text:
Is the net gain of ATP during glycolysis 2 or 8?
As I understand, 2 ATP are consumed during steps 1 and 3 (glucose -> glucose-6-phosphate and fructose-6-phosphate -> fructose-1,6-bisphosphate) and then 4 ATP are produced during steps 6 and 9 (1,3-BPGA -> 3PGA and PEP -> pyruvate)
So that's 4 ATP produced - 2 ATP used = 2 ATP gained.
However, 2 NADH are produced during step 5 (3GPA -> 1,3 BPGA), and as we know 1 NADH gives 3 ATP so these 2 NADH should yield 6 ATP.
So, if we consider the ATP produced from the NADH, the net gain is 8 ATP. Is this correct?

Possible duplicate of "Glycolysis - ATP production"? Try searching the questions tagged with cellular-respiration. I'm sure David has already written an answer elsewhere (citing Berg) that addresses this question.

Have you searched existing questions here?

@acvill i'm sorry but i dont think that answers my question.

@BryanKrause yeah i did, couldn't find any answers.

@Aditya That seems extraordinarily unlikely to me. Maybe you can link to them and explain why the questions/answers you found don't answer your question ?

@bryankrause after skimming through all the 153 questions tagged with cellular-respiration, i've found 3 q&a that are kinda related to my question this does not talk about the NADH, this does not talk about the NADH in glycolysis specifically

and this does not talk about whether the NADH should be considered during calculating the net produced during glycolysis alone

@Aditya That third link seems to cover it pretty well. How do we measure "should" in science? All that's important is to understand what happens. You can make your own "should" arguments however you'd like, as can anyone else - "should" is an opinion.

@bryankrause don't think my biology teacher likes my opinion of taking the NADH into consideration, just wanted to ask the forum on what would actually be the most "correct" opinion.

Are those reducing equivalents always converted into ATP?
When they are, is that done as part of the glycolysis pathway?

Presumably you have a text book. It most likely will have a section on glycolysis in anaerobic organisms, for example in yeast fermentation. This will include consideration of how the NAD+ needed for glycolysis is regenerated in these anaerobic conditions. There is a SE question related to this topic and my own answer. This provides an objective answer to your question of "should".

@david Just saw your answer, it was helpful. I spoke with my bio teacher again, she agreed that 8 could also be the answer along with 2. Thanks for all the help, appreciate it.

No! 8 can NOT be the answer, whether or not you have beaten down your teacher into submission. Glycolysis is a process that produces pyruvate, 2ATP and 2 NADH from glucose. It ends there. The metabolism of the pyruvate and NADH are separate processes, differing between organisms and between tissues in multicellular organisms.  Even in air-breathing organisms such as ourselves, one can demonstrate this by asking whether erythrocytes perform glycolysis, and then whether they can or do obtain ATP from the NADH. The answer is yes they do perform glyolysis, and no and no for ATP from NADH. Why?

@david thats because mature erythrocytes don't have mitochondria? so as i understand now, the ATP produced from NADH happens in a separate process independent of glycolysis (the ETS), so shouldn't be accounted for?

Indeed it does. Your course will, I imagine, deal with the Krebs tricarboxylic acid cycle and the process of oxidative phosphorylation that converts ADP to ATP. If it is a school rather than a university course it may not go into sufficient chemical detail to fully explain the process. But it would be worth waiting until you have finished covering the topic and then raise any questions you have.

And one last thing (perhaps I really should write an answer). Even changing your question to "What is that potential maximum net yield of ATP from the phosphorylation of ATP and the NADH produced in glycolysis, assuming the latter is oxidized in the mitochondria", the answer 8 is incorrect on two counts related to your statement "1 NADH gives 3 ATP". The minor quibble is that for most NADH generated in the mitochondrion it is now thought 2.5 ATP are generated. The major quibble is that cytoplasmic NADH enters the mitochondrion as FADH2 with an nominal yield of 2 ATP, now regarded as 1.5 ATP.


text:
What is the minimum light intensity that a human eye can detect?
By doing a quick search in Google, I find a series of pages dedicated to physics exercises claiming that the human eye threshold for light intensity is $10^{-10}$ W/m${}^2$. However I cannot find any reference for such a value. Is it even the right unit to use here? Considering the existence of the luminosity function and the difference between W, lumen and cd.
I am interested in the minimum light intensity (in W/m${}^2$ if possible) an average human eye can detect in the lowest part of the visible spectrum (red).

I would have thought the answer would contain a time component as well. (Although if it really is "the eye can detect as little as 1 photon" perhaps not).

@SoronelHaetir The watts should account for the time component, since power is energy over time.

@SoronelHaetir some papers, listed below, claim to detect a single photon.

@SoronelHaetir Actually, for 1 photon the time component is very important: specifically, detecting just 1 photon requires that there be effectively zero photons from the outside ahead of time to detect it as a 'flash'/'something happened'. Nervous systems and brains in general are difference detectors.

From Hecht, S., Shlaer, S., & Pirenne, M. H. (1942). Energy, quanta, and vision. The Journal of general physiology, 25(6), 819-840.:

Direct measurements of the minimum energy required for threshold vision
under optimal physiological conditions yield values between 2.1 and 5.7 X
10-10 ergs at the cornea, which correspond to between 54 and 148 quanta of
blue-green light

and

in order to produce a visual effect, one quantum must be
absorbed by each of 5 to 14 rods in the retina

They're talking about blue-green light, which rods are most sensitive to. I agree with you that light intensity in units of power density doesn't seem quite right, I'd think about it in terms of counting photons instead. Basically they estimated you need somewhere around 10 photons absorbed, with about 1/10 photons being detected. A more recent paper suggests humans can detect as little as a single photon:
Tinsley, J. N., Molodtsov, M. I., Prevedel, R., Wartmann, D., Espigulé-Pons, J., Lauwers, M., & Vaziri, A. (2016). Direct detection of a single photon by humans. Nature communications, 7(1), 1-9.
As far as "red", it'll depend how "red" you go. Rods aren't particularly sensitive to deep red light (I see quite a range of estimates depending on experimental conditions, but e.g. Lamb, T. D. (1995). Photoreceptor spectral sensitivities: common shape in the long-wavelength region. Vision research, 35(22), 3083-3091. shows about 4 to 510 less sensitivity of human rods at 700 nm compared to peak), and cones are far less sensitive to light because they require multiple photon hits on a single cone to detect; they're also sparse in the periphery. See for example:
Donner, K. (1992). Noise and the absolute thresholds of cone and rod vision. Vision research, 32(5), 853-866.
As such, when people are interested in the thresholds of human vision, they're not usually looking in the red spectrum.

Thanks for the sources, I will check them out. I was interested in red because of the definition of the Draper point. I was wondering if it could be predicted more exactly by knowing the human eye threshold in the longwavelenght red.

@Mauricio Got it; I really wouldn't recommend using human perception for approximating physical quantities. For one, human perception is extremely influenced by conditions. These sensitivity values are effectively in perfectly dark conditions (though the Hecht paper I reference had participants focus on a dim red light and then presented the flash stimulus on the periphery; the dim red light was needed to keep the subjects eyes still).

If you're looking at Draper you're not only looking at just the edge of the light emitted which is mostly in infrared, but you're also looking at a measure that's basically a dude in a room looking at a rock - 1800s science-worthy, perhaps, but not really modern-day.

A single photon...?? That's really "out there" yet it's what the publication is claiming. Remarkable, despite requiring a bunch of special conditions. Would be nice to see an SE-like summary of that paper, I didn't dig into it.

@OverLordGoldDragon It's probably better to characterize their result as a "single photo-isomerization", which is caused by a single photon. And this is not something noticed every time, mind you, it's that an observer can detect it (barely) above chance (about 52%). https://en.wikipedia.org/wiki/Stochastic_resonance_(sensory_neurobiology) likely applies. It's really not appreciably different from the Hecht result besides their technique.

Apparently that value is coming from a study by Clarke & Denton in 1962 where it is extensively cited in book1 about sound scattering in ocean.

The threshold intensity which the human eye can detect a small source of light is indicated as about 10-10 µW/cm2 (Clarke & Denton, 1962)

Beside the threshold has also been measured in terms of flux2.

The threshold for a steady, effectively point, source of light presented against a
zero intensity background, which represents the smallest energy flux detectable
by the human eye, has apparently not been recently determined. Walsh (1953)
gives a value of 750 quanta/sec entering the eye.

References

International Symposium on Biological Sound Scattering in the Ocean, Airlie House, G. Brooke Farquhar, U.S. Government Printing Office, 1970
THE MINIMUM FLUX OF ENERGY DETECTABLE BY THE HUMAN EYE, F. H. C. MARRIOTT,VALERIE B. MORRIS AND M. H. PIRENNE, J. Physiol. (1959) 145, 369-373 (PDF)
https://www.olympus-lifescience.com/en/microscope-resource/primer/lightandcolor/humanvisionintro/
https://sites.ecse.rpi.edu/~schubert/Light-Emitting-Diodes-dot-org/Sample-Chapter.pdf
https://people.cs.umass.edu/~elm/Teaching/ppt/691a/CV%20UNIT%20Light/691A_UNIT_Light_1.ppt.pdf
Light Detection and Sensitivity by Vasudevan Lakshminarayanan,
Handbook of Visual Display Technology, 2012, ISBN : 978-3-540-79566-7 (link)

It should be noted that $10^{-10}~\mathrm{\mu W/cm^2}$ is 100 times less than the value given by the OP, since $10^{-10}~\mathrm{\mu W/cm^2}$ = $10^{-12}~\mathrm{W/m^2}$.

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text:
Genetics question on recombination frequency
A space probe discovers a planet inhabited by creatures that reproduce with
the same hereditary patterns seen in humans. The phenotypic characters are
height (T=tall, t=dwarf), head antennae (A-antennae, a=no antennae). For
heterozygotes with tall and antennae phenotype, the offspring are: tall-
antennae, 47; dwarf-antennae, 2; dwarf-no antennae, 40; tall-no antennae, 11.
What is the recombination frequency for the experiment?
A)13%
2)2%
3)87%
4)11%
The recombination frequency can be calculated by dividing the number of
offspring with a different combination of traits than their parents by the
total number of offspring and multiplying by 100 to express the result as a
percentage. In this case, there were 47+2=49 offspring with a different
combination of traits than their parents, and a total of 47+2+40+11=100
offspring. Dividing these values and multiplying by 100 gives us
49/100*100=49%, but how we get 13%

Welcome to the site. Please take a [tour] and visit the [help] for more information on the Biology Stack. In particular note the homework policy - askers here, particularly for questions that are obviously homework, are expected to show some attempt at answering their own question.

You don't seem to have the original phenotypes for the actual parental types (F0s), only their children the F1s (all of whom are apparently tall/antennae, e.g. dominant characters one supposes), whose apparently random mating yields the F2 generation (with the 4 types you are counting). In the absence of other information, one supposes that the non-parental types are dwarf-antennae and tall-no antennae. Is that correct? Do your numbers really add up? Do you know the F0 (parental) types? Check again.

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Contrast Fluids in MRI: Which tissues "glow" first?
I am a bioinformatic and data scientist in progress, working on my Master Thesis about prostate cancer. Now I am at that point, I have a strong guessing, that contrast fluids in magnetic resonance images (of the prostate region) will first show their effect in blood vessels, and later in other tissues by a specific ranking/order/timing. But I can not find any good (scientific) source to flesh out this hypothesis.
I found some equations about relaxation times, but this seem to be more about "wavelength" then "when after injection will it start". Also I found a lot of equations for different transportation between cells and from blood to cell. But this is to specific.
My wish would be some kind of table, stating "after injection of contrast fluid, first blood vessels will be visible, then tissues nearby, then tissues with very active metabolism (like cancer), then tissues without fat, then tissues with i do not know..."
In which scientific source I can find some characteristics, in which order (in question of time) contrast fluid is transported into tissues in the prostate region?
Edit: In case it is as simple as the comments state, that I may need other terms for search, for example I tried: "tissue fluid transport"; "contrast fluid which tissue gets it first"; "how fast react tissues to contrast fluid"; "relaxation rate of different tissues" and combinations, more and less words, and so on.

This is possibly interesting, but I was readily able to find some relevant references  by googling ('"contrast fluid" penetration prostate'), e.g. table 1 here. I'd suggest putting a little more effort into your search.

@MaximilianPress Thank you! I did not have "penetration" as term in my search. Sometimes it is that simple, with the right words :) (I do not know, if this is because I am not full biologist, or not native english...) Would you make an answer out of it?

@MaximilianPress I had a closer look into this source, and it is not helpful for me. The times noted in the table are connected with the different contrast fluids and their different dosage. And it gives times for "when is the structure (ie whole liver, whole prostate gland) completely visible". I also tried the search term you suggested, and your link was the only one, matching in general my goals. The other results are about prostate infections or general health of male organs.

This isn't really my field, but I think you're not finding anything because what you're describing isn't how contrast is used. Contrast is used to differentiate tissues at a single point in time, it's not as if things light up one after another. You might look at search terms like "time course gadolinium" to find information about when certain tissue contrasts are most prominent, but that's not going to be because some tissue "got it first", these are smooth differential equations.

@BryanKrause Thank you for the help in search terms. I have a time series of MR images, so it is not one single point in time in my case.


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Is there a way to refine a low resolution Cryo-EM structure using high resolution partial crystal structures?
I'm working on running simulations of human topoisomerase IIa. These are best done by starting with high resolution structures to ensure the system is as accurate as possible. However, no crystals exist of the full TOP2A structure (catalytic & DNase domains).
What do exist are high resolution crystals of the separate catalytic and DNase domains and low res complete structures.
Is there a way, through simulations or otherwise, to impose the high resolution structural information onto the lower resolution full protein model?
Low-res full cryo-EM structure (~8 A)

High-res partial crystal structure (~2 A)

Not sure you’ll find an answer here. Quite a high-power question for this very broad group. If not, you might try SE Bioinformatics, although they tend to be more nucleic acid oriented. But you really need to talk to experienced protein structure people. Bite the bullet and email a biggie.

seems related, may be applicable: https://www.pnas.org/doi/10.1073/pnas.1506788112, https://academic.oup.com/bioinformatics/article/23/19/2558/185859, "fragment assembly" here: https://www.nature.com/articles/s41580-019-0163-x

@David I was aware that this isn't the standard type of question asked around here, but I figured I'd give it a shot. Perhaps I'll post this over on the bioinformatics exchange too!

@MaximilianPress Thanks for the articles! I'm actually very familiar with the nature pub you linked and its relevant, but tangentially! I will look into them, but I've found a few potential solutions that fall into the approach of "Hybrid Structure Modelling/Refinement". I'm looking into using a software I'm semi-familiar with, Chimera, that apparently has this capability. I'll report back here if it works out!

@Paul yes please answer your own question if you can! It seems like something that would be of interest to a lot of people.

Don’t cross-post. It’s frowned upon on SE.

You should use the original electron density map, not the atomic coordinates associated with it.
Other than that, what you are describing is fairly routine. Briefly, the high resolution structure is used as the starting point for a simulation, the atoms are moved around using the low-resolution information as a potential energy field, and the motion of the atoms is constrained with a level of granularity chosen by the user. I use the "Real Space Refine" program in the package PHENIX, but if you are familiar with VMD, you might prefer their flexible fitting plugin. Chimera can do "rigid body fitting" well, but that's not ideal unless you're certain the low-resolution and high-resolution structures are both of the exact same molecules.


text:
Does RNA of virus have poly adenylate tail before or after entry into the host cell?
I understand that RNA needs to have 5' cap and poly(A) tail to be recognised by eukaryotic ribosomes for translation.
Some viruses are RNA based(like influenza and HIV).
Does the RNA of these eukaryotic viruses come with 5' cap and poly(A) tail?
Or are the 5'cap and poly(A) tail added by host cell after entry of virus?

Just to clarify, you want to know if the RNA genomes of RNA viruses have caps and tails, not whether viral transcripts made during the course of infection have these structures?

Yes sir, that is what I would like to know

What research have you done to try to answer the question yourself? Have you consulted the Wikipedia entries on particular viruses or RNA viruses in general? If not, please do and indicate what you found in your question.

@david the presence and location of a polyadenylate tail on viral RNA can vary depending on the type of virus. In some cases, the RNA genome is already polyadenylated when it is produced within the virus particle, while in other cases it becomes polyadenylated after it enters the host cell. Is that right?

It depends on if the virus genome is dsRNA, -ssRNA  or +ssRNA (in the latter case the genome is supposed to be translated directly by the ribosomes, in the former two cases the virus usually transports its RdRp protein into the virions). Retroviruses are another case as the RNA genome is transcripted to DNA before being imported into the nucleus, though the genome is functionally mRNA as it was produced as such by the nucleus of the cell where the virion formed.


text:
Correct description of ALDH7A1 and other genes
A quote from a review paper:

ALDH7A1 gene (discovered in 2006), which is located at chromosome 5q32.2, contains a transcript of 4964 base pairs and 539 amino acids divided among 18 exons [1,10,16,17].

As I understand, a gene cannot contain a transcript, it can only encode an RNA transcript. I wonder whether the authors meant that the transcript-encoding sequence of DNA constists of 4964 base pairs, or that the RNA transcript itself consists of 4964 base pairs.
I think it's the first, because I more often read about DNA as consisting of "base pairs", but I've just read Wikipedia and started having doubts, because RNA also seem to contain base pairs. I haven't been reading about this a long time, so I'm confused.

I suspect that you're getting wrapped up in the terminology. Think about amino acid coding- the 539 amino acids * 3 = 1617 coding bases only. The transcribed portion of the gene might have 4964 base pairs. People get a bit loose with terminology, which can be annoying, but you can always go back to the iron(ish) laws of molecular biology.

@MaximilianPress — Genes encode RNA. mRNA encodes protein. The poster is correct in my opinion in saying that a gene encodes one of more transcripts. The code is dA=rA, dG=rG, dC=rC, dT=rU. Additional coding determines splice sites.

@David ... I guess. I suppose that I am responding more to genes "encoding" transcripts to the exclusion of other forms of relationship ("contain" is obviously chemically wrong, but from a genome annotation point of view is fine). Regardless, I'll delete my second comment as at best distracting from the real point, and at worst incorrect.

I think it better to say "a gene…specifies" and avoid "encodes". "Contains" is sloppy for a professional scientist, but it happens to the best of us.

It's the second: The RNA transcript of the gene (before editing) has a length of 4964 bases. The use of "base pairs" is wrong in this context since the transcribed RNA has no paired bases. This is a feature of the DNA.
This transcript (or better: the processed exon parts of it) code for the amino acid sequence of the protein which is translated from the mRNA.

Image from here.

I think the diagram is misleading. It suggests, wrongly, that the whole of the transcript exons encode amino acids, and compounds this by having the transcript start with AUG. (And there is a typo: "transcript are code for")

@David eh, the image is clearly not trying to be rigorously accurate. It's a doodle. I actually like it since it gets the main point across, let's not get hung up on the lack of UTRs and introns or the fact that no protein will ever be just three amino acids etc.

@terdon — The diagram may be appropriate in an answer to a question with a low degree of sophistication, but hardly to one that includes an explicit mention of exons.

Caveat Emptor
Scientific writing should be as precise and unambiguous as possible, and the poster is correct in implying that the language in the cited review is incorrect. A gene certainly does not contain a transcript. The sloppiness is further borne out by the incorrect reference to the length of the transcript in base pairs, as pointed out by @Chris. Finally, 4694nt is incorrect for the length of the transcript: it is 4765nt.
One can only say that this happens, especially in cases such as the present in which the authors appear to be specialists in brain function rather than molecular biology, are being obliged to write in a language other than their native one; and this is compounded by journals with inadequate editorial supervision.
Even worse, is the fact that mistake in citing the length of the transcript in base-pairs appears in the ENSEMBL entry for this gene, although not in that from NCBI, which gives the lengths in nucleotides (nt). I would, however, take issue with NCBI’s use of the term encoded in “The protein encoded by this gene…”, as a protein is encoded by a mRNA, not a gene, and the primary transcript of one gene can result in several different mRNAs, with different protein products — as in this case. I would recommend the use of the word specify rather encode in this case.
One must remember, however, that both ENSEMBL and NCBI employ temporary staff with qualification outside of molecular biology to compile these gene descriptions.
How to find gene details oneself
There are standard genomic resources where one can fairly easily find the details of any gene oneself, especially, as in this case, human genes. The two main sites are NCBI and ENSEMBL, for which the links to this gene are already posted above. To understand the data, one needs the basic knowledge of gene structure, transcription, splicing and translation of mRNA expected of those posting questions of this sort. From these sources I would list the salient information about ALDH7A1 as follows.

The human gene ALDH7A1, aldehyde dehydrogenase 7 family member A1, is located on chromosome 5.
It runs from nt 126,541,841 to 126,595,219 on the reverse strand, and hence it encompases 53,379 bp and its initial transcript are 53,379 nt.
The initial transcript contains 18 exons, which constitute a mature mRNA of 4765 nt (not 4964) after the introns are spliced out.
This mRNA is translated into (or “decoded to”, if you wish) a protein of 539 amino acids, the difference between the 1620 nt coding sequence (including the termination codon) and the 4765 nt of the mRNA being the untranslated 3′ and 5′ regions of the mRNA.

This is illustrated in the diagram of the gene below in which the vertical bars or boxes are the exons, with the translate regions solid and the untranslated regions blank.

Is this really the gene?
It seems to me that calling this the ALDH7A1 gene is rather dubious — or misleading, at least. The gene that gives rise to the transcript described above also specifies 36 other transcripts, many of which appear to be translated to different variants of the alcohol dehydrogenase protein. (See the transcript map in the page cited above.)


text:
What if all virus suddenly disappear?
Exactly as the question says:
Let's say that all the viruses suddenly disappear (it doesn't matter the cause, just evaporate!): what would happened with the life on Earth?
I know: if this question says "bacteria", that would be a cataclysm, but with virus?
Note: let me know if this is not a correct space for this question. Thanks!

As a new user to SE Biology it would be courteous to our community if you read to the end of the [Tour] where you would see that questions that are primarily opinion-based are not suitable for this site. This is expanded in the Help on questions to avoid asking, which specifically refers to the case: "you are asking an open-ended, hypothetical question: “What if ______ happened?".

I think it's a very interesting question because viruses have a major impact on many fields of global populations, climate and chemistry.

Viruses are the fungus of the bacterial world, they also naturally control invasive invertebrate, plant and pest populations, and have an effect on geochemistry and climate. https://www.google.com/search?q=main+effects+of+viruses+on+planet+earth&oq=main+effects+of+viruses+on+planet+earth&aqs=chrome..69i57j33i160.6752j0j4&sourceid=chrome&ie=UTF-8

ha - i'd say. more like its a viral world and the bacteria and fungi just live in it :)

I'm okay with speculative questions — they are often re-writeable into typical SE questions.
My short answer is that we guess but we don't really know.  Viruses do keep many bacterial and microbial populations in check.  They cause disease too but I'm guessing that they also transport information from one point in the ecosystem.  I remember some of the research into cholera showed that disease causing genes in Vibrio cholerae are transmitted by phage (a bacterial virus).  So that suggests that benign bacteria have reserves of phenotypes which they can pull out of the virosphere when they need to change their stripes.
How often does this sort of thing happen? We know so little about the estimated millions of bacterial species, much less how they might effect the microbial ecosystem.
I feel something would happen but it's really hard to say what.  Would viruses come back? there are quite a few viruses embedded in genomes, which reactivate at interval.  It's easier to imagine the earth scrubbed of all life before viruses would be gone!  Just sayin'

Their disappearance will not be much impactful because these are damaging to cells only, but we can also see this situation from another angle.
Many viruses act as 'bacteria eaters' such as bacteriophages. Most of these viruses are the main factors in slowing down the exponential reproduction rate of bacteria.
A typical bacteria duplicates every 25 minutes. On the other hand, the viral reproduction rate is extremely high. For instance, during the "lytic cycle", T-4 bacteriophage even reduces the number of bacteria in a bacterial population.
Moreover, the disappearance of all viruses will be dramatically beneficial for humans, as viruses are the main causative agents of many of dangerous diseases.Mian examples include influenza, small pox, AIDS, hepatitis, measles and mumps.

Welcome to SE Biology. This is an objective question and answer site, not a discussion site, so it would be better to ignore this sort of "What if?" sort of question. See my comment on the actual question for a more detailed explanation of this.


text:
Can someone help me identify what type of spider or insect builds a green nest that is black an gold
I had the same thing a spider like creature that was black and gold the size of a dime that was building a green sack like web that stuck to the windshield. Location south texas winter, any supspects?

The green web will be a nest for eggs. We would need high quality photos from several perspectives of the spider to ID.


text:
Help identify parasitic plant on oak seedling
See pictures below. I found five of them on a patch of oak seedlings in northern Turkey yesterday, they are about 2 centimeters in diameter and smell like grass.

Five months later:

I tried PlantNet and Google Lens before asking but nothing came up.

I've asked several botanists from North Caucasus, none of them know. Considering that it's green, it must be hemiparasite, like Viscum.

I wonder if these are galls formed by an insect. That may be who made the hole in the bottom in the third photo.

I second @Darlingtonia's comment. If you add your photo to iNaturalist, there is a user there, Megachiele (I don't know the name exactly), that is really good at galls. I've never seen a gall like that before. Really cool.

@JohnPolo Thank you both, I'll take a look.

I think these are galls produced by a wasp in the genus Andricus.
Here are some produced by A. polyceras:

However, there are many species in this genus so more detail would be needed to narrow it down.

This looks very much like it, thanks. What more detail would you like me to provide?

I'm not familiar with this group, but a positive ID might require dissecting the galls, or capturing the wasps that emerge for inspection. The other most similar species I saw was A. quercustozae, but most of the photos showed much more bulbous galls. I didn't see any with the really narrow bases that your photos show.

The oldest relatives of these found in amber are from about 50 million years ago. They inject up to 70 active mutagens and viroids that hey use to control hosts.

Couldn't find any more galls to dissect. I'll go ahead and accept your answer, thanks again.


text:
Are "antibodies" and "immunoglobulins" really the same things?
Wikipedia says that NCAM (CD56) glycoprotein belongs to Immunoglobulin (Ig) superfamily.
A the same time, its article on antibodies equates them with immunoglobulins. NCAM is obviously not an antibody, so are these words really synonymous?

See also https://en.wikipedia.org/wiki/Immunoglobulin_superfamily
What you have here is a bit of imprecise terminology, and a language problem equivalent to another familiar one: cats. A lion is both a cat and not a cat, because 'cat' refers both to a family of mammals and to what is more precisely referred to as a 'house cat'. To tell which you are talking about requires context or clarification.
Same thing here: antibodies are referred to as immunoglobulins, which are part of a larger family, the immunoglobulin superfamily, which you might also refer to as immunoglobulins but usually not. They share a name because the immunoglobulins (antibodies) are sort of the 'archetype' of the superfamily. Wikipedia is saying CD56 belongs to the immunoglobulin superfamily - that's clear because they specifically write superfamily - not quite the same as calling them an "immunoglobulin". They're also saying antibodies are called immunoglobulins, but that doesn't mean everything in the immunoglobulin superfamily is an antibody.

I don’t think your cat analogy is so helpful because we can say “a lion is a cat” but we can’t say “NCAM is an antibody”. I would have made the point that immunoglobulin is the technical name for a molecule of precise function, commonly known as an antibody. However “immunoglobulin superfamily” is a term used in structural classification of proteins which have a variety of different functions. It could equally well have been named something  like the Y family, but was named after the first structure of this type to be determined.

@David Eh, it would be better to argue that "we can't say 'NCAM is an immunoglobulin' " - I think that's accurate, in that "immunoglobulin" is only ever used for the antibody, and not in a broader sense to refer to the whole cat family/immunoglobulin superfamily, yet it's still used in that broader sense in the adjective form, e.g. immunoglobulin domain. The point of my answer is that you need to distinguish between the immunoglobulin superfamily and immunoglobulins/antibodies, just like you need to distinguish between the cat family and the household cat.

Whatever. But if you must make an analogy the it should be: Cat is the common name for Felis catus, a member of the family felidae. In the same way Antibody is the common name for immunoglobulin G (generally) a member of the immunoglobulin structural superfamily. But then it doesn't work as nicely. I prefer to stick to pictures of proteins, as in your Wikipedia link. May get round to it myself over Christmas.

@David I'll be glad to see your answer.


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Interphase is the process in which DNA is duplicated/replicated and is the longest phase
A test question that I completed as True just wanted to know if I'm right or not:
The Question goes as follows:
Please write True or False for the following question; if False, correct the Bolded portion!
Interphase is the process in which DNA is duplicated/replicated and is the longest phase.
Context: The test was to do with animal and human cells and mitosis
I would really appreciate a simple answer, as some google posts say Yes and some say no, so I kind of am confused.

As the interphase can be subdivided into three sub-phases (also, simply, phases or stages), namely Gap 1 (G1), S and Gap 2 (G2), the question can be misleading. DNA synthesis/replication occurs only in the S (from Synthesis) sub-phase.
The question seems wrong on two grounds:

Interphase is not "the" phase in which (only) DNA replication occurs. The "S" phase would be the subject of the sentence. To say Interphase is the phase in which DNA replication occurs is to forego cell changes during G1 and G2 phases, rendering this definition an improper one.

Cells may go in a quiescent, G0 phase. Some resources may consider G0 as part of the interphase. Depending on many factors, for a given cell, G0 may be transient or permanent. If it is permanent, well, the interphase in this case may never even deal with DNA replication.

Despite these intricacies, given the context, the question to your problem is nonetheless NOT FALSE (but, also, not true in a clear-cut, objective manner, as one would expect in an exam). You have not provided what the bolded part was (subject to change). Interphase is indeed the longest phase (the other large phase being the cell division - Mitosis/Meiosis - or M-phase, which is shorter). Thus, I cannot see how one may change only a part of the sentence to make it truer (it would take at least two amendments). Going with TRUE will most likely give you the points, unless other wrongful interpretations may have been approached by whoever created this test item.
PS
The G1, S, G2 are not "checkpoints", as in the chosen answer. Those would be G1/S, G2/M, or metaphase checkpoint (most important ones).

I have updated my comment to include the bolded part sorry for the misinformation

No misinformation here, only a lost piece of information. I would leave the phrase unchanged, giving me the best shot at points, but would not be extra-surprised if one phrased it wrong and his scale expects the student to replace "interphase" with "S-phase". To say "Interphase is the process in which DNA is duplicated/replicated" is a bit odd, but not incorrect per se.

It would be true, Because interphase takes about 90% of cell division and comes before Mitosis, and interphase contains three subphases, which are the following
G1 - the Cell PREPS to preform DNA Replication;
S - DNA Replication occurs;
G2 - cell makes protein and organelles in prep for Mitosis.
Cells that do not longer divide go in a quiescent, G0 phase.


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How many cuts are done during CRISPR-Cas9 in one cell?
In a CRISPR-Cas9 experiment, the protein cuts the site matching the cRNA part of the gRNA. My question is: How many cuts are possible if multiples sites matching the cRNA are found in the cell?
Especially, considering DNA is made of multiple chromosomes, if more than one chromosome have a site matching the cRNA, will they all be cut? Does it depend of the quantity of Cas9 protein brought in during the experiment (meaning is some Cas9 protein "consumpted" at each cut)?

The main limitation on guide RNA design is the availability of a PAM site (NGG for Cas9) proximal to the target sequence. Addgene has a great article on gRNA design that may address some of your questions.

@acvill Thank you I'll check the link. But I'm not sure that it adresses the question: the question is not about designing what sequence the gRNA should have, but what are the possibilities of sequence (everything - magic versus a pool of possibilities)

It seems like your question is less about gRNAs and more about oligonucleotide synthesis. Insomuch that gRNAs are just oligonucleotides, any gRNA sequence can be created by solid-phage chemical synthesis, either as a DNA construct to clone into an expression vector or as a ready-to-load RNA for use with purified Cas9.

@acvill thank you  the link you gave between oligonucleotide synthesis and gRNA does give me elements to search for. So every gRNA could be synthetized?

On a single molecule level, Cas9 from Streptococcus pyogenes cuts but does not move to other targets for a few days (Raper et al. 2018). In contrast, Cas9 from Staphylococcus aureus cuts multiple targets, though also it takes hours for a single round (Yourik et al. 2019). However, inside a cell, even S. pyogenes Cas9 is rapidly dislodged either by RNA polymerase (Clarke et al. 2018) or FACT histone chaperone (Wang et al. 2020). So even if only one Cas9-sgRNA complex enters a cell, it will be able to cut multiple targets. There are several methods to measure the efficiency of Cas9 cleavage of multiple target and off-target sites that differ in accuracy and sensitivity. The PCR amplification-free method, RGEN-seq, is the latest innovation in this field (Kuzin et al. 2021).
References

Raper et al. (2018) Functional Insights Revealed by the Kinetic Mechanism of CRISPR/Cas9. JACS, 140(8), 2971–2984.
Yourik et al. (2019) Staphylococcus aureus Cas9 is a multiple-turnover enzyme. RNA, 25, 35-44.
Clarke et al. (2018) Enhanced Bacterial Immunity and Mammalian Genome Editing via RNA-Polymerase-Mediated Dislodging of Cas9 from Double-Strand DNA Breaks. Mol. Cell, 71(1), 42-55.e8.
Wang et al. (2020) The Histone Chaperone FACT Induces Cas9 Multi-turnover Behavior and Modifies Genome Manipulation in Human Cells. Mol. Cell, 79(2), 221-233.e5.
Kuzin et al. (2021) RGEN-seq for highly sensitive amplification-free screen of off-target sites of gene editors. Sci Rep, 11, 23600.

Thanks but I have a misunderstanding: are'nt "However, inside a cell, even S. pyogenes Cas9 is rapidly dislodged either by RNA polymeras" and "So even if only one Cas9-sgRNA complex enters a cell, it will be able to cut multiple targets" contradictory?
I might have misunderstood, could you please clarify?


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What happens if we lose voluntary control of our breathing?
Breathing can be controlled voluntarily, even though it is automatic. What happens if a person loses voluntary control of their breathing? How much would it effect day-to-day life? What are its effects on exercise?

What specific problem are you trying to solve. broad hypotheticals are generally off topic. to start with how did they lose voluntary control.

Some sort of surgery that accidentally cut the "voluntary-control-nerve?"

That would entail severing quite a few nerves. This is only likely to happen in the case of a broken neck or something else of great severity - there would be issues with breathing at all, let alone voluntarily. Could you be a bit more specific about what it is you're trying to explore, and with what purpose?

It's basically the same purpose as that of Randall Munroe's What If book.

I'm afraid I'm not familiar with that. Could you [edit] the question to add details from the book which would be relevant, as comments are not intended to last. You're perhaps referring to some sort of brain-surgery? Might not [psychology.se] be a better place to ask about the consequences of that? You'd need to be clearer about what's going on in the story.

To quote Munroe, it is "thoroughly answer[ing] a stupid question can take you to some pretty interesting places"

I'm sure that's true. There are obvious things like difficulty eating and speaking - what have your prior researches into the topic shown you?

As for the Psychology & Neuroscience thing, I don't think it is worth creating an account on a new site for this question.

I know about the speaking thing, but I think that the body would involuntarily prevent choking while eating...

Maybe, it'd depend on the specifics of the lesion/malfunction.

It literally ttakes two clicks of a mouse to create a new account there......

I know, but there are the hurdles of adapting to handle the (slightly different) community of the new site...


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Why are green monkeys (West Africa, Barbados) green?
Melanin in fur, hair and bare skin (eumelanin, pheomelanin) does not create green colors, which is why green mammals are so rare....
Green sloths (Americas) are covered in some sort of algae, which explains their coloration....
But what about green monkeys?  I can find no explanation....


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Does all CO2 from the blood leave the body through the respiratory system?
I know that the primary way that CO2 leaves a healthy human’s body from the blood is by diffusing into the lungs during gas exchange and then being exhaled. Is there any other way in which CO2 from the blood leaves the body? Since CO2 is a gas, it only leaves the body when gas is expelled. As far as I know, gases are only stored in the lungs, stomach, and intestines, and they can only expelled by breathing, burping, and farting. Is the CO2 released during burps and farts from the blood? Is there any other way that I didn't account for by which CO2 leaves the body?
This link states that an average person exhales about 500 liters of carbon dioxide every day. How do the numbers from burps and farts compare to that?
This might be useful in identifying hypercapnia or hypocapnia unrelated to respiratory function.
Edit: Bicarbonate is a form of carbon dioxide, and it is excreted in urine.

What problem are you trying to solve/what's the significance of the question? Why would it matter if CO2 is lost some way besides exhalation?

I just want to know.

The [help] says "You should only ask practical, answerable questions based on actual problems that you face". We usually interpret that fairly broadly, but there really should be some motivation for a question besides mere trivia.

Here's a situation where that might matter: A doctor wants to measure rates of CO2 production in the body to very high accuracy by measuring average CO2 expulsion over a day by putting sensors on the patient's body, but if he didn't account for all the places in the body where CO2 is expelled, he'd underestimate the CO2 production rate.

Great, that seems like a good motivation to me. Ideally you could edit that into the original question, as it will help frame answers.

humans do uptake tiny amounts of oxygen through skin so it should be worth looking to see if they do the same with co2. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2290093/

It would seem (to me) only to be important if a person had hypercarbia unrelated to pulmonary function. Air in the upper GI tract is usually swallowed air; air in the lower GI tract is both swallowed air and gasses produced by bacterial fermentation of contents, so don't really represent CO2 produced by the body anyway.

https://biology.stackexchange.com/questions/94330/gastric-and-intestinal-gas-exchange might help.

Maybe helpful, maybe not. The only current source is the first, and it doesn't discuss gas in the GI tract at all. The others are ancient (from a scientific viewpoint). Some physiological processes may take millions of years to change, but knowledge about the processes advances quickly. PS: Is bicarb excretion in the urine significant? (Among other things, the kidney's job is to conserve bicarb.)


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Why does nitrification -oxidation consume organic matter?
I want to express some doubts regarding autotroph bacteria.
The question I want to ask is relative to wastewater treatment plants, more precisely at the nitrification/denitrification step.
I've studied that nitrification doesn't need organic matter, in fact the latter is an inhibitor of the process. In addition, there are autotrophs bacteria employed, which comsume inorganic carbon for the processes.
But books of environmental engineering also mention that denitrification, if preceded by nitrification -oxidation, can present the issue of not having enough organic carbon for their processes, and that's the main reason we use post-denitrification systems today. Isn't it a contradiction? Why is organic carbon consumed by nitrification -oxidation, if they are autotroph bacteria? What am I missing in my reasoning? Do autotrophs in reality need organic carbon for their vital functions , and that was just omitted in calculations?
Thank you in advance


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Availability of information on genes in Gnomad VCF data
Im new to gnomad and genetics in general and i was wondering does the gnomad genome data that is downlaoded in the vcf format on variants contains information of what is the nearest gene and is the genomic location available also: exome/intron..... , if yes then what are the columns that contain this data? is it the INFO column?
thank you:)

Can you paste a snippet of the first few lines of a gnomad file here for us to look at? Generally speaking VCFs can be annotated with genes according to your favorite annotation, here is one of many tools. Alternately, bioinformatics SE might be a better place to get an informative answer.

@MaximilianPress hi it is the regular VCF file for variants that gnomad has on the download page

can you reproduce or link it here so that we don't have to go remember the exact url for that file?

(I'd suggest going and looking at the file header or the first few lines of variants, which directly answer your question)

@MaximilianPress the first lines of the variants are chrom position ref/alternate allele i was wondering if the information is in the INFO column?

Given that the cross-posted question got answered, I am going to see if I can mark this as a duplicate.


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How are spacer sequences created in a prokaryotic genome?
The CRISPR/Cas defense mechanism uses spacer sequences between palindromic repeats to search for the sequence to cut by an endonuclease. But how are these spacers created?
Let's take Bacteriophages, for example, which insert and integrate their genome into the prokaryotic genome. How does this infected cell get rid of the viral genome so that only a piece of the virus remains between palindromic repeats?

https://academic.oup.com/nar/article/50/3/1661/6511979


text:
Why doesn't eating affect lung capacity?
The paper Recent consumption of a large meal does not affect measurements of lung function from 2010 claims what it states in the title. However, I don't see why this would be true, as an increased size of the abdominal cavity (caused by eating) would definitely push on the diaphragm, changing various lung volumes. Why doesn't this happen?

Original article here . It's odd and certainly goes counter to my experience and intuition.

Intuitively, as @JiminyCricket. (and you) express, it should matter. Maybe it does; the article referred to has only 4 citations, and the Pulmonology literature still uses a 2 hour wait after a meal for PFTs as a standardization a decade past that paper. However, the body's nervous system is a complicated thing, and feeling full/bloated may seem to affect lung capacity without actually doing so, something like how a bit of air under the diaphragm causes rather intense shoulder pain even though it's no where close to the shoulder.

Thanks for telling me a new fact!


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In drug discovery, what is an undruggable target?
The term "undruggable" is often use in drug discovery. As far as I understand it, it means "for which no inhibitor has been found so far".
It's a fuzzy, non-satisfying, definition.
What is an undruggable target?

Welcome to Biology StackExchange! Here, it is expected that you show some research on your own. Some relevant articles: Zhang, G. Strategies for targeting undruggable targets, Dang, C. V. Drugging the undruggable cancer targets.

I doubt a proper definition of the word "undruggable" would be found anywhere. The word is used throughout medchem books without any explanations, but the word "druggable" is more widely used.
As a note, I also found the word "druggable" used in conjuction with cellular pathways, genome, cell types, or binding sites, not only with molecular targets e.g. proteins.
As such, an "undruggable" target (or pathway, or cell type) is simply considered "unsuitable for pharmacological modulation". Check the following references, in regard to protein targets.
From Drug Discovery and Development – Present and Future, Edited by Izet M. Kapetanovic (2011):

In this context, one of the most challenging tasks is the identification of the right target and more importantly whether this target is ‘druggable’. For example, although we know that RAS mutations are an early component of tumorigenesis and are identified in
approximately 30% of human cancers, attempts to target RAS have been unsuccessful to date as complex molecular structures constrain binding to the active site or pocket

The successful development of such agents is of course complex but can be simplistically considered as having three key components: the right
target (strong biologic rationale, druggable), the right drug selective, right formulation, tolerable side-effect profile) and the right biomarker (reproducible, validated)

Many stones are still left unturned, perhaps due to the lack of interest or belief that so-called “undruggable” proteins can be successfully targeted.

From Burger's 6th ed. (2003):

A number of these molecular targets are considered "druggable" or suitable for pharmacological modulation, including the 5-HT-R..."

From Flow Cytometry in Drug Discovery and Development (2011, John Wiley & Sons):

a target may be identified from patient samples, but this
target may be known to be undruggable based on prior screening efforts.


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Why is China experiencing such a surge in acute cases of COVID?
The majority of western nations have lifted most if not all COVID restrictions, however we are not seeing a massive rise in serious cases of COVID-19.
Why is it different in China? Do they have a different strain?

The claim that "we are not seeing a massive rise in serious cases of COVID-19" requires reputable sources.  From all the publicly available data I have analyzed, there appears to be no data to support any such claim.  Of course, I suppose, one could define "massive" to mean whatever they want, which is why it is best to use scientific terminology and methodology and refrain from using such ambiguous terms.

There are a number of different reasons, all adding up to the current situation.

The strain: There is not a special strain going on in China, according to different references it is mostly the Omicron BF.7 substrain. This strain is highly transmissible (with reported $R_0$ over 10, meaning each infected person infects on average another 10; the Delta strain (which was also already seen as highly infectious) "only" came to an $R_0$ of 5-6). Additionally this strain has accumulated mutations which allow immune escape, a shorter incubation time.

Covid politics: China went from a very strict zero Covid politics to no restrictions at all in the matter of days. Additionally, testing almost completely stopped. This happened with the rise of the highly contagious variant. People started getting together and spread the virus very fast, leading to the current problems.

Vaccinations: In China only the relatively inefficient Sinovac vaccine has been used, as far as I know only two vaccinations are common, with no preference for the older part of the society. How this vaccination (which happened some time ago mostly) will be able to prevent severe disease and death remains to be seen. However, the vaccination status could be better.

Immune status: Curiously, this point is connected to the zero Covid policy. This lead to many people in the Chinese society having never had contact to SARS-COV2. Without this contact, immunity cannot be built (besides vaccinating), this may be an advantage for other societies which had more contact with the virus, although immunity wanes over time.

Population: All the areas where Covid surges now are urban centers with a really high population density. Additionally public transport leads to a lot of potential contacts.

Every of this point attributes a bit to the current problem, but only the combination made it so severe.
References

WHO concerned over increasing reports of severe COVID-19 cases in China
COVID spreading faster than ever in China. 800 million could be
infected this winter
China’s COVID Wave Is Coming
Omicron BF.7, major strain causing latest outbreak in Beijing, has
strong infectious ability: medical expert

All of them, plus a very dense population and a highly interactive urban dynamic.
In each of the biggest cities, subway networks transport more than 10 million passengers per day, and more than 108 billion domestic postal packages last year, etc.

@XZhang Right, I forgot to mention the high population density and dynamics. Thanks, I added this point.

I think 4. is especially relevant. In Most western countries, a vast majority of the population had Covid.  A lot of people even multiple times. Often enough more or less harmless (being out of order for a week) but still built immunity far beyond any vaccine (and most often on top of it). This constant natural re-innoculation keeps numbers low

with reported 0 over 10, meaning each infected person infects on average another 10; the Delta strain (which was also already seen as highly infectious) "only" came to an 0 of 5-6 => these estimates are likely to be overblown. See this article.

Indeed. Important questions when doing such comparisons: What is the vaccination coverage in China vs the countries you compare it with? What's the effectiveness of their vaccine vs the one used in the countries you compare it with? Don't forget to account for boosters and population density. The closer people are together, the more vaccines for such viruses matter.

Allegedly, the Sinovac vaccine is on par after the third dose. The source is somewhat controversial, but there is a reference to the primary source in it.

@Hobbamok wrote: built immunity far beyond any vaccine - I'm interested in reading about your claim.  What are your reputable peer reviewed sources?

@RockPaperLz-MaskitorCasket mate. Calm down. All curent Covid vaccines effectiveness decays. You'll find a source for that easily enough. Any further interaction with the virus (be it live or another shot) increases the immune systems effectiveness. Since anything beyond a 4th shot is not recommended for most people, the constant lowkey reinfections with covid (or successfully defended intrusions of the virus) keeps antibody count high. It's not rocket science.

Another important point is that a good bunch of the western world went, and stayed, remote. It's harder to get the virus if you're not stuck inside an office with someone sick.

Great answer to a challenging question! (potentially interesting/helpful in the NYTimes: How Bad Is China’s Covid Outbreak? It’s a Scientific Guessing Game. (In the absence of credible information from the Chinese government, researchers around the world are looking for any clues to determine the size and severity of the surge.)

@Hobbamok Please do not tell anyone to "calm down" when they politely ask you to cite sources for your unsubstantiated claim.  You want us to simply believe you and your claims and that immunology is not "rocket science" but you literally have earned zero reputation on this site.  Sorry, but you need to back up your claims with references or provide documentation of your expertise.  You are correct on one matter, however.  Immunology is not rocket science.  It's much more complicated and not as well understood.

however we are not seeing a massive rise in serious cases of COVID-19.

Because we've already had a huge Omicron wave in December 2021/January 2022 while China is only reopening today. This means that their population is highly vulnerable to becoming infected with the Omicron variant and they need to go through a massive COVID wave to acquire proper immunity. See the Boston Wastewater data tracking the presence of COVID in the city:

That giant spike in late 2021 is precisely what's going on in China right now. Note that they're in an even worse shape than the US because <1% of their population was infected prior to December 2022 and their vaccine efficacy is lower compared to Pfizer/Moderna's product. They'll go back to having the same baseline of cases as the US once the initial wave subsides and the herd immunity threshold is reached.

Did Boston reopen in dec 2021? or did something else caused this sudden rise?

@moshevi compared to China Boston was never locked down in earnest and the worst restrictions were dropped by spring 2021. The only thing that happened is Omicron.

1/ China hasn't built up natural herd immunity, only 0.1% has had it.
2/ Restrictions are lifting in winter, the worst time to lift them for a low immunity nation.
3/ Some Chinese populations are frustrated by extreme and unreasonable covid rules, they may not quarantine voluntarily after watching the world cup.
4/ China has administered 3,5 billion doses of a fairly effective vaccine, it reduces mortality by 90+ percent, however they may have administered the second dose too long ago in 2020 and 2021 to be very effective today.
5/ Everyone knows that the government gives false information, they don't know what is true and what isn't.

ad 1) As far as we know, there is no herd immunity to be obtained as the virus can mutate.
ad 3) Unfortunately, not following the orders can result in pretty hard restrictions in China, so I doubt this is a major factor.
ad 4) The vaccine is far less effictive than other available ones.

1/ that's a fair argument, however the global infection figures with unrestricted contact and without recent injections are 5-10 times lower on new year 2022 than they were exactly one year ago, when there was major vaccination and contact restriction... Even though herd immunity is less than i.e. smallpox, immunity is causing 10x less infections in previously infected populations one year on. 3/ Home quarantine apartment blocks are difficult to police and the restrictions are reducing 4/ the vaccine has 95% reduction in mortality according to current medical sources.

also consider the financial benefits to labs that announce "natural immunity may be insufficiant", because that plays exactly into the hands of pharma bosses that say "boost your immunity with our product (at 10x prices now)" ... Industries love false science that promots their product, i.e. cellulose insulation was banned for 40 years at the profit of fiberglass/rockwool because of a single false study promoted by the rockwool stating a fire risk, which was reverse when they found cellulose has mininal fire risk.


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What kind of skull is this - fish?
Skull found near Merrimack River, West Newbury, MA frequented by Eagles, Hawks. Some kind of fish maybe? It's about the size of a hand

I'll leave answering to someone who can tell for certain, but it looks more pelvis-like than a skull to me.

that is not a skull, it is a weathered bird pelvis. but without scale and how heavily weathered it is picking an exact bird will be tricky. some bird pelvises for comparison https://ecuador.inaturalist.org/posts/27974-peacock-chicken-and-duck-pelvis-comparison

Wow! You guys are fantastic - I never would have thought pelvis. Thank you for the help. It's about the size of my hand, including the fingers. Probably duck since that's what's in the area. Thank you!


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Molecular biology - Lewin's Gene Xi vs Molecular Biology of the Cell by bruce albert
I am an undergraduate and want to start reading about molecular biology. to anyone who has read both books please let me know your thoughts. which one should I go with?
Lewin's Gene Xi or Molecular Biology of the Cell by Bruce Albert

They are both good books and standard texts, but they are not equivalent. Albert's "Molecular Biology of the Cell" is an overview of many aspects of cell biology: metabolism, genetics, cellular structure, intracellular communication, cancer, etc. Lewin's "Gene" really only covers genetics. It's a subset of the material in "Molecular Biology of the Cell", but it goes into more depth on many of the topics that it does cover.
Which book you should choose will depend on whether you are interested exclusively  in genetics, or if you want to cover other aspects of cellular biology too.


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[IAL Biology]: Struggling to understand how pH and temperature affect haemoglobins affinity for oxygen

As seen in the graph above, why do we say that increasing pH increases haemoglobins affinity for O2, but decreasing pH reduces its affinity? If the pH increases above or decreases below haemoglobins optimum pH level, wont haemoglobins affinity for oxygen decrease either way? Same goes for temperature. Why do we say that decreasing the temperature increases haemoglobins affinity for oxygen and vice versa? If the temperature goes above or below the optimum temperature of haemoglobin, wont its affinity for oxygen decrease anyway? So how does this make sense?

I think you have the wrong idea about what "optimum" means - what's hemoglobin's job? What would happen if it bound oxygen strongly and never let go?

Does this answer your question? If during exercise the affinity of oxygen for haemoglobin is decreased, what are the general consequences for tissues?

Further to the comment from @BryanKrause, the idea that haemoglobin (Hb) has a pH optimum is nonsense. There is a normal tissue pH, which can act as a signal for lack of oxygen, to which Hb responds. I'd forget about temperature. Body temperature is normally maintained in a narrow range, but pH change is of the essence. The molecular nature of this response is dealt with in my answer to another question: https://biology.stackexchange.com/questions/55683/effect-of-2-3-bisphophoglycerate-2-3-bpg-on-haemoglobin.

I think you might be misunderstanding the term affinity, which is a measure of how strongly the two molecules (for example, haemoglobin and oxygen) bind to each other. High affinity means there is a strong bonding, and low affinity means the bonding is weak. Affinity can also be more formally defined via affinity (or binding) constant, $K_{\mathrm{a}}$.
Now take a look at you graph and choose some partial pressure of oxygen, say $P_\ce{O_2} = 30 \; \mathrm{mmHg}$. In the intermediate regime under physiological conditions (solid line), approximately $60\;\%$ of haemoglobin molecules have oxygen bound. However, when pH is increased (upper dotted line), the percentage of haemoglobin with oxygen raises to approximately $75\;\%$ – this is an indication of a stronger bonding (higher affinity). Conversely, when pH is decreased (lower dotted line), the percentage drops to only $35\;\%$ because the bonding is weaker (and we say the affinity is lower).


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Why is linkage disequilibrium high on either side of a beneficial mutation, but not between sites across the mutation, during a selective sweep?
I was reading the paper "A survey of methods and tools to detect recent and strong positive selection" (2017) and came across this:

Upon fixation of the beneficial mutation, elevated levels of LD emerge
on each side of the selected site, whereas a decreased LD level is
observed between sites found on different sides of the selected site.
The high LD levels on the different sides of the selected locus are
due to the fact that a single recombination event allows existing
polymorphisms on the same side of the sweep to escape the sweep. On
the other hand, polymorphisms that reside on different sides of the
selected locus need a minimum of two recombination events in order to
escape the sweep. Given that recombination events are independent, the
level of LD between SNPs that are located on different sides of the
positively selected mutation decreases.

I am having trouble understanding how this works. If I am understanding this correctly, if you took two sites on the left side of the beneficial mutation during a selective sweep, you would see high LD between them. The same goes for taking two sites on the right side of the beneficial mutation. (Provided they are close enough to the mutation site of course.) However, if you took one site 300 bp to the left of the mutation, and another 300 bp to the right of it, you may not see the same rise in LD. I am not sure why this would be the case: wouldn't the entire region linked to the beneficial mutation, regardless of which side of the mutation it occurs to, be co-inherited and thus display similar high LD across the board, provided it is overall close enough to the site of beneficial mutation?

High-level answer
Obviously, if the positively selected site occurs on a single haplotype, then all the polymorphisms on that haplotype "win" due to hitchhiking and will have some degree of LD, regardless of whether they are left or right. All that this scenario is asserting is that the left and right flanks have a higher degree of within-flank dependence in their fate than they have inter-flank dependence.
In other words, the right flank will be preserved by recombinations left of the selected site, and the left flank will be preserved by recombinations right of the selected site. The flank blocks' interests are to some degree independent or antagonistic, whereas the polymorphisms within each flank have a common interest.
More detail
For the purpose of discussion, I think it is worthwhile to include the figure that they show here (Figure 2 in the paper):

It is less that there is no LD across the site, but rather that the LD is less marked than between sites on either side and the focal positively selected site (in black, in this figure). Negative selection is removing left or right flank polymorphisms separated from the selected site by recombination. As your quote notes, you would need a compensatory recombination to preserve LD across the site, which is relatively rare. So negative selection is not acting to preserve LD from the left to the right flank.
Everyone on the left is co-inherited due to the selection against recombination in that window. Everyone on the right is co-inherited similarly. However right and left are not co-inherited.
Note: since all polymorphisms on the haplotype are hitchhiking along with the selected site, when I say "selection against" what I mean is that recombination will mean that sites on the other side of the recombination event from the selected site cannot hitchhike at the same time. That hitchhiking is (as expected) the ultimate source of this pattern. And all of these LD blocks will decay with distance as expected.
Omega calculation clarifies within-flank dependence
If you go on to look at the equation 2 that immediately follows in the paper, this becomes maybe a little clearer:

\begin{aligned} \omega = \frac{\left({l \atopwithdelims ()2} + {W-l \atopwithdelims ()2}\right)^{-1}\left(\sum _{i,j\in L}r_{ij}^2 + \sum _{i,j\in R}r_{ij}^2\right)}{\left(l(W-l)\right)^{-1}\sum _{i\in L, j\in R}r_{ij}^2}. \end{aligned}

$\omega$ is looking for two flanks of fairly high intra-flank LD within themselves that have relatively low inter-flank LD with each other.

Thank you, studying your answer I feel like I largely understand this now. May I ask you to clarify your ‘Note: ‘ paragraph?

done. that passage was trying yet another way (possibly superfluously) to express that hitchhiking on the haplotype is still the only relevant selection happening in these flanking polymorphisms (for a strong canonical strong sweep). Hitchhiking on a single site plus recombination should equal this pattern.

Thank you. Btw, I think your second "Everyone on the left ..." meant to be "Everyone on the right ..."

In addition to the other great answer, I would like to revisit my question because I came across a stellar explanation in another paper I am now reading that also answers the question very succinctly and which I share here:

The LD within both flanking regions of the selected site is compared
with the LD between flanking regions. Selective sweeps lead to high LD
within but not between the flanking regions.
...
Selective sweeps generate a very specific LD pattern at sites
neighbouring the beneficial allele, which can be captured by the ω
statistic (Kim & Nielsen, 2004). Owing to the fast increase in
frequency of the beneficial allele, genetic variation in the region
under selection is only maintained by recombination during the
selective sweep. When conceptually regarding a chromosome as two
flanking regions adjacent to the selected site, a recombination event
divides the chromosome into two parts: (1) the original genetic
background of the selected site including one flanking region, the
selected site and the second flanking region until the recombination
breakpoint; and (2) the alternative genetic background, starting from
the recombination breakpoint at the second flanking region. Hence,
recombination will always affect only one side of the genomic region
separated by the selected site per recombination event, leading to
independent recombination patterns at both flanking sites. Therefore,
LD should be high when comparing sites within one flanking region but
low when comparing sites between the two flanking regions.
https://doi.org/10.1093/zoolinnean/zly007


text:
Is a plant's own compost better for the plant?
Does it make a difference if a plant is composted and used for its own compost ?
Meaning, let's say there is a plant "X" (example Cucumber)
Would it grow better if the compost was made from the "X" plant itself ?
Has there been a study on the same ?

There are a lot of studies about composting and plant vigor. Have you looked for a study? If so, what did you find out? Some evidence (not your claim to have done so) of prior resesarch is strongly recommended on this site, and lack thereof is a reason for close vote and down vote.

you should ask a farmer this question,they have studied this for som time(10 000 years+).


text:
Is it possible to change an amino acid within a protein but not affecting that protein's functions?
In the answer(source - Campbell Essential Biology with Physiology, self-quiz question), it's given that "if the change doesn't affect the protein's shape in any way then it's possible to do so". But practically, is it possible to amend a protein without changing its shape?

The authors are right saying that one amino acid may be changed without affecting protein's function. It depends on many factors, such as amino acid position and what you change it to. What do you mean by practically? As in vitro? In the title you say 'function' but in the question, you say 'shape' (these are different aspects). What is the exact answer found in the book?

I recommend editing the question to make it more clear, and show your own research on the matter, as per site policies, then we may guide you. Otherwise, the question may be closed.

@danieldelrey I honestly have zero knowledge
I've never studied biology before( as my subjects are maths, electronics, thermodynamics, mechanics and computer science ) but my school is forcing us to and now it's getting really difficult to understand things for me
So I just need it to pass my exam

Not only can it happen it is one way we study what are the functional components of a a particular protein . https://www.ncbi.nlm.nih.gov/mesh?Db=mesh&Cmd=DetailsSearch&Term=%22Amino+Acid+Substitution%22%5BMeSH+Terms%5D#:~:text=The%20naturally%20occurring%20or%20experimentally,enhance%2C%20or%20eliminate%20protein%20function.

What the authors are describing here is the idea that function follows from form.  Meaning that a proteins 3D structure is, in many ways, responsible for it's actions.
And yes, it is possible to change a residue without changing the proteins shape.  For example, changing a residue that resides on the outside of the protein from a positively charged one like Lysine to a positively charged one like Arginine (both residues are very similar) will not have any effect on the structure of the protein, in most cases. Same thing when changing an Alanine to a Valine: they are so similar to one another that it would be difficult to find a case where swapping them would cause the protein to change shape or for its function to be destroyed.

Your answer could be improved with additional supporting information. Please [edit] to add further details, such as citations or documentation, so that others can confirm that your answer is correct. You can find more information on how to write good answers in the help center.

"a proteins 3D structure is, in many ways, responsible for its actions"? in all ways, not in "many"

@danieldelrey - There are proteins which are intrinsically disordered (https://en.wikipedia.org/wiki/Intrinsically_disordered_proteins) or that contain regions which are intrinsically disordered. In these cases it is the lack of a stable 3D structure that is responsible for their action.

@RiskComplex the discussion is not about stability. All proteins manifest conformational changes (small or large) and/or vibrations that allow them do their function. Their 3D structures (or potential attainable 3D structures, as in IDPs) are still responsible for the specific function e.g. binding to their specific substrate(s) or interacting partners.

@danieldelrey - When the original poster is asking about a proteins shape or conformation he's referring to a stable structure that persists through time (vibrations and all).  Of course the 3D structure of anything physical is responsible to some extent for its function, but that's a useless definition and irrelevant here.

Although the question is vague, there is value in it.
We have to distinguish shape from function. The function of a protein is mostly (but not only) attributed to certain discrete regions, called domains, which have a particular "shape" attributable to the protein's primary structure (i.e. amino acids) which arrange in a particular 3D spatial conformation (this is the protein's "shape", as explained in your book).
One may change an amino acid (mutate it) within a domain without it losing its shape and function. Such a change should be conservative (e.g. between similar amino acids), but sometimes even an additional carbon atom (e.g. Gly -> Ala) or carbon permutation (e.g. Leu -> Ile) may change a protein's function.
Could you change the protein's shape through a mutation? Certainly. It may or may not lose/affect its function(s). One can even delete entire portions of a protein without it losing its function(s). As John says in the comments, we do this in laboratory  (practically) to see the effects of amino acid changes (mutations).
As I can see, in your textbook, you see this, and here is where the value lies in:

Q: Is it possible to change an amino acid within a protein but not affecting that protein's functions?

A: If the change doesn't affect the protein's shape in any way then it's possible to do so.

I do not have access to your textbook, but the answer there is actually false (or incorrect). Why? Because a protein's shape does not dictate its proper function. We may change its "shape" (3D conformation) of a non-functional domain (or a linker, or an non-important loop) and its function(s) can be wholly preserved.
PS
I do not want to mislead you, but the answer provided there may be useful for beginners in Biology. A beginner's book may not dwelve into such intricancies, so it leaves its reader associate protein shape with its function. Albeit incorrect, it simplifies things by reduction. Nonetheless, it is hardly acceptable to do so.
PPS
Most Biochemistry textbooks cover these aspects through their chapters (e.g. Lehninger's Principles).
This study mentions exactly what I said:

A mutation in the amino acid sequence may alter the structure of a protein but it does not necessarily alter its function, although, the mutation at specific sites such as conserved residues can bring about a change in the structure and function of the protein.

Going in more depth, it is even possible to maintain the shape of the protein, but alter its function, for instance, through indirect, allosterical effects.

Although, the conformation of the mutant protein may be highly similar to the conformation of the wildtype, there could be alterations in their topologies at sites distant from the site of mutation.

In this category we also include active sites of enzymes, whereby proper amino acid residues interact with the substrate; their mutation does not change the shape, but can directly perturb/abolish the enzyme's activity (example).


text:
What is this large insect?
A large (body about 4 cm long) flying insect flew into my workshed when it was very dark, warm and humid outside, probably attracted by the lights. It fell onto the bench upside down and could not turn back onto its legs. Video here: https://www.youtube.com/watch?v=rQdFE4P-HHo

Can someone please identify the species? This is the very bottom of New Zealand.

For a full answer we would need to have further pictures of the back of the insect. However, NZ has few insects of that size range that are at all common, so I suspect that what you have here is a Huhu beetle (Prionoplus reticularis).
The Huhu beetle is a widespread, large, brown beetle that is often in the 40-50 mm (~2 inch) range, with a pattern of reticulated veins on the elytra. They have brown hairs on the head and thorax and long antennae, that are often 1/3 or up to as long as the body. The species are largely known as a "wild food", with the grubs (larvae) eaten raw or fried. They are also fairly heavy fliers and make quite a racket flapping around. Completely harmless to people.
Edited to add: Having watched the video; a couple of seconds from the end you can see the elytra with the patterns on, so I am confident that this is a Huhu beetle.
The larvae are commonly found in rotting wood, particularly conifers (pine, macrocarpa), so if you have those around, that's where they will be coming from.


text:
How are cells different depending on the ethnic origin?
I recently came across an article about the fact that cell-lines provided by merchant entities to give cells to researchers, were tagged by ethnic origin. The article especially speaks about ethnic origin of African and European. The article points out that the lack of diversity in available cells has consequences on the effect of the therapies made by researchers, since they can work only on limited European (which are the majority of the provided cells). I understand that this concerns stem cells (am I correct?).
I understand of course the problem, but what remains unclear to me is : How are cells different depending on the ethnic origin? (especially protein coats of the cells that affects the vulnerability to diseases) The first answer I have is that they could be distinguished by their DNA (obviously genes coding skin color will be different).
With my researchs I found other articles that gave some information:

This lacks of diversity has an impact on the prostate cancer, so does it mean that prostate cells are different depending on the ethnic origin?
Some viruses have different expression in different ethnic origins

The article is particularly concerned with personalized/precision medicine: tailoring therapy to specific individuals based on their genetic background.
The article is in particular talking not about stem cell lines, but about cell lines derived from patients with cancer. These cell lines are studied to understand what made those cells cancerous, to both understand mechanisms of cancer and develop treatment.

How are cells different depending on the ethnic origin?

The issue raised is not a specific difference, but rather the unknown. If you only study variation among European-derived cell lines, you cannot possibly understand human-wide variation. Further, if you have just one cell line labeled as "African-American" and use studies with this cell line to make decisions about how you're going to treat all Americans with Black/African ancestry, and that one cell line is also mostly of European origin, you shouldn't expect that research to result in good outcomes for African-American/Black patients.
An example of how this might work is that a bunch of study into cancer cell lines identifies some specific mutation associated with cancer, and some pharmaceutical treatment that is highly effective in cancers based on that mutation (perhaps an antibody-based treatment). The next step would be to identify patients who carry that specific mutation or where that mutation is present in biopsied tissue, to give them that customized therapy. However, if all the cell lines you study come from people with European ancestry, only people with European ancestry are likely to have any of those specific mutations, and everyone else is left out.
In particular, African populations are more genetically diverse than populations anywhere else, presumably because humans first evolved in Africa and subsequently traveled elsewhere. Therefore, studying mostly people of European ancestry merely because they are the dominant group in a specific high-wealth country like the US is leaving the majority of human genetic diversity out of study.
The article you linked about prostate cancer seems like a good place to further understand this: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7219314/
It describes how therapies developed because they are effective in a single prostate cancer line didn't actually work for most people with prostate cancer, and that subsequent efforts to study therapies in multiple cell lines have not benefitted "Men of African Ancestry" because those cell lines are predominantly derived from "Men of European Ancestry".

Can you clarify how it comes about that "you have just one cell line labeled as 'African-American'...and that one cell line is also mostly of European origin"? Is it typical or atypical for a cell line from a random African-American patient to be "mostly of European origin"? Are you alluding to a specific cell line (e.g., HeLa)? I do see mention that Lacks's family was mixed-race ("Many of the black Lacks family were also descendants from the white Lacks family"). If that is your point, perhaps you can say it more directly.

@nanoman This is from the article in OP's question, which links to this paper: https://aacrjournals.org/cebp/article/28/6/1003/71948/Genetic-Ancestry-Analysis-Reveals "For instance, the 22Rv1 prostate cancer cell line was recently found to carry mixed genetic ancestry using a much smaller panel of markers. However, our more comprehensive analysis determined the 22Rv1 cell line carries 99% EUR ancestry. Most notably, the E006AA-hT prostate cancer cell line, classified as African American, was found to carry 92% EUR ancestry"

@nanoman Here's another descriptive article you might be interested in: https://cen.acs.org/biological-chemistry/cancer/Genetic-tests-reveal-cancer-cell/97/i10 Overall, though, my answer isn't particularly concerned with testing the premise, and cancer biology or ancestry determination are not my fields. I'm just answering OP's question about why someone would find this concerning and what the implications are for personalized medicine.

Could be a difference between self-reported ancestry, and genetic ancestry. Could be deliberate choice when completing the donation forms, or could be a typo or other accident - click the first choice in a drop down for example. By genetic ancestry, I mean clustering within large-scale population genetics studies such as Thousand Genomes

Thank for the answer, but if the article raised the issue, I suppose it is because the article does not "suppose an unknown difference that would impact the treatment's efficenciency" but because this difference is already a known phenomenon (like we already know that cell X has mutation Y for European but not for African)?
And a subsidiary question: if treatment's efficiency could be that much lowered/increased by ethnic difference, why does'nt it impact viruses or bacteria the same way ?

@totalMongot "I suppose it is because ... this difference is already a known phenomenon" I disagree - the issue is if you don't study both you don't know what the differences are, plus that it is known that there are poorer outcomes for prostate cancer for Black patients. I don't understand your statement "why does'nt it impact viruses or bacteria the same way", my answer does not mention viruses or bacteria.

@BryanKrause For first part I might have wrongly expressed but that's what I meant: some differences like outcome of prostate cancer are already known.
The statement is an extension from your answer: if diseases act differently because of cell differences, do viruses or bacteria act differently as well?

@totalMongot Different people have different responses to viruses and bacteria, yes, both within and between populations.

@BryanKrause Ok but is there a specific ethnic criteria about these differences? As for the previous example of prostate cancer?

@totalMongot What do you mean by "a specific ethnic criteria"? A historical example might include the decimation of populations native to the Americas after exposure to European illnesses, notably smallpox. Sickle cell trait would be another example.

To supplement @Bryan Krause's excellent answer, I would add another with a very specific example of the kind of variation that could affect research.
Different people have very different responses to drugs, and in many cases this variation is genetic. This variation exists across human populations, but can also to some extent be non-uniform or "private" to specific populations, meaning that sampling populations unevenly will give an inaccurate estimate of drug response variation. For example, appropriate warfarin dosing varies dramatically across patients, based in part on genetic variation in known genes.
Thus, if all cell lines tested for response to a new drug candidate are of European descent, then you only understand the pharmacokinetics of that drug for a relatively small sample of overall human pharmacokinetic variation. This could lead to ineffective or lethal (!) drug dose guidance if initial studies in cell lines do not assay a representative range of human genetic variation. (Note: in general, many regulatory safeguards are in place hoping to prevent this kind of event.)
Expert reviews have in some cases explicitly counseled personalized genetic testing to avoid such adverse drug reactions. This indicates that surveys at the population level are in fact inadequate to this problem, as they are too crude. So the issue is not really ethnic population representation, but rather the large scope of human genetic variation, to which apparent/reported ethnicity is only modestly correlated.

Many of the works on "ethnic origin" are based on the chromosome Y. Majority of it (not all) does not have the pair to recombine (very small region still recombines with X), so essentially the same Y chromosome is passed from father to son, different only by infrequent mutations. Using these mutations, it is possible to construct a map of human origins, starting from Y-chromosomal Adam. This would reflect the history about how humans migrated, populating the Earth. The known "versions" of the Y chromosome are called "haplogroups", these are highlighted here by color (image credit):

There are obviously less groups than countries but very approximately this can be matched to the "ethnic origin" in cases like at least Russia, China, India or Australia, and to some ethnic groups that are known to be somewhat tied together, like the European region, for instance. In such cases, the origin of the parent line of ethnicity like Russian vs Ukrainian can be estimated by DNA sequencing of the Y chromosome.
These chromosome signatures cannot be "assimilated" by living for generations in a region where another type of Y is dominant. A hundred generations can pass and the simple scan of the Y chromosome would still show the true origins of the parent line.
There is obviously no reason to think that any version of Y chromosome is better than other. In general there not so many genes there. However anyway the Y chromosome is part of the cell.

The paper referenced in the OP's link is using SNPs from modern populations; so, if you have SNPs that are commonly found in people from Europe, and not commonly found in people elsewhere in the world, you can say you have a high probability of European ancestry. It's the same approach that commercial genome analysis companies offer to individuals. It has nothing to do with the Y chromosome or determining the migration of peoples in history/human origins. This answer also doesn't appear to answer the question asked about how the cells differ/what the concern is in this paper.

Please read the referenced sources, "has nothing to do with Y chromosome"

I'm talking about the OP's question, not your answer.

I think that my answer addresses the question well enough, sorry about this.

@h22 Thanks for the detailed answer. I understand that all (or at least significant part) of the difference between ethnic people is "coded" on the Y chromosome? Am I correct? Also, this means that these specificities are recurrent (not different between me and another guy of same ethnic origin?
PS: I upvoted because even if it focuses on the Y chromosom, it gives hindsights useful for the answer

@totalMongot no, ethnic differences are evenly spread over all chromosomes.

OK so Y chromosom is only one way to follow them. But in what do cells actually differ? Do their cell receptors, proteins differ?

@totalMongot there are all sorts of differences, depending on the genes we're talking about. Some populations with a certain genotype may be more susceptible to damage from a certain environmental toxin, for example, or get a certain kind of cancer more easily than another. The actual physical differences can be found at the protein level, or in the way genes and groups of genes are regulated in different ways due to differences in DNA sequences.

@h22 I honestly don't see how this answer addresses the question at all. OP was not asking about Y-Adam or the origin of ethnic differences at all.

Y haplogroups are good for tracking migration because they're strictly divergent (two Y hapologroups will never merge) and because they accumulate mutations at a predictable rate, giving information about timing.  They're not much good for anything else precisely because of that divergence: every other chromosome can get mixed up with others.  For example, an African-American male might be Y-hapologroup B-M150 (west African) with the entire rest of his DNA being European-typical variants.


text:
How do I construct sample-based rarefaction curves if the area (or volume) sampled is not consistent between samples?
My apologies if a similar question has been asked previously but I cannot find an answer.
I have data from multiple zooplankton tows from different study sites and I am trying to construct sample-based rarefaction curves for each site. So, number of samples on the x-axis, number of species on the y-axis.
However, nets were used to sample the plankton and the volume of water for each sample is not consistent.
How can I adjust the curves to account for the variability in sample volume? Can I replace the x-axis (number of samples) with the average volume of water sampled per tow?


text:
How are ray-finned and lobe-finned fish related in terms of their evolutionary history?
I'm trying to trace human evolution back to the first eukaryotic cells (as a tool to research the evolution of various bodily systems), and I understand that lobe-finned fishes are considered a key transitional group between early fishes and the first tetrapods. However, I'm struggling to understand the relationship between ray-finned fishes and lobe-finned fishes and how they fit into the larger picture of evolutionary history. I’ve tried using google, Wikipedia, and YouTube, but I can’t seem to find a straightforward answer.

[should possibly be a comment but can't embed images there]
The rather clear consensus is that tetrapods are a subordinate group within lobe-finned fish, which is a sister group to ray-finned fish. See diagram below from here. This should be apparent from the wiki article on lobe-finned fish.
Just to be clear, yes, we're all fish from a cladistic point of view.
.

What was their common ancestor like?

@SeanHolm https://en.wikipedia.org/wiki/Osteichthyes

i loved those armored fish as a kid!

@shigeta my personal favorite- phenotypic variation of the armor character!