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How does retinal ganglion cell receptive field affect the LGN neuron activity?
If we have a spot of light hitting the center of the ON center receptive field of a retinal ganglion cell, will the LGN neuron be activated? Will the V1 neuron be activated? I mean its receptive field looks different, see the image below. I am just so confused on what the receptive field of an LGN and V1 neuron even means. In other words, how is the receptive field of the retinal ganglion cell related to or how does it affect the receptive field of the LGN neuron?
If light shines in the center of the ON center LGN neuron receptive field that is not in the receptive field of the ganglion cell, then the LGN neuron is activated and the ganglion cell is not. How does that work? How can it skip a stage? Does not the RGC first need to get activated for the LGN neuron to get activated?
Since a V1 neuron to get activated for example needs a shine of light that is 45 degrees diagonal to the right, will it get activated if only a spot of light is shone to the ON of the ON center retinal ganglion cell? This RGC is connected to the V1 neuron is it not?
In conclusion, I think that I am confused in why is the ganglion cell connected to the LGN cell, which is connected to the V1 cell, when they all have different receptive field. What does the connection bring about?
Thanks sm in advance!

The picture is showing you how receptive fields are combined at different levels of the visual processing hierarchy. The activity of multiple cells is combined to influence the activity of the downstream cell. This diagram is a bit confusing in that it focuses only on one RGC to show divergence (connection from one to many from the RGC) from RGC to LGN and then only convergence (connection from many to one in V1).
Light doesn't only shine "on the receptive field of a retinal ganglion cell"; light shines on some spot on the retina, which will influence multiple retinal ganglion cells. If you want to understand what happens at the level of LGN or V1, you need to consider all of the inputs to a cell, not just one of them.

If we have a spot of light hitting the center of the ON center receptive field of a retinal ganglion cell, will the LGN neuron be activated?

Maybe? Who knows. Neurons in the LGN will be activated (fire action potentials) if they receive enough excitatory input (and little enough inhibitory input). If you have an ON-center RGC that synapses on an LGN cell, then yes, light at the center of the RGC receptive field will increase the likelihood that the LGN cell fires.

Will the V1 neuron be activated?

Maybe? Who knows. If light only lands on the center of one of the LGN cell receptive fields, it's also landing in the "surround" of the other adjacent LGN cells that also give input to V1. You'd expect the V1 neuron to be more active in response to a spot of light than if light only fell in the dark surround area, but far less active in response to a spot of light than to a bar/line of light that looks like the shape on the right hand side.
I would recommend working back the other way. Look at the way the receptive field is drawn: that tells you how light in different areas will influence that cell's firing. Light on the white background areas increases firing, light on the shaded areas decreases firing. Then, work backwards in the pathway to understand how those responses could have been created by adding together cells at the previous level of the processing hierarchy.

What does the connection bring about?

No light shines on any cells in the LGN or V1. These are deep in the brain. Light information needs to be transmitted to them in some way. Without connections between these cells, there would be no responses to light in the brain.

Whoa! Thank you so so much! So nice of you to spend so much time answering my questions to help me out, I greatly appreciate it

there is only one ganglion cell connected to only one LGN cell? But more than one LGN cells connected to a V1 cell? Does the receptive field of a ganglion cell superimpose with the receptive field of the LGN cell to which it is connected? Are their receptive fields identical? If not, lets say if that of the LGN is bigger and light is shone on a part that does not shine on the receptive field of the RGC, then how is the LGN cell activated when RGC is not? Since only this RGC is connected to that LGN cell so it is the only one that can activate the LGN cell (?)

and since V1 cells are only activated by bars of light, then if I am seeing a round spot of light, is any of my V1 neurons being activated?

@Maria Each RGC connects to multiple LGN cells; each LGN cells receives input from multiple RGCs. Each LGN cell connects to multiple V1 cells, and each V1 cell receives input from multiple LGN cells. There are also lots of different types of V1 cells and receptive fields, arranged in different layers of cortex; only the "simple cell" is being depicted here.

V1 cells are activated best by bars of light. How V1 will be activated will depend on the size of the spot of light; if it's small then yes, any V1 cells where that spot would fall on their 'bar' would be weakly activated. If it's a big circular spot of light, you'd expect V1 cells to be activated in a pattern consistent with a line of "bars" along the edge of the circle in a tangent orientation, where light lands on their center and one side of the surround, but not the other side. V1 receptive fields are also considered "edge detecting".

I highly recommend reading some of the early papers by Hubel and Wiesel that show how people learned these things before any of it was known by anyone.

cool! thank you so much! sorry to bombard you with qs, but how can an LGN cell be an ON or OFF center if it receives input from many ganglion cells that can be a mix of ON or OFF center? I thought that it went like if the bipolar cell is ON, the ganglion cell will be ON, and hence the LGN cell will be ON

@Maria I'm not sure whether LGN cells do get a mix of ON and OFF input, is there a reason you think that's the case? Hypothetically, there would be nothing wrong with assembling an "on-center" receptive field by summing aligned on-center receptive fields with offset off-center receptive fields, but I don't think this actually happens until V1.


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why do we use the glasses so that a different image is seen in each eye in the binocular rivalry experiment?
If we use the glasses so that in the right eye we see a house and on the left eye a face, we can see with a fMRI that the FFA is activated when seeing the face and the PPA activated when seeing the house. But if we did not use these glasses and just saw the house and face superimposed, how would the recording look? The recording for when you force yourself to see the house and then the face? The same as with the glasses? So what difference do the glasses basically make? Thanks in advance!

source of image: https://www.sciencedirect.com/science/article/pii/S0042698909000169

It would be helpful to include references/sources in your post. I would expect the source to explain the purpose of this experiment, what have you read and why does that explanation not make sense to you? I'm not really understanding what you mean by "just saw the house and face superimposed"; how would that happen, exactly, without the glasses?

I included an image into the post! That is what I mean by seeing the house and face without glasses, so you would see them simultaneously and only one of them if you force your brain to perceive only one of them.

How would that show binocular rivalry?

aah wait, so binocular rivalry is created when your brain perceives two alternative images because both eyes SIMULTANEOUSLY see something different.  Without the glasses, you would be able to control what to look at, there is no alternation of images as one image is perceived at a time. If we see the face by the right eye, I assume the right temporal retinal fibres do not participate for perceiving the image because that is for the left visual field, right? And so this means right temporal and left nasal retinal fibres do not get involved in this binocular rivalry experiment with glasses?

I'd recommend backing up a bit and looking at the big picture. What's the whole point of these experiments?
Binocular rivalry is an observation, like seeing that the sky is blue is an observation. That is, when you present two incompatible images to the two eyes, you typically perceive one or the other, not a combination: that's the observation/phenomenon.
The next step is to use this observation to try to understand more about how the brain processes information. Not necessarily just to understand this weird binocular rivalry paradigm, which isn't something that would normally occur out in the world (without someone messing around with some goggles your eyes are generally going to be viewing the same world, not different ones), but to ask how this little "malfunction" gives insight into how the brain processes information in general.
An fMRI experiment that shows the FFA is activated when someone perceives a face, and PPA activated when someone perceives a house, tells you something about the relationship between PPA and FFA and perception. The context of binocular rivalry presents an interesting and very useful control experiment.
Let's set binocular rivalry aside for a moment and just consider looking at pictures of houses and faces. Again, you'll see differences in FFA versus PPA with houses versus faces, great. But, you'll also see differences at the retina. In fact, if you had some machine learning algorithm, you could definitely use responses from the retina directly to figure out if someone is looking at a house or a face: it's really the same problem as doing it from a camera image. So, this test isn't really measuring anything about what's going on "inside your head"/inside the mind/conscious perception, its just measuring a biological representation of the outside world.
Now consider binocular rivalry: you're presenting a constant face image to one eye, a constant house image to the other eye. At the level of the retina (and, to some extent, in early visual processing areas in the brain like LGN and V1), you can expect exactly the same activity no matter what the perception is: the experiment lets you dissociate what is different because the perception is different from what is different when the outside stimulus is different. The outside stimulus stays the same, yet the perception changes, and the perception changes are associated with changes in activity in particular brain regions. That provides some evidence that perception of objects (rather than mere signal processing of visual patterns) involves brain regions like the FFA and PPA.

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

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how can a patient with conduction aphasia answer questions but not repeat words?
When we have a Q&A with someone, the path in the brain goes as such: auditory cortex to Wernicke's area (to be comprehended) which then activates the Broca's area to initiate a motor reaction (so to answer the questions). So if someone asks questions, is not the arcuate fascicle taken into use? Doesn't the Wernicke's somehow need to tell Broca what to say? Or does it just stop at Wernicke's and then a new path is initiated from Broca's?
When someone with conduction aphasia is asked to repeat a word, let's say "apple", they cannot as apparently this arcuate fascicle is necessary.
What is the difference with answering a question to repeating a word? Would the person be able to say "I cannot repeat the word 'apple'"? So it would technically be able to say the word 'apple'. Thanks in advance!

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Can several genes be edited at once and what is the name of that procedure?
In general, if there are multiple genes of interests, or edits at multiple points along a large gene are desired, can several edits done at once (or as many as is possible while minimizing off-target effects), transfecting cells with multiple gRNAs and possibly different Cas variants, or would the edits be done one at a time, with each edit being screened for one after another? Or somewhere in-between where you'd batch edits and screen for them in groups? Mostly interested in base edits and electroporation based transfection, but any information on workflow for editing multiple sites is welcome!
Per bob1, my goal is to edit multiple base pairs on sites adjacent to and within a gene for in vitro mammalian cell lines, to see how those edits affect protein expression.

How you go about it is dependent on what phenomena you are interested in and your reasons for looking at the products. Need more information on your aims to answer this. Also depends on organism.

The workflow you're talking about I believe is called multiplexing. Maybe this  article can help you out.

@pawelekzzz That's exactly the term I'm looking for, thanks! I didn't know the name of it and hadn't seen that term in any of my searches prior, this gives me what I need the find more articles, and the one you link gives a good intro to the concept too, much appreciated.

@bob1 Simultaneous base pair edits on sites, upstream, downstream and mid-gene for in vitro mammalian cell lines, to monitor changes in protein expression

@Gumpf You should edit that into the question. In that case I can see that intermediates might well be useful...

@pawelekzzz you could expand that into an answer.

One of the advantages of CRISPR/Cas9 is that it allows what is called multiplexing. In other words: transcriptional regulation of multiple different genomic loci in one single construct. I'm not sure if other biotechnological methods allow for a different strategy to obtain the same result.
Multiplexing using CRISPR/Cas9 has been documented several times expressing several gRNAs at once. Anecdotally, I can also personally say it works. The multiplexed CRISPR/Cas9 reagents are assembled into T-DNA vectors. This is done through reactions called Golden Gate cloning and Gateway reaction.
Bear in mind I'm talking about plants all this time.

References:
Lowder LG, Zhang D, Baltes NJ, Paul JW 3rd, Tang X, Zheng X, Voytas DF, Hsieh TF, Zhang Y, Qi Y. A CRISPR/Cas9 Toolbox for Multiplexed Plant Genome Editing and Transcriptional Regulation. Plant Physiol. 2015 Oct;169(2):971-85. doi: 10.1104/pp.15.00636. Epub 2015 Aug 21. PMID: 26297141; PMCID: PMC4587453.
Li JF, Norville JE, Aach J, McCormack M, Zhang D, Bush J, Church GM, Sheen J. Multiplex and homologous recombination-mediated genome editing in Arabidopsis and Nicotiana benthamiana using guide RNA and Cas9. Nat Biotechnol. 2013 Aug;31(8):688-91. doi: 10.1038/nbt.2654. PMID: 23929339; PMCID: PMC4078740.

What you should do is highly dependent on what you are looking at and why you want to make those changes. It also depends on which method you want to use
There are quite a few different ways of doing this for mammalian cells. One commonly used way is to have the gene expressed off a plasmid in a cell line that lacks expression of the protein of interest. This means you have an easily manipulable plasmid which you can make and confirm sequence changes easily and quickly. Plasmids are also easy to use and can get results quickly.  However, these are usually non-permanent changes, unless you have a selection mechanism like geneticin and maintain this on your cells. If you don't maintain the selection the cells tend to lose the plasmid. The downside is that you don't tend to get every cell transfected and the percent of cells transfected drop with plasmid size and/or method and can be variable between different transfections and different plasmid preparations. These methods are known as transient transfection and stable transfection respectively. For many sequential changes, looking at intermediates, this is probably the method I would use, but CRISPR/Cas (see below) is also promising.
For targeting of the genome of the cells you are looking at, conventional gene editing techniques by recombination between plasmid and genome are slow and best suited to smaller inserts and low numbers. They tend to have lower success rates and require things like antibiotic selection to ensure that they have happened. This includes things like Cre-Lox recombination. These tend to be quite slow relative to transient transfections and require you to have robust sequence checking methods in place (often done by PCR product size and/or sequencing), but are stable and don't require continued selection once stable. They can be done at a single-cell level and can be site-specific, depending on the method used.
Viral transduction is similar to both transfection and recombination methods. You usually work with relatively easily manipulated virus genomes expressed off plasmids to make the viruses, which are then used to do the recombination/expression. It does tend to have quite a bit of finicky set-up, but is robust and stable once it is working. Lentivirus and Adenoviral vectors are two common methods of this, but there are others.
CRISPR/Cas I don't know a lot about, but I know it is entirely possible to use this method to rapidly make site specific changes in genomes. I think this is the most promising technique for many genetic manipulations in the cell. This is very quick, but requires quite a bit of optimization.
In general, making lots of changes at once is entirely possible, though, as you will have realized from the above, this depends on the mechanism used to make the changes. Just be aware, that if you are manipulating the genome of a host, dramatic changes (i.e. many) might drastically affect the cells in some fundamental manner so that you don't get any cells survive. This is where intermediate steps might be useful, but is something you can choose or not at this point.

Really? :) You provided the animal cells answer, and I provided the, rather succinct, plant cell version.

@pawelekzzz To be fair, you can use the viral method and a bacterial method (Agrobacterium i think?) on plant cells too.

Yes, that's right, Agrobacterium tumefaciens is used in plant cells transformation.

@pawelekzzz excellent, having not worked on plants for over 20 years, good to know my memory of methods hasn't failed on me. Not that I used Agrobacterium at the time, just knew it was a possibility.


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What happens to the gamma motor neuron during too much contraction of a muscle?
Suppose a muscle is contracting too much, so we need a reflex to stop it from contracting too much.
Contraction of a muscle causes the muscle spindle to go slack, hence the Ia axons and II-axons do not fire action potentials. The Ib axon synapses with the alpha motor neuron via an inhibitory interneuron so that the muscle is stopped from contracting. But what happens to the gamma motor neuron? Is it also inhibited just like the alpha motor neuron is inhibited? If indeed, it is inhibited, is it the Ib axon that inhibits it? I mean if it was not inhibited, then it would activate the Ia axon and the II axon which would activate the alpha motor neuron. As a result, there would be conflicting messages sent to the alpha motor neuron (excitatory from Ia and II and inhibitory from Ib).
During stretching of a muscle, for example, during the patellar reflex, the Ia axon and II axon are activated, which activate the alpha motor neuron as well as the gamma motor neuron to get contraction and contraction over and over again until the muscle returns to its set point.
During stretching, is only the muscle spindle active?
During contraction, is only the Golgi-tendon-organ active?


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Which predator / prey pair of species have the most drastically different body size?
I'm trying to identify which 2 species, one predator species and one prey species that have the biggest size difference.  Specifically, which predator hunts the largest prey relative to itself?
I'm looking for the pair with the smallest predator taking the largest prey but relative to each other, not the other way around.
Some limiting factors to the question:

Parasites don't count.  Parasites will, ideally, repeatedly feed on the same host for as long as possible. Killing the host will, eventually, remove the resource, which is undesirable for the parasite (it can't keep feeding on the host if the host ceases to exist).  I'm looking for a predator prey relationship that does not do this in any way, shape, or form.  Even if the predator does not consume the majority of the prey, the portion consumed must be vital to the prey, or the prey must be killed in order to access it or overcome resistance to it.

Animals eating plants don't count.  Animals eating other animals only please.

Pack hunters don't count.  Lions, wolves, orcas, army ants, etc., don't count because packs can come in so many shapes and sizes that it makes it impossible to pin down a size ratio between the pack and the prey.  Single predator individuals only, please.

Scavenging doesn't count.  Predators might also scavenge, but prey species used in the size comparison should only include species that the predator actively hunts as part of its regular active hunting routine (even if intermittently or seasonally).

Intentional prey sharing doesn't count.  Sure, a predator might have it's prey stolen after a kill, that's fine.  In many predator species, parents will share kills with offspring until they are capable of hunting for themselves, that's fine too.  But nothing like the Tarantula Hawk that doesn't actually eat the "prey" itself, but rather leaves it to be eaten by offspring later.  But typical behavior, even in the presence of non-self-reliant offspring, and assuming another predator doesn't take the kill by force, should be for the individual predator that makes the kill to also be the individual that consumes the largest share of the nutritive portions of the prey.

Body mass is the primary measurement for "size".  Since length, width, height, etc., can vary widely based on body plan, let's use mass as the measurement for "size" for the purposes of this question.

Size of the predator should be the mass of a 'typical' or 'average' adult member of the species that performs the actual hunt / kill.  For species with significant sexual dimorphism in relation to size between male and female, use the size of whichever sex is generally larger.

Size of the prey should be the mass of the 'average' specimen taken in a predation event.  For example, Lions (yes, I know I excluded them in the 'pack' section earlier, but for the sake of example), lions will eat elephants.  This is most commonly scavenging, rather than hunting.  And when it is due to hunting, it's more often calves, not adult elephants, that are taken in the hunt.  So (if lions were allowed, and were compared to elephants) the scavenged elephants wouldn't count toward the 'average', only the hunted ones, and the average would be closer to the size of a calf, rather than an adult, due to the higher frequency of predation events involving calves.

The ratio matters, not the absolute mass difference.  I'm looking for the pair with the biggest ratio, or percentage difference, not the greatest sheer difference in mass.  For example, Pair A is a 20 pound predator taking a 30 pound prey, this is only a 3:2 ratio and a 10 pound difference.  Pair B is a 1 pound predator that takes a 5 pound prey, which would have a much larger ratio of 5:1 despite only a 4 pound difference.  Pair B is the winner here, by ratio.

Given all of this, which two species, that have a predator and prey relationship, have the greatest mass difference between the predator and the prey?

Have you googled this? Or "tiny animal predators"? Please give evidence of research have you done to answer this question yourself, which is a requirement on this site. Thanks.

@Darlingtonia  I'm actually looking for the pair with the smallest predator taking the largest prey, not the other way around.  I'll update the question to clarify.

@anongoodnurse  Yes, I attempted many such searches, but the question is too complex for that type of search, as far as I've been able to determine.  For example, your suggested search criteria, of "tiny animal predators" would be useless, as the absolute size of the predator isn't actually relevant.  The ratio of the sizes is the relevant factor here, which is all but impossible to put in to an internet search, and yields useless or no results at all, when attempted

I recently found a beetle larvae specialized to kill an earth worm that was 50+ times more massive than it. your question doesn't make sense to me totally... A parasite is just a predator that eats the prey slowly, and some parasites do kill the prey. If a tiny spider kills a human and eats a piece, where does that fit into the relativity of the query? it doesn't make sense to kill a prey which can supply so much food that it goes mouldy when only 0.1% has been comsumed.

@bandybabboon Parasite, parasitoid, predation...Yes, the lines are blurred. There are no spiders that hunt humans intentionally as a food source, so that would be a defensive kill, followed by opportunistic scavenging, not predation. Parasitoids do kill the host, eventually, but keep it alive as long as possible, for other reasons realated to their life cycles, such as feeding young, defense, or environmental concerns, etc. For simplicity, I'm looking for only those that are clearly not parasites or parasitoids, but rather clear and unambiguous predation.

I think the Black Swallower (Chiasmodon niger) is a good contender. This fish can (at least according to Wikipedia and reference therein) can swallow other fish that are up to twice its length and 10x its mass.
For land based predators, the Least Weasel (Mustela nivalis) is capable of killing prey 5-10x its weight, though these instances are believed to be rare (at least rarely observed), though they will take birds like Chickens occasionally too. Diet is normally much smaller - rats, mice etc.

Why would someone downvote this?


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Does interspecies breastfeeding occur in the wild?
Does interspecies breastfeeding occur in the wild?
Say, for example, a zebra feeding a wildebeest, or a bushbuck feeding a gazelle.
There is a Wikipedia page on this topic but it only shows animal-human and human-animal feeding.
https://en.m.wikipedia.org/wiki/Human%E2%80%93animal_breastfeeding

Not specifically "the wild" but pet cats and dogs have been known to nurse wild animals or other pet species, possibly inadvertently. There are several YouTube videos of cats nursing baby raccoons, for example. I'm unsure if they're aware the animal they are nursing is not a kitten or if they can't tell the difference.

Yes, interspecies adoptions have been observed. They're rare enough that study is limited to case reports, and the causes are guessed at but not fully understood. However, I think it's clear that there are strong biological drives towards participating in mothering for the species that do so, and it's not too surprising that these drives could be at times "misplaced" from a biological perspective and directed at non-offspring.
A couple papers:
Carzon, P., Delfour, F., Dudzinski, K., Oremus, M., & Clua, É. (2019). Cross‐genus adoptions in delphinids: One example with taxonomic discussion. Ethology, 125(9), 669-676.
Izar, P., Verderane, M. P., Visalberghi, E., Ottoni, E. B., Gomes De Oliveira, M., Shirley, J., & Fragaszy, D. (2006). Cross‐genus adoption of a marmoset (Callithrix jacchus) by wild capuchin monkeys (Cebus libidinosus): Case report. American Journal of Primatology: Official Journal of the American Society of Primatologists, 68(7), 692-700.

I didn't ask for adoptions, but specifically breastfeeding. Has this ever been recorded? If so, between which animals?

@Samid Read the papers in the answer. They involve breastfeeding. Do you think these animals would otherwise get milk from the grocer?

@BryanKrause while your comment is true, it'll be more proper as an answer to the question if you include at least the word "breastfeeding" in your answer :)

This video describes a cat feeding ducklings, and shows the ducklings subsequently still having the emotional attachment to their foster mother even after growing up.

Not "in the wild" and the ducklings didn't breastfeed.  The bit at the end about the lioness may qualify.

@JamesK: They did breastfeed; it was clearly stated that they were observed to be sucking at the nipples. Even though it's on a farm, one could argue that cats are kind of semi-wild, and there is no reason to believe that the same thing couldn't happen in the wild. No doubt the quality of evidence provided by this is low, but it's worth knowing.


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How do microbiologists decide whether two morphotypes on the same plate belong to the same strain?
Background
Colony: A colony, in microbiology, is a visible cluster or mass of microorganisms (such as bacteria or fungi) that has grown and multiplied on a solid agar medium. Each colony represents a population of genetically identical microbial cells that originated from a single cell or a small group of cells. Colony formation is an essential step in the isolation and identification of microorganisms.
Colony morphology refers to the visible characteristics of a bacterial or fungal colony when grown on a solid agar medium. It includes features such as size, shape, color, texture, and edge appearance. Each type of microorganism may exhibit distinct colony morphologies, aiding in their identification and classification.
"It should be noted that when a microbiologist examines an agar plate and determines that mixed bacterial
types are present, it is actually mixed bacterial colonial types (morphotypes) that are being observed. These
visually distinctive colonies often represent different species (or even genera), but they may also represent
phenotypic variants of a single genotypic organism."

Koneman's Color Atlas and Textbook of Diagnostic Microbiology. 7th.
Wolters Kluwer; 2017

Question
In diagnostic microbiology and in order to save time, how do microbiologists decide whether two morphotypes on the same plate belong to the same strain?
I'm not talking about great differences in morphologies as Lactose fermenters vs Non-Lactose fermenters on MacConkey agar, but ones like these: The center in Type A is purple while the center in Type B is pink.

Pure culture of Acinetobacter on MacConkey agar plate

They don't look any different to me from your photo. Perhaps a closer photo might help. All I see is some difference in thickness (depth?) of the colony perhaps, so one appears lighter colour than the other.

I will try to find a more clear example and I will add more essential quoted text to the background section about "Phenotypic Variants of Bacterial Colonies"

You have to remember that when a microbiologist looks at a plate, they are looking to observe a particular something, which depends on exactly what they are doing, and they will have some idea of the range of morphotypes expected for those species and/or strains.
They also aren't doing this in isolation - they will use tests to further confirm what they see, often starting with simple tests like Gram staining and going on to other biochemical tests, genetic tests (sequencing possibly or PCR), or even MALDI-ToF.
Experience also plays a part - if this is something being done routinely, say in a clinical lab, then the investigator know what species to expect, and which ones are things to further investigate for that particular sample type. This means they will have some idea (it may not be formal knowledge, as in taught, just experience) of the range of potential morphotypes for a particular species and be able to use that information to assess a plate quickly and accurately. Exact identification of a strain and/or species is often impossible without further testing  (e.g. you can't normally tell the difference between antibiotic resistant and non-antibiotic resistant strains without susceptibility testing, or even the difference between various Streptococcus species without testing), though pathogenic factors such as bacterial capsules in some strains of a species (e.g. capsules in *E. coli*), might be obvious from colony morphology immediately.
In the case of a pure strain streaked on a plate, as in your photo, changes in colony morphology might or might not indicate genetic changes reflected by phenotypic changes. An example might be loss of flagellae, means the bacteria are no longer motile, so the colony is less spread-out than ones with flagellae. Pigementation changes might also indicate a phenotypic and/or genetic change - perhaps processing a metabolite by a different pathway or able to do it only under certain conditions - no genetic change, just a phenotypic.

"There may also be variation in morphologies of colonies of the same
strain. Hence categorization if isolates based on specific colony
characteristics should be broad and based on several aspects of
morphology rather than on only one or two characteristics. "
What could be the variable characteristics that one should not always rely on? From my example color seems to be one.

@FreezingSoul Categorization based on colony characteristics is necessarily broad. It is usually the very first step in ID, followed by more specific tests to discriminate between species or groups of types.  If you were using a dichotomous key, it would be one of the first steps in ID it's that fundamental.

@FreezingSoul There's no one variable because it changes with each organism. An equivalent (at the risk of sounding racist; no racist intention here) might be comparing races of people - Asiatic peoples tend to have straight dark hair, so it's not a good characteristic to separate them internally into regions, but is useful to separate them from Caucasians and Africans (=genus from colony in bacteria), but in Caucasians hair might be useful for separating out groups internally (Germanic = blonde; Hispanic = dark, curly; Hibernian = red, equivalent to species within a genus for the bacteria)

Are you saying that one should learn about the possible colony variation for the potential species that could be obtained in a given case?

@FreezingSoul Yes. There's no "one answer fits all" here.

But in diagnostic microbiology, especially when the number of possible pathogens in a situation is high, there must be some terms that can be generally applied. I'm starting to become convinced that color and size are two characteristics that one should be skeptical of when interpreting. Do you have any personal experience or text that could go with this?

@FreezingSoul not really, if you know the sample type, then there are well known pathogens that are the prime candidates. E.g. for a throat sample, think streptococci, not E. coli, so looking for small creamy entire colonies +/- hemolytic on blood, then narrow down using specific tests. Try Mim's diagnostic microbiology.

Yeah, maybe i need to use this approach.

@FreezingSoul 100+ years (since the late 1800's) of diagnostic microbiology could have given you a hint that the processes and easiest ways have already been worked out. As I said in the answer, none of this is done in isolation, you have other information about the sample that can help to solve the puzzle.

Maybe, I might be wrong at some obvious cases as the throat sample. But what about the number of candidates that different types of nosocomial infections feature? Each type of infection (UTI, pneumonia....) can be caused by a good number and to make matters worse, causative bacterial species can overlap between different infection types.

@FreezingSoul You are overthinking it. In the medical training axiom: "If you hear hooves, think those are horses not those are zebras". Yes, some pathogens might be missed for rare cases, but that's where further investigation (repeat samples etc.) comes in. Overlap can be a problem, but the problem species is usually the most abundant species in the sample. Experience and training will tell you when this isn't the case!

Yeah, that's me honestly. I'm putting my hand in the jar and trying to get everything out, then end up getting nothing. Thanks for your time and help.


text:
Fate of GTP produced in the TCA cycle
As someone already mentioned in one of the following questions, the TCA circuit generates GTP in addition to NADH and FADH2.　The fate of NADH and FADH2 is clear: they are used to pump protons in the electron transfer system.
Why is GTP, not ATP, produced in Gluconeogenesis & TCA Cycle?
However, the fate of GTP seems less clearly described. I have seen a weak statement that "1 mol of GTP can produce 1 mol of ATP," but I do not know when, where, what, and how the energy of GTP is diverted to the production of ATP.
So.

My question;
When, where, what and how GTP generated in the TCA circuit is used to generate ATP

There are direct enyzme-catalyzed pathways for reversible conversions among nucleoside diphosphates and triphosphates, via nucleoside-diphosphate kinases. See also https://archive.org/details/biochemistry200100jere/page/476/mode/2up (link to Berg's Biochemistry from that Wikipedia page).
Note that all of the triphosphates are used for some things in the cell, RNA synthesis in particular, so it's necessary for the cell to be able to generate them all.


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Where is the source of H+ in the matrix that will be pumped during the electron transfer system?　Where does the OH generated at that time go?
In the electron transfer system, it has been mentioned in prior questions that complexes I, III, and IV are proton pumps and that these pumps pump protons from the matrix into the intermembrane space.

Does the formation of water inside the mitochondrial matrix help contribute to the proton gradient during the electron transport chain?
Electron Transport Chain Proton Pumping into the Intermembrane Space
How many protons are pumped out per pair of electrons from NADH in oxidative phosphorylation?

My question.

However, where are the protons in the matrix supplied from?
In other words, where does the OH- generated when the protons are generated in the matrix disappear?
Why is it not biased to the alkaline side to the extreme even though the number of proton is decreasing rapidly due to being pumped out or used to dispose of surplus electrons?

In particular, it seems that the Protons in the matrix are used to dispose of surplus electrons in the electron transfer system by combining with externally introduced O2 to produce H2O, but this seems to result in too much OH-. I would like to know the fate of the excess alkali.
See also,
https://bio.libretexts.org/Courses/University_of_California_Davis/BIS_105%3A__Biomolecules_and_Metabolism_%28Murphy%29/Electron_Transport_System

What "H2" are you referring to? Are you familiar with pH and dissociation of water into OH- and H+ (or H3O+)?

That typ. You're right, it's a proton.

I know that there exists a chemical equilibrium in which the ionization product is constant. Both H+ and OH- should be produced in the process. And if the H+ produced is pumped out, the OH will be left behind.
The protons may be used to dispose of the excess electrons, but in that case they will combine with externally introduced O2 instead of OH-. So there is even more OH- left over.
In the process, it is likely that there will be more and more OH- only.

I'm a bit unclear which part it is you're exactly trying to understand...is it that you're wondering where the "H+" comes from that combines with O2 to make H2O? Or are you wondering about the H+ pumped through the membrane?

Fate? Nothing. There is nothing in chemistry, thermodynamics or  Nature that says a cellular compartment cannot have a particular non-neutral pH. It remains alkaline until the pH gradient is used to make ATP.


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Does thermal shock apply to human bones?
I always knew that a drop of cold water would crack a hot glass. But does this apply for our bones tho? Obviously not instantly, but after repeating it for years?
I've always wanted to do cold showers and drink cold water but I instantly have these annoying thoughts that my bones would crack overtime or that my teeth would shatter.
A phobia of a thermal shock I guess.
However, I see people do ice plunges and spill iced water over themselves, and Islam makhashev going from laying on ice to the sauna: https://youtube.com/shorts/XFW29nSowAw?si=BkySqtRf2bKm5pjA
So I just wanna know does thermal shock apply to our bones? Would going from hot to cold or vice versa damage the performance of bones and joints eventually?
Also, I especially mean the spine. I Litterly cannot stand the thought that doing a cold shower would make my back like an old man's. Squicky and painful to move.

No is the answer to this - stop a think for a little bit. If this were the case, there would be many thousands of such incidents observed every year, and no-one would ever do such things as plunge into ice-cold water (there are plenty of videos of this on YouTube) or visit cold climates. Bones do not behave like glass. In addition, your bones are inside your body, where they are heated by your blood and body mass. Thermal shock does not apply.
Teeth on the other hand, can crack from cold, but it needs to be very very cold, much colder than you will ever experience unless you are visiting Antarctica in the depths of winter, or perhaps parts of the Arctic (Yukon, Siberia) in winter.
As far as I know, the only documented cases of this happening, happened to the members of Scott's Terra Nova party who went to Cape Crozier in the middle of winter to collect Emperor Penguin eggs in 1912. This was a side scientific quest apart from the attempt to be the first people to visit the South Pole, which was the main aim of the expedition. The best description of this trip to Cape Crozier is described beautifully in Apsley Cherry-Garrard's 1922 work The Worst Journey in the World (it is well worth the read, one of the best written memoirs ever).
During this voyage, the temperatures fell so low, that they weren't able to measure them accurately, but definitely below -75 F (-61 C), and resulted in their teeth cracking. For some frame of reference, your domestic freezer, where you might keep ice-cream and frozen meat runs at about -4 F (-20 C).  I suspect this was a result of a number of things, not simply cold - first and foremost being dental hygiene, which was rudimentary at best in those days. Secondarily, they had poor diet while sledding in particular, so might not have had the strongest teeth. They also were very cold (so cold they had ice inside their sleeping bags) continuously for about 3 weeks, so were chattering and/or clenching teeth almost always, so putting a lot of strain on their teeth.
To quote the book from a couple of places:

They talk of chattering teeth: but when your body chatters you may call yourself cold. | can only compare the strain to that which | have been unfortunate enough to see in a case of lockjaw...

...I don’t know why our tongues never got frozen, but all my teeth, the nerves of which had been killed, split to pieces.

Now this is exceptionally rare. You are very very very unlikely to experience anything like this, under conditions of hardship such as these men experienced, certainly not from drinking cold drinks or taking a cold shower.


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How are some plants and trees able to grow and thrive on little to no soil?
I was watching a documentary about abandoned soviet structures and cities. At the beginning of the documentary a piece of drone footage is shown featuring the abandoned flats of pripyat from above. While watching it i noticed something very peculiar, there were several fullgrown shrubs and even a tree growing on top of the roofs of the flats.

The red arrow points at a berch tree that's apparently growing on top of the rooftop as well. How is such a large plant able to grow there? I've seen plants grow in strange places in my own city Groningen as well. Here's an example of small shrubs that managed to grow out of asphalt.

Here are a couple of pictures of 2 seedlings that are growing out of a hole of a rotten piece of wood. The hole does not go all the way through the wood, so the roots are not in contact with the soil.

According to ChatGPT one explanation could be that over time, organic debris like leaves, bird droppings, and dead insects can accumulate on surfaces. This can decompose and form a thin layer of organic matter that serves as a growing medium for plants. But I can't believe that a tree such as the birch tree in the first video still could grow so large using only organic matter that deposited on the rooftop.
So how does this work? Can trees and shrubs use different materials like asphalt or roofpanels to extract nutrients from when there is little to no soil available? If so, how do they do it?

What two main things are plants made of (think of photosynthesis), and where do those things come from?

@BryanKrause, Plants need minerals as well..

Sure, but not in the same quantities. I'm not really sure what you're looking for in an answer: clearly plants you see growing somewhere are getting everything they need there, or you're assuming they need more than they actually do. Exactly how they get it will depend on the exact situation, and the plants will grow just as much as they're capable of in the conditions.

Plants mostly need air, sunlight, water, and the appropriate range of temperature to grow. Growing through asphalt is not uncommon; water seeps through a break in the asphalt, reaching a seed beneath it, which (believe it or not) when it swells with water is able to break up the asphalt. They also need nitrogen, potassium,  phosphorus, and iron, but not in great amounts.

I think the key is gene expression (specifically, plant response to stress). Plants are living organisms whose genetic material gets altered over time to express what is needed to grow in whatever environment they are.

Bromeliads are called air-plants because they don't need soil, just rain and run off from above.
Photo 3/ That is a plant with big cotyledon leaves which comes from a big seed with lots of energy resources. As the seed sprouts it transforms ambient water into a radicle (embryonic root) of 10-20-30cm that is biologically designed to survive challenging conditions, grow straight down and find soil. Wet rotten wood is a perfect medium for propagation of radicles, it has a PH of 4-6 after a few years, which is similar to the humic acid rich leaf humus of the forest, and is easy for the taproot to travel down 20-30cm at a rate of an inch per day, to find regular water.
Photo 2/ A growing root cell's turgor pressure can be up to 0.6 MPa, which is over three times that of a car tire. Roots can search their environment using micron-thin rootlets the width of individual cells that propagate forwards and under patches of wet leaves or moss where they sprout in the spring time. A tree just has to find a hairline crack through the tarmac to establish a lifeline to the soil. Once it is there, the cells can use chemistry to pump water like a hydraulic jack and push new cells upwards through tarmac. Redwood bark cells have 115m of water pressure, equivalent to a hose that ascends a 35 story building. 20m of water pressure in a hose is very difficult to stop manually.
Photo 1/ That roof collects a lot of water when it does rain, which can collect in pools, under cracked asphat roof linings, and can create pools and cool damp zones in the abandoned building interstices which last for some weeks in summer. They are as big as their access to soil permits.
Those trees require a lot of water for the summer and are sized relative to their resources, they are northern plants like birch who's white trunk is white flexible bark which protects from cold and fast temperature changes due to frost and sun, it also reflects summer sun so that the tree stays cooler in arid times.
Trees also meter their growth by available soil and water and make natural bonsais. There are trees in cliffs with a thousand years of narrow growth rings that are just 1-2 meters tall. Bonsai cliff trees are often prized for dendrochronology.

These are highly specific adaptations to an environment with specific traits. Organisms that are pushing their boundaries (pH, amount of needed water and nutrients and specific proportions, etc...) in some direction. This could be plant adaptations to salt stress, heavy metal stress, or to high temperature, low temperature, or even drought conditions.
The key is the regulation of gene expression to produce the gene products necessary for a given environment.


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What is the difference between added sugars and natural sugars in processed foods?
While buying juices, I came across two options, one with no added sugars, one with added sugars. The one with no added sugars had 11 grams of sugars, the one with added sugars had also 11 grams of sugar.
Hence my wonder, does it matter what is the source of your sugar intake, whether it is naturally occurring or artificially added?
I generally don't worry about how sweet something is as long as it’s natural, like mangoes are very sweet, but my mind tells me it’s a fruit hence healthy and I am neither diabetic nor fat, so mangoes are ok for me. But still I don't eat candies or other man-made sweet stuff because my mind says it’s artificial. Is my mind right or wrong?

One of the ways to measure the impacts of sugar in different foods is with the glycemic index, which is a measure of how quickly blood sugar rises after eating. Faster rises in blood sugar are thought to contribute to the development of diabetes and possibly contribute to weight gain, though as with most nutrition science the specifics are very difficult to study due to the difficulty of conducting true randomized trials over a long time period (people just won't stick to eating what a study assigns them to eat) and a vast array of potential individual differences in digestion and metabolism.
Generally, the glycemic index for a piece of fruit will be low despite containing sugars, because fruit also contains other things like fiber which slows the rate at which sugar is absorbed. Adding just sugar to any food will always increase the glycemic index, because added sugar isn't coming with anything to slow it down.
Sugar in juices are typically going to be absorbed quickly, whether the sugar came from the fruit (like an apple juice) or is added (like a lemonade), because you're typically removing the parts of the fruit that slow digestion (the fiber) when you make juice. If you have some hypothetical glass of juice, process it to magically remove just the sugar, and then add that much sugar back in, no, it won't matter that the sugar is now considered "added" versus not.
Labeling of added sugars is just intended to help you identify foods that have extra added sugars; it does not help you identify if the natural occurring sugars in something are going to contribute to a rapid increase in blood sugar or not. Manufacturers can use different tricks to avoid their sugars being considered "added", such as blending apple juice with a more sour fruit (the apple juice is mostly there to add sugar, yet isn't considered "added sugar" because it isn't added as sugar, it's added as sugary juice).

Sugar doesn't cause diabetes. However, being overweight is a risk factor for diabetes, and weight gain is caused by consuming to many calories. The biggest concern from added sugars should be consuming too many calories, since sugars are caloric, and manufacturers like to add a lot of sugar when they add sugar. If you're already diabetic, both added and natural sugars need to be regulated.

@Vaelus Ultimately diabetes is an insulin dysfunction; type 2 diabetes specifically is insulin insensitivity. Peaks in blood sugar result in peaks of insulin; not necessarily the same effect as total sugar in the diet. The cause and effect structure of weight gain and diabetes is not entirely clear.

Excess weight is not known to cause insulin resistance, but it's know to be a risk factor. None of the reputable health information websites I've searched (government health agencies, diabetic association's, etc.) even list sugar consumption as a risk factor. I do not regularly read literature on the topic, however, and perhaps you do. Are you saying you're aware of recent literature on the topic strongly indicating the possibilty of a causal link between sugar intake (binging, I suppose) and insulin resistance?

@Vaelus Like I said in the answer, it's hard to identify causality because of difficulty in doing experimental research and co-occurrence of potential risk factors. https://doi.org/10.2337%2Fdc10-1079 is an example paper that purports a link with sugar specifically beyond weight. I would not call this idea recent.

That particular study explicitly does not control for excess weight, and right in the conclusion, it says: "These data provide empirical evidence that intake of SSBs should be limited to reduce obesity-related risk of chronic metabolic diseases" (emphasis mine). To completely clear, I assert that government health agencies are competently communicating the best current scientifict concensus of risk factors for diabetes, and sugar intake independently from obesisty is not one of them. Therefore this answer would be improved by removing the focus on risk of diabetes.

@Vaelus: My comment on the question was inexplicably removed despite being relevant, and it also partially addresses your inquiry here. It linked to this study which of course some people wish to suppress. It is very well-known that there is a significant correlation between soft drink intake (e.g. coca cola) and diabetes, and also reason to believe that there is a causal relationship. Now we have evidence that sweeteners too are related.

@Vaelus: Indeed, I have searched hard too, yet nowhere could I find proper studies linking sugar intake and diabetes, when controlling for smoking, alcohol, and healthy diet excluding amount of sugar consumed.

The label is so you know how much sugar has been added, and juice just has issues with the label in the US.
It is put on the label so you can see how much sugar the companies are adding, compared to how much it contains normally. Most people would not have any idea how much sugar, say bread or juice, contains naturally, so it is important to know how many empty calories companies are adding.
Your mindset is the very issue. A loaf of bread or bottle of juice may have more than a candybar's worth of sugar added just to make it easier to sell. So you are eating lots of candy without knowing it. A bottle of juice may have just as much sugar as soda or other drinks we think of as "sugary". This is an issue in the US, because the US has little regulation on adding sugar (due to a powerful lobby), so many things are loaded with extra sugar. Your body does not care whether the added sugar is in a candy or or bread, or juice. This is one reason the US consumes 5 times the recommended amount of sugar.
From the FDA and CDC

The Dietary Guidelines for Americans recommends limiting calories from
added sugars to less than 10 percent of total calories per day. For
example, if you consume a 2,000 calorie daily diet, that would be 200
calories or 50 grams of added sugars per day. Consuming too much added
sugars can make it difficult to meet nutrient needs while staying
within calorie limits. Added sugars are listed on the Nutrition Facts
label so that you can make informed choices, based on your individual
needs and preferences.

If both juices had the same amount of sugar one was likely lying, again US crap regulation. They can put "no added sugar" on the label while still adding lots of sugar in forms like extra concentrate or honey, or agave nectar. Other countries are a lot more strict about what counts as added sugar. Added sugar is not bound in fiber or other things that slow the absorption.
To be accurate, the causes of diabetes are still being deeply studied because the complete mechanisms are not known. But one thing we have good evidence for is rapid absorption of sugar likely contributes to diabetes. Added sugar is essentially always rapidly absorbed and thus is a contributor to insulin resistance. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3836142/#:~:text=Diets%20with%20high%20glycemic%20index,risk%20of%20type%202%20diabetes.
There are other factors as well. Excess sugar is basically always turned directly into fat and for actual diabetics, added sugar is an even bigger deal, so knowing how much added sugar is present is important for making knowledgeable choices.
A final consideration: Much of the sugar in candy is made from vegetables (beats, corn, or cane), so just because it comes from something healthy does not make it healthy.

Your last sentence goes the other way too. Just because a sugar source is a fruit or vegetable (e.g. sugar cane) does not imply it is healthy to eat much of it!

@user21820 of course, as I said, the body does not care where the sugar comes from but how fast it makes it into the blood stream.

@John by that logic it seems that I could come up with a balanced diet that consisted of candy (or raw sugar) combined with various nutrients and fiber.  Regarding excess sugar "always" being turned directly into fat I'm wondering if that is "always" true - have there been any studies done on people who eat an excess of calories (even considering activity) but never seem to gain weight to see if they may be eliminating some of the calories unprocessed?

@Michael sure if you added the other macronutrients, and mixed it to get the benefit of the fiber, artificial compiled food sources similar to that exist. Also such people don't exist outside a few fatal cases, some people just burn more calories through higher basal metabolic rates. often through less efficient mitochondria. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5786199/ and https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4535334/

Natural sugars are mostly glucose, fructose, and saccarose. Added sugars can be anything, from glucose to a variety of syrups. There isn't much difference, although caramelized sugars (brown syrups) also contain longer carbohydrates, and if the caramelization process is not good, other complex molecules can form. Industrial sugars also contain extra additives, colorants, and stabilizers (https://en.wikipedia.org/wiki/Anticaking_agent , https://infinitabiotech.com/blog/sugar-processing-chemicals , https://en.wikipedia.org/wiki/Corn_syrup , https://hummingbirdmarket.com/blogs/news/what-are-the-chemicals-in-white-sugar). In theory, all safe substances. In practice, only time will tell... The calories are the same.

Can you please add some references for stabilizers in industrial sugar? The plain sugar you buy in the store is something like 99.9% saccharose. It is of biological origin, so not, there is not difference.

@Chris I have added a few links

@alec_djinn: All those links seem to be about agents added to table sugar not to sugars added in industrial sugar production.

@JackAidley, it is a general overview of sugar production. Not only table sugar, but in general powder sugar and syrups.

If you live in the E.U., a beverage labeled "juice" may not contain added sugar. If both beverages you compare are 100% juice from the same fruit, adding sugar to one would lead to it having a higher overall sugar content than the unaltered one. So let's assume that the drinks are from the same fruit, but the one with added sugar is diluted.
It is typical that the taste of diluted juices is improved with added sugars. The resulting overall sugar contents may add up to be the same as for the original juice, but obviously only half of the more desirable fruit components are present together with it.
Thus, the added sugar is not a bad thing in itself but rather an indicator for a bad thing: It indicates that the beverage contains less of the more desirable constituents; it is an inferior product.
That can be the case with many processed foods: Ketchup with more added sugar was made from inferior tomatoes, a ready-made meal with a lot of added sugar wouldn't have much flavor without it etc.

The FDA explains the nutrition label requirements.
https://www.fda.gov/food/nutrition-facts-label/added-sugars-nutrition-facts-label

Total Sugars include sugars naturally present in many nutritious foods and beverages, such as sugar in milk and fruits as well as any added sugars that may be present in the product. There is no Daily Value* for total sugars because no recommendation has been made for the total amount to eat in a day.
Added sugars include sugars that are added during the processing of foods (such as sucrose or dextrose), foods packaged as sweeteners (such as table sugar), sugars from syrups and honey, and sugars from concentrated fruit or vegetable juices. They do not include naturally occurring sugars that are found in milk, fruits, and vegetables. The Daily Value for added sugars is 50 grams per day based on a 2,000 calorie daily diet.
For most Americans, the main sources of added sugars are sugar-sweetened beverages, baked goods, desserts, and sweets.

Notice the order of ingredients (high to low) in Ocean Spray's Cran-Apple juice:

Water
Sugar
Cranberry juice
Apple juice

You can assume that the 23 (out of 26 total) added sugars are literal sugar added to the juice to make it more palatable. The other 3 are cranberry and apple sugars.

Aside from the Vitamin C, there is no reason for this food item to exist. It is literally an excess sugar beverage.


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EasyHLA HLA Upgrade Tool Website does not work
I'm trying to use Easy HLA, HLA Upgrade (https://hla.univ-nantes.fr/recherche/recherche.php) to impute my low resolution typings into high resolution ones but I have this error when I upload my file:

Has anyone ever used this tool? I wanted to use it because it is said to be better than HaploStats (couldn't find a reliable source though) but I couldn't make it work so I cannot even compare them.

This isn't really the kind of question we welcome here, though I can understand your desire for an answer and the logic to posting it on Biology.SE. I'm a technophobe, so when I'm frustrated by a product (if I paid for it), I call their customer or tech support. If it's a popular product, it may have its own forum for problem solving. No disrespect intended, just trying to help (with the full realization that help isn't likely to come from a technophobe!)

Oh I'm sorry, I was hoping someone might have been using it on a regular basis.

I’m voting to close this question because this is not about a problem in biology.

Not a problem at all; as I mentioned, it was a logical place to post. Please don't take the closure personally; it's a site issue. I forgot to say welcome. Welcome! I hope we can help you in some other way(s). :)

A 504 error is a server error caused by lack of response of an upstream server. The website owners are the only people who can fix it. You might be able to contact a webmaster for the page indicated (try going to the homepage and see if there is a webmaster contact).

I have used it in the past and you typically have to wait several hours between the moment where you upload the file and the moment you can download the result. The website will not be accessible in the meantime.
About a source proving it's better, there is a github repository I found a few weeks ago that benchmarks different imputation tools and does find better results for HLA Upgrade compared to HaploStats as you mentioned. However, it seems HaploSFHI yields better results overall. It's only one random github repository though, I wouldn't trust it blindly.

Oh yes you're right, my file went through!! Thank you

You can also contact them at easy-hla@univ-nantes.fr, it's hard to find but it''s written at the bottom of the page ;)

Huzzah! An answer!


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Is it rare for a virus to be similar to its host?
Halomonas bacteriophage vB_HmeY_H4907 discovered recently in the Mariana trench is apparently highly homologous to its host:

To our best knowledge, it is the deepest isolated siphovirus from the ocean. Its 40,452 bp linear dsDNA genome has 57.64% GC content and 55 open reading frames, and it is highly homologous to its host.

Naïvely, this seems to suggests to be an evidence in favor of a particular hypothesis of the origin of viruses - as runaway genetic elements.
Questions:

Is it common for a viral genome to be homologous to its host (or another cellular organism)?
Is such homology an evidence in favor of a particular hypothesis of the origin of viruses - as runaway genetic elements?

References:
Identification and genomic analysis of temperate Halomonas bacteriophage vB_HmeY_H4907 from the surface sediment of the Mariana Trench at a depth of 8,900 m
For laymen interpretation see, e.g., Virus from depths of the Mariana Trench uncovered or Deepest Virus Ever Detected Unearthed by Scientists in the Mariana Trench

Funny to see something "unearthed" in the ocean... Language can be wonderful at times.

Please read the paper and find out in what specific way the authors of the paper think the virus is “homologous” to the host (and indeed tell us what the host is). Then modify your question accordingly. By itself the word “homologous” is unclear.

@David I think the second sentence in the quote, where the first half of the sentence is talking about the genome, indicates sequence homology. I'm not sure any other homology would make sense in context. Sure, I think this could be clarified, but the authors are making a relatively qualitative statement here anyways.

@BryanKrause DNA, RNA, encoded protein? For how many genes? The question does not say and is therefore unclear. I have asked the poster to clarify and think that perfectly reasonable. Too many questions (and answers) are of little use here because their subject is not clearly defined. This can be because the poster assumes everyone knows what he is talking about, but often is because he is not clear about the problem. In this case going back to sort this out is an important learning experience. If the poster is not prepared to engage with us we should not engage with him.

Phage similarity to host
Briefly, yes. Generally speaking phage have relatively similar compositional features (e.g. k-mer frequency, see linked paper) and also direct homology (large regions of sequence similarity) to their host genome, compared to a null model. Methods leveraging this have been used (with some success) to predict hosts.
Support for hypotheses of origin
I think that there are multiple possible mechanisms for how similarity arises:

Gene conversion between phage-host
accidental packaging of host genome
phage integration as endovirus (possibly as a "dead" copy) and neofunctionalization.

I think that these mechanisms don't directly contradict your hypothesis. In fact, the presence of auxiliary metabolic genes in phage might argue in favor of it.
But at the end of the day, the phage and the host are just swapping DNA at a nonzero rate, and you'd expect them to be more similar than otherwise.

“Compositional features”? The question is not clear on what it means by homology, and your answer does not say what compositional features you are talking about. Size? An RNA genome surrounded by a protein coat? A genome that does not encode ribosomal components?

@David "composition" is usually used to refer to nucleotide, GC, or k-mer frequencies in the context of DNA sequences. "Homology" is generally understood in genomics to refer to regions of sequence similarity. (As described in the linked paper.) I have updated the answer to reflect this.

As I implied in the original version of my request to the OP, to the man with a hammer, everything looks like a nail. Composition means composition. In the context of a genome it could mean the number and functional distribution of genes, whether they were ss, ds, RNA or DNA, their base composition etc. And your answer ignores the vast differences between viruses in the same organism: simple RNA phages like Qbeta, v. large T5. Even human herpes viruses show vastly different GC contents, and, of course they are quite different from polio and from SV40.

@David certainly- variation exists. The question, as I understand it, is whether that variation shows any association to the host, or whether it is agnostic to the host. If you are frustrated with genomics terminology at large, and the discipline's attempt to reduce everything to sequence data, then I will happily agree that it is annoying.

I am not frustrated with genomics terminology, I resent imprecise terminology and lack of context that make statements ambiguous and scientific discussion pointless. I know about viruses, I know about relationships between viruses and hosts, viruses and viruses and genes within viruses. I have now read the paper, and have, I think, managed to fathom what the authors mean in their sloppy usage of the term "homologous". As their first language is not English they are only partly to blame for this — the journal editors should take their share. If I chose to answer this question I will explain.


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Are cytoplasm and collagen basic in nature?
Eosin is acidic in nature. Hematoxylin is basic in nature. What I have learnt about H and E staining is that the nucleus is blue in colour because it is acidic and takes up the basic dye, Hematoxylin. But I don’t understand why collagen and the cytoplasm appear pink? Is it because they are basic? Is collagen a basic protein which takes up eosin and appears pink? Is cytoplasm basic in nature? What am I missing?

Eosin generally stains anything with protein, and that includes the cytoplasm (full of dissolved protein) and collagen (made of protein).  It is also very nonspecific.  If you take a section or even live tissue/cells and put in eosin, almost everything will label to some extent.  When making H&E slides, they wash after staining to remove the less tightly bound dye, but even then almost all structures are labeled to some extent, with basic ones simply being brighter.

Hey Thanks a lot.


text:
Is it possible to reconnect a severed tree trunk and save a tree?
I ask this question because I saw in a the news recently (September 28, 2023) that some vandal cut down the famous Sycamore Gap Tree

I know people normally don't put trees back together, but from what little I know about plant biology and tree trunks, I thought it might be possible, with some extra effort. The inner part of the tree is dead wood anyway, so perhaps that could be fused with internal steel rods, sort of like how surgeons use metal to align broken leg bones. Then, perhaps, the sap-carrying outer layer, under the bark, could be realigned and protected in some way so that it could grow back together?
Has it ever been done? Do you think it could be possible?

Potentially, but the forces involved with a tree in wind are enormous, so I don't think it would work. Not certain though - grafting is certainly possible on trees.

I would try reattaching it with an specialized bioreactor pumping some nutrient medium, do periodic analysis, readjust nutrient input, etcetera, but it would cost a lot only doing the very much needed previous research on the topic. Maybe some A-Team of biotechnologists and physicists could pull it off.

I asked a similar question which was closed as a duplicate.  But my question really is, why does this not appear to even have been considered?  I get that there are challenges and it would be expensive, but for something that touches the public to this extent why not at least try?   Is it known impossible for some reason? https://biology.stackexchange.com/questions/113166/why-couldnt-grafting-save-the-sycamore-gap-tree

Maybe because Northumberland council is cash-strapped, but that'd be a question to ask them. @CrashGordon


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Determining the Length of DNA in a Human Spermatozoon
Hello everyone,
I’m currently trying to solve a problem related to DNA length in human spermatozoa and could use some guidance.
The problem states: “The DNA of one human spermatozoon contains 10^23 pairs of nitrogenous bases. Determine the length of the DNA molecule in a human sperm.”
I know that the distance between two base pairs in a DNA molecule is approximately 0.34 nm. So, I’m thinking that I need to multiply the number of base pairs by this distance to get the length of the DNA molecule.
However, I’m not entirely sure if this is correct or if there are other factors I need to consider. Also, I understand that this calculation will give an approximate value and the actual length can vary depending on the specific sequence of the DNA molecule.
Could anyone confirm if my approach is correct or provide guidance on how to accurately calculate this length? Any help would be greatly appreciated!
Thank you in advance.

Hi Wino, welcome! Is the question about bp length or actual length? If this is about bp length then I think the answer is in your question. Maybe there is some additional context to the problem?

This site is not a service for people to check their homework before submitting it. Please desist.

10^23 is an absurdly large number. Should be 10^9 ish. Approach seems correct. There is a book Cell Biology by the Numbers which you can use to verify your answer.


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Does this cryoEM micrograph show one or two macrophages?

Attribution: CC BY 2.0 DEED NIAID.
The image description says "Colorized scanning electron micrograph of a macrophage," implying this is just one macrophage. Is this true? If so, what is the cleavage-looking feature in the middle of the macrophage?


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Looking for literature that gives a systematic presentation of geometric and topological features of trees
Introduction
I am a software engineer specializing in procedural generation of 3D models, and currently I'm building a generator for 3D models of trees, founded on the theoretical work of Aristid Lindenmayer. Having successfully constructed the system framework, my next endeavor is to incorporate distinct tree species models for generation.
Challenge at Hand
Despite my proficiency in software development, I lack the comprehensive biological knowledge essential to accurately deduce tree morphologies from visual references. I feel like my unfamiliarity with botanical terminology and key morphological features of trees prevents me from "seeing" the important parts of tree morphology.
Request for Assistance
To achieve a high degree of biological accuracy in my models, I seek recommendations for literature detailing the fundamental principles governing visible tree features. This includes the distribution of branches and sub-branches, inherent regularities and anomalies of certain features, variations in tree girth across species, potential branch count and orientations specific to species, among other external features. It would be great if the resource is supplemented with illustrative diagrams. Currently, my primary interest lies in modeling Conifers, hence a dedicated section on this category would be nice.I'm not interested in chemical or developmental models. At the moment I'm just interested in the analysis geometric (quantitative) and topological (qualitative) features of trees.

Welcome to the Biology Stack. Please continue the [tour] and visit the [help] for more information on this stack and how we work. Please note the homework requirement.

I have a couple of questions about your question - 1) by "principles" do you mean how they form or just the different types of form (leaf arrangements, types etc.)? 2)What do you already know about the above (see homework...). Please also note there are roughly 73,000 tree species and about 600 different class Pinopsida species, so a general answer might not be possible, though going up a couple of divisions from species to family, might be able to generalize at that level. There will also be well studied species (timber ones) like Pinus radiata you should look into.

Not meaning to spam you at all... but a nice bit of nominative determinism in Aristrid's name - Linden is a type of tree; Tilia genus, and Meyer means "farmer" so (Linden) tree farmer.

@bob1 Thanks for the feedback sir! I added the homework tag since my question is of that kind -- it addresses a kind of basic biology concept that is trivial to professionals. Feel free to edit my question the way you see it fit. I'm new to the stack so please forgive is the question doesn't belong here.

@bob1 As for the clarifications: 1) currently I'm not interested in developmental models, so formation processes are of a lesser interest to me. References on the topic are welcome though, as I will be interested in learning about it at a future time. 2) As I mentioned, my background in biology is thin. Most of the things I know about the topic are things from computer science literature and papers. They mostly don't do a comprehensive analysis of tree features. They do a kind of pragmatical analysis that helps the models "looks good" without really diving deep into biological side of things.

@bob1 What I would like is some sort of a starting point literature for me to get familiar with the biology side of this multifaceted coin. An example of the type of "laws" I'm looking for is say how the cross section area of the branches changes at branching points. One other example would be what types of branchings are most likely to be found on tree species. By "types of branching" I mean qualitatively different types. Conifer trees usually branch away from one single main pole that doesn't change direction, while say apple tree's "main" branch changes the direction. That type of things.

@bob1 I'm aware that I can find this type of things sporadically on blogs etc., but I would like to have a comprehensive book(s) that goes through this topic in a systematic fashion, because blogs are usually focused on one topic and I have to know about the topic in the first place in order to find it. But since I'm a total beginner in learning biology and botany I don't even know the types of questions I can ask, so a list of books that I can study would be a gold mine for me. Also thanks for the bit of trivia you posted, it's always fun to find out about such unexpected connections.

Those sorts of information might be tricky to find, if they have been studied at all. I would start looking for forestry information on Pinus radiata, though there they are more interested in having a straight trunk and aren't interested in the branches so much, but cross-section of the trunk at branching might have been looked at.


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Why do damaged joints or ligaments experience inflammation? Why do physiotherapists try to stop inflammation as part of the healing process?
I have had the repeated experience of going to physiotherapists with injuries to ligaments or joints and they all expressly aim to reduce inflammation.
I don’t understand this. Our mammalian (and previously reptilian ?) bodies have been using inflammation for hundreds of millions of years (mammals have been around for 167-220 million years). Surely this is a tried and true response to injuries and healing injuries - those organisms that practice it have been selected for because it works.
Do all mammals experience inflammation in response to injuries? Do reptiles? Why is inflammation considered to be a bad response? Or in other words - why does my physiotherapist(s) actively fight hundreds of millions of years of evolution to stop this response?
I understand that stopping inflammation reduces pain- but surely it also stops natures tried and true native healing response?

Welcome to Biology.SE. There is a (very strong) recommendation to show evidence of research (a quote with a link) included with your question. What have you read about inflammation and how it is good/healing for the body? Is there a difference between acute and chronic inflammation? Why are anti inflammatories and physiotherapy helpful? Not everything that is natural is good.

Similar underlying question: What is the benefit of fever during infections?

Agoodnurse: This is my research. That’s why I am on this forum - to ask questions and get answers that inform me of the right view on this!

You're right, inflammation is a healing response-at first. Whenever we get hurt, such as an infection or a knee injury, inflammation is part of our healing response, and helps to recruit a further immune response-sort of a cause and effect. Problem is when inflammation doesn't cease. This can be caused by a number of issues, such as autoimmune disorders, arthritis, I'm forgetting a few. If the joint stays inflamed, then the added swelling caused by fluid can put pressure on the joint & nerves causing pain.
I like to think about it like a plant-if it's dry, we water it. But if we keep watering it the plant will rot, the best move is to cut the watering down.


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Can hybrids from closely related species with similar chromosomes reproduce?
Let's say the plant Triticum monococcum which has 2 sets of 7 chromosomes when diploid and 1 set of 7 chromosomes when haploid has the genome AA. When interbred with a different species that has the same sets and number of chromosomes when diploid and haploid but instead has the genome BB, the hybrid produced would have a genome of AB and 2 sets of 7 chromosomes as well, just that the sets of chromosomes would be genetically different although similar. This hybrid is known to be sterile.
I thought that because both parents had the same number of chromosomes which are similar, the hybrid would be able to reproduce, just not an offspring that is also like itself (unless an autopolyploidy event occurs).
To show what I mean, given that the hybrid has the genome AB, 2n=14, it would undergo meiosis and given that no variations occur the result would lead to gamete 1 which has recombinants of the chromosomes, and gamete 2 which has the remaining chromosomes. Would not these gametes be able to reproduce with others?


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How do molecular biologists typically get their oligos?
What's the typical route taken to obtain synthetic DNA/RNA samples in practice? Are they pretty much always custom ordered from a place that prints them using sold-phase synthesis, or can you cobble them together from random "common" samples?
Theoretically I could see an arbitrary 120bp oligonucleotide being made of 2-3 strands from random parts of across a genome or two, where you could separate out those parts with restriction enzymes and then anneal the snippets, but A) I don't know how you'd find those snippets reliably or whether my assumption that they'd exist in a random sequenced genome, or B) whether it's even efficient to try to digest, isolate, assemble and purify oligos that way when compared to buying a printed synthetic oligo

Depends on your application. For smaller to medium sized DNA oligos (<~120 bp) or medium sized dsDNA fragments (<3kb), I will always order them. What you're describing sounds a bit like Gibson assembly cloning (https://en.wikipedia.org/wiki/Gibson_assembly), and I would only go that route for fragments upwards of ~3kb, unless I needed to make several of them at once (also assuming I know the full sequence needed). Larger fragments can be purchased, but the price per bp can get high for very long fragments (still might be worth it for a one-off).

I see, is the same true for RNAs or would you just order a template DNA and run in vitro transcription?

@MikeyC i think that your comment is a different (and possibly more useful) answer from mine if you want to post it there

Depends.
For short defined sequences, IDT or a similar oligo synthesis provider is your best bet. It's very fast and straightforward, compared to trying to do something complicated with a genome. Recall that the number of possible e.g. 120mers is $4^{120}$, or $1.7668471*10^{72}$. That's an astronomically large number, and the probability of finding it in some random convenient genome is small.
For e.g. single well-studied genes, you might order a plasmid vector from AddGene or similar, which you can put into E. coli and grow up to make many copies.
If you are trying to isolate something a little less standard, you will usually clone it out of the genome though.


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Help identifying insect
I live in Milan, Italy in the city center.
I started seeing this insect in August after a long vacation. In this periods the temperature inside the house went up to 36°C (temperatures here range from -1°C to +35°C in average).
I find it mostly in my kitchen in particular in a cabinet where i store food.
The size is about 3mm in length and less than 1mm in width.
What is its name so I can research more about it (i.e., does it pose any risk to my health or to my belongings in the house?)?
I have tried to use a common bug spray to get rid of it (i.e., emptied the cupboard, got rid of food that was not sealed and sprayed the cabinet profusely). It was unsuccessful as after 10-15 days it came back.
Is there a more appropriate bug spray to get rid of this insect?
Should I be looking for nests or eggs?

EDIT
Additional close-up pictures with a cheap microscope.

Welcome back to the Biology Stack. Unfortunately that photo is too low quality to say anything about the insect, we would at least need to see photos of the back of the insect and they would need to have higher resolution to properly identify it. Your best bet is to contact a local pest control company and have them come out and do an assessment.

Thank you for the comment. I have added some pictures, I don’t know if they are very helpful.

Much better. Something in the beetle family I think, but there are a few experts on here, who I will leave it to.

Can't give a species but my first thought would be a grain/flour beetle; you might check your food again, especially any grain, flour, cereal, etc. They may be able to enter through packaging, depending on the packaging type. I wouldn't think you need any pesticides, just to identify the infested food and wipe up any remaining beetles/eggs/larvae, but if the problem persists you could consult a local expert.

Would you know what kind of bug spray should I try before I call pest control?

I don't think a spray is going to help. If I'm right, they're in your food. Spraying outside the food doesn't get the ones that are in your food. Spraying your food directly is not wise because you don't want to be eating the stuff you're spraying. You'll need to find what is infested before you continue. If there are beetles to wipe up, I'd think just a soapy rag is going to be better than any insecticide spray.


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Hypothetical violation of independence assumption for linear models
Let's say I have measured the abscisic acid content (could be any metabolite really) of 10 individual plants which we can consider biologically independent. Then I repeat that measurement for all 10 plants on 15 different days over the course of a year. I then want to correlate, with a linear regression model, the values of abscisic acid with the amount of rainfall (from publicly available regional data, say) on each of those days. What is statistically appropriate?
Firstly, I believe that a mixed model should be used, with individual plant as a random effect, to account for the fact that I am repeatedly measuring the same plant over time.
On top of that, am I not also in danger of pseudo-replication from the fact that my rainfall has only been measured once for all 10 abscisic acid measurements (i.e. the abscisic acid vs rainfall measurements are not really independent on each day either)?

Observations are assumed to be independent, not predictors. For example, if you were doing some chemical fertilizer treatment, you'd probably not apply a random chemical or random dose of chemical to each plant, you'd most often choose a small number of doses, and have far fewer values of the predictor than you have observations.
But, I do think you've identified a potential issue here, it's just that it isn't about repetition in the rainfall measurements, it's about additional repetition besides rainfall in your observations: there are going to be a lot of other environmental variables, besides the one you measured, that are the same for all the plants because you're measuring them on the same day, and that's potentially going to introduce correlations in same-day measurements.
It probably makes sense to account for that using a random effect for observation day, in addition to a random effect for each plant.
That approach may not work well if there are other specific factors that have a substantial impact (you should try to measure and account for those directly, instead), or if it's not really right to make the choice of day as a "random" feature, for example if there are seasonal variations you may need to track time explicitly. It all depends on what you know about the system you're studying.


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Induction of IFN-beta in HEK293T
I'm trying to increase expression of a protein we're attempting to study, UBL7, supposedly unregulated by Type I Interferon and particularly IFN-beta.
I've tried treating HEK293T cells (~60% confluence) with 0, 5, 15, 45, 90, 135ng/ml recombinant IFN-beta for 36 hours.
Based on the (quite vague) protocol we're following (Figure 7B) this should be well more than enough to observe a change in both UBL7 and our positive control ISG15. Instead, UBL7 levels are unchanged from 0ng/ml, and no ISG15 is observed. IFN-beta was added directly to DMEM media in a 6-well plate.
I'm quite new to cell culture so if there's some glaring issue please don't hesitate to call me out, I really don't see how no change at all is occurring :( thanks!
Note: the first figure uses PBMCs, but my figure (7b) uses 293T!

HEK293 cells (whatever the variety) are not an excellent substitute for PBMCs, as they are from a completely different cell lineage and behave very differently in a lot of ways. However, if the paper or protocol you're following uses them, I would also, at first, until you can get your hands on some PBMCs. I don't recall at the moment if 293T cells are sensitive to IFN-$\beta$, but I'll assume for the moment that they are.
I would first test your stock of IFN-$\beta$ to make sure it is active. If ISG-15 is supposed to be upregulated and it isn't, then your IFN treatment isn't working. Get a fresh supply of lyophilized IFN-$\beta$, reconstitute it according to the instructions, aliquot it into single-use portions, store the aliquots at -80, and avoid freeze/thaw cycles. Improper storage can kill cytokine activity. If you must store it at -20, make sure it is a manual defrost freezer (ice forms on the inside over time), as automatic defrost freezers change the temperature and cause the contents to thaw and freeze again. Don't store it at +4 or on wet ice except for during the day while you're using it.
Another line of investigation would be to perform cell counts of the different treatment conditions to ensure that your treatment isn't affecting the cells' growth rate, either positively or negatively. At the same time, determine the protein concentration of your lysates (if you're making them to do your analysis) to ensure they're not different across the conditions.
Finally, while this won't affect your current issue, I would strongly recommend making serial dilutions of your treatment concentrations. 2x, 5x, and 10x are all common dilution schemes. Make your most concentration dilution in one tube, then serially dilute it from that tube into another, then that tube into another, and so on. It helps reduce variability.
Don't worry about things not working the first time. Take a break, think carefully about possible reasons, and correct those issues one at a time so you're not trying to study multiple variables at once. Good luck!


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Can someone with albinism have red hair with very pale skin and blue eyes?
I have heard of a type of albinism that occurs in races with darker skin that can give people red hair, but in the pictures I've seen, they usually have reddish-brown hair, a medium skin tone, and brown eyes.
Would it be possible for someone to have the very pale skin and light blue eyes typically associated with albinism while also having red hair? I have seen a picture of someone with this appearance, but their hair looked like it could have been dyed since it was brighter than natural red hair usually is.
If there is no form of albinism that causes this, is it a form that could possibly exist, or is there a particular reason that those traits couldn't come together?

Just a terminology note: race is a social construct, not a biological distinction. The American Association of Physical Anthropologists' 2019 statement on Race and Racism may help you understand the issue more.


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How does blood flow to and from the brain when a choke is applied to one side of the neck
In the sport of Brazilian Jiu-Jitsu and Submission wrestling there are some chokes that only target one side of the neck, meaning only one of the carotid arteries. In the context of blood flow, how is this possible since we have two carotid arteries located on the "right" and "left" side of the neck?
A friend of mine gave an explanation that the neck, head and chest can be seen as a circular flow of blood and if one where to stop the flow in the left or right part of the neck than that would stop the "circular flow". Is this correct?
Here is a video showing an arm in guillotine which I believe (and the author states) only target one of the carotid arteries: video
To concisely summarize the question: How does a single sided neck choke work in the context of blood flow?


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Why does the medial hypothalamus cause affective aggression while it causes the release of serotonin?
Since aggression is inversely related to serotonin, why does activation of the medial hypothalamus, which sends axons to the serotonin-releasing PAG, cause affective aggression? Thanks in advance!

It would help to provide sources referencing the claims made in your post about serotonin, the medial hypothalamus, and aggression.


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Why couldn't grafting save the Sycamore Gap tree?
The Sycamore Gap tree in England was recently cut down by a vandal.  There is hope that the tree can be "saved" by nursing shoots that are hoped to come up from the roots.
Grafting is routinely done to propagate desirable trees by attaching branches to the root of a more hardy tree.  In these cases, the pieces being grafted come from two different individuals.  (Or more; my grandfather had an apple/pear/rose tree with dozens of types on a single root.)
So why is grafting not considered when a single individual is involved?  It seems to me (who has never grafted anything) that it should be possible to place a support (e.g. sturdy non-corroding metal bar) in the middle of the stump to replace the mechanical strength of the wood, then set the entire tree back upon it and allow it to graft back together.
Certainly this would be an expensive undertaking for a large tree, and would not be guaranteed to work.  But for a tree of such historical significance, there must be some reason that it wasn't even tried.
What am I missing?


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How to measure cytochrome P450 activity in owls?
I hope you're all doing well. I'm currently working on a research project focused on owls and their exposure to anticoagulation rodenticides such as brodifacoum. As part of my study, I need to measure cytochrome P450 enzymes activity in these birds to assess their ability to metabolize these toxins.
I'm curious to know if there are assay kits or ELISA kits commonly used for measuring cytochrome P450 activity in owls. Any insights or advice would be greatly appreciated. If there are alternative methods or techniques that may be useful in this context, I am open to exploring them as well.
Thank you in advance for your help, and I look forward to any insights you can provide.


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Water transport to the Shoot apical meristem in a seedling
I am familiar with how plants transport water from the roots to leaves. Specifically, Water evaporates from the leaf surface, generating a negative pressure gradient which pulls water up from the root.
What is unclear to me, is how water is transported to the shoot apical meristem of a seedling, where there is no leaf above it (see red arrow on image attached).
Are there stomata on the shootapical meristem from which the water can evaporate? Or is there some other mechanism which transports water up here? Thanks.


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Why are beavers not considered marine mammals?
They spend a lot of their lives in the water, they have fur, give live birth, have mammary glands etc...but my teacher mentioned that beavers have continually growing teeth (incisors) which supposedly excludes them from being marine mammals. The thing I'm confused about is that we also learned later that manatees & walruses (which are both considered marine mammals DO have continually growing teeth. I don't understand, any help would be appreciated :'(

It might help you to think carefully about the word "marine"...

@bob1 It might help you to think carefully about the fact that beavers sometimes brave the sea.

So do people, are we "marine"? @Araucaria

@Araucaria true, but does not make them marine any more than whales and dolphins coming into fresh water makes them aquatic.

Beavers are not Marine Mammals
According to Wikipedia, Marine is an adjective meaning of or pertaining to the sea or ocean: as Beavers can be found in a number of freshwater habitats, such as rivers, streams, lakes and ponds, they are not considered "marine".
Beavers are semiaquatic Mammals
Their wikipedia page mention that they be semiaquatic mammals (that dwell partly or entirely in bodies of water), as the European otter, the Baikal seal, the Capybara or the hippopotamus:

Beavers (genus Castor) are large, semiaquatic rodents
(...)
Other semi-aquatic mammals, such as water voles, muskrats, minks, and
otters, will shelter in beaver lodges.

Be nice to your teacher when you correct them about their answer: it's ok to be wrong sometime, even for a teacher! Hope it helps.


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Why is antheridiophore not considered part of the sex organ while stamens including filament are considered a sex organ?
In the majority of websites and textbook I have referenced, the antheridiophore is considered to be the stalk which extends the sex organ (antheridium) in bryophytes. Meanwhile, in flowers, the whole stamen, that is, the filament also is considered a part of the sex organ. Is there any reason behind this?


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What could be the cause of strange brown discoloration around some bacterial strains' colonies on macconkey agar?
Acinetobacter

Unknown (Yellow TSI, Oxidase negative, Catalase positive)

Unseeded plate

My only guess is that the initial pH of the poured agar is too acidic (too red), so any alkalinity is more marked. Could non-gram-negative contaminants with their normal unapparent growth on MacConkey agar, have an effect on the pH of the media?
I may have no way to check the pH of the liquid media prior to pouring and the presence of non-gram-negative contaminants.
So my only hope is that someone here is familiar with this scene and knows the reason behind it.