune globulin
  -Routine vaccination of all infants with the hepatitis B vaccine series, with the first dose administered at birth

The risk of HepB vaccine is low. The seriousness of the disease is high. It is not only the mother who might be a carrier. There are many unidentified carriers in the US. That makes the risk-to-benefit ratio low. Driving your newborn home in an automobile is probably more of a risk than the vaccine, but most people do so anyway, and do so many, many times over the course of the baby's life.
In the US, we do not routinely vaccinate against TB, so I cannot address that issue with any degree of expertise. The risk-to-benefit ratio is not as low as for HepB. It is given to children who are continuously exposed to someone (say, a parent) with active TB, or in certain communities where TB is very prevalent. Obviously, if the risk of SCID (severe combined immunodefficiency) is high, the risk of the vaccine is much higher, and some infants have died from it.
Discussing the risk to benefit ratio of all infant vaccines is too broad for this venue.
Separating Fact from Fiction in the Newborn Nursery: Hepatitis B Vaccine for Newborns
The benefits and risks of bacille Calmette-Guérin vaccination among infants at high risk for both tuberculosis and severe combined immunodeficiency: assessment by Markov model

I guess that also risk of HepB infection within first months of life is also lower than of a car accident due to its way of transmission. Of course given that we trust our healthcare to follow antiseptic guidelines, which was not the case in early 90' in Poland (as it was common practice to use dry-air autoclaves that time, which AFAIK do not inactivate HBV).


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Have the effects of hydroalcoholic gel on mosquitos have been studied?
It is well known that alcohol attracts mosquitoes [1] and the impact of alcohol in the blood sucked by these insects is very low on their nervous system:

But in reality, insects can be remarkably resilient to the effects of alcohol [2].

So it is likely the alcohol is neutralised before it hits the insect’s nervous system [2].

[1] https://pubmed.ncbi.nlm.nih.gov/12083361/
[2] https://www.bbc.com/future/article/20190313-will-mosquitoes-bite-me-more-when-ive-been-drinking
However, does the impact of hydroalcoholic gel on mosquitos has been studied? On my own (home-made) experience, several mosquitoes have resisted several hours in a closed box, but only few minutes once a piece of paper with some drops of hydroalcoholic gel has been introduced in the box...
Are they dying only because alcool has been breathed instead of sucked?

Have you thought about the concentration of blood alcohol much?

Welcome to SE Biology. It would help preserve the professional ethos of this site if you could edit your title so that it reads as grammatical English. Hint: replace “do” by the later “have”.

@David, thanks! Sure, I have edited the title.

When you say "hydroalcoholic gel" - are you referring to ethanol-based products or rather some other alcohol (eg. isopropanol)?

@JiminyCricket, I am speaking about hand sanitizer typically used during the COVID period and largely available in public shops (ethanol-based product)


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Fraction of methylated sites in restriction-modification systems
Given a strain that is expressing proteins of a restriction-modification system (like EcoRI), is there data to measure the fraction of metylated target sites? I am just looking for an approximation, so in vitro assays also should work.
For EcoRI, I have seen people measuring kinetic constants for the methyltranferase and couting number of molecules in a cell. But from that I do not think I am able to predict the fraction of modified sites, only the fraction of enzyme bound to DNA at a time.

I find it difficult to understand your question. When you refer to target sites, which DNA are you referring to — E.coli DNA or invading bacteriophage DNA? And why would you expect not all EcoRI sites in Ecoli to be methylated, if that is what you mean? Or in a phage infection, that would be related to the number of progeny phage. Or are you thinking of restriction enzymes in cloning? If so the problem is one of enzyme kinetics.

By target sites I mean the sites recognized by the Methyltransferase in the own bacteria DNA. I would expect almost all of them to be methylated, but probably a small percentage may remain unmethylated due to loss of the methyl group, or DNA replication before division. I expect this percentage to be small, but I have not been able to find any data about that.

Ok. That’s a fair question (to which I don’t have an answer). Perhaps you could edit the question to make that clear, or I will do it for you if you wish.


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Is this a harmful insect?
I found this insect crawling on my neck while standing under a tree. I am wondering if it's a harmful (to humans) insect. I live in Prague. It is small (not even a centi-meter I think).

Harmful to what? All insects eat something. But it seems unlikely to be harmful to humans.

Seems like a species of true bug. Some, like bed bugs or assassin bugs are harmful, but this one doesn't particularly resemble any of those.


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What insect is this? There are a lot of them in my apartment, but they don't seem to be either cockroaches or spiders
I keep finding these things in my New York City apartment, and I am very curious what species they are. I thought they were cockroaches at first, but couldn't find any pictures online that would resemble these insects.
(Added later):
Thanks for a comment--I am now convinced that these are, in fact, spider beetles. Mine look somewhat dissimilar to the ones shown on wikipedia--they are black in color and round in all three dimensions, they looked like balls with legs when they crawled, which totally confused me as to what those things were!

Where in the world do you live? Different insects are present in different places, that might help narrow it down.

You are absolutely right. How come I didn't think about it? I modified the question.

These look like spider beetles. https://en.wikipedia.org/wiki/Spider_beetle

Why not write that up as an answer @Rich ?

These look like spider beetles. see here Spider beetles are about 1-5mm long and there are 70 species of them here in N America.
here's more info from whatsthatbug. "They belong to the family Ptinidae and are not considered true spiders or arachnids, but insects." They're not apparently harmful, so I would categorize them as "Mostly Harmless."


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What is the use of male plants in nature?
If pollination is done by insects like bees and through the air, then what is the use of male plants in nature?

They are just the delivery service for Pollen

Pollen, spermatozoid, ovules and bees
The pollen is a coarse substance containing the spermatozoids. Males plant creates these pollens. As bees visit the flowers, the pollen get stuck on their body. When the bee covered with pollen visits female plant, then the pollen may randomly stick onto the female organ. The spermatozoid grow into a tube within this organ and goes to fertilize the ovule.
In short, bees are ...
In other words, you need females for the ovaries, males for the spermatozoids and bees for the delivery services.
Note that bees don't do this delivery services just to be nice with plants. They do so because they get nectar (substance full of sugar) in the flowers.
Reality is more complex and more diverse
Note also, that reality is more complex and more diverse than what I explained. Not all plant species are pollinated by bees. Not all plant species have flowers. Most plant species are hermaphrodite (have male and female flowers or even have male and female organ within the same flower).


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What are hyphal compartments?
The hyphae are the branching filaments that make up the mycelium of a fungus. Hyphal compartments are part of the hyphae. What are they exactly?

I did a quick lookup on google for "hyphal compartments" and the number of online texts/books/citations using this term is quite meagre to say the least. One of the images that I found was this-

And I have reached to the conclusion that--
Hyphae cells (only in septate species) are known as hyphal compartments.
Quoting from wikipedia (read if you don't know about septate and coenocytic varieties of hyphae)

A hypha (plural hyphae, from Greek ὑφή, huphḗ, “web”) is a long, branching filamentous structure of a fungus, oomycete, or actinobacterium.In most fungi, hyphae are the main mode of vegetative growth, and are collectively called a mycelium.
A hypha consists of one or more cells surrounded by a tubular cell
wall. In most fungi, hyphae are divided into cells by internal
cross-walls called "septa" (singular septum). Septa are usually
perforated by pores large enough for ribosomes, mitochondria and
sometimes nuclei to flow between cells. The major structural polymer
in fungal cell walls is typically chitin, in contrast to plants and
oomycetes that have cellulosic cell walls. Some fungi have aseptate
hyphae, meaning their hyphae are not partitioned by septa.
Hyphae have an average diameter of 4-6 µm.


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Could humans breathe if the average methane content of the atmosphere increased to 1%?
Below is a table of atmospheric composition. Could humans breathe if the average methane content of the atmosphere increased to 1%?

Table 7a-1: Current Average composition of the atmosphere up to an altitude of 25 km.

Gas Name          Chemical Formula    Percent Volume

Nitrogen          N2                  78.08%
Oxygen            O2                  20.95%
*Water            H2O                 0 to 4%
Argon             Ar                  0.93%
*Carbon Dioxide   CO2                 0.0360%
Neon              Ne                  0.0018%
Helium            He                  0.0005%
*Methane          CH4                 0.00017%
Hydrogen          H2                  0.00005%
*Nitrous Oxide    N2O                 0.00003%
*Ozone            O3                  0.000004%

* variable gases

Could you provide a link for the table?

1.0 what?  Percent, ppm, or?

Not sure what you had in mind, but if the atmosphere was 1% methane there would be a massive contribution to global warming. I don't know if anyone has run a model with that much methane but it could very well be an unsurvivable level for human's time on the planet, regardless of direct biological effects.

See http://www.sciencedirect.com/science/article/pii/S1871174X16300488

Methane is biologically inert and can only act as an asphyxiant at high concentrations by displacing oxygen. An environmental exposure limit has been set at 5,000 ppm, though 10,000 ppm (1%) had no effect:

It is obvious that an exposure limit that presents an explosion hazard cannot be recommended, even if it is well below a concentration that would produce toxicity; thus, exposure limits should not exceed 5% by volume in air.
Animals exposed to methane at 10,000 ppm showed no toxic [effects]; an uncertainty factor of 2 is suggested to derive an EEL—5,000 ppm. There is no evidence that duration of exposure is important in methane toxicity.

Source: Methane in Emergency and Continuous Exposure Limits for Selected Airborne Contaminants Volume 1 (1984)


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What is the relationship between complexity and organization in biology?
Is there any relationship between what we can call complexity and what we can call organization in biology? And if there is, what is it? Can we define these terms independently of each other or would the definition of one of them always inescapably include the other and vice versa? If the second is the case, what can such a relationship tell (or, at least suggest) us about life?

I would like to draw a parallel between my question and another question here on SE pertaining to the same notion-that of complexity in biology, to show how we can shape a question in a much clearer and precise style and get more information about the same issue. Here it is- http://biology.stackexchange.com/questions/13853/why-and-how-does-complexity-usually-tend-to-increase-through-time/57005#57005 I'm trying to show how the topic discussed there can be presented in clearer and more exact style if we concentrate on a particular issue instead of trying to cover everything in 1 question

I think if one starts out a question with a clause that includes "depending on the definition of the terms you use" one must be prepared to provide such definitions, otherwise it isn't possible for anyone to answer without using their own definitions and therefore making the question opinion-based.

Hi, @YordanYordanov. Complexity & organisation have specific meanings depending on context. For example, I work with sequences in terms of simple and complex depending on their linguistic entropy. Some people would call a protein structure complex if it was very disordered due to estimations of chemical entropy. Some people would call one cell more complex than another if there were more external forces interacting with it, others if the structures were more varied. Because of the vagueness of the term "complexity" in this question, I'm voting to close as off-topic.

I have edited my question. Are you happy now, @Bryan Krause ? In this form is it still "opinion-based" according to you?

Hey, how can you put it on hold? I just edited it! What is the problem now?

I and the others voted to put the question on-hold before your edits (I think @James gives a good argument for why, in addition to my own answer). I will review your edits - questions put "on hold" can always be returned to an open status after edits.

I will wait then and if you reopen it I will delete my comment and this comment, too.

Unfortunately I don't think the edits resolved the issues. Your question really contains a dozen different questions all going in different directions. "Can we define these terms independent of each other" - this is really just an opinion question. Sure, someone could do so if they wanted to, because they are choosing the definitions. I could define complexity as "number of photons emitted" if I wanted to. I don't think your question is uninteresting, but it is not suited to the question-answer format of this site - as written, it is more of a discussion question.

What about now? I managed to shape it into a question pertaining only to whether there is any relationship between the definition of complexity and organization in biology. The point is is it possible to define complexity  in biology without including organization in the definition of it and the vice versa? Are they interrelated in codefinitional circle we can't escape and if they are-why? How is this not an interesting topic for discussion in a biology Q&A? Don't you see implications if the 2 terms are mutually dependant on each other for their definitions?

The whole point is that questions for discussion are not questions for this site - questions should have a correct answer (within the bounds of existing knowledge, of course), not based on opinion, or they don't belong. I don't want to hijack your question, but consider something like the following, which I still feel is not ideal but it is not a question I would vote to close: "Are there any academic works that distinguish between complexity and organization in biology such that they need not be correlated with one another?"

Then do you suggest I make 2 new questions-1 is there relationship between the definition of complexity in biology in terms of the organization of the organisms and 2-is there relationship between the definition of organization in biology in terms of complexity? Would that be more "fit" for you?

I still am amazed how quickly you put this question on hold while other questions pertaining to the same field and also having many unclear questions mentioned in them like this one-http://biology.stackexchange.com/questions/13853/why-and-how-does-complexity-usually-tend-to-increase-through-time/57005#57005 are still standing active even after years have passed? What is so "unclear" here that is "clear" there to put my on hold so quickly?

@YordanYordanov the other question was asked during our beta. The community was a lot less clear on what constitutes "answerable". Now it's resurfaced I'll initiate a close vote. People may be hesitant to follow since it has 7 upvotes (people like the question) and an accepted answer that seems at least superficially satisfying. If in the future you have an issue with a question, it'll be best to raise it on that question rather than a different question. This site is vast.

@James , the issue I have is where is the place for Q&A about complexity in biology on that site. Should I use questions like the one I show you (which I personally-you're free to disagree-think is quite vague and broad)q should I make my own questions and use the tag complexity or may be something else, What do you think will be the best question for regarding the issue of complexity here on this site? What should be asked-what it is, how to measure it, problems regarding different definitions and/or measurements of complexity,its significance for evolution, ect.How to ask questions about it?

I'm ready to delete this entire question if you can provide me with better ways to ask about the problems associated with the discussion of complexity in biology. What do you consider would be appropriate question about complexity in biology on this site? If you manage to provide better question I'm ready to delete this one in its favour.

@YordanYordanov I agree the other question is vague and have opened a close vote on it. I see questions on complexity being more along the lines of "How can I quantify the complexity of system/thing X in a biologically relevant way?" This question is on hold and will be closed sooner or later unless it is successfully reopened.

I want to delete my question in favor of this one-http://biology.stackexchange.com/questions/57178/what-is-the-meaning-of-complexity-in-biology but the systems just will not allow me. I feel this one is better and if somebody wants to put it on hold it because it is a duplicate of this one I should delete this one, not my second question. What should I do?

Here's food for thought. Entropy is always considered to flow naturally in a direction of order, to disorder. That is, the higher entropy a system has, the greater degree of disorder it has, and the less amount of work it can perform.
Now, look at a cell. It is a biological system of organic molecules that are able to organise themselves in a way that outweighs the forces of entropy. To "fight" the natural tendency of the universe that moves toward a state of disorder requires a highly complex system. And, in the process of going against entropically favorable mechanisms, a cell is also able to produce its own energy (stored as potential energy, or ATP if you will).
I guess you could say, a more complex system is able to organise itself in a greater number of ways for the purpose (and I use this word very loosely, as nothing really has a purpose) of yielding entropic energy to do work.

I think you are on very right track here. The question, however remains can we define organization as the state which forces the system to go against the entropy gradient and if we can, then what is really complexity then? Does the increase in organization drives the increase in complexity or is it the vice versa? Or may be some even more intricate and "complex" relationship?

Another thing to consider is that complexity can sometimes be more apparent than real, because an underlying simple mechanism that is not understood by the observer can give rise to complex results.  For instance, consider how the growth of plants &c can be modeled by L-systems (https://en.wikipedia.org/wiki/L-system ), or how the widely different forms of mollusc shells conform to a few mathematical rules.  Or indeed, how a couple of simple principles produces evolution.

"Does the increase in organization drives the increase in complexity or is it the vice versa?" seems a lot like the question, "did the chicken or the egg come first?". I do understand why people voted to put this question on hold - because there isn't really any way to answer it. I honestly do not know because it is too abstract. I think I have somewhat of an idea about how it works, but I have no idea how it came to be.


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What would be the best dredging/trawling tools to collect macrofaunal priapulids?
Title says it all. I've been searching for the best way of collecting macrofaunal priapulids and would like advice on sampling methods and particularly sampling tools. Since large priapulids are usually found in low densities any form of grab-sampler would probably be inefficient and a dredge/trawl would be preferred. Any ideas on what tool(s) would sample at the right depth and filter efficiently?

The Ecology listserve (ECOLOG-L@listserv.umd.edu) would be a good bet to find expert responses to such a question; it would be useful to reference this question if you were to post there.

My first question would be is there any external indication of them such as air holes or anything else that you can assess from the surface?  I would think that if there is, you could use transects and a quadrat.  If you need to dive for them you can obviously make a weighted quadrat by filling pvc pipe with sand and gluing it together.  Then take an area and lay out transects and and randomly choose different lengths along each transect to put the quadrat down and that will give you an estimate of density.  If you actually need to extract them from the mud, I imagine that varies by species and you could make due with a grab sampler of the right size, something on the small end I would imagine.  That way you aren't dredging up tons and tons of mud to sort through.  If they are even rarer than I imagine, you could just lay out transects and swim them until you see something and do away with the quadrat.  Hope this helps.


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Long term storage of agarose-ethidium bromide gels that have already been cast
I have come up with what I thought was a clever idea: Store the agarose gels I pour, and only cut as many lanes as I need to run later, minimizing wasted agarose (and wasted effort/time) when I need to make many electrophereses using a small number of lanes.
I realized that over time, the EtBr would diffuse out of my gel into the buffer that the gels are kept in. Since I add 2 µl of EtBr to 50 ml gel, and the gels were kept in 400 ml TAE buffer, I added 16 µl EtBr to the buffer, reasoning that now concentrations are equal and no net diffusion will take place.
However, after several weeks, I noticed that the EtBr signal from the gel is severely weakened. What can I do to fix this? I can see the following options:

Use higher concentration of EtBr in the buffer (how much?)
Change buffer weekly, adding fresh EtBr every time
Cover the transparent container with aluminum foil to prevent hypothetical photobleaching

Which one is most likely to solve my problem? Should I just give up, and throw away gels that are older than a day or two (I want to avoid this option, because of the record keeping needed to track when the gel was last made)?

What I've seen is to keep a bottle of agarose gel, then heat it up to melt, pour what you need into a gel caster, add your ethidium. This way your large gel stock doesn't get contaminated with ethidium and you don't have to worry about loss of ethidium signal.

@user137 I am saving cast gels in order to avoid the hassle of melting and casting a gel everytime I want to run some samples. The bottle of agarose only saves me the work of weighing the agarose, which is quite insignificant in comparison.

did you see a reduced signal using the same DNA conc or construct after running it several weeks later in a gel containing no previously run DNA band? I think EtBr can photo bleach so just use fresh buffer with fresh EtBr. Even with a stock EtBr you are meant to wrap it around foil! Old gels are generally not good since they can become quite hard and fragile in my experience so using fresh gels is always best.

@Superbest You could store pre-cast gels without ethidium and then post-stain, but you'd end up with more ethidium waste to worry about.

@Bez Yes - what I do is, first make a gel with normal EtBr and wells etc., then put the gel into TAE buffer with EtBr in the buffer, keep it there for a few weeks, run. I'm comparing equal amounts of ladder, and it seems like my signal from a two week or so old gel is maybe 30% of a fresh (or 1-2 days old) one.

@user137 Yes, also an option. However, I want to specifically "pre-stain" - ie, apply EtBr after the gel is fully cast and ready to use, but before it is actually loaded with DNA. I am only asking how to accomplish this with minimal signal loss (your suggestions make sense - but which ones do I actually need to do?). If it is impossible, a good explanation for why would also be acceptable.

I have been told in order to maintain a gel I should keep it in a cold and dark place wrapped around a wet towel! But I think its the photo-bleaching which is the problem! so soak it in new buffer with fresh EtBr after you run your samples. Didn't you start getting mould in your buffer with gel in it for weeks?

Come on @Superbest it takes an insignificant amount of time to weigh and pour gels. Pour it before you settle down to check mails or facebook :P

@Superbest see my answer I've had to work through this before. Also if you are trying to save gels after they have been run you can use a gel dryer (one of those food vac bag kitchen utensils you can buy at Target work just as well as the $5000 commercial gel dryers fyi

@WYSIWYG true this is trivial but if your prepping a lot of gels like for 400 students for an undergrad teaching lab, it's a lot easier to cast them, cut them and store them.

To increase storage life: after gel solidifies, dampen it with running buffer. Wrap the gel in polyvinyl chloride. Place in plastic container with a lid. Store in fridge in dark. It will last for a year as long as you re-dampen it with buffer each time you access it. Don't keep it submerged in buffer as the etbr will diffuse out. this is probably the cause of your problem. Notice when you order precast gels (either agarose or acrylamide) they are sealed and only a small vol of buffer is added to keep it hydrated. Additionally, the etbr and EDTA in the buffer helps prevent most mold growth although I have seen black mold grow a few times at around a year.
You can always spike the buffer with etbr adding it directly to the electrophoresis chamber before you run the gel (etbr doesn't even need to even be in the gel for it to work) although I find you get a little more sensitivity with the etbr in the gel. If you spike it be sure to mix and let it sit for about 20 min for the etbr to diffuse.
If you are trying to cut down on cost you are probably using a higher grade agarose than you really need for the application your doing so I would take a look at that
If you end up needing to store gels for rna work, add plain old Clorox bleach to a final concentration of 1% to your TAE gel just after microwaving. It sounds crazy but it works extremely well. You will completely inhibit RNAse and your rna bands will look nice!!!. The bleach also helps  with storage of the gel.

OP has already stated that the concentrations of EtBr inside and outside the gel are identical.

@MarchHo To be sure, just because they are identical doesn't mean there will be no net diffusion.

I can confirm storage of the bleach gel as well - not only that, but despite not taking care to keep the bleach gel away from RNAse contaminants (keeping in the same box as normal gels, dirty electrophoresis tank) my RNA ran and stained just fine.

I think I have some evidence that the key factor is light.
Since asking this question, I changed the buffer for fresh TAE-EtBr (same concentration as in my gels) moved my gels from a well-lit area into a closed, opaque box so that they remain in darkness. After 1 week, I ran equal amounts of my ladder in the stored gel, as well as a fresh gel. The results (old gel on left, new gel on right) show very little difference in signal - I conclude that blocking the light is sufficient.

I'm not quite sure what you are doing. Are you running the whole gel each time and cutting off the lanes you've used, or only putting the lanes you desire into the tank and leaving the rest outside?
If the former then the ethidium bromide will be leaching out of the gel because it is positively charged so each time you apply a current to it some of it leaves.
If the latter, I'm not sure why you are storing your gel in buffer at all. Wrap it in clingfilm to stop it drying out and store it away from UV light to avoid the ethidium degrading.
Frankly, however, I'm not sure why you think this will be a big timesaver? You can store pre-melted agarose with ethidium bromide added for a period of weeks and pouring a fresh gel doesn't take a significant amount of time.

It's the latter. I have a big gel stored in a container (easier to open and close than film), and I cut off lanes I need and run only those lanes.

authors: Ольга Фарина