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Is there no good way to run the Vienna RNA tools on Windows?
I'm trying to get the Vienna RNA tools (particularly RNAfold) running locally (as opposed to using the web interface--because I have lots of sequences I wish to process in batch mode). On the website, it mentions that there are pre-compiled versions of the software available for all major operating systems, however the site seems to be down. All that's still accessible is the GitHub page with source code access.
From my experience, trying to get large C/C++ projects, that often have quite a few third party dependencies, to compile is a huge pain. And even the Python "version" (really a Python wrapper around the C++ code) doesn't install with pip, despite having a compiler available (and found by pip), there are quite some header files that aren't on my Windows system that it complains about--and I've generally never had a problem with pip not being able to install other Python packages, even ones that are internally mostly C/C++. Even installing Anaconda, then bioconda, and then trying to install "viennarna", it isn't found. I'm beginning to think that these tools are just broken other than on the sorts of workstations on which they were developed, which already have all the necessary dependencies and headers.
Has anyone else managed to get a local install of these tools working?

It think this question is ways better fitted for the bioinformatics community: https://bioinformatics.stackexchange.com/ Shall I migrate it?

I can access the website normally, and I have been using precompiled ViennaRNA on Windows without any problems.

@Chris I didn't know there was a separate bioinformatics community, yes it would be better migrated there.

Against my better nature (I think that this is a question about software, not biology), I offer:
https://www.tbi.univie.ac.at/RNA/#download

This download works for me to get the precompiled packages.
You could also try here (for a few days): davidleader.net/Wienershnitzel/index.html

I have edited the answer to remove the irrelevant pieces Domen is responding to.

And so we are left with the situation that a helpful and correct answer to a question, despite being off-topic, is sitting on -1. And all because I pointed out that most modern bioinformatics is written on and for Unix-type operating systems, which does not include MS Windows but does include another which also has widespread support for consumer software.

That website gives a time out error for me, and has been doing so all week. In fact all of tbi.univie.ac.at is inaccessible for me, not just /RNA or the download page. I can access the Github no problem since it's a separate site but the download links from there only lead back to that site.
If it works for you, then it must be an internet problem outside the site itself.

@biohacker I can also access the page. Unsure what the issue is on your end, I am looking on Firefox. Possibly switch browsers? If the download were smaller, I would simply link you to a version hosted elsewhere.

@biohacker I was using Safari on the Mac, which sometimes has trouble because of Chromocentric websites. Where are you trying to access from? North Korea? I’m in Britain.

@biohacker I wonder if you're on a network where someone has a bit over-aggressively limited which URLs are accessible, perhaps assuming that domains that are not ".com", ".edu", etc, must be hosting sketchy sites.

I'm on Chrome, in the United States. I can access univie.ac.at (which takes me to the main university home page) but not tbi.univie.ac.at. I will try accessing from other locations, but I believe I've tried also at home (where I'm not behind any sort of filter) instead of at work without success. I did manage to find Ivo Hofacker's faculty page by searching starting from the main university homepage, but it doesn't seem to have a link to the software.

@biohacker — I'll download again and mount it on a webpage for download.

@biohacker Try https://davidleader.net/Wienershnitzel/index.html

@David Thanks for that!

Another few options: run Vienna on a virtual machine with a (totally free) installation of linux - basic ones like Ubuntu or Mint are very easy to install. Run on a Linux distro designed to run from USB drives - Puppy linux used to be the goto there, dual boot a linux distro, or (best IMO) run one of the several docker containers for viennaRNA .


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How are on and off bipolar cells of the retina arranged?
In the retina, there are both on and off bipolar cells. But how are they spread out in the retina? Are they so, that there is one of each after one another? Or are there areas where there are clusters of just on bipolar cells and other clusters of only off bipolar cells?

source: Stack Exchange

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Identifying a plant in the botanical garden of Paris
I went to the botanical garden in the "Jardin des Plantes" in Paris. In a glasshouse with the name "Serre de l'histoire des plantes" on the natural history of plants (exhibiting some ancient members of plants like ferns, Cyatheales, etc.), I found the tree-like plant on the picture attached below (the one with grass-like looking "leaves"; unfortunately, I don't have a better picture because it was a bit hidden). There was no sign labelling this particular plant, or at least I was not able to spot any. Does anyone know what type of plant this is? It was rather small, roughly 2 meters in height.

It looks like a bromeliad called spanish moss, perhaps it's related to spanish moss, else it could be very different, a close up zoom of the leaves would be good.

Looks like Casuarina glauca ‘Cousin It’

@PolypipeWrangler thanks for the comment. That looks indeed very similar. But the plant on my picture has a stem, like a tree. On the first picture one can see it a bit.

Given the exhibit was about primitive plants, my best guess is a gnetophyte, most likely a species of Ephedra going on appearances.

@sir-thinksalot is correct. This is an Ephedra species. You can have a look at this PDF to get some spatial orientation - it should be with the Gnetales. You can look which species of Ephedra are known to be cultivated in French botanical gardens via a search on the BGCI database. I couldn't find a public database for the plants of the Jardin des Plantes, and it isn't mentioned on the accompanying MNHN website. If you are really interested, you can drop them a line and ask which species it is.

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What is the simplest known metabolic pathway?
What chemical process that can be defined as "metabolic" is the simplest found in any organism, and are there even simpler theoretical metabolic pathways, that are simpler than any found in known organisms?

How would one objectively identify a metabolic pathway as "simple"? What are the criteria for simplicity?

We don’t do definitions much in biology. Certainly we define our terms in any discussion, but generally in our own terms, rather than by appeal to some authority. “Pathway” is a synthetic human concept — we, not Nature —define the first step and the last step, draw a ring round connected reactions of our choice, and call it a pathway.  Please go back and finish reading the [Tour] to find out what questions are acceptable here, then the Help on asking — particularly the need to provide context. What is the biological problem you are facing. And, as Bryan requested, define your terms.

Trivially: the protonation/deprotonation of water.
This is a process that happens spontaneously without any other inputs or outputs or catalysis under physiological conditions.
It feeds into basically every other biochemical process, and cannot be reduced into any of them.
I really agree with the commenters, so this answer goes to show that your definition is more about how you choose to draw the box around your focal point than it is about how biology works.

I appreciate this answer a lot. While I understand the problem with my intitial framing, I think you were able to see through the inexactitude of my framing and get to the real point of my question. Thank you all for the input on how I can better express and think about my questions, and thank you for trying to see the real question beneath my shortcomings in asking it clearly.

@blacktopshaman don't be too harsh on yourself. this stuff is hard.

This will not wash. The protonation of water is not a metabolic reaction, much less a metabolic pathway. First, metabolic reactions are generally regarded (any hit from a Google search or text book of biochemistry) as enzyme-catalysed reactions reacting on metabolites — chemical intermediates in energy generations, anabolism or elimination of waste products. Water participates in such reactions but is hardly regarded as a metabolite and its ionization does not require catalysis. Similarly, definitions of metabolic pathways refer to reactions in the plural, generally using the word "sequence".


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Is there a reliable method to determine if heat fixation was inadequate before proceeding with further staining steps?
Background
Heat Fixation: Heat fixation is a technique used in bacteriology and other biological sciences to affix bacterial cells or other microorganisms to a microscope slide. This is achieved by carefully passing the slide, smeared with the specimen, through a flame. The heat kills the microorganisms, causing them to stick to the slide. Heat fixation helps to preserve the cellular structures and prevent them from being washed away during subsequent staining procedures.
Simple Staining: Simple staining is a basic microbiological technique used to enhance the visibility of microorganisms under a microscope. It involves the application of a single stain (usually a basic dye) to the specimen, which imparts color to all cells, making them easier to see. This technique is called "simple" because it involves only one staining agent. Simple staining provides contrast between the microorganisms and the background, allowing for better visualization and examination of their morphological features. Examples of basic dyes used in simple staining include crystal violet, methylene blue, and safranin.
Question
Is there a reliable method to determine if heat fixation was inadequate in bacteriology before proceeding with further simple staining steps and microscope inspection?

I work with a teaching group who has looked at this, specifically for the aim of making things easy for undergrad labs in under-resourced countries, where gas and/or Bunsens or alcohol burners might not be available.
It turns out for most commonly used bacteria (E. coli, Staphylococcus, Streptococcus, Bacillus etc.) and on regular glass slides with common stains  such as Gram stain, crystal violet, endospore etc. it is the drying that is most important, heat "fixation" just ensures that it is dry enough to not wash off during the subsequent staining steps. The vast majority of stains contain a step (often involving alcohols) that will kill many of the common pathogenic bacteria adequately for most purposes. The step where you are more likely to contaminate yourself is usually during the picking and spreading on the slide, before the heat fixation anyway.
Thickness of film helps here, if you have a thin film, it will dry quickly and adhere, but a thick layer (which you usually don't want anyway) won't dry adequately, and (assuming using the drop technique, not Coplin jars) acts as a barrier for liquid flow which means it is more likely to wash off during wash steps.
Most bacteria are too small to make out a lot of internal structure with basic stain techniques and using 100x oil immersion objectives.
So; let it dry. Instead of a 10 min wait, this might be a 30 min wait, but it works!


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What kind of moth is this? Why does it have a stinger?

Unfortunately, the moth died before I could photograph it.
The body length is approximately 2-3Inches. It was much bigger than the moths I usually see. And this is the first moth that I have seen which has a stinger. Does anyone know which moth this is?
This moth was found on Sep 16th in Bangalore, India. (Sorry, I missed this information before)

Welcome to the Biology Stack Shobana, please take a [tour] and visit the [help] for more information on this site and how it works. Please also edit your question with where you live in the world, as species present vary quite a bit depending on where you are. A large nearby city or a state, even country might be enough for us to get a good ID.

lots of things are unknown your location and the natur type is two of them.do you know for sure it is a stinger is an other unknown.

@trondhansen : I am guessing it is a stinger, I am not completely sure. It felt hard and sharp.

without knowing what country or region this is from, @shobanas it is hard to make any progress towards an ID

Without information about the origin and/or better quality photos of this moth, it reminds me of and could be a member of the subfamily Arctiinae.
What might look as a stinger, is part of its gential apparatus which is usually more or less retracted into the abdomen. Being not too familiar with moths, I guess it should be - depending on the sex - either the ovipositor or the claspers.


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Does this explanation hold good even in case of Mitotracker red?
When the fluorescence intensity is higher when the depolarization is high?
The more damage to the mitochondria, the more mitochondrial dysfunction and therefore more fluorescence intensity. So, in irradiated cells(), 2, 5, 20Gy); the Mitotracker Fluorescence intensity will be lowest in 0GY and highest in 10 gy.

No, the Mitotracker probes accumulate in active mitochondria, not in ones that are dysfunctional, as mentioned in the product page from Cell Signalling Technologies (emphasis mine):

...with MitoTracker® probes, which passively diffuse across the plasma membrane and accumulate in active mitochondria.


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What is happening to this moth cocoon?
We 'adopt' a catepillar each year and this year I believe we have a Buff Ermine Moth.
It seemed healthy and created a woven cocoon. It was at this point that I found out these moths overwinter.
We put it outside when we started to use the heating again to avoid it drying out.
Within 24hrs of being outside, two hard areas appeared outside the cocoon, actually poking through the dried leaf to which it is attached.
The following day one of these hard objects fell off!
This is completely different to the other catepillars we have observed and I wondered what is going on. Is the catepillar still OK??
Photos attached.
Thanks for your help!
Just to note, the woven cocoon is actually between those two leaves. It's not that clear on the pictures. The cocoon itself seems unaltered.

Maybe it died. Seems kind of like insect abdomen.  But I am not the expert


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Are parasympathetic nerves different from motor and sensory nerves?
So the nerves leaving the spinal cord are either motor or sensory (only?). But what about the cranial nerves? For example, the cranial nerve vagus is a parasympathetic nerve. Are parasympathetic nerves divided into categories of motor or sensory? Or is it just a parasympathetic nerve?
If it is indeed composed of motor and sensory nerves, then what about these nerves coming from the spinal cord? Should they not be of a broader name? Just like nerve vagus is of the parasympathetic nervous system.
So, it goes like this: parasympathetic -> n. vagus -> motor or sensory, right?
What about: ? -> n. median -> motor or sensory

There are many ways to divide and sort peripheral and spinal cord nerves and axons.
One division is into "autonomic" (further divided into sympathetic and parasympathetic) and "somatic" nervous system; the somatic nervous system is the part controlling the skeletal muscles and also involving the somatosensory system: touch/pressure/etc, as well as proprioception and proprioceptive reflexes.
Another division is directional: afferent versus efferent. Afferent nerves/fibers transmit information towards the central nervous system; efferent nerves/fibers transmit information away from the central nervous system, such as to control muscles.
Usually, when I hear "sensory" and "motor" I would assume someone is talking about afferent and efferent parts of the somatic nervous system. They're not necessarily considering the autonomic system at all (there's a bit of a tradition in some subfields in biology/physiology to forget that others exist). But there are also some sources that seem to prefer avoiding introducing the terms afferent and efferent for students and still use sensory and motor. I can't know what is being done in the specific text you're reading.
That doesn't mean that the autonomic part of the nervous system doesn't involve sensory or motor functions, just that "sensory" is often shorthand for "somatosensory" and "motor" shorthand for "skeletal motor".
If you want to talk about nerves within the parasympathetic system (or autonomic more generally) are carrying information into the CNS or out of the CNS, I'd recommend using the words "afferent" or "efferent", though nothing is wrong about calling them sensory and motor, you just want to be clear you are not talking about somatic nervous system functions. Using those terms, cranial nerve X/vagus nerve is primarily made up of both afferent and efferent fibers of the autonomic nervous system.
However, nothing is quite so simple in biology, and the vagus also carries some skeletal muscle efferent fibers and sensory afferents.
For the cranial nerves more generally, I think it's important to recognize that the cranial nerves are not all homologous even though they're numbered in sequence - someone just naively counted all the "pipes" coming out of the brain and ordered them. I would not attempt to generalize among them besides that feature (and even the simple idea that "cranial nerves leave the brain" is a bit suspect!).
Some of the cranial nerves are really no different from the somatic nerves coming out of the spinal cord, they just happen to come out really close to the brain. Others, like the olfactory nerve and optic nerve, are quite special: they don't come out of the brainstem but rather the cerebrum, and arguably the optic nerve doesn't even really leave the brain if you consider that the retina is embryonically brain tissue.
For a quick summary from Sonne J, Lopez-Ojeda W. Neuroanatomy, Cranial Nerve.:

Cranial nerves I (olfactory), II (optic), and VIII (vestibulocochlear) are considered purely afferent. Cranial nerves III (oculomotor), IV (trochlear), VI (abducens), XI (spinal accessory), and XII (hypoglossal) are purely efferent. The remaining cranial nerves, V (trigeminal), VII (facial), IX (glossopharyngeal), and X (vagus), are functionally mixed (sensory and motor).


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Why do we not develop tolerance to endogenous factors?
In pharmacology, we studied the development of tolerance to the therapeutic effects of drugs. It is defined as the diminished response of the body to a drug as an adaptation to its continued presence.
However, the factors like enzymes and hormones (either autocrine, paracrine, or endocrine) are also continuously present throughout the body in a steady state concentration or fluctuating concentrations (depending on the function and homeostatic requirements). So why, and how, does the body not develop tolerance to its own enzymes and hormones?

There's a false premise here. Sometimes we do develop a tolerance for our own enzymes, etc. Obviously, this is not healthy.

I find your question unanswerable without your naming a specific example of a drug to which the body develops tolerance, and a specific example of  a (preferably similar) molecule (what you call a "factor") that you think should invoke a similar tolerance but does not, explaining why think it should. The key to this, in my opinion, is the molecular mechanism for this "tolerance". I suspect you and others may be approaching this from the wrong angle and the question to ask yourself is why should another compound have such a mechanism, not why it lacks this.

Tolerance is just a special case of homeostasis. There definitely is some level of "tolerance" to endogenous substances: down-regulation or desensitization of receptors that are over-activated, negative feedback loops, etc, are ubiquitous in biology.
The mechanisms that manifest as tolerance to exogenous substances are often part of endogenous homeostatic pathways.
Commenter bob1 mentions insulin resistance as a classic case of "endogenous tolerance", and it's quite an important one as it results in type 2 diabetes.
For another example, the most common excitatory neurotransmitter in the brain is glutamate; too much glutamate release or excitatory responses that are too strong result in seizures. There are several pathways that you could consider contributing to "glutamate tolerance", including particular glutamate receptors that downregulate other glutamate receptors: when neurons are exposed to a lot of glutamate at once, they reduce their responsiveness to glutamate in the near future. Failures in this regulatory/tolerance pathway are one cause of epilepsy.
A third generalized example is that of receptor-mediated endocytosis, which can serve to import specific things into the cell when they bind with a receptor, but is also important in regulating the overall strength of signaling pathways. Whether a ligand is exogenous or endogenous, when binding a receptor causes internalization of that receptor there is one fewer receptor available to bind additional ligand.

Bryan “…are often part of endogenous homeostatic pathways”. How many people will have a clue what this means? You work hard for this site. Give it a rest.

The classic example would be insulin resistance. This leads to hyperinsulinemia and can result in type 2 diabetes if the resistance gets too high.

+1. I think a pharmacology student should be able to understand your answer, however I doubt most lay persons will. Please forgive me for explaining it/dumbing it down.

@David "Endogenous" is in the question; "homeostatic/homeostasis" is linked in my answer and also in the OP - I think it's reasonable to expect someone to understand that word or read more until they do; "pathway" is, hopefully, a word that someone studying biology would encounter regularly.

This does not seem to provide a good reason to the actual question. Yes, the body regulates its internal functioning properly to achieve some usually near-optimal -- under the given circumstances -- dynamic balance. But why does it find a balance with endogenous substances, like endogenous opioids, which does not involve developing a tolerance, while a tolerance is developed for synthetic opioids? Saying "it's the usual mechanisms, nothing to see here" does not seem to cut the mustard. (Oh, I see you edited the answer in the meantime. It is a bit more specific now.)

@Peter-ReinstateMonica What makes you think there is not a balance found with synthetic opioids? It may not be the "desired" balance for someone seeking a euphoric drug experience or a physician using opioids for pain relief, of course. And, it may be desirable to have more tolerance than actually observed for some common side effects like constipation.

A balance, yes, but one that involves tolerance. As opposed to the balance found with endogenous opioids. (IIUC the endogenous ones are scrubbed quickly by receptors etc., which is why no tolerance develops. Such specific differences are causal.)

@Peter-ReinstateMonica Here's an example of a paper about tolerance to endogenous opioids: https://link.springer.com/article/10.1186/s40360-017-0193-y They claim evidence that tolerance of NSAID pain relief is mediated through reduced sensitivity to endogenous opioids. So, it isn't that tolerance can't or doesn't occur with response to the endogenous signals. Just that, when everything is "working properly", the body is somewhere near a homeostatic equilibrium. You need to perturb it or find a case of dysfunction to notice the regulation happening.

@David This feels like an appropriately technical answer to a technical question on a technical site. I don't understand what rest you think Bryan is supposed to give.

I suspect that the Emperor is naked. Bryan, just because the poster used an imprecise word, doesn't mean you should. I think this is an unclear question which according to SE policy should not be answered until the poster clarifies (as I comment to him). I respect your work on this site, but expected a hard molecular answer from you. And @fredsbend —  I don't think this is a technical question, but a naive question from a student who should be encouraged to do more preparation and give more precision to his thoughts.

@David The concepts and accompanying jargon make it technical, both vernacularly and technically. A false premise from a learner doesn't change that. If something is specifically wrong in this answer you should focus on that.

@David I don't know, I think the question is a bit naïve to a biology professional, yes, but also insightful for a biology student given how these things are often taught in a biology/pharmacology classroom: it's likely that the concept of tolerance was introduced, and examples given, but the connection was not made between tolerance and regulation within biological systems more broadly. OP noticed that something didn't quite sit right, and asked a question about this conflict in their understanding.

I may be asking a naive question.  But I think the body has some ability to distinguish between foreign and self substances. It would probably perceive a foreign unusual drug as harmful and actually work towards building tolerance to it. A naturally found  substance in the body if useful will not stimulate body to build resistance Right? Otherwise people with allergies wouldn't have to suffer so much

Like the answer below says,  the body regulates endogenous factors so it is not noticed.  I think the body would create new receptors try to undo damage to the old ones and  more to reverse tolerance to something useful produced by the body. Otherwise hormone requirements and production should increase rather largely with age. Right? Insulin resistance is again a counter to what I said so IDK

Chemistry is chemistry. A given chemical is no different depending on how it's produced. Something exogenous might be different because it's in a different place or in a different concentration but otherwise there cannot be any difference in the effect of the same chemical. That doesn't mean that the response to any chemical is to respond less in the future - that's a response to "too much", wherever it's produced. Of course sometimes it's possible to get it "wrong" because our bodies are just chemistry, they don't have the ability to see the future.

Yes thats true. What i meant by foreign was something chemically similar or producing chemically simar effects as a substance produced by the body? Like body will probably promote tolerance, resistance to and removal of a drug but not whatever is it's analogue is in the human body.

@Aurelius Even endogenous neurotransmitters result in a regulatory response the same as tolerance, when they are present at a high concentration or for a long time. That's what I wrote in this answer. I'd suggest trying to grasp this concept rather than assuming it's not true. If you study biology you'll find these regulatory pathways absolutely everywhere. It's a basic defining principle of how biology works. See also the concept of "negative feedback loops".

@Brian Krause's answer is completely correct. I'm only going to simplify it.
Tolerance to drugs develops because the enzymatic pathways (which are already in existence in the body, i.e. "are... endogenous homeostatic pathways") responsible for its metabolism enabling its removal from the body are increased, either by increased rate of metabolism or increased production of the enzyme(s) responsible for the drug's metabolism, etc. One of the most widely known such enzymatic pathways is the Cytochrome P450 pathway. (These are not the only ways tolerance develop, just the easier ways to measure.)
Tolerance to drugs is more noticeable because most drugs are xenobiotic, i.e. substances foreign to the body (or "exogenous substances"), so we must ingest them to get the intended effect, and the effect is noticeable, so when tolerance starts to develop, the dosage must be changed. So it's easy to observe tolerance to drugs. However, substances produced by the body are regulated without our being aware of it, because we're not visibly or otherwise noticeably actively doing anything; our bodies are to constantly compensating for internal processes, e.g. regulating our blood pH, glucose levels, etc. In a healthy individual, this is normal homeostatis, e.g. through positive and negative feedback, up- or down-regulation of substances produces, etc.. You mentioned hormones; thyroxine is a good example. Thyroxine is needed by nearly every cell in the body. The pituitary gland monitors (and controls) blood levels of thyroxine through the production of thyroid stimulating hormone  (TSH) Low levels of thyroxine stimulate the  production of TSH, whereas high levels causes decreased TSH production. of We're just unaware of all the regulation our body does until it overwhelms our ability to maintain homeostasis and becomes a problem of some sort, e.g. hyper/hypothyroidism, T2D (type 2 diabetes.), etc.
Cytochrome P450 Structure, Function and Clinical Significance: A Review
Drug Metabolism
Physiology, Thyroid Stimulating Hormone

Thank you, this is a great companion answer. I think you stated the most important concept for OP to recognize when you write "the effect is noticeable, so when tolerance starts to develop, the dosage must be changed. So it's easy to observe tolerance to drugs". That seems to be the main difference with exogenous factors: they can be changed quickly and the effects observed. If you did the same with synthetic versions of endogenous factors you'd see the same behavior. The distinction is in the presentation of the factor rather than the response of the system.


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Sequence identity and coverage in multiple sequence alignment of proteins
This might be naive since I am very new to the field, but I wonder about the difference between sequence identity and coverage in multiple sequence alignment of proteins. I imagine the calculation would be simple, but I couldn't find strict definitions of these two terms and how they are calculated. Can somebody possibly provide an example showing how these two terms are calculated (preferably sequences with gaps and the terms not being 100%)? Many thanks.

I've never heard the term "coverage" used as in this area, and sequence identity is obvious until you start to deal with sequences of different length, when it is not. So the answer is that different packages will calculate on the basis of what seems reasonable to them. If you are asking about a particular MSA program you need to consult the documentation — or look at the results and work out for yourself what is going on. In extremis you could post an example here. Of more practical interest is "similarity" — scoring for similar amino acids. See posts on this list.

In high-throughput sequencing applications, we will often refer to "coverage" as the number of unique sequence reads (queries) that align to the same region in a reference sequence. This alignment problem is a subproblem of the alignment domain referred to as "local" alignment, and coverage makes sense in this context as a measure of how many local alignments of short sequences map onto some location in a much larger sequence.
However, the multiple sequence alignment context that you are referring to is likely a bit different, where you do not have a reference sequence and instead try to find some maximally good alignment of a set of query inputs. This is sometimes called the "global" alignment problem. Here you could plausibly compute the number of other sequences that have aligned residues at the same positions as some focal sequence. That would be a bit like "coverage".
But I agree with commenter David that measurements like similarity are probably more useful in practice- they will certainly be highly correlated with such a "coverage" measure in any reasonable example I can imagine.
Minor update: pairwise identity is a very simple measure that just measures the number of residues in one sequence that are aligned to identical residues in a second sequence. I'm surprised that you can't find anything on this, but here is one highly technical discussion that probably covers a bunch of cases that you don't care about.


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MSA cluster and MSA depth
I was reading the AlphaFold paper and had difficulty with a couple of terms introduced in the main text of the paper. I asked ChatGPT what these were but I'm not sure that it's accurate.
I had a hard time finding the definitions of an MSA (multiple sequence alignment) cluster and MSA depth. GPT-4 explains that an MSA cluster is a subset of sequences from an overall MSA that are closely related to each other, which seems to be simply the results from clustering analysis on MSA. GPT-4 also defines the MSA depth as the number of sequences in MSA. However, I want to make sure that these definitions are correct and are not just hallucinations from GPT-4.

Please finish reading the [Tour] and the Help on asking questions. Don't use non-standard abbreviations without definition. I have run MSA for years and never heard of GPT-4. Sure, I may be old and out of touch, but very few list members will have heard of it either. Say what it is and provide a link. If you can't find standard definitions for terms, say on Wikipedia, it is likely that there won't be any. Something like "cluster" and "depth" would seem so general that I doubt whether there can be any "correct" definition of them. What are you trying to do that you care?

Where did these terms come from? Are you just reading GPT-4 outputs, or did you find the terms and ask GPT-4 to explain them? If the former, I wouldn't trust the chatbot to understand differences between local/global alignment (see other answer), and thus it is probably mixing a lot of apples and oranges in a nonhelpful way. If the latter, it would be much more useful to see the original source, which we might be able to explain.

Hi @Maximilian Press, thanks for the reply and sorry for not providing more context. I was using AlphaFold and one of the parameters was for specifying the number of MSA clusters, I then asked GPT-4 for its definition. AlphaFold was introduced in this paper for protein structure prediction and is also where I saw the term "MSA depth": https://www.nature.com/articles/s41586-021-03819-2

@Jack: thanks for following up, I edited your question and provided an answer below.

I'd really recommend staying away from ChatGPT and similar for learning for now; these tools are really great at creating plausible text, but they can't cite sources so you can't follow up, and they have no concept of what is "correct" or not, they are just using a statistical model to predict which words should come next in a sequence. That means they can sometimes do a good job of summarizing content that is repeated over and over again in their training set, but also that sometimes it gets mixed up and confuses concepts, misses a negative, or confidently states something absolutely wrong.

For example, if the training data includes phrases like "People think cats are dogs. They are wrong", ChatGPT learns that "cats are dogs" is a reasonable pattern and if you ask it to tell you about cats and dogs it may confidently spit out "Cats are dogs" from that training data.

AlphaFold defines these measures in the supplementary information of the paper, as referenced in the main text.
Generally speaking, a lot of information for these highly condensed papers goes into the supplementary information, and that's the first place to look for more explanation.
MSA depth
Figure S10 legend:

MSA depth is computed by counting the number of non-gap residues for each position in the MSA (using the Neff weighting scheme with a threshold of 80% identity measured on the region that is non-gap in either sequence) and taking the median across residues.

This is not a standard measure, just to be clear.
MSA clustering
There is a section "1.2.7 MSA clustering" in the paper supplement that describes the clustering procedure at some length.
MSA clustering is a fairly standard thing to do, but there are many possible algorithms for deriving clusters, and a large family of implementations of each algorithm. I suggest looking into the field of phylogenetic inference for other examples.


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Would asymmetrically positioned eyes impair vision?
Assuming one eye is 5 cm further down compared to the other, would that somehow change perception if the brain has long enough to deal with that incoming information? For example, if you were born that way, would you be able to do depth perception and binocular vision just as well?

Welcome iwab. You'll notice the "do your research" stipulation in the [ask] section of the [help]. Please show that research. For example, if an eye were positioned in the maxillary sinus instead of the orbital socket, would there be an optic-nerve to connect it to the brain? What about muscles? What do your researches into stereoscopic vision lead you to conclude in this case?

If the eyes have the same distance then they geometric effect is the same. if the eyes were on top of each other, they would have less depth perception information when the person turns and leans their head, and they would have a greated change in depth perception when they are running. It's probably tested on robots, not animals.

Would you be able to do depth perception and binocular vision just as well? This is hypothetical question. Hypothetically, the answer is yes.
The human brain has an amazing ability to adjust to changes to an individual's physical body.  As evidence of this, consider the PD (pupillary distance) when you were born to what it is now.  You have the same brain (in all likelihood), but that distance has undoubtedly increased significantly.  Your vision continues to work exactly as designed.
This amazing flexibility is not limited to homo sapiens.  Some species of actinopterygii are born with eyes on both sides of their head, but develop into fish with both eyes on the same side of their head.  Their ability to hunt does not diminish after this change takes place.


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What is the difference between an immortalized human cell line and a cancerous cell line?
Many cell lines (like CaCo2) are derived from cancerous tissue, and hence, like any other tumor cell, they have an infinite replicative potential. However, many cell lines like HaCaT cells are not cancerous but still have infinite replicative potential.
What makes a spontaneously transformed immortalized non-cancerous cell line different from a cancerous cell line?
What are the key differences in phenotype/genotype/karyotype? How are they different in origin?

"This HaCaT cell line is obviously immortal (>140 passages), has a transformed phenotype in vitro (clonogenic on plastic and in agar) but remains nontumorigenic."
-Normal Keratinization in a Spontaneously Immortalized Aneuploid Human Keratinocyte Cell Line (Boukamp et al., 1988)


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Comparing the role of fathers in different species
In species where the male of the species is involved with the life of his offspring in what species is the role he takes is the same as the role of the mother, and in which species is it overlapping or distinct?

Wikipedia estimates there are 2.16 million described animal species and 7.77 million total. So, it seems an answer to your question is going to be quite long. Can you narrow/focus it a bit more?

Maybe take a quick look at wikipedia to start answering your question.

There was a magnificent book that looked at the role of females in several primate species.  it's not new.  the title is "The Woman that never Evolved" The Author, Sarah Hrdy decided to compare the gender roles of various near relatives to imagine how human societies could have been different.  Hrdy also wrote another book on Motherhood.  I'm sure there are many books on fatherhood but I like starting here for a couple of reasons.
By comparing these diverse primate societies she turned on its head previous generations of primatology that had imagined all near relatives live like humans do with a male hierarchy dictating social structure.  not only did she expand our concept of primate social structures, but she also made a statement that human society could be different.  Which, since then it has changed.
There are many diverse studies looking at male roles in primates but this is a good place to start to look at the roles of males.  Its a good comparative structure.  if you are interested in broader sorts of structures, there are so many species and different families you could start... you would have to pick one i'd think.

thanks so much! i'll get those books

This does seem useful to the OP, but I'm failing to see how it answers the actual question asked.


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Why does activity cause hypoglycaemia in diabetics?
(I'm from the UK so I'll be using mmol/L as units and taking <4.0 as hypoglycaemia.)
I remember being told that I should consume a small amount of sugar or reduce insulin dose sightly to increase blood sugar before any considerable physical activity. Only over the last year or 2 have I had to use this strategy regularly since starting at a gym. I remember being told that it was recommended to be >8.0 before exercise but in my own experience >10.0 is required to avoid hypoglycaemia after exercise. I'm simply asking why this is necessary. If my body does not produce insulin, how does the introduction of physical activity cause my blood sugar to drop? Are my cells absorbing the glucose without insulin? If not where is the glucose going?

While doing physical activity you are using your skeletal muscles. When the skeletal muscles are active i.e. contracting and relaxing during exercise, especially moderate or severe exercise, they (skeletal muscle cells) can take up glucose present in the blood, in the absence of insulin which will be used as a source of energy for the contractile process.
Thus there could be decrease in Blood sugar levels(BSL), i.e. hypoglycemia especially if you are taking insulin or any other tablets to maintain your BSL as you a diabetic. The dosage of these medicines/tablets is determined by assuming that you will be doing routine day to day activities.Any increase in quantum of physical activity such as exercise will result in hypoglycemia i.e. decreased blood sugar level during or after moderate/severe exercise.

Ref. Guyton, Textbook of Physiology.

Glucose is the primary fuel of cells. If you're diabetic and under medication, the doses you receive are calibrated for normal physical activity. If in case you engage in any unusually excessive physical activity, your blood glucose will fall due to two reasons:

The unusual physical activity
The diabetic drugs you're on

This combo of glucose-level-reducing factors may cause your blood sugar to fall to dangerous levels.  In essence the drug dose is too high (relatively) for that particular time you're engaged in unusually strenous physical activity.
In a nondiabetic the glucose level is kept at normal levels by controlling the level of insulin in the body + nondiabetic people's cells are responsive to insulin.
Last I checked, diabetic drugs are intentionally called hypoglycemic agents so that prescribers and patients are aware of the danger.


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What elements are affected when dehydrated?
I know that the blood vessels constrict and there is a decrease in water in the blood. Are there any other elements that increase or decrease when the human body is dehydrated?

When you say "element" what do you mean? It isn't clear from your question, because it seems like you're saying that water is an element, which it isn't (except I suppose in mythology). What efforts have you made to answer this elsewhere? e.g. does this page answer your question?


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If the very first codon of an mRNA strand is a start codon (ie, AUG) does no 5' UTR exist?
Apologies if this is too basic of a question, but from what I've learned all mature mRNA strands have both a 5' and 3' UTR. Normally this is just because the start codon has not appeared yet. However, I was given a complete strand of mRNA where the very first sequence was the AUG codon. Does the translation skip this codon to form a UTR and wait for the second, or does it immediately start translating with no UTR?

Welcome to SE Biology. Please take the time to finish the [Tour. You write “I was given”. By whom? What was it — a real mRNA or just something invented for a student question?  I suspect the latter. But you need to provide us with this context if we are to help you. There are questions about the initiation of eukaryotic (I assume it was this — it’s important to know) protein synthesis on this site. You should check them out. I wonder whether your question should be “are there eukaryotic mRNAs without a 5’ UTR?” Personally I doubt it, but I may be wrong.

It would be a student problem, yes.
The entire (very small) mRNA sequence encoded by the human XAM gene is given
below. The stop codon is capitalized.
5’-augucccauccuuuucaccaggaugggagagguugcuucccucccacauccggcaugcgcauuaUAAaagaugauaauauaaag-3’
The problem looks like this, and as it starts with AUG, I am wondering whether to skip that one to leave a 5' UTR. I apologize for the lack of clarity.

@FK18 There are a few ways of dealing with this - You could look up the gene and decide for yourself; you could BLAST the sequences and various translations and see what turns up.

If it is a student problem then it is just on interpreting the genetic code. I cannot find a human XAM gene and suspect it is entirely fictitious. In any case there can be no justification for missing the first AUG. Real bacterial mRNAs always have at least a ribosomal binding sequence preceding a start AUG, and eukaryotic mRNAs almost always have a cap sequence at the 5' end, where the ribosome binds and scans along to either the first AUG (generally) or a subsequent one. But clearly the question is not about this. This is often the problem with this type of contrived problem.


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Does a tree absorb carbon dioxide only by its outer growth ring?
I'm trying to understand how the amount of carbon-14 isotope is changing in a tree trunk, so I would like to clarify if a tree absorbs carbon dioxide only by its outer growth ring in a current year of its life.

Welcome to SE Biology. Please finish reading the [Tour] to learn about this site. As an apparent non-native English speaker, I advise you to do what I do when writing in a foreign language. Run your text — especially the title — through a spelling and grammar checker before posting. Even if you are highly intelligent and your science is good, simple errors of grammar give a bad impression.

I think you will find that the CO2 is absorbed at the leaf, converted into sugars and then may be stored as carbon. So no Co2 at the trunk.

Do you actually mean to ask about CO2, or about carbon-14?

Thanks to everyone and sorry for my English, I'll try to be more careful with grammar next time.

@BryanKrause, I'm interested in carbon-14. I just know that CO2 contains carbon-14 at a constant percentage.

the outer ring stores carbon from the last growt season but the leaves store a lot too.


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Which species of iron-reducing bacteria are hyper-sensitive to copper?
I would like to know which species of iron-reducing bacteria are inhibited in their iron metabolism by a copper concentration of less than 500 nano moles per litre.
Searching the internet, I can only find Klebsiella/Enterobacter/Aerobacter aerogenes, and I'm not even certain that that is an iron-reducing organism.
According to one reference, there are "other" iron-reducers which are similarly allergic to copper, but it doesn't mention which they might be.
I have done cultures in which iron-reduction appeared to be inhibited by a copper concentration of less than 100 nano moles per litre, and I am trying to identify the organism by a process of elimination.

Presumably these are environmental cultures? If so, work on eliminating the common ones first. You might need to do this by culture and test, though you may also be able to do it through next-gen sequencing and looking at abundance changes between with and without copper. Just because you can't find data on the internet doesn't mean that a particular species isn't inhibited, it might just be that it has never been tested.

Thank you for replying bob1.  The cultures were done in rainwater, though unfortunately I no longer have a sample of the organism.  At the time when I was doing this, I didn't know that iron reducing bacteria existed.

I don't have a list, but copper has a pretty strong antifungal and antibacterial action, at least against pathogenic species.


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How does the primitive streak disappear after gastrulation?
So, I am not a biologist or anything related to the field, but this question is indirectly related to something I am curious about.
I read some articles about the role of the primitive streak in the development of the human embryo. And it says in some of them that after gastrulation, the primitive streak regress caudally or disappears. So, my question is how does it disappear, what happens to the cells that constitute it?
And this might be a little strange, but does it have anything to do with the formation of the coccyx?

Welcome to SE Biology! It can help to take the tour, if you haven't already. It would help to see direct quotes from the articles you refer to and any links/references to such articles. Have you tried e.g. a google search, and if so, what did you find? e.g. wikipedia notes that the primitive streak becomes the mesoderm, the germ layer that gives rise to all bones (including the coccyx).

I am sorry, but I have read the wikipedia page before and I think it doesn't mention that the primitive streak transforms into the mesoderm. It says that after gastrulation, it regresses (which i don't understand where the cells that disappeared have gone) and by day 20, the remaining cells constitute a midline caudal cell mass (which i don't understand what it means either). And by day 26, it has seemingly disappeared(didn't explain how did it disappear). Please if I am missing something point it to me, as I am not a professional.

Fair enough- I did not read closely, and it is not as specific as what I said. Nonetheless, it would be helpful for you to excerpt the relevant sections in your question and explain what you don't understand. I would still suggest further research, for example when I google "primitive streak cell fate" I found articles like this that have a fate map for the primitive streak.

My shot in dark (read the Wiki article): The linea primitiva establishes 1)bilateral symmetry and 2) craniocaudal axis and 3)germ layer formation (gastrulation). I suppose it serves as some kind anatomicochemical landmark which embryonic cells recognize and serves as a cue as to 1. what they should do and 2. where they should do it. Once this function is served, the linea primitiva "disappears". The only features in an adult human that corresponds to the linea primitiva are the vertebral column (structure) and the spinal cord (central nervous system).


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Can a grasshopper jump with so much force that it could rip its leg off if it was stuck?
I live in Colorado Springs, Colorado, USA and I have noticed something interesting while walking and longboarding the many miles of paths of trails in the city. Grasshoppers seem to get stuck quite frequently in sideway cracks. I see this rather frequently, sometimes multiple times in a single walk, in certain areas, during the day. This alone is not interesting, but I suspect it I suspect that at least one of them may have jumped out of their leg, if you will. I'll explain.
First, I am reasonably sure they are stuck, because I can see them try to get away from me, while one leg remains fixed in the crack. Also, I see countless more (sometimes several dozens in those same areas), that appear to have been stuck, but have since been run over by something (bike, scooter, skateboard, etc.) or stepped on. I see VASTLY more grasshoppers smashed on cracks in the sidewalks, than on the flat surfaces of the paths. I counted a small (maybe 100-200 meters, I admit I am bad at estimating distance) stretch of path and counted over 25 smashed in cracks and only 6 on that flat surfaces. And, obviously, the cracks represent only a small fraction of the total area of pavement. So, as I said, I am reasonably sure they are getting stuck. That being said, it is possible the reason so many grasshoppers get killed in the cracks is due to something else. An example I can think of is that they seek nutrients filled within the cracks. Of course, I am not sure why they would be attracted to the cracks, considering the extreme danger, when they are surrounded by vegetation. Are grasshoppers smart enough to recognize a busy and dangerous pathway through their territory? IDK.
However, if they are getting stuck, could they jump out of their legs? My evidence for that is a lot more sparse. I have only a handful of possible clues. First, I have seen a few (maybe 4 or 5) incidents in which the leg was mangled. In a couple, the leg seemed to be dislocated and nonfunctional; the grasshopper would scurry using its other limbs while the nonfunctional leg was stuck, immobile, in the crack at an odd angle. A couple other times I saw what looked to be a pinkish-white "meat" (maybe coagulated blood?) popping out around where the "hip" was, where the leg connected to the thorax. That was on much bigger grasshoppers (like 4"-6" in length).
Finally, a couple days ago, I was walking again and I looked in a crack and I found what I believe to be a grasshopper leg. I pulled the leg out, and I thought it appeared to be missing the foot, so I guessed it was stuck in the crack. I did not have my phone at the time, so I could not take a picture, and I did not even think to bring it home. I just tried to memorize what it looked like, then when I got home, I looked up grasshopper anatomy and I found this GRASSHOPPERS OF WYOMING AND THE WEST by the University of Wyoming. Judging by that drawing on the leg anatomy, the tarsus (everything from the spur down) was missing.

I never planned on asking a stack question, I just let it go until a friend in California mentioned seeing a grasshopper stuck in a crack in Hacienda Heights, California, USA. I do understand there could be other, good explanations for why a grasshopper's leg was left stuck in a crack, such as predation, but from what I remembered, there was that pinkish-white stuff showing at the coxa, so the predator took it off cleanly at the joint, or at least it seemed. I don't know if it was the coxa or just something protruding out of the trochanter after the coxa was ripped off. Or it could have been something protruding from the coxa, I just remember the end tapering down like that in the picture with the reddish-white stuff coming out.
In order to answer whether or not a grasshopper could jump out of its leg, I believe we need to know two things: 1) the amount of force produced by a grasshopper during a jump; and 2) the breaking strength of a grasshopper leg. The first was rather easy. Now, this does come from a University in the UK, (St. Andrews), but I imagine the grasshoppers in America are somewhat similar regarding the amount of force they can produce. If I am wrong about this, please correct me. The figure it gives is about 30 g (which I believe is grams-force and not the unit of acceleration). I am not sure if this is even the correct figure to use, because I am not sure this is the stress the leg feels, or if this is the right unit of measure for reasons I will explain. Even if this is the right figure, is this enough to break a leg off? What does it take to break off a grasshopper's leg?
Well, that is pretty much the question I need answered. I Googled variations of "breaking strength of grasshopper legs" using different variations and synonyms, and the most relevant of which brought up an NIH National Library of Medicine paper Fracture toughness of locust cuticle. The abstract says,

Our results show that the fracture toughness of cuticle in locust hind legs is 4.12 MPa m(1/2) and decreases with desiccation of the cuticle.

Can someone explain what that measurement is? I type "4.12 MPa m(1/2)" into Google, and this comes up:

Is this the conversion to something? How does this play into the 30 grams force that is possible to be produced to by grasshoppers?
Also of note, I found an article on JSTOR (which frustratingly I cannot read, despite having JPASS) which on the Google search page has the following quote:

The grasshopper's leg muscles are so powerful that at maximum tension they can snap the tendons like threads.

Which is also quoted verbatim here without attribution: How strong are grasshoppers? - About Bugs.
One final thing before I summarize, I realize that if a leg were in a degraded state, such as after several attempts at jumping with a limb stuck in the crack, as well as possibly moving around, twisting it, breaking it more, it would take less force, and how much less would depend on the state of degradation. But, would jumping alone be enough to rip its leg clean off?
Okay, so the questions are:
Can a grasshopper jump with such force that it rips a stuck hindleg off, even after repeated attempts?
In order to answer that I believe knowing the answers to some other questions will help :

How should the force applied to the joints of a grasshopper during a jump be measured?

Is the amount of force produced on the ground during a grasshopper's jump, the same as the amount of force experienced on the legs of the grasshopper?

2a) If the legs experience a different force, what forces do they experience?

What is the measurement of force on the ground in the St. Andrews paper? grams-force, g's, something else?

I found that fracture toughness, mentioned in the NIH abstract is measured in Pascal m^(1/2) (pascal square root meter) not just m(1/2). But is this the measurement needed to determine the breaking strength of the leg. I THINK that would be tensile strength, but that is a wild guess.

Could repeated jumping attempts reduce the leg's strength so much as to be ripped off?

5a) Any idea how many jumps it would take to finally rip it off?
5b) Is a grasshopper capable of this effort?
Any help anyone could give would be awesome. This is something I think about whenever I see these poor creatures grasped by what appears to be death's maws. Kinda breaks my heart a little when I see them. Anyways. Thanks.

4.12 MPa m(1/2) is a textual rendering of $4.12, \text{MPa}, \text{m}^{1/2}$. You can guess it from other units where m(-2) appears, and you can read it properly written in the actual pdf article. MPa is of course megapascal. https://journals.biologists.com/jeb/article/215/9/1502/11309/Fracture-toughness-of-locust-cuticle

Yeah, I figured that out when I put that text in Wolfram Alpha. It made more sense. Thank you for that article.


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what does concentric antagonistic areas in the retina mean?
"concentric antagonistic areas seen in retinal and LGN receptive fields." (Source: Neuroscience: Exploring the brain)
So the receptive field of a ganglion cell is either ON or OFF center. What does this "antagonistic area" mean in the ganglion cell receptive field?
I did not know that the surround can be called ON or OFF, I thought it was just the center. Doesn't the OFF and ON for the center stem out from depending whether the bipolar cell in the center is connected to the ganglion cell is either an ON or OFF bipolar cell? The photoreceptors in the surround are connected to the same bipolar cell (image below).

Image sources: https://azretina.sites.arizona.edu/node/241
https://nba.uth.tmc.edu/neuroscience/m/s2/chapter14.html

Antagonistic means opposite/opposing.
The receptive fields have ON and OFF areas that oppose each other; that is, light on the surrounding area has opposite effect of light on the center.
It gets clumsy to always say "on-center off-surround" or "off-center on-surround" to describe bipolar cells or retinal ganglion cells, so when you hear "on" or "on-center" to describe one of these cells, this is just shorthand for "on-center off-surround".


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how many bipolar cells connected to a ganglion cell?
Is it that only one bipolar cell is connected to one ganglion cell (which (ganglion cell) is connected to only one LGN neuron cell)?
I mean if more than one bipolar cell is connected to a ganglion cell, then how can the ganglion cell be ON or OFF center? Because what if two ON center and two OFF center bipolar cells are connected to the ganglion cell? Is the ganglion cell ON center or OFF center? Thanks in advance!


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Chimera generation rate between mouse and other animals
I have a question about the chimera generation rate of the mouse compared with other animals.
Before asking the question, I need to define the following terms:
ES cells: Embryonic stem cells
The procedure of generating chimera mice and other chimera animals should be similar, where I am supposed to do genetic modification, such as gene knockout, on the ES cells and implant them back into the animals' blastocysts. However, I found the following statement interesting:

The mice's chimera generation rate is higher than that of other animals.

and

Where chimera production with ESL cells has been attempted, both the rates and the levels of chimerism are typically much lower than found with murine ES cells."

From Gardner, RL (2014) Pluripotent Stem Cells from Vertebrate Embryos: Present Perspective and Future Challenges.
I am not sure why that is the case. Could anyone kindly give some directions? Thank you.

where did the statement come from? Did it provide a reference?

"Where chimera production with ESL cells has been attempted, both the rates and the levels of chimerism are typically much lower than found with murine ES cells." From Pluripotent Stem Cells from Vertebrate Embryos: Present Perspective and Future Challenges. ESL cells from other animals are very, very similar to murine stem cells. The only difference is the higher nuclear-cytoplasm ratio compared with the murine ES cells.

I am editing your question to include the relevant quotation and citation


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I need help identifying the source of my contamination in my viral titration experiments
I am relatively new to what I'm currently working with and as the title suggests, I am currently having some issues with my experiment (viral titration).
So, what I have been doing is the following:

Seeding cells on a black grenedier 96-well-plate, by extracting cells from culture flasks with Trypsin, counting and diluting them to a sufficient concentration for seeding.

The day after, a virus dilution series was performed in infection medium, and the cells in the grenedier well plate were infected in different concentrations, including negative controls.

After incubation, all the cells were fixed using the reagents: PFA, Methanol, PBS.

After fixing, the plates were stained using a primary, and a secondary antibody attached to a fleurophore. The primary binds to a viral protein of interest. The antibodies were diluted in PBS, and the second one also with Hoechst. The staining was performed with standard conditions, including incubation and washing 3 times with PBS after each antibody. The plate was stored in a fridge over night before analyzing it.

The infection was visualized using a Cytation 5 plate reader.

Now, the issue Im facing is that I have kept seeing some infection flourescence in my negative controls, (which should have un-infected cells only), according to the images which showed the flourescent dye in these wells. I am trying to figure out what I am doing wrong.
I have been pipetting from lowest to highest concentration, when adding media or PBS, and used separate liquid plastic containers for the control-wells and the infected ones, to avoid contamination. I am going to redo it once again using new infection media, in case the old flask had contamination.
But apart from this, what other factors could possibly help explain why I keep seeing flourescence from the secondary antibody in my negative controls? ANY type of mistake I could possibly have been making I would love to have pointed out. Or other factors which could cause contamination in the lab.
Could PBS/the other reagents possibly be contaminated as well?
Could it be I am not washing away secondary antibodies sufficiently?
Any tips would be much appreciated!! :/

Welcome to the biology stack. Please take a [tour] and visit the [help] for more information on this site and how it works.

To answer your question we would need to know a few more experimental details - have you performed titration of these antibodies to determine that they are working as expected? Have you performed any epitope blocking experiments for antibody specificity? Are you using a block of some sort in your staining? Is the 1ry suitable for PFA fixed samples? Is the 1ry antibody suitable for native protein? What controls are you using in your experiments? You should have primary and secondary antibody controls in each plate you run. Why are you using 2 fixatives?

Hello! Let me try answering your questions:

No I havent performed any such titration but my supervisor has and it has worked before for her. She has also said blocking is not necessary. since these antibodies should be specific enough to the virus in question, but what specific type of blocking were you thinking of? I dont think a block is used in the staining, since the primary antobody is specific for a viral protein of interest, and the secondary antibody is specific to the primary.

What do you mean by "1ry"? Primary antibody? And as in "suitable for native protein", are you referring to unspecific binding to other proteins of the cells? They antibody used should be specific enough to the virus Ive been told. The negative controls used are just wells with seeded cells, that have been treated the same, but not infected with any virus. Its the same cells, treated with both the primary and secondary AB. Do you mean I should have controls that have ONLY been treated with the primary OR the secondary AB, respectively? Too see if the 2dry are specific enough for the 1ary?

good, so long as you are using her conditions exactly as she did, this should be fine. Block is used to block non-specific binding of antibodies. It is very very very common that they can bind non-specifically, depending on the conditions used. Secondaries less commonly bind non-specifically. You should have appropriate controls in each experiment you perform to ensure that you can detect these problems if they occur.

1ry = primary. Native protein is that found in cells - not denatured as in western blotting/ SDS PAGE. Many antibodies on the market will work for denatured proteins, but not native, or vice versa, or even occasionally both.  Not all antibodies work on aldehyde fixed proteins, not all on methanol fixed. You should read up on immunocytochemical staining. The controls you need to have until you are certain of your technique are to detect problems in your experimental processes....

... In your case I would recommend that you have for both infected and not-infected cells controls with primary only (tells you if you get signal with no secondary - serious problem, could be caused by many things), and secondary only (non-specific secondary binding, needs optimization in concentration most likely, could be a few other problems). I would also test fixation methods to see what works best for your samples and make sure you read the product information sheet to see what they recommend for concentrations, fixation, binding conditions.

There is no one answer to this still. You will need to work through the conditions and see what your problem is.


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What kind of spider is this please? Southern Indiana. Very strong web

It never comes out during the day so it's been hard to get a decent picture. We have been battling over ownership of my mailbox. It's a house box and every morning it's covered in cobweb from it to the siding or across the top of it if the lid was left up. Very strong web, it takes effort to get it off. I was going to put up a new one with a sealed lid but would kind of like to know if it's poisonous before I go messing about the battle grounds.

Even with lightening your photo:

It is difficult to ID this to genus. If you are only interested in knowing whether it is a medically significant spider, you can rest assured that it is not. The (few) markings and shape of it are enough to rule out widows and recluses.
From its shape and habitus, it is likely a cobweb weaver of some kind (family Theridiidae), but there are many possible choices for genus unless you can get a clearer photo. While black widows are also Theridiidae, the medically-significant female widows have solid black legs while we can see leg banding in this specimen. As @anongoodnurse points out in the comments, the legs here are shorter than a black widow's legs, so I would even rule out a male widow. The abdomen here is rounder shape than the tear-drop abdomen with a tapered end that a widow has. (Similarly, recluses do not have banded legs and do not hang in webs like this Araneoid is. And there are no other medically significant spiders you need to worry about in your geographic area).
The leg banding, general shape, and the slight white marking on the abdomen we can see in the lightened photo make this a little reminiscent of Enoplognatha marmorata (like this one https://bugguide.net/node/view/646186/bgimage). It is very rare to find Enoplognatha indoors.
Here is an example of an E. marmorata found in Indiana: https://www.inaturalist.org/observations/107343897

It would be helpful if you could explain how/why you know it's not a widow-type spider, and even better if you could actually identify the spider. I'm not an arachnophobe by any means, but I would approach this one with some caution, as it's habitus is similar (though the legs don't appear to be as long.) Good answers on this site are backed by sources. Thanks!

@anongoodnurse thanks - added additional info with my best hypothesis of a feasible ID.

The globular abdomen, posture in the web and general shape certainly suggest a Theridiid.  The glossy black body and banded legs are consistent with both the pretty harmless Steatoda species of "False Widows"and their more problematic cousins the Black Widows.  In both cases, the abdominal stripes and leg bands fade to black as the female matures, and while it would be unusual, I bet that having an all-black abdomen and still have traces of the brown banding on the legs is not too uncommon. However, Latrodectus mactans, which I think is the more likely Black Widow species in Indiana, would be expected to still show some of the red spots on the abdomen at this point in its growth. So I'm leaning toward a Steatoda.  Both are noted for strong webs, with the real Widows having a particularly strong silk; the simple ID solution is to check the underside - a real Widow will have the classic red "hourglass" marking, while a Steatoda will not.
The image below is Steatoda grossa, the bigger of the common "False Widows".  Steatoda borealis females commonly feature a white midline on the back, but I'm not sure if the photograph shows a real feature or just an artifact of the flash.


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Is there a way to measure the handicap principle?
The handicap principle is used as an explanation for some genetic traits, such as bright tails in male peacocks. However, it seems that this principle could be used to justify sexual selection of almost any trait. Consider the following examples justifying selection of two opposite traits:

Assuming everything else equal, an individual with a larger body has higher nutritional requirements, which are harder to meet. Therefore individuals with larger body sizes were selected because that signals higher fitness.

Assuming everything else equal, an individual with a smaller body can't protect itself as effectively. Therefore individuals with smaller body sizes were selected because that signals higher fitness.

Does this discredit individual applications of the handicap principle? Or is there a way to measure the extent to which the handicap principle has affected selection of any given trait?

I don't have any expertise in this realm, but I will agree that your example does indicate that at the least, one should be rather careful applying this kind of theory to real data, due to the risk of building a just-so story. I think that a more nuanced view of the principle could argue against your second case, considering e.g. conspicuous consumption, so a strong case would need to engage with that IMO (just as one example).

@MaximilianPress This is more about how one would support the idea that the trait has evolved due to the handicap principle and not something else. Would that require an exhaustive argument considering all possible alternatives?

@rus9384 Yes, more or less. None of these principles occur in isolation so to get the full picture, you need to consider all the relevant factors. Compare "island gigantism" with "island dwarfism" for examples; both are things observed in animal populations on islands - why one way and not the other?

@rus9384 I agree with bob1. If you are arguing for or against a specific instance, you need to include detail from natural history, consider alternate hypotheses, and evaluate each argument in light of available data. The kinds of statements in your question are very difficult to evaluate when isolated from data; there isn't a purely logical solution. You could probably write down some fancy differential equations arguing either way with equal elegance.

@MaximilianPress It's more so that even if, say, handicap principle explains peacock tails, it's not clear if it explains it 100% or maybe there are other factors. So, the expanded question would be "Is there a way to estimate how big of a factor the handicap principle is for a given selected trait?"

@rus9384 Oof, quantitative causal inference in evolutionary reasoning is extremely tricky. In no case will it be 100% one factor. Peacock tails couldn't happen outside of the context of birds, or of having tails, or of feathers, or of pigment biosynthetic pathways. Your best bet would likely be something like comparative method: in the bird lineage, how often did peacock tails arise (or be lost), and can you find correlations with other features indicating "handicap principle"? For one-off cases, it's very hard to make robust arguments.

One recent phylogenetic methods pub: https://academic.oup.com/sysbio/article/67/6/1091/4985805

Let me give two separate answers.
First, for your example specifically, you could design a test to see whether body size has any selective effect from your proposed mechanisms.  There are 4 tests, you'd need to do to establish the hypothesis. First you have to test whether the opposite sex finds your proposed trait attractive.  For example, inject half the animals with growth hormone so they become large and see if the opposite sex prefers them or not.  Second, stunt the growth of half the animals so they become small and again test to see whether the opposite sex actually finds them attractive or not. It's possible the opposite sex won't even notice the difference much less make mating choices based on them.  You need two more experiments to establish the cost of the trait in natural selection.  Test whether larger animals have more trouble surviving harsh winter by measuring the amount of food they each eat and seeing if animals that eat less food actually suffer health consequences.  Maybe they just hibernate an extra week and everything is fine.  Similarly with the small animals, test to see if small animals really do get caught and eaten by predators more often.  Only once you have shown that the trait of interest has a negative effect on the animal's survival but a positive effect on its mating chances, does the handicap principle come into consideration as a possibility.
Unfortunately, before you can come close to concluding that's the reason, you have to look at all the other possibilities.  For example, maybe the reason larger animals have better mating success isn't because they signal being healthy enough to compensate for their size disadvantage.  Instead, if animals grow large BECAUSE they eat lot's of food, then perhaps the opposite sex will select them for mating because the animal sends a signal that they are good at finding food and thus will find a lot of food for the children they have together.  There is often a strong incentive to find a mate that can find enough food for your children.  There could also be genetic linkage between traits that control size and traits that control some other gene of interest.  For example, if the size genes are next to the genes for pheromone emissions, then maybe it's completely by luck that the larger animals also have genes that emit more mating pheromones to attract mates, and actually the opposite sex is selecting on that.  There could also be linkage between the gene for body size and gene for mate preference.  I don't want to write  a super long explanation, so look up "runaway sexual selection."  And of course, there are many, many other possibilities.  For example, the sexy sons hypothesis posits that females will select sexy males not because they find the males attractive, but because other females do.  And they want their own male offspring to be found attractive, so therefore they decide to mate with a male that is considered handsome so that her sons which carry her genes will be able to mate a lot.  And there's a lot of complexity with any specific real world example.
So this brings me to my second answer which is that while it's fun to think about these concepts, and its certainly useful to study these things in terms of being able to explain the natural world. That is, find evidence for the hypotheses, try to find examples, etc.  At the end of the day, I wouldn't put too much stock into these types of considerations.  It takes a lot of work than can actually be done in most cases to prove one specific reason is why a species has its mating habits, and once you do prove it, so what?  It was all just random to begin with, and other times, other random things will happen, so its not too impressive to say "hey, this time the random thing that happened is the handicap principle because of all these interesting reasons, circumstances, and coincidences."  Biology is a very unsophisticated science, and evolution (my area of expertise) is probably the least sophisticated of all the fields within biology, so as long as you don't buy into these theories hook line and sinker, you can have a lot of fun bullshitting about what might or might not be and even trying to actually test these things when possible (which it usually isn't; I mean who's cruel enough to inject animals with growth hormone just to see if the opposite sex finds them more attractive?)

Does this discredit individual applications of the handicap
principle?

Both support the handicap principle.

Or is there a way to measure the extent to which the handicap
principle has affected selection of any given trait?

No, there is not a good way to do this yet.


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Does Dr. Sinclair's Epigenome Resetting in ICE Mice Also Repair Telomere Length?"
Dr. Sinclair's team at Harvard University has published a paper this year on rejuvenating ICE mice by reprogramming cells to reset the epigenome. Does this cellular reprogramming also repair the length of telomeres?

Welcome to SE Biology. Please finish reading the [Tour] and the Help on asking questions. Regardless of who was the captain of the team and where they play, without a link to the paper, most list members will ignore your question. You can't expect us to go searching for it. The second point is whether you are asking if the information is in the paper, in which case you should point out where this isn't clear, or whether you really expect someone on this list to know about the group's unpublished work.

Thank you very much, it was very informative. I will take measures from now on.


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Identify a hanging plant with spherical leaves

This plant was found in the "drylands" section of a public conservatory (you can see a potted cactus in the background).  It did not have a label, and there was nobody around to ask about it.  The plant has hanging stems about a meter long, with spherical leaves about five millimeters in diameter -- the leaves appear to be genuinely spherical, not curled-up flat leaves.
Any idea what it is?

you could have googeled "hanging plant with spherical leaves"

Top result was a Wikipedia article for a plant with spherical fruit, and the next several were plants with curled-up leaves.  Google doesn't have all the answers.

It seems that this might be Curio rowleyanus, sometimes called "string-of-pearls".  The Wikipedia article indicates it has spherical leaves about 6mm in diameter on trailing stems up to about a meter.  It is a succulent and the spherical leaves reduce evaporation for volume contained.  It grows in the dry parts of southwest Africa.

BTW, my Google query was simply plant with spherical leaves.

Looks correct to me. Incidentally, there are a bunch of similar "String of..." plants in the same or very closely related genus Senecio, and they are all very easy to propagate from the leaves and stem, so are incredibly popular houseplants at the moment.


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Is there a specific book or textbook that lists all of the specific concepts of the theory of evolution in one place?
By specific concepts I mean those such as Zahavian signaling, the "sexy son" hypothesis, Mendel's peas, Lamarckism etc.
Essentially I am looking for a book that helps visualize evolution in a practical way that is simpler than actual scientific literature but more in depth than just popsci Dawkins fare.

Have you tried the wikipedia categories pages?


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Clustering collection of PDB files based on 3 dimensional structural similarity in python
I have generated a set of 3-dimensional structures of the peptide AGAGAG with different structures. Total number of PDB files are 300. I need to cluster the peptide structures based on their similarity. Is it possible to do Kmeans clustering and get the total number of clusters in Python? The issue is that the RMSD-based distance matrix requires reference PDB which is not available here. Kmeans does not do clustering based on the distance matrix.

First, there are versions of k-means that can handle k-medoids from distance data.
Second, there are plenty of clustering methods that are fine with distances (see e.g. hierarchical clustering). Is there a reason you don't want to use this?
Third, is there a reason that you need to cluster them based on their similarity?
Fourth, you may be interested in approaches like FoldSeek that describe differences between structures using a structural alphabet to yield a sequence, making it a lot easier to do structural comparisons. Your example is admittedly a lot simpler than what they are trying to do with full proteins, but nonetheless may hold some points of interest. It is being used for larger-scale protein clustering tools like ProteinCartography.


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Risk with cultures taken from stagnating water?
Necessary foreword: I'm an amateur and just starting with microscopy and microbiology.
Wanting to observe some protozoa, I collected samples of dirt and water from some pools here in the city and nearby, and started keeping them in jars to see if something changes over time (different protozoa and small animals, quality of water, etc.). Stuff happens, which is great, but also means that a lot is going on in there.
The jars sit mainly indoor and I wonder if I should be more worried about them: apart washing my hands with care after handling them, is there any other measure I should take (some guidelines maybe)? For instance, I will for sure breathe nearby the water when I observe at the microscope.
I hope that your answer will be "take it easy", but you know, safe is better than sorry.

First off, without knowing the specifics, it is very hard to say, but in general, so long as you are careful and don't ingest (i.e. drink) or breathe in aerosols/droplets of the water, it should be OK. Washing your hands and spraying down work surfaces with hand sanitizer after you finish your observations is a good idea too. The risks probably aren't substantially greater than digging in the soil in your garden. Other standard lab practice is also a good idea - don't eat/drink/smoke/apply lip gloss/makeup while doing this, keep your hair tied up, clean up spills immediately, keep your hands off/away your face.
What is in the water strongly depends on your water source. If you got it from the local duck-pond, it could contain all sorts of things associated with bird faeces, such as Avian botulism, Salmonella, Cryptococcosis and Histoplasmosis (though these last two are more associated with soil than water), even viruses, such as avian influenza, though you'd only likely get this by handling sick birds or the feces directly.
Water that runs off a farm, might have a range of bacterial species, such as E. coli, and Brucella, as well as eukaryotic pathogens such as Giardia, Pinworms (we carry these too, 30-60% of children has these at any given time) and a whole range of other parasites.
Water from a puddle in your back-yard, on the street, or an actively flowing stream (collect the water from a still-water spot) is less likely to contain parasites that might harm you, but bacteria will remain in suspension. Again it depends on source - the neighbour's (or your) cat/dog can carry pinworms, tapeworms, even Toxoplasma, as well as a range of bacteria similar to those listed for the farm above. Any wild animal that visits your place can also carry a range of things.
the highest risk places are areas with a lot of people. We carry a huge range of native and non-native pathogens that you can pick up from people's dirty habits and leavings. These include bacterial species (E. coli again, but also several others), viruses such as norovirus and rotavirus, and the aforementioned parasites. However, you are much more likely to catch these sorts of things from shared facilities such as toilets rather than water, unless you are collecting from a high-traffic area such as a popular forest walk which doesn't have toilet facilities nearby.
These are the worst-case scenarios, follow good hygiene practices and good laboratory practice and you should be fine.

Thanks @bob1, this makes me more aware of what I'm handling and what the good practices are


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How much of life expectancy gender gap is caused by social vs biological factors?
I can't find any data/study bringing some light to the components of the life expectancy gender gap. But this should't be difficult:

Men suffer many more accidents and suicides, these are clearly not biological factors, it should be easy to calculate life expectancy gap excluding these.

Men abuse alcohol and tobacco more than women, it should be possible to compare life expectancy for non-smokers and non-drinkers only.

Please let me know if you know of any study.

Men suffer many more accidents and suicides, these are clearly not biological factors debatable. Perhaps men have a higher 'biological' instinct to commit suicide or do risky things. Fundamentally, I don't think there's a possible distinction to be made between things which are 'purely' biological or social.

Agree with user438383. Social factors are biological factors manifested in interpersonal behaviors. If what you mean is something about physiology that intrinsically differs between men and women, somehow excluding (or at least statistically adjusting for) social factors... maybe. (This isn't a judgment on you, people in general are sloppy when they talk about this.) In any case, there are multiple studies that can be found readily, in one second of googling I found this. There are a ton of references in there.

I like your question, and it got me looking for some answers to similar questions I've been thinking about too.
I don't have the full answer; the exact disparity between specific hormones and the differences between mood regulation, but I do have a pretty good research paper that looked into this.
I'd highly recommend anyone and everyone to read it - it's free to access, and even if you only read the abstract you may hopefully take something from it.
In summary though, to answer your question, there seems to be due to (as you said) riskier decision making, but just in young men, and increased stress levels in middle aged men.
I guess the men who make it through to old age (due to socioeconomic, genetic/epigenetic reasons or just pure luck) managed to not be situated on the upper end of either of these spectrums of risk taking and physical stress response, as is most likely thanks to selection pressures. However, these high mortality-linked traits have not entirely been bred out of our populations around the world as many of these high-mortality-associated men do live long enough to pass on their genome, of which some, (roughly half, on average), will be inherited.
These physical, inheritable traits are a bit like radioactive decay: They will decline in the population over many many generations if nothing else happens, but they will never truly disappear. And the problem is that the way that society works is it does in fact exert an external force on many people, pushing them towards making risky decisions (e.g. gambling, impulse buying expensive items on a pay £0 today finance deals et cetera) and to experience much higher daily levels of stress than people can cope with day-to-day. There may even possibly be epigenetic modifications occurring in individuals that would possibly be passed down to offspring if that is the case. This, I believe, alongside the increased media attention recently on mental health, is why we are seeing much more of it these days than ever before, unfortunately.
Anyway, here's the paper: Economic Transition, Male Competition, and Sex Differences in Mortality Rates
I hope you enjoy reading it, and if you have any follow-up questions I'd be more than happy to try to answer them.

The paper is so close, yet never gives the ratio of internal to external causes.

I dug into Eurostat's Causes of Death statistics to come up with this napkin calculation. (I am not a statistician, do not take this data at face value.)

2010 Norway - all LEGG: 4.54
2010 France - all LEGG: 7.14

Minus mechanical causes: suicides, assaults, accidents and drug and alcohol overdoses, etc.

2010 Norway - all LEGG: 4.54 | non-mechanical LEGG: 3,51, decrease by 29.5%
2010 France - all LEGG: 7.14 | non-mechanical LEGG: 6.19, decrease by 15.3%

Assuming that smoking reduces the life expectancy on average by 10 yers and smoking rate among French men and women are 0.349 and 0.319 and smoking rate among Norwegian men and women are 0.17 and 0.154, I reduced the LEGG further:

2010 Norway - all LEGG: 4.54 | non-mechanical, non-smoking LEGG: 3,35, decrease by 35.7%
2010 France - all LEGG: 7.14 | non-mechanical, non-smoking LEGG: 5.89, decrease by 21.2%

It should be possible to do this for alcohol, meat consumption, and many other causes. Again, I am surprised that I can't find any such research.


text:
What does "the scaffolding of biology" mean here?
In Zoltan Torey's The Conscious Mind, the author discusses the emerge of self-awareness:

Turning to the changes that the acquisition of language instantiated, Damasio reflects on these changes in some detail:
To hold extensive memory records not only of motor-skills but also of the facts and events, in particular of personal facts and events, those that make up the scaffolding of biology, of personhood and the individual’s identity, these depending on the ability to reconstruct and manipulate memory records in a working brain-space, parallel to the perceptual space, an off-line holding area where time can be suspended during a delay and decisions freed from the tyranny of immediate responses.

What does this mean?

It's just a metaphor. Look up scaffolding in a dictionary.

This sort of question actually has nothing to do with biology, and would be more appropriate on SE English Language Learners. However, in addition to it being pretentious twaddle, I don’t find it a very good metaphor, given that scaffolding only supports something (and not necessarily even that) until it is built or repaired. “Framework” strikes me as better. But, again we are in a realm other than biology — perhaps philosophy.

I agree with David that the specific meaning here is not really worth dissecting or understanding from the perspective of biology; it won't bring you any closer to any knowledge or understanding of biology.


text:
How often do birds steal from fish traps?
Does anyone have any solid information about how often birds (e.g. cormorants, mergansers, gulls etc) steal fish from any sort of fish trap? Fish traps include, but are not limited to, fyke nets, pound nets, gill nets etc. I'm not looking for info on birds getting caught in the traps, rather any cases where the birds actually take the fish in the trap.
Ideally I'm looking for published articles, but grey literature or any reports are useful.
If you can think of anything more or less suitable, please let me know.

taken that fish and fishtraps are under water it is unlikely that birds can open a trap under water.

@trondhansen Cormorants and mergansers at least do their hunting under water normally. These are not necessarily closed traps that need to be "opened"; I'm not familiar with all of them but a gill net for example is a net where the fish swims partway through and then gets stuck past the gills, so that they cannot move forward (body too big) nor backward (gills caught). There's a half of a fish sticking out either side.

@BryanKrause i was unaware that a fishing net can be seen as a trap,but atleast i now know  the definition of a trap.maybe this question can be narrowed down by focusing on just a few types of traps.birds do take fish from nets every single day and many birds get trapped in the nets and drown.

@trondhansen OP specifically listed the sort of instruments they are considering.

@trondhansen, Could you provide any reasearch or reports about birds taking fish from nets? Especially if you have info on the amount of fish taken and what species of birds took it.

I think that would be a pretty nice line of research. Thievery in birds (corvidae and psittacidae especially) has to be well documented. However, something as specific as what you're asking seems hard to find with some initial research. I'll try to give it a shot tomorrow.

@pawelekzzz Thnaks, I appreciate it. I've been looking for a while now, but with no luck.

Since kleptoparasitism, that is, stealing food from other entities that have procured that food earlier for themselves, is a widespread strategy in animals, it is no surprise that birds also engage in this kind of behavior (up to 856 accounts of some sort of interspecific thievery). Food stealing skills is even related to parental quality in Sterna dougallii. Honest parents had lower productivity. Additionally, in parrot-owner behavioral problems dynamics, stealing human food got a 2.34 in a 5-point Likert scale where 5 = always.
On top of that, theoretical ecology tells us that behavioral dynamics are characterized by a cooperation/conflict tension where a behavior such as theft may thrive (while also depending on many other factors, e.g.: larger thieves tended to get the highest payoff, and bear in mind size is but one factor). So I think a bird will maximize stealing if the opportunity is present to it and whether it's physically capable of doing it.
In Larus argentatus, head turns, approaches, and angular body position were three behavioral markers identified in an ethogram to measure attention to anthropogenic food-based contexts. I think this article is the one that is key to your question, considering how difficult it is to find statistics for how often thievery from anthropogenic sources happens. It is key, because combined with theoretical ecology, and the amount of bird intelligence research nowadays, it shows intuitively that birds will probably steal from human fish traps 1) if they have knowledge about it, and 2) as much as they can.
Anecdotally, birds, (both known and unknown to me) have also stolen from me several times in varied environments (many of them could be considered "traps" or at least "food containers that require a certain degree of skill to operate or get to"), but not fish traps.

References
Anne Tygesen & Björn Forkman (2023) The Parrot–Owner Relationship and Problem Behaviors in Parrots, Anthrozoös, DOI: 10.1080/08927936.2023.2238434
David A. Shealer, Jeffrey A. Spendelow, Jeff S. Hatfield, Ian C. T. Nisbet, The adaptive significance of stealing in a marine bird and its relationship to parental quality, Behavioral Ecology, Volume 16, Issue 2, Mar./Apr. 2005, Pages 371–376, https://doi.org/10.1093/beheco/ari008
Feist F, Graham P. An ethogram identifies behavioural markers of attention to humans in European herring gulls (Larus argentatus). Biol Open. 2023 Jun 15;12(6):bio060016. doi: 10.1242/bio.060016. Epub 2023 Jun 13. PMID: 37309817; PMCID: PMC10281265.
Hadjichrysanthou C, Broom M, Rychtář J. Models of kleptoparasitism on networks: the effect of population structure on food stealing behaviour. J Math Biol. 2018 May;76(6):1465-1488. doi: 10.1007/s00285-017-1177-7. Epub 2017 Sep 18. PMID: 28921258; PMCID: PMC5840298.
Morand-Ferron J, Sol D. and Lefebvre L (2007) Food stealing in birds: brain or brawn? Animal Behaviour, 74, 6, 1725-1734. https://doi.org/10.1016/j.anbehav.2007.04.031
Phillips JA, Peacock SJ, Bateman A, Bartlett M, Lewis MA, Krkošek M. An asymmetric producer-scrounger game: body size and the social foraging behavior of coho salmon. Theor Ecol. 2018;11(4):417-431. doi: 10.1007/s12080-018-0375-2. Epub 2018 May 1. PMID: 30931016; PMCID: PMC6405016.

Thanks, I'll look into the references you provided