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Why don't people seem to die from salmonella in bites?
As far as I know, reptiles have salmonella in their mouths as part of their digestive process. Every time I hear about someone being bitten by an python or alligator or monitor either at a zoo or in the news or from a private owner, it seems like whoever is bit recovers with ease.
How come something as virulent as salmonella that can evade an immune response doesn't cause whoever gets bitten to nearly immediately become septic? Is it because salmonella only attacks epithelial tissue and there isn't much of that deep in an arm or leg?

Important to considera as welk that a Salmonella infection isnt always that bad, even the gastrointestinal salmonella infection can be mild depending on the serotype. Salmonella is actually very common in some parts of the world and it isnt super deadly or anything.

@MikeKatz45 Others and myself been through enough food poisoning to know everything you just said is total BS.

nop, look at my answer

@MikeKatz45 I looked at the first few words and figured it was a waste of time and ignored the rest, especially considering the question is already answered. You can't speak against people's personal medical history and there is plenty of documentation that people have died from salmonella in the past. I am going to take a rare opportunity to downvote for the first time ever, congratz on being the only one to earn that.

Yes, those like you who make the mistake of assuming they are omnipotent gods. This is not a religion site, this is a biology site.

I provided all the sources to backup what I'm saying (which is relevant to responding the question because Salmonella doesn't always kill you or cause severe disease). The one who is being unreasonable is you and I haven't seen a single source to discuss this matter from your side, in that sense you are acting in a dogmatic way, not me. I commented this question because I thought it was a good question and that the answer given previously was oversimplified and I don't know why you took it like I was being an "omnipotent god" lol.

You arbitrarily mixed personal opinions with references, which doesn't change anything. If you want to go into denial over deaths across the globe, you have much bigger problems than this site.

What part exactly is a personal opinion? I never denied Salmonella can be as severe to kill you, I was only pointing out that it isn't as simple as saying Salmonella infection = dying or almost dying. The bacteria can cause a wide spectrum of things,  really don't get why you have this attitude when there is reason in all I said.

Not even ebola=dying, but that doesn't mean it isn't an enormous problem for whoever contracts it. Seeing as how that's true, your presence here has lead to no good, you clearly have no intention of contributing, you are only here for your own personal insecurities of your own intellect and nothing more. In far fewer words, Stephanie has accomplished what you failed to and without any emotional bickering, the topic is resolved and you have no purpose here.

In the case of salmonella yeah sometimes it isn't a problem at all cause you can be completely asymptomatic (as I have repeated until tireness now). I invite you to read this whole series of posts again and figure out who doesn't have the intention of contributing at all, you are the one who has been in a defensive position all the time (since you mentioned insecurities lol) . I won't make further posts here since you clearly have no interest in the question anymore whatsoever and it was all a waste of time for both you and me

Yet again you've proven my point. Whether or not it "can" be asymptomatic is regardless, the fact is that it isn't always and unless you have proof otherwise, you have no reason to be here. You are yet again reported for trolling.

Guys: First, please tone down. Then stop excessive commenting and move over to chat.

Salmonella infect via the fecal-oral route. They have proteins on their surface that match our gut cell surfaces, allowing them to attach and invade the gut. Those cell markers aren't present when you are bitten. it's the same reason that plant virus dont make us sick.
https://www.ncbi.nlm.nih.gov/pubmed/17593246
this is a bit heavy if you dont usually read primary papers, but looking for "Salmonella route of infection" or similar will yield the same kind of information

You can have Salmonella without actually knowing it, the reason behind this is that there is a group of salmonellas known clinically as non-typhoid Salmonellas (this means they are still S: enteritidis, but different serovars other than the more popular S. typhi). These most of the time cause mild infections as noted by the World Health Organization non-typhoid Salmonella. These infections can even be completely asymptomatic (carrier state) as it has been known for more than 2 decades Old paper on treatment for asymptomatic salmonellosis. We also now know thanks to modern genomic analyses that even within different strains of S. typhi some strains are more virulent than others.
There is even an atlas provided regarding the "less popular" Salmonella serovars, I suggest checking it out if you are truly interested in this topic CDC Salmonella Atlas.
Also regarding your original question there is an useful review here that mentions human-infecting serovars of Salmonella reported in relationship with snakes & lizards A Review of Salmonella and Squamates (Lizards, Snakes and Amphisbians): Implications for Public Health. As you will see the species reported belong to the group that can cause mild or asymptomatic infections so that could be contributing to the fact that people don't have that much trouble with bites from these animals in general. Of course what Stephanie said in his answer is true but also the implicated serovars are less virulent in general than the well-known S. typhi. More in favor on this last point you will see that in the review they mention that some people did develop extra-intestinal disease from reptile-derived Salmonellas like the man who got sinusitis, this means that if the strain is virulent enough in will cause disease even outside the gastrointestinal system.


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What is the reason behind that children can cry but can't laugh?
I have a cousin who is almost 1 months old. As a normal child of her age, she cries a lot. But I noticed first that she doesn't laugh. So I noticed and found out that other children of her age also don't laugh. So how is it possible that childs can cry but can't laugh? What is the explanation for this?

Because life isn't funny yet. Sometimes, though, they smile in their sleep very early on, and smile socially as early as one month of age. They laugh when they can appreciate something funny - a funny face, a funny sound, a funny feeling (a 'zorbit'). Discomfort is present from the beginning, hence crying.

@anongoodnurse Why is discomfort present from beginning?

Hunger is a kind of discomfort. Cold, or being too warm, intestinal gas, uncomfortably wet diaper, being alone, having a startle reflex triggered, ad infinitum. Discomfort likely begins in utero, but believe me, every baby I ever delivered cried on delivery; I never had to slap a single one (nor did I hold them upside down. Being born is uncomfortable. Is it really a mystery?

source: Stack Exchange

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

sort: votes


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Modularity score comparison between different algorithms in network analysis
I used different algorithms for splitting my large gene network into different sub-networks using Cytoscape. I compared the modularity scores and decided that the algorithm with the best modularity score will be used for clustering the network.
My colleague came up with the argument that modularity scores can only be compared for different number of clusters being created by the same algorithm.
So, my question is if modularity scores can be used to compare between different algorithms or only in the case of the same algorithm producing different number of clusters.

If you don't get an answer here, you might do better to transfer your question (delete and repost) to SE Bioinformatics, which would seem more appropriate.

Since the goal of modularity estimation algorithms is to find the community structure that maximizes modularity, it is valid to compare different algorithms based on their modularity estimate. However, i) it is not the only consideration for choosing a community detection algorithm, and ii) the obtained modularity estimate will depend on the particular structure of each network, e.g. its number of nodes. For a principled comparison between several different algorithms, see Yang et al. (2016). Based on multiple criteria, they identify the multilevel (or Louvain) algorithm (Blondel et al. 2008) as the overall best choice.

References
- Yang, Zhao, René Algesheimer, and Claudio J. Tessone. “A Comparative Analysis of Community Detection Algorithms on Artificial Networks.” Scientific Reports 6, no. 1 (August 2016). https://doi.org/10.1038/srep30750.
- Blondel, Vincent D., Jean-Loup Guillaume, Renaud Lambiotte, and Etienne Lefebvre. “Fast Unfolding of Communities in Large Networks.” Journal of Statistical Mechanics: Theory and Experiment 2008, no. 10 (October 2008): P10008. https://doi.org/10.1088/1742-5468/2008/10/P10008.

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


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Bug identification - Beetle, grasshopper, moth-like and it also flies
 Could anyone please help me identify this creature? It can fly and seems to like crawling as well. It has mandibles that are beetle-like.  Approximately 3cm/2inch. Location: KwaZulu Natal, South Africa

Hi Ari13, and welcome to Bio.SE! Please update your question with the approximate size of your specimen, and please provide any additional information or pictures that are possible. See [tag:species-identification] tag question guidelines here. Doing so will increase the positive voting response your question receives as well as increase the odds of receiving a good/accurate answer. Thanks!

Thanks! Updated with approximate size and location.

That is a mole cricket, Order Orthoptera, family Gryllotalpidae
https://en.wikipedia.org/wiki/Mole_cricket

Thank you! Odd that I would've found it down here though? Don't you think?

You mean in South Africa? No, they are cosmopolitan. Cool bugs!


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How can skull size difference alone explain behavioral differences using evolutionary theory?
I just started Robert Sapolsky lectures series on Youtube on Human behavior biology, and on the second lecture, at this point, he is explaining how evolutionary biology can be used to predict lots of animal behaviors just through the differences on the skull size of adult males and females.
He considers two groups of primates, one in which the skull of the adult male is quite bigger than the female and the other where they are about the same size. He then asks the student: "which group would display higher male aggression?" I am lost at this point. How can the size difference alone be used to answer that question? The students answer the question: "the first group (in which the males are bigger)", and the reason provided is that their body is built for it. Why and how?
Following up, the next question is: which of the species has more variability among males in reproductive success? The answer provided: "obviously, it is the first one because the males are aggressive for a reason, and that is they are competing for reproductive access." Couldn't it be that the second group had a biological variation in sperm productivity, that greatly outmatched the fight for reproductive access of the first group? I mean, how can it be this easy to conclude such a complicated process? Shouldn't you carefully consider millions of other things before concluding that one group will have higher reproductive variation simply because of differences in the size of the skulls?
Thanks!

it's an "all others things being equal" kind of statement. If I were writing an exam question based on this idea, I would certainly phrase it as "which group would we expect  to display higher male aggression"?

Having a large difference between the sizes of the skulls between males and females is strong sign of sexual dimorphism, particularly of males that are larger in general.  Knowing which form of sexual dimorphism there is allows you to predict several other features. In particular large males is seen almost exclusively in animals in which the males fight each other for control of a harem AKA contest competition. This means high male aggression, since they are driving away other males. Since they drive away other males they have little to no sperm competition so they also don't need competitive sperm. These species also show drastic difference in male reproductive success, males with a harem produce many offspring males without one produce few to none.
https://www.intechopen.com/books/sexual-dimorphism/the-evolution-of-sexual-dimorphism-understanding-mechanisms-of-sexual-shape-differences

Thank you for the answer.
So, the reason we can say that the species with the larger male skull will show greater male aggression is because "large males is seen almost exclusively in animals in which the males fight each other for control of a harem". Or basically, "It is so, because it is what we see in nature." I thought, there would be some evolutionary explanation? I mean, equal size males could also, in theory, be aggressive and dangerous.
I come from engineering, and I might be missing some fundamentals here, so, please bear with me.

absolutely equal sized males could be, the question  is asking "given X we can extrapolate Y" not "What all conditions can cause Y". This actually is an evolutionary explanations, sexual dimorphism needs a reason to evolve, and for large males that situation is basically only direct male to male competition favoring large males who more reliable win said competitions. There are no other reliable reasons, evolutionarily speaking, to have males larger than females.  Given X we can extrapolate Y, it is not a guarantee but it is a fairly robust assumption.

I see. But it could also be that the bigger male could be a sexual selection (that females are just attracted to big males)? I guess, it could be, in theory, but that is not what we see in nature? So, looks like, like you said, X doesn't imply Y, but it is what we regularly see in nature. If it is so, I find it quite 'wrong' for Dr. Sapolsky  to expect new-coming student to be able to extrapolate Y from X (because there is no definite logical route from X to Y; only one of the many plausible route); that gave me the impression that X implied Y.

Since I don't know what support material or prerequisites the videos have I can't say how fair it is. But it would not be out of place if there is an expectation of competence in evolutionary concepts or primate in general. Contest competition is a pretty standard concept used when discussing sexual dimorphism and reproductive strategies. It is actually well studied in primates, and correlates with things like tesitical size, sperm production, and reproductive strategies.

I suspect the answer by @John is exactly the answer Dr. Sapolsky would be looking for. However, without supporting data from behavioral observation and actual genetics to rule out say, sexual selection, I'd remain skeptical.
The scenario posited by Dr. Sapolsky strikes me as the sort of ad hoc story telling that shows up so often in evolutionary psychology. It might be a good starting point for investigation, but the story by itself is not dispositive. We all "knew" for over a century that the longs necks of giraffes were an adaptation to grazing the upper levels of trees. It's an obvious and plausible story, but apparently the genetic evidence is more complicated and it may be an example of sexual selection (female giraffes acquired a fairly random preference for long necks), or the trend started as an adaptation for grazing higher vegetation, but was then hijacked as a tool for sexual competition (male giraffes fight by whacking each other with their necks).

This is really well studied in primates, it is not ad hoc.

@John it may be, and I'd trust those studies a lot more. I've got no problem with field studies and actual genetics. What I object to is Sapolsky encouraging a popular audience to believe that  it can be derived from hand-wavy principles of evolutionary biology. It's a plausible story, but a story is not dispositive.


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What does it mean by “end effects can be ignored”
I have been reading a book ( Statistics for Biology and Health) and i encountered many of following bold text.

Consider a long DNA sequence of length N, where N is assumed to be
so large that end effects can be ignored in our calculations.

In Shotgun sequencing also the saw similar thing :

The fragments are assumed to be taken at random from the original
full-length sequence, so that if end effects are ignored, the left-hand ends
of the fragments are independently distributed with a common uniform
distribution over [0,G].

What does " end effects can be ignored " means?

They are considering a model of a DNA sequence of quasi infinite size. They consider a case where the DNA sequence is so long that the fact that it has ends will only negligibly affect the conclusions of their model. This is likely the same as considering the DNA is circular.
To give you a similar logic, imagine a species where individuals live in different populations. All population can be placed on a one dimensional axis. The migration rate from one population to the neighbouring population is 0.1 (this is called a "stepping stone model" btw). Hence, the probability of not migrating is 0.8 (1 - 0.1 - 0.1). I can draw conclusions from such a model but it would be important to specify that I neglected the end effects and hence, I assumed there are a lot of populations (or that the population form a loop). Why did I neglect the end effects. The last population on each side cannot have a migration rate of 0.1 toward a population that does not exist. Hence, their migration rate must differ from the other populations. This is commonly called edge effects (rather than "end effects")

Out of curiosity, do people actually call these end effects in the context of DNA when this comes up? The more common term for these issues in a broader mathematical context in English is usually "edge effects."

@BryanKrause I agree the term edge effect sounds more common, esp. in its use in population biology (info added in post). I am not sure I had ever heard "end effects" before but the term makes the meaning quite intuitive.

Thanks - I suspect the author (or translator) of the text the OP refers to made a bit of a mistake here. I think if they had called them edge effects it would have been more easily investigated by the OP. That said, anyone familiar with the field would probably quickly infer that they meant 'edge effect' when writing 'end effect.'

Perhaps end-effects is strictly correct when considering a one-dimensional object, such as a DNA-sequence. If you were considering a two-dimensional object, as you might in ecology when looking at a particular geographical area, then the area would truly have an edge, whereas a DNA molecule could be said to only have 'ends', not edges.


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What species is this orange mushroom in Romania?

So I've found these mushrooms near a ditch on a field a few days ago in Romania. Can anyone help me with identifying what species of mushroom is this? The size of a mushroom is about 3-6 cm in diameter. Thanks and a happy new year.

Hi griffinwish. Please update your question with the approximate size of your specimen, and please provide any additional information or pictures that are possible. Images of both the tops and undrsides of mushrooms are preferred for accurate ID. See [tag:species-identification] tag question guidelines here. Doing so will increase the positive voting response your question receives as well as increase the odds of receiving a good/accurate answer. Thanks!

This is most likely Kuehneromyces mutabilis or sheated woodtuft. It is quite common in Romania where it is named Gheba ciobanilor.
Quote from Wikipedia about the diagnosis:

The clustered shiny convex caps are 6–8 cm in diameter. They are very hygrophanous; in a damp state they are shiny and greasy with a deep orange-brown colour towards the rim; often there is a disc of lighter (less sodden) flesh in the middle. In a dry state they are cinnamon-coloured.
  The gills are initially light and later cinnamon brown, and are sometimes somewhat decurrent (running down the stem).
  The stipe is 8–10 cm long by about 0.5–1 cm in diameter with a ring which separates the bare, smooth light cinnamon upper part from the darker brown shaggily scaly lower part. This type of stem is sometimes described as "booted".
  This species always grows on wood, generally on stumps of broad-leaved trees (especially beech, birch and alder), and rarely on conifers.
  It is found from April to late October, and also in the remaining winter months where conditions are mild. It is often seen at times when there are few other fungi in evidence.

Further details can be found here in English
or here in Romanian


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Why don't rates of cancer increase generation to generation?
As cells divide, they accumulate mutations that can sometimes cause cancer. Gametes have to divide like any other cell, and thus generation to generation mutations should accumulate in people's genomes. However, it doesn't appear to be the case that cancer rates increase as a species ages. Why isn't this the case? Is the process of development itself a filter that ensures that most of the cells in the body are "far from cancer"?

If an organism grew from a mutated gamete, they will carry that mutation. And if the mutation is sufficiently debilitating, they won't properly develop or survive as well as other non-mutated members of the species. So the mutation would, in theory, be filtered out by natural selection.

This Wikipedia page is relevant. Individuals can inherit germline mutated forms of the TP53 gene and have a higher cancer risk. But organisms with a high cancer risk are less viable than those with a low cancer risk so their form of the gene is filtered out.

@Jam presumably this selection pressure will decrease as medical treatments become better - so we would see cancer rates increasing for younger patients in the future?

I see what you're suggesting but I don't really know. In theory, you might be right but I think the incidence rate of the mutation would need to stay constant, and the cancer would need to affect people early enough to not affect whether they can have children.

Species age

However, it doesn't appear to be the case that cancer rates increase as a species ages

Species don't have an age. All lineages on earth are about 3.5 billions years old. No, lineage is younger or older than that. A lineage does not get its genetics magically reset when the lineage gets a new species name. For more information about the standard misunderstandings about the concept of species, please have a look at the post How could humans have interbred with Neanderthals if we're a different species?
In all cases, there is some equilibrium between the selection pressures brought about mutations that are linked to cancer (whether mutations on oncogenes or on tumor suppressor genes).
Individual age
Individual, do have an age though. Cells, within multicellular individual replicate in order to ensure the multicellular individual growth and maintenance. Those cell lineage can accumulate mutations that could be linked to cancer development. Within the individual, these mutations are not deleterious and are therefore not selected against. Actually, in case of a cancer, those mutations are, by definition, beneficial as cancerous cells proliferate (have a large fitness). As a result one should expect that old organisms are at greater risk of developing cancer than younger organisms. In humans, this correlation exists, however, the statistics are slightly more complex than that. Typically, different types of cancer seem to show different age associations. See this article from the NIH as a start for more information.

I understand that species don't age, my question is "why don't they age? why haven't all species gone extinct from cancer?"

@Mike Flynn: Basically, because the individuals carrying the cancer-causing mutation die before they can reproduce, and thus pass the mutation to their offspring.  A current example is the Tasmanian Devil, which seems likely to be rendered extinct by a particular cancer to which they're subject.

@MikeFlynn Is your question something like "How does selection gets rid of deleterious mutations?", then?


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Home bacteria culture at home?
Can simple bacterial culture be done at home using food agar as the medium (with some additives found in the store)?

what exactly are you trying to achieve?


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What are mutator genes which cause copying errors in other genes?
Reading Dawkins' book "The Selfish Gene," I came across this line: "There are even genes--called mutators--that manipulate the rates of copying errors in other genes." (The context is his argument that such a gene is looking out for its best interest by killing off the competition.)
What are these "mutator" genes, and how do they function?

Most obvious examples are the genes directly involved in DNA mismatch repair (MMR) such as mutS, mutL, mutH, MLH1 and MLH2.


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Learn biology without experimentations
I'm a high school student in a third-world country (Algeria).
My problem is with the way we are been taught biology. It's all about memorizing facts and procedures from a textbook without any application whatsoever due to the unavailability of laboratory equipments(there are some but they are either expired or useless).
My question: does this way of learning have any benefits at  all? Are we even learning?
I know what a lipid is because I've read its definition, but, is this enough? Is it enough to only read a paragraph that describes lipids and then see a model of it in order to know  what a lipid really is? Would it be useless if I go to a laboratory, extract some cholesterol, study its characteristics and see it with my own eyes to have a rough idea of what it is?
I've been seriously thinking about dropping out of school because I think the world doesn't need another indoctrinated kid who knows a bunch of facts and want to  earn some money with that knowledge.

there is a big difference between "no experimentation" and "only memorizing facts and procedures"  Are there explanations, examples, and discussion? Also what level of schooling is this? There are not many suitable experiments for the biology at the lower school levels.

There is typically little to no "experimentation" in math education, yet few would consider math as a boring list of facts to learn. You are definitely putting in opposition two concepts that should not be. Studying biology is much more than learning a boring list of facts (and it does not necessarily implies making any kind of experiment). That being said, if you find your class boring it might be a result of poor teaching skills of your instructor (it might be for some other reason).

If you want to study biology by yourself, you will find some ressources on this post.

I'm voting to close this question as off-topic because it is not about biology but about teaching practices. It is also slightly unclear by opposing two concepts that should not be opposed. The last paragraph of the post is clearly off-topic.

Not to be discussed on a biology Q&A site but earning money with your acquired knowledge is really not fundamentally wrong. Not being interested in class or not finding the point of studying can be a challenging sentiment. I would personally tend not to recommend dropping school but I am not trained to give such advice and would not know enough about your situation. In all case, you have my sympathy and I wish you good luck with whatever you'll end up choosing!


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About. Autosomal recessive diseases in genetics
What happens if homozygous dominant  alleles are present in an individual for an autosomal recessive disease will he be affected ?

What are your thoughts? Knowing your thoughts on the subject would help us understanding what could be unclear to you

You are talking about an extremely simple system of inheritence that is a single bi-allelic locus with simple dominance relationships. You are talking about a autosomal recessive disease. In other words, let a and A be the two alleles, where A is dominant of a. By definition of your model, the individual expressing the disease is the individual carrying both a alleles (a aa individual). Anyone carrying the dominant allele would not express the disease (by definition of the term dominance and because you define a model where a and not A is causing the disease).
In short aa express the disease, while aA, Aa and AA individuals don't express the disease. aA and Aa are carrying the allele causing the disease though and might have kids expressing the disease if they mate with an individual that carries at least one allele a.

No. Because you said it's homozygous, meaning that two alleles are identical, both dominant in this case. Hence, there's no recessive allele at this locus so he won't be affected.


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What is the genetic background for fast metabolism?
I am wondering if it is possible that people with very fast metabolism have some genetic mutation. There are people who can eat a lot while others would definitely get fat with such a diet. In other words, they seem to have very fast digestion and never feel so much full after eating but what's surprising is that they still stay very skinny?
Can it be a result of some disorder/mutation?

Are you asking about the genetic background for fast metabolism or for underlying diseases? I am asking, because a) not all genetic deviance from the 'norm' is a disease and b) not each possible underlying diseases are caused by genetics. Could you please edit your post (and/or title) to clarify this?

For medical advice, it is better to ask a physician.

The expression "fast metabolism" is very general and makes the question hard to answer. I will hence answer in the most general sense possible and then just give one example.
Yes, it is most definitely the case that there is genetic variation underlying the variation in metabolic abilities in the human population (btw, this post summarizing the partitioning of phenotypic variation might be helpful to you). For example, Greenlandic Inuits have a series of mutations that affect their ability to digest polyunsaturated fatty acids allowing them to cope with the impressive amount of animal fat that is/was found in their traditional diet (Fumagalli et al., 2015).


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Shrimp in rainwater puddles
After rain, we often find shrimp-like creatures in the puddles left on our concrete patio. We have also found them in the cat's water bowl (on the same patio). They are pink in color, and around 3mm long.
The idea of shrimp on land seems absurd, but that's certainly what they look like.
We live in Okinawa, and even long-time local residents don't seem to know what they are. We're on a cliff 10 meters tall, right next to the beach.
My questions: what are they, and how do they magically appear after rain? From eggs that are lying dormant on my patio, waiting for rain??
The alleged duplicate is quite helpful. My question is slightly different because I live beachside in Okinawa, not in central Florida, and my creatures are much smaller. Probably a related species, though one that doesn't seem to be familiar to the locals.

Is there any chance you could take a good picture and add it in your post?

I thought someone would ask for a picture. I'll try next time it rains. But meanwhile, after some research, I suspect that they are some sort of amphipod. Weird that the local folks don't know about them. Maybe a new arrival in Okinawa??

or maybe water fleas...

@BryanKrause: Thanks. I saw the post you cited. My creatures are quite similar, but about half the size. Just another species, I suppose.

does any match https://openi.nlm.nih.gov/imgs/512/352/3253665/PMC3253665_ZooKeys-163-013-g017.png


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Is the mesenterium a synonym for the mesocolon?
On biodigital anatomy browser I found a structure called the mesocolon. I didn't find the term in Uberon and I'm unclear whether it's simply a synonym for mesenterium or whether it's a separate concept.

Mesentery is the name of a whole set of tissues attaching the intestines to the abdominal wall.
In human anatomy, there are three different portions of the mesentery:

Mesenterium sensu strictu, also called Meso
Mesocolon transversum
Mesocolon sigmoideum, also called Mesosigmoideum

Two smaller mesenteries can be found at the appendix (Mesoappendix), and at the cranial part of the rectum (Mesorectum)
So... Mesocolon is a part of the mesentery, but no synonym.

Could you specify what the term Mesocolon includes?

Mesocolon includes all mesenteries of only the pelvic colon (Sigmoid colon) and transverse colon. All other parts of the intenstine are held in place either by the Meso or the smaller mesenteries named above.


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Ligation without purifying insert
I am planning to insert a 45 bp sequence in a vector. After restricting my insert to create compatible sticky ends, I am finding no way to clean it up. Is there any way for cleaning this fragment after restriction or should I proceed without clean-up?

Proceeding without cleanup will reduce your efficiency but may still work. Have you tried purifying via gel extraction? A high density gel should allow you to separate the band to some degree.

Hi Joe, I can locate the band in high density gel, but would it be possible to extract 45bp sequence through gel extraction protocol?

I think so, though you may need to ensure you use a column designed specifically for small fragment retention. There are columns for purification of miRNAs, so I’d have thought there might be a column you could source which will do a similar thing for dsDNA, but I am guessing somewhat. I believe there are some old-school chemical techniques for precipitating away melted gel without needing a column too that you could try. You could then concentrate with a rotorvap or heatblock.

“GeneClean” which involves adding powdered glass and potassium iodide solution to an agarose gel slice would work for this.  I believe QIAgen sells a matrix like this.  The glass is extremely fine, and has to be prepared by boiling in nitric acid.  Once upon a time there was a company named Bio 101 that sold a product named GeneClean, but they may have been bought by somebody else.  For unknown reasons, nucleic acids will bind to glass in the presence of a chaotrope.

A much simpler way to insert sequences that are really small is to order the DNA as oligos and anneal the complementary oligos such that they have compatible overhangs with the overhangs from  your restriction digest

Thanks all for your comments guys. I tried purifying using PCR purification kit. I could recover 120 ng of purified fragment from 500 ng. It is ok for my further work.

That's not too bad for a fragment of this size, the efficiency of the column kits (actually almost all DNA preps) goes down with decreasing size. If you wanted higher efficiency you could use a magnetic bead based kit such as Dynabeads or  AMPure XP ($$$, but the best).


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Bacteria resistant to antibiotics?
If I use antibiotic on a specific type of bacteria, some will survive because it is resistant. Was this bacteria resistant to this antibiotic before it was even used, or did the bacteria develop resistance after the antibiotic is used?
How or why some bacteria can simply mutate to form beneficial alleles which will help in survival and others can't?

Antibiotic resistance comes from selection pressure: any bacteria that are resistant will survive and replicate, so in the next generation of bacteria you will find more resistance.
Bacteria do not simply mutate to form beneficial alleles, the alleles or genes that confer drug resistance must already be in the population; by using antibiotics, however, you're killing off their competition by killing the bacteria that don't have the resistant allele(s)/gene(s).
It's very unlikely that one individual using one antibiotic for one illness will lead to detectable antibiotic resistance. However, antibiotics aren't used in just one individual: they are used repeatedly, in many individuals, often in multiple species, etc. It is this broad use of antibiotics over time that eventually "finds" strains that are antibiotic resistant. Once these strains with resistant alleles become more prevalent, it becomes more likely that they will be present in some quantity to be selected for in the future.

Not that you said otherwise, but I'd like to emphasize that there need not be a dichotomy between complete resistance and no resistance. Some population with partial resistance could have a selective advantage, especially if the antibiotic dose is low (or short), and then continue to mutate towards higher resistance.

@canadianer Of course, I think this is a fortunate case where we've actually picked a linguistically informative word as a scientific community: resistance refers to being less susceptible to the antibiotic, that is, resistant to it, rather than invulnerable to an antibiotic, and so resistance to a given drug can be on a spectrum. It could be thought of as just a shift in the LD50 for a given drug.

I think there is too much emphasis on alleles in this answer. Resistance to antibiotics is not a purely genetic phenomenon. Some cells may resist the antibiotic pressure through epigenetic mechanisms, e.g. upregulation of efflux pumps etc. There need not necessarily even be a specific mutation required.

@JoeHealey I'm not sure I follow. An ability to upregulate of an efflux pump is going to be due to some allele, an epigenetic mechanism is just that: a mechanism. If one organism has a different propensity towards epigenetic modification of an efflux pump, that's still an allele.

@BryanKrause an allele is specifically a variant form of a gene, but the efflux pumps (or whatever other mechanism we are discussing) may only be deployed differentially - any mutations arising (which isn't always necessary) need not even be in the gene, so calling this an allele isn't wholly accurate. So, one bacteria that is killed, may simply not have responded sufficiently to the selection pressure and therefore dies, whilst another cell survives. The response could be affected by any number of other things going on in the cell such as quorum signals, nutrient levels etc.

For me 'must already be' sounds confusing. When did 'already happen? Are you talking about already drug-resistant strain (if so - where did it come from?), or any mutation that happened to happen at moment when antibiotic was poured over, or, let's say, plasmid?

@JoeHealey We're talking about evolution of gene resistance, not the variables that affect survival of individual cells and cause not all cells to die exposed to the same drug. If it isn't heritable it isn't meaningful to drug resistance. The allele need not be in an efflux pump, it could be a regulator. I suppose using a very strict definition of allele you could say that "allele" cannot refer to insertions of additional genes, etc, but I feel like that sort of terminology is unnecessarily pedantic and leads people astray to the idea of "gene for A, gene for B."

@MaximKuleshov All of the above.

@BryanKrause I'd disagree with "if it isn't heritable, it isn't meaningful". With the question as posed, it is meaningful if it allows at least some cells to persist through that specific round of selection, leaving at least some of the population viable on the 'other side'. What happens beyond then is anyone's guess, but the population has survived, and will almost certainly have used many different 'dirty tricks' over as many rounds of selection as it takes in order to survive. You don't necessarily suddenly get resistance and have it hang around forever, its much more fluid than that.

@JoeHealey If it isn't heritable, no additional resistance is carried to the next generation, and no selection has taken place. What happens beyond then isn't just anyone's guess, it would be the only thing that matters (beyond the effects of the infection on the individual we're talking about). If the "dirty tricks" are heritable then there is some gene/allele there mediating that dirty trick. Even if it's epigenetic, as long as it's heritable it counts.

@BryanKrause from the perspective of any single cell, I agree. But from the perspective of a population persisting through selection, the resistance does not need to be inherited. It can re-emerge on each exposure (though I concede this is less efficient and therefore less likely). Selection has taken place because the population will have been bottlenecked by the fact that many cells will not have survived.

@JoeHealey Starfishes (at least some of them, not sure of the exact extent) can regrow limbs that are removed. We do not say that starfishes that do not have their limbs removed lack the arm regrowing trait just because they haven't had any limbs removed. A population that has an ability to upregulate a pump for resistance has a resistance trait that has to be encoded by some heritable factor. The difference between that population and a population that does not have that ability is a gene or allele.

I think that's a bit of a false equivalency, but perhaps we will just have to agree to differ on this one. I still believe that playing fast and loose with the term 'allele' is not a triviality - terminology exists for a reason.

Let us continue this discussion in chat.


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Which mammal produces the most milk?
I'm searching for the mammal species that can produce the most milk during lactation. I Googled it, but it says dairy cattle which biologically speaking is not right answer, because a baby whale can drink up to 150 gallons (> 550 litres) of milk per day (according to whalefacts.org). So which mammal can produce the most milk?

I'm looking for volume but if you can tell about fat content too it would be appreciated : )

Define "most", because I think you will find that dairy cows which produce everyday will outperform whales which only do so for part of the year in total milk output.

By "most" I mean a mammal who can produce most milk whenever she lactate. I'm  editing my question to make it more specific.

What happens if you “normalise” but dividing by body mass for example? Ie remove size...

Blue whale should be the answer. You can deduce it based on given info and if you compare to other mammals. It is also mentioned in this (non-credible) source: https://www.intoyard.com/do-whales-have-nipples/

In animals, such as the blue whale, that fast during lactation, nutrients are mobilized from tissues (maternal reserves). Supply is mainly limited to body fat; thus, total available supply is proportional to body mass. Body weight of a blue whale is approximately 120,000 kg (at the start of the nursing period) and lactation duration in this species is 210 days (7 months). According a published paper (Oftedal 1993, J. Dairy. Sci. 76), "a female blue whale arriving at the feeding grounds weighing 80,000 kg might gain 40,000 to 50,000 kg before migrating to low latitude waters to give birth. This stored mass is assumed to be lost during the 7 mo of lactation; thus, milk production can be predicted to be 27,000 to 33,000 kg, which is equivalent to about 23 to 25% of initial maternal BW. During this period, suckling calves gain about 81 kg/d, or a total of 17,000 kg, which corresponds to a predicted milk intake of at least 26,000 kg. These two estimates are reasonably similar and indicate milk production of about 30,000 kg milk, or 140 kg/d". Production per cow is lower (in the United States it averaged 23,391 pounds for 2019, United States Department of Agriculture (USDA)).
About your second question (fat content), true seals (Phocidae) exhibit the shortest and most intense lactations, with extremely rapid weight gain in their pups. Hooded seal lactation duration is only 4 days (briefest lactation period in mammals). Hooded seal mothers secrete milk, which contains 60% fat, at rates of 10 kg/d (Iverson et al. 1995 J. Comp. Physiol. B 165).


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Difference in frame rates of normal and peripheral vision
I recently encountered an incident in my laboratory. It was evening and the sunlight entered the lab through a window with exhaust fans. So the ray kept flickering at fixed intervals.
I noticed that the flickering was more noticeable when it was viewed through the side of my eyes.
Is it a fact that the frame rates of the two visions are different?

Vision doesn't have frame rates.

I believe the persistence of vision puts an upper limit for the no. of distinct images that can be seen in a second. That is what I meant by the frame rate of vision of human eyes.


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Why are higher doses of atropine required to produce central effects?
Reason given in my book is restricted entry into the brain..is it something to do with the chemisty?

Can you give more context as to how the book is referring to atropine being administered? If you are talking about IV administration this is wrong. Could you provide a citation and quote from the book?


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Etymology of eccentric/concentric contractions
I was wondering if anyone knew why the terms eccentric and concentric were chosen to refer to lengthening and shortening muscle contractions?
The basic etymology of the words are to do with alignment with the centre of something. Eccentric is derived from the Greek for "off centre" and is also commonly used in bio-mechanics, another branch of sports science, to refer to a force applied out of alignment with an object's centre of gravity. I couldn't see how this definition applied to a lengthening muscle contraction, and haven't been able to find any information on why the terms were chosen.
I'd appreciate any help.

Try a Google search for a video demonstrating sarcomere contraction.

Are you suggesting it's just to do with the direction the z-lines are moving relative to the m-lines? ie. eccentric would mean 'away from centre' as in away from the m-line, therefore lengthening?


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How to identify whether something is in linkage disequilibrium?

If the following loci indicated the presence of an SNP in flu strains, is Locus 2 and Locus 3, which are located 10 bp apart in linkage disequilibrium?
"When alleles and molecular
markers are associated with each other at a frequency that
is significantly higher than expected by random chance, they
are said to exhibit linkage disequilibrium" Brooker's Genetics
Both loci seem to be linked, but how do I determine if it is significant enough to be considered in disequilibrium or not.

As per the definition you gave, you check whether there is a statistical association between the two. If knowing when allele is present at a locus does not affect the probability of finding a given allele at the other locus, then they are independent (there is no association). Otherwise, there is an association and hence the two loci are in linkage disequilirium.
See wikipedia > Linakge disequilibrium for more info.


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Why doesn't peritoneal dialysate leak through the fallopian tubes?
It is my understanding that the female peritoneum does not form a closed (potential) space due to its puncture by the uterine tubes. If that is indeed the case, why is peritoneal dialysis in women not typically complicated by vaginal leakage of dialysate? Similarly, why do we not expect surgical insufflation (e.g. in laparoscopy) to suffer from CO2 leakage via the same route? Does this have to do with muscle tone in the fallopian tubes, or a duckbill valve effect where intraperitoneal pressure effectively seals them off? There seem to be only a handful of case reports of PD dialysate leakage, but more suggesting flow in the other direction where sexual activity, for example, resulted in unintended pneumoperitoneum.


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What's the relationship between oxygen consumption and ambient oxygen concentration for a lobster?
I was looking at a research paper by Thomas (1954) and came across a graph with ambient oxygen concentration plotted against oxygen consumption rate of a European lobster kept in water.

As we can see, this is a linear relationship, but I'm unable to figure out the reason behind this direct linear relationship.
I would be glad if anyone out there can suggest a possible reason, because just rote learning the graph is not something which should be done.

Did you read the summary? Given explanation seems legit to me: "6. Increase in oxygen uptake with temperature in sea water is mainly brought about by an increase in the gill ventilation rate. In addition, the degree of utilization increases. The relationship is a direct reflexion of the increased metabolic activity".

I read the summary and I understand why increase in temperature leads to higher oxygen consumption rate, but I can't figure out how oxygen consumption rate is dependent upon the ambient oxygen concentration.

That's how blood flow works. Gills are not 100% effective and can absorb only certain percentage of oxygen. So the lower oxygen concentration is the lower amount of oxygen is absorbed.

Now I understand. Thank you very much Maxim Kuleshov.

Increasing the ambient oxygen concentration increases diffusion of oxygen across the gills, thereby increasing the oxygen uptake by the lobster.
This can be proven by the fick's law of diffusion-
r=[-DA(P2-P1)/L]
L=thickness of diffusion membrane
D=diffusion coefficient
A=cross sectional area of diffusion membrane
P2-P1=pressure difference


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What are the effects of oxygen toxicity in human blood?
I was reading some text on deep sea Physiology, and for to know that diving to do could cause oxygen toxicity in the blood. This was the exact text from the book Textbook of Medical Physiology by Arthur Guyton and John E. Hall:

A  column  of seawater  33  feet  (10.1  meters)  deep  exerts  the  same  pressure  at  its  bottom  as  the  pressure  of  the  atmosphere  above the  sea.  Therefore,  a  person  33  feet  beneath  the  ocean surface  is  exposed  to  2  atmospheres  pressure,  with  1  atmosphere  of  pressure  caused  by  the  weight  of  the  air  above the  water  and  the  second  atmosphere caused by the weight of  the  water.
When  the  PO2  in  the  blood  rises  above  100  mm  Hg, the  amount  of  O2  dissolved  in  the  water  of  the  blood increases  markedly. Note  that in  the  normal  range  of  alveolar  PO2  (below  120  mm  Hg), almost  none  of  the  total  O2  in  the  blood  is  accounted  for by  dissolved  O2,  but  as  the  O2  pressure  rises  into  the thousands  of  millimeters  of  mercury,  a  large  portion  of the  total  O2  is  then  dissolved  in  the  water  of  the  blood,  in addition  to  that  bound  with  hemoglobin.

I understand that high pressure causes more oxygen to dissolve in blood, but cannot figure out how excess dissolved oxygen in the blood disturbs the normal physiological balance of the body.
I'd be grateful if someone knowing the answer can help me.

This is from a Wikipedia article:
Central nervous system oxygen toxicity manifests as symptoms such as visual changes (especially tunnel vision), ringing in the ears (tinnitus), nausea, twitching (especially of the face), behavioural changes (irritability, anxiety, confusion), and dizziness.
Oxygen toxicity - Wikipedia
https://en.wikipedia.org/wiki/Oxygen_toxicity
It says there's hemolysis of red blood cells - i.e., they lyse = break open.


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How to recover all protein ses into refseq database
I'm actually trying to download all the virus protein sequences available in the NCBI database.
I guess the link is this one: ftp://ftp.ncbi.nlm.nih.gov/genomes/refseq/viral/
How could I get all the protein sequences in fasta format into one file ? Does someone have codes to do that easily?
Thank you very much.

I believe that this question belongs to StackOverflow, as it's not about biology or related interdisciplinary subjects. Also for such tasks I recommend using Scrapy for Python

@MaximKuleshov — Better on SE Bioinformatics than Stack Overflow as nobody on SO will know anything about the file format of Genbank files. And leave it at that. Recommending a package in a particular language is not appropriate in a comment and not much use anyway if the poster doesn't use the language.

As with most things, there are multiple ways to do this. Here are two of them:
Download from the NCBI Assembly portal

Go to https://www.ncbi.nlm.nih.gov/assembly/ and search for 'Viruses[Organism]'. For our purposes, I am going to restrict this search to Virus assemblies that are latest RefSeq and reference genomes. The query for this will be: "Viruses"[Organism] AND "latest refseq"[filter] AND "reference genome"[filter]. It will return 46 results.
To download the protein FASTA sequences for all of these, click on the big blue Download Assemblies button, choose RefSeq as source and Protein FASTA as File Type.
Click the Download button and a tarball with FASTA files - one for each assembly - will be created for you to download. You will then have to combine them all into a single file.

Download using wget

Go to ftp://ftp.ncbi.nlm.nih.gov/genomes/refseq/viral and download the assembly_summary.txt file. This is a tab-delimited file with information about every RefSeq viral assembly located in that FTP path. Column 20 has the FTP path for the assembly which you can parse out and use wget to download the protein FASTA file for each assembly, followed by combining them into a single gzipped file as shown below:
## download the assembly_summary.txt file
wget ftp://ftp.ncbi.nlm.nih.gov/genomes/refseq/viral/assembly_summary.txt
## download the protein FASTA files
grep -v '^#' assembly_summary.txt \
    | cut -f20 \
    | while read -r url ; do wget $url/*_protein.faa.gz ; done
## combine all files into a single one
zcat *_protein.faa.gz | gzip > all_viral_proteins.faa.gz

Hi, thank you for your help, it did work. Unfortunalty when I try zcat *_protein.faa.gz | gzip > all_viral_proteins.faa.gz I get : -bash: /usr/bin/zcat: Argument list too long

Finally I found I way by doing : for i in $(ls | grep "_protein.faa.gz");do cat $i >> all_viral_proteins.faa.gz;done

Interesting. I never had to concatenate so many files! Is there a reason why you want such a large number of sequences in a single file? Can you not work with multiple files? Presumably, the single file would be very big and may not be the easiest to handle for downstream usage.

It is because I'll make a blast with those sequences as queries, so I'll make a blast database with them.

Maybe you can help me again, I would like to download a list of genomes, I have their ID number (list with one ID number by line) and I would like to get all the genomes in .fa format do you know if it is possible with the same script?

What kind of IDs do you have? Can you give me a couple of examples?

Yes of course:
'Genome ID:  12051
Genome ID:  39971
Genome ID:  44840
Genome ID:  55512
Genome ID:  39899
Genome ID:  65382'

Where did you get these IDs from? They don't seem to be the NCBI Assembly UIDs because when I search for 12051[All UIDs] in the NCBI Assembly I don't see any results. Would it be possible to get GCF or GCA accessions for these genomes?

Let us continue this discussion in chat.


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why can a queen wasp sting many times but a worker bee can only sting once?
wasp queen and workers can each sting you several times but a bee can only sting you once. As all of the stings have barbs on them, how can this happen?

Your question is unclear. You seem to have partially answered your question (bee stingers have barbs while wasp stingers don't) . What do you mean by "how can this happen"?

It's not true that all stingers have barbs. Wasps, and many other species, don't have barbed stingers, and therefore they can afford to sting you repeatedly without being killed. Worker bees, on the contrary, have a barbed stinger that gets stuck in your skin.
Although wasps have a more powerful venom than bees, with bees usually the venom sack remains attached to the stinger and will keep pumping venom even after the bee itself has run away and died, causing the sting to be more painful. However, because bees died after stinging, they are less likely to sting you compared to wasps, hornets, yellow jackets and bumblebees.


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Why does water stress lead to alkalinity of xylem sap in plants?
I was reading this book: Plant Physiology and Development, Sixth Edition by Lincoln Taiz, Eduardo Zeiger, Ian M. Møller, and Angus Murphy when this doubt came to my mind. Abscisic acid, the stress hormone, works to prevent water loss from a plant. Its mechanism of action requires the xylem sap of the plant to be alkaline. I can't figure out how water stress in the plant body causes alkalinisation of the xylem sap. The section in the book stated as follows:-

During the early stages of water stress,however, the pH of the xylem sap becomes more alkaline,increasing from about pH 6.3 to about pH 7.2.
  Stress-induced alkalinization of the apoplast favors formation of the dissociated form of abscisic acid, ABA–, which does not readily cross membranes. Hence, less ABA enters the mesophyll cells, and more reaches the guard cells via the transpiration stream.

I'd be grateful if anyone out there can help.

According to recent studies, drought stress does not consistently lead
to increases in the pH of xylem sap. One article which discusses
interspecies differences is Vit Gloser, et al., "The dynamics of
xylem sap pH under drought: a universal response in herbs?," Plant and
Soil 409, nos. 1-2 (2016): 259-272.
As to what may have prompted the textbook authors to assert this, see an
earlier article by two of the coauthors of the Gloser essay: Sally
Wilkinson and William J. Davies, "Xylem sap pH increase: a drought
signal received at the apoplastic face of the guard cell that involves
the suppression of saturable abscisic acid uptake by the epidermal
symplast," Plant Physiology 113 (1997): 559-573. Wilkinson and Davies
summarize an earlier study: "Hartung and Radin (1989) found that the pH
of xylem sap from water-stressed Phaseolus vulgaris roots increased
from control levels of 6.3 to 7.2." (560)

Welcome to Biology.SE! It would be very helpful if you could elaborate on your answer.  For example: How do changes in the cation/anion ratio affect the pH?  Also did you mean to say that lower nitrate uptake causes the cation/anion ratio to decrease? ——— You may also wish to take the time to go through the [tour] and the help pages starting with [Answer] questions effectively on this site. Thanks!

Pls elaborate. Don't just give references


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Do unique communities of bacteria form inside water storage in plants?
I assume that plants, like animals, have an ability to fight off bacteria that invade their cells (support: here and here.
However, water often harbors quite a bit of bacteria in even unsuspecting locations (e.g., see here).
Moreover, plants store a lot of water in their vacuoles.
I was wondering, whether the water stored in plant cells tends to harbor bacteria...
If so, are the bacterial communities in such water-storage organelles unique to plant vacuoles or do bacteria get transferred with the water as it moves through the plant?

As stated in Plant Signal Behav. 2010 Dec; 5(12): 1568–1570:

Phytopathogenic bacteria do not enter plant host cells, but proliferate in the intracellular space.

But as they can reach the apoplast, pathogenic bacteria can take advantage of environmental humidity levels and manipulate water content inside plant leaves to reproduce and spread infection as shown in
Nature volume539, pages524–529
So yes, bacteria can infect water inside plants but usually not inside the plant cells themselves. As they infect the intracellular space, they can spread in the water and infect the whole plant. It is also to mention that we are not speaking about the same bacteria as in standing water or something else. Viruses on the other hand can infect the plant cells themselves.


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How do booklice avoid dessication?
I often find booklice (aka psocids) in old paper notes I have in semi-storage. These pages of paper are intentionally left in dry conditions on my desk to avoid damage. However, if the psocids live and feed totally within these pages, how are they getting any water? How do the booklice avoid drying out and dying?


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What is this tiny lizard?
This tiny guy stumbled into our house in the suburbs of Sydney. What species is it?
It's dark and has two yellow stripes going along the length of its body. They start on its head and go right above its eyes.

This looks like a Common Garden Skink (Lampropholis guichenoti)
Further information can be found here and here
The description is a quote from the first source:

The colour of the skin of a common garden skink is mostly a brown-grey colour, and it usually has a black or dark coloured stripe down either side of its body and a copper coloured head. The diet of common garden skinks generally consists of insects and vegetation, and can include caterpillars, spiders, slugs, cockroaches, crickets, worms and ants, and fruit and vegetables. Small and enclosed spaces, such as rocks or trees, are the sought after home for common garden skinks, and they are commonly found in urban gardens, hiding in among plants or leaves. Common garden skinks generally grow to a length of 9 centimetres (3.5 inches), and they have five toes on each of their four legs, as well as a long tail. Common garden skinks can release their tails when caught by predators, such as birds, cats and larger reptiles like snakes.


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What is the max amount of photons per second of the rods and cones in our eyes?
The title says it all. I just cannot find any information about this - I have tried for so long now. Therefore, I figured that I could reach out to some clever guys in this forum for help instead:)
Also, if it is possible, I would love a link to read more about it.

what did you find? It's much better if you show the information that you've found so far, it may help others to know how far you've got and where you're stuck.

Nothing, quite simple :(


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Can blood that has had an anticoagulant added to it be boiled without coagulating?
If I understood the information I've found elsewhere correctly, you can't boil untreated blood without it coagulating, right? But what if you added an anticoagulant to it? Would it be possible to boil that blood or would it coagulate in spite of it? Thank you in advance!

Coagulation, or clotting, is a proteolytic cascade that generates an insoluble fibrin based protein net, or mesh.
Anticoagulants are things like EDTA (?) that chelate divalent cations required for the clotting cascade.
Boiling blood will denature most, if not all, of the soluble serum proteins, forming an insoluble precipitate.  This is structurally different from a blood clot.
Think about what happens to the white part of a chicken egg when you boil (or heat) it.  That is protein denaturation.


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What is the distribution of gene polymorphism levels across human genes?
Of the approximately 19,000 human genes, about how many have one allele that occurs with appreciable frequency in the current human population, how many have two alleles, and so on? (By "appreciable frequency", I mean, say, is found in at least 1% of the population, which seems to be the rule of thumb for classifying a gene as polymorphic in the population.)
I'm not looking for an exact breakdown for every single number of allele variants - I'm just curious, does the typical human gene have only one (frequently found) allele? Or two, as is often implied in elementary genetics texts? Or five, or 10, or 100? What does the approximate distribution look like?
According to the Wikipedia article linked above, the most polymorphic genes known are those coding for the Major Histocompatibility Complex (MHC), with the HLA-B HLA-DRB1 loci having 200 significant alleles, so I guess 200 is the upper end of the spectrum. (Although I don't know whether "the HLA-B HLA-DRB1 loci" refers to a single gene or several, so maybe 200 alleles is higher than any single gene has.)

Also, when Wikipedia says that the MHC genes are "the most polymorphic genes known", do they mean the most polymorphic human genes, or the most polymotphic genes across all species? I would assume that e.g. bacteria display a much higher level of gene polymorphism than humans, because they have a much higher rate of mutations per base pair.

Ah, I might have misunderstood what you are after. Are you interested in 1) the distribution of the number of alleles per locus or in 2) the distribution of frequencies per allele. The second one is the SFS. You can totally consider a SFS for loci that have more than one allele. Although, most often SFS are drawn from SNP data, as such there is rarely more than two alleles at a given SNP.

@Remi.b I'm after distribution (1).

Ok, I've removed most of my comments, then!


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How can a child be blood type AB, if both of the parents are blood type A?
Basically, both of my parents are blood type A (both are confirmed and it's also certain both of them are my biological parents). I recently found out my blood type is AB. How is this possible? I tried reading about different mutations in blood type, but I couldn't find anything that was similar to my case.

Blood type A has a variety of subtypes, which have different features in terms of their antigens. This leads to people with different A subtypes having somewhat different kinds of antibodies in their blood (for a technical article, see here). I don't know the population prevalences well, but I read somewhere (can't find it now) that as many as 20% of blood type A people actually have one of the subtypes. And these are themselves going through their own mutations. It is possible that you have an A subtype of some kind.
Testing blood types usually consists of testing which antigens and antibodies are present in your blood (see e.g. here). So if you have some kind of A subtype that didn't fit well into the blood test's expectations, you might have shown up as AB. I'm not a hematologist or physician, so I'm not sure how plausible that is.
But if you are really interested, you might consider getting a DNA test that will identify which type/sub-type you have, as this will add a different source of information on top of the standard blood test. In the jargon, the standard blood test is for "phenotype" (what are your blood cells actually doing), whereas DNA tests are for "genotype" (what is your DNA sequence). Often genotype and phenotype have less to do with each other than you might expect, or they don't fit in all that well with the cut-and-dried tests. In particular, a lot of medically underserved populations have variation that isn't really accounted for by standard medical typology.
Hope that helps.

Of course this, while possible, overlooks the most obvious cause.  As Homer put it '“My mother,” answered Telemachus, "tells me I am son to Ulysses, but it is a wise child that knows his own father."'

@jamesqf : Well, we have to trust OP: "Basically, both of my parents are blood type A (both are confirmed and it's also certain both of them are my biological parents)". (my emphasis).


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What are the sources of molecular hydrogen in human breath?
In the BBC News article CES 2019: Tech preview of the expo's hottest new gadgets there is a new product that one can use to measure the hydrogen in ones breath, and this is supposed to have some connection to diet:

By contrast, FoodMarble's Aire measures the hydrogen in your breath and combines this with a log of what you have eaten, to warn you of foods you should avoid and possible substitutions.
Aire is designed to discover which foods are being passed to the large intestine without being fully digested

There also exist air quality monitor chips that measure both TVOC (total volatile organic compounds) and "eCO2", where "eCO2" is really a measurement of H2 in the air, and via some electronic algorithm uses it to calculate the expected rate that people are exhaling CO2.
Question: Both of these are examples of interpreting the presence of molecular hydrogen as having some indication that we are alive, breathing and eating. Here I would like to understand the sources of hydrogen in human breath, and how that hydrogen makes it from source to breath.
potentially related: Where does molecular hydrogen in the atmosphere come from?

They explain on their website.

@canadianer Thanks! I'm not sure how to judge the validity of foodmarble.com could you consider writing a short answer and quoting that page? That way other readers can comment and possibly add more information or other sources.

If I have some free time I will. They do link to scientific articles on that website. The gist of it is that this isn’t new technology (all they’ve claimed to have done is make it available to consumers) and it is based on hydrogen fermentation by bacteria in the gut.

@user1136 thank you for the link, and I see what you mean. Pardon me a moment, I'm going to brush my teeth now... ;-)

Hydrogen in breath arises from normal intestinal bacteria, mainly in the colon, which break down (ferment) the undigested nutrients that have passed through the small intestine. Hydrogen is absorbed from the intestine into the blood and exhaled via the lungs.
Conditions in which intestinal bacteria produce hydrogen:

Normal digestion in which soluble dietary fiber is not digested in the small intestine. Examples of soluble fiber: beta-glucan (in oats and barley), pectin (in apples) fructo-oligosaccharides (in red onions), raffinose (in beans), etc.
Lactose intolerance in which lactose remains undigested due to lack of the enzyme lactase (gas is produced mainly after ingesting milk)
Fructose malabsorption in which fructose absorption is reduced due to lack of a certain molecule in the intestinal lining (gas is produced after eating foods high in fructose: apples, pears, honey, agave, etc.)
Sucrose intolerance due to lack of the enzyme that digests sucrose
Small intestinal bacterial overgrowth (SIBO) due to various malabsorptive conditions

Hydrogen breath test is an established method for diagnosing various intestinal disorders. It includes drinking a solution high in certain substance (lactose, fructose..., depending on which disorder is expected) and measuring hydrogen in the exhaled air.
To properly interpret the results of a hydrogen test you need to consider the time in which hydrogen appears in breath after ingestion of a certain substance.
Food Marble provides a relatively thin explanation of their breath test. The question is if this test can distinguish between the hydrogen produced during normal digestion of the soluble fiber and hydrogen produced in the mentioned intestinal disorders.
Business Insider made a review of FoodMarble in which they mention some other reviews...In summary: it's not proven reliable, yet.

Wow, this is a real surprise! Thank you for taking the time to explain all of this and source well.  It looks like the rises are of order tens of ppm, so it's not a profound amount of gas.

The breath tests in hospitals are established and considered reliable, but the results need to be explained by a gastroenterologist. BreathMarble does measure hydrogen, but it is not clear how reliably you can explain the results.

yep I understand. Until now I had no idea of the order of magnitude of the amount, ppt? %? This is very small compared to what I first imagined.

Most of hydrogen goes out of the intestine at the back side... https://en.wikipedia.org/wiki/Flatulence


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Genetics, sickle cell anemia
Sickle cell anemia is autosomal recessive. Then Why is it an example of codominant alleles? I thought a person with sickle cell trait is heterozygous because one of his/her alleles is recessive and the other one is dominant which is not codominant.

Whether alleles are "codominant" or "recessive" or "dominant" depends on the level at which you look at it.
If you look at it from the organismal "healthy vs sick" point of view, then sickle cell anaemia is "recessive" because the individual is only sick when they have both sickle cell alleles.
If you look at it from again the organismal point of view, but this time looking at the trait as well, then you find that (if we say "A" is the anaemic allele and "N" is the normal allele) AN has a different trait (called sickle cell trait) than NN, so you could say the alleles are codominant because both the A and the N "do something" in the heterozygote.
If you look at the molecular level, again you will find that sickle cell anaemia is codominant. The gene codes for the haemoglobin beta gene. So if you have AN, then one of your alleles will be coding for the defective haemoglobin, and the other will be coding for the normal one. So you would have 2 types of haemoglobin in your blood, which means that it is "codominant."


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Should I be concerned about health (bacteria/lice) after having birds fly directly over me?
Yesterday a flock of birds (crows) passed over my head. I've heard that there are many bacteria and lice in the feathers of birds. So I'm thinking about whether to wear or launder the clothes that I wore. What do you recommend I do? Is it ok to wear it again?

Yes, you're fine wearing the same clothes again.

@Remi.b Thank you for you answer, Sorry for asking one more question, But can I ask If you are answering that it's ok because there is no pathogens on my clothes or It's ok because the pathogens on my clothes can't infect me? I'm sorry for making you to answer twice.

I'm answering (commenting actually because I don't think of my comment as a full trustworthy answer) in the sense that most people have birds flying over their heads regularly and no one has never seemed to really suffer from it. You probably don't have any pathogens on your clothes. If you did, those would be crow pathogens, not human pathogens anyway.

@Remi.b Sorry for late reply. I see! Thank you for your additional comment at my a bit vesatious request. Thank you

The situation and context is of some minor importance: Did you encounter the birds in close proximity, such as startling them from the ground and receive a cloud of dust and feathers as they departed? Did they fly dozens or hundreds of meters overhead?
While it's true that many birds have some population of feather lice (Mallophaga), even in healthy birds, they are harmless to humans.1
All animals, including humans, are hosts to vast populations of bacteria. Of these, the majority are innocuous or even necessary or helpful. That said, microorganisms can be the cause of illness and moreso if they are unfamiliar to your immune system.2
Wild animals can be carriers of disease, and one should always exercise caution when handling or working with animals. Getting bitten, scratched, or even removing a carcass from a roadway, for example, has certain risks associated.
Note that most situations where illness or health problems arise usually involve contact with fluids, breaks in your skin, etc. Our skin and immune systems are remarkably efficient at keeping pathogens out or neutralized. Unless you were in direct contact with the animals and/or were injured in some way, or had a sneeze or excretion come your way, you should be fine. (And even if you were in direct contact you would likely still be fine. An injury such as a scratch from a wild animal should be disinfected and monitored.)
References

Temple, S. A. 2001. Form and Function: The External Bird. In Handbook of Bird Biology (S. Podulka, R. Rohrbaugh, Jr., and R. Bonney, eds.) The Cornell Lab of Ornithology. Ithaca, NY.
https://en.wikipedia.org/wiki/Bacteria

Sorry for late choosing the best answer. Thank you for a very specific answer, and your proofreading of the title as well. And well, the crows were right above my head. My question would sound more too much worrying than now If the crows were several hundred meter over my head X) Thank you for your consideration again.


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Does cheese contain cells of animal stomachs?
When cheese is made with calf rennet, is it possible that the cheese contains cells of this calf (stomach)?
Dried and cleaned stomachs of young calves are sliced into small pieces and then put into salt water or whey, together with some vinegar or wine to lower the pH of the solution. After some time (overnight or several days), the solution is filtered. The crude rennet that remains in the filtered solution can then be used to coagulate milk.
Does this filtering exclude all stomach cells of the calf?

Somehow I doubt any whole cells exist after the process, the whole thing seems designed to break living tissues down and to denature protein. That being said calf stomach cells may be tough so +1.

@Duckisaduckisaduck - One would hope it doesn't denature protein. the whole puropse for the sacrifice is to obtain a complex set of enzymes. Denatured enzymes would be useless.

@anongoodnurse My error, I read too much into the adding vinegar part.

I’m voting to close this question because it relates to food analysis rather than a biological problem.

95% of cheese does not use animal rennet.
Many cheeses use no rennet.
Of the cheese that do use rennet the vast majority use rennet derived from bacteria, fungi, or plants. often because it is cheaper, easier, and more humane.
Of cheeses that do use rennet 5-10% of it makes it into the final product, so yes if your cheese uses calf rennet the cheese likely contains calf enzymes.
https://www.vrg.org/journal/vj2008issue3/2008_issue3_update_renet.php

Yes it is possible, filtering is unlikely to be fine enough to remove all cells (though the presence of intact cells based off of the culturing methods is unlikely), note though that modern methods of rennet extraction from stomachs are different than what you described. There are also non-calf rennet made with everything from fungi and bacteria to vegetables. Source

It all depends on the filter. Standard filters for preparations of this sort will be 0.45 micrometers (um), which is definitely smaller than a mammalian cell at 100-300 um, and even smaller than most bacterial cells at 0.5-10 um.

Please post references (ideally to primary literature) that support the part of your answer that is actually relevant to the OPs question. Without that support, your answer is indistinguishable from opinion and thus not a good fit for this site. Thanks.


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Actual definition of cardiac output
Is cardiac output the amount of blood pumped by both ventricles in 1 minute or only by the left ventricle in 1 minute?

Cardiac output is the amount of blood pumped only by the left ventricle, per minute.

Cardiac output (CO) has also been defined as the amount of blood pumped out by each ventricle in one minute. I've seen it both ways. Maybe a source would be good.


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Could deutrium oxide be used to make organic compounds with Deutrium instead of hydrogen?
I am wondering for prokaryotes if Deutrium Oxide could be made into Deutrium Glucose or other biological compounds with Deutrium.

Homework questions are off-topic on Biology unless you have shown your attempt at an answer. For more information see our homework policy. Moreover, this question is not really about biology.

I am sorry that this is not for biology but this is not homework. I am a Freshman in High School. I am currently learning about Meiosis and Genetics. If this is not biology then what would it be? It relates to living organisms, and it ain't physics.

We don't mean homework just in the literal sense. For any query that you have out of interest or as a result of your academic courses, you should make an attempt at finding out the answer yourself with whatever resources that you have and can understand. Did you try simply googling this query? Your query relates to isotope exchange which I would consider a chemistry question. If your query was more about whether organisms can survive and function properly with deuteriated biomolecules, then it may be considered a biological question.

Yes, this is possible and inter alia used to clarify biosynthetic pathways.
For example in this study. Rats were given deuterated water and the average number of D atoms incorporated in cholesterol and fatty acids was determined. Also deuterium was found in plasma glucose and liver lactate and pyruvate.


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Sweating at all temperatures
Is sweating possible if surrounding temperature is below the body temperature? How the sweating occur due to the combustion of food?

Most people most of the time live in the environments that have lower temperatures than it is their normal body temperature (36-37 °C). And most people sweat sometimes at these temperatures.
In the summer, when it is 30 °C and you wear only swimming trunks, even light walking can make you sweat. The same can occur in the winter when the ambiental temperature drops below 0 °C and you wear warm clothes. This is because the muscles, when working, can generate more heat than you need and sweating is the way to get rid some of it.
When you eat food and the food is broken down to release energy, some of this energy will be released as heat. If the food generates more heat than your body needs, eating foods, especially ones high in protein, can make you sweat.
Some people get sweaty after eating certain spicy foods. This is called gustatory sweating, which is not related to food combustion, but it is a neurological phenomenon.
Capsaicin in red hot chili peppers can also trigger heat generation and sweating.
Drinking alcohol dilates the blood vessels in your skin, which results in increased flow of warm blood through your skin, which can signal the thermoreceptors in your skin to trigger sweating.

Indeed, I've been known to work up a good sweat while cross-country skiing in nothing but light pants and a T-shirt.


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Does diamond tblastn exist?
I actually want to use diamond instead of blast because it is faster with small sequences and big genomes, but I actually want to make a tblastn with several protein sequences as queries and the database which will be the genome transformed by makedb.
Do you know if diamond have the tblastn option? I cannot find it.
Thank you.

We welcome new posters to SE Biology, but I must say that the obvious place to ask such a detailed technical question about software that few people will have heard of is on the website or documentation for that software. Failing that, I would email the authors of the paper cited on the website. (If you must post on SE you would be better trying SE Bioinformatics.)

Biostars.org is another very helpful Q/A site for bioinformatics.


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PCR and Semiconservative replication
Why does PCR use heat as opposed to helicase like in semi-conservative replication in order to separate the double DNA strand?

Simply because it is ways more practical and there is no need to use a helicase. Heating is fast and convenient and denaturation is reversible. Also all the DNA is denaturated, so afterwards, primers can bind to their target sites, setting up the start point of the polymerase.
If you want to do this with and helicase, you need to make sure that you have a heat stable polymerase (at least at 72°C), you need to have the right places on the DNA unpackaged and finally, you need two enzymes in the reaction (which is more expensive than just having one).


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Will new proteins incorporating new amino acids trigger an immune response?
This article reported that scientists have succeeded in adding two new bases to the quartet of A, C, G and T, resulting in non-canonical amino acid. Additionally, the bacteria in which this was done were able to produce new proteins using the newly added bases. The article quotes the scientists as saying that the extra amino acids “might become building blocks for new drugs and novel materials”.
My question is that if new proteins are made from amino acids that don’t naturally occur, won’t the body reject them?

The body's mechanism for detecting foreign object has a built-in failsafe that minimizes the likelihood of misinterpreting a self-derived antigen as foreign.

Immunologic tolerance (unresponsiveness) normally prevents reactions
  against self-antigens; if immunologic tolerance is broken, autoimmune
  reactions may occur. Much of the development of tolerance occurs in
  the thymus by the elimination (clonal deletion) or inactivation
  (clonal anergy) of self-reactive clones of T cells. Other mechanisms
  of tolerance occur extrathymically and include activation of
  antigen-specific T suppressor cells and clonal deletion, which results
  in the elimination of self-reactive B cells or T cells, and clonal
  anergy.

https://www.ncbi.nlm.nih.gov/books/NBK7795/
Basically, before a T cell starts looking for potential antigens, it generally first spends some time in the thymus being tested against antigens which are native to the body. If it responds to such an antigen, the T cell will either be destroyed or deactivated.
Having unnatural amino acids as part of this process is unlikely to change its efficacy. T cells which would target peptides with these unnatural amino acids will still be checked against the body's cells before being sent out to do their work; the mechanism would work the same way. I suspect that the rate of autoimmune diseases would be unchanged compared to normal organisms.

@Astrolamb The question asks whether the body will reject proteins containing unnatural amino acids. Your answer focuses on the mechanism of tolerance, indicating that this will continue to operate as normal and that synthetic proteins will be treated by the immune system as non-self, a conclusion that few would disagree with. However it does not address the concern of the poster that synthetic proteins would be rejected by the body, implying that their use as "new drugs" would be doomed to failure. Please provide more information on this point. Does your argument imply rejection or not?

Introduction
This question has two components. The first is the near rhetorical question whether proteins with unnatural amino acids will be considered by the immune system as ‘non-self’. Unless, by chance, the unnatural amino acid resembles some normal macromolecular component, the answer is obviously that it will be regarded as ‘non-self’.
The second question is, to my mind, much more interesting, but does not appear to be considered (or has been taken for granted) in the answer by @Astrolamb. This is whether the immune response would cause such artificial proteins to be eliminated, if  administered therapeutically. It is important, at this juncture, to emphasize that proteins containing unnatural amino acids as the result of expanding the genetic code do not, in principle, raise any problems of immune ‘rejection’ that have not already been seen in ‘unnatural’ proteins containing normal amino acids. Any immune response should therefore be regarded as being to ‘non-self protein’ and rather than to ‘non-self amino acid’.
As there have been many such studies with the latter proteins (and with proteins containing unnatural amino acids introduced by chemical modification) there are extensive studies on which to base an answer. An immunologist would be a better person to do this, but in the absence of any “immune response” I will attempt an answer from my perusal of the literature, leaning particularly on:
K. Wals and H. Ovaa “Unnatural amino acid incorporation in E. coli: current and future applications in the design of therapeutic proteins” Front. Chem 2, 1–12 (2014)
and
B. Leader  et al. “Protein therapeutics: a summary and pharmacological classification” Nature Reviews Drug Discovery 7, 21–39 (2008)
I welcome comments suggesting improvements or corrections.
Summary
The question asks:

“if new proteins are made from amino acids that don’t naturally occur,
  won’t the body reject them?”

which I take to mean:

“if new proteins are made from amino acids that don’t naturally occur,
  won’t they induce an immune response which will render them
  ineffective?”

The brief answer to this is:

It depends — the immunogenicity of foreign proteins varies.
Even if an immune response is elicited this may not necessarily render such proteins ineffective.
In some cases the therapeutic intention is actually to provoke an immune response — to make a weakly immunogenic protein more so.

Foreign proteins vary in immunogenicity
The crux of the answer to this question lies in the following:

The fact that a protein used for therapeutic purposes differs from
  those in a human subject does not in itself mean that it will invoke
  an immune response.

Let us consider two examples to illustrate this.
The first is the case of porcine insulin, which has been administered to patients for many years, but has one amino acid different from human insulin. Regarding such non-human insulin this review states that “severe immunological complications occur rarely, and less severe events affect a small minority of patients”.
The second example is taken from more recent work by D-A. Silva et al. in designing artificial proteins. (See also Nature News & Views summary). They designed mimics of the cytokines, interleukin-2 and interleukin-5, that had extensive differences in helix organization and amino acid sequence from the native proteins. However they reported that “Immunogenicity against the de novo designed proteins appears to be low”.
It turns out that  a wide variety of factors affect the immunogenicity of foreign macromolecules, so that even if a therapeutic protein elicits an immune response it may be weak enough to allow the therapeutic action to occur. In the work just cited, Silva et al. suggest that the reason for the low immunogenicity might be “the small size and high stability” of the proteins on the basis of previous work they had performed with 20,000 mini-proteins.
Admittedly, in some cases a strong immune response will occur and can obviously be a problem, so that measures need to be taken to reduce the immunogenicity. This is widely recognized and discussed in the following paper:
V. Brinks et al. “Immunogenicity of Therapeutic Proteins: The Use of Animal Models” Pharm Res (2011) 28:2379–2385
Sometimes chemical modification of proteins can actually reduce their immunogenicity, as is the case for polyethylene glycol in relation to interferon (B. Leader et al. review, cited above).
Use of therapeutic proteins to provoke an immune response
One use envisaged for modified proteins is in cancer immunotherapy. In brief, the objective is to try to make the body mount an immune response against cancer cells, which may exhibit ‘foreign’ tumour antigens. However, in many cases these differences from normal cells are not sufficient to provoke an adequate immune response. It is has been shown that modifying retinol binding protein by introducing an unnatural amino acid can help overcome the self-tolerance to tumours in mice, suggesting a possible use in cancer immunotherapy  (J. Grünewald et al. “Mechanistic studies of the immunochemical termination of self-tolerance with unnatural amino acids” PNAS (2009) 106, 4337–4342).
Conclusion
Proteins containing unnatural amino acids as the result of expanding the genetic code do not, in principle, raise any problems of immune ‘rejection’ that have not already been seen in ‘unnatural’ proteins containing normal amino acids or chemically modified amino acids. The problem of potential immunogenicity is widely recognized and has been extensively studied by those wishing to develop the considerable therapeutic potential of all such proteins.

This is a lovely answer, and I'm not sure why someone downvoted it.

I think this answer is good, but sort of following from the cleaned up discussion in the comments, the problem I see is that you don't answer the interesting part of the question until your conclusion. The key important concept here, in my opinion, is that Proteins containing unnatural amino acids as the result of expanding the genetic code do not, in principle, raise any problems of immune ‘rejection’ that have not already been seen in ‘unnatural’ proteins containing normal amino acids. If there is an immune response issue, it's with non-self protein, not with non-self amino acids.

@BryanKrause — Thank you for your suggestion. I have edited my answer accordingly.


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What are these tiny, swarming, jumping bugs?
I built a small plywood box in my yard (on Long Island, NY, USA) for some stray cats about a year ago. I didn't bother waterproofing the box, and so over time the box has gotten damp.
About two weeks ago I started seeing small reddish brown bugs on the box, and in the food/water dishes near the box. Can anyone help identify them? Here are some details:

there are 100s of them
they're really small, the biggest ones are about the size of a sesame seed
they jump when disturbed, usually in an upwards direction
they don't seem to go on the cats
some venture 2-4 ft from the box to find food dishes on the ground (concrete patio)
they drown themselves in the water dish by the dozen
they're more active when it's warmer (~ 45°). When it's cold (25-35°) they mostly hide somewhere

All of this makes them sound like fleas,  but they're not fleas -- they don't jump as high or have the flat body of a flea. They actually look like arachnids. OK that makes them sound like baby jumping spiders - but I've seen baby jumping spiders at work, and these look different (they're reddish brown, not black, and they don't jump in an "across" direction, they jump upwards, kind of randomly). Maybe they're a different type of jumping spider, but why haven't they moved on? Why are they taking up residence on the box, instead of spreading out and going their separate ways like baby spiders usually do?
They're are about the size of a sesame seed so it's hard to get a good picture.
EDIT: new picture collage:

Related to: Bug Identification: Tiny Bugs in Fairport NY, Help identifying tiny jumping bug, Can Anyone Identify This Insect?, Taxonomy: Categorising Collembola, What kind of small insect is this?, Unknown aquatic larvae

Very useful image updates! These are actually not arachnids but hexapods called springtails (order Collembola). Although springtails are often very tiny and hard to see without a lens, you happen to find some "larger" specimens. Specifically, these appear to be some species in the family Dicyrtomidae.

 Credit: M. Bertone (source)
Your species resembles the image of Dicyrtomina minuta seen here or Dicyrtomina saundersi seen here (though I can't be certain of these source's accuracy).
In general, springtails usually feed on decaying matter, and -- you guessed it -- they're known for their ability to jump!

Springtails are so-called because they have a unique structure, the furcula, that allows them to jump for considerable distance relative to their tiny size. [source].

 Springing mechanism of a generalized springtail. Credit: Marianne Alleyne [Source]
According to NC State Extension:

Rarely springtails may become exceedingly abundant and may congregate in heaps several inches high on driveways, sidewalks and poolsides.

Collembola.org has many excellent close-up images as well as detailed descriptions of nuances and sexual dimorphism seen in the Dicyrtomina group of springtails.

I found some close-up pictures of similar lookign species here


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What does differential consumption mean?
I have not been able to find any definition of differential consumption online. What does it mean in this quotation?

Vertebrates can influence natural fire regimes in several ways. First, herbivores limit fuel quantity by consuming and recy- cling plant matter that would otherwise accumulate as litter, and by reducing the density of vegetation [3]. Second, differential consumption of plant growth forms can enforce changes in the composition of vegetation and thereby alter the type and arrangement of fuel. Third, herbivory can gen- erate large-scale habitat heterogeneity, as a result of variation in herbivore activity in response to factors such as terrain and water availability [3,11], and this can mean that zones of low and high flammability are interspersed in arrangements that could impede the spread of landscape fires. Finally, herbivores and other animals may alter the abiotic environment in ways that affect flammability: by forming trails, dust-baths or leks, large animals create lines or patches of bare ground that can act as fire breaks, while some species forage by turning over or digging through the litter layer and surface soils, and in the process bury fine fuels and thus reduce fuel loads. In the sections below, we explore the evidence supporting these effects of herbivores on fuel and fire regimes, in the past and present.

Johnson, Christopher N., et al. “Can Trophic Rewilding Reduce the Impact of Fire in a More Flammable World?” Philosophical Transactions of the Royal Society B: Biological Sciences, vol. 373, no. 1761, Dec. 2018, doi:10.1098/rstb.2017.0443

Welcome to SE Biology. I am afraid we cannot answer this question unless you provide us with the context in which you met this term, which might relate to anything from shoppers to livestock. We need a full quotation and source. See the section of our Help entitled Be Specific.

A differential consumption is a difference between two consumption levels. This is all one can tell without a direct quote and a context. I am VTC as unclear.

Thanks for editing your question. It’s allowed @BryanKrause to give you an answer.

Second, differential consumption of plant growth forms can enforce changes in the composition of vegetation and thereby alter the type and arrangement of fuel.

This sentence means that herbivores eat more of certain plant growth forms than others. "Differential consumption" just means "different consumption." This can be important in the context of fire risk because herbivores will tend to not eat certain types of plant biomass, such as full-grown trees, but will eat new growth, grasses, etc (therefore the total amount of fuel by type is different).


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What is difference between light harvesting complex , reaction centre and photosystem
my book says light harvesting Complex are made up of hundred of pigment molecule bound to protein. Is photosystem has all the pigment (except one molecule of chlorophyll A )forming light harvesting complex also called and dinner this pigment help to make photosynthesis more efficient by observing different wavelength of light the single chlorophyll A molecule forms reaction centre.
These things are very confusing for me . I doesn't understand is light harvesting complex is present inside the photosystem or the photosystem is present inside the light harvesting complex.
Is reaction centre not a part of photosystem?