text:
Repetition of "Clade" in a taxonomic tree
Animals and plants are somtimes classified (organized) into a taxonomic tree data structure. The term "tree data-structure" comes from the fields of computer science and software development.

On Wikipedia this taxonomy sometimes has more than one field named "Clade". How is it possible for more than one tier of the taxonmic tree of life to be named "Clade"?
Kingdom:
Clade:
Clade:
Clade:
Clade:
Order:
Family:
Genus:
Species:

Why would "Clade" be repeated more than once?
Are the instances of the text "Clade" supposed to be "phylum", "class", and "Order"?

Have you read about what a clade means?

Possible duplicate: https://biology.stackexchange.com/q/55457/27148

Minor note: the tree structure for representing knowledge does not derive from CS/software. CS/software probably adopted it from biology and related disciplines (would be interested to know where exactly). Recall that biological taxonomy in its modern sense derives from Carolus Linnaeus, who had no knowledge of CS or data structures.

Wikipedia employs multiple taxonomy databases. The page gives an idea of conflicts of consensus and for official species classification. The ball python has 10 levels of classification and the rose has 11. One is a plant, the other is a reptile. Biology didn't give them tidy class and phylum ranks.

I don’t think we need to get rid of [taxonomic ranks]
[...]
What we need to abandon is the unwarranted connotations that higher-level taxa are comparable. Because they aren’t. They are abstractions. They are information storage boxes. That’s all they are.
Ronald Jenner, a phylogeneticist

Linnaeus invented ranks (uniform levels of nesting that he applied across groups of organisms) to organize his understanding of diversity. The original ranks designated by Linnaeus were kingdom, class, order, genus and species, and others, including the phylum, have been added since. As phylogenies improve, some have called for the abandonment of ranks to avoid implying that different clades given the same rank are comparable.

There have never been clear objective criteria for designating a clade as a phylum. There is, for example, no known property that is shared by all echinoderms or all molluscs, both of which have been designated as phyla, and that would distinguish these clades from more or less inclusive clades that aren’t phyla, such as deuterostomes or bivalves. This has provoked considerable discussion about whether the categorization into phyla says more about the way humans perceive animal diversity or the biological processes that generated this diversity
 Ref.: Andreas Hejnol, Casey W. Dunn, Animal Evolution: Are Phyla Real?, Current Biology, Volume 26, Issue 10, 2016, DOI: 10.1016/j.cub.2016.03.058

UK and USA textbooks don't have the same number of kingdoms, one has 5 and the other has 6, other theories have 32.
Super and sub ranks also exist, like superfamily and subphylum.
Taxonomy is most often a spectrum of variety with unclear or overlapping divisions, like a rainbow, and words are attempts to put labels onto the divisions of the spectrum.
Different cultures and regions employ words that segment the spectrum of knowledge into different compartments, artificially. That is especially mired by the complexity of taxonomy grouping.

For taxonomic hierarchy, there’s some sense in which the phylum and the species both have rigorous currency, however the intermediary levels are a kind of construct.
Ref.: https://www.quantamagazine.org/phyla-and-other-flawed-taxonomic-categories-vex-biologists-20190624/

The idea of a clade and taxa (phylumn, class, order, etc.) are two different, but sometimes overlapping approaches to the classification of organisms. In short, a clade is any group of organisms that contain a common ancestor and all of its descendants, and is sometimes said as monophyletic. On the other hand, a taxon is a group of organisms that fits in to the taxonomical ranking system. Due to the limitation of technology and molecular evidence in the past, not all taxa reflect the evolutionary relationship.
On the wikipedia page, many clade are included as a result that an organisms can fit in groups within group. Take the clade Angiosperms and Monocot, an angiosperms is any flowering plants and this clade contain another clade within. That is, the Monocot, which are flowering plants with a single cotyledon (embryonic leaf) in the seed. Keep in mind the Angiosperms and Monocots are clade, meaning that is a natural group in the sense that it reflects the evolutionary history of the organisms within the group.
So, to answer your question, a clade does not always represent, or equal to a taxon. The purpose of including the clades is to provide finer details with regard to the evolutionary history and phylogenetic relationship to a given organism.
Suggested readings and relevant question:

What is the difference between these terms: clade, monophyletic group and taxon?
Monophyly (wikipedia)
Clade (wikipedia)

Hi MKJ, I don't understand the last phrase of the first paragraph, if clades are related, "and technology hasn't always confirmed the eveoltionary relationship of taxa" that should be the same with clades?

@bandybabboon Hi, I was refering to some taxa like the class Reptilia traditionally didn't include birds. I made an assumption that birds were excluded due to limited molecular evidences, but I might be wrong and tbh I haven't really researched about it before I answered. I'll edit it out of this answer if this is not the case. Apologize for the confusion.


text:
How Difficult is Artificial ATP Synthesis?
One way of making ATP requires:

A membrane (would probably have to be a phospholipid bilayer)
A difference in H+ chemical potential across the membrane
ATP synthase anchored to the low-potential side of the membrane
Some reasonable concentration of ADP on the low-potential side of the membrane

Now, I know ATP has a short half-life, but if we wanted to run some step of a biological process that requires ATP, would it be possible to create an artificial ATP synthesis "cell" that would convert ADP to ATP for use by enzymes in solution?
If not, then are those four steps sufficient? If so, then which step is the hard part? Thank you.

Welcome to SE Biology. As a new user we expect you to do us the courtesy of at least finish reading the [Tour]. You have not done so. Please do, and look at the Help on asking questions. Questions that relate to hypothetical situations can generally only be answered by opinions. Creating cells is usually considered in the domain of God, or perhaps evolution. What precisely do you mean by “is it possible to create an artificial ATP synthesis cell”? What exactly is the biological problem you are faced with? Questions here are expected to fulfill the latter criterion.

Hello David. When I said "cell" I wasn't referring to a biological cell but an electrochemical cell. I do not know why you would have interpreted as the former. Regarding what I meant by "is it possible to create an artificial ATP synthesis cell?” I meant precisely what I wrote. My problem is synthesizing large amounts of ATP in vitro. My question does conform the the tour guideline which you can see because it's already been given a non-opinion answer.

I’m not much the wiser. What’s an electrochemical cell? Sounds like something in the chemical domain. And why do you want to generate large amounts of ATP? The fact that someone posted an answer, means nothing, especially as the answer is in terms of a biological cell with a lipid bilayer membrane,and amounts to no more than touching on the main features of the biological system. If I wanted to generate ATP I’d use a single reaction that performed substrate-level phosphorylation, but I don’t answer questions which are unclear to me. Btw we use @johndoe type references for alerts to replies.

If your just trying to mass produce ATP there are several known production systems, why do none of those work for you?

The four steps you listed are the basic requirements for ATP synthesis, and a simplified artificial ATP synthesis system can be created using these components. However, there are some additional factors that need to be considered in order to create a functional system, such as the stability of the lipid bilayer, the efficiency of ATP synthase activity, and the availability of energy sources to generate the proton gradient.
One of the key challenges in creating an artificial ATP synthesis system is the efficient reconstitution of functional ATP synthase in the lipid bilayer. ATP synthase is a large, multi-subunit protein complex that is composed of both membrane-bound and soluble components, and it can be difficult to reconstitute the complex in an active form in vitro.
Another challenge is the generation of a stable proton gradient across the membrane, which is required for ATP synthesis. This can be achieved using different energy sources, such as light, electrochemical gradients, or chemical reactions.

there are many TP production methods that do not need ATP synthase and use enzyme cascades instead.

source: Stack Exchange

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

sort: votes


text:
Has the approach of any protein digesting enzyme has been trialled for Progressive Supranuclear Palsy against a protein accumulation in brain cells?
PSP -the degenerative disorder is attributed to accumulation of a protein in brain cells. Has any work been done to approach it by digesting this protein?

We ask that questions show evidence of prior research effort.

How would you digest such a protein without also digesting other proteins in the cell. How would you get this protease into the brain and into the cells?

I think the word "digesting" is the wrong choice. You digest a meal (non-discriminatory/encompasses almost everything in your stomach. Same with your example using proteases/other.) You want to research "tau-targeted therapy".

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


text:
Sigmoidal Curve in Geometric Growth
Here is an excerpt from my textbook:

Let us now see what happens in geometrical
growth. In most systems, the initial growth is slow
(lag phase), and it increases rapidly thereafter – at
an exponential rate (log or exponential phase). Here,
both the progeny cells following mitotic cell division
retain the ability to divide and continue to do so.
However, with limited nutrient supply, the growth
slows down leading to a stationary phase. If we plot
the parameter of growth against time, we get a typical
sigmoid or S-curve.

The exponential growth can be expressed as  $W_1 = W_oe^r{^t}$

$W_1$ = final size (weight, height, number etc.)
$W_0$  = initial size at the beginning of the period
$r$ = growth rate
$t$ = time of growth
$e$ = base of natural logarithms

The first paragraph makes perfect sense to me, but what bothers me is the formula given. When I plot the given equation $W_1 = W_oe^r{^t}$, this is what I get;

Which is clearly not sigmoidal (s-shaped) as my textbook says.
What I think should be the correct equation is:
$$W_1 = \frac{W_o}{1+e^-{^r{^t}}}$$
When I plot this equation, this is what I get:

Which is slightly better than the previous plot. Though this formula might also be erroneous as I just made it up from the general formula of a sigmoid function $S(x) = \frac {1}{1+e^-{^r{^t}}}$
Why is there a discrepancy between the in-text statement and the plot of the mentioned formula and is there any better formula to depict this growth?
Also, I have referred to various sites but could not find any satisfactory answer.
Any help is appreciated. Thanks!

If this statement is true (The exponential growth can be expressed as 1=^^), which seems to be the case, then this is a mathematics question. Probably acceptable on Mathematics.SE. I'd love to help, but I stink at math, and am exceedingly impressed that you even bothered to plot this out. I predict you have a bright future in STEM fields!

I’m voting to close this question because it's a mathematics question. (I did upvote you, though, because wow!)

It is presented confusingly, but they aren’t giving you the equation for the sigmoidal curve. They are giving you the equation for the exponential phase of the sigmoidal curve (Fig 15.6). See wikipedia for the sigmoidal (logistic) growth curve equation.

@canadianer - D'oh! I even stated that, but didn't see it.

I agree with @canadier. The formula given corresponds only to the exponential phase of the growth curve, which is also clearly indicated on the corresponding figure 15.6.

@anongoodnurse Thank you for your comment. Before even posting the question, I knew it was borderline Math-Biology, though I chose to ask here since it was from my Biology textbook  (ps: I'm aspiring to be a doctor, but I'm interested in a whole lot of other things too :)

@canadianer Yeah, that seems to be it, I think. Maybe the authors thought a sigmoidal function would be too complex for the grade level?

I discussed this question with my biology teacher and he confirmed that the equation $W_1 = W_oe^r{^t}$ just represents the exponential phase of the sigmoidal growth, but not the entire growth period. This was also helpfully pointed out in the comments.
Though I did find an article talking about the mathematical functions of sigmoidal growth which includes both the exponential and linear phases of growth.

Within the life cycle of an organ, a plant or a crop, the total growth duration can be divided into three sub‐phases: an early accelerating phase; a linear phase; and a saturation phase for ripening (Goudriaan and van Laar, 1994). Therefore, the growth pattern typically follows a sigmoid curve, and the growth rate a bell‐shaped curve. While the sigmoid pattern can be represented piecewise using an exponential, a linear and a convex equation sequentially (e.g. Lieth et al., 1996), a more elegant way is to use a curvilinear equation which gives a gradual transition from one phase to the next. For example, based on principles of light interception and leaf area expansion, Goudriaan and Monteith (1990) derived a single equation, the expolinear equation, for both the exponential and linear phases of crop growth:
$$w=\frac{c_m}{r_m} ln [1+e^{r_m(t-t_o)}] \tag{1}$$
where $w$ is mass, $t$ is time, to is the moment at which the linear phase effectively begins, $c_m$ and $r_m$ are maximum growth rate in the ‘linear phase’ and maximum relative growth rate (RGR) in the ‘exponential phase’, respectively.

YIN, XINYOU, GOUDRIAAN, JAN, LANTINGA, EGBERT A., VOS, JAN, and HUUB J. SPIERTZ. "A Flexible Sigmoid Function of Determinate Growth." Annals of Botany 91, no. 3 (2003): 361-371. Accessed February 26, 2023. https://doi.org/10.1093/aob/mcg029.

But, this equation too does not achieve the smooth sigmoid curve I wanted to see. With this equation you get a plot like the following:

The equation I suggested is almost close to an equation mentioned in the paper and is not entirely incorrect. The equation uses the logistics function and gets the smooth sigmoidal curve I was hoping to see on the plot.

Alternative, but simpler, functions that can produce two smooth transitions in a single formula are the classical growth functions. The first is the well‐known logistic function (Verhulst, 1838):
$$w = \frac {w_{max}}{1+e^{-k(t-t_m)}} \tag{3}$$
where $k$ is a constant that determines the curvature of the growth pattern, and $t_m$ is the inflection point at which the growth rate reaches its maximum value. At time $t_m$, the RGR is $\dfrac{k}{2}$. As can be seen from eqn (3), the weight at $t_m$ is half of its maximum value, $w_{max}$.

Now, when I plot equation $(3)$, I get what I was hoping for! The smooth sigmoidal growth curve:

NOTE: All the graphs in this Q&A take the growth to be on the y-axis and the time duration to be on the x-axis. The values on the graphs are completely arbitrary.
27-02-2023 EDIT: Added equation which depicts sigmoidal growth.


text:
How to figure out when my hot (but cooling) drinking water will go bad
I have a 200 liter electric water heater in a secondary building.
The time periods between me visiting the building and using the water vary and do not follow any schedule.
I can be visiting as rarely as once every 6 months or as often as once every two weeks.
The heater is turned off during periods when I am not at the building to save on electricity, but the heater is well insulated and the water stays warm in the heater for up to two weeks, while slowly cooling down.
The issue is that around 3-4 weeks the water goes bad due to being in the sweet spot for bacteria creation temperature wise (30-40 degrees celsius it seems) for a while.
Then the water starts smelling bad and obviously needs to be discarded, which is wasteful and cumbersome.
The question: I want to install a smart plug (and possibly some temperature sensors) to turn on the water heater every once in a while to keep the water from going bad. I want to hit the sweet spot where the water heater is on as little as possible to conserve the most electricity and still keep the water from going bad.
Obviously there is no one perfect answer for this (e.g. "dont allow the water to go below 40 degrees for more than 8 hours and the water will be safe for consumption forever"), as the water contents will be different based on location, filtering setup, etc, but are there any general guidelines on how to approach this? or a way to figure out what the perfect balance would be for my specific setup without resolving to trial-by-error?
I've googled around using "how long does it take for warm water to go bad" query, but this returns results only on how long you need to wait until the water heater reheats cold water, not how long it takes for warm water to go bad.
Reason for me not wanting to go with "just replace with a flow-through kind of water heater instead of tank kind" is this water heater is hooked up to the fireplace of the building (i.e. fireplace warms up pipes with heating water in them that are circulated by a pump through the tank without mixing with the drinking water), and if I am already in the building, I will be running the fireplace and the water in the heaters tank will be heated for me, without needing to use the electrical function of the water heater.

I’m voting to close this question because it's not really an answerable Biology question (even though it's about bacteria). As you stated, it somewhat depends on factors we cannot guess at. There are answers, but they don't work for you, so it's more about water temperature regulation, efficiency and personal economical considerations.

I'd say it's a practical application of theoretical concepts and knowledge of bioligy, but fair enough, I understand why you would think this way. Could you suggest a better stack exchange site to ask this question on rather than bioligy?

DIY maybe? Home improvement? I don't know. Potential biological solutions include keeping the water heater on at 140° all the time/heat the water to 160° for several hours when you return after an absence (hard on the heater, shortens lifespan)/shock chlorinate the tank, hot water pipes (you have to drain off all the sediments first, as it can harbor and protect bacteria insuring you always have a ready supply of contaminants)/get a hot water on demand system/etc. etc. But you will reject them, so it's not really biological at all. Your requirements make it otherwise.


text:
What is the difference between a semi-permeable membrane and a selectively permeable membrane?
What is the difference between a semi-permeable membrane and a selectively permeable membrane in cell biology? Is a selectively permeable membrane a type of semi-permeable membrane? Please help.
I think the semi-permeable membrane allows passage to only solvent molecules while a selectively permeable membrane permits the movement of solvent molecules along with some selected solutes. Am I correct in my understanding?

Welcome. I can understand your confusion, but there is a lot online about this. Using your exact phrasing, the top Google hits explained the difference. What do you understand about each type of membrane? (Asking to understand exactly the point where your confusion starts.) What were your search terms? If English is your first language, how do you understand semi and selective in general? Please click the edit button to include details and a quote from one of your sources. Thanks!

Not quite. Semi-permeable membranes permit diffusion of anything limited only by size. Anything bigger than the pore size can't pass (there are different pore sizes in different membranes.) Selectively permeable membranes allow certain select molecules/substances to pass and nothing else, independent of size. They are made to allow a particular substance to diffuse through. Does this answer your question?

Yes, thank you very much.


text:
Random X-Inactivation and Duchenne
I'm reading about X-inactivation and I can't reconcile some things with it being truly random. In only a small percentage of female carriers Duchenne's will be expressed. But if this was truly random, wouldn't 50% of female carriers expressing the disease?
As one of the X-chromosomes is silenced at random, this seems sort of contradictory. Then, in females that do express the disease phenotype it's because of non-random X-inactivation. For me, this sounds like it's the other way around, so clearly I'm not up to speed and am in need of a bit of clarification on the subject.

Duchenne muscular dystrophy (DMD) is caused by the body's inability to make the protein dystrophin, which is needed for proper muscle function (1, 2). In an individual carrier, half of the cells that would normally make dystrophin cannot, but the other half still can. This leads to two explanations (AFAIK) for why carriers do not express DMD:

The cells that can make dystrophin make twice as much, so the total amount produced is the same as a normal individual.
Only half as much dystrophin is produced, but that is enough to prevent symptoms from manifesting.

This is actually the stock explanation for why female carriers exist for X-linked recessive diseases. You can substitute 'DND' and 'dystrophin' with another X-linked recessive disease and the associated protien (e.g. 'hemophilia' and 'factor 8 or 9') and it would still be mostly true.
I say mostly true because DMD is actually an unusual. Its carriers do sometimes exhibit symptoms (3, 4). Different studies give different rates for how often this happens, but the NIH says it is about 20%.
EDIT: I am still a little unclear on what your asking, but I think you are confused about why any carriers for Duchenne express the disease. The answer to that is a phenomena called skewed X-inactivation, which is when either the paternal or maternal X chromosome is inactivated and turned into a Barr body more often than the other. This can happen for 2 reasons:

Primary: When Barr bodies are forming, the paternal or maternal chromosome is selected more than 50% of the time.
Secondary: After Barr bodies form, cells with the paternal chromosome active reproduce less than cells with the maternal chromosome active, or vice versa.

Both types of skewing can be happen for genetic causes (e.g. the Xce locus in mice can cause primary inactivation) or stochastic causes (i.e. by pure chance some people will have unlikely things happen to them).
I spent the last few hours reading up on which type happens specifically during Duchenne and I am still not 100% sure. What I am confident about is that carriers for Duchenne can have a translocation, which causes the skewed X-inactivation and therefor symptoms in carriers:

A few cases of translocations involving DMD have been reported22; these translocations will cause DMD in both males and females, the latter owing to non-random X-inactivation of the unaffected X chromosome. In these cases, cells with inactivation of the mutated X chromosome (cells that could, in theory, produce dystrophin) are not viable owing to the inactivation effect of the chromosomal translocation on the autosome. Only the cells where the unaffected X chromosome is inactivated will be viable. However, these will not produce dystrophin owing to the chromosomal translocation affecting DMD. Therefore, females with these translocations are unable to produce any dystrophin.

What I cannot figure out is if the translocation happens on the chromosome with the functioning DMD gene or the chromosome with the defective DMD gene.

Thank you for your answer, my question was more about the seemingly confusion naming of (non) random X inactivation

Would it be helpful if I rephrase to include the relation between X inactivation and dominanc?

Thank you for your elaboration, my question is about naming, I think. I understand the process of (skewed) x-inactivation, in principle, but the thing that's not clear is why it's called random inactivation if only a few % of carriers express the disease phenotype. If it would be truly random, 50% of carriers would express the phenotype, as one chromosome at random gets silenced. This probably has to do with dominance, but I find it a bit counterintuitive and would like to know a bit more about this.

Having read your comment again, I think it brings me closer to an understanding. I'm gonna do some more reading on non-random X inactivation. Thank you!

Random/ stochastic just means that the event is non-deterministic. As long as we are talking about probabilities we are describing a random process. The uniform distribution, where every outcome is equally likely, is not more random. The lottery is random and there are only two outcomes (you win or you lose), but that does not mean you have a 50-50 chance of winning. No matter what the probability of a carrier for Duchenne has for will presenting the disease, that fact we are describing the process with probability means that we are describing a random process.

Thanks for your elaboration!


text:
Why is SF3B3 gene annotation missing in chm13_v2 gff3 file, and is it temporary?
In the annotation gff3 provided for CHM13 v2, I noticed that for the SF3B3 gene there's no entry with type "gene" (third column).
However, transcripts and other annotations are still available. I checked on UCSC genome browser and transcripts still appear annotated:

I was not able to find if this is associated with other aliases. I am trying to understand:

why the "gene" annotation is missing in the gff3
if this is temporary, i.e., the "gene" annotation will be updated later

Note that all of your transcripts for SF3B3 have a source_gene=ENSG00000189091.13 tag in the GFF3 file. A gene with that annotation does exist in the gff3 (see the grepped output below), though for some reason it has the identifier MSTRG.2232. That gene almost but not quite overlaps with the transcript SF3B3-201 and perfectly overlaps with the transcript CHM13_T0084548 represented in your browser shot.
# gene annotation
chr16   CAT     gene    76334966        76388859        .       +       .       source_gene_common_name=MSTRG.2232;source_gene=ENSG00000189091.13;gene_biotype=protein_coding;gene_id=CHM13_G0022147;gene_name=MSTRG.2232;transcript_modes=transMap,exRef;ID=CHM13_G0022147;Name=MSTRG.2232;source_transcript=N/A;alternative_source_transcripts=N/A;collapsed_gene_ids=N/A;collapsed_gene_names=N/A;paralogy=N/A;unfiltered_paralogy=N/A;alignment_id=N/A;frameshift=N/A;exon_anotation_support=N/A;intron_annotation_support=N/A;transcript_class=N/A;valid_start=N/A;valid_stop=N/A;proper_orf=N/A;extra_paralog=False
# transcript annotation
chr16   CAT transcript  76334997    76388857    10000   +   .   source_transcript=ENST00000302516.10;source_transcript_name=SF3B3-201;source_gene=ENSG00000189091.13;transcript_modes=transMap;gene_biotype=protein_coding;transcript_biotype=protein_coding;alignment_id=ENST00000302516.10-0;frameshift=nan;exon_annotation_support=1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1;intron_annotation_support=1,1,1,1,1,1,2,2,2,2,1,2,2,2,1,2,2,2,2,2,1,1,1,2,2;transcript_class=ortholog;valid_start=True;valid_stop=True;adj_start=76337842;adj_stop=76383007;proper_orf=True;level=2;protein_id=ENSP00000305790.5;transcript_support_level=1;hgnc_id=HGNC:10770;tag=basic,MANE_Select,appris_principal_1,CCDS;ccdsid=CCDS10894.1;havana_gene=OTTHUMG00000137582.8;havana_transcript=OTTHUMT00000268972.3;paralogy=nan;unfiltered_paralogy=nan;source_gene_common_name=SF3B3;transcript_id=CHM13_T0084551;gene_id=CHM13_G0022147;Parent=CHM13_G0022147;transcript_name=SF3B3-201;ID=CHM13_T0084551;Name=SF3B3;gene_name=SF3B3;alternative_source_transcripts=N/A;collapsed_gene_ids=N/A;collapsed_gene_names=N/A;extra_paralog=False
# transcript annotation
chr16   CAT     transcript      76334966        76388858        .       +       .       source_gene=ENSG00000189091.13;transcript_class=putative_novel_isoform;novel_5p_cap=True;novel_poly_a=True;transcript_biotype=protein_coding;gene_biotype=protein_coding;intron_rna_support=1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1;exon_rna_support=0,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,0;transcript_modes=exRef;exon_annotation_support=0,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,1,0,0;intron_annotation_support=1,1,1,1,1,1,2,2,2,2,1,2,2,2,1,2,2,2,2,2,1,1,1,2,2,0;alignment_id=exRef-MSTRG.2232.2;source_gene_common_name=MSTRG.2232;transcript_id=CHM13_T0084548;gene_id=CHM13_G0022147;Parent=CHM13_G0022147;transcript_name=CHM13_T0084548;ID=CHM13_T0084548;Name=MSTRG.2232;gene_name=MSTRG.2232;source_transcript=N/A;alternative_source_transcripts=N/A;collapsed_gene_ids=N/A;collapsed_gene_names=N/A;paralogy=N/A;unfiltered_paralogy=N/A;frameshift=N/A;valid_start=N/A;valid_stop=N/A;proper_orf=N/A;extra_paralog=False

I'm not sure why those genes aren't tagged with the common name, and I'm not sure why it's not in your browser shot (whereas the alternate systematic gene NM_012426 is represented there; a quick grep suggests the NM_012426 IDs are not in the GFF3, and are interpolated by UCSC). But in general it's a good idea to always use the systematic identifier, because the common gene symbol/name won't always be trustworthy. If you use the systematic identifier, you should find the right gene.
Most likely explanation is a clash of competing methods, and a failure of the annotation method to hook the actual gene to the common name that you are looking for. It looks like some of the transcripts are longer than the gene, so maybe that's the reason. Possibly those transcripts derive from RNA-seq, and the gene annotator didn't find a good overlapping gene so it didn't get all the way linked. But I'm not enough of an annotation method expert to say for sure.
It looks like the annotation was done using CAT, so you could look there for more info. You could contact the author or post on the github if you want to learn more.

Thank you! Yes, the issue was reported on github. Your explanation is reasonable, should the Ensembl gene ID solve the issue, too?
I tried to lift the coordinates from hg38 to chm13. After that I noticed that the sequence for SF3B3 (ENSG00000189091.13) is ~93% identical (through blast) between hg38 and chm13, so I believe that 7% difference might also have affected the annotation?

@gc5 Yeah, I would guess that something went weird with liftOff based on the difference, I would be curious to know if that 7% difference is due to real difference or different slices of highly similar sequence. But regardless I think the Ensembl gene ID should fix it.


text:
What bug could this be?
I found a bunch of bugs, approximately 2-3mm in my kitchen, most of them dead and with a throughout search i found a bunch of them living in my gluten-free flour and on some other products like fried batter peels (idk if this is correct, excuse my english) I live in Germany and found them during winter time.
I dont know what those are and google doesnt really help me.
Does anyone know?

Please include better pictures. Also pictures of the "top" side of the insect would be beneficial. thanks.

It's difficult to be certain, but this could be a drugstore beetle, Stegobium paniceum. They commonly infest kitchens where they feed on dry plant matter. In addition to eating various grains and spices, they are capable of feeding on material from plants like tobacco that are toxic to most other insects.


text:
Why does an Enzyme-Substrate Complex have slightly less energy than the substrate alone?
In some books the graph of the change in free energy during an enzyme-catalysed reaction is depicted as shown below, where S = substrate, E = enzyme, P = product, and T* represents the transition state.

In this depiction the free energy of the enzyme–substrate complex (ES) is shown as having a slightly lower free energy than the substrate (S).
What is the explanation of this?

Welcome to SE Biology. I have tidied your question up a bit, decreasing the graphic to a more reasonable size, improving the presentation, indicating that the type of graph is only found in some depictions (where did you find it? You should say) and defining the terms. Is this question an assignment of some sort? If so you should state this and present your attempt to find the answer yourself. See our Homework policy.

The diagram presented in the question is only one of many variations found in text books and the like. It is unsatisfactory to the extent that it shows one of the intermediates (ES) in the catalysis, but not the other (EP), and that it does not label the species present at each stage. Such energy diagrams are considered in a paper by Aledo et al. in Biochemical and Molecular Biology Education, from which I reproduce their favoured example, below.

Explanation: A simple first order reaction in which a single substrate (S) is converted to a product (P) is shown with intermediates, ES and EP. The transition states between the various conversions in the sub-reactions are shown in red, and that for the uncatalysed reaction (E + S≠) in dark blue. (I am not sure why the E is included in this, except to allow use of a unified diagram.) ΔG is the overall free energy change of the reaction and ΔGUC≠ and ΔGC≠ are the free energy changes to reach the transition state in the uncatalysed and enzyme-catalysed reactions, respectively.
This diagram reflects the key point made by the authors of the paper:

“For an enzyme-catalyzed reaction, it should be stressed that, under conditions where the overall reaction is spontaneous, each elementary step must exhibit a negative free energy change, and this must be properly reflected in the progression profile of the reaction.”

So, to answer the poster’s specific question, for the reaction to proceed not only must the overall free energy change from E+S → E+P be negative, but that of the intermediate stage, E+S → ES must also be negative, i.e. the free energy of ES is lower than that of S — or E+S, to be precise.
(And the free energy of E+P must be less than that of EP, the violation of which principle is apparently a common failing of many diagrams.)


text:
Identification of cells containing the gene of interest at a double strand break instead of undergoing recombination
If I tried to knock in a gene for example KANMX and want to swap it with say some gene "x", but, since, there can be double strand break in the DNA and KANMX may get inserted within the ds break instead of undergoing homologous recombination with gene x, in that case how can we identify the colonies which can be a mixture of the following :-
A.) Undergoing proper recombination and now having KANMX but not gene x
B.) Having both gene X and KANMX (how can we specifically identify these?)
C.) Undergoing no homologous recombination (one way is using G418 sulphate).
This question was asked in my class, one possible reasoning given was that we can make forward primers upstream of gene x, which won't work for KANMX and only reverse primer will work.
But I was thinking how we will screen so many colonies and can we use probes instead of primers or even a simple thing as gel electrophoresis to see size differences?
I will be very thankful if anyone can clear up this doubt!
I was troubleshooting the question with designing probes upstream of gene x and also only specifically for kanmx to differentiate the two or even observing size differences through AGE.


text:
Do lobsters form social hierarchies and is the status in hierarchy reflected by serotonin levels?
In his book 12 rules for life Jordan Peterson claims that:

Consider serotonin, the chemical that governs posture and escape in the lobster. Low-
ranking lobsters produce comparatively low levels of serotonin. This is also true of low-
ranking human beings (and those low levels decrease more with each defeat). Low
serotonin means decreased confidence. Low serotonin means more response to stress and
costlier physical preparedness for emergency—as anything whatsoever may happen, at
any time, at the bottom of the dominance hierarchy (and rarely something good). Low
serotonin means less happiness, more pain and anxiety, more illness, and a shorter
lifespan—among humans, just as among crustaceans. Higher spots in the dominance
hierarchy, and the higher serotonin levels typical of those who inhabit them, are
characterized by less illness, misery and death, even when factors such as absolute income
—or number of decaying food scraps—are held constant. The importance of this can
hardly be overstated.

at another passage he claims that:

A lobster with high levels of serotonin and low levels of octopamine is a cocky,
strutting sort of shellfish, much less likely to back down when challenged. This is because
serotonin helps regulate postural flexion. A flexed lobster extends its appendages so that
it can look tall and dangerous, like Clint Eastwood in a spaghetti Western. When a
lobster that has just lost a battle is exposed to serotonin, it will stretch itself out, advance
even on former victors, and fight longer and harder.

For the second passage he cites the following paper
While there are many papers linking position in the social hierarchy in primates and humans I could not find a paper supporting the first passage.
The best I could find to support the first passage is an interview with Bret Weinstein where they mention that Peterson is indeed correct claiming that social hierarchy of lobsters in linked to serotonin levels. Interview with Bret Weinstein
A review paper claims that:

Is the marine environment less conducive to the establishment of dominance hierarchy structures, or does this just underline the lack of detailed behavioral information about most marine invertebrates?

Which suggests that not much is known about the relationship between serotonin levels in lobsters and the position in the social hierarchy.
Peterson basically argues that since the injection of serotonin leads to aggressive behavior in invertebrates, which is dominant trait in the animal kingdom this is proof that serotonin is indicated by the status in the social hierarchy. However It could just as well be that serotonin just leads to aggressive behavior in lobsters without being an indicator of the position in the hierarchy.
Are there any studies which specifically investigate whether the position of lobsters in a hierarchy is reflected in their serotonin levels?

https://pubmed.ncbi.nlm.nih.gov/33772639/

Comments have been moved to chat; please do not continue the discussion here. Before posting a comment below this one, please review the purposes of comments. Comments that do not request clarification or suggest improvements usually belong as an answer, on [meta], or in [chat]. Comments continuing discussion may be removed.

The paper Peterson cites about serotonin and lobsters explicitly contradicts him in two major ways. First, although serotonin plays a role in aggression across many species, its role is not the same across those species:

The nature of the linkage [between serotonin and aggression], however, is not simple, and it has proven difficult to unravel the role of the amine in the behavior. In vertebrates, lowered levels of 5HT (endogenous or experimentally induced) or changes in amine neuron function that lower the effectiveness of serotonergic neurons generally correlate with increased levels of aggression (19, 20) whereas in invertebrates, the converse is believed to be true (11–13). Genetic alterations of amine neuron function also can change aggressive behavior in animals (21–24) and in people (25–27) although, again, in most cases, it is not clear how the genetic change is linked to the behavior. ... Finally, direct injections of amines like 5HT into animals also cause changes in aggression, but even here the relationships are complex. For example, in ants, injections of 5HT and its precursors lower interspecific aggressiveness toward intruders but raises intraspecies aggression (28, 29).

Clearly, the role of serotonin plays in aggressive behavior is not conserved between lobsters and humans. The most we could say is that serotonin plays some role in regulating aggression, but that role changes between species.
Secondly, the same study observed that although lobsters injected with serotonin will fight for longer, but are not more to start a fight or to win:

Thus 5HT selectively decreased the likelihood that subordinates withdraw from the attacks of their dominant opponents without altering their locomotor activity, the rules of escalation of fights, or the eventual outcome of an encounter.

Peterson is directly contradicting the conclusions of the paper he is citing:

A lobster with high levels of serotonin and low levels of octopamine is a cocky, strutting sort of shellfish, much less likely to back down when challenged.

Either he is a liar or does not understand the paper he is citing, and I can't decide which is worse.
P.S. Here is a video thoroughly dismantling Peterson's entire philosophy. The part about him being incorrect about lobsters at 40:00.

You did not answer the question if there are studies linking the position in the social hierarchy to serotonin levels.

Comments have been moved to chat; please do not continue the discussion here. Before posting a comment below this one, please review the purposes of comments. Comments that do not request clarification or suggest improvements usually belong as an answer, on [meta], or in [chat]. Comments continuing discussion may be removed.


text:
CSF types in humans
There are several blood types such as A, B and O. Crossing these blood types such as in a transfusion, the results can be fatal. Along these lines, issues can arise when an organ or bone marrow are placed in a new host, issues can arise if certain markers aren't met.
With these examples in mind, are there multiples types of CerebroSpinal Fluid (CSF)?
In attempting to research this subject, I did not find anything answering this question, included is an article discussing CSF, but not mentioning different types of CSF. Science Direct Article on CSF

https://biology.stackexchange.com/q/94/5198

@David: Thanks for the edit.


text:
Why is my spirulina biomass getting destroyed in my new photobioreactor?
I have a 500L flat plate photobioreactor in my backyard. Whenever I add my culture to the PBR, after 3-4 days of growth, the culture becomes transparent and my biomass is wasted.
I add the stock at a 1:10 ratio (50 litres). My culture medium is Baum. The temperature varies between 12 to 25 degrees Celsius in 24 hours, and the pH is between 9 to 10. Circulation is done by an air pump and a water pump (for circulation of the biomass across the system, from one flat plate to the next).
Maybe it is caused by shock or the sheer stress of the water pump? Or something (like brass valves) releasing some toxic substance into the culture? What should I do?

Are you only growing spirulina? sounds like an infection of some kind to me.

Things to try - can you grow the spirulina elsewhere (i.e. not in your reactor, but in a jar or something similar)? This tests whether it is something to do with the reactor. Can you sub-sample from the reactor on days 1 -4 and get growth from those samples outside the reactor (also check pH etc at same time)? This tests whether there is a problem like infection in the reactor. Is your ratio too high - given log growth a 1:10 will consume all the nutrients pretty quickly - do you need more light. Does the temp rise too high inside the reactor (not air temp)? How about O2 concentration?

please add a bit more details about your setup,do you aerate the water,how do you fertilize your algae,where do you get water from for your setup?

please enlighten me what is baum?

@MaximilianPress It seems under a microscope. Only spirulina, but their springs were straightened by self-shading. We also changed the stock and water several times.

@bob1 Thank you. I'll work on it. The ratio for the first time was 1:20. The light is perfect (flat plate in the backyard). The mentioned temperature was the temperature inside the biomass. Aeration is done by an air pump and circulation is done by a water pump.

@trondhansen Same as before. We grew spirulina under the same conditions (water from water refinery kiosks (they are common in my city, as our drinking water is full of arsenic). We add all the materials (Baum) needed by the biomass at the beginning and aerate the system every 20 minutes with an air pump.

@trondhansen Baum culture described in Heinsoo, D. (2014). Cultivation of Spirulina on Conventional and Urine Based Medium in a Household Scale System. I do not recommend it.

Cyanophage? https://link.springer.com/article/10.1007/s10811-012-9853-x

@acvill Thanks, but I don't think so, since the sample is growing in the lab.


text:
Do we need to underline the name of a gene while handwriting?
While teaching about the cry genes and the Cry proteins in Biology class, my teacher told us that the names of genes are always written in lowercase and should be italicized, and the name of protein coded by that gene should always start with a capital letter.
Now, while reading the notes taken in the same lectures, I am wondering whether the name of the genes should be underlined while handwriting, as we use to do while writing the biological names; or are there some other rules related to it?
Moreover please tell me that is it really necessary to write the name of a protein (I am talking about every protein) always with a capital letter at start?

Do you get graded on your notes? They're your notes; if you'll remember the difference between the gene and the protein, write them however you want. I had an extensive shorthand system (10 years of notetaking will do that); no one ever corrected me about my unique symbols.

@anongoodnurse Actually they are my own notes which I took during the lecture!

@anongoodnurse There are no grades for those notes, but I asked the question for myself knowing the right way!

They're your notes. There is no right way or wrong way to take notes. The purpose of notes is to help you remember what was said. Formal writing is different.

@anongoodnurse Actually, my question is about the formal writing only! Are there any rules for the aforementioned?

Handwriting and notes
How you handwrite is totally up to you. No important information in research science is disseminated widely with the use of handwriting anymore; whatever the conventions were, you'd be wise not to care about it one bit.
Nomenclature in scientific research
The nomenclature can be different across fields. In Drosophila genetics, the prescribed norm, which is admittedly not really often followed, is as follows for capitalizing the first letters (contrary to what you were taught):

1.2.2. Selection of lower or upper case of initial letter. Gene symbols/names begin with a lowercase letter if the gene is FIRST named for the phenotype of a recessive mutant allele, and begin with an uppercase letter if they are FIRST named for the phenotype of a dominant mutant allele. Gene symbols/names also begin with an uppercase letter if they are FIRST named for an aspect of the wild-type molecular function or activity of the gene product, which includes genes named after an ortholog or paralog.

Rules of thumb

Keep in mind the distinction between nucleic acid and protein; this usually differentiated by formatting (e.g. italics).
Keep in mind that macromolecule formatting nomenclature often specifies capitalization (entirely capitalized, first character, if non-first characters are allowed to be capitalized, etc.)
Keep in mind the difference between symbol (ID or shorthands) and full gene names.
Keep in mind that synonymous gene names and symbols exist for many genes.

The search engine is your friend. This is a good landing page on the topic.


text:
Do lions crabwalk?
Cats turn sideways arch their back and puff their fur, to apppear bigger, when trying to intimidate someone. Do lions do that? What is the largest feline that does that?

As apex predators who can also run away if necessary, it would seem to be an unnecessary tactic.

with a mane turning sideways might actually make you look smaller.


text:
What is the origin of mammals X/Y sex determination system and what/when was the last common ancestor to possess these chromosomes?
I know many animals use an X/Y sex determination system, but not all of these animals use the same X/Y genes.  That is to say the X/Y sex determination system has convergently evolved in many species, and they often use different chromosomes as their X and Y than humans do.
I'm interested specifically in the variant of the X/Y genes that humans and most mammals use and their origin.  (side note, is there a better term for referring specifically to therian x/y genes vs the X/Y genes of say snakes or insects?)
I'm frankly curious what we know about how the sex chromosomes we use now evolved and when it happened.  For example do we know of any non-therian mammals that have autosomal chromosomes that look similar to our sex chromosomes that presumably suggest where our sex chromosomes split off from?
I'm aware that monotremes have their own odd variant of X/Y sex determination system, but it looks like neither the platypus, nor the Echidna X/Y chromosomes are similar to our own.  So clearly our sex determination system came after we split from monotremes, but are there any therian mammals that don't share a last common ancestor with us that used our X/Y genes for sex determination?
Not sure if this is asking for more then we can know, but if the monotremes' similarity to Z/W chromosomes in birds suggests pre-mammal ancestors used z/w sex determination system then how come we now have only one non-autosomal chromosome now?  How would a theoretical pre-mammal z/w sex chromosomes have become autosomal?

As I am sure you know by now, the Stack Exchange format works best with one question per question. I count 3 related questions in yours. You could split them up into 3 questions or re-word to make what you actually want to know clearer.

try googling "vertebrate sex chromosome evolution": https://www.nature.com/articles/nrg.2015.2


text:
Different enzymes catalyzing the same reaction but in opposite directions

Nelson, D. L., & Cox, M. M. (2017). Principles of Biochemistry 7e. W. H. Freeman. 13.3: Phosphoryl Group Transfers and ATP: Inorganic Polyphosphate Is a Potential Phosphoryl Group Donor.
(This part has been removed from the eighth edition of the book.)
PPK-1 and PPK-2 are essentially catalyzing the same reaction, however, PPK-1 is used when polyphosphate synthesis is thermodynamically favorable and PPK-2 is used when the reverse reaction(ATP synthesis) is favorable. What is the need for having 2 different enzymes if 1 enzyme is enough to catalyze the forward and reverse reaction?

Welcome to SE Biology. Please indicate the source of the graphic, with date.

Oops, I forgot that! thanks for reminding me. Nelson, D. L., & Cox, M. M. (2017). Principles of Biochemistry 7e. W. H. Freeman. 13.3: Phosphoryl Group Transfers and ATP: Inorganic Polyphosphate Is a Potential Phosphoryl Group Donor.
(This part has been removed from the eighth edition of the book.)

Thanks. I’ll have a look at this. You have written polypeptide synthesis, but I presume you mean polyphosphate.

Thank you. Yes, I meant polyphosphate.

I don't see the mystery. Having 2 enzymes doing opposite things allows for better activity or specificity (each can be much better suited than a "general" catalyst) and regulation, over multiple levels (e.g. localization, transcription, post-translational modification, inhibition, degradation, etc.). Don't you think a single enzyme catalyzing forward and reverse reactions would be rather difficult to regulate, or be very functionally limited? For purposes of ATP production, I think an enzyme strictly producing ATP would have viability over another enzyme simultaneously producing/degrading ATP.

Well, what you said about the different regulations of the two enzymes makes sense. I'm looking for a more specific answer, however. Also, I have a comment on your last sentence. In reversible reactions, all the enzymes catalyze the forward and reverse reactions simultaneously and equally. And in this case, since these two reactions are reverse of each other, any enzyme catalyzing either of these two reactions would catalyze the other too. The existence of an enzyme that strictly produces ATP contradicts what I have in mind about enzyme function. Am I right?

This is a complex area that I was completely unaware of and know nothing about. The first question that I ask is how you reverse a reaction with a ΔG˚ of -20kJ per/mol? Two possibilities occur to me — either a high ratio of polyphosphate to ATP or that there has been some mistake and the two reactions are not the reverse of each other. The few papers I looked at on PPK2 did not address the thermodynamics. Without further information I cannot be of any help.

The textbook is either incorrect or very poorly worded. You are correct that all enzymes catalyze both both the forward and reverse reactions. The enzyme could only lower the activation energy of this given reaction, affecting both the forward and reverse reaction rates. To drive them in the forward direction, enzymes must couple endergonic reactions (i.e. $\Delta G > 0$) with exergonic reactions (i.e. $\Delta G < 0$).

Please add sources to support your answer


text:
Is there a dataset for the optimum conditions (Temperature, humidity, light intensity, etc.) for plants growth?
I'm a student working on an automated greenhouse. I wanted to add a database for the most commonly grown plants and the optimum conditions needed (I'm mainly looking for temperature, humidity, and light intensity) for the plants' growth. I have already found a dataset on Kaggle, but I was wondering if there are any datasets that include light intensity. Any recommendations are appreciated.

All the info is out there, but you need to search for the specific plants you're growing as their optimal growing conditions may vary widely. "Commonly grown plants" is a pretty broad category, not one-(x)-fits-all and varies widely by culture and purpose.

@Belal Bahaa Did you have any luck finding what you were looking for?

The best one I found was the one in Kaggle. Thankfully, I'm done with that project!


text:
Bimodal melting point of animal fats?
This could fit into Chemistry, Seasoned Advice or other SE forums. The largest number of "close" questions seems to be here; apologies if I'm in the wrong place.
I've noticed when cooking some meats - most notably real mutton, from older sheep - that quite a bit of fat renders out long before the meat is cooked, while some remains even after high-temperature grilling or sautéeing. When working with ground meat (patties/burgers, sausages, patés), the effect seems more dramatic, with a distinct separation in fat release between two rendering-temperature ranges.
Assuming that the phenomenon is real, and not an experimental or observational artifact, can someone here explain the cause? Some possibilities:

Distinct populations of fat types, whether by glyceride number, aliphatic chain length, cis/trans isomers, mixed within each fat-body?

Anatomically distinct (perhaps microscopic) fat bodies with different functions, hence compositions?

Other anatomic factors, like encapsulation of fats with varying degrees of containment by membranes or other structures?

As a cook, one often wishes to maintain high fat content. Expensive Wagyu ("Kobe") beef must be cooked very lightly to retain all the marbling. And there are many distinct ways to cook hamburgers to retain fat while adequately cooking the meat for safety and organoleptic properties. So insight into this kind of melting/rendering behaviour might be useful in recipe design and execution, in the same way that making puff pastry requires careful temperature control when mixing fat into détrempe and beurrage, as well as paste temperature during folding/rolling.
Thanks for any thoughts.

Not going to answer formally because I don't have the ambition to research this. My guess is that it's a combination of factors, including anatomic factors (encapsulation of fats with varying degrees of containment by connective tissue) and physiologic, i.e. we make a number of fats, some that melt at lower temperatures and higher temperatures and everything in between, and maybe you're noticing two of the more common triglycerides melting. I used to make soap (a lot for a long time) and rendered fat from everything from deer/goats to bears ( lots of hunters around here)...

...and there was definitely a range of fats in any one animal fat, and definitely some encapsulation such that pulverizing was necessary to get it. Interestingly (or maybe not), the same is true of plant fat production: it's not just one kind of fat. Sometimes there is a very wide mixture that includes fats that are liquids at room temperature right to fats that you need a chisel and hammer to break up at room temperature (these would be long, very highly saturated fats. Pure coconut oil can be fractionated into several groups with different melting points, one a liquid, another a goop, etc.)

One last comment. Adult sheep have seen more extremes in temperatures than lambs. Animals produce different fats in cold temperatures than in warm. Maybe you're seeing this phenomenon as well. If there were an Organic Chemistry site, this would be a good fit there, I think.


text:
Are giraffes living on Calauit island an example of Island dwarfism?
When I traveled to Calauit island I was stricken by the small size of giraffes living there. The giraffes are the descendants of Africa animals imported in the 1970s.

Like Noah and the biblical ark, a boatload of animals was shipped from
Africa to remote Calauit Island in the Philippines in the 1970s
The descendants of these animals—20 giraffes, along with dozens of
zebra and antelope—are now among the most intriguing legacies of the
late dictator Ferdinand Marcos.

The following picture will give you an idea of how small they are (my wife's height is 160cm). I asked the local guides why they were so small (around 3 meters height, some even less than 3 meters), they told me because they are island born and they have become smaller compared to their ancestors.

To me this seems to be a perfect example of Island dwarfism. But when I google it I can't find any result of this. The only result I got was the dwarf giraffes found in Uganda. The science.org even used the title "World's first dwarf giraffes spotted in Uganda and Namibia", also check NYTimes article "Dwarf Giraffes Discovery Surprises Scientists" for detailed information of that finding.
So are Calauit giraffes an good example of Island dwarfism? If not, what is the explanation of their small sizes, e.g. does the NYTimes article's words "The condition, also known as skeletal dysplasia, affects bone growth, often resulting in short stature." apply here ?
PS. the original article NYTimes refers to was published at springer nature under a Creative Commons Attribution 4.0 International License, so you should be able to read it free.

Update
Updates to question and comments clarify:

3m high giraffes (small)
locals say giraffes are smaller because they are "island born".

The first data point indicates that the giraffes are in fact smaller than usual (usually >4m).
Being "island born" would be considered as an environmental perturbation. This would indicate malnutrition or something similar, covered under my 4th hypothesis below. Granted, it is not clear to me what exactly the local folks meant.
Original answer
Island dwarfism is a natural macroevolutionary process that is presumed to take a very long time due to long-term ecological pressures. The example you provide appears to be one in which humans took some giraffes to the island 50 years ago, or ~5-10 generations of giraffes (estimates differed in their generation time).
The body size evolution of distinct island varieties is measured in the millions of years. Based on Table 1 from the linked paper, I think that I interpret that the expected rate is something like a 10% size change per million years.
In other words, if those giraffes were island dwarfs, that would be an astonishingly fast natural adaptation. I can think of several possible explanations other than island dwarfism as we generally think of it:

The giraffes you observed were normal sized. Average height for a female giraffe is ~4-5m, or ~3m at the shoulder. Their shoulder height at least does seem a bit short in the picture, but it might be a weird perspective thing.
The giraffes you encountered were small, but that's because they were immature and had not reached full stature. (No dwarfism.)
The giraffes you encountered were derived from a variety with relatively small stature. (There is some variation, especially the females are not so tall, at 14 feet maximum height). Supposedly the animals were from Kenya which I believe are one of the bigger varieties, but who knows.
The giraffes you encountered were dwarfed by poor nutrition due to a suboptimal habitat (developmental loss of stature, not evolutionary).
There is genetically determined dwarfism / short stature, but it's due to genetic drift (the original giraffes had substantial dwarfism, as has been observed in natural populations, as you note).

I would probably want to exclude all of those hypotheses (and perhaps more) before I would say anything about island dwarfism. Evolution usually happens really slowly, unless it's acting on existing variation!
For a general description of the evolution of island dwarfism/giantism, see here.

When I first saw those giraffes I didn't know the term "Island dwarfism".  I asked the local guides why they were so small (around 3 meters, some even less than 3 meters), they told me because they are island born and they have become smaller compared to their ancestors.

Hi is your 4th reason, poor nutrition basically the same as the NYTimes article (I attached) words "The condition, also known as skeletal dysplasia, affects bone growth, often resulting in short stature" ?

@Qiulang Thank you for updates, I will update my answer. I don't have NYTimes access so I can't evaluate exactly what it says, but skeletal dysplasia is usually considered a genetic disorder, as noted in the freely accessible publication that I linked to regarding dwarfed giraffes. This would then be similar to my 5th point. Either poor nutrition or genetic skeletal dysplasia could lead to small stature.

Hi thanks for the update. The original article NYTimes refers to was published at springer nature under the Creative Commons Attribution 4.0 International License, so you should be able to read it free. I added this information to my question too.

@Qiulang- thanks, yes, this is the same BMC Research Note linked to in my answer. In that paper, as well as more generally, skeletal dysplasia is considered a genetic disorder. I consider it most likely that the short stature of your giraffes is environmentally rather than genetically determined, and is probably not due to such a disorder.


text:
Happiness from sunlight is from IR or UV?
I found this study that shows that UV light makes our skin release feel-good endorphins. This is the pop-sci writeup.
On the other hand, it seems like IR is what causes the sense of warmth in the skin when you feel sunlight.
So are there two effects that make us happy when we see the sun? One being physical - IR heat - and the other chemical/biological - endorphins from UV? Is one more important than the other in that feel-good sensation?


text:
Can We Determine the Cell Types Ab initio?
Is it possible to find all cell types in the human body and their respective transcriptomes by analyzing the human genome (and doing no physical experiment)?
If such a thing is possible in principle, how close (or far) are we from achieving it? Is there any active research in this area? And what is the name of this research area?

No.
Cell types are identified by differential gene expression. Every cell has (effectively) the same genome, but different expression patterns give you different functions.
You could attempt to identify cell types from gene products: the transcriptome (RNA) or proteome (protein), though there would be some challenges as cells we typically consider of one "type" do not necessarily have the same transcriptome/proteome at various time points. A neuron, for example, is distinguishable based on recent activity (for example Benito, E., & Barco, A. (2015). The neuronal activity-driven transcriptome. Molecular Neurobiology, 51, 1071-1088.).
"Cellular differentiation" is the general topic of studying how cells become different types.
Note that even if you attempted something like this (and I'm sure someone has, though likely in some narrower field like deciding whether some cell type should actually be considered multiple types), you'd still need to rely on experimental evidence to verify the result. We're nowhere near being able to abandon actual biological systems in studying biology, and I'd argue it's not even something we should be attempting to do.

Yep, every time someone has said "XX science is dead, nothing left to discover" as has happened in Biology a few times (including with the advent of whole genomes), they have been completely and utterly wrong!


text:
Has Darwin's abominable mystery been solved or not?
When I research Darwin's abominable mystery, the abrupt origin and rapid diversification of the flowering plants during the Cretaceous, I read different conclusions about whether it has been solve or not. The following 4 articles are the top results I googled for the subject.

New light shed on Charles Darwin's 'abominable mystery', published 23 January 2021 said "In short, no. "One hundred and forty years later, the mystery's still unsolved," says Prof Buggs. "Of course, we've made lots of progress in our understanding of evolution and in our knowledge of the fossil record, but this mystery is still there."

SCIENTISTS FINALLY SOLVE CHARLES DARWIN'S 'ABOMINABLE MYSTERY', published Jan. 12, 2018 said yes

Darwin's abominable mystery, published May 24, 2017 said "many of the solutions we are seeking for the mystery today - such as pre-Cretaceous angiosperms - even if they were found, would simply restore the mystery to the depth that it appeared to have for Darwin. They wouldn't solve it."

The meaning of Darwin's “abominable mystery”, published 01 January 2009 said "it is worth briefly addressing whether Darwin's “abominable mystery,” specifically with respect to angiosperms, has been “resolved” in the interim between 1882 and the present."

So has Darwin's abominable mystery been solved or not?
BTW, I asked a related question at history SE "How often was the 'abominable mystery' used to attack Darwin's evolution theory?"

Why would you think the rapid diversification a plant that evolved a completely new way to exploit animals, thus decreasing its need for gamete production at the same time drastically increasing the efficiency of its seed spreading mechanism, would need special explanation.   Its like asking why there is a rapid diversification of animals once they evolve the ability to lay eggs on land.

I am a layman and that is why I asked.

Short answer:
No, it has not been solved.
Long answer:
To briefly summarize:

2/4 of your citations (1,3) definitely state that the mystery is unsolved.
1/4 definitely states that the mystery is solved (2).
1/4 does not provide a clear answer (4).

Looking more into your citation (2), it refers to this paper (Simonin and Roddy, 2018, PLOS Biology). However, it does not look like that paper actually resolves the problem, that appears to be a journalistic exaggeration. What the paper actually does is present some hypotheses for how a hypothetical angiosperm ancestor's genome might have been well-disposed for rapid diversification. The pop science article also somewhat misstates what the mystery itself is: "why angiosperms replaced gymnosperms so abruptly", as opposed to "how angiosperms diversified so rapidly" (the paper itself appears to more or less accurately summarize the mystery). So we can probably discount the reference that claims that it is solved, because it is a somewhat overhyped presentation of interesting but incremental work.
I think that your citations 3 and 4 comes the closest to a nuanced view here, neither of which appears to be very optimistic about a solution, and both of which appear to be quite skeptical of claimed solutions of the mystery. This is a classic case where the more you know, the more confused you get.
Overall, it's worth noting that "solving" the mystery is probably not something that we can do beyond a general inferential fashion, at least without a time machine. The early evolution of angiosperms (or dicots, with respect to your citation 4) happened a very long time ago, we can't directly observe or measure it. We are obliged to look at the fossil record and make guesses based on that.
Our guesses might be very good and highly quantitative, but they're still just guesses based on a very incomplete and non-representative dataset. And that's ok! That's what a lot of paleontology is, you can get very far with that kind of analysis (for example, we are now quite sure that birds are dinosaurs). But "how did this extremely complex evolutionary process occur?" is a much more difficult question than "how can I best classify this object?".
For these reasons, we are unlikely to ever get a complete picture of the process by which angiosperm radiation occurred. What we might achieve is a good general idea of when the radiation's major events occurred, what its major lineages are, and a statistical guess at the causal factors behind it.
Based on your references, I think that we have a good idea of the major lineages and the timing of the radiation, but the causes of the radiation are still very up in the air.

Thanks for answering my question but other than my citations is there any consistent conclusion in science community ?

@Qiulang I think that the consistent conclusion is what you've already found: no we have not. The sophisticated commentators that you've found go on to say that we probably can't solve this mystery, you yourself have quoted the relevant passages. We don't know why or how the radiation of angiosperms/dicots happened. As I say in my last sentence, we have more paleontological data points but do not know much about causes. Claiming to solve this kind of question is a good way to hype up your work, so people make those claims (as with your citation 2). But those claims appear to be unfounded.


text:
Is somatic fusion/hybridization off-limits to DIY-ers? ELSE: how can an infertile plant's characteristics be salvaged to a fertile one?
I was amazed to discover plant tissue culture could be performed relatively easily at home.
I have been wondering, what's the likelihood of a DIY-er being able to setup and learn a crude and basic lab setup for somatic hybridization?
I haven't had the chance to ask an actual molecular biologist, but amongst non-specialists I was met with pious contempt for my naivete or told in a very politically correct manner "you're not smart enough to do that".
Now, assuming the worst case (somatic hybridization being 100% off-limits), are there any other possibilities/strategies for achieving gene transfers between an infertile plant and a fertile one of same genus but different species in hopes after due selection and testing a fertile plant could be obtained carrying some desired characteristics from the infertile one?

Not 100% impossible, but highly unlikely (upwards of 99% impossible) for the average home experimenter to be able to do.
Your biggest barriers will be

Cost - you need extensive, very expensive equipment and lots of it to get these sorts of things to work. You also need lots of reagents, many of which are expensive (roughly in the 100's to 1,000's of dollars for a single attempt), temperature sensitive, and unavailable to the average person (i.e. you need to be working at a registered business or research institute before they will sell them to you; you can't just get these off the shelf somewhere). To equip a lab for equipment alone will be in the \$10,000 - \$50,000 range, depending on what you buy and exactly what you need.

Time - this is not something the average person could pick up a book or watch a video on and do, it takes years of training to a post-graduate level before most people attempt this sort of thing.

Regulation - this is an advanced technique for genetic manipulation; you may not have any malicious intent; but there are environmental laws in most countries that regulate the use of genetic manipulation. If you get caught the penalties will be very high.

Assuming you have enough of 1 and 2, you still won't be able to get around 3.
Having said that - techniques/areas you would need to learn: Plant cell culture, sterile technique, preparation of reagents, molecular biology techniques such as PCR (you have to have some way of determining if it worked...), plant physiology (to make sure that it is something feasible biologically and to be able to work out if something is going wrong, and exactly what that is), plant anatomy (where to source the protoplasts).
Scientific method will also be a big one - you would need meticulous attention to detail, recording everything, so that when something goes wrong (and it will; I'm a research scientist writing this) you might have some idea of what went wrong and maybe why and what to do next. Empirical technique (i.e. trying one set of conditions -> didn't work -> alter single factor in the next one) seems to be the way most people do this , but there is a whole field of literature with several hundred scientific papers on somatic hybridization, and what works for one species might not work for another.

It might be appropriate to also mention that it's illegal to propagate a patented plant. I have no idea if the OP has a particular plant in mind.

The plant I was interested in is inferrile as it is found in nature, no patents whatsoever ;)

Thanks @bob1 for your thorough answer. Although utteely disheartening, at least I now have a clear answer. This is very sad indeed. Are there any other methods to cross an infertile plant with another?

@geeheeb not that I know of, but many plants have been brought back from the brink of extinction by simple propagation methods.


text:
CRISPR-Cas9 system, DNA repair
As a critical stage in the CRISPR-Cas9 system, two different mechanisms of DNA repair can occur in the target DNA after RNA has been introduced: non-homologous end joining (NHEJ) and homologous recombination (HR).
Can these repair mechanisms be intentionally controlled or manipulated, and if so, what effects do they have on the target DNA? If the repair mechanisms cannot be controlled, how can we determine which mechanism has been employed in the target DNA, and if an undesired repair mechanism has been performed, can it be distinguished from the desired one?

This is a pretty broad question. From the [help/dont-ask]: Your questions should be reasonably scoped. If you can imagine an entire book that answers your question, you’re asking too much. The regulation of DNA repair is a huge subject, and books have been written about it. Please [edit] your post so that it focuses on one discrete, specific question that can be answered in a few or several paragraphs. Additionally, please include the research you've done so far to try to answer the question on your own.

I would recommend reading some basic resources on current Cas9 technologies. Here is one such review on prime editing, which illustrates one mechanism by which you can force cells to use a favorable precise repair mechanism. The way that you do this is by providing a repair template as part of the guide RNA that can be directly incorporated (see figure illustrating mechanism).
Properly, this mechanism uses neither of the two pathways that you mention:

Since almost all precise repair strategies generally require repair templates, they must exploit the endogenous HDR machinery, restricted to dividing cells. This has been a bottleneck in therapeutic applications of gene editing, especially for the many neurological diseases involving mutations that affect post-mitotic neurons. However, as [prime editing] bypasses the need for HDR machinery, precise genome substitutions were observed (albeit at low frequency) in primary mouse cortical neurons.

Note that this is only one example of how you can control repair mechanisms. I suggest reading that review (Scholefield and Harrison 2021, Gene Therapy), which includes information on other methods such as base editing.
As for distinguishing NHEJ vs HDR, there are a variety of references on this that can easily be found by google, such as this one. I'd recommend doing some cursory research there as well.


text:
Do whales really sleep "head down"?
Currently there is a broadcast in German TV (see https://en.wikipedia.org/wiki/The_Swarm_(TV_series)) where there was a scene of multiple whales sleeping in suspended state, vertically heads down.
The whales were not moving any fins.
The scene looked impressive, but I wonder:
The lungs had some air inside, and when being in suspended state the other parts of the body must have a tendency to sink, as otherwise the whale would surface (by the rules of physics).
Assuming that the lungs are in the front part of the body, I'd assume that that part of the body would have a tendency to surface, while the tail has a tendency to sink (submerge).
So the scene in the film was just opposite to my expectations.
Thus my question: Was the scene real, or was it just artistic fiction?

Welcome to the site. 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.

Well, the best resource that I could find (https://marinepath.com/why-do-sperm-whales-sleep-vertically/) was that sperm whales do sleep vertically, but the text did not mention whether "head up" or "head down".


text:
Need help identifying this microbe

Sorry for the bad image, we don't have a camera hooked up to our culture room microscope yet. But Has anyone seen these kind of (what I'm assuming are) contaminating bacteria before? We see these from time to time in our transgenic A431D/MDA cell lines. They're not motile. They're not visible by eye so I'm assuming they're not fungi either. The media we maintain these cells in is supplemented with geneticin (G418) antibiotic for selecting the transgenic clones.
If you've come across these, could you also share how you dealt with them?

Have you searched the literature for geneticin resistant bacteria? Did you do a gram stain? I doubt anyone can identify the bacteria from that photograph. A wild guess might be possible (Acinetobacter?), but I don't see how that would really help you.

From a practical perspective, if you have contamination like that, the best course of action is to just dump the cells and start over. Go back to earlier passages in your frozen stock. If they're all contaminated, you may have to re-derive the cell line. It is extremely difficult to rid cells of contamination 100%. If even one viable cell remains, it can start multiplying again in culture. It's not impossible, it's just a lot of work.

What magnification are we looking at here? Many fungi (especially yeasts) are microscopic, and significantly smaller than your mammalian cells. If they are bacteria, you're not really going to narrow it down with much confidence by looking at microscope images alone. I'm seeing a couple of potential diplococcus pairs, but that doesn't get you much closer to a positive ID on it's own.

I'm assuming you are meaning the blob-like thing in the middle of the picture, below the senescent cell? If so, does it get bigger over time or you find a lot more of these with time? If not, then there's a good chance that it's not contamination, but something like an apoptotic cell or a lump of something from the FBS.

please update with 1) magnification of image, 2) which object your are asking about, 3) and other relevant information about media/culture/storage/etc.

@MattDMo - I agree with you completely. It would be nice to know what got in, though. There might be a clue as to how it got in.

@anongoodnurse but sometimes, you don't want to. I once worked for a pharma company doing QA investigations of environmental monitoring failures. In one case, they identified contamination in the air (in a non-critical area, fortunately) as Gardnerella vaginalis. No one had any desire to further investigate its source. We just called it "resulting from human presence in the area" and left it at that...

@MattDMo  - Oh my word, lol! That is a bit awkward...

Couldn't you draw  a circle around the microbe in question? Like, with whatever basic image software your computer  has.

I am assuming you are referring to the blob thing in the middle of the pictures. Very hard if not impossible to say what is it. If I was you I would do a PCR on the 16S rRNA gene and send it for Sanger sequencing. the results can then be blasted against nrNuc databases in NCBI, you will have then your answer.


text:
Why low noise / low light camera on microscope?
I see plenty of back illuminated CMOS cameras, low noise cameras, high sensitivity cameras for microscopes.
What's the point? Is there a use case for it or is it pure marketing?
We have a lot of light available for microscopy imaging.

I've used such cameras for fluorescence microscopy and had to deal with very low-light, high-noise conditions, especially when looking at transient signals like calcium imaging or flavoprotein autofluorescence.
In many of these applications additional light would cause photobleaching, and for live-cell imaging additionally cause phototoxicity/death of the imaged cells.

so it's very specialized. and for fluo it should be CCD, right ? not a CMOS ? or cmos works too ?

@ker2x I'm not an expert in sensor engineering/physics, but I believe CMOS is more sensitive and can get you single-photon detection which is then amplified immediately, which is necessary to overcome the noise added in digitization.

@ker2x I wouldn't call fluorescence microscopy "very specialized". It's used in numerous fields, and in some areas of cell biology it's used quite extensively.

possibly confocal as well ? i don't know the intensity of the lasers

Confocal cuts light by a ton, yes. Effectively you get two attenuations of the light: going through the confocal first cuts it into a tiny window, then going back through it again cuts the emission light into a tiny window.

@MattDMo I suspect that ker2x was meaning specialized application for the camera, rather than the technique.

Nearly all modern image sensors are CMOS, and most reasonable-sized sensors are also back illuminated.  Even if you don't need the sensitivity, you're probably still going to use one because that is what you can buy.


text:
Sports of western sword fern: descriptions or resources?
I found a western sword fern (Polystichum munitum) growing in a home garden that appears to be showing a sport. Notably, the sportive fronds come off the same rootstock as more normal-appearing fronds (see image).
Prominent features include duplicated frond apices and pinnae, and a "lacy" appearance with marked serrations (see images). There is also possibly some chlorosis and/or necrosis, suggesting that the sportive leaves are unhappy in some way.
Fern sports are a well-known phenomena, and have been described in the Polystichum genus previously.
Questions:

Is this truly a sport? If not, how could I tell?
Are spores from this fern likely to be viable?
Is anything known about the mechanism, other than mutation? I know that fern karyotypes and genome sizes can be pretty unwieldy, I suppose ploidy change is a good hypothesis.


text:
Which species of bird does this feather belong to?
I found a feather at work when cleaning, a pleasant surprise. However, I cannot identify which bird species it belongs it. Between a friend and I, we deduced it to most likely be a falcon feather. However, even with online tools, we are uncertain of which type of falcon it originates from. I am intensely curious. The United States is where I live, in the Midwest.
Here are photos from numerous angles.

Welcome to the site. Please take a [tour] and visit the [help] for more information on the Biology Stack Exchange. If you could supply a closer photo of the back edge, thin side (as in your second photo, that'll help with ID and eliminating a couple of suspects.

@bob1 Added some photos.


text:
How do shoot apical meristems know which leaf arragement to set out based on DNA?
Shoot apical meristems are responsible for leaf and stem growth.
However when developing, how does the meristem develop the arrangement of the leaves? Like, alternate, opposite, whorled or basal.
Ive tried to search for any answers but to no answer.

Very briefly, leaf growth inhibits the growth of newer leaves.
Aspects related to this inhibition (distance from the old leaf, inhibition over time, architecture of the growing shoot, etc.) influence where on the stem the next leaf will appear. By varying the details of these parameters, one can model leaf arrangements that match most of the common leaf arrangements found in nature. Presumably there are genes that control aspects of these parameters.
https://phys.org/news/2019-06-unusual-japanese-recalculation-equation-leaf.html
https://journals.plos.org/ploscompbiol/article?id=10.1371/journal.pcbi.1007044


text:
Linearising plasmids for CRISPR experiment
I am currently designing a mock CRISPR knock-out experiment, and I’m wanting to insert a plasmid for selection. Using a restriction enzyme at 2750bp for cutting, would the location of the cut site then be considered position 1?
I’m wanting to run PCR after insertion to confirm it has been successfully transfected, and I have been supplied PCR primers - would these primer locations have to be shifted to fit in with the new linearised plasmid from location 1 at cut site?
E.g primer at location 3320 would now become location 570 after the plasmid was cut at 2750?
I’m very new to this!

No. Plasmids should generally be considered as a circular DNA rather than linear. However, no matter where you cut it, the positions don't change.
The position of the cut site is still the position on the plasmid at which the RE cuts. The numbering on plasmids is based on the position of a common restriction site, which depends a bit on which plasmid you are using. For pBR322 based plasmids, it is in the middle of an EcoRI site. This is because when plasmids were first discovered and used, we didn't have sequencing so the sequences were determined by restriction fragment mapping. Thus the start site was determined based on the position of a cut site in one of the restriction enzymes.
The positions of your primers are relative to the sequence you are inserting  - if you are using something like SP6/T7 from the plasmid, those are sites on the plasmid and would be noted as such at the relevant sites when publishing the sequence. If you are sequencing off sites internal to your insert, then you would add on the bases of the plasmid when reporting these sites. You can also report the bases position on the insert; as an example:

We inserted gene ABC into plasmid pBR322 between HindIII and EcoRV and sequenced using primer specific to insert ABC, at position XX on the plasmid (YY on the insert).

However, if you take your linear (cut) sequence and put it into a sequence manipulation program (e.g. Snapgene, Lasergene, Genious, etc. (no affiliations or recommendations for any of those, just commonly used ones)), then it might annotate your plasmid as having position 1 at the cut site, but this is an artificial annotation based on what you have told the program. If you circularize the sequence, the program may well recognize the plasmid and annotate the sites of interest (e.g. resistance markers, MCS, Ori) correctly with their proper positions marked.
Edited to add: Some positions on the plasmid do change once you have put an insert into it. These are the positions after the insert. For example, let's say you have a (hypothetical) plasmid of 500 bp in length, which has a promoter at position 50 and a resistance marker starting at position 300. If you insert a 100 bp fragment at position 250. The plasmid is now 600 bp long, the position of the promoter is still 50, but the resistance marker now starts at 350.


text:
How can Nematodes be the most numerous animal species when their habitat is smaller than that of other species
Wikipedia says Nematodes represent no less than 80% of the animals on earth.
I don't know anything about biology, but I've had this thought: isn't their habitat much smaller (in terms of volume) than the one of other species (for example: fishes) ?
Indeed, the volume of Nematodes' habitat is about $10m × S$ where $S$ denotes the surface of the earth, whereas the volume of fishes habitat is about $3 700m × S$. (considering $3700 << \sqrt S$).
So, how come Nematodes be the most numerous species on earth ?

If only the universal language was my mother tongue...!

Where are you getting your numbers for habitat volume for each? Seems likely there are some unfounded assumptions in there. Also fish are really big.

I took the average depth of oceans (I Googled it but don't remember the link) and for Nematodes I've just guessed the number. However, I just asked chatGPT (the artificial intelligence) the depth at which Nematodes can live: it answered me $15$ to $20cm$.

Never ever ever take information from chatGPT like that. ChatGPT does not "know" anything. It cannot check or understand information it gives. It has no concept of "correct" or any concept of concepts at all.

Fish don't live at all depths of ocean, certainly not with uniform abundance. Nematodes live in aquatic environments as well as soil. The Wikipedia page you started your question with talks about nematodes living very deep. Did you read the page that you yourself linked here?

"They are found in every part of the earth's lithosphere,[16] even at great depths, 0.9–3.6 km (3,000–12,000 ft)". Yes, I should have noticed this part of the Wiki page, I did read rapidly the page but I think I skipped this part.

For future reference, the exact Wikipedia quote is: "Their numerical dominance, often exceeding a million individuals per square meter and accounting for about 80% of all individual animals on earth, their diversity of lifecycles, and their presence at various trophic levels point to an important role in many ecosystems."
I could not look at a free online copy of either source, but I have a guess where the 80% figure comes from. Imagine giving every living individual animal a number and then holding a lottery where every number you gave out has an equal chance of being picked. What I believe this quote is saying is that there is an 80% chance that the winner of the lottery will be a nematode.
The reason so many individual can live is so small a space is because most species are extremely small. This site offers data on the average weight of individuals in each nematode families and the largest was steinernematidae at less than 115 micrograms. Wolfram Alpha says that is less than half the mass of a grain of sand.

Half the mass of a grain of sand seems to me a bit small. Actually this picture from Wikimedia let me think they have a length of a few ( more than 5) centimeters. It's also possible that I'm not reading correctly the ruler next to the Nematode's picture

@niobium indeed that is one of the larger species - Females of this species are up to 35 cm I think.

Nematodes can actually get quite a bit larger. The largest species (according to my first link) can be up to 13 meters long and is a parasite of sperm whales. However, these species are the exceptions, not the general rule. It's like ostriches are birds, but that does not mean the most birds weight over 200 lbs. Those nematodes species are a few centimeters big, but the vast majority are microscopic.


text:
What happens when someone is subjected to extreme pain beyond any pain tolerance?
What happens in extreme medical scenarios when a individual is subjected to extremes of pain far beyond any pain tolerance?

Can you include a link or quote for this definition of 'pain tolerance' from a peer-reviewed source? This study (https://www.jpain.org/article/S1526-5900(22)00031-1/fulltext) defines the phrase as "the maximum pain an individual is willing to tolerate".

Comments have been moved to chat; please do not continue the discussion here. Before posting a comment below this one, please review the purposes of comments. Comments that do not request clarification or suggest improvements usually belong as an answer, on [meta], or in [chat]. Comments continuing discussion may be removed.

The full definition for pain tolerance provided by the link you gave is:

The maximum intensity of a pain-producing stimulus that a subject is willing to accept in a given situation. [emphasis added]

In other words, a person's pain tolerance is how much pain a person will endure before they decide that they do not want to experience more pain. A person can absolutely experience more pain than this limit. I do not have any data to back it up, but it seems clear to me that most common response to exceeding this limit is to try and lessen the painful stimuli.

While this answers the question, it would be helpful if you can back your answer with some references or data.


text:
Are channel proteins considered a type of integral protein or peripheral protein?
I have conducted research, and unfortunately, I am unable to conclude whether channel proteins are considered a type of integral or peripheral protein. Based on my understanding, channel proteins are located on the peripheral surface of the cell, however, they have the function of integral proteins. Is my understanding correct?
All input in helping me distinguish between whether channel proteins are integral or peripheral proteins will be much appreciated.

Channel proteins are located on the peripheral surface of the cell, however, they have the function of integral proteins. Is my understanding correct?

No.
In this case of nomenclature, the context/reference point is the plasma membrane, not the cell - peripheral does NOT mean outside the cell, and integral does NOT mean inside the cell.
Integral proteins are integrated into the membrane, i.e. are embedded in the whole phospholipid bilayer that is the cell membrane, and peripheral means the protein is docked nearby, or associated adjacent to the membrane, and interfacing. They are still "at the membrane" but not integral to it.
By channel proteins, you are likely referring to membrane-spanning (transmembrane) proteins which feature pores that conduct molecules and ions. For example, aquaporins conduct or facilitate the transfer of water molecules across cell membranes, and ion channels such as Na+/K+ exchangers/pumps move cations in and out of the cell across the plasma membrane.
Transmembrane proteins such as (ion) channels or transporters are integral proteins (they are integrated into the membrane, not peripherally associated).
Personal aside: I will say that I don't often hear biologists refer to proteins as integral or peripheral... usually one would simply indicate whether they are transmembrane proteins or not. I guess this may vary by field but this practice is less ambiguous and less likely to throw someone off (as unfortunately was the case with you and plenty of others).