text:
What are the differences between different strains/types of Cre?
Reading from Hedgehog signaling reprograms hair follicle niche fibroblasts to a hyper-activated state:

Lineage-specific genetic tools are necessary to precisely study HF
fibroblasts; however, their repertoire remains limited. Embryonic
dermal condensate progenitors can be targeted with Tbx18-Cre (Clavel
et al., 2012), whereas adult DS fibroblasts, with
Sma-CreERT2 (Rahmani et al., 2014) and Acan- CreER (Heitman
et al., 2020). DP fibroblasts activate Sox18- CreERT2 at
birth (Legrand et al., 2016), Corin-Cre soon after birth
(Enshell-Seijffers et al., 2010a), and CD133-CreERT2 in
adult skin, albeit only with low efficiency (Zhou et al., 2016). Here,
we confirm that in mouse skin, Leptin receptor (Lepr) is a faithful DP
marker gene (Greco et al., 2009; Rezza et al., 2016) and show that
isoform B-specific LeprB-Cre (DeFalco et al., 2001) and LeprB-CreER
can be used to efficiently target postnatal DP fibroblasts. Using
these genetic tools, we uncover how DP fibroblast lineage and
signaling niche are regulated by the Hedgehog pathway.

I watched this video as a refresher on Cre recombinase. I attempted to Google the question with no luck. I also glanced back at one of the papers referenced. It seems it would take considerable effort for me to teach myself this answer and I'm sure there are members here who know off-hand. My understanding of Cre is that we will put it under the expression of tissue-specific promoters, as is stated in the video. I covered this technique in a paper I read last semester. I assume ER stands for endoplasmic reticulum, possibly? Where additional confusion is arising for me is that in the sentences describing "at birth" and "soon after birth" it seems in the way it's presented that these Cre could be native to the organism but we add Cre to the genome in all these cases, right?

FWIW, to find a reference to include in my answer I searched "CreER cre recombinase" (to avoid false positives with "creer") in Google and found an example paper to cite immediately. Perhaps it helped that I'm familiar with the system and knew what I was looking for.

Your answer is absolutely helpful, thank you for typing it up and for the quick reply. I definitely am in a much better position to complete the investigation myself if need be. Instead of accepting your answer, I am going to leave the question open as while your answer is a start there is quite a bit going on in that paragraph I quoted from the paper.

CreER is Cre coupled with a binding site for the estrogen receptor ("ER") to make an inducible version of the Cre system triggered by tamoxifen. CreERT2 is just a particular variety of this system with some mutations that improve the function.
Feil, S., Valtcheva, N., & Feil, R. (2009). Inducible cre mice. In Gene knockout protocols (pp. 343-363). Humana Press.
Some quotes from this paper:

To add inducibility to the Cre/lox system, ligand-dependent chimeric Cre recombinases, so-called CreER recombinases, have been developed (3–6). They consist of Cre fused to mutated hormone-binding domains of the estrogen receptor. The CreER recombinases are inactive, but can be activated by the synthetic estrogen receptor ligand 4-hydroxytamoxifen (OHT), therefore allowing for external temporal control of Cre activity.

The properties of CreER recombinases were continuously improved to decrease the background activity in the absence of inducer and to increase the sensitivity and efficiency of tamoxifen-induced recombination in mice. The CreERT2 recombinase, which contains the human estrogen receptor ligand-binding domain with a G400V/M543A/L544A triple mutation, is currently the sharpest tool in the CreER box and its use is highly recommended for inducible mutagenesis in the mouse (4 , 9 , 10).

Briefly, the two common ways to use the Cre-Lox system these days are either 1) You have a gene you want to knock out in only certain cells; you've modified this gene to be surrounded by LoxP sites (often referred to as 'floxed' as a shortening of 'flanked by LoxP sites'), or 2) You have some genetic construct you want to express in only certain cells (for example a reporter like green fluorescent protein/GFP), so you start with an inserted gene with a 'floxed' stop codon that comes before the GFP.
You then express Cre under a desired promoter (let's call it YourFavoritePromoter), Cre cuts out the floxed section: either the gene to conditionally knock-out (1), or the stop codon so your GFP is produced (2), but only in cells that have YourFavoritePromoter expression.
However, this is a permanent change in a lineage. If Cre is ever expressed at any time during a cell's lineage, all subsequent daughter cells will have had the floxed part removed. That means the cells you mark with GFP are not necessarily those expressing YourFavoritePromoter now, but cells that sometime in the past expressed YourFavoritePromoter.
You can use CreER to get around this, as Cre will only be expressed with tamoxifen present. That allows you to control the time window in which Cre is expressed, and therefore the time window in which you are identifying cells with YourFavoritePromoter.
You'd want to follow up with all the individual references in your paragraph to see what they are doing specifically. For example, in the "Legrand et al 2016" paper:

Sox18 is expressed specifically in the DP in all dorsal hair follicle types; however, at birth its expression is restricted to zigzag hairs lacking Sox2 expression in the DP (Driskell et al., 2009, Pennisi et al., 2000)

So, if you want to tag "zigzag hairs" (I really have no idea what these are, but it doesn't matter for understanding the system), you use Sox18-CreER and give tamoxifen at birth. If you used ordinary Sox18-Cre, you'd label "all dorsal hair follicles" instead.
All of these are artificially introduced constructs. A frequent method for efficiency is to have some homozygous mouse strain that expresses the gene you want to see (say, floxed GFP in our example), and a different mouse strain that has the Cre construct you want (say, Sox18-CreER). Each are created using standard transgenic techniques; many researchers don't need to bother with those details because you can just buy the mice, but if you want a particular unique line you have to make them. You then breed them together to get mice that have Cre and the floxed gene.
Here's what they did (quotes from Legrand et al):
Make mice with floxed version of gene they want to control expression of (STAT5A/B; note here they're actually doing a conditional knockout, so rather than have Cre remove a stop codon it's removing the entire gene):

STAT5A/Blox/lox mice (Cui et al., 2004) were first crossed with Flash/+ reporter mice to generate mice homozygous for the STAT5 floxed allele containing the previously described Flash Wnt-reporter transgene (Hodgson et al., 2014)

Breed these with the Sox18-CreERT2 mice so they have tamoxifen-controllable cre expression under the Sox18 promoter (extra complication here that these mice also express a reporter gene; that one works with the stop codon method I described above):

These mice were then crossed with B6;129S-Sox18tm1(GFP/cre/ERT2)Pzg/J (Sox18GCE/+) mice to generate Sox18GCE/+ mice homozygous for the STAT5A and STAT5B floxed alleles, although also containing the Flash reporter transgene

Give tamoxifen at birth to express cre in a specific population of cells which will knockout STAT5A/B and express the GFP reporter.

Recombination in these mice and their appropriate control groups was induced at birth using a single dose of 1mg tamoxifen.

Thank you, Bryan, for your well-thought-out answer. My only suggestion would be to define acronyms before you use them (I think I also made this mistake in some of my earlier content). I know what GFP is but it's about making it easier for the next guy. Anyhow, I definitely feel up to my neck with this paper and am going to pause, step back, and read the chapter you referenced.  Where I struggle is with visualization of the crossing of mice, and like anything needs practice. I am open to any specific literature (or exercises) you feel may be helpful before I continue reading this paper.

@neurosciencecalc I think it'll come with experience. Crossing mice is just like Mendel's experiments with pea plants, I'd go re-read those sections of a biology textbook for a refresher.

Sounds good. Thank you, Bryan.

I feel kind of silly for my question now that I am understanding more, but that's all part of the learning process. I see now that the notation is 'tissue_specific_promotor-CreERT2' and you did such a great job explaining the CreERT2 and that chapter you linked to is great as well. Thanks again for your help.


text:
Genetic modifications to produce blue hair
The following animals are known to produce blue pigmentation:

Linckia laevigata (blue star, study reveals blue carotenoprotein, linkiacyanin)
Nessaea batesii (obrina olivewing, study reveals blue pterobilin pigment)
Synchiropus splendidus (mandarin dragonet, study reveals blue chromatophores ("cyanophores") and blue organelles ("cyanosomes"), but "the chemical nature of blue pigment remains to be determined")
Synchiropus picturatus (picturesque dragonet, ibid.)

Given:

Alpha-keratin is a fibrous structural protein of mammalian hair.
Human hair is pigmented by eumelanin and pheomelanin.
Eumelanin is associated with black or brown hair.
Pheomelanin is associated with red or blond hair.
The ratio of eumelanin to pheomelanin determines colour.
MC1R provides instructions for making a protein called the melanocortin 1 receptor, which is a key gene for regulating hair colour.
Keratin genes are found in chromosomes 12 and 17.
The MC1R gene is found in chromosome 16.

What biological structures would have to be modified (or introduced) to produce pigmented blue hair in humans?
First example: Adding carotenoids to human hair (made from keratin) could be directed to deposit lipid droplets (fat molecules) within the cells of the hair follicles. As cells exit the follicle, the lipid solvent dissolves, leaving the carotenoid pigment dispersed throughout keratin that was genetically modified to offer a larger binding site for the blue protein. Intermingling yellow carotenoids and linckiacyanin at various ratios thereby provides a spectrum of blue hues.
Second example: Create a new cyanosomes organelle responsible for producing blue pigment that latches onto the eumelanin receptor. Change the epigenome for the MC1R gene to modify eumelanin with cyanophores produced by the organelle, such as by reprogramming the keratinocytes that regulate the function of melanocytes.

source: Stack Exchange

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

sort: votes


text:
Volunteer/seedling in Toronto garden
What species of plant is this?

Location: Toronto area (Ontario, Canada)
Date: July 7, 2022
Conditions: Acid soil in shade
Height: Approx. 11 inches
Description: Younger leaves resemble tomato leaves. Main leaves are serrated. Opposite.

August 25, 2022

September 6, 2022

I think the leaves are simple pinnate and alternating, though it is hard to tell from the photo. I want to say Dahlia, but the leaves don't look quite right.

@bob1 Thanks. If you click on the photo a couple of times in your browser, it should show the full photo, which is quite large. From there, you can zoom in. When we do that, I think it's a bit clearer that the leaves are opposite, not alternating.

Thanks. Opposite is correct. Not Dahlia - too hairy.

Can you post more photos of this plant? Closeups of the stem, roots (if you decide to kill or move it), and both surfaces of the leaves may help; however, flower photos are likely necessary for you to get a definitive identification (ideally from multiple angles).

Nice updates. Should help quite a bit.

I think that this is one of the beggarticks, in the genus Bidens. There are several possibilities in your area, including B. connata, B. frondosa, and B. vulgata. I think more detail would be needed for a finer identification.
The main features pointing me this way are the opposite, compound leaves, and the distinctive shape of the leaflets (ovate-lanceolate, serrated margins, attenuate tips).

Based on the number and type of bracts beneath the flowering head (aka "calyculus bractlets", about 8, not "foliaceous" but merely herbaceous), and the shape of the leaves (3-foliate), I think this is probably Bidens frondosa.

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


text:
Confusion regarding the location of myelinated and unmyelinated nerve fibres
So, what I understand by neural system terms is

Central nervous system [CNS]- consist of brain and spinal cord

Peripheral nervous system [PNS] - consist of cranial and spinal nerves (all the nerves in the body)

A further classification of PNS is
I) Autonomous nervous system
II)somatic nervous system

(Here, my understanding is that both the system [somatic and Autonomous nervous  system] are made up of cranial and spinal nerve, and they are just classified based on the different organs that they are functioning upon [i.e for somatic it is skeleton muscles and for autonomous, it is heart, smooth muscles and involuntary organs] and not on composition ,since both systems consist of cranial and spinal nerves)
Now,i read the lines that are there (beside the red line) in picture below and I am highly confused now.

Now, it says that myelinated nerve fibers are found in cranial and spinal nerves i.e all the nerves in the body a.k.a Peripheral nervous system.
And on another note, it says unmyelinated nerve fibres are found in autonomous nervous system and somatic nervous system.
but isn't autonomous and somatic  nervous system makes up the peripheral nervous system?
so according to the first point (myelinated nerve fibres is present in peripheral nervous system.)
Therefore, It( somatic and autonomous nervous system i.e the peripheral system) should contain myelinated nerve fibres but here ,in just the next line ,it states that it contains unmyelinated nerve fibre?
By my understanding of the above mentioned terms......
My confusion here is.......
Does it contain both (myelinated and unmyelinated nerve fibre)?
or is there a printing mistake?
or is my understanding of terminology is wrong?
If so, please correct me.
Thank you so much

Where is this text from? Does it happen to be an Indian textbook? It's been a long time since I've seen one of these Indian textbook translation questions but I suspect this may be one...

@BryanKrause       Yes. This (confusing and unclear)text is from  "NCERT Biology" 11th std Indian Textbook. I will be highly grateful if you can clear this or anyone. Thank you so much

I don't know where these textbooks come from, but they aren't written by anyone who knows what they are talking about. I don't know why many Indian textbooks work this way. I'd highly recommend getting a different book or just learning from Wikipedia.


text:
Human Evolution Chromosome 2: Fusion or Break?
I have a question regarding Chromosome 2.  I've heard that there is evidence that the Human Chromosome 2 is a fusion between the two ancestral chromosomes 2a and 2b, but could it be possible that it is the other way around?  That is, could it be possible that what we call chromosome 2 in the last common ancestor between humans and other great apes could have broken in some offspring of this ancestor and preserved the broken copy in their descendants. Meanwhile other descendants of this ancestor kept an intact chromosome?  Can someone please point me to evidence/papers that ruled out this possibility?  I'd like to hear why they thought it was a chromosome fusion and not a chromosome break, especially with an incomplete archeological record available.

I've heard that there is evidence that the Human Chromosome 2 is a fusion between the two chimp chromosomes 2a and 2b -- a small but important correction: human's didn't evolve from chimps, so human chromosomes cannot be derived from chimp chromosomes. It is more correct to say that chromosome 2 is hypothesized to have formed by a fusion of two ancestral chromosomes after the divergence of the "human" lineage from the most recent common ancestor of humans and other primates.

Related: Evolutionarily speaking, why do humans have 46 chromosomes.  There is very good evidence that human chromosome 2 is the result of a telomere-to-telomere fusion of two ancestral chromosomes (ref is here)

The way you answer these sorts of questions is by looking at other, further relatives because that gives you more hints about what the "ancestral" trait is.
Since other apes (gorillas, orangutans) also have the separate "2a" and "2b" chromosomes (see, e.g., Fan et al 2002), we can conclude that the common ancestor to all of the great apes had separate 2a/2b chromosomes. That makes humans the outlier, and therefore suggests the fusion occurred somewhere between the most recent common ancestor of chimps and humans and modern humans.
The alternative would have to be that the ancestor had a single "chromosome 2", and then separately in every other great ape lineage that chromosome broke in the same place. That is effectively impossible to have occurred in the same way like that by chance.
I've annotated the cladogram from the Wikipedia page on great apes to show how this works:

If the great ape ancestor has separate 2a/2b, then one fusion event is required to explain why humans differ from the others (top diagram).
If, however, the great ape ancestor has a single chromosome 2, which then broke to make 2a/2b in chimps, that's a perfectly reasonable hypothesis if you just look at the chimpanzee/human branch. However, when you also consider gorillas and orangutans that have separate 2a/2b, that would mean that the ancestral chromosome 2 would have had to break at least 3 separate times in 3 separate lineages in the same place. That doesn't make much sense.
Fan, Y., Linardopoulou, E., Friedman, C., Williams, E., & Trask, B. J. (2002). Genomic structure and evolution of the ancestral chromosome fusion site in 2q13–2q14. 1 and paralogous regions on other human chromosomes. Genome research, 12(11), 1651-1662.

there is also structural evidence in the chromosome itself, chromosome 2 has telomere like sequence in its center and a second inactive centromere. those only make sense if the it was to different chromosomes in the past. https://en.wikipedia.org/wiki/Chromosome_2

It's important to emphasize, I think, that the unfavorability of the "break" hypothesis arises not merely from the pattern of occurrence in contemporary apes and humans alone, but from that pattern together with the fine details of their past evolutionary relationships. If it were the case that all non-human apes shared their own common ancestor after the one for both them and human apes, only one break would be required, even were the distribution at the leaves identical. But because Hominina splits off where it does, instead of before the first fork in the diagram, 3 breaks are required.


text:
How does one derive a KD from an equilibrium titration experiment?
If I have an antibody A and a target B, and experimentally titrate the antibody against a single concentration of B, and then measure the % of B that is bound after the solutions reach equilibrium, I should be able to determine the KD of the interaction.
Source below (and others) shows that determining KD is as simple as determining the EC50 of such a curve. Source.

How does that square with the following equation for KD?
$KD = \frac{([A]*[B])}{[AB]}$
where A is unbound antibody, $B$ is unbound antigen, and $AB$ is the bound complex.
Let's say I have 10 pM of target antigen, 50% of which is bound when incubated to equilibrium with 10 pM of antibody. That would mean the antibody and antigen are each 50% bound and 50% unbound.
$KD = 5pM * 5pM / 5pM$
$KD = 5 pM$
So I have calculated a 5 pM KD, not the 10 pM that I would think would be similar to the graph below (assuming they had pM units on the X axis) I'm assuming these types of example graphs refer to the input concentration, right?
Even more confusing, what if the antibody is a really tight binder, such that 10pM of antibody is able to essentially bind 100%, such that 10 pM antibody is able to bind 50% of 20pM of antigen. (1:1 binding assumed)
$KD = ~0.001pM * ~10pM / ~10pM$
Now you have a KD of 0.001pM, but the graph would suggest that 10 pM of antibody is necessary to bind to 50% of the target antigen.

Welcome to Biology.SE. Unfortunately, general chemistry questions without a strong biological component are off-topic. Just mentioning enzymes or antibodies as reactants isn't sufficient. Please delete your question here and ask it at [chemistry.se] (cross-posting is frowned upon), or flag it and request that it be migrated.

Are you sure? Protein-binding, which is definitely the most relevant tag, is not even an option in the chemistry stackexchange.

The models you are using are based on the Langmuir Isotherm. The classical use of this model is for gas adsorption to a solid. In these experiments, the pressure of the gas is measured against the fraction of sites bound.
This model is easily transferred over to aqueous systems, but you have to be careful about making the correct analogies. The pressure of the gas is related to free concentration of the gas, not the total concentration. So the X-axis of your plot must be the free concentration of your ligand.
Most experiments are done where the ligand is in major excess of the receptor. Therefore, the free ligand concentration is roughly equivalent to the total ligand concentration. However, when this isn't the case it is not hard to adjust based on a known ratio of ligand to receptor.
At 50% binding we know that:
$K_d = [L_f]$, where $[L_f]$ is the free concentration of ligand
From conservation of mass we know:
$[L_f] = [L_t] - [LR]$, where $[L_t]$ is the total ligand in the solution and $[LR]$ is the concentration of bound ligand
Since we are at 50% bidning we know:
$[LR] = \frac{1}{2}[R_t]$, where $[Rt]$ is the total receptor concentration.
This lets us solve:
$K_d = [L_t] - \frac{1}{2}[R_t]$


text:
Is bacterial respiration a continuous process?
Respiration in micro-organisms is the process of releasing energy from food. There are two ways of doing so: Aerobic respiration occurs in the presence of oxygen and produces ATP from the complete oxidation of carbohydrates or fatty acids. Anaerobic respiration involves incomplete oxidation in the absence of oxygen. No matter the method, bacterial respiration is thought of as a continuous process that releases energy continuously. However, the word "continuous" is ambiguous.
My question is:

Is the respiration continuous without rest (e.g. DC signal) where the bacteria are releasing energy at every stage of the respiration process.

or

Is it alternating (Like human breathing (inhale & exhale)) where the bacterial cell produces energy during one stage of the respiration stages and takes a rest in a periodic rhythm (e.g. AC signal) before releasing energy again?

Please clarify your specific problem or provide additional details to highlight exactly what you need. As it's currently written, it's hard to tell exactly what you're asking.

The question is still lacking enough context to form a coherent answer. Like, in what setting are you interested in this problem? And on what scale? I suppose any reaction could be divided into discrete steps at atomic or molecular scales. Like, a single enzyme may only catalyze one reaction at a time, and then it has to release the product, change conformation, and bind a new substrate, which takes a non-zero amount of time. But in a cell each reaction might be happening millions or billions of times each second, asynchronously, such that the metabolic process is effectively continuous.

Please respond to comments from other users by [edit]ing your posts — we are trying to help you craft better questions. Not doing so is likely to be perceived as rude and generate down and close votes. This can result in you losing the privilege of posting further questions.

"Respiration" in this context has nothing to do with breathing, it refers to cellular respiration. These are the chemical reactions that make ATP to be used in energy-requiring processes in the cell. Human cells do cellular respiration, too, and while we require breathing to replenish oxygen (and carry away carbon dioxide), this is not part of cellular respiration. Don't confuse them just because they have the same word in the name.
These processes occur more or less continuously in all cells; the rates can vary with conditions (for example, your muscle cells are going to do more cellular respiration when you run than when you sleep), but cellular respiration isn't breathing so don't expect it to be rhythmic the same way breathing is.


text:
blackberry: what morphological features suggested the species epithet "bifrons"?
What morphological features suggested the epithet "bifrons" in Rubus bifrons? The scientific name of the familiar invading species "Himalayan Blackberry" (or "European Blackberry" or "Armenian Blackberry") in the US is Rubus bifrons (with Rubus armeniacus as an alternative if the two species are considered same).

Following the links given in the NCBI Taxonomy Browser, the International Plant Names Index gives the author abbreviation Vest, likely indicating that this species was named by botanist Lorenz Chrysanth von Vest sometime around 1821.

As @acvill pointed out, R. bifrons was named in 1821 by Lorenz Chrysanth von Vest. The original description can be found here (pages 163-164).
The latin bifrons translates to "two faces". I'm not sure, but I suspect this references the leaves of the plant, with the upper surfaces being dark green and the lower white (or much lighter)

Foliis subrotundo-ovatis subtus albentibus saepe villosis, tenue et confertim serratis...

[Leaves roundish-ovate, whitish on the underside, often villous
thin and serrate...]

However, I can't translate his comments after the description, so maybe there is another explanation included there.

As far as I can see, nothing in Vest’s comments offers any further explanation of bifrons.  The Latin description reads in full: ‘Foliis subrotundo–ovatis subtus albentibus saepe villosis, tenue et confertium serratis, caulium fertilium plerumque teretibus, caule tereti rarius per intervalla subangulato, aculeis validis rectis, petalis obovatis stamina subaequantibus.’ — I don’t know botanical Latin enough to properly translate it, but nothing seems more relevant than the part you already translate.  [cont’d]

The German note reads: ‘Er ist häufig in den Wäldern um Gräß, und wird gewöhnlich für den R.fructicosus gehalten, der ein aufrechter Strauch ist, mit eckigem Stamme und krummen Dornen u.s.w. der unsrige liegt am Boden, sowohl der blühende Stamm, als der unfruchtbare (flagellum, stolo).’ — this translates roughly as ‘It is common in the woods around Gräß, and is commonly mistaken for R. fructicosus, which is an upright shrub with square stem and crooked thorns etc., whereas ours [i.e. R. bifrons, I guess] lies on the ground, the flowering and non-flowering stem alike.’


text:
What is the evolutionary purpose of citric acid?
According to Dr. Paul Saladin, fruits are brightly coloured and sweet because they want to be eaten to spread the seeds of the plant. Unlike roots stems seeds and leaves that don't. To deter consumption they produce chemicals that have extreme tastes like bitter or spicy (ginger, black pepper, chillis) etc. But lemons are brightly colored, however, they have their own extreme taste. What is actually the function of this?
And, come to think of it, chillis are often also brightly colored. What is the evolutionary function of that too?

Welcome Joe. This is not simply a Q&A site, here we are expected to show the results of our own investigations into a subject here, you can [edit] to tell us what your searches found and where the sticking points are. You should also take our [tour] and refer to the [help] for guidance as to the ways of any site you post on, see our section on how to ask and see our homework-question policy. Enjoy the Stackexchange network.

It’s worth remembering that many/most fruits have been selectively bred to taste a certain way by humans, so trying to infer evolutionary reasons may be hard.

Please consider that the question of how best to assure seed viability is not an either/or proposition. That’s a bifurcation. There are many ways to help seeds become seedlings besides color and taste of fruit.

As far as your question about chilis is concerned - bright colors in nature are also used as warnings. Look at the various types of poison dart frogs, for example.


text:
How long is the typical peptide sequence recognized by a T-cell?
A naive T-cell recognizes either a certain sequence of amino-acids (even if that sequence occurs as a part of a longer sequence of amino-acids(*)), or a small set(**) thereof.  Only T-cells that do not recognize any sequences native to their own organism are allowed to mature.  Then they are released from the thymus and start searching for the amino-acid sequences they recognize, assuming that their occurrence within the body would indicate proteins synthesized, and possibly forming, another organism (a parasite).  I wonder what are the shortest, longest, and typical lengths of the sequences recognized by a matured T-cell, as counted in amino-acids.
(I suppose that if a naive T-cell recognized any very short peptide, it would be unlikely to survive in the thymus, and if it only recognized very long peptides, it would be overspecialized and evolutionarily unstable.  So there must be some limits.)
If the answer varies across vertebrate species significantly, that would be interesting, too.
Footnotes:
*: In this sense I used the term "peptide" loosely in the title formulation of my question.  Please correct me if such usage was simply wrong.
**:I don't have a good understanding of how the "sets" are represented in the T-cell, and consequently, how they can be structured - whether they tend to form a single "pattern with wildcards" or multiple independent patterns, or anything in between.


text:
Examples of subvarieties and forms in botany or other biological nomenclature?
So I found a fairly complex Rhododendron subgenus to subsection classification list, and despite there being genus > subgenus > section > subsection > species > subspecies > variety > subvariety > form, the only parts that seem to make up a name when things go beyond the species level is picking the last one after that (so subspecies, variety, subvariety, or form). So we have examples like Capsicum annuum var. glabriusculum or Rhododendron campylogynum var. leucanthum.
https://en.wikipedia.org/wiki/Infraspecific_name
You can also have the cultivar epithet added after species.
So my question is, is it always genus species [possibly one deeper]? Or are there any other situations I missed? Also, it sounds like you can insert arbitrary number of levels between the ones you are taught in grade-school (kingdom / phylum / class / etc.), you might insert a few layers there when necessary like phylum > subphylum > superclass > class sort of thing. Like for family we added 4:

Superfamily
Family
Subfamily
Tribe
Subtribe

So in the end it might be something like this, or even more!?:

empire
kingdom
superphylum
phylum
subphylum
superfamily
family
subfamily
tribe
subtribe
genus
subgenus
section
subsection
species
subspecies
variety
subvariety
form

So from 7 to about 20 levels! They don't make that obvious in your initial pass at learning this. Do I have the naming system correct then? If there is anything below the species it gets a 3rd item in the name. If there is anything between genus and species, that is ignored in the name.

Binomial nomenclature is the name for the formal naming of species in "Genus species" form. Genus species should always be a unique identifier (also see Are All Taxonomic Groups Uniquely Named?), so this is the "official name" of a given species.
However, as you've pointed out, sometimes after a species is described it is found useful to differentiate between subspecies or smaller varieties, especially in agriculture where artificial selection has taken one native species and transformed it into many cultivars that have become so distinct from each other that they'd hardly be considered the same species had they been discovered that way in the first place (and very unlikely to evolve those discordant traits naturally without some of the reproductive barriers that lead to speciation).
Note that all of these designations are somewhat arbitrary, besides their order. They are all just a way of imposing a categorization for the convenience of humans in describing relationships between different living things.
Some more reading:
https://en.wikipedia.org/wiki/Phylogenetic_nomenclature
https://en.wikipedia.org/wiki/Evolutionary_taxonomy
https://en.wikipedia.org/wiki/Taxonomic_rank
How could humans have interbred with Neanderthals if we're a different species?
Usage of "lineage" over "species"
Why is traditional rank based taxomomy considered by some as logically inconsistent with phylogenetic knowledge?
Difference between Category, Rank and Taxon
Imagine life as a very, very big tree. You can call a part the "trunk", that's pretty well-defined. That might be the original common ancestor of all life, or perhaps all eukaryotes, or perhaps all vertebrates; you can choose where you want to start. The leaves, also, are relatively well-defined. Those are the species. But some leaves have a complex shape and you might even debate when a leaf is one leaf and when it's actually a collection of leaves. In between, though? We use some names for tree parts. Limbs, branches, twigs, etc. But if you want to get into more detail, you may eventually find yourself needing a word to describe something between a branch and a twig, and then sometimes between that thing and a proper twig, etc. There is no real behavior of the universe that is based on these classification points, it's just convenient to draw a line somewhere to say "okay, I want to talk about all parts of the tree past this branch, so I'll give them a name". Nothing constrains the tree of life to grow in any particular pattern where there are a set number of branches between particular extant species; you can easily have leaves that grow directly out of the trunk and serve as their own branch, their own twig, etc.

Does NCBI not use the new PhyloCode system then?

@Lance I have no idea, I assume PhyloCode is some sort of new standard? See https://xkcd.com/927/ and also note that just because there is a standard does not mean it is not ultimately arbitrary in some fashion. For example, the length of a meter is both entirely arbitrary and also exactly the distance light travels in 1/299792458 of a second. Of course, a second is also an arbitrary unit of time, even if it is also precisely 9,192,631,770 periods of the radiation corresponding to the transition between the hyperfine levels of the unperturbed ground state of the 133Cs atom.

(from https://en.wikipedia.org/wiki/Metre and https://en.wikipedia.org/wiki/Second )

The rules may be different for zoological names, but for botanical names:

Is it always genus species [possibly one deeper]?

This is governed by the International Code of Nomenclature for algae, fungi and plants, Article 24.1, and the answer is yes, the name is always genus species [connecting term infraspecific epithet].
The Code provides the following example:

Ex. 1. Saxifraga aizoon subf. surculosa Engl. & Irmsch. This taxon may also be referred to as Saxifraga aizoon var. aizoon subvar. brevifolia f. multicaulis subf. surculosa Engl. & Irmsch.; in this way a full classification of the subforma within the species is given, not only its name.

Here, the name is "Saxifraga aizoon subforma surculosa" (where subforma can be shortened to subf.), and it is common to list the authors who described that taxon (here, Engler and Irmscher). However, that taxon is placed within a hierarchy of variety, subvariety, and form, which may be listed if the full classification is needed.
One consequence of this is that no other subform within Saxifraga aizoon may have the epithet "surculosa", even if its classified in a different variety, subvariety or form.

It sounds like you can insert arbitrary number of levels

Also yes. Article 2 states, "Every individual organism is treated as belonging to an indefinite number of taxa at consecutively subordinate ranks, among which the rank of species is basic."

If there is anything between genus and species, that is ignored in the name.

Correct, if you're naming a species or infraspecies, only use the genus, specific epithet, and infraspecific epithet.
You can, of course refer to those intermediate ranks if you need to, such as Primula section Dodecatheon.


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Where to find all "authorities" for taxonomic names?

https://en.wikipedia.org/wiki/Author_citation_(botany)
https://en.wikipedia.org/wiki/Author_citation_(zoology)

I am using NCBI to get a fairly complete list of organisms and their taxonomic name. Going to look further how to find the common name programmatically. Next is where can I find the author / authority name and date, is that stored in a publicly accessible database anywhere? Where does it get stored in the first place as well, if not a central db?

https://species.wikimedia.org/wiki/Catalog:Taxon_Authorities/A

That's the best I've seen so far.

Admittedly, I haven't had the need to look for it, but I have not been able to find a common list of all authorities, partly because the vast majority of these sorts of things were done a long time ago - dating back to Carl Linnaeus in the 1700's.
You could try the various authorities on naming of organisms. International Committee on Taxonomy of Viruses, International Committee on Systematics of Prokaryotes,  International Association for Plant Taxonomy, and the International Committee on Zoological Nomenclature, but even these might not work.
You may have to dig through some very old literature to find the authorities. I've done so for similar posts in the past looking at finding primary authorites, such as this one, but it is very time-consuming and not easy without a very good local reference library and academic access.


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Does beta-actin have to be consistent in Western Blots?
I have been running Western Blots on rat brain tissues from rats that have been subject to neurological disorders.
I loaded the samples on the gel to ensure that for each tissue, I had a constant mass of protein (30 ug). The volumes were determined via BCA analysis. However, the BCA analysis was performed years ago (approximately 4-5 years ago). Also, the tissues have undergone multiple freeze and thaw cycles.
In addition to the tissue, I also loaded the same volume of Laemelli buffer as tissue and I used RIPA buffer to make the volumes of each sample constant.
I probed my membrane for my protein of interest and a housekeping protein (actin). I have attached a photo of my membrane down below.

top band is actin and bottom one is my protein of interest
However, I noticed that my actin bands are not consistent (some are fainter or darker than others).
Do the actin bands have to be the same darkness for each sample? Could I still use these results and instead do a normalization?
Or would I need to rerun this sample again?
Thanks for your help!

The long and the short of it is that your actin bands do not need to be consistent so long as you can normalize and have met the quite stringent conditions for normalization to be effective. For normalization you generally need to have loaded less than 10 ug of protein, have not over-exposed any of the bands, and have them all loaded on the same gel and blot for comparison. You can not compare results across more than one blot without running inter-blot comparison controls!
Please note that this image would not probably not meet most publication requirements (in my opinion).
Please read the PDF here from Li-Cor on western blot normalization. It are the best descriptions of the conditions needed that I have come across.
However, for publication, you may have a harder time convincing reviewers that your results represent real data if the actin bands are so variable. Having a plot of normalized results is all well and good, but the eye is not very good at determining changes of less than about 50% (i.e. 2-fold) without careful consideration, so for instance your lanes 4 and 5 (not including ladder) have faint actin, but the POI is more or less consistent with the surrounding lanes - meaning that in 4 & 5, you have much more POI than in those other lanes, but it takes some thought to realize this.


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Are there any Biology research classification systems?
There are research classification systems for mathematics (MSC) and physics (PACS and subsequently PhySH) which help the researchers to navigate through codes composed by letters/numbers made by associations that specialise in those pieces of human knowledge. Are there any classification systems of research in Biology?

You need to explain what sort of classes these systems produce, who operates them, and in what circumstances, as they do not immediately convey anything to me.

These classes are made by big associations in a try to make a classification of a piece of human knowledge, for example in the case of Mathematics the American Mathematical Society has made an effort since the last century to classify all the Mathematical research areas into a "simple" system of classes where one can access all areas of Mathematics just by a system of numerical/letter codes.
These classes are usually updated from times to times due to human knowledge evolution.

I discourage people answering in comments, but when the answer is a simple 'no' it is difficult to provide rigorous documentation in support. There are obviously different disciplines that lead to different academic departments, and British and (I imagine) US grant authorities divide biology up for the purposes of targeting resources and assigning experts, but trying to make a classification would be like trying to catch a greased piglet.

Please clarify your specific problem or provide additional details to highlight exactly what you need. As it's currently written, it's hard to tell exactly what you're asking.


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Have lions, tigers, and cheetahs begun to lose or not yet fully gained tree climbing traits?
Leopards, jaguars, and the domestic cat all regularly climb trees, but lions and tigers rarely do. From what I can tell from a basic online search, the latter are inexpert tree climbers, but they theoretically can.
My question is about the direction of evolution of tree climbing among the felidae. Did the ancestor of felidae have the ability to climb trees, and lions and tigers lost the agility necessary to do so with ease, or is this an example of convergent evolution, and jaguars and leopards happen to excel at it for physiological reasons? If so, what are those reasons?
What makes me unsure of the former is that cheetahs, not nearly as large as tigers and lions and quite agile, also have difficulty climbing trees. Is this a primordial behavior of the cats' ancestor or just a learned behavior among cats?
Some studies at least suggests it's that scapular shape is indicative of climbing skill. Canids are not regularly known to climb trees, though many bears do.
To be clear, I am not asking "why do A have Y ability but not B." I'm asking about historical priority. Was this a characteristic that existed in e.g. Proailurus, or did it evolve separately? I'm aware that the "why" questions are speculation and meaningless, but instead I'm interested in the history of this family of species.

small cats climb trees to hunt or to protect themselves against predators,lions and tigers have no need for protection against predators.

@trondhansen I thought about that, but as I mentioned in the question,  cheetahs also have trouble climbing trees, and they are preyed upon by lions, hyenas, and even jaguars. That's why I was unsure.

Related: https://biology.stackexchange.com/questions/35532/why-do-some-bad-traits-evolve-and-good-ones-dont?rq=1

Does this answer your question? Why do some bad traits evolve, and good ones don't?

Welcome to Biology.SE. The Biology.SE community has agreed that questions that show little or no prior research effort are off-topic on this site. Please [edit] your question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Under researched questions may be subject to down-voting and closure. You also seem to have multiple questions, which is another reason for closure. Thank you for taking the [tour], but please consult the [help] starting with [ask] for details and edit or delete your post accordingly.

@BryanKrause No, that doesn't answer my question at all. I'm asking about historical development. Did big cats slowly lose the ability, or is it a factor of convergent evolution? I'm not interested in so much in ad hoc guesses of "why" (though I do enjoy speculation, thus that one throwaway line).

@tyresome Fair enough. When I get a chance, I'll add in a few articles I read on this topic. Is there a requirement concerning the quality of the sources? Must they all be peer reviewed studies?

FYI: I've seen multiple videos/accounts of tigers in trees -- especially cubs. Adults are certainly known to climb a tree once in a while, too (a Google search I'm sure will pull up many images/videos). I think the infrequency is much more due to their large size: 1) bigger cats need bigger branches ; this is supported by cubs being more frequent climbers than adults. 2) being an apex predator doesn't really require going into trees for safety.... I think your question is ok and could receive a useful answer. But at least some of that answer likely will challenge your premise to some degree.

@CMW regarding quality of sources : no there is no official requirement. However, poor quality sources don't improve any post, and such poor quality sources may do little to improve community response to a post. Certainly, many posters here simply cite non peer-reviewed sources such as web pages in questions. That's often ok (depending on source). But please use sources that reflect your level of competence/experience. Thanks for the question and effort to respond/edit.

@theforestecologist That's certainly fair. An answer that is basically your two points isn't unwelcome. It wouldn't tell me too much about felid ancestry, but I'm happy to be wrong about my initial observation.

https://whyevolutionistrue.com/2022/03/12/caturday-felid-why-dont-lions-climb-trees-cat-butt-pencil-sharpener-and-a-refugee-cat-from-ukraine/ . If you actually had good records of tree-climbing ability you could do character mapping on a felid phylogeny to try to find out ... Mattern, Michelle Y., and Deborah A. McLennan. “Phylogeny and Speciation of Felids.” Cladistics 16, no. 2 (June 1, 2000): 232–53. https://doi.org/10.1006/clad.2000.0132.


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Help identifying possible fossil found in coastal northern Iran
This was found in Jangels near by the sea, in North Iran:

can  you add something for scale or give the dimentions and please edit this into your question.

Pictures from the side and bottom would also help. Having said that the term "echinoderm" springs to mind. Which one, I have no idea.


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What causes Erythroblastosis fetalis?
So this is what I understood about the disease by researching about it
When a Rh-ve mother has a Rh+ve baby in her womb,

The placenta prevents mixing of fetal and maternal blood preventing antigen detection by her immune system.
There are no pre-made antibodies that can attack the fetal RBCs to kill them
At the time of birth, the placenta breaks thereby exposing the fetal RBCs to her immune system
The WBCs get sensitised and begin antibody formation which takes atleast 6 months
The first baby is born safely
In the event a second Rh+ve baby is conceived, the antibodies aleady present in the blood
cross the placenta and destroy the fetal RBCs killing it.(secondary immune response)
To prevent this an injection of Rh antibodies is given to the mother after first birth which
destroys all fetal RBCs before they sensitise the immune system preventing secondary immune
response.

My Question is
Why does this happen only with the Rh antigen?
I know many people whose mothers have B+ve/A+ve blood but their children are born normally even when they have A+ve/B+ve blood(opposite of the mother). There even are people whose mothers have O+ve blood while they have B+ve/A+ve blood groups.
The body has pre-made a and b antibodies which should kill the fetus unlike in case of Rh where 1st birth is safe. Also much lesser time is needed to produce these antibodies which is why there cannot be any blood transfusion between incompatible ABO system blood types while one transfusion is possible between incompatible Rh blood types
My take on this will be that antibodies against ABO blood groups can never cross placenta but most antibodies do so this seems less like a solution
A lot of research failed me a solution.
I found a somewhat similar question here but it does not address my query completely
Erythroblastosis Foetalis

You may find this helpful: https://www.exxcellence.org/list-of-pearls/management-of-pregnancy-with-abo-incompatibility/


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How can children scream so loud and so long?
Recently I saw a small baby shrieking extremely loudly (my ears hurt) for at least 4 minutes .
How is it possible? If I yelled so loudly, I would be defeated by throat ache after less than a minute. I know that heavy metal vocalists are capable of such feats, but it takes them a lot of practice.
So how can children yell so loudly for so long? Do they ignore pain? Does the pain cause the feedback loop of discomfort->yelling->more discomfort->more yelling? Or do they have vocal chords of titanium?
I tried google search, but answers are generally "why do children scream", not "how can they scream".

4 minutes are not long,fb suporters can keep it going for 45 min.

@trond screaming and crying is a bit more physically strenuous than singing football songs, no?

I seem to remember that this question — which seems to me rhetorical — has been asked on this list before (and in life by countless parents including myself). I suspect that your real question is how to stop it, in which case I believe there is a Parenting SE. Or Doctor Spock. From memory, you let them scream themselves out.

Children are more energetic than you. Is it so surprising that this also applies to screaming? Square cube law is also probably involved.

@David this isn't a rhetorical question. I don't care how to stop crying baby. I don't have one. I'm just surprised it can go for so long and so loud.

If not rhetorical, your question seems to me to address something that has not struck others as enough of a problem to investigate.


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Albino pedigree question
https://www.proprofs.com/quiz-school/playquiz/?title=pedigrees-quiz is a link to the website containing this question.

I'm not sure how you came up with your table, but I encourage you to start over.
Among other things it appears to me that you've made an unwarranted assumption about the unaffected sister's genotype.

I suggest you start by making a Punnett square for the albino's parents and think about what that means for unaffected sister.

Next think about what must be true for the unaffected sister to have an albino child with the unrelated non-albino man.
• Once, you've calculated the probability of that situation you're one step away from your answer.

Finally, given the situation in (2) what is the probability that the couple will have an albino child?


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Species extinction attribution
In climate sciences there is the new field of extreme weather event attribution (EWEA). It investigates quite successfully on the one side how climate change (i.e. rise of global and regional mean temperatures) leads to an increase of the frequency and intensity of extreme weather events (of different types: droughts, floods, hurricanes, at different places). On the other side EWEA investigates for a given extreme weather event (a specific drought, flood, hurricane) how climate change contributed to its causes (making it more probable in a sense).
I wonder if there is a corresponding field of species extinction attribution (SEA) which investigates how climate change and extreme weather events contribute to the causes of the extinction of a species. Both on the statistical (frequentists') and on the anecdotal level. Anecdotal means: considering a specific species that's gone extinct recently (so we know the circumstances quite well) and investigating how the rise of mean temperatures and/or extreme weather events have caused it.
On the one side SEA might be "easier" than EWEA because the extinction of a species is a better defined event than extreme weather events. On the other side there may be more and more complex additional causes (next to climate and extreme weather events), mainly the destruction of habitats and interruption of migration routes.
So my question is: Is there something like extinction attribution science with a focus on climate change as a main driver of species extinction?

Maybe species extinction is too much, and (severe) decline of species population (species decline for short) would be more appropriate?

I am afraid this is not a question about a problem in biology, but about the catagorization or directions of development of biological research. Although not without interest, I do not feel it is appropriate to this list. Please re-read the [Tour] and Help pages.

There used to be a whole journal devoted to this question: Climate change responses

https://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.2001104

I’m voting to close this question because it is not about biology in the terms of SE Biology (as I wrote at the time).

Even though without focus on climate change, this paper is about extinction attribution in the sense that the relation between traits and extinction risk is investigated:
A review of the relation between species traits and extinction risk (2019)
And of course the impact of climate change on species populations is investigated carefully (only under another umbrella term: "climate attribution science", not meaning "what contributes to climate change" (as in weather event attribution science) but "to what does climate change contribute"), for example
Climate attribution science and the Endangered Species Act (2021)


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Are there flies that can spray their eggs while flying?
While I was reading a few articles about parasitic infections caused by flies, to be specific Myiasis, I read something saying that some flies can spray their eggs when they are flying around their target instead of having to stay on it and lay the eggs there.
Is this true? What's the name of these kind of flies?
PS1: I include part of the source translated to English:

Dr. A. Khazani ,entomologist &  an expert in charge of the vector control program of Isfahan province, emphasized that environment hygiene is particularly important in preventing people from contracting myiasis, added: Some flies spray their eggs while flying, which may get inside the ears, nose, and eyes. and... penetrate and cause disease

Source: IMNA, A Metropoitan News Agency, June 8th, 2019
Names of the species were not mentioned in the source article.

Welcome Merlot. "Almost"? Personally I can almost afford a new car. I'm not sure if such a creature exists, but if you were to add the results of your investigations to the body of the question (even if inconclusive) that would definitely improve the question. I find that Google Translate is handy for translating quoted, why not give it a try.

@JiminyCricket. I translated that part of the source & put it in here.


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What is the technical term for a combination-mouth-anus?
Some organisms have a single hole that is used both for food intake and for waste excretion. Does the scientific community have a name for that hole? What is it called? Or is it simply called the mouth-anus?

The mouth.
This is sometimes referred to as the hypostome (most sources, though Wikipedia disagrees). It is usually muscular.
The Pharynx.
This is the muscular part of the tube leading to the gut which contracts in waves (the familiar peristalsis), pushing the meal into the gut. Sometimes undifferentiated from the mouth such as in the hydra where the mouth leads straight to the hollow interior.
Proboscis pore.
Some sources have it that Planaria have just a pharynx, in others the structure the food enters before the pharynx is also referred to as the proboscis within a proboscis sheath, the "mouth" being referred to as the proboscis pore.

The intestine to cap it off.
This is referred to variously as the gut, the gastrovascular cavity, the digestive cavity and, of course the intestine.

If an organism has a single pore for both ingestion and excretion then it is known as incomplete digestive system. Primitive organisms like  Platyhelminthes (flatworms), Ctenophora (comb jellies), and Cnidaria (coral, jelly fish, and sea anemones) has this type of digestive system. It contains only one opening, the "mouth" which also serves as "anus". Ingested material enters the mouth and passes through a hollow, tubular cavity called gastrovascular cavity. Cells within the cavity secrete digestive enzymes that break down the food. The food particles are engulfed by the cells lining the gastrovascular cavity.

(image source)
There is no specific term for this orifice although there is this statement from the Wikipedia article of GI tract:

A through-gut (one with both mouth and anus) is thought to have evolved within the nephrozoan clade of Bilateria, after their ancestral ventral orifice (single, as in cnidarians and acoels; re-evolved in nephrozoans like flatworms) stretched antero-posteriorly, before the middle part of the stretch would get narrower and closed fully, leaving an anterior orifice (mouth) and a posterior orifice (anus plus genital opening) ...

Technically, digestive system of Sponges is also primitive, having pores all over the body called ostia where food is entered but excretion happens at a dorsal pore called osculum. (See image here)
Related: Why porifera is classified to have an incomplete digestive system although it has no organs?


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Isolation of viruses and Koch's Postulates in connection with terrain theory and claims that viruses don't exist
If, as a physicist, I were to be told that quarks have never been isolated, and so they are not actually real particles, it would take some effort to respond.  I'd have to talk about the Standard Model and Asymptotic Freedom, and thus admit that they do have some properties that are not like other particles.
If faced with insistance that this proves the case, that they are actually some sort of epiphenomenon of particle accelerators, I might have some difficulty knowing how to proceed.  It's true that they manifest an as yet new characteristic, and so perhaps we have to expand our conceptualizaiton of what a particle is.
That may not be a perfect analogy for my question, but I have a medical friend who would like to tell me that no virus has ever been isolated, and that as opposed to some kind of transmissible, infectious organism, they are actually some kind of waste product of cells. I am told that any attempt to satisfy Koch's postulates involves the injection of materials in addition to the viruses at issue, and the claim is that it's these combination of materials that is making the animal sick.
I see a lot of varied "viruses don't exist" claims around the web, focused on HIV, measles, and CV19, and associated with names like Drs. Stefan Lanka, Andrew Kaufman, Tom Cowan, etc. Associated claims are that in any context that involves supposed exposure to a virus, less than 100% of the animals get sick, and so whatever may be going on, it's the animal itself at issue. In some quarters this is called "Terrain Theory." I would like to not have to dig too far into this.
How can I respond in a coherent way that doesn't require becoming a virologist?

Comments are not for extended discussion; this conversation has been moved to chat.

It is very easy to disprove their claims, but the burden of proof doesn't lie with you, it lies with the person making the claim. If they want to claim that there is a "cell waste product" that causes the widely varying symptoms and viral effects (in cells, model organisms etc) we see with different viruses (compare say chickenpox with SARS-CoV-2), then they need to prove that this is the case. They need to do the science and have it passed through peer review etc. Also remember that extraordinary claims require extraordinary proof - they need to prove the whole scientific consensus wrong in this case!
At its most simple, you can purify viruses via a range of methods (e.g. ultrafiltration, ultracentrifugation, chromatography etc) and resuspend in a simple salt solution of varying compositions (e.g. phosphate buffered saline, ringer's solution, tris buffered saline) and use that purified virus to infect. I would hope that even the most science-denying person would see that these solutions are very simple and don't contain anything special that could be "cell waste" or "its the fetal bovine serum" (another virus-denier claim). I would note that most of these denier people wouldn't understand the principles behind the above methods, but using them you can get pure preparations of viruses and other materials, down to separating out single molecule types from a crude solution.
You also run controls of the solution alone and easily see that the animals/cells don't infect at all with these controls, but do infect with the virus containing material. You can also run controls on your sample prep - for example, treat uninfected cells to the same virus preparative procedures as you did for the virus and show that this also doesn't result in infection.
If it were a product of cell waste you would expect to see these effects from all cells, not just virus infected ones.  For a cell waste you should also see some sort of dilution effect that is non-propagable (i.e. can't be passed on) - take your purified virus and dilute it in your solution of choice and it will still infect, but "purified" material from un-infected cells won't.
An additional note: You can also take the genetic material of the virus and use that to produce more virus. In some cases (as with positive sense RNA viruses and DNA viruses) you can use the genetic material directly and produce more viruses with the same characteristics as the source of the genetic material. Now, it doesn't work for some viruses - some genomes are too big, need special conditions, etc., but it does surpass some of Koch's postulates, as in you can synthesize this genetic material in the lab and using that material along with cells to produce a virus with exactly the characteristics of the original source of the genetic material.

The trouble is, the "burden of proof" claim may be formally correct but it is not necessarily rhetorically persuasive - and moreover it leaves any third parties to the dispute who are ignorant of the arguments on both sides hanging as to becoming better informed about what and why certain things should be believed. Someone could say, "sure, they haven't proven their case, but because xyz, why should I believe the 'mainstream' side either? "

@The_Sympathizer I totally agree - and it definitely is a problem, which is why the rest of the post is there...

Very good answer.  Much appreciated.  The various forms of "isolation" and the control methods are sufficient to what I was looking for.  Also, I've read some history of koch's postuatels, and see that they were criticized almost right away.

This may be too brief or simplistic, but a short discussion of electron microscopy might be in order; the different viruses are consistent in morphology in the diseases they cause (e.g. Ebola virus, smallpox, COVID, etc.)
It’s hard to argue with your own eyes (or a mental picture of what your eyes would see…)
To quote from a paper on the subject:

Using TEM, viruses can be differentiated by their ultrastructure: shape, size, intracellular location and for some viruses, by the ultrastructural cytopathic effects and/or specific structures forming in the host cell during their replication. Ultrastructural characteristics are usually sufficient for the identification of a virus to the family level.

And

For some viruses, TEM can be conducted on contents of skin lesions (e.g., poxviruses and herpesviruses) or on concentrated stool material (rotaviruses and noroviruses). For successful detection of viruses in ultrathin sections of infected cells, at least 70% of cells must be infected, so either high multiplicity of infection (MOI) or rapid virus multiplication is required.

If you know any cell biology. Viruses can’t be mistaken for cells or detritus.

What cell or piece thereof can the above be? Great picture of bacteriophages.

Ebola virus. Always present in Ebola, not present in other illnesses.
Electron Microscopy in Discovery of Novel and Emerging Viruses from the Collection of the World Reference Center for Emerging Viruses and Arboviruses

+1, best way to prove something exists is to go take a picture of it.

Excellent - the beauty of EM is that the capsids are so consistent with the species - and of course phages are only found in bacterial preps and look nothing like exosomes. I also really really wonder how the capsids of the filoviridae evolved, must be some significance to be so distinct.

@bob1  A bacteriophage is a wondrous thing, isn’t it? Such a tiny, ‘simple’ thing, but so elegant and dangerous to the bacteria it targets. Amazing!

@anongoodnurse absolutely, couldn't agree more. The diversity is incredible too, not to mention the abundance

At this point, anyone who doesn't accept the existence of viruses has reached flat-Earther levels of delusion and probably cannot be convinced otherwise by any evidence you would show them or any argument you can make. To believe that viruses are not the explanation for most diseases attributed to viruses, you have to believe in a vast conspiracy among government institutions, scientists, hospitals, pharmaceutical companies, and various commercial enterprises. If you think such a conspiracy is more likely than viruses doing what science says they do, then your method of weighing evidence is quite strange and, I'd say, wrong. There are many compelling sources of information that viruses are real. Even if you refuse to accept one of these sources, the others should be enough to convince you that the existence of viruses is more likely than such a massive conspiracy.

First-hand knowledge. Believing in a flat Earth requires rejection of evidence of an approximately spherical Earth that can be obtained firsthand (ships on the horizon, lunar eclipses, flights from Santiago to Auckland, flights from Johannesburg to Perth). Even more so (and unlike quarks), most people have first-hand experience with viruses, observing spread of colds, flu, chicken pox, and COVID-19 within families and people in close contact. It's pretty hard to explain this fact without proposing some kind of microscopic replicating organism-like thing that passes from person to person. Even if you don't believe that the viral particles are carrying these diseases, it should be clear to everyone that they are contagious diseases.

Changes in society in recent memory due to understanding how viruses work. Major early support for the existence of viruses came from the fact that vaccines work, which I am guessing virus-deniers don't accept. Vaccines are based on treated viral particles or components of viral particles (viral proteins, sometimes called toxoids). There are people living today who remember a time when people lived in fear of polio and measles was a common childhood illness. You can easily find history discussing the small pox and measles epidemics. What happened to those diseases if viruses aren't real and we don't understand how to combat them?

Pictures of viruses. If you think they are computer generated or something, you can probably talk to someone at your local university who has taken a picture of one. Taking pictures of viruses is easier than taking pictures of a round Earth. You only need a relatively low quality electron microscope, which you can get for less than $100,000.

Understanding viruses enables other technology. For many viruses, we understand the components that make them work. Besides vaccines, there are other technological uses of viral components. Retroviruses such as HIV must have a protein that copies RNA to DNA. You can buy such a reverse transcriptase to copy RNA yourself. Viruses are also used in gene therapy and you can contract with a large number of companies to create viral vectors with your custom gene. If we didn't understand viruses, why would people buy and sell this stuff?

Koch's postulates are only somewhat more relevant to modern medicine than insisting that electromagnetic waves must travel in some medium (luminiferous aether) is to modern physics. They do not describe necessary and sufficient conditions for proving that viruses cause disease, they're postulates that someone came up with over a century ago and were proven insufficient by subsequent investigation. They're not laws of nature, and any argument assuming that they are necessary and sufficient conditions to prove that a given pathogen causes a given illness is meaningless.

I'd argue that Koch's postulates are sufficient but not necessary to prove that a given pathogen causes a given illness: if you've got a pathogen that meets the criteria, it's reasonable to assume that it's the cause, but if you've got a pathogen that doesn't, you can't rule it out as the cause.

It's worth noting that Koch's postulates don't always apply to viruses, and that alternative postulates have existed for nearly a century to better identify putative viral pathogens. See Why did Rivers replace Koch's postulates?

I read about this, thanks @acvill .  Beyond Rivers, I also found Koch's Postulates in the 21st Century.


text:
Does centrifuging the bacteria culture removes bacteria leftovers?
Usually, we centrifuge bacteria culture to either replace the media, control its density (OD), ..etc. I know that when centrifuging the cells are pushed to the bottom while the media (solution) remains at the top. However, let's say the bacteria was left to culture for a few days and the bacteria metabolism releases some carbohydrates as an output (e.g. Cyanobacteria).
Would those carbohydrates remain at the bottom with the bacteria cells or will they stay with media at the top where we can pour them?

What research have you done on your own to answer this question? The Biology.SE community has agreed that questions that show little or no prior research effort are off-topic on this site unless you have shown your attempt at an answer. Please [edit] your question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Our goal is not simply to be an answer site, but rather a site that promotes self-learning with some expert help along the way.

Centrifugal pelleting is density based. Under general media conditions and centrifugation, most secreted carbs will remain in the supernatant.

Correct answer, +1. The only way to pellet ("precipitate") dissolved compounds is a low enough temperatures, in conditions where sugars would crystallize out of solution. It would then be possible to centrifuge them into a pellet. Also, routine centrifugation in my experience leaves some viable bacteria in the supernatant, so if you wish to have a cell-free supernatant, it is always good practice to additionally filter it post-centrifugation. PS. I see you've been downvoted, likely by someone looking for the addition of credible reference/citations.

@SPr There are methods to pellet dissolved compounds.


text:
What is the deepest living underground organism?
A quick search reveals Halicephalobus mephisto which was

detected in ore recovered from deep rock fracture water in several gold mines in South Africa [...] 3.6 km (2.2 mi) under the surface of the Earth.

Have any deeper living organisms ever been found?

I suspect the answer to this question is the same as to the answer as to how deep underground we've ever actually looked for living organisms.

Halicephalobus mephisto, the "devil worm" (actually a nematode) was, as of 2017, the deepest discovered species -- found living at 3.6 km below the surface! However, this species ties another deep species: Plectus aquatilis found a number of years before (~2011 I think; don't quote me). I know of no recent updates regarding multicellular organisms. Looks like acvill's answer covers fairly recent (2021) "deepest" cellular evidence

Have any deeper living organisms ever been found?

In 2021, researchers recovered microbial cells and DNA from rocks retrieved from a depth of 4,850 m below the surface.1 The New Scientist covered this finding in an article titled "Deepest land microbes ever found".

Dong and Huang say that, to the best of their knowledge, these are the deepest known microbes ever found on land. Demonstrating that the cells are living will be a challenge as microbes that live deep below the surface often operate on such a slow timescale that they show few typical signs of life such as movement or reproduction.
But there are reasons to suspect the microbes may be alive. Most importantly, they are intact rather than just cell fragments, which might hint they are carrying out basic cellular repair.

Dai X, Wang Y, Luo L, Pfiffner SM, Li G, Dong Z, Xu Z, Dong H, Huang L. Detection of the deep biosphere in metamorphic rocks from the Chinese continental scientific drilling. Geobiology. 2021 May;19(3):278-291.


text:
What is the conjugation capacity of the liver?
Our liver conjugates 250-300 mg bilirubin per day under normal circumstances but it is capable of conjugating much more. What is the upper end per day after which it won’t be able to conjugate leading to increased unconjugated bilirubin in serum?

Welcome. What have been your research efforts to answer this question so far? Cn you share it with us?

I’ve looked everywhere I’m dying I need help :(

If you mean that in the very real sense, then you should speak to a member of your medical/surgical team as questions regarding personal medical advice are off-topic here. If it's just an expression of frustration of not being able to find what you're looking for, then I get it. The limiting factor (or a limiting factor) seems to be the process of glucuronidation by the enzyme glucuronosyltransferase (UDPGT), the rate of production of the enzyme being limited. That should be a starting point for research.


text:
How to fix outliers in Ramachandran plot using Coot
I have the following Ramachandran plot generated by Coot:

Notice that it has high outliers content (red dots). I want to manually drag those
red dots into some part of the region. Eventually, I expect it to be reflected
in the coordinates so that I can save it as a new PDB file.
How can I achieve this?
G.V.

Surely the first place to ask would be the mailing list for this very specialized software. Have you done this?

https://www.jiscmail.ac.uk/cgi-bin/wa-jisc.exe?A2=ind2207&L=COOT&O=D&P=2725

This was asked also on chemistry and mattermodelling


text:
What does "sect." mean?
For example, Centaurea sect. Microlophus

Section, a taxonomic level. In plants it's a possible level between genus and species.
See also https://en.wikipedia.org/wiki/Section_(biology) as the term is used differently in zoology.

So in my example above Microlophus is a Section? And is this different from Genus - Species - Subspecies?

@AlLelopath Yes. It's different because Microlophus is a group of species within a genus. If you have subspecies, those are within a species. All of the levels are quite arbitrary, but are used to avoid having to rename things every time you discover or want to emphasize some particular aspect of taxonomy.


text:
Performing histology on undecalcified tissue
Performing histology on tissue containing calcification - without performing decalcification of the tissue - is a challenging problem. There are currently a few methods to overcome these challenges including epoxy embedment, methacrylate embedment, and stabilization of tissue followed by partial decalcification. However there are drawbacks or limitations to each method as each may require specific infrastructure to perform effectively, such as a specific style of microtome.
Besides these challenges, how might you approach sectioning of calcified tissue with the aim of preservation the soft-hard interface along any calcified region? The following are objectives and demands of a successful technique:

objective 1: perform sectioning of a tissue containing thin wall calcification while preserving the spatial arrangement of soft
tissues in the region adjacent to calcified tissue - analogous to
periosteum-bone interface

objective 2: preserve molecular composition and spatial arrangement throughout process

objective 3: produce thin sections

demand 1: limit as much as possible any decalcification of to-be-sectioned tissue

demand 2: perform technique with minimal specialty equipment

demand 3: no paraffin

I will provide an initial option to begin: Tissue will be embedded in a high monomer content neutral aqueous polymer solution and chemically crosslinked following adequate diffusion time (akin to CLARITY protocol). Tissue will be cryostabilized and placed on a cryostat near -40 for sectioning.

This seems more like a research-level question someone might spend several years developing a PhD thesis to address; the techniques you mention exist because they're the best that people have come up with. If someone came up with something better that lacked the drawbacks, that's what everyone would do instead. Have you attempted the option you propose? What happened? I think it's okay to have this question here in case someone does have an answer, but I'm highly doubtful.

I think thats the purpose of asking the question isn't it? As well, getting answers which may not necessarily outright provide a method that encompasses the objectives and demands but might provide ideas toward a successful method would still be useful.


text:
What are the structures that make pixel-like patterns in wood?
Some wood seems to have structures that are squarish in cross-section. I've often noticed that these are distributed in arcs or sinusoid shapes on guitar fretboards, for instance.
Here's an example I was able to find online:

Edit: here's a better picture, you can see the pattern as it rotates with respect to the cutting plane I think:

Are they channels or just fibers of a different color? Why are they distributed in this way?

Welcome to Biology.SE. I see a lot of different patterns — I think it could be helpful to indicate (e.g. by adding markings like arrowheads) exactly what structures you are interested in. It also would be clearer if you showed a plain piece of wood (ideally a closeup of a small section of wood) rather than a fretboard, which complicates the issue. Next, if you are using some else's image it should be public domain and properly credited. Finally, have you tried looking up "wood anatomy"? Demonstration of prior effort on your part is one of the site expectations (see: [tour], [ask], and [help]).

I suggest looking for wood cell patterns online. also is that a natural pattern or is a veneer which involves cutting a wood in a rotary slice. https://www.google.com/search?q=wood+grain+patterns+microscope&tbm=isch&chips=q:wood+grain+patterns+microscope,online_chips:forestry:NiLTcVs6464%3D&hl=en&sa=X&ved=2ahUKEwiXw5Pt5_74AhW5rXIEHce0BeQQ4lYoBHoECAEQKQ&biw=1215&bih=571

Wood is composed of a variety of longitudinal cells (those running parallel to the axis of the trunk or limb) and ray cells (those running perpendicular to that axis, from the center of the trunk to the edge).
Longitudinal cells produce the regular ring pattern (you can see them aligned vertically in the fingerboard photo). Rays (also called medullary rays, vascular rays, or pith rays) are producing the darker squiggles.
The ray cells help conduct sap and other materials radially in the trunk, between the center and the bark.
Different types of wood produce more or less prominent rays, with different characteristics. Different cuts of wood also make the rays more or less visible.


text:
Are, or how are, polyuria and diuresis different?
http://wikidiff.com/diuresis/polyuria and http://neetprep.com/subject/U3ViamVjdDo1Ng==/topic/VG9waWM6NzEx/doubt/RG91YnQ6MTQ0MDc= appear to state that the terminology is identical, or provide unhelpfully similar and potentially automatically generated description of each:
http://wikidiff.com/diuresis/polyuria states that diureses is "excessive production of urine", and refers to polyuria as synonymous. It additionally states that polyuria is "production of an abnormally large amount of urine" and that diuresis is synonymous.
http://neetprep.com/subject/U3ViamVjdDo1Ng==/topic/VG9waWM6NzEx/doubt/RG91YnQ6MTQ0MDc= very directly states that their definitions appear to be identical, but anecdotally that they may be utilized during different conditions.

You state that "most websites appear..." so some websites don't provide identical definitions, have you considered those?

We expect questions to show some evidence of the effort you've taken to understand the problem. If you've found definitions of these terms that seem the same, could you cite those? Perhaps quote them briefly with a link, and point out why they seem the same, and why you think they should be different?

@BryanKrause, I believe that I have added what you request.

Probably better on SE Medical Sciences.

@David, are you able to transfer it? Nobody appears to be able to answer this.

No, only the mods like @BryanKrause (the diamond indicates he is a moderator). So what you can do is raise a flag and under "other" ask for the transfer. But it would be a good idea to first modify your question as he suggested. Alternatively, delete and post there.


text:
What percentage of the mass of green plants / algae is carbon?
Wikipedia says that the human body is about 18% carbon, but I can't find any percentage on how much of green plants / leaves or algae is carbon? I assume it varies, so if an example is needed, what percent (by mass) of duckweed or grass is carbon?

Why do you care?  Context helps us to determine whether questions are worth answering.

I was just interested, some questions get stuck in my head when watching documentaries or reading things. If people do not find the question worth answering, I am afraid my reasons will not make it more worthwhile. Sorry.

See table 1 here.

Life form
reprod organn
reprod organmean/sd
rootn
rootmean/sd
leafn
leafmean/sd
stemn
stemmean/sd

Herbaceous plants
83
42.56± 4.57
749
42.45± 5.12
5181
44.73± 3.45
162
42.41± 3.54

Crop
42
42.40± 5.11
56
38.20± 5.23
85
41.32± 3.38
69
43.26± 3.15

Woody plants
57
48.56± 4.07
1392
47.43± 3.94
12 064
47.83± 3.81
3461
48.16± 3.27

Deciduous broad-leaved
17
46.81± 3.93
513
46.59± 3.55
5074
47.25± 3.42
1581
47.69± 2.68

Evergreen broad-leaved
29
49.64± 4.42
520
47.72± 4.14
4490
48.48± 3.86
1212
47.78± 3.58

Conifers
8
48.25± 2.56
252
48.43± 4.16
560
50.25± 3.33
502
50.48± 3.07

Fern

2
43.64± 3.83
98
44.47± 3.33
–
–

Vine
2
45.83± 0.33
38
46.25± 4.46
251
45.74± 4.77
82
46.73± 2.69

Bamboo

23
45.06± 4.28
30
42.98± 5.09
39
49.20± 3.54

All
142
45.01± 5.23
2306
45.64± 4.95
18 124
46.85± 3.98
3754
47.88± 3.49

For an algal estimate, see here:

Carbon is obtained from the post-carbon-capture flow and compressed to 1 MPa for transport and supply to the growth volume (requiring 248 kJ/kg of gas). Carbon uptake efficiency is 79%. The algal biomass productivity is 82.5 t/ha-yr (23.8 g/m2-d) with an elemental composition consisting of 48% carbon, 6.3% nitrogen, and 0.6% phosphorus (Huntley et al., 2015).

I guess it's not a coincidence that it hovers around 45%, since cellulose is 44% carbon? :) C6H10O5: (612.0)/(612.0+101.0+516.0)=0.44

I guess the issue then becomes how much is cellulose!

I could not find easily understood numbers on algae? The table was great for anything else, thank you!!

@HenryStone see edit pulling a direct quote

@Maximillian Press Thank you for an absolutely excellent answer!


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Primer design for site-directed mutagenesis
In our practical course about modern cloning methods, we performed point mutations on a promotor via site-directed mutagenesis.
As far as I understand that method you need forward and reverse primers with a partial overlapping sequence to perform point mutations. For deletion and insertion you need forward and reverse primers with a back-to-back orientation.
In the practical course, we already performed that step of the mutation. However, after taking a closer look via CLC workbench where we performed that reaction in silico, I saw that our used primers had no overlapping sequences. Instead our forward and reverse primers had a back-to-back orientation.
Our mutation did work out.
Therefore, I was thinking that point mutation via SDM is also possible with back-to-back primers. However, I did not find any source that can prove that theory of mine.
So I am hoping that someone with more experience than I have, could help me out.

It would be useful it you could make an example drawing/figure to explain what you mean. I'm currently having a hard time understanding your question.

Thank you for your comment! I now edited my question and included some screenshots of my analysis in the CLC workbench. Even though I found the solution now, do you understand what I meant?

Yes, I understand now. Since you have no primer overlap, you probably used 5' phosphorylated primers, amplified the entire plasmid, and then ligated the resulting PCR product to create the new, mutated plasmid. You might want to remove your edit from the question and instead post it as an answer. Also, you did not perform permutations, you inserted mutations. Permutations is something different.

I found the answer! Apparently, it is possible to perform a site-directed mutagenesis with back-to-back orientated primers.

In that picture, the green mark represents a part of the lacZ gene. There, we performed a point mutation by using the forward primer "Cand2 M5 Fwd" and the reverse primer "Cand2 M5 Rev". The forward primer is in fact longer: it includes the purple highlighted part as well. There we exchanged some nucleotides.

In this picture, some nucleotides in the once highlighted part are now exchanged. I was confused as I was tought that the primers should have a partial overlapping sequence with each other. But now as they are back-to-back orientated and have no matching sequence with eacht other, I discoverd that it is possible to perform point mutations like this in a template sequence.

This doesn't really answer your question though. Like I pointed out in my comment to your question, my guess is that you used phosphorylated primers and then went through a ligation step to seal the plasmid before transformation into bacteria. But whether that's what you actually did or not is not clear from your answer.

Hello there! Maybe you understand something wrong. We indeed used back-to-back primer which were phosphorylated and then ligated the plasmid with the wanted mutations. However, with my question I was focusing on the POSSIBILITY to use back-to-back primers for point mutations. Maybe I misunderstood that in class, but I thought you have to use overlapping primers. Therefore, I was very confused as I saw our in silico experiment and reached out to get an explanation from more experienced people (my prof didn't answer my mail...).

Got it. Thing is that in traditional site-directed mutagenesis (with homologous primers) you don't use phosphorylated primers, nor do you depend on a ligation step. Two completely different methods.

Hi there!
Thank your for your response. Do you mind telling me more about this? Is there a possibility to write something like a private message?

There is not, but you can look for the QuikChange method.

Just thought i'd clarify for anyone who is reading this.

Typically site directed mutagenesis uses two complementary, overlapping primers which each contain the mutation desired in the plasmid.  then PCR will generate the entire plasmid.
There is a second method with only one primer for each desired mutation.  The primers are phosphorylated by a kinase enzyme to make the primers work to accept ligation.
This requires a high fidelity polymerase because PCR is copying the entire plasmid else unwanted additional mutations will occur.  This sounds simpler but you have to sequence the mutation sites of several colonies to get full results.


text:
Are there any examples of social animals which show collective behavioral change in response to disease?
When Covid-19 happened, collective behavioral changes were taken in order to curb the spread of the virus by the human race. Do things like these happen in other animals as well? Like isolating a person who gets sick and such.

Interesting question. Here we are expected to show the results of our own investigations into a subject here, you can [edit] to tell us what your searches found and where the sticking points are.

Welcome to Biology.SE. As stated by @JiminyCricket we are expected to demonstrate prior research when posting. Please [edit] your question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Under researched questions are subject to down-voting and closure. Please take the [tour] and consult the [help] starting with [ask] for details and then delete or edit. ——— For example, I did a quick search and came up with this article.


text:
Is DNA a Language?
I’ve been thinking about attributes that are unique to humans (not just far more developed in humans than other species) and aside from trivial things like chins, the only ones I can think of are art and language, but I’m not certain of either of these. Some songbirds sing for no apparent reason, which might suggest they have an intrinsic aesthetic sense.
As for language, what separates it from communication, I would argue, is grammar. It seems fairly clear that the other examples of what we would typically call communication in nature are not grammatical. But then I thought about DNA. People often speak metaphorically about DNA as a “programming language”. So, is that more than just a metaphor? That is, does DNA have clear lexical units, whose arrangement determines the relations between them? That is, is DNA, in whole or in part, grammatical?
There is a similar question here, but the answers are too ambiguous in the use of the word “language” for my purposes. For example, English is undeniably a language. We could take all valid English sentences and order them as in a dictionary. This assigns each sentence a natural number. We could then assign the number the meaning of the corresponding English sentence. It would be fair to call this a “code”, but hard to call it a “language” in the strict sense: the digits of the numbers and their organisation would not really have meaning. In comparison, in English, the word “biology” has a specific reference, or placing an adjective before a noun has a specific meaning. I’m not talking about DNA “meaning” what it’s encoding in the sense that it knows what it’s doing, that is of course nonsense. Rather I’m using the word meaning in the sense that lexical units of DNA and ways to organise them would denote specific things, for example, specific ways to fold part of a protein, or bond amino acids. Just like how a computer doesn’t know what it’s code says, but still, in the psuedocode:
while n>1:
    if n even:
        n = n/2
    else:
        n = 3n+1
print “Yes”

every term has a clear meaning, and their arrangement combines these meanings according to clear rules.
This may be an incredibly misguided question. I’m not a biologist.

It would not be fair to call anything to do with DNA a "code" unless you are referring to the Genetic Code. In molecular biology (which predates modern computer programming) it does NOT mean encoded information and cannot be used in this way in scientific language.

Welcome to Bio.SE, Thomas. If you haven't yet, please take the site tour and read the guide on asking a good question. Generally, this forum is dedicated to answering specific questions about biological systems or concepts. Your question strikes me as philosophical, and your edit, while clarifying your point, does not do much to rectify the fact that any and all answers would be speculative and/or opinion-based.


text:
What is mechanism of action of ellagic acid as an antimicrobial compound?
Ellagic acid (a polyphenol) works as an antimicrobial compound. But what is its mechanism of action?
I found these 2 research papers related to this, however the mechanism of action is not clearly explained in either of them. Is there a paper that effectively explains the mechanism of action?

doi:10.3389/fmicb.2019.00829(in page 2, it is mentioned that the compounds are known to involve many sites of action at the cellular level, but why does it affect the site of action?)
doi:10.1002/chem.202000354 (In page 3, It has been postulated that ellagitannins inhibit the growth of microorganisms by sequestering metal ions critical for microbial growth, but direct bacterial targets remain unidentified.
Is there a paper which explains why it inhibits growth more clearly?

What do you mean by mechanism of action? I would argue that those papers both present possible mechanisms of action related to cellular adhesion. Why does that not answer your question?

@MaximilianPress Indeed, in the first one, the entire second paragraph is entirely about this question; in the second one, it's a picture within the abstract - pretty rare to find a picture in an abstract, for sure, but certainly not hidden information. OP - can you clarify what is missing/where the gap is between these papers and what you want to know?

Thank you for editing, but I don't think you've adequately addressed the above comments and thus have voted to leave closed. For example, as noted by Bryan the abstract of the second paper you link shows a clear mechanism that you seem to be ignoring. ——— Also note that questions on this site work best if they are narrowly focused — an example would be asking why biofilm disruption is important for antimicrobial activity, or better yet how biofilms contribute to infections in Streptococcus (including a summary with references of what you've learned about the question from your research).


text:
Please help me identify this plant. Is the fruit edible?
When free, could the experts here please help me identify this plant.
Location: Puget Sound, Washington State, US
Height: 3-4 feet
Date: July
Is the orange colored fruit edible?

This is a huckleberry or related vaccinium, Vaccinium parvifolium probably.
It looks unripe to me. I'd wait till August or September.
Some are unpalatable/sour but they are nominally edible.


text:
Identifying a Texan horned butterfly
I found this butterfly on some late-season bluebonnets in Fort Worth, Texas, this evening.  You can get some sense of scale if you know how big bluebonnets are; the body is probably about the size of my thumbnail, but the 'horn' made it longer.

Great job on providing enough detail for an ID. I've edited your post a bit (including taking out the moth part since the antennae are clearly butterfly-like). One helpful tool for identifications is "Google Lens".

This appears to be an American (or common) snout (Libytheana carinenta).
The "snout" of this butterfly is very distinctive as is the squarish tip of the forewings (the part projecting furthest back to the left in your picture.
Did you see the top surfaces of the wings? They should have had a dusty orange and brown pattern with white spots.
These butterflies are found from Texas to Canada and related species are seen in the Caribbean.

Image: Judy Gallagher CC BY 2.0.

I only saw it perched, so I didn't get to see the top surface, but, as you say, the snout is hard to miss, and the wings also had that squarish tip that you mention, so this seems like it must be it.  Thank you!

You're very welcome :-)