text:
How many atoms has the smallest known bacterium?
Background thoughts before this question: is it feasible to simulate a complete bacterium, atom by atom, in a computer simulation? On modern systems, either in an  upcoming exascale computer?
In current research they've simulated an organella with 100M atoms but I don't know on which infrastructure.
On Quora, there is an estimation of E.coli to have about 9x1010 atoms. With 4m base pairs it is though still quite big and possibly would produce too high computational workload in a simulation.
See also:
https://scicomp.stackexchange.com/questions/33941/is-a-complete-bacteria-simulation-with-an-exascale-supercomputer-possible
If they have simulated an organella with 100M atoms atom by atom, possibly you could already completely simulate some viruses, but they are not independent organisms.
So there has been an atom by atom simulation of the polio virus capsid in 2014 on the K computer with 10 petaflops. To include enough water molecules to fill and surround the capsid, Okazaki and colleagues needed to model the dynamics of nearly 6.5 million atoms, which they did for a simulated 200 ns.
Question - which order of magnitude would a small bacterium count on atoms? What about the smallest known bacterium Nasuia deltocephalinicola with its 112K base pairs? How many atoms has it got?

Do you perhaps mean pathogens? I imagine you can classify pathogens by dozens of criteria, but number of atoms strikes me as little more use than the day of the week in which they were discovered. Molecular science is past the descriptive phase today. It is concerned with mechanism.

There are literally hundreds of "well known pathogens". Their molecular weight is known, but their pathogenesis is much more important.

Please edit your post to clarify why you want this information — it isn't clear to me how this could possibly be useful.  If you are just trying to get a sense of scale then you may find this website helpful.

@tyersome I try to understand the physical complexity

I'm not sure number of atoms really helps with that — for example, a diamond has many more atoms than a virus, but to me it seems clear that a virus is much more complicated ... You might find the wikipedia article on complexity helpful for organizing your thinking on this subject.

changed question to narrow down and be more specific, with more background information.

I am sorry to sound harsh but this question is absurd. It does not matter how many "atoms" an organism has. You cannot model the organism by the number of atoms it contains. Two proteins may have exactly same number of atoms but their functions may be worlds apart.

@WYSIWYG it's just about order of magnitude. For sure you need a more complex model than just a set of atoms. I'm just trying to understand the computational gap between the already successful organella atom level simulation with 100M atoms and a complete small organism.

A droplet of radius 1µm will have ~1.7×10⁷ molecules of water (three times more atoms). This is an easy calculation. A typical protein molecule may have ~10³ atoms. Molecular dynamics simulation of a crystalline virus particle may tell nothing about it's infection dynamics. Typically, these models are used for studying molecular structure changes. It can be used to study how viral proteins bind to receptors but not the entire infection cycle. The scale of those processes are different.

It is akin to modelling motion of large objects using quantum-mechanical models.

I really wonder why it's not known how many atoms does a bacteria species can have, roughly. Or why it should not be asked on a Q&A site. I think, now the question is not too broad and quite specific.

@J.Doe It can be calculated. It is not explicitly reported because nobody thinks that it would be useful. Your question is not broad but the purpose of it is not clear. It certainly is not very useful. Moreover, a cell can change its structure in response to the environment and can drastically alter the number of molecules it contains. The importance of the number of atoms in the context of the paper that you linked is because of the technique they use. MD involves calculation of intra/intermolecular interactions. It makes sense for molecules/supramolecular complexes, not organisms in general.

I agree wholeheartedly with @WYSIWYG, I feel a layperson can misinterpret the notion of complexity far too readily. It's actually a very deep topic of discussion even for specialists. I have provided an answer for the sake of closing this question. As you can see, a bacterium is made of a great big number of atoms. Alright, so is a perfect crystal (a simple configuration), or a perfectly disordered gas (also a simple configuration). In biology, all simplicity is obfuscated by emergence and by chemistry (not physics). Knowing about atom number is a most useless and uninsightful bit of info.

Let's take the example of the model bacterium E. coli, for which one can find the numbers for a wet cell of a dry mass of 0.28pg. If you have a feeling for how much smaller the smallest known bacterium is compared to E. coli, you can ballpark things.

The number of carbon atoms in a single E. coli cell is approx. 7x10^9 carbon atoms.
The ratio of elements in E. coli is C : H(1.77) : O(0.49) : N(0.24) .

More simply, if you multiply the ratios by 4, you get the ratios of approximately 4 carbons, 7 hydrogen, and 2 oxygen atoms for each nitrogen atom.
Taken together, there are approximately the following number of atoms in an E. coli cell:
C: 7 x 10^9
H: 1.23 x 10^10
O: 3.5 x 10^9
N: 1.75 x 10^9
That is around 2.4 x 10^10 individual atoms. As you may have noticed, these numbers do not have any bearing on the complexity of the system whatsoever. They also do not provide any insight into the intrinsic biological plasticity and dynamics of the system.

but how many atoms does the supposedly much smaller Nasuia deltocephalinicola have? most references I can find refer to its genome size.

@J.Doe as I mentioned before, the composition and size of a bacteria will not remain constant. The paper in the question talks about a supramolecular complex, not a cell. If you assume that composition of all bacteria is more or less the same then you can simply calculate the values for your bacterium by scaling the volume accordingly.

@WYSIWYG so what is the size of the Nasuia deltocephalinicola compared to E.coli?

@J.Doe that's a separate question and is also something that you can Google easily.


text:
How does species diversity vs Earth total biomass relate?
Are there any laws/theoretical foundations about how diversity of species relate with total biomass on Earth?
While there is a lot of esoteric sort of talk "humanity dis-balances the live on the Earth", I thought, there are formally seen the following hard facts (correct me if I am wrong):

biomass of human species and species we need (plants/cattle etc) is increasing;
diversity of species is decreasing

So it looks like some sort of global system change (correct me if I am wrong), but how does biology science discuss them (in case my inquiry can be anyhow scientifically formulated)?

Biomass includes algae, plants, and insects. Humans are almost certainly negligible.

There are quite a few papers out regarding this topic e.g. this is a more recent one I've found that showed diversity and biomass being positively related.

Here's an older one focussing on theoretical foundations. I think the main idea is that a system rich in species is generally more efficient in resource use and also more stable resulting in a long term higher level of biomass.

I don't work in ecology, but my first thought is that I would not expect any relationship whatsoever between diversity and biomass. Biomass simply means the combined mass of all life on the planet. If that mass consists of one extremely fat goat the size of the moon, or several trillion different organisms doesn't make a difference, mass is mass.
Now, it is undoubtedly true that loss of diversity is a huge issue. However, the way this works is usually that we replace the local ecosystem with its several, varied species with a monoculture. For example, grasses like wheat and barley are taking over the world. Destroying a forest to plant wheat might easily result in no net change in biomass or even a net positive, but it will certainly be a significant loss in the diversity of the local ecosystem.
Finally, humans are a teeny tiny part of the world's biomass, most of which consists of unicellular life, plants and insects:

Note that the axes in the image above are logarithmic. You can get a clearer image, perhaps, from this:

(both images taken from Bar-On YM, Phillips R, Milo R., The biomass distribution on Earth, PNAS, 2018 Jun 19;115(25):6506-6511. https://www.pnas.org/content/115/25/6506)
See how all animals, let alone humans, are just a tiny part of the image on the right? That gives you a pretty clear indication of just how irrelevant we are in terms of global biomass. So yes, diversity is indeed decreasing, but there is no reason to think that the accumulated mass of living organisms will decrease, only the diversity of said mass will decrease.

thank you! wow did not think there is so much fish as one could think we have "fished out" seas!?

@J.Doe the idea of "fishing out seas" really is a major ecological/economic issue, but not to the point of eliminating life (biomass) from the seas. The concern is that extending beyond a maximum sustainable yield, we can cause an individual species to be extirpated or to go extinct. This presents 2 problems. 1) we rely on that fish species for a reason -- perhaps ease/cost of capture, nutrition, etc.. 2) I invite you to investigate further concepts of food webs, keystone species, and trophic cascades. A short summary: what you do to 1 species can and will impact the rest of the ecosystem...

source: Stack Exchange

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

sort: votes


text:
What is this insect in Southern California?
I saw this insect flying around in Southern California, USA during the summer. It is about 1.25 cm in length. When it flies, it opens up its wings like a ladybug's.  What is this?

You want to add the species-identification tag to your question, and say something about size; this will bring your question to the attention of those most likely to be able to answer it.  If you have better photographs, adding the best of them will also help

The observation about the way it opens the wings, like a ladybug, is a good one. Both are Coleoptera: https://en.wikipedia.org/wiki/Beetle. "Coleoptera" means something like "with shielded wings". Like most insects, they have two pairs of wings, but the front one is hardened and has a protecting role. The animal has to open this "shield" to allow the rear pair of wings to do the flying job.

It appears to be a type of beetle, most likely a May beetle (genus: Phyllophaga).

I have seen that bug for years, I know its a type of beetle and you are not suppose to smash em. This is just coming from my own research and talking with friends. I think they are called June Bugs.
Heres a descriptor I found.
mahogany-colored beetle of the scarab beetle family, widely distributed in North America and especially abundant in the NE United States and the adjacent parts of Canada. It is also known as June bug, although true bugs belong to a different insect order. The adults, which may swarm in great numbers in early summer and are attracted to lights, feed by night on the foliage of deciduous trees and hide during the day. The eggs are laid in the soil, where the larvae, called white grubs, remain for two or three years, eating the roots and other underground parts of grasses, grains, and trees. The grubs cause great destruction to lawns and fir trees. Many birds and small mammals, such as skunks and pigs, root out the grubs and eat them. The insects pupate underground in the fall and emerge as adults the following spring. June beetles are sometimes called cockchafers, a name used primarily for some of their close relatives in the Old World. They are closely allied to the leaf chafers, including the rose chafer. June beetles are classified in the phylum Arthropoda , class Insecta, order Coleoptera, family Scarabaeidae.

For the people down voting my response, its better than nothing.  If you know what this is then post otherwise stop being a keyboard warrior troll.

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


text:
What promoter is required for expression of a human protein Y in bacteria?
This is the actual question. It's from an entrance test for a research institute:
A scientist wants to express human protein Y in bacteria. For effective expression of this protein he should use
(A) promoter of human gene Y. (I think this is the correct one)
(B) promoter of bacterial gene.
(C) operator of any human gene.
(D) operator of any bacterial gene.
I think my answer is right although I am not sure if my thinking is entirely correct.

Homework questions are not allowed unless you show your attempt at an answer, so please share your thinking.

I am pretty sure there is no way to convince you but this is not a homework question. It's from an entrance test for a research institute in my country.

I believe you, though some level of effort is expected for all questions. Here's a leading question: why would bacterial transcription factors recognize a human promoter?

My guess is that they probably wouldn't? Instead the prokaryotic RNA polymerase is more likely to recognise a bacterial promoter. But I don't know if a bacterial promoter could work with a human gene, hence the confusion.

Yes, that's correct. The promoter essentially directs RNA polymerase to start transcription at a specific point, but transcription initiation isn't generally concerned with what comes after the transcription start site. Bacterial promoters (and viral promoters, which have coevolved to be recognized by bacterial transcription factors) are used frequently for heterologous protein expression.

That clears it up. Since prokaryotic RNA polymerase doesn't recognise an eukaryotic promoter AND promoters aren't concerned with what comes after the transcription start site, a prokaryotic promoter should be employed for the expression of a human protein in bacteria. Answer should be B. Thank you for helping me arrive at the answer. Although I didn't know about heterologous protein expression, I could answer (after some prompting by you of course) it by using the knowledge of prokaryotic and eukaryotic RNA polymerase.

I am sorry. I was not aware of that. I will correct it right away.

I'm afraid that "My query has been solved… details in the comments" just will not do. This is not how SE works. The poster is allowed to accept an answer, but the votes of the list indicate general opinion on the answer. If there is no answer the question has not been answered. Either withdraw your question or arrange with @canadianer for an answer to be posted. Please.

I have removed that last line.I hope there are no further transgressions on my part.

Canadianer has very deftly enabled me to arrive at the answer with knowledge I already had. I attempt to explain the same here.
We know that eukaryotes and prokaryotes have different RNA polymerase (enzyme responsible for transcription) enzymes. Eukaryotes have three different RNA polymerase, each responsible for synthesis of the three different types of RNAs. RNA Polymerase II is responsible for mRNA synthesis in eukaryotes. It recognises the eukaryotic (or say, human) promoter present in an eukaryotic cell. On the other hand, in prokaryotes, there's only one RNA polymerase responsible for synthesis of all the types of RNA.
Coming to the question, using a human promoter is probably logical since it would be ideal for initiation of transcription of the said human gene Y. But this is not true because a promoter is only responsible for recognition by RNA polymerase and allowing it to move further and transcribe the DNA sequence i.e. it doesn't matter what comes after a promoter. Also, prokaryotic RNA polymerase is unlikely to recognise the sequence of a human promoter. It is much more likely to recognise a bacterial promoter. Since a promoter's function is limited to allow recognition, it doesn't matter that it's a bacterial promoter as long as it can be recognised.
The two options about operators weren't a confusion for me since I already know that they don't have much to do with expression of gene as much as regulating it. Besides, any operator used would also require a promoter in any case, since that is how transcription is initiated.
Thus, the scientist should use a bacterial promoter.

You're welcome. Credit goes to you.

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


text:
Which components grow in size but not in number and which grow in number but not in size?
During growth of an individual animal some components of the body grow in size but not in number (type 1) while some others increase in number but not in size (type 2). Which of the following is correct?
(A) type 1: bones and muscle cells; type 2: hair follicles, red blood cells and epithelial cells.
(B) type 1: bones and red blood cells; type 2: hair follicles, muscle cells and epithelial cells.
(C) type 1: hair follicles and muscle cells; type 2: bones, red blood cells and epithelial cells.
(D) type 1: epithelial cells and bones; type 2: hair follicles, red blood cells and muscle cells.
I know muscle cells only grow in size. I am unsure about hair follicles, which is why I am confused between options A and C. I am also confused about bone growth. Does it ever increase in number? It would be nice if someone could clear that up.

Welcome to Biology.SE! Did you ever see giant hair follicles in adults? :)

I'll admit I didn't think of it that way. So do they increase in number then? And what about bones?

Well, either they grow in number, or, if they stay the same size, they become less and less dense when we grow up. Which option do you think is the correct one? Also, have a look at this page. Can you tell something about bone cell growth?

(It's not that I don't want to give you the correct answer straight away; it's just, you know: "Give a man a fish, and you feed him for a day. Teach a man to fish, and you feed him for a lifetime.")

Clearly they become less and less dense, duh. Also a new bone would require more osteoblasts and since they don't divide, bones don't grow in number? I like that you want to me to learn to think for myself but you pretty much gave away the answers. :D So bones, muscle cells and hair follicles don't grow in number? None of the options are correct in that case.

No, come on, if they become less dense we would have the same number of hair as babies and as 2 metres tall individuals, and it seems unlikely to me that a basketball player and a newborn baby have the same number of hair, isn't it?

This means that the number of hairs you had on your head when you were born and now is the same. I don't think so, right?

You're right. I got confused. I'm not thinking straight. They grow in number. I think that solved my question. Answer should be A. Thank you for being so patient. You're a good teacher. :)

You're welcome, Fenil. Remember: common sense before biology ;)

I posted an answer summarizing the process we underwent to get a solution, so that you can upvote and accept it and the question can be regarded as solved :D

I am not sure if I can upvote. The +1 seems to go away after a bit. I think it's because I don't have enough reputation. This feels like a dystopia movie. Not complaining, though.

Strange, according to this you should be able to upvote answers on your own questions... Well, surely you have the privilege of accepting the answer by marking the tick sign at the left of the answer. :)

Done. BTW, is there any chance I can talk to you properly somewhere? I don't have anything in particular to ask. I would just like to get to know you a bit, since I plan to pursue to biology in college as well and probably head into research.

Sure! We can talk in chat here. You still don't have enough reputation to talk there; I'll proceed and up vote two of your question so that you gain it.

We navigated through this question with Fenil in comments, I'll resume the answer here:
Osteocytes
We know from this page that "osteocytes have an average half life of 25 years, they do not divide" and that "when osteoblasts become trapped in the matrix that they secrete, they become osteocytes. Osteocytes are networked to each other via long cytoplasmic extensions that occupy tiny canals called canaliculi".
We can thus conclude that bone cells don't grow in numbers, but in size by their cytoplasmic extensions.
Hair follicles
Well, we draw the conclusion that hair follicles grow in number and not in size based on the following common sense observations:

We don't get to see tiny hair follicles in babies and giant ones in adults;
If they don't grow in size, either they grow in number or they become less and less dense as the skin surface grows with age. If the latter, we should see the same hair number in babies and in adults, whichever their height is, and this is obviously not the case.

So, they grow in number.
The answer is $A$.


text:
When is Semelparous reproduction most likely to be favoured?
Under which of the following conditions is Semelparous reproduction (where organisms produces all its offspring in a single reproductive event) is most likely to be favoured? (A) Adult survival rate is low. (B) Adult survival rate is high. (C) Breeding is perennial. (D) Breeding is seasonal.
Adult survival rate being low makes the most sense since only would an organism want to reproduce as soon as it could and also all at once. At the same time, seasonal breeding also doesn't seem far off meaning an organism would only produce all its offspring in one particularly favourable season a d in it, it produces all of it.
This is from an entrance test for a research institute. I am confused between A and D. Reading about Semelparous reproduction didn't help. Please help me solve this one.

Please do not post text as images. It discriminates against blind and partially sighted people who use screen readers. And if you post this sort of homework question we require more evidence of effort than "reading about Semelparous reproduction didn't help". What did you read? Why didn't it help?

I feel like you're just out to hound me, David. You have been nothing short of uninviting until now. You told me about the images in my other question and I then wrote the question in the details. You could've just said remove the images as well. About the question, I did say that I was confused between A and D, both of which are almost correct and should tell you that I at least know what I'm talking about and am not just here to get the answer. In any case, I have complied to both your complaints.

I know you're just following the rules and that my opinion doesn't matter to you but if you could just be a bit nicer with the tone, it would be more fun. If you see the comments on the first answer you'll even see that I discussed the answer with JayCkat who further cleared it up for me.

I commented on this question unaware that the other question I had commented on was also from you. (Easy not to notice on the phone.) Otherwise I would have probably held off. It's not you I have it in for, it's MCQs in general. They are allowed here with certain provisos, but I feel that these must be strictly adhered to, as they are really not  biological questions of general interest.

Duly noted. I disagree about MCQs though. I think well-formed MCQs are very good fuel for discussion and for checking concepts of school students/undergrads.

All its offspring in a single reproduction event.
All and single are the key words here. Ie this organism produces all its offspring that it will ever have in one event.
When breeding is seasonal- however this does not exclude organisms that can produce several batches of offspring over several seasons. Animals like deer and bears. They reproduce seasonally but are able to live several seasons and thus are able to produce several batches of offspring.
For an organism that only reproduces once, the important factor is survival of the adult animal. If the adult animal does not live long (due to predators, climate), you could expect the animal to reproduce only once and die.

This was my thinking as well. But don't you think the predation pressure could be present on the younger forms as well, and not only adults? That adds a bit a of a twist. Although, for all intents and purposes, A seems to be the most appropriate answer. Thanks.

Not really. Offspring are cheap. If there isn't so much pressure on adult form, the adults can continue to produce offspring.


text:
Concentration calculation of Factor VIII for Elisa
I have the following problem. I'm trying to get the concentration calculation for an Excel sheet that will calculate values from an Elisa plate.
The basis is a standard curve with the following values:
Std: PreDil factor 1: 40
PreDil factor 2: 55
---> Total Predilution = 2200
Concentration: 2123  µg/ml
Dilution  1:20      1:40    1:80
Std 1     1,3910    0,6360  0,2850
Std 2     1,4020    0,6360  0,3140
Std 3     1,3500    0,6250  0,2880
Std 4     1,4470    0,6810  0,2900
The sample values are the following:
Predilution: 15
Dilution 1:20   1:40   1:80
Sample   0,4060 0,1940 0,0760
According to the program that has been in use earlier, the concentration shall become 4,786 µg/ml. How do I calculate this in the best way? Unfortunately, I can't seem to get the right answer.
To add more context to the question. I work on a project to move an old program that calculated the concentrations to a new excel sheet. Unfortunately, I do not perform these analyses myself as I work on another part of the lab.
However, the question is based on how to get the concentration value of the undiluted sample. The standard used have an undiluted concentration of 2123 µg/ml. It is pre-diluted in two steps, first 1/40 and then 1/50 giving a total dilution of 1/2200.
The Standard is then analysed for three different doses 1/20, 1/40 and 1/80. Two times at the beginning of the run, and two times in the end.
The Sample is pre-diluted 1/15 to then be analysed for the same three doses as the standard.
What I have done now is that I used the Parallel Line model to try to calculate the concentration. Unfortunately, I don´t get the same answer as the earlier calculation program (Which is 4,786), and I have been able to figure out is that the problem is that I get a slight shift in the relative potency. Unfortunately, I can´t find where the problem lies.
Hopefully, this clears it up a small bit.

This just doesn't make sense. You say that the undiluted sample has a higher concentration than the undiluted standard. The assay values are of the same order of magnitude for standards and sample. But the standards were prediluted x2200 while the sample was only prediluted x15. If the sample is more concentrated and is prediluted less then it should give much higher readings. Or I don't understand your experiment.

Hi sorry for the late reply. The undiluted standard got a concentration of 2123µg/ml while the sample got a concentration about 4,8 µg/ml.

My answer: 4.79 µg/ml

(All values below are µg/ml)
Calibration data
Determine the mean of the four absorbance values at each dilution.
The calibration curve is then a plot of concentration (x-axis) against mean absorbance. Note that the actual concentration in the assay is (2123/2200)/dilution where dilution is 20, 40 or 80. If you chart this you will see that the data fit well to a straight line.
Use the Excel SLOPE and INTERCEPT functions to derive the parameters of the trendline. (I get SLOPE = 30.59; INTERCEPT = -0.8225)
The equation for converting an observed absorbance value to a concentration is:
concentration = (absorbance - INTERCEPT)/SLOPE
Sample data
For the sample measurements the only one that is valid is that for the 20x dilution because the other absorbances lie outside the range of the calibration data (see note below).
Using 0.406 as the absorbance value in the equation above gives a value of 0.01596 for the concentration in the assay well. This sample was diluted 20-fold for the assay, and the source for that dilution was derived from a 15-fold ‘pre-dilution’ so the original concentration of the sample is 300x the assay value which is 4.788 µg/ml.
Note
I don't know the nature of the discrepancy between your calculations and the target value, but if you try to incorporate the 40x and 80x dilutions for the sample you will get higher values for the sample concentration. Presumably the assay becomes non-linear at low concentrations.

Hi Alan, Thank you´so much for the response. It really helped a lot and I have been able to work out how to perform this when only one of the samples are in range. Now I´m stuck instead on how to incorporate the values when all of them are in range.
Example: Predilution for standard = 1, conc = 1,04
Avg ystd =  1,1585 0,611 0,3205
Y sample = 1,16 0,687 0,345    with a dilution of 30.
I try to put them on a common slope, get a value for the relative potency and then calculate the concentration. The problem is that I get a value of 31,88 when the "correct" result is 33,50.

@Martin    Not sure that I fully understand the numbers you mention, but if you have more than one assay of the sample that is in the range of the standard curve then you can simply use all valid readings to derive separate measurements of the [sample], remembering to vary the dilution factor as appropriate (e.g. x20 above but if the 40x dilution had also been valid then use the same formula but multiply by 600 (15x40) at the last step). You can then take the average value of all of your estimates of [sample]. (Apologies for using 'mean' and 'average' interchangeably here.)

Thank you so much, Alan! Got confused with the common slope that is mentioned in my papers, this helped me out fantastically!

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


text:
What is the half-life of dNTPs at 95 °C?
I'm looking for the half-life of dNTPs, either as a whole or broken into individual bases, at 95 °C (or similar). A titration would be great if that exists. I can provide more specifics if need be, but broadly the idea would be 'able to polymerize' vs. 'unable'.

Interesting question. FWIW, I was able to get strong bands on a 6 hour long PCR reaction with Pfu polymerase, so it is unlikely that dNTP stability would be a very big concern under most circumstances.

@MarchHo Thanks for the insight. To confirm, when you say 6 hour long PCR, that is the total length of the program, and not a total time of 6 hours at 95C (or 98C perhaps with Pfu)?

The total time was 6 hours long, most of which was extension at 72C. I would say the time taken at 98C was roughly 25 minutes (30s per cycle)

I think almost every molecular biologist must have wondered about this (as we always assume that (d)NTPs are unstable) but there seems to be no study that checks the stability of (d)NTPs at different temperatures. The closest I could find is this article which says that 40% of ATP survives after 1h at 95⁰C (10mM in distilled water). Mg²⁺ would increase the stability and stability of dATP may probably be higher.

Instead of searching for the stability of dNTPs, consider the stability of their constituent parts.
Caveat: ignoring the bonds between the different parts of dNTPs likely misrepresents the stability of the intact molecule, given that the covalent bonds between the nucleobase, sugar, and phosphate pieces each have their own relative stabilities. See my related Chemistry.SE post: Do the phosphoester and glycosidic bonds of dNTPs increase thermal stability?

Hydrolysis of Purines and Pyrimidines

In The stability of the RNA bases: implications for the origin of life,1 there is an Arrhenius plot showing the rate of decomposition of the most common nucleobases (A,T,C,G,U) at pH 7 in 50 mM phosphate buffer.  According to ThermoFisher, the pH of PCR buffer is between 8 and 9.5, though the authors of the paper linked above observe that the pH rate profile for the decomposition of purines (A,G) is relatively flat between pH 5 - 10.
At 95° C, the least stable nucleobase has a half life of 10-1 years, or about 1 month.

Fig. 2. Arrhenius plot for the decomposition of A, U, G, C, and
T, pH 7. ∆, data from Garret and Tsau (10). Equations are as follows:
log k(A) = -5902/T + 8.15; log k(U) = -7649/T + 11.76; log k(G) = -6330/T + 9.40; log k(C) = -5620/T + 8.69; log k(T) = -7709/T + 11.24. [red lines added for emphasis]

Decomposition of Pentose Sugars

The same research group investigated the stability of the sugar moieties of nucleic acids in Rates of decomposition of ribose and other sugars: implications
for chemical evolution.2  The analysis is slightly obscured by the use of deuterated water, though the authors observe that the rate of decomposition of ribose in H2O at 100° C and pH 7.0 is identical to that in D2O at 100° C and pD 7.4.
At 100° C and pD 7.4, ribose, the sugar component of RNA, has a half life of less than 2 hours.  Interestingly, the authors note that 2-deoxyribose, the sugar component of DNA, decomposes 2.6 times slower than ribose with a half life just shy of 4 hours.

Fig. 1. Rates of ribose decomposition as a function of pD.
The curves were fitted by assuming a functional form k = k0/(1 +
[H+]/Ka), where Ka and k0 are adjusted constants. [red lines added for emphasis]

Hydrolysis of Triphosphate

Getting to the heart of your question, i.e. at what point are dNTPs no longer "polymerizable", the stability of the triphosphate is vital, as the hydrolysis of the two distal phosphates and the creation of a phosphodiester bond with the remaining proximal phosphate is the rate-limiting step in DNA polymerization.
An older publication, The Hydrolysis of γ-Phenylpropyl Di- and Triphosphates,3 investigates the hydrolysis of nucleotide analogs at 95° C, over a pH range of 0.3 to 10.  For the ATP analog, the rate of spontaneous hydrolysis to ADP is very low, 17.5 × 10−5 s−1 at pH ~5.  Assuming first order kinetics, the half life of the triphosphate form is ~4000 seconds, or a little more than an hour at 95° C.  In a buffered solution closer to a neutral pH, we can expect triphosphate to be even more stable.

Table 5. A Comparison of the Rates of Hydrolysis of γ-Phenylpropyl Di- and Triphosphates and ADP and ATP at 95°

A worked example
A PCR with one 2-minute initial melting and 20 cycles with 15-second melt steps will expose dNTPs to 420 seconds at 95° C.  Considering only the hydrolysis of triphosphate, which is the least stable component of the 3-component dNTP molecule outlined above, the equation for exponential decay can be used to calculate the proportion of unincorporated dNTPs that are still "polymerizable" at the end of cycling, using the rate constant provided in Miller and Westheimer.3
$N_{\text{final}} = N_{\text{initial}} × e^{-kt}$
$N_{\text{final}} = e^{(-17.5 × 10^{-5} s^{-1})(420 s)} = 0.929$
For some perspective, a 50 μL PCR with 0.2 mM dNTPs contains enough raw materials to create 1.51 × 1013 copies of a 200 bp dsDNA amplicon, ignoring the contribution of primers to the amplicon body, and assuming perfect fidelity of the polymerase and primers in excess.  A 20-cycle PCR with 106 molecules of template will yield 1.05 × 1012 amplicons, assuming perfect duplication at each cycle, meaning dNTPs are supplied in more than 10-fold excess and heat decomposition is unlikely to have an effect on PCR fidelity in this system.

References

Levy M, Miller SL. The stability of the RNA bases: implications for the origin of life. Proc Natl Acad Sci USA. 1998 Jul 7;95(14):7933-8.
Larralde R, Robertson MP, Miller SL. Rates of decomposition of ribose and other sugars: implications for chemical evolution. Proc Natl Acad Sci USA. 1995 Aug 29;92(18):8158-60.
Miller DL, Westheimer FH. Hydrolysis of Gamma-Phenylpropyl Di- and Triphosphates. Science. 1965 Apr 30;148(3670):667.


text:
Finding phylogenetic distance between sequences?
I'm working on a piece of software that does comparative genomic analysis; and I found out in homology methods for functional annotation, it's preferable to pick the high scoring homolog from a distant sequence (i.e. not closely related to the query sequence in the phylogenetic tree).  My question is: why? and also could NCBI taxid for each taxon be used for approximating this distance? if not, then is there a simple way of making this binary decision (close, not close) when given two sequences.

No, because it is really not a binary decision. There are attempts to associate percent pairwise difference with taxonomic ranks (particularly species), but this is problematic because every independent lineage can vary according to its own rate. You could use sequences from different families, or orders, or even phyla, but these two can depend on whether specialists in the field are lumpers, or splitters. For example, all ants are in the same family, and Formicidae is over 100 million years old, while birds that may have diverged from a common ancestor within the last 10 million years are in a different family. You can use pairwise distance OR higher-level taxonomy as a proxy. But it would be crude. Why not program your software to make hard decisions about homology, and then find the closest most distant homologue in terms of pairwise differences?

are you referring to these methods: https://en.wikipedia.org/wiki/Distance_matrices_in_phylogeny

and also what about the reason for picking a homolog that is not closely related to query sequence? is the sequence taxid useful at all?

Yes, distance can be calculated simply by counting the differences between pairs, and then sometimes correcting those distances with various models that assume some of these changes will be masked by multiple changes at the same sites. The taxid tells about classification. Picking a distant homolog far from the query gives you more information about how much a gene can change over time.


text:
Affinity for oxygen and carbon dioxide in animals
I'm currently reading Treatise on Invertebrate Paleontology (A) and don't understand the following fragment:

The affinity for oxygen in lower animals is many times that in higher ones, whereas conditions are the reverse with regard to carbon dioxide.

What does it mean by "affinity"? Affinity of hemoglobins (in blood)? Affinity of oxygen-transporting molecules, whatever they are? Something else? The book doesn't provide a source of its claim here.
EDIT: @Will - I'm more interested in what kind of affinity they are speaking about in regards to carbon dioxide (I can't comment due to not having enough reputation yet.)

Can you include more of the surrounding text to help with context?

@AlanBoyd "Their [i.e. aerobic organisms'] needs vary according to degree of activity and environmental conditions. In any given case, oxygen requirements can be extremely different, and such variations are usually determined by the affinity of special hemoglobins for oxygen. [The quote above is here.] Humans require an oxygen to carbon dioxide ratio of 250 to 1. In contrast, Arenicola marina needs only a ratio of 50 or 70 to 1. Many lower organisms, especially polychaetes, can tolerate considerable decreases in the amount of oxygen that they take in without the slightest organic damage."

In your comment it says "affinity of special hemoglobins for oxygen".  That is not the same block text as your question.    I think they are speaking to the ability of worms and the like to scrounge O2 out of environments that would be much too hypoxic for vertebrate life.  They can do that because their hemoglobins have greater affinities for O2.  You can read up on bloodworms for an excellent example.

In English "A has an affinity for B". We know what B is (oxygen) but you are expecting us to be able to guess what A is. I'm afraid that you are not supplying enough information for anyone to be expected to help you.

The phrase "lower animals" is so vague as to be completely useless.


text:
What species is this lizard?

A small green lizard (20 cm in size). It was found in the direct neighboorhood of a house, in a small village in the Hungarian hills south of the Balaton lake. It was found in the middle of the day.
Our first guess would be Lacerta viridis. Is this correct?

By the picture and the official distribution it looks to be as you said a Lacerta viridis.
Some references and distribution here:

https://www.iucnredlist.org/species/61530/12507156
https://commons.wikimedia.org/wiki/Lacerta_viridis
http://reptile-database.reptarium.cz/species?genus=Lacerta&species=viridis

In Western Europe we have a brother specie Lacerta bilineata.
Example in Geneva:

The distribution maps shows that Lacerta viridis is mainly present in Easter Europe (including Hungary) and Lacerta bilineata is present in the Western Europe.
Both species are similar and the male get the throat blue generally during the breeding season.
This site have also a description of the specie.

I think it's the biggest lizard locally in most places, i.e. in France it's the biggest lizard i have seen, up to 40cm. the ones with the most blue are the best, they vary a lot.


text:
Why there is no blood in a bird's egg?
Egg consists of some albumin and yellow colored yolk.
But it is a living organism with red colored blood, it should contain red blood.
so why can't we find the blood in the egg (specifically bird's egg)?

Simple: You don't see it, because there is no blood in eggs.

@user60306 seriously, at least show some research effort and instead of calling the egg white 'transparent gel', use its proper term (albumen).

It is not a living organism. It is a live cell. There is a vast difference.

You do not see blood because you are looking at unfertilized eggs.  These are the chicken eggs that one gets from the supermarket.  The hens are bred to lay these even with no rooster.  No chick will ever grow from these eggs.
If you have a fertilized egg that is about to hatch and open it, you will find a chick.  Inside the chick there is blood, should you wish to check.
If you have a fertilized egg that will hatch eventually and open it, you will find signs of the developing chick.

If the egg has been laid very recently you may see only what looks like a tiny spot of blood.  Occasionally you will find this in a farm egg.  That is what will become the chick.  Depicted is a day 4 egg.


text:
Implanted neural recording system vs Electroencephalography
Can someone help me to understand why in nowadays the scientists develop implanted neural recording system to measure and collect neural signals? Why the use of the electroencephalogram is not sufficient to record neurons? Which is the difference between these systems?
Thanks in advance

EEG records a rough average of activity from a large area of the brain, because it is located far away from the actual neurons. There is no way to separate out the activity of individual or even small groups of cells; instead, you record lower frequency synchronous activity among whole populations.
Implanted systems can record from small groups or sometimes even single neurons, which greatly increases the amount of information available.
Depending on the purposes of the recording or research, EEG might be sufficient; in other cases, implantable electrodes are required. EEG is sufficient to monitor sleep/wake cycles, for example; there is no need to record intracranially to monitor sleep (unless perhaps you are studying mechanisms of sleep itself). Implanted electrodes are often used before surgery to remove parts of the brain that are causing seizures. Using ECoG (basically an "EEG on the dura" rather than on the skull) or depth electrodes allows the surgeon to know more precisely which area is causing seizures, hopefully leading to a more successful surgery and needing to resect less tissue.
Implanted electrodes are also commonly used in animal experiments to learn about how single neurons and small populations encode or process information.

Perhaps the OP was more likely referring to brain-machine interfaces, where recording from single neurons or populations may offer some advantages.

Perhaps; the answer is the same. I gave just two examples.

Thank you so much, Mr. Bryan Krause.Very good explanation!


text:
Question to the color scientists
I have a question.
if you look at these two spectral diagrams (SPDs) from two different televisions that is calibrated to the same white point (D65) 6500K with a spectrometer.
The problem is that white still looks different to the eye here.
why does white look different is my question.
Television1
(pictures from avsforum)

Television2

A logical explanation would be great as i trying to figure out whats causing it.
is it the spectral power differences that causing it or is it the different distribution of the GREEN and RED with its more narrow peaks on television1 that causes it?
what i can see and what i understand is that Television1s spectral power will produce a more natural light as its more close to the warm light from an incandescent bulb.
Television2 reminds more of an typical LED lamp that we all know have a more harsh and poor light.

First: What is TV in this context? Then: LED lights are not necessarily cold, they can be produced in almost all color temps you want to have.

Tv=Television and ok cold is maybe the wrong term. poor and harsh is the right description.

The difference between both images can by explained with the spektrum. The upper one lacks most of the colors between green and red (more or less) while the lower one is more complete here. Both also differ in green.

Thanks for the input but i think its more about the different energy of Green and Red on the first television thats makes the difference. higher energy for Green and Red compared to Blue should make whites "look" more warm..while television 2 only has high energy for Blue it will give whites a more cold tone.  i have already captured the differences on whites with an DSLR camera but the differences on photo is not the same as i see them.. the camera sensor picks up the correct white for television 1 but not for television 2 for some reason.

i have already captured the differences on whites with an DSLR camera but the differences on photo is not the same as i see them.. the camera sensor picks up the correct white for television 1 but not for television 2 for some reason.. here is the differences for white with similar televisions models but not the exact ones from these photos..television 1 to the left..whites "looks" correct on the photo but white on television 2 looks too much Blue/Green. http://privat.bahnhof.se/wb192876/500M%20B7_2.jpg

it has nothing to do with computer graphics. where do you think its related to graphics from a computer?.. its more about how our eyes see light and colors different compared to spectrometers and cameras.

This is probably caused by the imperfection and/or mismatch between what your eye thinks white and the calibration device's white...color perception from spectrum can be nonlinear and have individual variations.

A simple observation: whilte points are a single dimension: temperature.  Color itself is a 3 valued thing (for human eyes).  Thus it will always be possible to have two colors with the same temperature.  Color temp is more useful if your source is blackbody.

After more reading and information its quite simple.
our eyes picks up the energy from the primary colors.
if a television has higher BLUE energy than RED and GREEN that picture will have a blueish cold look to it even if its calibrated to D65
the SPD from television nr1 has higher energy for GREEN and RED and so whites on this television will look more warm and less blue.
how distinct and separate the cones are can also matter here.
television nr1 has no clear separation between GREEN and RED while television nr1 has.


text:
New speciations among Darwin's finches
In this video it is claimed that Darwin's finches arrived at Galápagos Islands just a few hundred years ago. Have there been new speciations over the past 200 years?

According to oneZoom.org (see the node of interest here), the large ground finch and the large cactus finch share a common ancestor about 170k years ago. Looking among Darwin finches on oneZoom.org, I could not find a more recent speciation event. I could not find their references for their estimates though.
However, part of the difficulty here lies in the exact definition of species one is willing to use (see this post). While it is not reported in oneZoom.org, grant and grant (2009) reported an evidence of reproductive isolation within the G. fortis species.

Speciation, the process by which two species form from one,
  involves the development of reproductive isolation of two divergent
  lineages. Here, we report the establishment and persistence
  of a reproductively isolated population of Darwin’s finches on the
  small Gala´pagos Island of Daphne Major in the secondary contact
  phase of speciation. In 1981, an immigrant medium ground finch
  (Geospiza fortis) arrived on the island. It was unusually large,
  especially in beak width, sang an unusual song, and carried some
  Geospiza scandens alleles. We followed the fate of this individual
  and its descendants for seven generations over a period of 28
  years. In the fourth generation, after a severe drought, the lineage
  was reduced to a single brother and sister, who bred with each
  other. From then on this lineage, inheriting unusual song, morphology,
  and a uniquely homozygous marker allele, was reproductively
  isolated, because their own descendants bred with each
  other and with no other member of the resident G. fortis population.
  These observations agree with some expectations of an
  ecological theory of speciation in that a barrier to interbreeding
  arises as a correlated effect of adaptive divergence in morphology.
  However, the important, culturally transmitted, song component
  of the barrier appears to have arisen by chance through an initial
  imperfect copying of local song by the immigrant. The study
  reveals additional stochastic elements of speciation, in which
  divergence is initiated in allopatry; immigration to a new area of
  a single male hybrid and initial breeding with a rare hybrid female.

Thanks. The second question is not much necessary to me, so I will remove it.

It is some kind of a rule though that the OP cannot just change the question (or only for mild clarifications) after someone has answered it though. You're now realizing part of the problem of why one must always restrict a post to a single question!

I would rather advice, restricting the current post to the second question only as it has already been answered (although relatively poorly answered) and open a new post for the first question.

You're right. I edited the question.

I think this article implies there have been new speciations? https://evolution.berkeley.edu/evolibrary/news/100201_speciation

I read your post about the definition of species. I was curious what's the definition of lineage, but I don't have enough reputation to comment there. Doesn't lineage refer to an individual?

From wikipedia, An evolutionary lineage is a temporal series of organisms, populations, cells, or genes connected by a continuous line of descent from ancestor to descendent. Lineages are subsets of the evolutionary tree of life Feel free to open a post if anything is unclear. I've added a link to the wikipedia page onto my answer to "How could humans have interbred with Neanderthals if we're a different species?"

I opened a new question: https://biology.stackexchange.com/questions/72521/usage-of-lineage-over-species
Not sure if it's not against the rules, since it looks kind of personal.

I think it is totally fine to cite someone (whether the cited text was published on biology.SE or anywhere else) and ask for more information. Don't worry about that


text:
Which information can be extracted from time course RNA-Seq Data?
So I am very new to the area of biology so I am sorry if this is a stupid question.
I have RNA-Seq data carried out over a span of 100 days and I have gene expression data in the following format. Each expression value is the mean of
3 replicates.
           Day 1         Day 10     Day50     Day 100
Gene 1      12             42         35       12
Gene 2      50             53         23       100
.           .              .          .        .
.           .              .          .        .
.           .              .          .        .

so on, the above data is just something I came up with, but can you tell me what information I can extract from this type of data ? Such as differential gene expression. Thank you very much

Note that there is also a bioinformatics.stackexchange.com site.

It can be complicated because RNA-seq data is looking at gene expression, in the form of mRNA. But there are thousands of housekeeping genes that are expressed constantly, as long as an organism is alive. So the real interesting genes in a time course are those that are differentially expressed. So gene 1, in your example is not that interesting. Gene 2 however shoes a 4-fold increase between day 50 and day 100. Still, that is not that huge. You need computer programs to sort all this out. But what you want is to be able to associate a huge change in mRNA (gene expression) that can be distinguished from background.

Hello Karl, thanks for your answer, I need to mention that each expression value I have is the mean rpkm value of 3 replicates. So the change in expression is not due biological noise. Yes, I was thinking of using R to perhaps classify the genes by the time points during which they have maximum expression.

Even though there are replicates that doesn't mean you've eliminated noise -- just reduced one of the many different sources of noise. You should have data for housekeeping genes that you can use to normalize gene numbers against; see for example this question and answer

I have never seen people extracting data from data, maybe you meant which type of information you might want to extract and the answer is "genes differentially expressed". You should check whether your data are normalized or not if they are you can use popular R package like DEseq2 or Limma to detect genes differentially expressed. In case your data have not normalized these tools have the proper way to normalize your matrix.
Here is the link of limma:
https://www.bioconductor.org/packages/devel/bioc/vignettes/limma/inst/doc/usersguide.pdf
at page 46 you have an example of how to handle with time-course analysis

Yes, that is exactly what I mean, I want to know what information I can extract. But since each data point is the mean of 3 replicates is it possible to find the differentially expressed genes? Thanks for the lead on DESeq and Limma !!

Yes, of course, you can, it would have been better if you have all the replicates for each sample, but you have to do with what you have unless people in the lab can give you the raw data. Please check the new answer. I have pointed you to which page you have to go to perform the analysis.

if this reply answered your question, mark the question as answered. Best


text:
How to troubleshoot in vitro formaldehyde fixation for nucleosomes?
For an experiment, I am trying to fix the mononucleosomes (100ng) using formaldehyde as crosslinking agent in HEPES buffer. I have been using 2% formaldehyde in a reaction buffer containing 1mM EDTA, 25mM NaCl and 50mM HEPES, pH 7.5 (same as nucleosomes suspension buffer) to fix mononucleosomes.
In my first reaction, I added 100ng of nucleosomes, 2% formaldehyde and incubated at 4degC, 30', then I added 0.4% SDS and incubated for 30' at RT. I observed less intense but equally sharp band for nucleosomes (less smear) as compared to unfixed nucleosomes.
When I performed the same reaction again, the gel showed a huge smear covering the entire lane instead of a sharp band.
I have been reading about the fixation reactions and encountered an emphasis on using methanol free formaldehyde (while I was using 10-15% methanol containing formaldehyde). Do you think that can be one factor for not being able to get similar results?

Same reaction protocol giving undersirable result may simply be because of some sample prep errors. See this protocol. The final concentration of formaldehyde is 1%. Most protocols suggest that formaldehyde be prepared fresh. This is because formaldehyde gets oxidized to formic acid.

Thanks for the suggestion. The chance of adding errors while making the reaction is relatively constant since I prepare it in the same manner, every time (except for the pipetting errors). I agree with you about the oxidation of formaldehyde. The protocol you suggested uses 11% of final formaldehyde, is it because they are using certain mammalian cell lines?

Their fixation buffer contains 11% formaldehyde. They add 20ml of this buffer to 200ml of cell suspension. So final concentration of formaldehyde is 1%.

Yeah, I figured. Thanks though.

Since formaldehyde is the matter of discussion here, I wanted to ask that I have an 1ml aliquot of pure formaldehyde sealed with inert gas in a glass. Now, in one reaction I am only using 10ul from that 1ml. Ideally since these aliquots are for  one time use, I shoud discard remaining 990ul but if I want to store, is there a feasible way to preserve the rest of the formaldehyde while taking care of its exposure to air?

That is a different question and should be asked in [chemistry.se]. That said, I think that most people who do these experiments prepare "fresh formaldehyde" by heating paraformaldehyde solution. You should look at the protocols for more details.


text:
Knockout and knockdown of gene
Out of curiosity, I got this question whether knocking out (deletion) of a gene on one side and knocking down (RNAi) of the same gene on the other side will affect the cell in a similar manner or not.
If not why?
If yes, is it applied to every gene?
Knock out of a gene will correspond to no expression (gene deletion) in the cell, which can be appropriate to confirm the functional specificity, to observe processes which are affected in its absence and some other processes which are compensating the absence of the gene.
Knockdown of a gene will result in expression defect by decreasing the level of the transcript (mRNA silencing).
Now, the points which I am wondering upon are:

no mRNA presence and silenced mRNA will create two different environments for the cell to deal with or not.
whether the whole amount of transcript should be targeted to have the same phenotype as of gene knockout.

As I understand KD, it is a significant reduction of gene expression (the gene is "down"), while KO (in a homozygote/haploid organism) results in no expression of the gene (it is "out").

@abukaj This sounds like a good start for an answer. Why don't you write one?

This is a fascinating set of questions.  The only one I can comment on is: is KD qualitatively similar to KO?
My answer is: sometimes yes, in general no.  To understand why, I like to think of a hypothetical plot of "phenotype of interest" on the y axis, and "expression of gene" on the x axis.  You can imagine that this plot could be monotonic, i.e. that the phenotype continuously increases or decreases as expression increases.  Or it is also possible that this plot could have one or more minima or maxima in it.  One example of KD giving dissimilar results from KO is for essential genes.  If they are knocked out, they of course kill the organism.  However, there may be some levels of essential gene knockdown for which the phenotype is actually increased relative to wild-type!
I will selfishly share one of my articles where I observed something like this.  We found that ADH1 knockdown improves butanol tolerance in yeast, but that ADH1 knockout was highly detrimental to butanol tolerance.  http://dx.doi.org/10.1007/s10295-015-1713-7

Naively you would expect that they should have about the same effect, but in reality a lot of things can happen. Gene knockout can induce compensating upregulation of other genes and RNAi can have off-target effects. See e.g. this paper
"Genetic compensation induced by deleterious mutations but not gene knockdowns" https://www.nature.com/articles/nature14580

As I understand KD, it is a significant reduction of gene expression (the gene is "down"), while KO (in a homozygote/haploid organism) results in no expression of the gene (it is "out").
Quoting Wikipedia:

Since RNAi may not totally abolish expression of the gene, this technique is sometimes referred as a "knockdown", to distinguish it from "knockout" procedures in which expression of a gene is entirely eliminated.


text:
What does (deaths / (resolved + deaths)) describe in an emerging epidemic?
It would seem in a emerging epidemic, where the time to resolve a disease is long, an evaluation might be used such as:
(predictive mortality rate) =  (deaths) / (deaths + resolved)
Is this a standard metric?  And if so what is it called?
It would seem that this kind of metric would be a predictor as to the ultimate mortality rate, unadjusted for treatment advances. The intent is to describe the demonstrated mortality of those who have acquired the disease, without influencing of the number of people who have acquired the disease.  This would be helpful where R0 is large and/or Specific Interval is small. However I cannot find references to a metric similar to this.  Pointers appreciated.

The problems with the measure you've proposed have been addressed on MedicalSciences.SE:
https://medicalsciences.stackexchange.com/q/20970/8728
The short version is that this measure isn't very informative while there are unresolved cases, because it ignores what is known or expected about those unresolved cases, and it is not a standard measure.
In the long run (when almost all cases are either recovered or dead) it approaches the case fatality rate because the denominator of (resolved + deaths) becomes equal to the total number of cases. Until then, it doesn't tell you much at all.
You could track the case fatality rate over time based on time of initial diagnosis to look at effects of new treatments.


text:
Best fundamental books?
I’m looking for internationally applauded  textbooks on fundamental biology. Books that are a must for a pre-medicine student/high school advanced. Currently, I study Biology by Neil Campbell, Jane Reece(and team) and I really like it. What I’m looking for is 21st century pedagogy and a modern writing style(as opposed to a stiff, unfriendly writing style that reads like a fact presentation pamphlet); books so good you don’t need an amazing teacher(which I definitely do not have.) Thanks.
P.S.- If you have come across amazing books in branches of biology like say biochemistry or neuroscience or immunology, even those suggestions are welcome.
P.P.S- My question is distinct from the “Books for beginners” question asked by user31782 because: 1.cost is no bar 2.I am not a beginner in biology, I’m studying pre medicine; and 3.All the resources suggested in the answers, I already know about them/have used them.

How can one study pre-medicine (note the hyphen)? Or is this an example of the modern writing style you yearn for? And as for 21st century Pedagogy, sounds like a film company or a rock band. I would suggest that you explain yourself more clearly.

@David, a number of universities require a year of basic biology, biochemistry, calculus, biostatistics and psychology after high school for admission to medicine. That preparatory year is called pre-medicine (hyphen duly noted). Pedagogy means the method of teaching; both an apathetic school teacher and an ivy league professor know that DNA is transcribed into RNA and RNA is translated to protein, but their methods of presenting that to a student is what creates the difference. That’s where pedagogy comes in.

My criticism of your use of words is because the lack of precision makes your request unclear, so that all that happens is people express opinions about books they like or use, which is both off-topic here and does not answer your question. Pre-clinical medical courses differ throughout the world and within countries (and in some ‘21st centurary pedagogy’ has replaced them completely by ‘problem-based learning’ — although this is clearly not what you mean by the term). The problem is that the adjective you use describe your emotions towards the books, rather than the books themselves.

To clarify further: What do you find ‘amazing”? (Do you really mean this or just good?) How is a book ‘unfriendly’? (Author frowning in photo?) What do you consider a ‘modern writing style’?  And when you have ceased to be a beginner, biology is not a single subject. Do you want to understand one branch at a less superficial (more chemical and mathematical) level, read something in which the science is related to medicine, or be inspired to do something about the apalling maternity mortality statistics in the US? Or do you, like most students, just want a book to pass an exam? Tell us.

For fundamental mammalian cell biology, and molecular biology, and fundamental biochemistry: "The Molecular Biology of the Cell" by Bruce Alberts and colleagues.
It is mostly written for first semester students at university and thus summarizes the basics in a very clear way. Moreover they state whenever findings have some ambiguity, and they use many nicely drawn pictures to convey abstract concepts.  Despite its approachability it covers most fundamental topics of many domains (also diseases).
While the ~2,000 pages of the complete edition might seem a bit intimidating they rarely provide unnecessary detail, and the individual chapters are written in a very concise way (even allowing you to skip some of them).

Biology by Brooker (and now additional authors Widmaier, Graham, and Stiling) 4th edition is one which I used, and I quite liked it. Great presentation of information, in my opinion.
Textbook of Medical Physiology by Guyton and Hall, though not friendly, is a decent book.
I mostly have recommendations in the field of biopsychology, etc.
Neuroscience: Exploring the Brain by Bear, Connors, Paradiso (2016 ver) is colourful, inviting and VERY friendly! Great for high school advanced or pre-med, though I suppose if you want more details in neuroscience, you'll need something like Kandel.

Have you ever had a chance to compare Neuroscience by Bear, Connors and Paradiso and Neuroscience by Purves, Augustine and Fritzpatrick? Are they the same level or one is more in-depth than the other?

Both seem to be on more or less on the same level. Presentation of the matter is better in B,C,P. Neuronal signalling is really good in P,A,Z, as in, it goes pretty in-depth. If you're a high-school student, I'd recommend B,C,P as your text book and P,A,Z as a reference book because B,C,P teaches better and that is what you want.

I really like The Molecules of Life: Physical and Chemical Principles from John Kuriyan. It does a good job of introducing basic to intermediate principles in biochemistry. In particular it is a great introduction to protein biochemistry and pharmacology.

I just got the book last month, I find it very helpful. Thank you.

My pleasure. Good luck!


text:
Can someone identify this spider?
Saw this on the street in the UK. To my eyes it looked and moved distinctly tarantula-y (although I don't have any firsthand experience with them) which I'm pretty sure we don't have any of natively. Most of the spiders you commonly see here are thinner generally and move much faster. This guy lumbered.
For scale, it didn't span more than a couple of inches.

@Charles Did you want to post this as an answer? Having researched more thoroughly, I think you probably linked the exact species.


text:
What causes the blue color seen in baboons?
Based off of this question from Worldbuilding SE.
In that question, I talked about how the scrotum and buttocks of various animals have a blue color because of thick deposits of collagen in those areas. I wanted to make a race of elves that used this mechanism to achieve blue skin all over their body.
Now, I thought that the thickness of the collagen layer was what was behind the structural coloration of animals like baboons and vervet monkeys. However, I have since learned that it is also the way the collagen is arranged that makes that color occur. That made me think that to achieve my desired effect, I wouldn't need to make the skin exceptionally thick. I could just rearrange the collagen humans already have and not change the thickness at all.
I'm having a hard time understanding the underlying mechanisms behind what makes the arrangements of collagen different, and why it wouldn't occur over the whole body.
Thus my question is twofold:

Is it the structure, or the thickness of this collagen layer that makes the structural color work?
Does the way the collagen is structured in these areas make the skin function differently than normal skin? (I.e. Is it less stretchy? Is it more fragile?)

(I'm sorry if this is off topic, I was thinking that since the focus of the question is on how the collagen works that it would be better suited here than on Worldbuilding)


text:
E. Coli metabolization of paracetamol
For my science fair project, I did an experiment on how paracetamol and ibuprofen affected the growth of bacteria. By day 5, however, parts of the paracetamol blackened (image below). I am wondering if E. Coli can metabolize paracetamol and if so, what operon in the K-12 genome is responsible for this.

EDIT: I realized it may be metabolizing other ingredients in the medicine I used. I am including a list of the ingredients in the medicine I used.
Acetaminophen 160 mg in each 5 mL (duh)
Other ingredients (33.015873 mL):

Anhydrous citric acid
FD&C red no. 40
glycerin
high fructose corn syrup
microcrystalline cellulose and carboxymethylcellulose sodium
purified water
sodium benzoate
sorbitol solution
sucralose
xanthan gum

I thought it might be the fructose, but is the byproduct really black? Still confused...

I thin, you are using blood agar plates, isn't it? In this case, it could also be the heme which can cause the black colour.

No, the medicine I used colored the agar red. I used regular agar.

Is it possible the dye changes colour as the pH decreases?

Sorry that my answer is not a real answer, but this would be a good starting point for some more science.
Several of the questions you might ask and could answer (with some more experiments):

Does this happen in plates without E.coli?
You have a contamination on the right side, perhaps also on the black part. Could this be the culprit? Only half the plate is black, the rest is (still?) red.
You used a paracetamol tablet with red dye and a lot of sweeteners, does the same thing happen if you use one without the red dye? A dye would be a likely source, because it already contains an absorbing moiety. It only needs to be slightly modified to absorb different wavelengths.
What kind of agar are you using exactly? There are many kinds, often selecting for certain types of micro-organisms, with indicators for pH or other colored markers to detect and identify strains.

For your metabolic question you can take a look at https://ecocyc.org/ where you can find a database with all known metabolic pathways for E.coli K12. Unfortunately I couldn't find anything for paracetamol (or synonyms) but you could try to see if it produces a colored product for any of the additives.


text:
Anaerobic Respiration vs Aerobic Respiration during physical activity
So I was wondering about the difference between aerobic and anaerobic respiration on the context of burning calories. While swimming we can choose to keep our head up and breathe, or keep our head below water for a stretch. Which will burn more calories for that time and why? And does anaerobic respiration cause fatigue of the brain due to insufficient oxygen?

Anaerobic respiration releases much less energy than aerobic respiration. Anaerobic respiration leads to a buildup of lactic acid in muscle tissue, which can feel like fatigue. Swimming is an aerobic exercise whether you head is at the stage of being under or over water. Exercises that count as anaerobic are those that require a lot of energy being produced by the cells in a short time (like sprinting).

@P.SN yeah but ultimately it is incomplete breakdown of glucose due to less oxygen availability... Shouldn't it affect the brain also?


text:
How do you find probabilites of carrying an X linked recessive disease in a blank pedigree given only one phenotype?

In the above pedigree, the black square indicates the male
affected with Hemophilia which is a X-linked recessive trait. What is the
probability that the proposed child, which is a male (indicated as ?), will carry the disease?
I started off by trying to figure out the probability that the sister has an X chromosome carrying the disease, which I got as 10/16 (Since the mother must be XcXc or XcX and the father either XY or XcY; possible genotypes are XcX, XcX, XcXc, XcXc, XcX, XX, XcXc, XXc)
I then repeated the procedure for each generation and got the final answer as 9/16. However, the correct answer is 1/8. How do you obtain this? Are my assumptions flawed?
Source: https://biolympiads.com/wp-content/uploads/2016/08/inbo2009-Q.pdf

Assume the disease is rare. The parents of the affected male are thus probably X/Y and Xc/X. Their daughter (the sister of the affected male) has a probability of 1/2 of being a carrier (Xc/X). Her daughter also has a 1/2 probability of being a carrier. Her son has a 1/2 probability receiving the mutant X chromosome. Therefore, the probability that the son is affected is 1/2 * 1/2 * 1/2 = 1/8.
I can’t right now, but I’ll try and make it clearer with a figure tomorrow.


text:
Measure of relatedness between two animals
So I am aware there is such a thing as inbreeding coefficient which is a number allocated to an individual as a result of taking the average of it's parents' inbreeding coefficient.
(Note that I am working in terms of pedigree based relatedness, not genomic relatedness.)
Is there a number that quantifies the relationship level between 2 individuals?
If so how is this calculated? Can it be done in R using the pedigree package?
Where say a sire and ewe have a 0.5 value or something similar?

There are about an 25 thousands ways to measure relatedness between two individuals. The most obvious coming to mind  based on your description is the coefficient of relatedness. Relatedness is the probability that two individuals share an allele due to recent common ancestry. There are probably tens or hundreds of online tutorials. Consider this one for example.

I believe a good word for what I am after is "kinship," or a "kinship matrix."

Consider having a look at the kinship2 package.


text:
Measuring Enzyme Kinetic constants
Is it possible to experimentally determine $k_1$ and $k_{-1}$ of the Michaelis Menten model:
$\ce{E + S <-->[k_1][k_{-1}] ES ->[k_{cat}] E + P}$,
or their ratio?


text:
What is this grainy surface on my two-week-old sourdough starter?
I'm baking bread at home as a hobby, using sourdough. After skipping one baking day, I haven't used my sourdough starter for two weeks. When opening the jar in which I keep it, I saw the surface had taken on this unusual look. When viewed from the side through the glass, the contents looked normal below the surface.
The sourdough starter consists of whole rye flour at 100% hydration (flour:water = 1:1). I had removed it from the ripe sourdough on the last baking day and have since kept it in the refrigerator with a lid (only loosely screwed on) for 13 days.
Normally I'm using it already after keeping it for 7 days, and I'm used to the surface turning light gray and dry (but smooth and soft) after that time, which didn't ever seem to be a problem. Now the color of the surface was identical, but it has become grainy, like tiny worms.
I have removed and discarded the top layer (3 mm). It was soft (unlike dried out, crusty, dough) and smelled a bit like fresh yeast. Below that, the contents smelled normal, like very ripe sourdough.
The jar is about 6 cm in diameter and was filled to about 2 cm (→ volume of the starter ≈ 60 ml).

What are we looking at here? Could it be actual yeast cells (or other microorganisms normally found in sourdough)?
Is it harmful?

After 13 days (click for full-resolution version)
Reference pictures
After only 2 days, the starter looks like this:

(click for full-resolution versions)

You're not seeing cells, as you would need a microscope to see them.

I'm not talking about whether we are seeing individual cells. It is clear to me that a single cell is too small to see with the naked eye. But if there are many cells forming colonies, we can see them. My question is if a colony of yeast or other organisms found in sourdough would look like in my picture.

Thanks for the link! I hadn't seen that before, it looks very similar.

Naturally, when you create dough you expect it to rise in size the following few days. That's just a chemical reaction that allows air to enter the dough body and traps it in tiny bubbles. My theory is that if the dough is not as high as expected that the air has escaped it because of the extra time you left it.
The pattern is not unusual and is the result of the deflation I'm talking about.
It's probably still safe to eat, but the bread won't be as good(eat at your own risk)

The sourdough starter doesn't rise much (because it is taken from already ripened sourdough) and collapses relatively soon after 2 or 3 days. But then the surface is still glossy and darker as in the picture I've included. The starter collapsing is not the issue here.


text:
Are there biological reasons why life expectancy is lower for men in most countries of the world?
I've been checking life expectancy figures for men versus women in many countries of the world and the figures for men sometimes are terrifying. Countries like Russia have a 12 years gap in disfavor of men. Developed countries have usually a 4-5 years gap in disfavor of men. My country Argentina has a 7 years gap. African countries and middle east countries where supposedly women have a harder life because of religion have usually a 3 years gap in disfavor of men. So far I haven't found a single country where men lives more than women.
Now I know there are more men than women who dies in homicides, suicides, work accidents, wars, etc. men are more likely to get addictions because of depression, etc. but aside of all that, is there any biological reason why men lives less than women everywhere?

Here is a recent review: http://www.cell.com/cell-metabolism/pdf/S1550-4131(16)30237-6.pdf

If I recall correctly from my US history class, in colonial America the life expectancy for men exceeded the life expectancy for women, but you are correct about the general trend.

Three little words... "Hold my beer".

@omegacron Non true. Women now drink as much alcohol as men, global study finds https://www.theguardian.com/society/2016/oct/24/women-drink-alcohol-men-global-study

@Pablo You missed Omegacron’s point - it refers to the effect of testosterone (and alcohol) on men’s judgement. See: The 21 Greatest Moments In "Hold My Beer" History

There are both biological and  social factor for that:
Biological

Females have two X chromosomes. When mutations in genes of the X chromosome occur, females have a second X to compensate. Males, on the other hand gave just one chromosome X and all genes its genes express themselves, even those lethal or deleterious.
Females have better resistance to biological aging and hormones and the role of women in reproduction are known to be associated to greater longevity (e.g. estrogen offers some protection against heart disease because it facilitates elimination of bad cholesterol while testosterone has been linked to violence and risk taking).
The female body evolved to accommodate the needs of pregnancy and breast feeding hence deals better with making reservation. This ability has been linked to a female's better ability to cope with overeating and eliminating excess food

Social
This "advantage" women seem to have was once nullified by the status and life conditions they had back then, as the risks and the burden of pregnancy and the lack of attention to health and rights women had in a way more misogynist world.
Given the economic, social and political changes that the world experienced, a general progress in female life conditions took place and women have not only regained their biological advantage, but have gone beyond it, achieving higher life expectation. Social and comportamental factor are involved in this higher longevity:

Women tend to engage in fewer risky and bad for health behaviors than men do, e.g. men have more problems than women with alcoholism, smoking and road accidents.
The world is still very sexist and the gender roles to be played would expose men to higher risks. Regarding to work, for instance, although women nowadays participate in the work force, their professional activities remain different and are less prejudicial to their health (on average).
Also regarding to  very sexist gender roles, men are expected to be strong and manly and powerful and women are expected to be gracious young and beautiful. As a result of that, women are more attentive to their body and health, engage themselves in more healthy activities and benefit more from medicine and science. Men on the other hand submit their bodies to challenges from early ages and tend to neglect their bodies needs.

You can have access to detailed statistics (male/female, country by country, life expectancy and other health data) here:
http://www.who.int/gho/publications/world_health_statistics/2016/Annex_B/en/
And also, read more about the issue here:
https://www.scientificamerican.com/article/why-is-life-expectancy-lo/
http://www.who.int/mediacentre/news/releases/2016/health-inequalities-persist/en/
https://en.wikipedia.org/wiki/List_of_countries_by_life_expectancy#cite_note-10

Do you have research to share that supports your claim that "women have not only regained their biological advantage, but have gone beyond it"? In general, the answer could benefit from references in the scientific literature on the issue. The only one of your references that is not just stating the existence of the phenomenon, is the one from Sci. Am. that @rotaredom linked before you, and we have no way of evaluating it as there is no scientific literature cited in it. That is especially true for the discussion on the social factors you mention, which does not sound scientific at all.

Good answer, could you clarify the line "and all genes its genes express themselves"?

@vkehayas considering social "sciences" dont use the scientific method because many times they dont do experiments but try to assert their theories with observations or interpretations, or they dont use valid methods for validation because they cant isolate what's going on in the mind, because there are no tools for doing so, asking for an answer in regards to social disciplines to be "scientific" is asking for the impossible.

@Pablo I thoroughly and vehemently disagree that social sciences cannot be scientific a priori! I only disagree with the verbiage used in the linked article, and consequently the answer since it is basically echoing the points therein. The issues can be in principle empirically addressed but I found no evidence in the linked article. Also my request for references was for the whole answer, as none were given for any of the claims made.

I also disagree that social studies are not science and are not done with scientific methods. @vkehayas, life expectancy studies in past years are not easy because this data were not recorded in early ages. But this conclusion comes from interpretation of a few data (e.g. life expec in  royal family of Wales and their related ones, which shows that men in early ages lived longer)... There is also a very well known issue: maternal death. Nowadays, every day, more than 800 women die from pregnancy or childbirth related causes. Can you imagine how it was in early ages?

Also, there are some studies linking higher female mortality with traditions leading to discriminatory treatment against females... If I'm not mistaken they were gave India as example, but this is a real issue everywhere

Mortality aside, and selective breeding aside, is there also a reason why there are (naturally) more males are born than females? Is the gestation period changing over time?  Women live longer? These questions reach back to hunter gatherer times when "work accidents" were probably somewhat more serious.

It's arguable that the greater risk-taking of men is attributable to testosterone and other biological differences, as well.

Women have two X chromosomes but only one is active in each cell, see Barr body - https://en.wikipedia.org/wiki/Barr_body

I found this article https://visual.ons.gov.uk/how-has-life-expectancy-changed-over-time/ . Life expectancy for women was higher than men 2 centuries ago. Now the gap duplicated.

Is there a reference for "This "advantage" women seem to have was once nullified by the status and life conditions they had back then, as the risks and the burden of pregnancy and the lack of attention to health and rights women had in a way more misogynist world. Given ... changes that the world experienced, a general progress in female life conditions took place and women have not only regained their biological advantage, but have gone beyond it, achieving higher life expectation." @Pablo lists evidence the gap still favors women in less developed countries today & developed ones in the past

@Silverfish - as a wholly random single (out of hundreds) examples, look at funding and attention for breast cancer vs prostate cancers.

@Silverfish - another one is that the much-mentioned in the answers risk-taking isn't only biological (testosterone) but also social (sexual competition between males). This is largely sociological, based on what kinds of mates women choose to both date and procreate with (compare: Mick Jagger vs. Bill Gates).

There are a lot of factors playing in here.  You've pointed out the surface reasons that can sometimes contribute: work accidents, style of life, etc.  However, there are biological causes as you suspected.
Probably the most obvious has to do with the difference between their hormones.  Testosterone (male hormone) is associated with violence and risk taking.  This would tend to contribute to men having at least a slightly shorter lifespan.  Estrogen, on the other hand, is associated with the removal of cholesterol from the blood.  This may lower the risk of females dying from heart diseases, raising the average female life span.
Some hypothesize that a large section of the difference simply comes from lifestyle resulting from those hormones, per American Scientific: Men tend to want to be caricatured as strong and tough (result of testosterone), whereas women tend to be more concerned with maintaining their bodies, keeping themselves beautiful, etc.  Obviously, this is hard to measure in a conclusive way, so scientific articles and measurements are hard to produce.
However, there are also diseases which men are more prone to because they can lose the Y chromosome in their blood (this is suspected to be induced by smoking, along with other potential causes), such as cancer, and even some forms of Alzheimer's.
Edit:
Another reason hypothesized that women tend to last longer than men is that they are less prone to serious genetic mutations on the sex chromosome, since they have a double X instead of two totally different XY chromosomes (See Why women live longer than men: Sex differences in longevity (2006) by Steven N. Austad: Gender Medicine 3(2): pp. 86-88).

It is noteworthy that sex differences occur for infants as well, so I'm not sure that a behavioural explanation like this explains the phenomenon. Your paragraph starting "A large section of the difference..." should be backed up by research papers, otherwise you may be accused of parroting the stereotype-promoting language used in the Sci.Am. article you linked to. An alternative theory is that lifespan simply depends on body size

@vkehayas you have a very good point.  Unfortunately, I have to run for a biology seminar right now, but I'll try to scratch up some references afterwards.  :)

Men get a lot more heart attacks. Perhaps 2% mortality per year after 50!!! https://archive.cnx.org/resources/b32e423e49c72ec63021d4c65847d375433a2888/CNX_Psych_14_03_HeartAtt.jpg   ..............
https://www.google.fr/search?q=heart+attacks+in+men+vs+women&num=100&source=lnms&tbm=isch&sa=X&ved=0ahUKEwiT7_S57Y7XAhWQDRoKHdZYBlEQ_AUICigB&biw=1026&bih=606#imgrc=9KXzzK1p17V8tM:

One reason for that delay in onset of cardiovascular disease could be that women are relatively iron-deficient compared to men — especially younger women, those in their late teens and early 20s — because of menstruation. Iron plays a very important part in the reactions in our cells that produce free radicals, which damage cell membranes and DNA, and may translate into aging the cell. Postmenopausal women lose this benefit https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2821138/
Here is a well researched article on why women live longer than men https://ourworldindata.org/why-do-women-live-longer-than-men

One of the dominant causes of death is atherosclerotic heart disease. Males are susceptible to this disease for their entire adult life with atheroma detectable as early as late teens and twenties. Females are moderately protected from developing this disease until menopause and the decline of estrogen, etc., after that point, they develop ASCVD as well. Therefore, if average duration f ASCVD is 20-30 years until death, men die in their 50-60's, women in their 70's-80's.