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What is a fungus formally?
Fungi are immotile eukaryotes that do not have chloroplasts or perform photosynthesis. Yet there are other organisms that fit this definition that are not fungi, for example slime molds. What is the formal definition of a fungus? Wiktionary, Wikipedia, and other dictionaries provide informal definitions.

Some fungi produce zoospores, which are motile.

A fungus is formally a fungus, a base divergence of Eukaryote, a plant is a plant. An animal is an animal.

Formal definitions aren't really a thing in Biology or anywhere outside of mathematics.
For cladistics, the closest you will get is that species are arranged based on common ancestry. Fungi are a group of organisms sharing a common ancestor. This is present, not absent, in the definition on Wikipedia:

These and other differences place fungi in a single group of related organisms, named the Eumycota (true fungi or Eumycetes), that share a common ancestor (i.e. they form a monophyletic group), an interpretation that is also strongly supported by molecular phylogenetics.

If you have some organism and you want to convince other biologists that it should or should not be classified as a fungus, you would want to make arguments about its ancestry.
Before modern molecular biology techniques, these groupings were entirely based on phenotype. Linnaeus is the individual most recognized for classifying organisms this way and many of his conventions and groupings are still used today (though many others have changed, as well). Darwin's contribution to biology was recognizing that the groupings based on phenotypic similarity originate from common descent (that is, shared ancestry). But, even with that knowledge, it's possible to make mistakes in classification based on phenotype alone. When you hear about some organism previously classified one way whose classification has changed, it's likely that the previous classification was based on assumed relationship based on phenotype, but molecular phylogenetic methods have since suggested a different ancestry and therefore a different classification is more appropriate. Because we do not have all the ancestors (or, really, any of them) to examine, these relationships have to be inferred.

So if I find a new mold, how am I supposed to know if it's a fungus or something else?

@imrobert New to you, or new to science? How do you know it's a mold? If you're sure it's a mold, for whatever reason, then congratulations, you have a fungus! If it's a slime mold, well, that isn't a mold at all, any more than a bat is a bird.

If I find an organism of any kind that I suspect to be a fungus, how am I supposed to determine whether it is or not...

@imrobert You can probably assume it's a fungus if it shares the phenotypic characteristics of other fungi. It's helpful to know about other types of organisms that you might possibly confuse with a fungus so you can consider or dismiss those alternatives. If you have a key for identifying species, and you can use it to classify what you've observed, you'll have a better answer. If a definitive answer is critical you could sequence the genome and use that to either identify the species or find which known species it is most closely related to.

@imrobert: It might be worth asking a followup question, something like “What phenotypic characteristics distinguish fungi from other similar organisms?”  This answer gives the correct theoretical answer to your original question as written — that the formal definition of fungi is cladistic, not phenotypic.  But asking about distinguishing characteristics is also a valid and important question, and it sounds like that’s more the question you care about and maybe meant to originally ask, you just didn’t quite hit a technically correct phrasing of it.

@PLL I'd like to leave my question open to a cladistic definition but "The monophyletic group where true fungi go" is obviously not a definition

@imrobert "Fungi" is the name for that monophyletic group; that's the definition.

@BryanKrause What defines that monophyletic group?

@imrobert Phylogenetics: common descent. They share an ancestor. That's what "monophyletic" means.

Not liking an answer doesn't make it wrong... Life evolves from previous life. We can organize all life into a "tree" of related organisms. It's useful to name parts of that tree to refer to groups of organisms together. Fungi are one of those groups. There are no features that make something a fungus or not besides being in that related part of the tree. If you find something that seems to share every characteristic you can think of, but then find out it's not actually related, then it's not in that group.

Similarly, if you find a member of that "family tree" of organisms within that group that has some feature that you didn't think any fungus has, you wouldn't declare it "not a fungus", instead you would say "aha, this particular fungus has a new feature we didn't think any fungi had". There is no definition, besides membership in that clade, that describes it and would not change with new discovery.

If you want a definition, here is a not very formal cladistic one: If you found an organism and determine that the most recent common ancestor of that organism and a mushroom is neither your ancestor nor the ancestor of a potato, that organism is a fungus (probably the potato part of the definition can be discarded as redundant).

Thanks guys, I understand the concept of a monophyletic group. My question is, how can I determine if an organism is inside the group Eumycota? If you don't know it's okay

It's hard to be sure.  You need to reconstruct a tree using the available features of that organism and other members of the taxon (and also other non-member), and that features can be of all kinds, although nowadays genetic ones are the most useful when available. From here: https://evolution.berkeley.edu/phylogenetic-systematics/reconstructing-trees-cladistics/reconstructing-trees-parsimony/

Of course, if the organism you found is of a known species or at related to know taxa, it becomes a lot easier. For example, if you found a mushroom with all the parts mushrooms usually have, you can be sure that it's a fungus.

@imrobert You can see my comment above about using phenotype to get a pretty good idea but if a definitive answer is needed you'll need to look at the genome. As far as which phenotypic characteristics, the Wikipedia page you previously rejected is a good place to start (for example the "characteristics" section). Fungi are a huge group with a lot of variety, so it's not as if you'll be able to just check one or two boxes to decide. Like Pere suggests it might make more sense to start more focused e.g. to ask "is this a mushroom?" - if yes, it's a fungus, too.

@BryanKrause "how am I supposed to determine whether it is (a fungus) or not"?  Didn't there used to be books where they asked questions about what you saw, and it sent you to a different page?  Eventually, after X number of questions, you got your answer.  I remember doing this once in high school at an insectarium: catch a bug, and then identify it using a huge book.

@RonJohn Sounds like a "dichotomous key". It's a lot like following a phylogenetic tree: each time the tree branches, there is some characteristic that is different in one branch from the other, though as a practical tool they don't necessarily need to follow phylogeny at all, just go through enough characteristics within a limited group (usually limited by geography as well as overall "type" of organism, a literal tree perhaps). The thing is, fungi are a huge group many many steps removed from the common ancestor, so they don't necessarily look very much like that ancestor.

@RonJohn at the end of the day, the ancestry-based definition means that kind of thing only works as an approximation. If it walks like a duck, talks like a duck, but (e.g.) its DNA tells us its ancestry branched off earlier, when then, its not a duck.

@mbrig in practice, how far does DNA move creatures?  For example, moving the Giant Panda from Ursidae to Ailuridae then back again seems reasonable, but "We thought this was a really weird bat, but DNA says it's really a bird" seems a bit extreme.

@RonJohn I think that's partly a question of how "bad" the initial identification is and partly how close convergent evolution comes. You could imagine that somebody guessing that some Multituberculata is part of Rodentia, but obviously people try not to make that kind of mistake (and its harder when the thing is extinct and you have less evidence to go off of). Maybe more realisticly, I could definitely see some kind of bacteria getting reassigned to Archaea based on DNA, and that's a whole nother domain!

@RonJohn Adding to what mbrig wrote, some initial classifications were extremely wrong (eg: archaea used to be classified as bacteria), and have been revised substantially as various new information is available, and there are still open debates about fairly substantial parts of the overall tree, especially around microorganisms. But, mostly what keeps things consistent are the closer relatives; every time you discover a new bat, you can see how it relates to other bats and that immediately tells you roughly where it falls, you don't have to start from scratch.

does anyone know the genetic data required to classify something as a fungus, or where i can find out?

@imrobert: As per my first comment, I really suggest asking that as a new followup question.  I appreciate your disappointment with this answer — it’s technically absolutely correct, but it’s also kind of a gotcha, saying “you phrased your question technically wrong” and explaining how, but never answering the actual question you wanted an answer to.  But you’re much more likely to get a useful answer by asking a new question, now you know a technically more correct wording for it, rather than going on in comments here.

thanks @PLL i'm going to ask a new question. do you have a suggestion on specific wording to include to make sure i get what i'm looking for in the answers


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How long does therapeutic mRNA last in vivo?
How long does mRNA delivered therapeutically to cells last in the human cell once it's gotten there? I've seen sources say that endogenous mRNA lasts around 8-10 hours in humans, but wasn't sure if anything about the currently used mRNA therapeutics extended their halflife in vivo. For example, some of the COVID vaccines used a human α-globin fragment for one of their UTRs, and similar specifically selected UTRs show up in mRNA therapeutics presumably to enhance either transcription or stability.

This is a very broad question which is unlikely to be answered in this form. Can you please restrict yourself to one question at a time?

@Chris Understood, question scope restricted, thanks

mRNA half-life varies markedly, with a variety of stabilising features (or the reverse). Viral structural RNAs that act as mRNA differ again. Regardless, mRNAs are not transcribed. If you want to know how long a particular viral RNA or a particular vaccine RNA persists, that would be a valid question. Likewise the purpose of introducing particular sequences in vaccines. But at the moment your question seems to me misconceived.

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How does comparing shuffled proteomes to the unshuffled ones help us understand independent protein adaptation?
From 'Protein and DNA Sequence Determinants of Thermophilic Adaptation', by Konstantin B Zeldovich, Igor N Berezovsky and Eugene I Shakhnovich (Published: January 12, 2007 | https://doi.org/10.1371/journal.pcbi.0030005):

Proteins are encoded in the nucleotide sequences of their genes, and
thermal adaptation presumably leads to increased stability of both
proteins and DNA. Therefore, signatures of thermal adaptation in
protein sequences can be due to the specific biases in nucleotide
sequences and vice versa. In other words, one has to explore whether a
specific composition of nucleotide (amino acid) sequences shapes the
content of amino acid (nucleotide) ones, or thermal adaptation of
proteins and DNA (at the level of sequence compositions) are
independent processes.
To resolve this crucial issue, we applied the following logic. If
amino acid biases are a consequence of just nucleotide biases and not
protein adaptation, then proteomes translated from randomly reshuffled
genomes will feature similar “thermal adaptation” trends in amino acid
composition as observed in real proteomes. In contrast, if amino acid
compositions are selected independently, then such control calculation
will result in apparently different amino acid “trends” in randomly
reshuffled genomes than observed in reality.

Can someone explain the logic of these authors in the second paragraph? Because I do not understand.
Firstly, I understand that DNA can adapt somewhat independently from proteins due to codon bias, and protein expression can adapt independently from DNA due to epigenetic factors (epigenetics is not mentioned in the article). However,
how does comparing the amino acid composition of a proteome translated from a randomly shuffled genome to the original, unshuffled proteome provide insights into independent protein adaptation?

I think they explain themselves pretty clearly; think about the two possible scenarios they identify, and how their shuffling experiment will give different results in the two scenarios.

@BryanKrause thanks Bryan I have several times, but I still do not understand how the second scenario in particular suggests what the authors are claiming it suggests. This is probably me at fault, but for some reason I can not understand.

Firstly, the researchers say: "proteomes translated from randomly reshuffled genomes will feature similar “thermal adaptation” trends in amino acid composition as observed in real proteomes", this is only a chance, there is a chance that the thermal adaptation trends will be entirely different. I suspect this is probable, because DNA only has four unique nucleotides, read in codons, if one nucleotide in a codon is changed then the entire amino acid could change. This is why I would actually expect "apparently different amino acid “trends”" in the first scenario.

Furthermore, if the genomes are randomly shuffled, how would this suggest: "In contrast, if amino acid compositions are selected independently, then such control calculation will result in apparently different amino acid “trends” in randomly reshuffled genomes than observed in reality."? I would expect the opposite, if the genome was reshuffled and we observed the same amino acid composition, then I could see how protein adaptation is somehow independent from DNA adaptation, as I would expect the amino acid composition to be different, due to new codons being created by the random DNA shuffle.

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Which planktonic foraminifera are found in both the Arctic and the Antarctic?
I want to investigate the influence of glacial melting on the 18O signature of foraminifera shells. I want to compare the Arctic (which is melting rapidly) and the Antarctic (which has just started melting). For this I need a foraminiferal species that occurs both in the Atlantic in the Arctic and in the Antarctic.
For the Arctic I have found Neogloboquadrina pachyderma and Turborotalita quinqueloba but I don't know if they also occur in the Antarctic. Does anyone have a publication or database on this? It does not have to be the mentioned foraminifera species, it can also be other species.
By the way, we are talking about planktonic foraminifera and not bentonic foraminifera. This means that they must live close to the water surface.
Many thanks :D

Did you come across the FORCIS database?


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How many pyrophosphate groups are released during dinucleotide formation?
I can't seem to fathom how a dinucleotide is formed.
My textbook says that initially both nucleotides have 3 phosphate groups before the join but the formation releases only one pyrophosphate
If dinucleotide formation releases only one pyrophosphate, where did the two phosphates of the upper nucleotides go?
Also does this mean it releases 2 pyrophosphates? How many pyrophosphate are released during trinucleotide formation?

I’ll answer your question if you 1. Give title, author and publication date of your textbook, 2. The title of the chapter and section from which this picture is taken — DNA replication I presume, in prokaryotes or eukaryotes or doesn’t say.? 3. Finish reading the [Tour] — which we can tell you haven’t yet.


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Do nerves grow out from within or in from the skin?
The Question:

Do nerves grow out from within or in from the skin?

Thoughts:
My guess is outwards.
However, I have a vague memory of a study involving frogs that I read about in a pop science book - I forgot which - that took skin from the back & chest of a bunch of frogs, swapped them, then tested their reactions. If I remember correctly, some of the frogs wiped their chest when the skin on their back was stimulated (and/or vice versa). That would suggest that they grow inward from the skin.
Some vaguely formed hypotheses:

Nerves grow inwards from skin.
Nerves grow outwards from, say, the brain.
Some combination of 1. and 2.

Background:
I have no formal training in biology. I read a handful of textbooks on evolution for fun though, like "99% Ape", "Why Evolution is True", and some of Dawkins' work, including "The Selfish Gene".


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What is meant by increased vagal tone?
Smiling ,for example,can stimulate vagus nerve as written in the following quote:

Whether it’s through mindfulness, paced breathing, sports, sex or
simply smiling, increased vagal tone is important for good health and
wellbeing. There is a lot of hype online and some of it may be over
the top. But reduced stress and greater relaxation are safe for
everyone and have positive effects for our body and brain.

In above quote vagus nerve is stimulated by increased vagal tone.
My question is - What is meant by increased vagal tone ? Can pain also stimulate vagus nerve and increase vagal tone ?

Welcome Dheeraj. I'm not sure that this site is the best fit for this question. We have a [psychology.se] sister-site as well as a [medical.se] one. You might want to check them out, but before posting, ensure to take their tour and read their help centres to ensure that your post is on-topic.

@JiminyCricket ok.

Hi, that was supposed to read: [medicalsciences.se] in my previous comment.


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Reverse protein biosynthesis in nature
This is more of a funny question to think about, but I am wondering, theoretically if it is possible in cells to synthesize nucleic acids(DNA, RNA) from proteins.
What might this be useful for and how could it be working?
Good luck and thanks for your time.

In biological systems, the central dogma states that genetic information flows from DNA to RNA to proteins, and the reverse process, synthesizing DNA or RNA from proteins directly within cells, does not occur. It has not been observed, and I doubt some hidden reactions exist, as a lot of enzymes would be necessary for this process. Since we do whole genome sequencing today and also have extensive knowledge about genomes, I think we would have discovered these enzymes. If you think of reverse transcriptase, this has even been discovered before all these methods and data where available.
However, in the realm of theoretical and synthetic biology, scientists have been exploring the possibility of creating artificial biological systems where unconventional processes could take place.
In terms of how it might work, it would require the development of enzymes or chemical processes that would reverse work somehow like the processes necessary for the synthesis of proteins. You would need some enzymes (or reactions) that "read" the protein sequence and have a way of converting it into a DNA or RNA sequence. This has a lot of challenges connected to it, including the specificity (choosing the right sequence for a given amino acid), steric problems (amino acids vary quite a lot in size and charge), the degenerated code (choosing the right codons) as well as the stability of the resulting nucleic acids.


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How many base codes are in DNA? Two or four?
We know there are four bases found in a DNA: adenine (A), cytosine (C), guanine (G), and thymine (T). We also know that A always pairs with T and G always pairs with C. Can we say that the DNA is coded binary with two options: AT and GC?

Your question is not about either genes or the genetic code, so I have removed these tags.

Please explain what you mean by “base code”. It is not a term that means anything to me as a molecular biologist. And then how such a thing (or apparently things are “in DNA”. I have answered your question from what seems a fair interpretation of it. But I really don’t know. And what do you mean by “coded binary”? Does this have a meaning in informatics or have you invented it by analogy with its use in terms of sexual relationships? Please rewrite your question, clarifying these points.

Can we say that the DNA is coded binary with two options: AT and GC?

Sort of, but really in one aspect. DNA is double stranded. It is replicated by splitting the strands apart and generating two new molecules using the existing strands as a template. The binary pairing you point out guarantees that the two new DNA molecules will be faithful copies of the original molecule.
However, replication is only one aspect of DNA. Translation is the conversion of DNA -> mRNA -> protein. Generation of the mRNA from DNA is also governed by the binary pairing, (except that mRNA uses Uracil, so an A in the DNA will be paired with a U in the corresponding mRNA). However, when it comes to generating a protein from the mRNA, each possible triplet of mRNA bases (which corresponds to a triplet of DNA bases) codes to one particular amino acid in the protein. It's this correspondence between triplets of mRNA bases (and the underlying DNA bases) and amino acids that's referred to as the genetic code.

This does not appear to be a question about biology but a semantic question in the realm of information technology. However, the answer is NO.
First, linguistically I would never use the word “coded” to describe or specify the sequence of DNA — which is what the poster appears to wish to do — any more than I would use the word to do likewise for proteins (I would not say that “a protein is coded by 20 amino acids”). The use of the word is poor — you can say “RNA is coded by DNA”. (I prefer to say “DNA encodes RNA”, as it is a single word that only exists as a verb.) But “DNA is composed of four different bases”. Keep the two ideas (template and composition) separate.
From a computational standpoint one can say that a DNA sequence can be described or specified using four characters and hence represented most compactly as a number to the base 4 — a quaternary number. NOT a binary number.
The fact that the poster’s logic is incorrect is simply demonstrated: the single strand of a DNA with the sequence ATGC is not the same as AAGC, TAGC, TTGC, ATGG, ATCG, ATCG etc.
The logical flaw is in an implicit assumption that because the sequence of the second strand is specified unambiguously by that of the first strand this somehow influences the numerical complexity of the first strand. It does not.

Thanks David. Quote: the single strand of a DNA with the sequence ATGC is not the same as AAGC, TAGC, TTGC, ATGG, ATCG, ATCG etc. My question is exactly how is it even possible to have AAGC sequence when we know that A always pairs with T.

Unless it is the case that when talk about ATGC sequence, we are actually talking about the bases on the one side of the DNA, that is complimentary to the TACG sequence on the other side of the DNA. I'm sorry about my poor terminology, I'm quite a stranger in this field.

I saw this and everything is clear now: https://www.youtube.com/watch?v=dijqYyFY1GM


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Are all humans related to one mother and one father?
Are all humans related to one mother and one father ?
What is proof for that?
If that is case,that mean brother and sister reproduce, this is incest, so how population survived?

Welcome to the Biology Stack. Please take a [tour] and visit the [help] for more information on this site and what makes a good question and answer. Please note the requirement for showing us your research into this question as outlined in the homework part of the help section.


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Are there different species that profoundly changed the earth?
In the narration of the first episode of the new Netflix series Life on Our Planet it says that one species (humans) “would go on to change our planet like nothing before.” My immediate thought was the Great Oxidation Event and how cyanobacteria changed the earth in a way far more extreme than anything humans have done.
Are there any other species that have profoundly changed the earth?

It's ironic that cyanobacteria may have ushered in the first ice age, and humans may have done the opposite.


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Twin with one boy and one girl with single placenta
I am 27,male and just become father of twins.
One baby boy and one baby girl.
According to my wife’s medical report both of the babies were sharing a single placenta.
I am not an expert in medical science but through internet I have read that the twins will be either boy or girl.
So is it a rare case that I got a baby boy and a baby girl who were sharing a single placenta?
Just curious to know. If yes then what was the probability of this case?

First and foremost, congratulations!
Yes, it is extremely rare for dizygotic twins (two eggs/zygotes, fraternal) to share a single placenta. This is referred to as monochorionic (one placenta) dizigotic twins (MCDT). This is the rarest of all twins.
It was a well known occurrence in cattle, but until recently not recognized in humans. For this reason, articles you find online will often still state that twins with shared placentas are monozygotic (identical) twins. The rate is influenced by assisted reproductive technology (ART) e.g. IVF, which itself increases the rate of twin births. The exact rate is not known, but it is probably more common than estimated, as more testing is now being done on monochorionic twins.*
This happens because the two placentas happen to implant too closely to each other in the uterus, and sharing a relatively small space grow together to form one whole. The degree to which they grow together is variable.
Without IVF, twin birth (in the US) occurs in about 2% of births, so 1 in 50. Including IVF, twin births increase the total to about 3 in 50 births (numbers vary from country to country). In one study of 31 MCDTs, 87% followed assisted reproductive technology; only about 18% were conceived naturally. So, 18% of (2/100) is about 1 in 250 naturally conceived twin births. If ASR twins are included, it increases, but it's still uncommon.
*In one case, a pair of monochorionic twins were found to be dizigotic at 14 months of age after testing because the parents believed they were not identical.
Unusual Twinning Resulting in Chimerism: A Systematic Review on Monochorionic Dizygotic Twins
Chimerism in monochorionic dizygotic twins: Case study and review


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Was it a mucus or a spider's web? How can a mucus look like a spider's web?
Today I found a small slug, 35-40 mm dangling on a shiny thread from a branch 175 cm above me. I thought that the slug had slid on a spider's web, so I touched it and it instantly snapped and the slug fell on the floor. I think it was wet and was mucus. How can a slug mucus, in 5-12'C, become 2 meters long, 50 microns wide and hold a slug from a branch?

Fascinating, I do not understand why down voting has become more prevalent in this community. Nonetheless, this question pertains to biophysics, materials science and biochemistry. I am by no means an expert in any of these fields. I assume the phenomenon you observed was due to the unique physical and chemical properties of the mucus, as well as the temperature experienced (5-12°C is quite cool) which would have altered the properties of the mucus.

Using Google Scholar, I was able to yield these results: 'The Physical Properties of the Pedal Mucus of the Terrestrial Slug, Ariolimax Columbianus', 'The role of mucus in the locomotion and adhesion of the pulmonate slug, Ariolimax Columbianus', 'Mechanical Properties of Pedal Mucus and Their Consequences for Gastropod Structure and Performance' and 'The role of gastropod pedal mucus in locomotion', which may provide interesting information to your question, but not answer it, such is the nature of science, we can not 'know' something.

Lastly, if you do not have a background in these fields, it can be extremely frustrating trying to read and comprehend scientific articles. This is by convention and in my opinion by mistake, since articles narrow their audience significantly, by lacking explanations of prerequisite concepts and critical background information, and context.  For example, in science often people will tell you that something is, not how we figured out or have reason to believe that it is. Meaning readers can not formulate an idea on the level of human understanding of a specific subject.

This is a separate matter, hopefully someone answer your question by using logic and outlining the limitations of our knowledge on the subject.

Hey thanks a lot for the comments, I will look into it. I just had an idea that the slug gelatin became some kind of organized cylinder of organized organic chemistry called mucins and when I touched it with my hand the dryness and oil of my hand instantly disrupted the organic chemistry and it just exploded like when glass that is under pressure erupts. I was stupid not to examine if the mucus was had conpletely sprung up or if was a web cos I was just confused.


text:
Can anyone identify this bug please
We had just gotten a new kitten from a not great home. It was her second night here, and she was laying on my chest when I noticed that where she had been lying on me was really really itchy. When I looked down I thought I was looking at dust, but it was moving and there must have been like 5 or 6 of them. I can barely see it, they just looked like little brown spots and I'm hoping to god its not bed bugs.
It looks like it has antennae and 6 legs maybe I'm really sorry about how blurry the photos are. The YouTube video is easier to see here (youtube video). I'm not good at identifying insects so please help me.
Thank you!

[

Do they live huge big pimples on you ?
Put the cloth your cat has been on in the freezer overnight first. You can get some "diatoms earth" (I am not sure what the name is in English) as a way to kill a few on your cat before resorting to hardcore chemicals.

Very hard to say definitively from your photos and video. To help with ID, a location in the world, and some indication of the environment where you got your kitten - urban, rural etc, would be helpful. Bed bugs don't tend to remain on the host animal, so I suspect something more like a tick or a mite.

Shes only been here for two days, i got welts after the bugs were on my chest and i found a dead adult in the blanket she came home in, im going through the process of heating and freezing every fabric thing i own because im overly paranoid. We live in a smaller town in the north of Vancouver island and its common here, she also came from an apartment which i know had a problem with bugs and rodents etc.

Not a bed bug. Really grainy video; can't be absolutely sure of anything. If you have any specimens, try to get a higher quality picture. Freeze or put in ethanol one if necessary.

what you have is most likely some type of tick,the best way to get rid of them is to treat your cat using one of the tic repelling products out there,ask your cat`s vet what the recomended treatment are.some of the products can be used to get rid of fleas,ticks and mites at the same time.

May be rat mite - https://en.wikipedia.org/wiki/Ornithonyssus_bacoti
When the tropical rat mite bites its host, it causes an inflammatory reaction to its saliva and then pruritic nonspecific dermatitis, known as rat mite dermatitis.

I agree they look like mites, but a better (more enlarged) photo would help there.  Definitely not ticks and probably not bedbugs, though.


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Monoclonal Antibodies
In this paper, the authors say:

We demonstrate that for a considerable number of eplets, the
antibody-verified status is solely based on polyclonal serum
reactivity of multiparous women or on reactivity of murine mAbs.
Furthermore, we noted that a substantial proportion of patient sera
analyses and human mAb data presented in the HLA Epitope Registry
Database has never been published in a peer-reviewed journal.
Therefore, we tested several unpublished human HLA-specific mAbs by
luminex single antigen beads assay to analyze their HLA reactivity for
eplet antibody verification. Although the majority of analyzed mAbs
indeed verified their assigned eplets, this was not the case for a
number of eplets.

I don't understand how did they have access to the monoclonal antibodies that were published but not in peer-reviewed journal. Surely those authors of non peer-reviewed journals did not ship the antibodies to the authors of this article, right?
Is there something I'm not understanding?

This is not a question about biology but speculation about the provenance of material described in a paper — a question that nobody can answer other than by further speculation.

@David I think this is a reasonable question covering techniques in a biological laboratory. It's very helpful that OP provides enough source material to help answer the question, including a reference to a specific paper. You don't have to answer it.

@BryanKrause I will. It is completely trivial and the only methodology involved would be seem to be navigating a database and sending an email . The poster seems to labour under the misaprehension that it is only possible to obtain antibodies when they are described in a publication. The database is too specialized for me to check, but I imagine that anyone can submit, publication or no, and there are details for each eplet (whatever that may be) deposited by the depositors, including names and institutional addresses, regardless of publication. Protein and Gene databanks work that way.

I believe the eplets are the target of the antibodies (the variable region of the epitope) so whilst we have their sequence I'm afraid we do not have the sequence of the antibodies themselves. But there could be a way that the authors skimmed through the articles of the non-peer reviewed articles in which there might have been description of how to get the antibodies (maybe they could be ordered commercially?).

Update
It was pointed out by OP in a comment that the sequences/structures provided in the db are not antibody but antigen sequences, which I overlooked. Therefore, no clear sequences of the antibodies are provided directly in the db.
Original answer
Your confusion is warranted, given that the authors of the paper simply do not describe how they obtained the antibodies (as far as I can tell, though I only skimmed a few sections).
However, I'll note that many researchers would respond to reasonable request for reagents- specifically if it were publicly reported in a database somewhere, which is not too different from publication (peer review not being necessarily any particular mark of distinction; and presumably there is some minimal vetting before database inclusion).
Furthermore, it does appear that for at least many of the antibodies in that database, either full sequence information is available, or the antibodies can be directly ordered commercially.
In such cases, obtaining antibodies would not be an obstacle (though possibly expensive).

For the "sequence information is available", I'm afraid that's the sequence of the protein targeted. I don't think that's the sequence of the antibody.

@FluidMechanicsPotentialFlows ah I see, sorry I misunderstood the db and assumed that the provided structures were antibodies. I would probably remove your "answered" thing if possible, if not I'll delete the answer.


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Are bacteria members of Kingdom Monera or a separate domain by themselves?
The openstax biology textbook by Rice University says: "For example, after the common beginning of all life, scientists divide organisms into three large categories called domains: Bacteria, Archaea, and Eukarya."
But the latest edition of the Indian biology textbook (grade 11) speaks of a Five Kingdom Classification: Monera, Protista, Fungi, Plantae, and Animalia. It also says: "Bacteria are the sole members of the Kingdom Monera."
Which of these is correct? Are bacteria members of Kingdom Monera or a separate domain by themselves?

A domain is a higher level of organization than a kingdom, so they do not necessarily conflict. Please see this lecture for more context. Wikipedia also describes this at some length. There are additionally other questions on this site that discuss the issue, though none directly seem to answer your question.
The domains were introduced instead of the 5-kingdom model due to molecular work establishing the very very large differences between bacteria, archaea, and all other forms of life to be more representative of the actual biological relationships, and particularly the large molecular differences between the otherwise very similar-seeming archaea and bacteria.
The 5 kingdom are an older, more qualitative and less precise grouping. There are now other models that have a larger number of kingdoms under the domains (which are sometimes called other names like superkingdoms). These kingdom models nest more or less naturally under the domain model.
Of course, all taxonomies are somewhat arbitrary. The domain model is an attempt to make the groupings resemble evolutionary history more, and outward organismal characteristics less.

So, which kingdoms are currently under the domain Eukarya?

@Thomas Did you bother to follow any of the links in Maximilian's answer?


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How do T cells recognise the own bodies's infected cells?
A dendritic cell engulfs an antigen and presents it on its membrane with MHC II. This then binds to an antibody on the membrane of a T cell. It activates the T cell, let's call this X. This X then becomes X1, helper T cell, and X2, cytotoxic T cell.
A B cell with its antibody on its membrane encounters the same antigen and engulfs it. It starts producing IgM (right?). It then presents this antigen with MHC II (or I?), let's call this B cell Y. To the helper T cell, X1, the activated B cell, Y, presents the antigen and MHC II complex to X1 and then the X1 releases cytokines to Y, which then starts producing IgG antibodies (right?).
Now my main question is, what happens to the cytotoxic T cell? It goes and kills the pathogens but how does it know which one is a pathogen? Are the pathogens recognised by simply that the cytotoxic T cell realises that the pathogen has a different MHC? So is the point of the MHCs so that the cytotoxic T cells do not kills their own cells? So do cytotoxic T cells also kill infected cells? But the infected cells have a own body MHC so how does the cytotoxic T cell kill it when it recognises it as the own bodies cell? In other words, how does it recognise it as infected? And why must infected cells be killed anyways? Why not just prevent the pathogen from spreading to other cells? Or I mean do normal healthy cells even present MHCs? Or only the viruses, bacterias, and the infected cells? Is then the dendritic cell also killed since it presents MHC?


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Caffeine tolerance
I researched about caffeine tolerance and found out that regular consumption of coffe can build caffeine tolerance even if it's 1 cup per day, within few days or a week at most. Supposedly the body builds more adenosine receptors to cancel it's effect. My question is, is there any limit to it above which it can't neutralize the effect like a sweet spot say 3 cups which is neither unhealthy nor gets canceled by the body.

Hi and welcome. This question is kind of unanswerable as posed; how strong is the coffee? How large is your cup? These vary from country to country, and even just  how it's brewed matters. Caffeine isn't "neutralized", if it were, it would not work, and absolutely there's a limit to how much one can drink, which is why caffeinism is a thing. Finally, this reads to me as a request for personal medical advice, even though it's not phrased that way.

Maybe I was not very clear, I am not asking a personal health advice or the likes of that. It is a general ques and you are free to assume anything not stated specifically as  it may seem fit to you in  a way that it helps with the ques

I think you want a frequency rather than a quantity, that is, how long do you need to wait between caffeinated beverages so that any tolerance from the previous one has decayed.

No, how much is the upper limit above which the body can't build tolerance.

"The upper limit above which the body can't build tolerance" depends on the frequency too, which is why frequency has been suggested instead of a quantity. You need to know the frequency and the caffeine concentration.

Caffeine has several effects on the human body, and as far as I recall, while some of those things can build up a tolerance, other's can't. This is true even within the brain itself.


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Does communication with new parts of body requires internal changes in brain?
I am not a biological scientist and have low biology knowledges in general, but I want to know some thing.
Most of us probably can't even imagine what it feels the sixth finger to be touched. Because we do not have one. We can't imagine what should we do to move the sixth finger, although we can imagine same for the finger we have.
I can assume, that people with anomaly additional part of body, like finger or even hand, can fully control and feel it, independently and separately from the "trivial" one.
Analogy
Now, let's consider another world for a while. You probably know about USB - it is a protocol for data communication. There can be USB-device with any type of functionality, and USB-port, situated at some another device (PC, for example), where USB-device could be plugged in.
Number of USB ports of some device, where USB-devices could be plugged in (PC, for example) is finite, so if a user already used them, another device can't be used, without changing some PC internals.
But, USB protocol provides a concept of the USB-hub: this is a device, that concentrates multiple usb-devices, it has several USB-ports in the output, that can be used.
So, with such device, user can use even single built-in USB-port with multiple devices. So, although internally, PC provides only one port, the technology itself can provide many devices, without changing internals of host device (PC).
Back to biology
I was thinking: the person, that is born with additional part of body, that completely functionates, can be felt, can be controlled, and the mainly - separately and independently from others, during ontogenesis obtained some "internal", "core" changes somewhere in the brain, or it is just peripheral stuff, i.e. brain provides some analogy of hub functionality?
If second statement is true, that should mean two interesting things:

Theoretically, even for a person born, with 5 fingers we can emulate feelings of the six's finger.
Again, theoretically there can be infinite, or at least pretty big number of degrees of freedom for such feelings.

This is a site in which we attempt to provide objective answers to biological problems faced by our constituency — students and professionals in biology. Your question fails on all criteria. The 100 reputation granted to members of one SE site when posting to another is based on the assumption they are familiar with conduct on SE sites and will respect sites outside their many area of interest. Please do this.

@David, as You write, that my question fails all criteria, I can argue that: 1) why can't I be considered as biology researcher? 2) Why there could not be given objective answer to the question?

@David, 1. Prove that please. Provide the definition of what researcher means, and prove that I do not satisfy the criteria of definition. 2. Because it is not a question - You are wrong from the start. It is question, and it is a question objectively. What does objectivity means? Objectivity - that, which doesn't depends on opinion, on interaction. So, what I wrote is objectively a question, since it satisfies a definition of what question sentence is, and not satisfies what declarative sentence is. What You wrote next is subjectively, since it depends on Your opinion.

I quote "I am not a biological scientist and have low biology knowledges in general".

@David, Fine, I assume, You mean, that since I wrote, that "I am not a biological scientist and have low biology knowledges in general" I could not be a researcher. This statement is wrong, because researcher, for example, according to Cambridge dictionary is: "someone who studies a subject, especially in order to discover new information or reach a new understanding.". If You visit this site tour page, You'll see, that in the middle of the page it is written: "Biology Stack Exchange is a question and answer site for biology researchers, academics, and students" - they are separated.

@David, so if I am not an academic or a student it does not mean, that I could not be a researcher. As for my arguments for Your second complaint (about objective answer), as I can see You did not mention them, so I assume, that You have nothing to oppose.

What types of questions should I avoid asking?. You can either read this and try to understand the modus operandi and ethos of a site on which you are new user, or continue to play the barrack room lawyer or behave as if you had joined an undergraduate debating society. But do make sure you have the last word, which will be easy enough as I have no more to say on this topic.

@David, okay, so we ended up with Your complaints about objectivity and reasearcher. Now You have next. I have read the link You provided, and some further included links. Please quote exact statement that I violated by adding this post, so I could argue, or agree with that.

I think you'd benefit from reading about the concept of "critical periods" - basically, at different times during development, the brain is learning specific tasks, associating sensory stimuli and motor actions and more complex things, as well (like comprehending and producing language). Some of these things are best studied in model organisms where we can take it apart, but you can also watch a lot of this development in human infants since they are born so early relative to their developmental progress. A newborn really has no voluntary muscle control in their limbs and trunk at all. Arms and legs flail wildly, and only over time do their brains learn and refine how to control those limbs.
I would drop the USB analogy entirely, I don't think it's helping you at all in this case.
Experimentally, it's a bit of a challenge to just "add on" new limbs; it's not like you can tape a new digit on a hand because the developmental processes that connect the nervous system to a digit happen while that digit is growing. The nervous system connections are being made at the same time that the limb or digit is growing. However, there has been study of what happens when you take something away: taping digits together, for example, creates a unified representation in the brain. Occluding one eye causes the brain to use the remaining eye for the entire visual cortex. Some of these experiments are described in this Wikipedia article. These experiments tell us something about the relationship between the brain and the rest of the body: brain regions are dedicated to the parts of the body that sensory stimuli and motor connections are available from. They do not have a pre-ordained accounting of exactly how many or where those sources of information are at, when you take away things that are normally present, brain regions are proportionally dedicated to whatever inputs and outputs are available.
Conceptually, rather than thinking about extra parts, all of your same questions apply just as much to what is "normal". There is no evidence that brain development has any assumption built in that there will be 4 limbs or 5 digits on a hand, rather, connections are made with the nervous system as the limbs and digits develop, and these connections carry information between the CNS and sensory neurons and motor neurons, and the brain develops in response to those connections.

I got the third paragraph of the answer, but in the first one, it seems there is some misunderstanding from You, or from me. It seems to me, like You appeal to concept\part of brain not like some deterministic biological machine, but rather to a "personality", something, that learns after being born (sorry, I probably expressed what I wanted to write badly). I meant, as well as You wrote next, that fingers, skin surface on them, anyway (as I understand) at the time baby is born (comes out from mother normally) already are connected to the brain.

Probably we can consider a spine as USB-hub, but I asked rather about something more internal, i.e. brain: where all of the "connections" from body comes from to the brain - is there are kinda like sockets, and all "connections" from different parts of body have dedicated socket for, so they all connected separately, or there is one interface in the brain, where all connections come to, sending data maybe on a queue, or maybe all it ones generate some superposition data signal and brain decodes and selects from it many different "packets"?

And the third thing - I did not consider any specific part of the living, i.e. when the brain (human) is developing, not being born yet, or already being born, but rather when a baby is already born and grown.

@Stdugnd4ikbd I don't know what you mean by "personality", but the way we use the word "personality" in neuroscience and psychology it does not mean "learned after being born". Lots of things that are not personality, including motor control, are learned after being born, but a lot of learning happens before birth, too. "Learning" in a biological sense is all of the "software" that the CNS operates on; it is all learned.

@Stdugnd4ikbd I think you are taking the computer/brain analogy way too far (this is very common, you're not the only one to do it). You will be much better off starting from scratch, reading about brain development and biology, rather than taking everything you know about how a computer works and trying to find the biological equivalent. There's so much different in the architecture that it just won't help beyond an extremely abstract level.

I absolutely agree, that I need to learn something to understand something, however, I consider it as the case, when a generalized question can be ansked, and generalized answer can be given, the way both understand each other. So, summarise: can feelings of additional parts of body, like sixth finger, or generally, any kind of feelings, experience, can be simulated for a grown person, that already walks, talks, works, etc.? Clarify: I am not interested in will it possibly be difficult to achieve or not. I am interested in is it possible or not

(Additional comment) 1. I've just read critical period Wikipedia article, You provide, it was really interesting, but I rather meant "adding new feeling" not naturally, but artificially, "in vitro". Not as the result of natural development, studying, learning, etc., but forcely

So, if consider critical period conception, it seems like USB-hub analogy is not proper, and the correct is that internal "CPU" changes are needed to interact with new "device". Or maybe not, or true is another variation at all. I will read the article once again tomorrow.

@Stdugnd4ikbd What do you mean "simulated for"? In biology we almost never can speak of what is possible versus impossible; it's definitely possible if it's been done before, but can never be said to be impossible, the best that can be said is "hasn't been done". It's hard enough to regain neural control of a limb which has had neural connections severed yet that the CNS is already familiar with, let alone adding a new part, yet at the same time there are many ways we can learn to interact through existing motor systems to entirely new appendages, like a tool or vehicle.

The former (reconnecting a limb) requires plasticity in the periphery: physical neural connections between the CNS and the peripheral appendage. The latter (driving a car, using a new tool) requires plasticity in the brain.


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Can your T lymphocytes be activated by dendritic cells that have different MHC II alleles?
So it is clear that a T cell is activated by a dendritic cell by presenting to the T cell the MHC II and the foreign antigen. This is because T cells are taught to have high affinity for MHC II when bonded to a foreign antigen. Is it true that MHC II molecules never bond with the cells' own proteins? But the MHC I molecules can bond with the cells' own proteins AND with foreign antigens, right?
Are the MHC I types identical in all cells of the human body since all cells in an individual have the same MHC I alleles?
Can our T cells in the lymph nodes be activated by any MHC II type? Or does it have to be a particular type? For example, could a strangers' MHC II type which is different to mine activate my T cells in the lymph nodes? In the Janeways Immunology textbook it says "unless the graft shares at least some HLA alleles with the recipient, the T cells that are selected on host thymic epithelium cannot be activated by graft derived antigen presenting cells". So the answer must be no? Then what are alloreactive T cells?
If it is a no, why is there then transplantation acute rejection? In the same textbook it says "Donor dendritic cells in the graft (in this case a kidney) carry complexes of donor HLA molecules and donor peptides on their surfaces. The dendritic cells are carried via the blood to secondary lymphoid organs (a lymph node is illustrated here), where they move to the T‐cell areas. Here, they activate the recipient’s T lymphocytes, whose receptors can bind specifically to the complexes of allogeneic donor HLA (both class I and class II) in combination with donor peptides. After activation, the effector T cells travel in the blood to the grafted organ, where they attack cells that display the peptide:HLA molecule complexes for which the T cells are specific."
If I understood that correctly, it says that the T cells in the lymph nodes can be activated by MHC II molecules even if they are different from the recipients HLA alleles. But if I understood this incorrectly and it meant that the T cell are only activated if the recipient and donor share HLA alleles, then that makes more sense since it complements the first extract from the textbook that I quoted.
So then why do we try and find the donor that shares the HLA alleles with the recipient if it will lead to this acute rejection? Oh no, I am so confused.
But then could this, again from the same textbook, shine some light "Before naive alloreactive T cells can develop into effector T cells that cause rejection, they must be activated by antigen-presenting cells that express both the allogeneic MHC and co-stimulatory molecules. Organ grafts carry with them antigen-presenting cells of donor origin, sometimes called passenger leukocytes, and these are an important stimulus to alloreactivity". SO THERE ARE ALLOREACTIVE T CELLS? So there are T cells that react to a dendritic cell that do not have the same HLA II alleles? Then going back to the first extract that I quoted, why were the alloreactive T cells taken into use and hence activated (and hence allowed to go kill the infected cells) by the donor dendritic cell even though the dendritic cell has different MHC II alleles?
So the T cells can only recognise the infected cells that have the same HLA I alleles? So they cannot kill infected cells of the donor if those cells have different HLA I alleles? But the T cells can be activated by antigen representing cells of any HLA II allele? And so in transplantation the alloreactive T cells are activated and then go and kill the like cells of the donated tissue? Why is this not taken into use in hematopoietic stem cell transplantation when there is an infection? Apparently in this case the T cells can be activated by any MHC II type of the APCs (or not?) and it can only kill the infected cell with the same HLA I alleles? But then in the acute rejection the T cells can kill cells that have any MHC I type alleles? Yeah, so many conflicting sentences over here, please help...<3
In the attached image it shows that in hematopoietic stem cell transplantation the T cell can be activated by any APC but then in the first extract that I quoted it says otherwise. Images are related and from the same textbook I have been mentioning.


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Any idea what type of hawk this is?

Would like to know what this hawk is. Ground in So Cal

It is most likely a Red-tailed Hawk (Buteo jamaicensis). This is consistent with your location and the general markings on the bird:

The primary feathers are dark on the tips. There are "commas" (dark comma-shaped markings at the base of the primary feathers just under the alula). The patagial area is dark. There is a mottled/dark "belly band." You can sometimes use the "dark head, light crop, dark belly band" to identify Red-tailed Hawks when passing perched birds quickly and you have little other useful clues, such as the tail.
The bird's left leg looks somewhat unusual in this image, but I think this is due to having a bit of a strange posture in the moment. Buteos are not "booted", meaning the leg feathers end at the tarsus (analogous to your heel) which is the first joint above the toes. The right leg is sloping away from the camera position so it is not appearing to show the same length as the left leg.
There's a useful quick guide at Hawk Migration Association of North America that has this guide:

(Source PDF)
I can also highly recommend Hawkwatch International's Raptor ID page. I rely a lot on Jerry Liguori's books, which you can find at Hawkwatch's shop among other places.
Affiliation disclosure: I am an active volunteer of Hawkwatch International.


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How do I assess the conservation of a protein function across different homologs, isoforms, biosimilars?
I am studying toxicology where the presence of a "toxic" function is more important (in context) than a protein's ancestry. After scanning the lit, homology modelling seems to be the best way to infer (via structural conservation of functional domains/motifs) whether a function has been conserved or a protein has a similar action to another. Based on this my questions are:

Is there a better term for "functionally similar" than homolog, isoform, or biosimilar? Homolog implies common ancestry which isn't always the case. Isoform doesn't include homologs which may be the case. Biosimilars is very much tied to pharmaceuticals, which I would prefer to avoid.
Does anyone have any recommendations for models that can indicate/estimate the functional similarity between proteins? I realize this is a long shot, but the closest I have found so far was CSM-Toxin, which predicts toxicity, but doesn't alone the comparison of multiple protein sequences.

All of your three alternatives are unsuitable and should not be used. Spell it out in full, although how similar is similar is the crux of the matter.


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Why in organ transplantation the dendritic cells can activate the T cells but not in hematopoietic stem cell transplantation?
In the both following cases let's consider that the donor has different HLA type from the recipient.
When someones let's say kidney is transplanted into someone that has different HLA alleles, the dendritic cell from the graft goes to the lymph nodes and the T cells recognise that the dendritic cells have a foreign HLA type, hence the T cells are activated and go to kill the cells of the kidney --> rejection
This showed that even different HLA molecules are able to activate the T cells. Then how come in hematopoietic stem cell transplantation, the dendritic cells (during an infection) of the donor which have the donors' HLA type, are not able to activate the T cells of the recipient that has its own HLA type?


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Do multiple alleles undergo crossover?
For a reference, point 3 of this article: https://www.biologydiscussion.com/genetics/multiple-alleles/multiple-alleles-meaning-characteristics-and-examples-genes/35452
According to google Bard and some other sources: Crossing over does not occur among multiple alleles because the alleles are present in the same locus of the homologous chromosome.
But I dont understand why can't they undergo cross over? In my slides of population genetics, it is written as a characterstic of multiple alleles, that is they can't undergo crossover.


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Can human hair, animal fur and birds feather get cancer?
Hair, fur and feather protect skin from cancer(sun UV light).
I am interested can human hair, mammal fur or birds feather get cancer?
(Some migration birds like swifts spent 10 months in year in the air, without landing, but I never heard that birds get feather cancer.)

Hair and feathers are not living tissue, they are just proteins, mostly forms of keratin. Some skin cancers may start in hair follicles.


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qPCR precipitation
I have performed DNA precipitation using two methods on an amplified 194 bp PCR product:

using a PEG method
with just cold 80% ethanol

PEG worked much better for me.
Can the same methods be applied to qPCR products? If not, could someone propose a way of doing that? I am in the exploration stage, and I am trying to learn different experimental techniques.

You need to provide some more information: What is your PEG protocol? How big are the qPCR products you want to precipitate? How much yield do you expect (this can make a big difference in the methods you can apply)?

@Chris thanks for your reply.  To answer your questions. 1) First stage, 1:1 Peg/ PCR Product volume and two washing stages with 75% ethanol. At the end of each stage, I performed spinning at 4oc / 15000rpm for 15 mins, disposing of the supernatant, and finally, letting the pellet dry (open tube lid for 15 mins at room temp). 2) The qpcr product is also 194bp. 3) The yieldiest, the better. I just want to practice.

I would say, in general the answer is yes, with caveats.
Firstly, remember that the optimal amplicon size for qPCR is small, so you can expect lower yields.
Secondly, what is the primer concentration that you use in qPCR? If the primer concentration that you found to be optimal for the purposes of quantification is low, then the amount of the final product will be that much lower, as at some point, qPCR will run out of primers to produce new amplicons.
Thirdly, if you’re using probe-based qPCR, remember that you might have non-specific amplification there that doesn’t show up on the amplification plots, because there is no probe hydrolysis when the non-specific product is amplified. If you’re using DNA-binding dye-based qPCR and your melt curve gives you a single peak, you can be relatively sure that you have just the one PCR product (although, theoretically, you could still have two that just happen to be of the exact same size).
A tip I can offer is that for the precipitation of tiny amounts of DNA (or RNA) it is a good idea to add some molecular biology grade glycogen (or glycoblue, which is glycogen stained blue to make the pellet more visible) – provided your downstream applications aren’t glycogen-sensitive. Although I only used glycogen in isopropanol/ethanol precipitations, I’m not sure whether / how it would interact with PEG.
Hope this helps.


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Storage of bacteria in MgCl2 at 4 degrees
I have a small question to which I am unable to find a proper answer.
Will bacteria in a MgCl2 buffer (or similar solution) at +4 degrees Celsius survive storage for 1-2 days? Or will they die?
What about at -80 degrees Celsius?
I am guessing that they can be stored at -80 degress but not at +4 degrees because they will continue to be metabolically active in the latter scenario but will die as they will have no nutrients to consume.
I would be grateful for your comments and inputs.

Highly dependent on the bacterial species and the buffer composition. Unanswerable in current form. We would need the above to give a sensible answer .

Speaking generally, a cryoprotectant is usually needed when storing bacteria at -80C. Even then, it's normal to see upwards of 90% viability loss with common protectants like glycerol, PEG, and Trehalose. Some bugs will survive for days or even weeks +4C while others will almost completely die off overnight. Some bacteria can even be stored for long periods of time at room temperature with little to no change in the viable population size.


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How long can a hand be submerged in freezing water?
How long can one's hand be submerged in freezing (0°C) water before cell damage starts to occur? What causes the cell damage?
I know exposure to temperatures below freezing can quickly cause frostbite, and a decrease in core temperature can cause hypothermia, but I couldn't find any information on how temperatures just above freezing affect extremities.


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

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

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

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

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

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

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

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

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

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

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

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

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

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


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Does anyone know the name of this insect?
Living in São Paulo, Brazil. Thanks for helping me.

No guarantuee due to the low photo quality, but the habitus of this specimen looks like a weevil (Curculionoidea) to me.
This beetle superfamily has characteristic elbowed (geniculate) antennae and prominent snouts. Their bodies are usually rather compact and robust.
If you still have the specimen, you could check, if you can recognize these characteristics (on the right photo (Hectonichus CC-BY-SA-4.0) is a specimen of the similar-looking genus Polydrusus as comparison):


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Why is tautonymy forbidden in botany?
From Merriam Webster:

tautonym: a taxonomic binomial in which the generic name and specific epithet are alike and which is common in zoology especially to designate a typical form but is forbidden to botany under the International Code of Botanical Nomenclature

(My emphasis)
From basic research on Google I couldn't find a reason as to why this is.
Q: Why is tautonymy permitted in zoological nomenclature but forbidden in botanical nomenclature?

this should be helpful. https://www.jstor.org/stable/1219048

Thanks John, I will look through this. How do you know this is the meeting where they set this rule?

I'm not 100% sure I searched tautonym in the taxon database and it was the latest article discussing them, this one may be more relevent https://onlinelibrary.wiley.com/doi/10.2307/1218008 and Volume19, Issue5 October 1970 Pages 787-788 may be even more relevent but I don't have access to a hard copy. thats why I dropped it as a comment not a na answer.

Short of someone from either one of those committees being on here and seeing the question the answer is "Because we said so".
The respective committees are the authorities on the subject and get to make their own rules, even if they aren't consistent with committees covering similar aspects in other areas of biology.
For those interested, the committees have their rules available online and the ones relevant to the question are 32.1c and 23.4 from the International Code of Nomenclature for Algae, Fungi, and Plants and 23.3.7 (under Chapter 6, Article 23, section 23.3; no direct link possible) for the International Commission on Zoological Nomenclature.

I suspect they said so because they're trying to avoid the way that tautonyms are used to identify the "prototypical" species of a genus, given that there isn't really a fair way to choose a prototype so it'll always be based on some human bias. But I agree it is likely difficult to find any source that explains this rather than just stating the rule.

@BryanKrause quite likely true. In botany at least, type is often indicated by "vulgaris" meaning "the common one" rather than a tautonym, and vulgaris was used in several examples, but I didn't put 2 and 2 together. However, usually a type is the first identified species, which I guess is typically the most common one, but not always, so vulgaris might not be appropriate in all cases

Thanks bob and Bryan, this is helpful. Do the taxonomy commission meetings have public transcripts?

@imrobert No idea; you could try searching their websites.


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Skull of which animal ist it?
Hi someone found this skull in ancient city of iran I'm just curious to find out which animal belongs this skull?

Welcome - if you think that I have given the correct answer, use the check (tick) mark next to my answer to indicate that.

This will be one of the two-toed ungulate mammals (Artiodactyls), I think one of the smaller ones, probably in the family Bovidae, which includes the antelopes and goats as well as cows and sheep.
Furthermore, because the laws of frequency tell us that it is rare to come across a rare species, therefore this is most likely to be a common species. So, what species are common in Iran, that have two horns curved gently towards the back of the skull?
Goat (Capra hircus) or sheep (Ovis aries) are the most likely animals, though I lean towards goats in this case because of the shape and position of the horns.

Having had many goats (of several breeds) and having to guard my rear around some of them, that was the first thing I thought of when I saw that partial skull.


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How come SSBPs in RPA don't bind primers?
I've started reading about the recombinase polymerase amplification (RPA). I'm learning that in RPA, recombinase enzyme binds to primers, then makes them anneal to the complementary target DNA strand, and the displaced strand of DNA is bound by single-strand binding protein (SSBP) to prevent reannealing and promote extension of the bound primer. But how come the primers aren't bound by SSBP thus preventing them being bound by the recombinase? How come it's not recombinase that binds the displaced DNA strand? Materials that I'm reading don't mention anything about adding some kind of recombinase-recognised tags to the primer sequences, how do these two enzymes "know" which single stranded DNA to bind to?

From a 1994 review of E.coli single-stranded binding protein (SSBP) in Annual Reviews of Biochemistry, it would appear that at least 35 nucleotides (nt) of single-stranded DNA are required for binding of SSBP to occur.
From a paper in Trends in Analytical Chemistry  describing recombinase polymerase amplification I read that the first step in the procedure (A, below) is to add the primers to the recombinase, forming a complex between the two, and that it is only at a subsequent stage (D) that SSBP is added.

As the length of primers normally used is also apparently ca. 35 nt, I presume that the length of primer available to the SSBP is less than 35 nt, and it is for this reason that SSBP is unable to bind to it. (In the cartoon there would appear to be no primer available, except, presumably, for the DNA.)
An alternative would be that the recombinase hinders the binding of the SSBP.

Thanks for the reply. Yes, I read that article, but it doesn't actually say that the SSBPs are added at a later stage. They only show up in panel D of the figure because that's where they're relevant, not because that's where they're added. Like the DNA polymerase is not added after the SSBP (panel E). Also, the manuals for commercial RPA kits do not specify that SSBPs are added after the primers, recombinase and template. However, your "less than 35nt" theory does make sense!
And thanks for the edits to my question, but they weren't necessary.

@AndrewRoots — If you found part of my answer helpful you should consider upvoting or accepting it. As regards your opinion that my edits weren't necessary, I provide an explanation of the reasons for such edits on Meta. It is, of course, your prerogative to disregard them, and I do not wish to discuss this matter further.


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What allows ovaries to fuse to form a multiple fruit?
If these ovaries are from different flowers but from a single inflorescence, what makes it possible for these ovaries to fuse or produce a single mass? Furthermore, what exactly is the process of forming a multiple fruit?


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How do male seashorses give birth?
It's a commonly known 'fun fact' that male seahorses are the ones that give birth, but that does not make sense to me. As far as I am aware, the biological definition of male and female relates to their role in reproduction. During the pregnancy a male seahorse has a pouch similar to a uterus and a placenta that contains the embryos, does that not just make it female? How is it still a male seahorse?

Related, possible duplicate: https://biology.stackexchange.com/q/112927/27148

Seahorses are not mammals; only placental mammals have placentas.

https://www.sydney.edu.au/news-opinion/news/2022/09/06/new-research-discovers-the-elaborate-and-unique-way-seahorse-fat.html

If you go on Wikipedia and search for 'female', you will see that the sex defined as female is the one which produces the ovum.
Male seahorses produce sperm cells.
To answer your question in the title, if you search for 'seahorse'on Wikipedia, you will see that the females deposit the eggs in the breeding pouch of the male, who incubates them until they emerge and are released in the water.


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Why is nickel affinity chromatography not used in production of proteins for clinical purposes?
Is there a reason why this specific method of chromatography is not used for extracting proteins that will be used for clinical purposes? I saw an article saying that it could be used in many other biological applications, but my professor told me that it's not used in the specified cases above. What would be the reason for being so? Is it a problem of costs?


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Roses are red ... and have thorns
Just had an unpleasant encounter with a wild rose. Not her fault, should've kept my distance.
Roses are some of the plants that have anatomical defenses (I'm talking about thorns). Well, what transpired was I walked into it and as I was leaving I felt the tug of the thorns. That is to say their morphology was similar to shark teeth (curved backwards towards the gut to prevent prey from escaping), which at some level means rose thorns are designed for a "similar purpose" (offense in a weird sense because roses are not carnivorous, instead of defense like e.g. cacti thorns).
Any good reason why this is the case?

The offense is to day that they are designed really. You probably meant to say that they evolved this way.

@CaroZ, spot on! Why would rose thorns evolve like shark/python teeth instead of like cacti thorns? Turns out rose barbs are technically prickles. Do you know what the difference is between them?

I think the size of the thorns indicate the type of animal they defend against. Like a lot of plants have fur, which is like insect-sized thorns, but roses don't have fur as far as i know. so the thorns are probably mostly to prevent large herbivore predation.  It doesn't seem to deter the deer in my backyard though, they're always licking the thorns with their tongues to get the juicy leaves.  but probably for animals with weaker tongues, the thorns would be quite painful.

They are considered natural defense and they have evolved like that way only: https://www.birdsandblooms.com/gardening/flower-gardening/why-do-roses-have-thorns/ and yes, thorns and prickles are different: https://huntington.org/verso/2020/07/spines-thorns-and-prickles

@NilayGhosh, interesting

I think a good way to think about this is to analogize it to something closer to home.  Imagine if someone approached you with the following hypothesis:

The tread on my tires is there to make sure the car doesn't slip when
it moves.  The bumps on my shower mat are similar in design and so
must serve the same purpose.  Does that mean that shower mats were
originally designed to be mobile?

The flaw in this logic is clear.  The common selective factor here is grip, not motion.  The car needs grip to facilitate motion.  The shower mat needs grip to hold your feet in place.  They share common features because they are doing similar things but for a very different purpose.
Now think of that in reference to the thorns vs shark teeth question.  The shark has curved back teeth so that its prey will get stuck on them, and they can't get away while the shark is chowing down without tearing themselves up even more.  The rose also has curved back thorns so that they will stick into animal skin, but the rose isn't trying to hold you down.  It just doesn't want you to eat it.  But if it uses the same kinds of thorns then, likewise, an animal that gets caught on them is going to tear itself up getting uncaught, which is going to hurt more than it would if the thorn slid right out, making the animal even more averse to that plant in the future.  Both sharp curvy barbs serve to get stuck in your skin and do damage on the way out, but the shark is trying to prevent you from moving, while the rose just "wants" it to hurt.

Arigato gozaimus for the answer, but it still don't make sense to me.


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Postulate that one sex will put more resources into reproduction than the other
What is the name of the idea that because one sex will put more resources into reproduction than the other, that sex will try to minimize the number of mates (choosing the best one) and the other sex will try to maximize the number of mates?

Welcome to SE Biology. Please finish the [Tour] to learn about this site. I have taken the “law” into my own hands, as the term is alien to Biology. Let’s leave it for the physical and mathematical sciences.

I don't know if a named "law", and even where those exist it's a bit misleading to use that term because the things called laws in biology (which describe things that often have many exceptions) are nothing like laws in physics (where finding exceptions would be treated as rewriting our basic knowledge of physics).
Anisogamy means differently sized gametes. That Wikipedia page mentions some papers that discuss reasons that one would expect a tendency (but not guarantee) to evolve anisogamy:

Geoff Parker, Robin Baker, and Vic Smith were the first to provide a mathematical model for the evolution of anisogamy that was consistent with modern evolutionary theory.[4] Their theory was widely accepted but there are alternative hypotheses about the evolution of anisogamy.[9][1]

(1) Lehtonen, J.; Kokko, Hanna; Parker, Geoff A. (October 2016). "What do isogamous organisms teach us about sex and the two sexes?". Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences. 371 (1706). doi:10.1098/rstb.2015.0532. PMC 5031617. PMID 27619696.
(4) Lehtonen, Jussi (2021-03-05). "The Legacy of Parker, Baker and Smith 1972: Gamete Competition, the Evolution of Anisogamy, and Model Robustness". Cells. 10 (3): 573. doi:10.3390/cells10030573. ISSN 2073-4409. PMC 7998237. PMID 33807911.
(9) Majerus, M. E. N. (2003). Sex Wars: Genes, Bacteria, and Biased Sex Ratios. Princeton University Press. pp. 7–8. ISBN 978-0-691-00981-0.

You are probably thinking of Bateman's principle.
It states that since males are capable of producing millions of gametes that are much "cheaper" than female gametes, males maximize their reproductive success by increasing the number of females they mate with. On the other hand, females are limited by the number of eggs they produce.
Following this, the result would be sexual selection, where males compete for the access to females whereas females are more choosy. By doing so, females might maximize the quality of the male they mate with, and potentially the success of their offspring.

Can you please not just drop a link but actually explain something in your answer? This is more a comment.

I'd describe Bateman's principle as explaining why anisogamy should be expected to produce certain characteristics like increases variance among individuals of the smaller gamete sex, rather than explaining why anisogamy exists at all.

But this was not the question though. The person asking was thinking of Bateman's principle. I elaborated instead of providing a simple link.


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How can Clostridium tetani proliferate in relatively minor wounds?
It is often reported (NIH) that some of the most common infections by Clostridium tetani are in minor wounds where, in theory, blood (hence oxygen) supply should not be completely disrupted.
How can this obligate anaerobic bacillus proliferate in such conditions? Are concomitant necrotizing infections (such as, for example, Staphylococcus aureus) to blame?

SE Medical Sciences might be a better fit for this kin of question. In addition, it would improve your question if you cited a reference for your “often reported”.  (Also the number agreement in your question is ungrammatical, but I’ll fix it for you.)

Also, please note that there's a big difference between minor wounds and tetanus-prone wounds. Differentiating between the two will help your question.

Another piece of background information: Even for organisms classified as obligate anaerobes, there can a spectrum of oxygen sensitivity. Some strains of C. difficile can grow in up to 3% oxygen, and this trait may be associated with increased virulence. I don't know of any C. tetani research in this area, but I imagine a similar spectrum of oxygen tolerance exists, enabling some isolates to grow in microaerobic conditions.

Nondisruption of blood supply seems to be a heuristic/rule of thumb/approximation of the survival of oxygen supply to tissue in and around a "minor" wound. What I mean is, it's not a 100% confirmation of persistent oxygenation, especially if we consider every relevant locus at the wound site. Remember we're talking of microbes here and at that scale, anerobic pockets can exist even in the presence of macroscopically visible redness/bleeding/oozing (signs of good circulation) and that's all clostridium tetani needs to proliferate, synthesize and release its deadly toxin.


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The amount of heat produced in muscles. A wrong answer
I'm trying to find how energy is released during muscle contraction. Seeing how no work is being produced, the issue is, after working out how much heat was theoretically produced by the heaviest deadlift. First, to give context, the heaviest deadlift I know of is 502.5 kg. Assuming he lifted it up at a acceleration of .5 m/s^2, we can add the gravitational pull to get a rounded answer of 11 m/s^2. Multiplying by the weight gets 5527.5 N. Assuming he lifted it for 1 meter, we get that in joules. Then, taking that he took a second to lift it, gives an answer of 5527.5 Watts. Now, I know a lot assuming was done to get this answer, but all guessed values were rather small, so it shouldn't effect anything. Not only this, but I read that are muscles are around 25% efficient, so the amount of heat produced would be 16582.5 Watts. That's 16 kilowatts. Maybe its just me, but that seems like way to high an answer. Could someone explain?

A workout where no work is being produced would need to be isometric. Lifting barbells is work.

Welcome to Biology StackExchange! You seem to have slightly confused the basic terms in physics. To lift a weight with mass $m=500 , \rm kg$ for a distance $h=1,m$ up, you need $A=\Delta W_p=mgh = 4900 , \rm J$ of energy. With some rough assumptions, we can say that the muscle efficiency is indeed $25,%$, which means that approximately $3A=15,\rm kJ$ of heat was produced. This heat warmed the body, and also gets transfered to the environment. Note that Watts are units of power, which is $P=A/t$.