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Would it be possible to sequence human DNA from wastewater treatment plants?
I know that there are some efforts from scientists working with bladder cancer to perform  liquid biopsy from urine for detection and monitoring of the cancer such as this one.
I've been searching online - but the "wastewater" search term gives me tons of hits about "microbiome" and several types of pathogens.
But I'm really interested in sequencing the sewage to find and analyze human DNA. I have been wondering about liquid biopsies to get an estimate of the cancer status of a population.
I immediately think of several problems:
1. Technical Feasibility

Would we expect to find enough human nuclear DNA within the samples (taken across several days)?

2. Law and Bioethics

Is it legal in the US or European Union?
It could be difficult to get informed consent of all people who are connected to a certain sewage system. You may get informed consent from all residents but what about visitors?
It could be difficult to opt out of such study the
wastewater without a) moving to a different place b) using a septic tank.
I only found this elaborating other privacy issues: its just about Cov-19 and drug testing; both of which are not able to identify individuals at a genomic level.

I'd appreciate your experience and thoughts and references!
[Edit] as suggested in the comments: I have posted part 2 of the question to the law stack exchange here

Given the availability of sets of human reference-haplotypes I think it should theoretically be possible to gather some additional information to common mutations like SNPs even from sub-optimal waste-water. Just you have to be aware how incredibly polluted human DNA would be by incomparably higher DNA-concentrations from other species like microorganisms. Still, as it is possible to identify the whole range of micro-organisms from soil-samples using NGS, one can easily evaluate whether sequenced stretches are uniquely human. Anyways, why not directly get high-quality human DNA samples?

I once met a lady working at a waste water plant and she told me about the different samples they take. I found it fascinating and wondered about other applications that would only consider human DNA in particular as acquisition of participants for a study  is probably one of the bottlenecks. The question became 'hot' for me now as I'm doing an applied genomics course where we must invent a project with the requirement to do "very smart" and cheap sampling (his words). The project must be feasible and we are required to calculate a budget. --> why would not use high-quality human DNA :)

The U.K. tests wastewater for COVID currently https://post.parliament.uk/monitoring-wastewater-for-covid-19/

@Tim That is a totally different story as this is not looking into human DNA which can identify people... Thats the most personal data the any of us have to offer. Given you could make a Data Base of this human DNA. There are many ways this data could be matched to a region/community (where you poop) and to a network you belong to, possibly identifying you. That makes labeled DNA data. Given your computer science back ground I'm sure you can see why this is a totally different story and ethically concerning. Downstream one could even identify your relatives...

@ilamengl The bit about the practicalities of DNA sequencing are on topic. However, the edits which ask for a discussion on the law/ethics side of this are off-topic here. It also reads a bit like a discussion question rather than one with a specific, objective answer.

@user438383 they are 2 yes no questions in the post: The concrete answer to question is 1: yes it is legal - 2: No it is illegal. Question 2 can be answered as follows: 1: yes it is possible (see answer below) or  2: no its not

@ilamengl Either way, questions about the law and ethics are off-topic, and so is having multiple questions. Stick with the original bit about the scientific aspect of sequencing from waste-water and if you are interested in the legal aspect, maybe ask a question in https://law.stackexchange.com/

@user438383 given that people who have written proposals for scientific project had to think about those things and ask their local bioethics commission I feel like I got more chances here than in law...

@ilamengl Any "philosophical or ethical questions related to biology" are explicitly off-topic here, per the site help page.

As it turns out, you are not the first to have this idea. Prior research claims that it is, at least in principle, possible to conduct epidemiology of cancer by sequencing on wastewater DNA for biomarkers.
The ethics of this approach also need not be problematic because narrowly targeted sequence amplification focused on biomarkers like SNPs will not typically produce enough information to identify an individual.
The practicality of this approach is a major open question, however, given the small and variable nature of the signal.

Grate idea and grate paper -They are however using mtDNA. I am still wondering about the first part of my question is is ethically and legally possible to extract human cellular DNA.

If you can get mtDNA, then in principle you can get other DNA as well. The key issue remains signal levels.

@ilamengl a sewer grate? Sorry, couldn't resist.

@BolucPapuccuoglu LOL a Freudian slip.

@jakebeal thanks for answering the technical part. About the other part of the question: are you aware of any US or European laws that would prevent scientists from sequencing human DNA from the sewer without consent given it would be hard to get consent?

@ilamengl that might be a better questions for [law.se]

As already hinted in the answer by @jakebeal, the low concentration (high dilution) of human DNA in waste water would mean that we need huge sequencing depth in order to detect something. This is not the case when dealing with urine or feces. This is also not the case when sequencing bacteria in waste water, since we are dealing then with the strains that can live and multiply in water, i.e., they are present in important quantities. Moreover, we are interested in them only when they are present in high quantities, when they are potentially harmful.

The research group of the paper jakebeal linked used filters -> less water more cells...

@ilamengl it seems that their main achievement is precisely overcoming the problem that I described in my answer. It is a strong claim - if this is really the case, we might expect this done commercially in a few years. Note that they didn't do sequencing, and that they look only at mitochontdrial DNA (a small part of the DNA contained in a human cell).

@ilamengl it is human mtDNA. I think the catch is that they have a library allowing to amplify mtDNA. I am not sure, whether the same can be done for all of the nuclear DNA. If not, you have to shotgun sequence everything that is found in the water, which is the premise of my answer.

Again, I am aware that it is human mtDNA because I've actually read the article ;p but we both know that we cant find the same kind of info as within the nuclear portion of human DNA

@ilamengl if one is looking for a specific biomarker (e.g., a specific type of cancer) one is concerned only with this DNA fragment. I don't know what is special about mtDNA in this respect.

What if I wanted to find novel SNPs? And maybe their distribution within the population?

@ilamengl in most cases one can sample such data in less complicated ways.

Reputedly Osama bin Laden was tracked this way
... according to Water and Wastes Digest citing Time Magazine, but few of the details are known.  Given that 10 milligrams of feces is sufficient to amplify desired markers from DNA, you would need only consider the number of people living "upstream" to determine how much material you should need to collect overall, and how many sequences you would need to run to find the right one.  Maybe with some clever efforts to separate material into microwells you might be able to isolate one or more cells from the target of the search away from all others.


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If we evolve from microbes then why so many microbes are still here?
Researchers say that we evolve from microbes then why there are still so many microbes ?

https://blogs.iu.edu/sciu/2017/09/26/why-are-there-still-apes/

To answer the intention of the question: evolution works by branching. To use this language of 'microbes', imagine a world with only microbe A. Say there are 100,000 individuals of the species microbe A.
Now let one of the microbe As reproduce and produce a mutation leading to the first microbe B. This evolutionary step would not transform every microbe A into a microbe B. The change would only be in the offspring of one of the 100,000 microbe A. This would create a new branch as the new microbe Bs reproduced, but would not affect the 99,999 other microbe As.
There is no reason for microbe A to die out just because a small portion of them had children that eventually became microbe B (unless they were in direct competition for limited resources, or one was a predator for the other, etc.). The other microbe As can just go on living as before, and either stay the same or branch into even more species-- say microbes C, D, E and F.
Let this run for hundreds of millions of years and you get more and more complicated life eventually resulting in what we see around us, including many species that have evolved into other species.
Note that this is very simplified for the sake of clear explanation. A mutation does not necessarily result in a new species.

As noted in the previous explanation, but said in other way:
Our evolutionary lineage may have a common ancestor (aka, a "parent species", say, another microbe [a microbe that no longer lives today, probably]) with some of today's microbes many years ago.
In this scenario, if we look at the "childs of that parent species", we may find a variety of genotypes, which will express different phenotypes.
If we look at the different childs generated in the previous step, and iterate that process, eventually you could get some organisms more similar to the common ancestor between us and microbes (aka, the microbes), and some individuals with a great amount of divergence from the common ancestor (aka, us).
This divergence process has to do with genetic mutations generated at reproduction of each individual.

source: Stack Exchange

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

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What is the interchange of nutrients between plants called?
I've heard about how fungi is the nutrient super highway of the plant web. What is this interchange between plants and the fungi called?

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

Since all the exchange takes place at a molecular level, it can be called  Bidirectional transportation/ Bidirectional transfer of minerals, carbon, and other nutrients.
During the symbiotic association, the fungus grows either inter- or intra-cellularly in the host plant's root system to create certain interfaces between both symbionts. These interfaces are often termed as symbiotic interfaces, which are simply membranes of both the symbionts' cells separated by an interface space.
Like a normal bio-membrane, these membranes/symbiotic interfaces also have different types of transporter proteins, channels, ion-gates which have their regular role in the transportation of molecules across the membrane. The compositions of these symbiotic interfaces differ from species to species.

The process of interchange of nutrients is similar to what takes place between two cells. It depends on the concentration of molecules, charge, size etc.
For more info- http://www.davidmoore.org.uk/21st_Century_Guidebook_to_Fungi_PLATINUM/REPRINT_collection/Ferrol_etal_nutrient_transport.pdf

Mycorrhizal associations. These are mutualistic associations between the roots of plants and the mycelium of fungi. The plants and fungi both benefit. The plants gets improved access to nutrients deep in the soil and the fungi get access to the photosynthetic carbohydrates made by the plants.
Here is a good source: https://www.pnas.org/content/116/46/23163

what 1 or two words is the specific interchange between 2 plants, or fungi and plant called, since the whole system is the mycorrhizal network?

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Could the problem of overfishing be solved by throwing fertilized fish eggs at the right place and deepness into the sea?
I hear sometimes about over fishing and I wonder if the following idea could help to solve the problem.
My idea is to throw fertilized fish eggs at the right place and deepness into the sea. These eggs would then grow by themselves and be the fish to catch sometimes later on.
Instead of the fertilized fish eggs a few days old fish could be used. This should increase the chance of survival by a multitude.
My question is: Could it be done?
In case the answer is yes the next question would be how could it be achieved?
In case the answer is no I am curious: Why would it not work?
Just to be on the save side. The idea is meant to produce more "baby" fish. The "baby" fish should grow in its natural way. Just as if the "baby" fish would have been born in the natural way.
The person putting the eggs into the sea would not be the owner of the grown fish. No monitoring of the way from "baby" fish to grown fish would be done. Anybody could catch the grown fish. Just as it is now the case for natural born fish.
I am looking forward to your answers.

Apparently it works better with young fish ( fingerlings ) rather than eggs . Fingerling stocking is very widely used.

Please read the [Tour] to find out what kind of questions are acceptable here. Floating ideas that are only answerable by subjective opinions are not.

Most fish produce extremely large numbers of eggs anyway.  (Google says tuna can produce 10 million eggs/year!)  Most are, of course, eaten by something before they grow to maturity.

and where do you get enough fertilized eggs on a renewable basis?

Welcome to Biology.SE. This is not a forum or tutorial service; it is a Q&A site where specific questions relating to biology get specific answers. Thank you for taking the [tour], but please carefully read through the [help] to learn more about the site, including what is on-topic and what is not, and how to ask a good question. Thanks.

The answer is a lot more complex than simple yes or no: it depends on the environment, the type of fish in question, the aspects of fishing, etc. Just to list a few points:

availability of food, shelter and other resources necessary for the eggs to grow - I suppose that this was implied by the phrase at the right place and deepness into the sea, but it is more complicated than it seems.
the preferences of predators/parasites relevant to this species of fish: do they prey on the eggs, the babies or the grown-up individuals?
the competition for resources with other similar species of fish
the life history strategy of the species: are they investing in the massive reproduction with high mortality rate of the young? or do the specimen produce relatively small offspring, but live for many years? Do the parents care for their young?
is this more economically efficient than enforcing fishing quotas? How soon these fish become big enough to be of practical interest for fisheries? Do we expect them to reproduce naturally?

These are all questions that may be answered by conservation ecologists, familiar with the particular kind of fish, environment and the economic situation. But there is no one-fits-all-sizes answer.

References
L. Rockwood, Introduction to Population Ecology

Arguably, there's an easy answer to this one: "No!" As Roger points out, there are many complicating factors implicit in your question, but I can't think of any fish species off the top of my head where we could do anything similar to your solution that'd be successful. Consider, for example, Chinook salmon on the west coast of N America. We've been trying to supplement wild populations for decades by releasing juveniles that were spawned and raised to varying ages in hatcheries. There's a legitimate argument to made that this has been successful in that the fisheries for several runs are largely supplied by hatchery-produced fish, but this has come at multiple, complex costs (eg loss of genetic diversity). Perhaps more importantly, many if not most of these runs are still threatened, less due to over-fishing (US fisheries are heavily regulated) than to the loss of spawning habitat and climate change. Ultimately, the "answer" to your question (I'd say) is that the biological and ecological complexities of what you propose are far more than what we can over-come given our state of knowledge and our resources for most species. There are definitely on-going efforts to use hatcheries to supplement or restore wild populations, some of which have had a measure of success, but this is just one (expensive and difficult) tool we can use to address 'over-fishing'. By far the easiest solution (though not without consequences) is to regulate those fisheries--essentially, restrict the quantity of fish caught.

Welcome to Biology.SE. Please take the [tour] and go through the [help] starting with [answer] and [ask] questions effectively on this site. In particular, this was not a good question for this site since it is soliciting opinions and discussion. It is also multiple questions rather than a single one. From How do I write a good answer? in the [help], Answer well-asked questions. Not all questions can or should be answered here. Answering such questions encourages more inappropriate posts so please delete your post. Thanks.


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Why can't I swallow the entire (liquid) contents of my mouth at once?
I've tested this out using water - I manage to fit a certain amount of water in my mouth, but if I try to gulp it all at once, I fail: I feel like spitting the water out (gag reflex?) There's a certain limit, say 60%, of the full amount of water, that I can insert into my mouth and then gulp it without drowning myself. Why is that? What sort of muscle coordination causes this?

Normal swallowing triggers a peristaltic motion towards your stomach.
However, as demonstrated by young "scientists" (search "water chugging tutorial"), one can train to  voluntarily keep the esophagus valve open and poor down liquids without triggering peristaltic waves.


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Fairy little bug
Can someone please enlighten me what kind of a creature is this sweet little friend?

Welcome to Biology.SE. Please [edit] your post to include the size, approximate geographic location, and anything else you observed about this insect — e.g.s: behavior, what kind of plants are in the area. Where you saw this is essential to and the size may be very helpful for getting an accurate identification. You may also find it helpful to take the [tour] and then go through the [help] starting with [ask] questions effectively on this site. Thanks.

related: https://biology.stackexchange.com/a/93176/16866

This is a planthopper nymph. These are a quite diverse group of insects found worldwide. Which one you have is open to further answers, and will be based on your locality and the species of plants and insects in that location.
The furry "tail" and the fish-like mouth-parts/head give it away.


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How did Aposematism evolve?
Disclaimer: I know nearly nothing about biology.
My understanding is that camouflage evolved gradually with individuals that looked more like their environment even slightly being less likely to be eaten.
I might be understanding this wrong, but it seems aposematism could not have evolved like this because you really can't distinguish slight aposematism from just being bad at camouflage.

@MaximilianPress  are you saying there was a period of very low evolutionary pressure when  aposematism  evolved?

@MaximilianPress aposematism is not a "bad" trait it is a direct advantageous adaptation, the question is completely valid.

@John Fair enough, I seem to have misunderstood the original question.

The noxious element of aposematism evolves first.
Take a second to think about how  aposematism works, you will notice the underlying mechanism works even without distinctive coloration.
Bad at camouflage means more likely to be spotted which also means more likely to be identified.
If a wolf eats a pale green frog and gets sick it is likely to avoid pale green frogs. Avoidance works by itself regardless as long as the thing doing the avoiding can identify the toxic animal, aposematism just makes it work better by making identification easier. Even if the frog is well camouflaged avoidance still works if it is toxic, but it works better if the wolves can easily tell what it is.
If the coloration is distinctive enough, or is used my several toxic organisms, predators just start avoiding that color or pattern entirely.
https://www.sciencedirect.com/science/article/abs/pii/S0169534705002521
https://royalsocietypublishing.org/doi/abs/10.1098/rspb.2004.2968

Another really interesting aspect of aposematism, from an animal behavior perspective, is that some predators seem to evolve a genetic predisposition to avoid the aposematic prey, while others still need to learn through experience. I suppose it has to do with whether the poison is deadly to the predator or simply noxious and unpleasant.

Then there are 2 problems 1) animals that look poisonous but aren't  and 2) wouldn't it take several generations to be able to look distinctive enough  before you're just bad at cameoflauge?  During which time you still get eaten more often?

@user122938 mimicry is a separate issue, but yes is should reduce the effectiveness of aposematism. and many predators can identify animals even when they are camouflaged before they eat them, so yes you still get eaten but less often than if you were not noxious in the first place. like anything in evolution the advantage does not have to be huge to be favored. even making your camouflage worse can keep you from getting attacked as often since for many predators attack and eat are not the same action.

But isn't not being spotted better than spotted and recognized? Since it's guaranteed survival vs not guaranteed survival.
Clearly a 0% chance of being spotted is best so what you are claiming is that while 0% being spotted is best 1% chance of being spotted isn't better than 2% or 3% etc  why would that be?

@user122938 but a zero chance of being spotted is impossible, you still need to move around to find resources so there is no such thing as a zero percent chance of being discovered. So it is better to be avoided than risk being seen as prey, consider 20% chance to be spotted vs 30% to be spotted but 50% chance to be avoided.  also evolutions is about good enough not hypothetically perfect.

@John that wasn't the point it was that   while 0% being spotted is best 1% chance of being spotted isn't better than 2% or 3% etc why would that be?
You can't assume the percentage of avoidance that's some function of the the percentage of being spotted.

@user122938 even the best camo has a solid chance to be spotted, all that needs to happen is for avoidance to result in less chance of being eaten. remember aposematism usually evolves with something kind of defense like a sting or poison but an organisms can still be injured or killed while having those before the predator realizes that is why aposematism evolves because being avoided reduces this. no camouflage is perfect and it can work against you if you are noxious. aposematism and camouflage have to part of the same equation, they have to be linked. Have you read the sources I provided.


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Does human DNA code for enamel multiple times?
Given that DNA provides instructions for multiple parts of the body as a general representation, how is that about the number of teeth with regards to the enamel code?

there are 32 teeth but they are referenced as a "shape" that is there is no such a thing like "number 32" in our genetic code
is then the enamelin gene encoded 32 times in all corresponding places, or just once  and referenced somehow?

Morphogenesis doesn't work in either of the ways that you propose.
To understand better, let's shift the focus from teeth to something that's easier for me to explain and visualize: extra fingers, also known as polydactyly. This is a surprisingly common condition, appearing in approximately 1 of every 500 births, and for many people the extra digits are fully functional. More importantly, the causes, even when genetic, are subtle and typically involve very tiny changes in DNA code.
In the embryo, the hand starts out as an undifferentiated blob of tissue. At a certain point in development, it starts patterning and splits into fingers. When the patterning goes wrong, the split happens too often (polydactyly) or not enough (syncdactyly). Once those splits into "stuff that will become fingers" has occurred, however, then the "make a finger" system encoded in the DNA starts running in each and does its best to make a finger, leading to the final outcome.
Thus, the genetic code doesn't need multiple copies of the "make a finger" system or multiple independent invocations of the "make a finger" system: it just needs a system for making a pattern. The specifics for teeth (and any repeated structure) will be different, but the general principle will typically hold (with some caveats; evo-devo is complicated)
If you're a computer person, you can think of it as (very) loosely analogous to calling "split" on a string, then using "map" to apply a function to each of the components that comes out.

thank you: indeed the split can be referenced by computer persons to be an invocation in parallel thread execution. So be it a "split" into 5-fold fingers either 32-fold pre-teeth areas (which activate later, after birth), is there anything like genetic code capturing the actual number, for fingers, "make 5 fold split"?

@J.Doe To the best of our understanding, there is generally no encoding of a numerical value as a number in natural genetic materials. Number can be tightly or loosely controlled by a large variety of other mechanisms, however, and in some cases there are literal duplications of genes. The relationship of any of these things to the count of large-scale morphological features, however, is typically complex and indirect. I suggest reading up on evo-devo to start learning about it in more depth.


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How does DNA encode high level features like animal behaviour and language?
We know there are complex features which animals supposed to develop based on their genes as opposed to learning from the environment and the collective, also sometimes being very specific to certain species:

Concepts how to build homes
Animal languages including social insect interactions responsible for information transmission (or do they have to learn them through an acquisition process, let's exclude languages of ape tribes where "term" creation has been demonstrated?)

Valid answer: if already known, one or to examples to corresponding research.
Constraint: we are not talking about genes responsible for some sort of tendencies in behaviour but situations where there seems to be a more or less complex "blue print".

I suppose we are yet very far from understanding these things. Relation of genotype to phenotype is teh subject of much contemporary research, but it is mainly limited to simple phenotypic features, explainable by action of a few genes, such as the colors of zebra fish mutants: see, e.g., this paper and the related publications by Nüsseln-Vollhardt group. Perhaps closer to your question is circadian rythms, which also have genetic determinants.
The complex behaviors are likely a result of the complex interactions of many genes, which are a very interesting, but also a very difficult problem to solve.


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Turnover number of the enzyme catalase
My textbook says that catalase is the fasting acting known mammalian enzyme and it can act on 40 million molecules of hydrogen peroxide per second.
Does that mean that is acting on that number of molecules during normal conditions or does it mean that one “act” takes one 40 millionth of a second?
This fact is truly incredible. The speed at which these molecules are clicking in and out of the active sites must be near light speed.

Yes, it means that each individual enzyme molecule, under ideal conditions, is able to perform its reaction in one 40 millionth of a second.
But, the reactants aren't moving at even close to the speed of light. 40,000,000 reactions per second works out to 25 nanoseconds per complete reaction ($2H_2O_2$ entry into active site, catalysis reaction, and $2H_2O+O_2$ leaving, clearing the way for the next set of reactants to bind). The speed of light is 299792458 m/s, which means it travels approximately 7.5 m in 25 nanoseconds. Catalase is about 6x10 nm in size. Even if the molecular reactants had to each travel 10 nm, that's still about 1 billionth the speed to light.

Wow , numbers both big and small are truly mind boggling in science.

That's one of the reasons we use scientific notation. 2.5e-8 seconds is a little easier to wrap your head around than 25 billionths of a second.

l upvoted your answer, but now think you have fallen into a trap over the speed of light. See my comment to the poster. Think about it. Even if you say that catalase is affecting collisions, the colliding molecules are not moving any faster, they are just colliding more frequently. Speed and catalysis are both rates but speed is distance per time, whereas catalysis is events per time.

@David I think you might have misunderstood the last part of my answer. I wasn't trying to conflate the act of catalysis itself with the speed of light. Based on the last sentence of the OP's question, I was just trying to show that even if the reactants had to travel the entire length of the enzyme to get to the active site in 25 nanoseconds (a much longer distance than they likely would have to travel in reality), they still would only be moving at 1 billionth the speed of light, which travels on the order of ~10m in the same length of time. Does that make sense?

Sure. But I'd like to make the OP think more carefully about his use of words in science.


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

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

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

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

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


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What arthropod with a distinctive yellow and black colored body is this?
I found this outside my window, today morning, on a clothes peg;

I live on the eighteenth floor, so it probably is a good flyer.
I have noticed that the antennae are almost as long as its body and the legs are yellow, not dark.
Nothing peculiar about the behavior-- it moved around on the peg, for a while, and then flew away.
Location- Bangalore, India.
Length - ~2cm

This appears to be a Glenea multiguttata, a beetle species found in India.
Compare:  from https://commons.wikimedia.org/wiki/File:Black_and_Yellow_Longhorn_Beetle_005.JPG


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What is the relationship between a "main" strain genome and its variant genome in archaea?
I am going to analyze DNA sequencing data in order to try to extrapolate some information about the survival strategy of Pyrococcus Furiosus to gamma irradiation, as maybe you already know from all the previous questions that I published .
In particular, among my previous posts there was the one titled as What does genetically tractable strain mean? in which I asked the meaning of genetically tractable strain because I was reading the article about Genome Sequencing of a Genetically Tractable Pyrococcus furiosus Strain Reveals a Highly Dynamic Genome in which they compare the Pyrococcus Furiosus reference genome sequence (the one that was firstly sequenced in the year 2000) with the sequence of a variant in a lab strain population, designated COM1 and that is the genetically tractable strain which has undergone targeted gene disruption of the pyrF gene (I have clarified the meaning of this process here What is targeted gene disruption?).
Now, what I still can't really understand is why do they compare the "modified" genome sequence of the variant with the reference genome sequence ? I would have aligned the "modified" genome sequence of the variant with its sequence before the targeted gene disruption. Then, of course, I would have all the properties of the variant and not of the "main" strain ( the reference Pyrococcus Furiosus genome).
Instead, in the article they compare first the reference genome sequence with the one of its manipulated variant and then they also compare the sequences of some particular genes, obtaining some properties as if they were discussing of the same genome. For example:

the protein products of 102 of the total 2,134 genes in the NCBI reference sequence are disrupted in COM1 at the translational level through nonsynonymous mutations. These result in amino acid changes, insertions and deletions introducing premature stop codons, and frameshifts producing longer or shorter products with alternate coding sequences. These were subdivided into 36 major changes (Table 4) and 66 minor changes (see Table S1 in the supplemental material) based on the Needleman-Wunsch global alignment identity compared with the protein sequences in the NCBI reference sequence.

This and many other extracts show that they compare the reference and the variant as if they were, respectively, the "control" and the sample that has been treated, ignoring the fact that they were actually distinct genomes.
In the post What does genetically tractable strain mean?, the answer to the question "why do they do this comparison?" was essentially that results obtained by manipulation of the tractable strain can inform your understanding of the reference form. But why are we allowed to treat them as if they were the same genome? And so, can we consider the properties refered to the COM1 valid also for the reference Pyrococcus Furiosus and for all its existing variants ? For instance, here they say:

a number of genes involved in DNA repair, including an uncharacterized RadA domain protein (PF0872), DNA repair helicase Rad3 (PF0933), 5'-to-3' exonuclease NurA (PF1168 [23]), and DNA repair helicase (PF1902), could potentially be inactive in COM1 as they fall into the minor protein-level differences category (see Table S1 in the supplemental material). However, COM1, Parent, and DSMZ showed no significant differences in their ability to recover from exposure to UV or gamma irradiation under conditions previously reported for P. furiosus (14).

Can I say that this could be valid also for the reference Pyrococcus Furiosus, in the sense that if the mentioned set of DNA repair genes are inactive, it will show no significant differences in its ability to recover from exposure to UV or gamma irradiation ?
My conclusion, months ago, was that a variant can be considered as if it was the main strain since the definition that I read in Wikipedia is:

In microbiology and virology, the term variant or "genetic variant" is used to describe a subtype of a microorganism that is genetically distinct from a main strain, but not sufficiently different to be termed a distinct strain.

Now this conclusion does not satisfy me anymore and I would like to really understand the reason of this comparison and how to interpret the relationships between genomes. Can we consider the main strain and its variant simply the same since the last one is not "sufficiently different to be termed a distinct strain"? Are all the phenotypic properties observed for the variant COM1 (like for example the fact that although a set of DNA repair genes are inactive, the ability to recover from exposure to UV or gamma irradiation, under certain conditions, is still the same) valid also for the "main" strain (that is the NCBI reference genome) ?
Thank you in advance.

... I was reading the article about Genome Sequencing of a Genetically Tractable Pyrococcus furiosus Strain Reveals a Highly Dynamic Genome in which they compare the Pyrococcus Furiosus reference genome sequence ... with the sequence of a variant in a lab strain population, designated COM1 and that is the genetically tractable strain which has undergone targeted gene disruption.

Instead, in the article they compare first the reference genome sequence with the one of its manipulated variant and then they also compare the sequences of some particular genes, obtaining some properties as if they were discussing of the same genome.

I think this is from where your confusion originates. From my reading, the paper you link is a comparative genomics paper, and the authors do not perform any genetic manipulations of the tractable COM1 strain. All mentions of "disrupted" genes are referring to the effects of naturally occurring insertion sequences or nonsynonymous mutations. "Natural", here, meaning not purposefully disrupted. Based on the comparison with the Parent and DSMZ strains, it seems like COM1 accumulated its various disruptions and rearrangements while it was propagated as a wild-type lab strain.
For more on how the COM1 strain was "discovered", I suggest reading the original paper in which it was described.

Thank you for your answer @acvill but I do not understand many things: 1. Where is the term "natural" that you mention ? 2. So coming to the main question: why do they do this comparison ? Is it just to describe the difference between the two genomes ?

@Manuela (1) "natural" is in reference to my use of "naturally" in the previous sentence. I wanted to avoid confusion concerning the origin of the COM1 mutations. I'll italicize for emphasis. (2) Yes, they are describing the differences between the COM1 genome and the reference genome, as well as structural variants in the Parent and DSMZ genomes.

Ok @acvill in fact it makes sense, thank you. But I am still confused because in the part of the article that I posted, when they align the COM1 with the reference they say something like "these proteins in COM1 could be inactive because the protein sequences are different with respect to the protein sequences of the reference". Why do they expected to be the same ?

Let's continue this discussion in chat.

Finally, I do not really understand the utility of what they do (both the original paper and the latest one).

@acvill Moreover, when I said "the sequence of a variant in a lab strain population, designated COM1 and that is the genetically tractable strain which has undergone targeted gene disruption." I wanted to say that the COM1 strain was obtained by targeted gene disruption of the pyrF locus (PF1114) using a plasmid designed for double-crossover recombination (37) which are words written in the article. I did not want to say that they purposefully "disrupted" genes...

Then I found this definition in Springer about targeted gene disruption that tells that it is Experimental replacement of an endogenous gene by a mutated (non‐functional) version within the otherwise unchanged genome is called targeted gene disruption. So I said that they did genetic manipulations . But honestly now I do not understand if this was done by the authors of the original paper that you linked or it occured naturally. The original paper is too much complificated for me :/


text:
Found a bug looks like a true bug but it has a mowhak
It looks strange found it today what is it?

Looks like some kind of treehopper.

Welcome to the site. Please take a look around the [help] and take a [tour] to see what is considered a good question.  For species identification, we at least need a location (not just country - more specific) and at least one high resolution photo,  preferably several as ID is tricky without being able to see all the parts of the insect. Leafhopper of some sort, which one, I don't know - there are ~20,000 species worldwide.

Please [edit] to include your location, or this is just not detailed enough to narrow efficiently.

This inscent is a treehoppper or thorn bug (Membracidae). They belong to the Auchenorrhyncha.
Membracidae have a distinct transformed and enlarged (sometimes larger than the body itself) pronotum that often forms unusual structures - such as the "mowhak" on the photo or horns as the buffalo treehopper. These unusual shapes are thought to be camouflage or mimicry.
Besides, their body shape is typical for planthoppers: an inclined head, their "rooftop" wings, a proboscis to suck plant sap, short antenna and relatively short, but powerful jumping legs.


text:
What kind of bug is this on my curtain?
These bugs are frequently found hanging on a curtain next to my window.

This is a carpet beetle, although identifying the exact species is difficult. Compare for example the varied carpet beetle, Anthrenus verbasci:

from https://en.wikipedia.org/wiki/Varied_carpet_beetle#/media/File:Dermestidae_-_Anthrenus_verbasci.JPG

To add to @AL's answer.
This is a beetle of the Dermestidae family. These are a failry diverse group of beetles with a variety of names based on what they are most commonly found eating. Some of the species are specialist eaters of decaying animals. As you have found this one inside it is likely that you have one of the species known as Carpet Beetles. I would go so far as saying that what you have here is a member of the Anthrenus genus. To quote the Colorado Edu site I linked for carpet beetles:

The smallest dermestid beetles found in homes are in the genus Anthrenus. These are typically about 2-3 mm long and have a round body form. Adults have colorful body patterning produced by scales of yellow, browns and white. The larvae are spiny, with a body that is slightly narrower at the head end, which is often tipped with a small tuft of hairs. Species that occur within homes in Colorado, in approximate order, are the varied carpet beetle (Anthrenus verbasci), furniture carpet beetle (Anthrenus flavipes), and common carpet beetle (Anthrenus scrophulariae).

Carpet beetles are common destructive pests eating a wide range of items from clothes (cotton, silk, wool) to dust. If you have these in your house, expect to find holes in some of your less-used clothes, especially if they are stored in dark places.
The larvae are covered in hairs and look like small caterpillars. You may find them crawling along the floor in a quick humping sort of motion, much faster than a caterpillar/inchworm action.
You can control them with regular flysprays, but it is best to get an exerminator in to kill off the infestation and spot-control from there.


text:
Sediment Size and Mayfly (Explanation + Literature)
I am doing investigation into association of sediment size with the movement of mayfly nymphs in a choice chamber, sampling the organisms from a stream. I will be doing a chi square test to determine statistical association. I have three species of mayfly to choose from - swimming, burrowing, and flattened and I will investigate two. My question is this: biologically speaking, either from your knowledge or from the literature etc., where and why would you expect there the different mayfly nymphs to migrate towards, in terms of size of rock/sediment (e.g. categorically speaking, small, medium and large which I will categorise in the field). I'm really looking for for a biological reason for why there might be an association - any at all!
Thank you in advance.
UPDATE: I'm now also looking for sources of secondary data/published papers in journals/literature which might talk about this topic/have similar data/anything at all that I might be able to use. A google search of 'sediment size distribution swimming mayfly nymph' for example hasn't yielded very much so far, but I'm hoping an expert might be able to find such research more quickly.

What is your goal in doing the experiment?

@BenBolker - to find an association between these two variables to see if the type of sediment in a river will affect the distribution of these invertebrates. NB - It is only a introductory undergraduate based project.

@Rushi - an interesting question. I will see what I can find. Don't give up - the community will eventually come to your aid!

@vugpt - any luck?

@BenBolker - any luck?


text:
Washing buffers for protein identification?
I am currently learning protein identification techniques and come across ELISA and Western Blot. In these methods, a washing buffer is required to wash out the antibodies that are not bound to the plate (the specific antigens).
Questions:

I understand that detergent (E.g. Tween-20 (T)) is usually added since it can wash away the non-specific binding of antibodies. (ref) However, from what I have known, we are also adding blocking buffer to block the unoccupied sites on the membrane, which also prevents non-specific binding of antibodies (ref). I would like to ask if this is true, why do we need to add Tween-20 to the washing buffer?

I have heard PBST and TBST are 2 common washing buffers, where TBST seems to be much better. From ThermoFisher:

Determining the proper blocking buffer can help to increase the system’s signal-to-noise ratio. Occasionally, when switching from one substrate to another, the blocking buffer may need to be changed in order to avoid problems with diminished signal or increased background. For example, with applications using an alkaline phosphatase (AP) conjugate, a blocking buffer in Tris-buffered saline (TBS) should be selected because phosphate-buffered saline (PBS) interferes with AP activity.

This seems to me that TBST is always the preferred option (also ref). Then I would like to ask in what specific situation, that PBST is preferred than TBST, otherwise, it will cause a major problem to the result e.g. signal/noise ratio?
Thank you.

All the unoccupied sites on the membrane are saturated in the blocking step after the transfer of the protein gel to the membrane. You can prepare the antibody solution in pure buffer, but you should expect a slightly higher background (this of course depends also on the antibody used), since there still may be some binding possible. When you have a much higher amount of blocking agent in this solution it is much more unlikely that the antibody is able to bind non-specifically, since these sites are occupied already.
Some low affinity binding occurs between the antibody and other proteins which you will not be able to wash away without a detergent.

In my experience it doesn't really matter for most cases which buffer you use as long as you do it consistently. There are of course a few exceptions:

When working with phospho-proteins PBS can give a much higher background - but it can also work. It needs to be tested and optimized, but it is probably easier with TBS.
When using alkaline phosphatase in your detection step, you cannot use PBS since free phosphate inhibits the enzyme.


text:
Read neural activity only having access to the brain from the "outside"
Is it possible to read neural activity from the outside of the head and if you had an machine learning algorithm that could learn what the signals "mean" (for example moving the right arm)? Could that be achieved with having receptors at special places on the head? And what type of receptors that would need. I don't have any experience or knowledge with/from the brain. Sorry if this is a stupid question.

It's not a stupid question in my opinion.
However, it is perhaps naive. Brain function is very complex and how the different parts of the brain exactly relate to memory and function is still being worked out.
We can monitor neural activity outside the brain by a number of methods. The most common one you might have come across is an electroencephalogram (EEG). This measures physiological electrical activity at the surface of the brain (remember, the brain is a 3D structure), so this can't measure activity within the folds of the brain. It is generally done with electrodes placed outside the skull, so non-invasive and produces no harm, even if used long-term. It's closely related to the electrocardiogram, which measures electrical function of the heart. You will have seen an ECG on TV or in a movie - it is often portrayed as a regularly beeping device that goes emits a long sustained beep when someone dies.
A similar system, though invasive is electrocorticography (ECoG), which uses electrodes implanted inside the skull. It requires surgery to be performed so it is much more risky to do. Like the EEG this measures physiological function and can not be used to read purpose into the signals.  I believe this system can be used as an interface/controllers for prosthetics such as hands/fingers, but I don't know how advanced this is and what is involved in getting it to work. I don't think, however, that this is a true reading of function as such, rather that the user is trained to set off a signal for the ECoG to read.
There are much more complex and functional  methods of actually reading brain function and applying it to precise signals within the brain. All of these methods require the use of large equipment such as Positron Emission Tomography (PET) or Magnetic Resonance Imaging (the particular application here is called functional MRI or fMRI). These all require the patient to lie very still inside a large noisy piece of equipment to measure some aspect of the brain interpretable by equipment/software in question. These methods can be quite specific and do show the interior of the brain.
I don't know much about these methods other than general principles. However, fMRI measures blood flow to a particular area of the brain and requires the person being scanned to concentrate on the topic at hand while the scan is being performed. PET and the related technique Single-Photon Emission Computed Tomography (SPECT) often require the use of an injectable material that the scanner can pick up - this is usually (always?) a mildly radioactive one, often conjugated to a specific biological molecule (see here for a list of radioactives and localizations) so that it is trafficked in the body to a specific location.
In conclusion, people are still working on brain function and assigning particular things to particular locations, so we are still a fairly long way from having methods that can be used to natively control devices via brain function.


text:
Is the respiratory substrate oxidised?

Cellular Respiration is a biochemical process in which food materials present in cell are oxidised slowly in presence of enzymes with the release of ATP and small amount of Heat.

I am not able to relate this to the process of Fermentation(more specifically Lactic acid formation)

$$C_6H_{12}O_6 \rightarrow 2CH_3CHOHCOOH + 36kcal$$

The average oxidation number of C in $C_6H_{12}O_6$ is $0$ and the average oxidation number of C in $CH_3CHOHCOOH$ is $0$. So, C is not oxidised according to oxidation number concept. So, can we say that all types of cellular respiration involve oxidative breakdown of substrate?

In lactate fermentation, there is no net oxidation or reduction: free energy is obtained from the "splitting of glucose" (glycolysis). But of course, there is an oxidation  step (GAPdh that generates NADH) AND a reduction step (pyruvate reduction by LDH to 'regenerate' NAD(+)), where the 'carbon skeleton' that is oxidized in the GAPdh reaction is reduced in the LDH reaction (so do no net ox/red).


text:
Numbering of C atoms of pyrimidine rings in nucleosides
For a presentation of my work I wanted to show a structural representation for dihydrouridine with numbering of the C atoms of the pyrimidine ring, according to this numbering convention.
Then I found this Paper, where the numbering in 5-methylcytidine is consistent with this convention but that in N1-methylpseudouridine is not.
After some more research I found this paper (fig. 1 A), where uridine is numbered according to the nucleotide numbering convention, but pseudouridne is not.
So why is the numbering of modified cytidine according the the convention (m1C), whereas the numbering of pseudouridine (which is a modification of urdine) is not?

You would probably be best to ask the chemistry SE.

Welcome to SE Biology. I have answered your question, but can I make a suggestion for improving the way you could have asked it. 1. Your question only showed the numbering for uridine, which made it difficult for readers to know what the situation was with pseudouridine. You should have included a comparative picture — the red dihydro atoms in the diagram you provided are a distraction. 2. Most important, you should then have stated clearly what you thought the numbering convention was that was being applied inconsistently. This might have made you consider whether your assumption was correct.

Although this question should probably have been asked on SE Chemistry, as the molecules are of biochemical importance — and the question is based on a misconception — I will answer it here.
Answer
The numbering of the carbon and nitrogen atoms in uridine and pseudouridine is perfectly consistent. The numbering is for the pyrimidine ring, which is the same — uracil — in each case. The different positions of attachment to ribose (N1 or C6)) results in two different structures (and hence names) for the resulting nucleoside, but does not alter the numbering of the components.

[Modified from https://commons.wikimedia.org/wiki/File:Pseudouridine-synthase.jpg‚ Surundu]
Thus N1-methylpseudouridine has the methyl group attached to the N1:

Basis of numbering
The numbering of the atoms of pyrimidine bases derives ultimately from that of the parent, pyrimidine in which the two (indistinguishable) nitrogen atoms are numbered 1 and 3:

The relation of uracil to the parent pyrimidine can be seen from the IUPAC preferred name Pyrimidine-2,4(1H,3H)-dione and a perhaps more easily understood alternative as 2-Oxy-4-oxy pyrimidine i.e. the oxygen substitutions are at positions 2 and 4 (as shown for both uridine and pseudouridine, above).
The preferred IUPAC name for uridine is:
1-[(2R,3R,4S,5R)-3,4-Dihydroxy-5-(hydroxymethyl)oxolan-2-yl]pyrimidine-2,4(1H,3H)-dione
and that for pseudouridine is:
5-[(2S,3R,4S,5R)-3,4-Dihydroxy-5-(hydroxymethyl)oxolan-2-yl]pyrimidine-2,4(1H,3H)-dione
i.e. The formal nomenclature for the two nucleosides only differs in the designation of the position of attachment of the base to the sugar ring (1 or 5 — emboldened above).


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How Fast can the Electrochemical Gradient on a Neuron be Reestablished?
The electrochemical gradient of Na+, K+, Ca2+, and Cl- between the inside and outside of a neuron is vital for its function. When a neuron fires, this gradient reverses. How long does it take for the gradient to be re-established?

Does this answer your question?: https://biology.stackexchange.com/q/57064/27148 Gradients don't reverse during an action potential, only permeabilities chance substantially. Yes, a few ions do move and pumps are needed to restore concentrations, but it's very few ions.

Also https://biology.stackexchange.com/a/76167/27148

Thanks for the clarification. Although I knew the voltage change, I didn't realize how few ions are actually needed to cause that change. If you post an answer saying the same thing I'll pick it as correct.


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Cumulative synaptic transmission delay
Assume the following:

there are at least 10^11 neurons in the human brain
there are approximately 10^14 synaptic connections in the human brain (because on average each neuron gets inputs from approximately 1000 other neurons)
synaptic delay is approximately 1-2ms (but for the sake of it we can also assume an order of magnitude less, so 0.1ms)

A problem that revealed itself to me:
It would "only" take 1000 (or 10000 if we use 0.1ms as synaptic delay) serial synaptic connections in order to generate a lag of 1s. Considering that there are 10^11 neurons in the brain, the number of neurons you need  firing sequentially in order to generate significant lag (>1s) seems tiny compared to the overall amount of neurons in the brain.
My questions:
Are there series of neurons (firing from the time of input to the time after processing) greater than 1000 (or 10000)?
How are there series (not) greater than 1000 (or 10000) neurons?
P.S. I'm talking about chemical synapses which I assume to make up the bulk of neural transmission in this case

Welcome to the site.  Where did you get your information? Particularly, where did you get the idea that all the neurons in the brain are connected in series?  How on earth would the brain process information at all if there weren't millions of different short pathways that the "signal" could take?

The information is from the Springer Handbook of Bio- and Neuroinformatics. I do not (!) think that the neurons in the brain are all connected in series. I'm just asking how come that there isn't significant lag as it would take only a series of 1000 or 10000 neurons in order to create a lag of 1s. My question is more like: how aren't there series of neurons that are greater than 1000 or 10000?
I basically have an idea how to answer my question but I want to compare it with what people on here say. I'm not a neuroscientist and my reasoning doesn't suffice for me personally.

To clarify even further: I'm particularly interested in:
Are there series of neurons greater than 1000 (or 10000) Yes or No?
And subsequently: how are there series (not) greater than 1000 (or 10000) neurons?

Okay I'm starting to catch your question now; it would be great to [edit] this information into your question for clarity.  Not an answer here, so I'm just putting it as a comment, but there are definitely large variations in the number of neurons in a given circuit - think of reflex arcs which respond extremely quckly - there can be as few as 3 neurons implicated. Once you get into higher processsing estimating how many neurons are in series could be exceedingly complicated, since you (almost) never have isolated neuron-neuron connections (look up convergence and divergence).

...rarely would it be the effect of one neuron alone causing another neuron to fire; the whole idea behind processing is not to send information through the most processing centers possible; it's to take information from the most sources possible and integrate it into a single response.  That said, some processing does take much longer than 1s if it has to go through lots of circuitry, sometimes multiple times - think of doing mental arithmetic - you have to store numbers and recover them, process them, etc.

...and some series of neurons are indefinitely long - for instance, you can close your eyes and start imagining a story, and technically there is no limit to the number of neurons in circuit which you can make fire.  You could spend two hours imagining a story (or whatever) and there would be way more than 10000 neurons that fired dependant on others.  Anyway not an answer; just food for thought which will hopefully help you clarify the question a bit

Lags of 200-600 ms are pretty common. Have you ever read studies that measure reaction times? That said, total synaptic delays are typically much longer than 0.1 ms (that number is just for one step in the process). 1-10 ms is a better lower estimate.

I'm aware of these lags (200ms-600ms), I also encountered them when looking for an answer to my question. However, let's say this roughly equals 200-600 Neurons or synaptic connections, I'm still astounded it's that few. I would have expected it (sequential neurons) to be orders of magnitude higher and I'm asking myself how it is the way it is.

The brain is massively parallel. There are a lot of recurrent connections and feedback loops that are important for setting expectations, building a model of the world, and learning, but the pathway for stimulus to response is quite simple (see the diagrams in Grossberg & Pilly, and the latency profile in Schmolesky et al). It has to be, because if you are slow you die.
For example, a commonly used psychophysical task is to detect a motion stimulus and response with a saccade (eye movement). For this path you have a couple synapses in the retina, then the LGN, V1, MT, LIP, FEF, then a couple synapses in the brainstem and the muscle. For some of the cortical stops you might have responses that themselves depend on multiple synaptic steps. So let's say on the order of 10-30 synapses for that sort of rapid task with a response within a couple hundred ms. A good chunk of that is actually phototransduction in the retina which is quite slow (which is why you don't see still images a 24-30 fps movie).

DiCarlo, J. J., & Maunsell, J. H. (2005). Using neuronal latency to determine sensory–motor processing pathways in reaction time tasks. Journal of neurophysiology, 93(5), 2974-2986.
Gold, J. I., & Shadlen, M. N. (2007). The neural basis of decision making. Annu. Rev. Neurosci., 30, 535-574.
Grossberg, S., & Pilly, P. K. (2008). Temporal dynamics of decision-making during motion perception in the visual cortex. Vision research, 48(12), 1345-1373.
Schmolesky, M. T., Wang, Y., Hanes, D. P., Thompson, K. G., Leutgeb, S., Schall, J. D., & Leventhal, A. G. (1998). Signal timing across the macaque visual system. Journal of neurophysiology, 79(6), 3272-3278.

Parallelity indeed solves the problem of massive difference in magnitude between overall neuron count in the brain and serial neuron count from input to result of process for me. However, do you have more insight or a source about counts of serial neurons? Your answer probably is enough to resolve my question, I'm just dumbfounded why neural transmission is so slow and long serial neural transmission has the potential to be excruciatingly slow. Our brains are amazing but a complex instruction in Assembly like ldw (loading a content) takes only 100 ns with simpler instructions being much faster

Brains are biology. I would recommend learning how they work from the ground up (get a neuroscience textbook) rather than trying to understand them like you would silico computing. The brain-computer analogy breaks down really fast.


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Reasons for the existence of symporters and antiporters
I'm wondering what is an evolutionary adaptation to the evolution of symporters and antiporters instead of just uniporters.
Antiporters might help preserve electrical neutrality by pumping in/out an ion of the same charge as is the case in H+/K+ ATPase, and perhaps transporting 2 ions at the same time is more efficient than just one.
But the same can't be said for Na+/K+ ATPase, which actually contribute to a net negative charge, so why not instead use a uniporter here?
Additionally, could the efficiency hypothesis also be applied to symporters or are here other reasons at play?
Hence in brief, what justifies the existence of symporters and antiporters as compared to uniporters?

The Na/K ATPase hardly contributes to any charge. The (lack of) importance of the 2/3 ratio is often misleading to students. There are many questions here about this.

Uniporters function as passive transporters and can not achieve concentrative accumulation. Symporters and antiporters are examples of active transport (they couple the movement of a subtrate to an additional process that yields energy). Since some solutes are present at very low concentrations on one side of the membrane (e.g. in the blood) systems had to evolve which can achieve concentrative uptake (as opposed to equilibrative uptake as mediated by passive transporters). Therefore, it makes sense that not only uniporters exist, but also symporters and antiporters (and primary active transporters as well).

For me the more interesting question is, why do uniporters have to exist when you have pores and channels? (Uniporters differ from the latter two in that the function according to the alternate access mechanism and are not open to both sides of the membrane)

Uniport: a membrane transport process in which a single kind of sub-
strate is transported across the mem-
brane, either by the mechanism of mediated diffusion where the
substrate equilibrates at the two membrane sides (e.g., monosac-
charides in mammalian erythrocytes; TC 2.A.1.1.12), or by active
transport where an external source of energy is used to achieve
movement against a chemical potential or an electrochemical po-
tential gradient (e.g., plasma membrane H+-transporting ATPase
TC 3.A.3.3.1 or EC 3.6.3.6). Such transport systems may be designated as uniporters.

The above quote comes from Oxford Dictionary of Biochemistry and Molecular Biology and according to this definition active uniporters seem to exist.

@RtoR Most channels are specific to certain very small molecules and ions like sodium. If there were channels that were large enough to accommodate molecules like glucose, many other molecules would be able to pass through as well and the membrane would lose its selective permeability, and would be unable to maintain concentration gradients.


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How are electrodes working? (EEG)
How do electrodes receive signals from the brain when using/doing an EEG? Is there some "circuit" for it? Is it harmful if you have many (more than 50-100) on your head?
I found out that there are small disks used as electrodes to pick up the brain waves. What I didn't understand was how the circuit behind that worked. I mean each electrode has to have an individual circuit, right?

command to bump question

Welcome. What did you find out when you researched this question and what didn’t you understand? There is a lot of information about how EEGs work online.

Also please don't bump questions with meaningless edits.

I found out that there are small disks used as electrodes to pick up the brain waves. What I didn't understand was how the circuit behind that worked. I mean each electrode has to have an individual circuit, right?

The circuit is typically made with one or more "ground" wires for EEG, though it's possible to use other EEG contacts as references (more often this is done virtually - the original recordings are made and digitized with a common ground, and later an average reference or Laplacian is used to isolate more local signals).
EEG measures extremely weak signals and doesn't have any impact on brain activity itself, any more than listening to the radio impacts the broadcast tower.

Thanks for your answer. Is there any schematic for the circuit?

@Jakob An op-amp in your recording equipment with one wire to each EEG contacts and one to the ground wire.


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Is it possible to see some renal pyramids in a transverse section those which cannot possibly be viewed in one longitudinal section at the same time?
This is just a random image I found on Google.

It is showing that, in cross-section, several renal pyramids can be viewed. Is it so?
According to the following longitudinal section of the kidney, I think it is not possible to see more than two or three pyramids in a cross-section. Can anyone throw some light on this?

EDIT:
Apparently there are more pyramids in a kidney than what we see in a longitudinal section of this organ (?). Is it possible to see some pyramids in a transverse section those which cannot possibly be viewed in one longitudinal section at the same time?

Why don't you think it would be possible? Can you cite a source or show another figure?

Consider that both of these are two-dimensional images. Not sure how you think the bottom two-dimensional image rules out structure in the other dimension.

The figure seems about right
In these conference notes the figure posted from Diagnostic Ultrasound (CM Rumack), labelled as a cross section, seems to match your illustration fairly well; I think I count six pyramids.
It makes sense because pyramids are, well, pyramids, so if they are round and evenly spaced, a kidney should have room for about that many when imaged at the level of the ureter.  Unfortunately, I didn't find a good 3D model searching, and while I feel like it should be possible to infer the 3D locations of the pyramids from an image of the vasculature, I am not sure how to do so.
(I should note that the Visible Human Project data can now be downloaded without a license.  The files are large and they now require a helper application for FTP such as Cyberduck.  I should return to this if I can pull something useful out of them)

You see, I am not sure whether the pyramids that are visible in a longitudinal section, are the only pyramids of the kidney or there are more.

This paper about goat kidneys mentions that humans have seven to eighteen pyramids per kidney.  Given the variation of kidneys and figures I'm not sure if you want to chase that figure to its origin.  Logically though, pyramids are all over the kidney, including on the sides, so a longitudinal section can miss them.  Textbook figures like yours, with every renal papilla in the plane of section, are improbable - sometimes you would see just a piece of a pyramid.  The image I want ... is in "SGI RAW format".

That's just it. You've answered my question. So both longitudinal and transverse sections can miss some pyramids.

What if there are just these seven pyramids (textbook figure) that are present in the kidney in all sides of the kidney, but continuous?

They're pyramids.  They come to a point called the renal papilla because it looks like a papilla, though the milk it yields wouldn't go well with morning coffee.  They are approximately round.  This image of unknown provenance illustrates it.  But on any kidney image/model, note that the calyx is shallow - not a groove going all the way around the kidney.


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How are monosaccharides and amino acids absorbed in jejunum?

Duodenum receives bile from liver and Pancreatic juice from pancreas. Intestinal glands secrete Intestinal juice which acts at the ileum. Most of the absorption of food materials takes place in the jejunum, except for iron(duodenum) Vit $B_{12}$ and bile salts(terminal ileum).

I am learnt in high school text books that the succus entericus(intestinal juice) helps convert disaccharides to monosaccharides, dipeptides to amino acids and emulsified fat into fatty acids and glycerol. Then that implies that carbohydrates(monosaccharides) and proteins(amino acids) cannot be absorbed in the jejunum since they are not yet in the absorbable state(due to absence of succus entericus in jejunum). Then why only absorption of Vit $B_{12}$ and bile salts take place in ileum and not end products of digestion? How can they be absorbed in jejunum?


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dilutions in bacterial culture
In overnight bacterial culture, why do we put bacteria in a small flask to culture before moving it to a larger flask? Why not just put the sample in a large flask to begin with? This is in reference to growing e. coli to produce proteins in a 125mL flask overnight first, then over a liter after that. For recombinant protein expression.

Not sure, but it may have to do with equalizing/standardizing the size of the initial innoculum for the large culture.  Normally you want to harvest the large flask while it is still growing in log phase or otherwise appropriate condition. If your initial innoculum varies widely in number of cells, time to harvest of the large flask can also vary substantially. It might also have to do with maintaining selection for a plasmid, as partially permissive culture conditions under many generations can lead to selection for faster growth/loss/deletion of plasmid.

@Val Can you please give a specific example of a protocol you're working with? With what you've written right now, there's too much unknown to be able to answer your question clearly.


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What kind of spider is this? From New Zealand
Found this spider in my bin, sorry for poor quality photo, has a massive red bum, haven't seen one like it, can anyone identify it?, around the size of my finger or thumbnail. I am from New Zealand

Welcome to Biology.SE! Please [edit] your post to include as much of the following essential information to improve your chances of getting a good answer: 1) one or more clear closeup photos of the organism (photos from multiple angles if possible)); 2) the location (e.g. country and region — the more specific the better) where you observed this organism; 3) habitat information; and 4) an estimate of the size of the organism (human nails vary significantly). ——— Please also take the [tour] and then go through the [help] pages starting with [Ask] questions effectively on this site. Thanks!

This appears to be the False Widow Spider (Steatoda grossa), which is a cosmopolitan species found over much of the world.

The female S. grossa is 6-10.5 mm in length and dark coloured with a round, bulbous abdomen. Typical colouration ranges from reddish brown to black, with light-coloured markings.


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This graph about logarithmic and arithmetic plots. Shoudn't it be the other way around?

From the textbook 'Brock biology of microorganisms, 15th edition'
The black lines points to the linear graph with the caption 'Logarithmic' and to the curved graph with the caption 'Arithmetic'. Isn't this the reversal of what they are?

No it's correct. The arithmetic plot uses the left side of the graph and if you take the log of the values on the arithmetic plot (log10) it'll plot out a straight line; the red one which use the right side as the y-axis.

To add to @m4rio's comment: As someone once said "biochemists worship at the alter of the straight line" (It is the logarithmic plot that is linear, as is the Lineweaver-Burk plot, the Eadie-Hofstee plot, the Hanes plot, and quite a few others: they are all linear transformations of non-linear 'primary' plots)

It's always a good idea to carefully examine the numbers on the axes and draw your own conclusions before looking at the labels.

The image is correct, although the presentation is confusing because the association of the lines with the axes is not indicated clearly.
Plotting on an arithmetic scale (the "normal" sort of axis we all first learn about), an exponentially growing number of cells will result in a line that starts out looking pretty flat and then suddenly shoots up.
If you're interested in knowing the rate of growth, this sort of line isn't very useful, because the same rate will have different slopes, while the same slope indicates different rates, depending on the number.
If you instead plot the growth curve against a logarithmic axis, then you get a graph that focuses clearly on growth rate, with the same slope always indicating the same rate, no matter how many cells are present. Thus, if the growth rate is consistent, you'll see a straight line, as in the example presented.


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How do scientists create an environment that favors the selection of a microbe with higher production of a certain enzyme?
Let's say you want to create a strain of bacteria that is resistant to heat. You expose all bacteria to high heat and those who have mutated to survive this heat will be the survivors. Then you allow this group to reproduce and continue to gradually raise the heat until you are left with a population of highly heat-resistant bacteria.
Let's say you wanted to do the same but instead of selecting heat resistance you want to select for the production of a certain enzyme, for example amylase. How do you manipulate the environment so that only those with higher production would survive?
One thing that comes to my mind would be introducing all the microbes to an environment where the substrate they need to break down to survive is scarce. So the specimens that would create the most enzymes to break it down would survive. But then all of the other specimens would benefit too because the enzyme from the high-producing specimen would also give them the substrate they need to survive - so it would not be isolated but rather would 'carry the entire population on its back' (I have no idea whether this is how it would work, this is an idea)

Interesting, has there been a case where the enzymes did change shape to adapt? Also, wouldn't the poor enzyme producers also use up the product of the enzymatic reaction and therefore the high-producers won't be isolated?

No. Most substrates for growth have to be taken up by the cell before being metabolized. The lac operon mentioned by @user338907 contains a permease gene for this purpose.

@user338997 ? Lac permease doesn’t transport lactose into the cell?

@David Are you saying enzymes are working within the the cells? I'm pretty sure some enzymes are excreted to the environment where they break down their substrate. To clarify what i meant in the above comment i'll give an example: let's say 1 High-Amylase  producing microbe is put in an environment of scarce starch - and survives thanks to its ability to make the most out of the scarce nutrients around it - the problem is the glucose it will produce will also be available to the Low-Amylase producing microbes - who didn't contribute to survival whatsoever but still get to live on

I suggest you do a little reading on this yourself. Some substrates like proteins or polysaccharides are too large to be taken up by cells so they do excrete extracellular proteases and glycosidases to break them down into smaller molecules that can be taken up and metabolized internally. Ok, starch will not be permeable, but I was considering the general situation. If you need a group of enzymes to metabolize starch, other bacteria can only hitch a ride on the extracellular ones, which is no use if they lack the intracellular ones.

But if we take glucose for example, isn't glucose the final form of sugar needed for cellular respiration? And if there is a secretion of enzymes to the extracellular environment, and the activity of these enzymes results in free glucose in the extracellular fluid environment, then it seems these bacteria could soak it up and hitch a ride., preventing natural selection (they weren't the fittest but they were always around the fittest)

@Anonymir, It's really going to depend on your organism, the phenotypes you're selecting for, and on the goals of your experiment. I don't think there's one methodology that will work in all circumstances. As for the amylase example, I would first ask why you want to select for this? Are you planning to harvest an enzyme for specific applications downstream? Is maximizing yield important? Or are you doing simply interested in experimental evolution via positive selection?

I am interested. In the fermentation industry they use mold to make many foods taste sweet (thanks to amylase) and savory (thanks to protease) and in japan where mold-fermentation is common, they specially select spores for genetic qualities such as amylase production - in order to create the best taste of the final product. This interests me and i wonder if the process can be automated or made more efficient.


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Is it possible to put 100 live black ants and 100 live fire ants in a glass jar without them fighting each other immediately?
Background:
There is a claim falsely attributed to David Attemborough:

If you collect 100 black ants and 100 fire ants and put them in a
glass jar nothing will happen. But if you take the jar, shake it
violently and leave it on the table, the ants will start killing each
other.

The origin of this urban legend is possible this part in the novel Cat's Cradle of Kurt Vonnegut:

"What he was doing was spooning different kinds of bugs into the jar
and making them fight. "The bug fight was so interesting that I
stopped crying right away--forgot all about the old man. I can't
remember what all Frank had fighting in the jar that day, but I can
remember other bug fights we staged later on: one stag beetle against
a hundred red ants, one centipede against three spiders, red ants
against black ants. They won't fight unless you keep shaking the jar.
And that's what Frank was doing, shaking, shaking, the jar."

Since this is only a novel, not a scientific paper, we cannot be sure if it is possible or not in the real life. Some people argue that ants can identify each other by means of pheromones and automatically start to fight if an "enemy" is identified. But they are also not biologists. Is this argument correct?
I'm also not a biologist so please forgive me for the poor quality of my question.

This seems like it would be a very simple hypothesis to test, regardless of whether you're a biologist. Gently combine separate containers of the two kinds of ants, see if they start fighting within a minute or so. Then, combine another two separate containers and immediately shake it vigorously, then monitor for commencement of fighting.

I've found an article in Scientific American that states that newborn ants of different species mixed together do not harm each other.


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What is targeted gene disruption?
I am a bit confused about what targeted gene disruption means. I was reading this article in which they compare the Pyrococcus Furiosus genome with a genetically tractable strain P. Furiosus variant genome, called COM1. When they described how COM1 strain was obtained they say:

The COM1 strain was obtained by targeted gene disruption of the pyrF locus (PF1114) using a plasmid designed for double-crossover recombination (37).

Since the definition from Springer about targeted gene disruption is simply:

Experimental replacement of an endogenous gene by a mutated (non‐functional) version within the otherwise unchanged genome is called targeted gene disruption.

I concluded that it is the replacement of the gene, that is called pyrF in this case, by the experimenter with a non-functional version within the genome of the genetically tractable P. Furiosus variant. So I thought it was a sort of "inactivation" of a gene.
Then, in this discussion about What is the relationship between a “main” strain genome and its variant genome in archaea?, someone kindly suggested me to read the original paper about how the COM1 strain was discovered. Here I find some contradictions with the idea that I built about "targeted gene disruption of the pyrF locus".
In this paper, they say that

In attempts to develop a method of introducing DNA into Pyrococcus furiosus, we discovered a variant within
the wild-type population that is naturally and efficiently competent for DNA uptake. A pyrF gene deletion
mutant was constructed in the genome, and the combined transformation and recombination frequencies of
this strain allowed marker replacement by direct selection using linear DNA.

Then also that:

there have
been no reports of genetic manipulation of the P. furiosus
chromosome. Here we used simvastatin and 5-FOA selections
to generate a ΔpyrF strain, designated COM1

And, finally, an other important extract:

Here we report the construction of a deletion of the pyrF
locus in the P. furiosus chromosome and the discovery that this
strain, designated COM1, is remarkably efficient and naturally
competent for uptake of both circular DNA and linear DNA.

I have to say that this article was too difficult for me and full of details that I am not interested in, so I did not read it in deep, but I selected these extracts that describe in simple words how COM1 was obtained. However, from these I get an idea of how COM1 is obtained that is different from the one I thought at the beginning by Springer.
Since the Wikipedia definition of gene deletion mutant is:

In genetics, a deletion (also called gene deletion, deficiency, or deletion mutation) (sign: Δ) is a mutation (a genetic aberration) in which a part of a chromosome or a sequence of DNA is left out during DNA replication. Any number of nucleotides can be deleted, from a single base to an entire piece of chromosome.

Considering this and the other two extracts that I reported, now my idea of how COM1 was obtained is that the pyrF was deleted (by the scientists) and that part was (naturally) substituted by a marker (that is "a DNA sequence with a known physical location on a chromosome") which is a linear DNA since this COM1 strain is remarkably efficient and naturally competent for uptake of both circular DNA and linear DNA.
Now my question is: is the Springer definition (linked above) "universal" or by targeted gene disruption one can intend not only "artificial" genetic manipulation but also deletion of a gene and natural replacement that could also lead to a new pyrF gene (in this case) that is functional (so not non-functional) ? What does it mean when I say "The COM1 strain was obtained by targeted gene disruption of the pyrF locus (PF1114)"?
I apologize for the long question and I thank you in advance.

You have it mostly right, however, you are misunderstanding what has gone on here a little.
The definition from Springer is correct - a targeted gene disruption is a direct replacement of the gene with a non-functional one. However, to do so you also need some method of detecting that your gene disruption worked and will persist. This is most commonly done by introducing marker(s) along with the disrupted gene in a form known as a cassette.
In the case that you present it seems that they have used simvastatin as a selection agent and 5-fluroorotic acid (5-FOA) as a reporter to show that while the gene has been disrupted (i.e. non-functional), expression from that location is still happening as it should.
The method they used for introducing this cassette is a recombination between a plasmid and the Pyrococcus genome. This is (or was) a common method of altering the genome of many organisms to effect some functional change. The plasmid will have sites flanking the cassette that match the host (in this case Pyrococcus genome) and these are used to get the genome to recombine in the manner described in the pictures here.

Thank you so much @bob1 !


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Evergreen ornamental shrub identification
These images were taken in the middle of April in central Poland.
Plants are between 0.5 and a meter tall, and around a meter in diameter.

Welcome to Biology.SE! I've edited your text to make it clearer (e.g. I assumed that state was meant to be date) — please check to make sure I haven't changed your intended meaning. I'm very short on time right now, but this looks like a laurel of some sort (genus: Prunus), which are common garden shrubs.


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Is there any way to identify if chromosomes are inherited from the same parent?
I'm a PhD student in bioinformatics working on genomic data, and I was wondering:
If I have access to a person's chromosomes, is there an assay that can determine that two chromosomes come from the same parent, or do I need to sequence their DNA, refer to statistical genomics and infer the ethnic group of each chromosome?

‘Have access to their chromosomes’ - what does this mean? What kind of data do you have?

@user438383 I meant more theoretically - if I had access to samples of a person's DNA. My current dataset it mutations under the form of a vcf file.

Does this answer your question? What can you learn about someone's mother and father by examining their DNA?

@MaximilianPress although your answer to that question does provide some information towards answering mine, I don't think they are duplicates as such. For starters I am looking for quite technical answers, preferrably based on current literature, whereas OP in the linked question was looking for much broader information.

If that is your goal, I would suggest posting instead on bioinformatics.stackexchange.com. Biology SE is more likely to address your question at a higher level with a range of methodologies, such as the linked answer.

@MaximilianPress This could be a bioinformatics question yes, but I feel like it does ride the line between the two. The answer to this could be found in bioinformatics analyses, or it could lie in molecular biology assays.

@Whitehot sure, and that is more or less the answer that was provided at the link, was suggestions of both bioinformatic and wet-lab methods for examining this problem. If those methods are not adequate to answer your question, then it is good to know exactly how your question is not addressed!

There is an implicit assumption in the question that current technology can obtain the correct sequences for each of the two homologous chromosomes (for all chromosome pairs) of a diploid individual.  That is beyond the state of the art today.
In a few special circumstances, the latest methods can begin to approach that goal.  For instance, where the parents of the individual are from highly distinct populations such as subspecies, and the populations have good sequence characterizations, then some have come close to resolving the separate sequences of homologous chromosomes.  See, for example, "Haplotype-resolved genomes provide insights into structural variation and gene content in Angus and Brahman cattle" and "Ultracontinuous Single Haplotype Genome Assemblies for the Domestic Cat (Felis catus) and Asian Leopard Cat (Prionailurus bengalensis)".
Even when the genomes of the individual's two parents are also available (a set called a "trio"), correctly resolving the complete sequences of the individual's homologous chromosomes is difficult.  See for instance, "Accurate haplotype-resolved assembly reveals the origin of structural variants for human trios".

Interesting, I knew that it was a complex task but not that it was that challenging! I am using 1000 Genomes project data, and in this paper https://wellcomeopenresearch.org/articles/4-50 they describe how they created SNP data for both chromosomes in each pair, in the "Phasing and imputation" section. Do you think that this data is unreliable?

I would quibble with this answer: obtaining phased diploid assemblies is an active research area and has been more or less achieved at quite good accuracy, e.g. https://www.nature.com/articles/s41587-020-0711-0. See also https://www.nature.com/articles/s41467-020-20536-y

@Whitehot the phasing/imputation approaches that you mention are reliant on the linkage of alleles in the population- they are likely to be more or less accurate at the level of the population, but not terribly accurate at the level of the individual. Full, reasonably accurate individual-level haplotypes require long reads or in vivo linkage data (e.g. Hi-C), or ideally both. See refs in my other comment.


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Apportionment models, niche theory, neutral theory
I am trying to understand the relation between apportionment models, niche theory, and neutral theory of biodiversity. Wikipedia seems to suggest that the first two are the same thing, whereas the last one is controversial

The theory has sparked controversy, and some authors consider it a more complex version
of other null models that fit the data better.

This impression is further enforced by the fact that the Hubbell's original books seems to be almost the only source of information about this model.
On the other hand, this article suggests that modern niche theory is a synthesis of the apportionment models and the neutral theory

Niche-based theories have emphasized the role of competition for resources, while neutral theory has
highlighted the role of stochastic effects, and several works have investigated the interplay
between stochasticity and competition.Many of these theoretical insights have been synthesized
in what is commonly referred to as contemporary niche theory. Contemporary niche theory highlights
the role played by equalizing mechanisms, processes that decrease fitness differences between
organisms, and stabilizing mechanisms, processes that decrease competition for resources. These basic
organizational schema have been successfully applied to understand community structure in a wide range
of settings.

I am looking for guidance in this theory landscape, comments on what is mainstream and what is not, and suggestions for deeper reading (math is welcome).
Remark:  It is understood here that neutral theory of biodiversity is not the same as the neutral theory in population genetics (although the latter might have inspired the former).
Additional references:

The unified neutral theory of biodiversity and biogeography at age 10 - Article by Hubbell, outlining successes of the neutral theory.
Conceptual synthesis in community ecology - this articles draws extensive parallels between the community ecology and population genetics, but light on math.
The transition between the niche and neutral regimes in ecology - a physics-minded model, demonstrating a transition between niche and neutral behavior depending on the population size and environmental factors.

I think I would start with Letten et al.  https://doi.org/10.1002/ecm.1242  . BTW I wouldn't say "modern" niche theory, "contemporary niche theory" appears to be the standard terminology ...  I wouldn't say Hubbell's book is the only source - there are lots of research papers ...


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Bug Identification - Is this a bed bug?
What kind of bug is this? Side of a penny for size. Found on basement floor in a bedroom. Pleaase tell me this isn't a bed bug

Does this answer your question? Insect identification - Is this a bedbug?

No not a bedbug. ID is impossible without a location in the world (e.g. nearest big city, state). Likely a weevil of some sort.