text:
If longer wavelength color is perceived faster by human, what about non-spectral color (black)?
Related to human vision, I read the hypothesis about how longer-wavelength color is perceived faster by human eye than shorter-wavelength color source : A Brief Classification of Colour Illusions. But what if the other color is a non-spectral color like, black ? Black is achromatic color, it's the absence of colors and has no wavelength. Does this perception hypothesis still apply ?
Because I've been doing a color comparison by putting a layer of colors on top of each other. In this case I tried with black - green (~549nm) and black - yellow (~570nm), and it seems like black is always dominant against other colors. But I can't find any scientific reference for this. The closest I found is the hypothesis I mentioned before. Any suggestion ?

It would be helpful if you provided a citation for your claim about faster longer-wavelength perception. It's also not at all clear what you mean about putting a layer of colors on top of each other. If you are talking about absorbance, then yes of course, black is always going to dominate because it absorbs everything else. It doesn't matter what other color is there, when you see an object that has color that's based on the light reflected off of it. It has nothing to do with perception speed.

Hi, I've updated my question. So I've been doing some kind of experiment by putting a different color pattern for each eye to see. Because human vision will see the scene from 2 eyes as a whole one, so they will perceive these 2 colors overlap with each other. What I'm trying to find out is the information about color perception according to human vision. In case if there's black in the pattern, why is it always dominant when it's overlapping with other colors ? I hope I explain clearly.

Might be nice to post some of those illusion pictures; I have an idea of what you are talking about now thanks to the link you provided, but previously it was unclear from the text. Thanks for the edits

Thanks ! I'm not sure to put one of that illusion picture. I'm afraid it will mislead because what I've been doing is quite different. Not some kind of optical illusion.

Oh okay - still it might be helpful to show what you're doing. After all, I thought you were creating illusions similar to what was on that page. It's going to be hard for someone to help you with a hypothesis if they don't know what phenomenon you are trying to hypothesize about.

That link is not about perceiving some colors faster than others, so that reference is misleading, or distracting at best. What do you mean with faster? Quikcer, or perhaps better?

I couldn't find any mention of wavelength-dependent latencies in perception


text:
Can light destroy auxin?
In my biology textbook, it says that plants grow towards light because auxin is laterally transferred from the light side to the shaded side, so more auxin stimulates growth and hence the plant bends towards light. My textbook also specifically states that light doesn't destroy auxin. Yet, recently I searched online and find that light will actually destroy auxin by photo-oxidation. I am confused, can someone tell me which is the correct mechanism (or both)? Thanks!

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RNA polymerase and DNA helicase
Is DNA helicase or RNA polymerase responsible for breaking the hydrogen bond between the 2 strands during transcription for eukaryotic cells? My textbook (WJEC Biology for AS level) says it is DNA helicase that breaks the hydrogen bonds while RNA polymerase catalyses the formation of bonds between RNA nucleotides.

The enzyme DNA helicase breaks the hydrogen bonds between the bases in a specific region of the DNA molecule. This causes the two strands to separate and unwind, exposing nucleotide bases. The enzyme RNA polymerase binds to the template strand of DNA at the beginning of the sequence to be copied.

However, when I searched online, for example on https://en.wikiversity.org/wiki/Effect_of_hydrogen_bond_on_RNA

Transcription can be explained easily in 4 or 5 simple steps, each moving like a wave along the DNA. RNA polymerase unwinds/"unzips" the DNA by breaking the hydrogen bonds between complementary nucleotides. RNA nucleotides are paired with complementary DNA bases. RNA sugar-phosphate backbone forms with assistance from RNA polymerase.

Then do RNA polymerase break hydrogen bonds? If RNA polymerase can break hydrogen bonds between strands then what is the role of DNA helicase in the transcription process?

Good. I was answering the question while you were updating your answer, but I hope it clarifies things. Read the section of Berg et al. carefully. Successful text books are big earners for publishers, who put a great deal of effort checking each new edition. So you are likely to get a clearer account from such texts. The only problem is fast-moving fields where the material goes out of date. Wikipedia entries can be a dog's breakfast.

Disclaimer
As I have pointed out in my comment, it is not clear whether the sources mentioned relate to eukaryotes or prokaryotes, assuming they are correct. I am a translation man, rather than a transcription man, and so am answering this from the 2002 edition of Berg et al. ‘Biochemistry’, as I happen to have a copy of my own (a freebie from when I was still teaching) and this edition is freely available online. List members with more expertise in this area are encouraged to post comments to correct any errors in my answer or supply updates.
Answer

in neither prokaryotes nor eukaryotes is the DNA helicase that operates during DNA replication involved in transcription although other proteins necessary for transcription have DNA helicase activity.
In prokaryotes it appears that the RNA polymerase holoenzyme (made up of just four subunits) is responsible for unwinding about 17 base-pairs of template DNA. Quoting from Section 28.1.3:

Each bound polymerase molecule unwinds a 17-bp segment of DNA, which corresponds to 1.6 turns of B-DNA helix

There may be some ambiguity caused by the description of how this value was determined experimentally as it involved addition of topoisomerase II. However it is clear from discussion elsewhere that this is an enzyme of DNA replication and is not involved in transcription.
In eukaryotes transcription is much more complex, involving separate polymerases for different classes of RNA product and a variety of auxiliary transcription factors in the case of RNA polymerase II, which transcribes mRNA. According to Section 28.2.4:

The TATA box of DNA binds to the concave surface of TBP [the TATA-box-binding protein]. This binding induces large conformational changes in the bound DNA. The double helix is substantially unwound to widen its minor groove, enabling it to make extensive contact with the antiparallel β strands on the concave side of TBP.

So the initial recognition of the TATA box causes some unwinding. However the major player appears to be transcription factor TFIIF:

an ATP-dependent helicase that initially separates the DNA duplex for the polymerase

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PFU/mL count formula in the virus plaque assay
I do virus plaque assay on the cell culture layer. The source of the virus is an animal tissue homogenized in a culture medium (stock). Sometimes I should make series of x10 dilutions, 10ul from stock+90 ul medium and from it again, 10 + 90 medium. So, I have x100 dilution. From that, I plate 0.2 mL. I have got n = 12 plaques, I need find PFU/mL in the stock.
I was told to use formula
PFU/mL = (n * 10e6)/0.2 mL
Could someone explain where 10e6 comes from?
In the case I had m-fold dilution, my formula is next:
PFU/mL = (n * 10e6*10e-m)/0.2 mL
So, my PFU with 1/100 dilution = (12 10e610e-2)/0.2 = 6*10e5 per mL
If I would have 12 plaques at 1/1000 dilutions, that because stock has 10 times more virus, that I am expecting from the formula, but I get:
So, my PFU = (12 10e610e-3)/0.2 = 6*10e4 per mL
What results of my formula is showing to me?
How calculate the initial stock PFU/mL?

Welcome to the Biology Stack Exchange. Please take a [tour] and visit the [help] for more information on this site and how it works. You should also note the [homework policy}(https://biology.stackexchange.com/help/homework) and as such - have you looked up the formula and do you know what each component of the formula means? It looks to me like you are just working blindly off someone else's notes... It is always better to go and understand the fundamentals before attempting something.

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Which approach is the common one in the literature for determining the bacterial growth rate?
I have the following data, which is OD600 (the second component) vs. time (the first component):
data = {{0, 0.046}, {40, 0.111}, {80, 0.291}, {120, 0.808}, {160, 1.742}, {200, 3.319}, {240, 5.017}, {280, 5.503}, {320, 5.897}}

I want to obtain the growth rate of bacteria from the above data.
If I fit a logistic function, that is, $$f(t) = \frac{L}{1 + e^{-k(t - t_0)}},$$ where $k$ is the growth rate, I obtain the following curve:

In this approach, the growth rate is: $k = 0.028$.
Now, if I fit the natural logarithm of the logistic function to the natural logarithm of OD600, I obtain:

In this case, the growth rate is: $k = 0.025$.
Which of these values (or, approaches) is the correct and common approach for determining the growth rate of bacteria?

Welcome to Biology.SE. I’m voting to close this question because this isn't really a biology question — it seems closer to statistics to me. Some questions for you: How much uncertainty is associated with each of the estimates? Based on that are they actually different answers? When measuring things you typically aren't finding the "correct value" you are estimating (with some amount of error). For details see the [tour] and [help] pages starting with [Ask] questions effectively on this site.

@user68022, this seems to be a continuation to the/your question on MSE. I also think that the question is not about biology or directly related to biology (even after your edit), but falls under data analysis/statistics. You have clearly defined your model, which is a nonlinear model. You have also clearly defined $k$. Therefore, there is no question anymore about what $k$ is because you have defined it in your model. What remains is how to properly estimate $k$.

If  given a chance, I would prefer the first approach. Reasons being: It looks similar to a normal Bacterial growth curve ( I can see different phases lag, log etc.), Easy to track the growth pattern, easy to understand.

@Domen tyersome I strongly disagree, and attitudes like yours generate a lot of terrible data-handling in biology papers that I read.

@jakebeal, I don't understand: Which part of my comment is it that you strongly disagree with? I don't see how your answer (below) contradicts with anything I said in the comment. In your answer, you advise to use more datapoints and obtain error estimations. But both of these are, once again, in the scope of how to properly estimate model parameter $k$. You see, everything you said in the answer will naturally follow from what I commented: When you start to think about how to properly estimate parameters, things like replicates, error estimations etc. will naturally emerge.

@Domen I disagree with your statement that "I also think that the question is not about biology or directly related to biology". Please note that critical portions of my answer have to do not just with data per se, but about thinking through the relationship between data and the underlying biological system (e.g., media effects, how OD measurements actually work).

The simple logistic function that you are using here is a fine first-order approximation for modeling microbial growth. Both logarithmic and linear scales are reasonable, with different tradeoffs as explained below. It is unsurprising that these two scales will give slightly different numbers, however, as the exponential approach gives more relative weight to fit errors on the lower values. I wouldn't be too concerned about the difference in numbers, though, since they are only 1.1-fold different, and that's within the likely limits of your assay precision.
Thinking about this from a biological perspective, however, there are a number of key limitations to fit accuracy that you need to take into account when you consider and present your data:

You show only a single replicate. I would not trust this data without at least three replicates, which will give some understanding of the degree of variability encountered with your protocol.
At the low end of the scale, precision will likely be limited by instrument precision and media density. What are your control blanks? Are the OD values that you present with or without media subtraction? Since you are showing a high final OD, I would guess that you are working with rich media, which typically has a significant OD even without any cells present.
At the high end of the scale, remember that OD itself is a logarithmic measure. Once the level of light penetrating is very low (below ~1%, i.e., above OD 2.0), most instruments will start having difficulty quantifying the penetrating light. Are you actually measuring an OD of 6, or is this a compensated measure from a much shorter path length? If it's a compensated measure, that will again imply decreased precision on the low end.

These questions can be addressed by using controls that determine the effective linear range of your instrument with respect to your media and path length, such as the method that we validated  in this interlaboratory study.
Once you know the range in which you can trust your data, then you can determine your answer on how to fit:

Since your primary interest is growth rate, you want to focus on the exponential portion of the behavior. For this, the log-scale fit is better, since it places more weight on the range where the exponential growth dominates the behavior. Based on what you've presented, this is likely the approach that will work for you.
If your low data is mostly outside of the effective linear range, however, you can fall back to the linear-scale fit, which will de-emphasize the low data.
If your primary interest were the saturated level, then you would want to prioritize the linear-scale fit instead, for the converse reason.

Bottom line: you need to figure out your data limitations, based on the interaction between biology and instrument, then see if that supports the log-scale fit or if you need to fall back to linear.

This answer suggests fitting the same equation to the same data on different scales to get better results. This is a very poor scientific practice. Note also that logistic is an ad-hoc choice - one could propose any number of curves with any number of parameters that rise exponentially in the beginning and flatten in the end, and have extremely good fits - mainly because one downweights the results in non-exponential region and "fits the noise" with extra parameters. This is no different from trancation, but uncontrolled and subject to arbitrary errors due to the curve choice.

@RogerVadim Every scientific data fit is done with respect to a model, and part of that model is the expected distribution of errors and outliers. Consider, for example, the difference between mean and median household income which are two different interpretations of the same dataset aimed at extracting different knowledge. For OP's data, different goals (e.g., focus on growth rate vs. focus on level) and knowledge about instrument range entail different choices.

Likewise, you are incorrect about the logistic function being an ad-hoc choice. The logistic function was derived specifically as the solution for constrained population growth ODEs, and remains the standard starting point for modeling for that reason.  Since you are not familiar with the derivation of growth models, here is a Khan Academy article that can serve as a starting point for you.

@jakebeal I know where the logistic function comes from - and this is precisely why I call it ad hoc - the basis for this ODE is that it is easy to solve, i.e., it is mathematical convenience rather than biology. Biology only tells us that the equation is $dN/dt=f(N)$, where $f(N)$ has two zeros and is positive between them: $f(N_{1,2})=0, f'(N_1)>0, f'(N_2)<0$. The early exponential growth than can be shown to be a general feature when expending near $N_1$, just like the saturation. The rest is completely arbitrary.

@RogerVadim Sounds like you've got a more general argument with population biology then, which supports the use of this model as a first approximation on the basis of far more than mathematical convenience. I will prefer to follow the scientific consensus until given reason to believe that it is incorrect.

The approach depends on what is known besides the data points. Non-linear regression for parameters $L, k, t_0$ is certainly a thing to try, as the OP author has already done in MSE - judging by the shape of the curve logistic is a good candidate and it is hard to think, how one could improve upon it without introducing additional parameters (and therefore weakening the results).
Fitting the log would make sense only if $L$ (the saturated value of the population) is known. In this case one could rearrange the equation as
$$
e^{-k(t-t_0)}=\frac{L-f(t)}{f(t)},$$
the logarithm of which is
$$
-k(t-t_0)=\log\left[\frac{L-f(t)}{f(t)}\right].
$$
That is, plotting the logarithm of the expression on the right against $t$ and performing linear regression one could determine $k$ as the slope of the line. Taking log of the logistic function itself does not make much sense to me...
Comments follow-up
Far from the inflection point ($t=t_0$) the curve approximately behaves as an exponential one, and for $t\ll t_0$ it indeed makes sense to make a linear fit to $\log f(t)$:
$$
\log f(t) =  \frac{L}{1+e^{-k(t-t_0)}}\approx
\log\left[Le^{k(t-t_0)}\right]= \log{L} + k(t-t_0), t\ll t_0
$$
That is, one do first rough fitting using non-linear regression to estimate the inflection point $t_0$ and $k$, and choose to do linear regression of $\log f(t)$ against $t$ only for those data points that satisfy $k(t_0-t)\gg 1$.

@user68022 Indeed, this makes sense, but you use only the part of the data points, where the grow can be viewed as exponential. I added a discussion to my answer.

As an alternative to simple logistic (with more parameters obviously): https://www.pnas.org/content/116/29/14698 They seem to be doing non-linear regression though.

Fitting log-logistic vs. log-OD is perfectly reasonable as a data-handling choice: it's just an effective rebalancing of error weighting and doesn't require restriction to "far from inflection point"

@jakebeal please give more math details or a reference - I am interested to know.

@RogerVadim Mathematically, it simply depends on your expectation of distributions. If you are expecting variation to be dominated by +/- errors in the measurement, then you want to stick with an arithmetic scale. If you are expecting variation to be dominated by fluctuations in the exponential process, however, then the fit error magnitude will scale with the value, and you want to switch to a geometric (log) scale in order to avoid overfitting on the highest few data points.

@jakebeal I'd rather see formulas. While I agree about the errors, the main idea is to be able to replace the non-linear regression by a linear one - so I want to see the transformation that one has to apply in order to use the linear regression.

I would not advise attempting changing to a linear regression at all. I am also disagreeing with your comment about the non-linear regression: "Taking log of the logistic function itself does not make much sense to me..."

@jakebeal I guess we have different idea of why people do log-transformation. As for your last criticism - this is simply not serious, please read my answer to the end, as well as the relevant comments.

I have indeed read it carefully, and I disagree with your recommendation, since it entails disregarding more data than necessary from a dataset without many points to begin with.

@jakebeal Just saying I disagree is not an argument - please support your disagreement by solid mathematical/statistical arguments or references. I see no point continuing discussion on the current level.

Let us continue this discussion in chat.


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Is this tailed butterfly a coral hairstreak?
I spotted this butterfly feeding on some lantana in Fort Worth, Texas.  It looks exactly like a coral hairstreak, but it has these two tails (?) on its hind wing, whereas I thought coral hairstreaks had none.  Is it just a slightly unusual specimen, or is it some other butterfly?
Thanks to @tyersome for the suggestion to estimate the size.  I'm bad with estimating sizes, but it was a small butterfy, with its height (from the flower to the tip of its wing) perhaps more than my thumbnail but less than the diametre of a US quarter—maybe 2 cm.

Welcome to Biology.SE. Your question looks good, but it may be helpful to add an estimate of the butterflies size. Not an expert on this, but to me the 'coral band' looks very reduced compared to a typical Coral streak — combined with the tails I'd guess this is a different species.

@tyersome, thanks!  I have estimated the size (perhaps 2 cm high).

Oh my goodness, you just posted a picture of my favorite butterfly! It's not a coral hairstreak.

It's a Gray Hairstreak Butterfly (Strymon melinus).
It can have one, two, or even three "hairs" on each wing. How much coral is on the wing varies, as does the amount of coral on the antennae.
Hairstreak Butterflies Identification Guide

That is certainly it; thanks!  I thought 'hairstreak' was an idiosyncratic name for the coral hairstreak, but it seems to be part of a theme.  Do you know why hairstreaks are so called?  (One might guess it's after the hairs that you've mentioned, but the coral hairstreak doesn't have those, so I am confused!)  I also don't know how to tell that these things on the wings are properly called hairs, rather than tails ….  Any further light you can shine would be much appreciated.

@LSpice - You're right to be confused. Until I saw your question, I didn't know Coral Hairstreaks didn't have a hair. Hairstreaks are actually named for that "hair"; most of them have it. If you'd like to see it from a different angle, try ere. So cool! And I agree; swallowtails aren't called swallowhairs... but "gray hairstreak" is purely descriptive.

@LSpice - Btw, that's a beautiful photograph! I have tried many times to photograph one, and have never come close to that.

Thanks for the clarification, and the compliment!  The age of basically-free digital photography has upgraded me from "no pictures ever come out" to "fortunately, I can throw away 20 or more pictures that didn't work out for 1 that did."

I got a picture of the wriggling behaviour described in your link, though it didn't come out as sharp:  https://i.imgur.com/g8pxeOJ.jpg .  I see a lot of these butterflies on my local trails, so I'll have to see if I can get a picture from below!


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Is it possible to "triangulate" the location of a termite colony in a horizontal space using light sources as attractive bases?
So we have termites and I noticed that one of the can lights in our subfloor (the 1.5 foot vertical space between our first and 2nd floor) was a lift off point for many swarms. I put some tape over the can light and was able to catch the swarmers each time they did it. The termite guy wouldn't touch the area (useless good for nothing) because it was an "electrical" area and out of risk or harm I had to remove the can light first before he can investigate the area. Left before we figured out how to open it (I wish I was good at this kind of stuff... took less than 30 seconds once you understood the trick to remove it). In any case, the termite specialist says since the colony has spread in between the floors he can only offer tenting since other methods will be ineffective but he also knows we are an attached home and that means the only way we can do anything is if all neighbors agree to the tenting of which we are all unable to do at the moment due to a long story I won't get into here. In any case, I've been endoscoping the heck out of the area... plenty of other things I found in there except termites, I was wondering is it possible for me to "triangulate" the nest source?
It seems like that specific can light has a direct line of sight to the colony because all the swarmers go straight for it and none other. I was wondering would it be possible for me to place three different light sources in the space and see which ones will trap the most termites and maybe use that information to zero in on the nest location. Anyways, a bit of a wild idea but maybe its possible. I already know that triangulation and trilateration are useful if you are at your own location so that would mean the nest needs to be known but maybe there is something I am missing where I could locate the nest using light sources and traps and wait until swarm season. Anyways just a thought..

Perhaps better in the Biology Stack.

Because termite behavior under changing lights conditions is not Home Improvement…

Termite behavior is better asked about on Biology.

My approach with termites is to spray every possible place with poison . We get the type that build tunnels to the ground so I have a pretty good idea where they are . I have had them in the garage twice as they are common here .  Apologies for the political incorrectness of insecticide.

Thanks for the comment! Wish I had the same problem, unfortunately they are in the area that doesn't touch the ground - we believe they are drywood termites and yours sound like subterranean termites. Subterranean termites create those tunnels and come from the ground so that is a great tell!


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Why would the stroma have a higher pH during photosynthesis?
Here is a question form my test.

If you could measure the pH of the interior of thylakoids and the
  surrounding stroma during active photosynthesis what would be the
  relative pH of each?

The answer is C.

the stroma would have a higher pH

I understand that proton gradient is from stroma to thylakoid space, but that does not mean stroma would have less protons than thylakoid space, if stroma would have a higher pH, then the proton will never flow from stroma to thylakoid space, right?

Energy from an electron transport chain is used to actively transport protons from the stroma to the thylakoid lumen. Thus the lumen has a relatively higher proton concentration and therefore a lower pH than the stroma.
Higher [H+] means lower pH.
Lower [H+] means higher pH.
Keep in mind that the flow of actively transported protons from the stroma to the lumen is against their concentration gradient. There wouldn't be a net flow of protons this way without active transport.

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DNA sequencing problem
First off, let me start by outlining the problem:
Your laboratory has established a technique for examining DNA replication in a cellular extract. To the cellular protein extract, you add nucleotides, a small amount of radiolabeled 32P-dGTP to aid visualization of the synthesized DNA, and a 4000-base-pair linear double-stranded DNA molecule that contains an origin of replication in the middle. After allowing the reaction to proceed for 30 minutes at 30°C, you boil the mixture to denature the proteins and the DNA strands, separate the components on an acrylamide gel, and detect the radiolabeled DNA products. This complete reaction is shown in lane 2 on the gel in the Figure below.

Problem A:
You perform the assay by yourself for the first time with no one else is in lab. The tube labeled “nucleotide mixture” has only enough for a single reaction, but you find a tube with a label that reads “dATP, dTTP, dGTP, dCTP” and you use this in a second reaction. You find the first reaction looks like lane 2 and the second reaction looks like lane 3. Why was no DNA synthesized in the second reaction?
My answer:
Because deoxyribose triphosphates do not have a –OH group to attach. You essentially can’t build with them.
Problem B:
Your lab partner has recently isolated a mutant strain that can replicate its DNA normally at 30°C but exhibit no DNA replication at 40°C. He calls the mutant tsr1, for Temperature Sensitive Replication. The wild-type strain replicates efficiently at both temperatures. You believe that you can use the biochemical assay of cell extracts to identify which genes are defective in the mutant. You grow wild-type cells and tsr1 cells at 40°C, make the extracts, incubate the DNA replication reaction at 40°C, and detect the products on a gel. You observe the pattern shown in lanes 4 and 5. You are so excited by the results that you run to your lab partner and tell him that you know what enzyme is defective. He is delighted by your results but says that there are three different enzymes that can account for your results. What are they?
I am 100% lost on this one.
I understand from the figure that the wild-type at 40 degrees has 4000 nucleotides so it's not being cut off. The mutant, trs1 is being cut off one into two slices of 2000 and one of these slices has been cut off into slices of 500? Am I understanding this correctly?
I also don't understand why the 500 line is so thick compared to the others?
Anyhow I feel really confused on this. I've been learning about Sanger sequencing and it makes 100% sense with ddXTP added into the mix to view the length of each sequence and therefore be able to read the sequence, but I'm not even sure if that's what's happening here.

The title of the question is a bit misleading as the problem/ question you have detailed is not really a sequencing problem

Even though you - or the problem did not clarify, I assume in my answer that you work with eukaryote system, even though the principle of the replication is the same.
dNTPs do have an OH group on their 3rd carbon atom (for eg. check this wiki-page for dCTP) so I don't think that's the issue here. My guess is that the first tube contains the radio labeled GTP and the second does not, so even the DNA is there, you cannot see it - even though the question specifically asked why DNA was not synthesized, my opinion is that it's a tricky question to confuse you.
For the second problem we need to dig into the replication process a little bit:
In the replication fork the two strands are synthesized differently. The so called leading strand is made continuously, without interruptions, however the other strand - the so called lagging strand is synthesized by ligating small fragments - aka Okazaki fragments. These small fragments require their own RNA primers that need to be removed after synthesis is done.
Now since the origin of replication is in the middle and replication can proceed both ways, on a linear fragment such as yours you can get two 2000bp fragment from the two leading strands. Would it be a circular DNA, then you could still get 4kbp fragments since the replication could go around the DNA circle.
The smaller 500bp fragments that are quite abundant in the tsr1 lane, are the fragments that cannot be ligated. That being said I must admit that 500bp Okazaki-fragments would by atypical for eukaryotes (usual is around 100-200bp). So the enzymes responsible for this could be:
DNA Ligase - the one responsible for ligating (joining ) the lagging strand's fragments.
Polymerase delta (Pol δ): That is responsible for lagging strand synthesis and primer removal - in this case the primer removal function might be defective, this causes that the primers stay on the DNA and complete synthesis and ligation cannot occur.
The last protein although it is not quite an enzyme is the DNA clamp complex (PCNA). This complex stabilizes the polymerase to DNA, but when reaching a previous fragment the polymerase should dissociate. But if the clamp is dysfunctional than the polymerase gets stuck on the end of the fragment thus no primer removal and ligation can occur.
If need more info read this wiki-page.

You need not assume a eukaryotic system. The principle is same for prokaryotes also (the Okazaki fragments are longer in prokaryotes though ~2000nt).

yes it is. It stated it only to indicate my logic in the answer. That being said the 2kb fragments could easily be Okazaki fragments of a prokaryotic system, but then what about the 500bp fragments? Plus if explicit enzymes are required for the answer that you must know which system does the assay use. I am going to edit my answer to indicate that the principle is the same for both eukaryotes and prokaryotes.


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Why does the open tree of life have 2600 species of rose?
The open tree of life has 2754 species and subspecies with the prefix Rosa.
Wiki says:

There is significant disagreement over the number of true rose
  species. Some species are so similar that they could easily be
  considered variations of a single species. Lists of rose species
  usually show between 100 and 150.

The thing is that a subspecies in the open tree taxonomy (OTT) should be written with a different latin name, and I can find at least 400 OTT rosa that are listed as individual species and not subspecies.
Is the OTT not very coherent in terms of accepted species?

OTT does not claim the taxonomy to be perfect, as it was generated by a synthesis of a lot of existing taxonomies. This might lead to an overrepresentation of some species/subspecies, because they have been classified differently in different taxonomies.


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How to learn molecular biology through pubmed research articles?
Instead of using a textbook, is there an alternative curriculum, that simply lists a set of pubmed research articles for each topic covered in a typical undergrad molecular biology course?
I am currently learning molecular biology by reading a textbook.  Different chapters focus on different topics such as Cells and Genomes, Cell Chemistry, Proteins, DNA, Gene Expression, etc...  However, I'd prefer to learn these topics directly from research papers on pubmed.

For example, I would imagine the DNA "chapter" of such a curriculum would include the Watson Crick paper on DNA.
As another example, searching for "Protein" in pubmed reveals a ton of research papers, but which subset of them cover the topics taught in an intro molecular biology course?

Note: The pubmed articles don't have to be free or open access, I'm ok with getting the papers through my university library.  Also if an alternative curriculum such as this doesn't exist, maybe there is a supplemental one?  Or maybe you can recommend a set of papers that you'd include in such a curriculum?

I love this idea, but I think some things may just be better learned from a textbook, like the basics. But if you find something interesting I highly encourage you to look for a review article on that topic. The problem is that journal articles, even reviews, are meant to be specific. You may not be able to find a review on just 'mRNA' for example, but you can easily find reviews on topics like mRNA decay and mRNA splicing.

Tom Silhavy would use a similar method in the first year graduate Molecular Biology course.
His text was basically a set of papers bound into a book "The power of bacterial genetics: a literature based course".  I'm not sure its in print anymore, but a used copy can be had.  If you find a copy you can just fetch the papers if you like.
You can't do much better than finding excellent papers to read.
Briefly, the class covered the development of selection for mutations and mapping them onto genes - use of bacteriophage and replicate plating.  The papers started in the 40s and went on from there to the heyday of molecular biology.
It was an awesome course to take... an awesome baptism of fire.
As they say... Whatever doesn't kill you, will select you for a distinguishing phenotype.

If you are interested in quantitative/systems biology, the reading list for a course like this at Princeton has been published (with some context for each paper). I know this course reading list has also been taught at Stanford. They definitely look like good papers, and some of them are fairly recent.

Edit: I remembered another book of classic literature I've heard is good: Landmarks of Cell Biology. If you look at the Table of Contents, you can get quite a few of the articles straight from PubMedCentral, and with a reasonable university license you can download the rest. It's been an inspiration to at least one rising star professor at UCSF (link to a fun bio-sketch).

this is cool - Silhavy's class was there too.

There are in fact various books where each chapter is written like a published review. These are not text books, but they are very technical. Off the top of my head I can think of this one for example:

Hatfield DL, Berry MJ, Gladyshev VN. Editors. (2011) Selenium: Its molecular biology and role in human health, 3rd Edition. Springer.

Like all such books, it consists of various chapters, each of which is a short review of the relevant topic by leading authors in the field. The problem with this is that a certain level of knowledge is assumed. Using your example, you won't be able to understand the original DNA paper if you don't understand the results of X-Ray crystalography experiments. Published articles assume that the reader is already an expert and they won't explain basic concepts.
A better way would be to read your textbook and then, once you have read and understood a chapter, look into that chapter's references and read through those. Most serious textbooks include published articles at the end of each chapter, if yours does not, get a new textbook.
Finally, another choice would be to read a review article. Those of the Trends and Current Opinion series are particularly good. They tend to be very well written and, most importantly, highlight the seminal papers in their references. Just pick one that is about a subject you are interested in and then look at the references. The important papers in the field will be marked with • and seminal works with ••. So, read the review and then read the •• papers.


text:
Why Can Varied Species Live Together in Particular Ecosystems?
Consider the following question:

The Piney Woods of Eastern Texas is home to a wide variety of organisms ranging from the grass Longleaf Oats to coyotes. Which of the following best explains why these varied specifies can live together in this particular ecosystem?
  A.) Each species lives in a slightly different habitat B.) Each spices occupies a different niche C.) Each species functions at a different trophic level D.) A and B   E.) A, B, and C

I chose answer choice E with the reasoning that: Oats and Coyotes do not share the same habitat; they occupy a different niche -- Coyotes eat organisms, oats use photosynthesis; coyotes are at a completely different trophic level when compared to oats -- oats being primary producers. The answer choice E however is incorrect and I'd like to know why and what the correct answer should be. Is there a flaw in my logic?

The answer to the question as asked is E. If anyone (even the teacher) says otherwise, they are wrong.

Supposedly the answer is 'B'.

@ChinmayKanchi It isn't the best question in the world but E should not be correct.  Variation in habitat and trophic level are not mechanisms that explain species coexistence in a community.

Variation in habitat and trophic level form part of the niche that a species occupies.

The answer should be B "Each spices occupies a different niche" because this is the only answer that reflects a model of species coexistence.  Niche theory proposes a mechanism that allows multiple species to occupy the same space and time any yet avoid competition for limited resources.  Briefly, the model says that a species niche is the total suite of resources that it requires to survice and reproduce and that coexisting species will limit their niche overlap to avoid competition (and its requisite reduction in fitness).  Species can limit niche overlap by preferentially using a subset of resources that are not shared with potentially competing species (this is called the realized niche) or by evolving a new niche that does not overlap with the competitor (this is called character displacement).
Note that your reasoning is incomplete because the question does not specify that the organisms listed are the complete set of organisms  in the community.  For example if the community contained another species of grass, then choice "C" would be false.  Most importantly though, habitat or trophic variation are not mechanisms of coexistence, so they should not be used as general hypotheses explaining coexistence.


text:
Possible Genotypes -- Linked Genes
Please consider the following question:
Genes A and B are located on the same chromosome. If two individuals with the genotype shown below are crossed, which genotype could be formed?

Let / represent the line in the image above.
a.)AB/ab
b.)Ab/Ab
c.)aB/aB
d.)AB/Ab
Why can't the answer to this question be all of the choices? I thought that recombination was completely randomized through the process of crossing over. Why is only one of the choices correct and how would I go about doing this on my own?

The answer is for Genes A and B on the same chromosome is
a.
AB/ab

One of the alleles for each gene must come from the parent on the right hand side. That parent only has a and b alleles (is homozygous) - meiotic crossing over will not change this. So the offspring must inherit at least one a and one b. That should point you to the answer.


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Why do changes in preload not cause changes in end systolic pressure?
I am trying to understand why changes in preload do not cause concomitant changes in end systolic pressure. If you have preload enhancement than this should lead to an increase in cardiac output..increased cardiac output at a constant heart rate I would think would lead to increased end systolic pressure. Why doesn't this occur?

remember that blood pressure is not solely dependent on heart rate and stroke volume. Total peripheral vascular resistance is important too. If you increase your cardiac output, your body may have a transient increase in end systolic pressure (i.e. systolic blood pressure) - but this is going to be balanced and decrease total peripheral resistance to maintain what the body is perceiving as "normal" systolic blood pressure.

One more thing to keep in mind is when talking about increased preload, you should note which ventricle is concerned. The left ventricular preload would increase only if the pulmonary blood return increases. However, the pulmonary vasculature is extremely compliant and can accommodate vast amounts of blood without significantly affecting the preload to the LV. The blood pressure, on the other hand is measured in the systemic circualtion which might not be affected that much if the preload to the RV increases.

Preload is defined as the volume of blood that stretches the ventricle at the end of diastole. Therefore, when preload is increased, the end diastolic volume is increased. In simpler terms, there is more blood in the heart just prior to contraction. Even though there is more blood being ejected from the ventricle during systole (that is, there is an increased stroke volume), the increase in preload alone will not affect the end systole volume or pressure.
When preload is increased while afterload and inotropy are held constant, the cardiac muscle fibres will still shorten to the same length. This means that the end systolic volume is unchanged, therefore the end systolic pressure is unchanged. This is best visualized by a pressure-volume loop. On the first example on the diagram below, you can see that the end systolic pressure and volume at point 3 are unchanged with increased preload:

Since cardiac output is equal to the product of stroke volume and heart rate, with increased preload the cardiac output is increased due to the increase in stroke volume. The reason why the end systolic pressure is unchanged with the increased cardiac output is because the end diastolic volume is increased.


text:
Is there a blood panel lab test that measures all the hormone-producing glands?
I understand that there are gland-specific hormone tests, such as:

Secretin: for the pancreas; and
Prolactin/ACTH: for the pituitary; and
PTH: for the payathyroid, etc.

However, are there any "composite" blood panels that test the "entire gamut/spectrum" of organs/glands, similar to what composite metabolic panels do for your cell counts?

There are no composite tests that measure all the clinically important hormone producing glands. There are too many hormones produced by too many hormone producing cells/tissues in the body to test for all of them all at once (i.e. in a panel).
For illustrative purposes only... if you go to wikipedia they have a list of all hormones in the human body which is definitely far from complete! But it gives you an indication of just "how many" hormones there are and why testing for all of them is impossible in a panel.
Even with regard only to pancreatic hormones, there are several hormones produced (e.g. insulin, glucagon, somatostatin) that aren't necessarily a marker of the glands overall function (because they are not necessarily involved in the same function). Each of these hormones has different functions even though they are produced by the same gland.
Regardless, from a medical perspective you would never have a reason to test for all of them anyway. If you tested enough of them you'd find at least one of them that would - by chance - be abnormal.
Additionally, if you asked a handful of scientists to name fifty hormones there would be a lot of different hormones on each of their lists. The definition of hormone is vague, and we are learning more about new hormones every day. In the last decade we have learned that bile acids - chemicals predominately produced by the liver that are involved in dietary fat absorption - also act as hormones. There aren't clinical reasons to study all of these molecules just yet, but this demonstrates that it would be impossible to measure all of them all at the same time in one particular "panel".

Good answer.  Lipase and amylase are enzymes to my knowledge. Also many hormones are difficult to measure at all due to instability or low concentration.

+1 - Not to mention new hormones are being discovered constantly, it seems. They are actually pretty hard to keep up with.


text:
What is the lower temperature limit for ion channels function?
What is the cold-block temperature of ion channels? (not of nerves or axons)

The lower temperature limit of ion channels likely is dependent on various factors, including the type of channel and the recording conditions (tissue type, medium etc.). Reports on the suppression of voltage spikes (i.e., the inhibition of action potential firing) range from 1 to -20oC in squid axons, dependent on the species (Leuchtag, 2008). I couldn't find information on specific channels.
Reference
- Leuchtag, Voltage-Sensitive Ion Channels: Biophysics of Molecular Excitability (2008)

thanks, "suppression of voltage spikes " you mean stopping of action potentials right? The fact that an action potential cannot propagate doesn't mean that the channels are blocked but that the threshold cannot be reached right?

@george. Yes, correct on the AP firing, I edited the answer to make that more clear. Isn't threshold increase a consequence of inhibition? I.e., I don't follow your dichotomy posed. As a rule, if you find the answer useful, we upvote the question to let others know it's a useful answer. If you think it is the answer you can accept it too. You can also downvote it when it's a poor answer.


text:
How to determine sensitivity in a dose-response curve?
In a dose-response curve the % inhibition can be plotted against concentration antagonist. In our case, the effect of the antagonist is tested in different genetic variants of a microbe.
When trying to determine the potency of a drug on the different variants, I compared the IC50 values. The lower the concentration required for 50% inhibition, the more potent the drug.
When comparing drug efficacy, I compare the concentrations required to reach Emax or the maximum inhibition that each drug can exert - which turns out to be 100% inhibition.
To compare sensitivity, how does one proceed?

Wouldn't it be a sensitivity assay like Kirby Bauer?

You could do percent viability of the microbe at MIC50 versus control over a time course. The lower the percent viability, the more sensitive the strain is to the compound. There are other factors you would need to test such as biofilm formation prevention, killing of sessile versus planktonic microbes, but % viability should tell you the sensitivity of the strain to the compound.

I think you are after the slope of the dose-response curve:

Dose-response curve. Souce: Merck
The slope indicates the change in response per unit dose, which translates to sensitivity.


text:
What is the mechanism of folic acid deficiency and neural tube defects?
I am having difficulty finding the mechanism by which folic acid reduces the risk of neural tube defects. I know that it does so, but what in particular actually occurs with folic acid deficiency to cause the neural tube defect? Is that completely unknown and merely a strong association, or is there a putative mechanism?

You are having difficulties finding the mechanism because it is as of yet unknown.
Now of course comes the hard part where I need to prove that statement. Often, it's just apparent by papers not saying anything about the mechanism, even though you'd expect then to include a brief section if it was known, for example Folic acid supplementation for pregnant women and those planning pregnancy: 2015 update or the various Cochrane reviews on the topic of how much folic acid supplementation is optimal, or the WHO and CDC documents on the topic
Here's a few relatively recent ones that state it outright:
Folic Acid Supplementation and Pregnancy: More Than Just Neural Tube Defect Prevention, 2011

The mechanism by which folic acid prevents structural anomalies in the fetus is not known, but may involve the regulation of homocysteine metabolism

Folic acid supplementation in pregnancy and implications in health and disease, 2014

as FA deficiency may be a risk factor for NTDs additional studies will be required to determine the mechanistic role of the FA pathway in the onset of neural tube defects

FA = Folic Acid, NTD = Neural Tube Defects
Neural Tube Defects, Folic Acid and Methylation, 2013

To date, animal studies have not provided
  sufficient information to establish the metabolic and/or genomic mechanism(s) underlying human folic acid responsiveness in NTDs.

There are some putative mechanisms to do with folic acids effects on the homocysteine metabolism and its effects on methylation. I can't really tell how well-established those are yet, but maybe this can be a starting point for you.


text:
Could drugs promoting angiogenesis be used as a treatment for burn victims?
From what I've learned from my textbooks and in class lecutures it seems that inducing angiogenesis for people with severe burns would be an excellent way to speed up the healing process. Is this already being done? If so or if not what are (if any) challenges that are presented to doctors and surgeons trying to use this self-healing method?

good question, interesting idea... obviously angiogenesis is necessary for skin grafts to grow to previously burned and debrided areas. It loos like angiogenesis is measured/quantified in research in this area, but I'm not aware of actual drugs/pharmaceuticals that act in this way directly.

A quick Google Scholar search yields a number of papers looking at this through a variety of angiogenic factors such as leptin, EPO, and dextran hydrogel scaffolds, mainly by topical application.


text:
How does heat generated by metabolism differ compared with heat generated through exercise?
I am from a mathematical background so I don't have much knowledge on biology. I'm building a mathematical model to predict heat generation with parameters of metabolic heat generation and exercise heat generation.
Metabolic heat generation as far as I understand is the heat produced through body's chemical processes, digestion of food, and elimination of waste.
In this article here, the value for metabolic heat generation is given as 33800$W/m^3$. But the exercise intensities as given here only has values of around $582 W/m^2$.
I think we produce more heat when we exercise than through metabolic activities alone. Is this correct?
If so, why does this huge difference in values of 33800 and 582? Why would the heat generated via exercise be such a low value? (Of course they are not measured in same units.)
Is there any other unit other than $W/m^2$ that measures the heat generated through exercises so that it gives a resonably at least closer value to metabolic heat generation?

I tried to clarify your question and make the text easier to understand...you can change things back if I have unintentionally changed the meaning of your question.

You did notice that the units you listed are different right?  One is W/volume and other is W/area.

@akaDrHouse Yes the units are different. I am asking if there a way to compare the metabolic heat and energy from exercises? metabolic heat per volume is so higher than the exercise heat per surface. Shoudn't exercise generate more heat?

First, you have to convert your numbers to the same units for any comparison to make sense. Consider that the average human body has a surface area of about 1.8m$^2$ and a volume of about 66L = 0.066m$^3$. Then your numbers are equivalent to 2230W metabolic heat and 1050W exercise heat for an average person.
The value 2230W for basal metabolic rate (from Table 1 of the Bagum et al paper) is nowhere near what's measured in practise. Basal metabolic rate ("metabolic equivalent", 1 MET) would be 105W for an average person according to the wikipedia page you cited, which equals 2150 kcal / day. That's about the recommended daily calorie intake, so it makes sense. I don't know where their value of 33,800 W/m$^3$ for "metabolic heat generation" comes from, perhaps it's meant represent something else (can't say I understand the article) but it's not the metabolic rate for an average human tissue.


text:
Why ketoacidosis is less common in patients of Noninsulin Dependent Diabetes Mellitus?
The other day my teacher said ketone bodies are mostly formed when insulin is less and NIDDM type diabetes mellitus has less chances to grow ketosis. https://medlineplus.gov/ency/article/000320.htm
P. S. I had read the difference between the type 1 and type 2 diabetes.

Did you read this already? If so, could you please edit your post and explain, what remains unclear? Do you know the differences between Type 1 and Type 2 diabetes mellitus (formerly called insulin dependent or non-insulin-dependent)?

btw: there is a  diabetes-mellitus tag, while your editing your question, you should add this one :)

@Marzipanherz I don't think that Wikipedia article is very helpful in answering this question. The answer is certainly not obvious (or fully understood), and it's not really addressed there. In type 2 diabetes, insulin fails to work at some sites but not at others.

@DeNovo I agree that Wikipedia doesn't cover everything. However, in this case the article is more informative than the article linked by the OP. With my above comment, I was trying to figure out, how much background knowledge the OP has, since this isn't clear to me from the question. And I think, knowing this enables us to write an answer that is helpful for the OP.

@Marzipanherz The difference between the two types are clear, not wholly though, as you can see this question arising.

This is a good and important question. The answer is not obvious, or necessarily well understood. Hyperglycemic crises occur in both Type 1 and Type 2 diabetes. In type 1 diabetes, the crisis is more likely to be diabetic ketoacidosis (DKA). In type 2 diabetes, it's more likely to be something called hyperosmolar hyperglycemic state (HHS), though type 2 diabetics can develop DKA, especially later in the course of the disease. Both can be brought on by similar precipitating events (for example, infection) in an individual who has had diabetes for a very long time (and this is where we often see these patients now -- pneumonia or the flu in an older diabetic). With type 1 diabetes, though, it can be how diabetes is discovered in a young, otherwise healthy individual.
The key difference between type 1 and type 2 diabetes is that type 1 is an absolute loss of insulin production, typically due to autoimmune destruction of the cells of the pancreas that produce insulin. Type 2, on the other hand, starts as insulin resistance. In fact, insulin levels may be high early in the course, but the tissues do not respond appropriately.
Insulin actions in glucose and fatty acid metabolism
Broadly, a key role of insulin is to respond to increases in blood glucose by shifting energy metabolism from fatty acids to glucose.
In a healthy individual, insulin is secreted as blood glucose rises, and causes peripheral tissues, especially fat and muscle, to take up and use glucose. It also causes the liver to release less glucose into the bloodstream from glycogen stores and gluconeogensis, and instead to store it (in glycogen).
At the same time, since there is plenty of glucose available, insulin diverts fatty acids to fat cells, promoting their storage in and inhibiting their release. Insulin indirectly prevents fatty acid catabolism in the liver by promoting its storage in fat cells, but also directly inhibits liver ketogenesis, a process by which byproducts of fatty acid and protein catabolism are converted to ketone bodies that can be used by, among other tissues, the brain.
Impaired insulin signaling
In both DKA and HHS, despite high levels of blood glucose, the muscles, fat cells, and liver act as if the organism is starving. In response to this state, counter-regulatory hormones (catecholamines, cortisol, glucagon, and growth hormone) are released. The liver releases glucose from glycogen stores and generates even more glucose from other metabolites through gluconeogenesis.
The difference between DKA and HHS is how lipid metabolism is regulated. It is unclear why, exactly, in HHS insulin fails to regulate glucose metabolism but seems to succeed in suppressing lipolysis and ketosis, but that is the current hypothesis. In DKA, fatty acids are released from adipose tissue and delivered to the liver, where massive unregulated lipid catabolism and ketogenesis occurs. In HHS, the existing insulin seems to be effective at suppressing lipolysis and ketogenesis.
You can read more about the pathophysiology of both these diabetic hyperglycemic crises in this excellent review.

Are cells completely resistant to insulin? I construe if there might be some, albeit reduced action of insulin on adipocytes suppressing lipolysis.

@user73023 that's the theory. If this answered your question, you should mark it the answer by clicking the gray checkmark next to it (it will turn green). If it was helpful, and you have the upvote privilege, you should upvote it. See someone answers


text:
Why are only few cigarette smokers prone to cancer?
It's tacit that only a few populace of smokers get cancer. What spares the others from it or what specifically cause cancer in those populace? See this Washington Post Article

Those 5% are unlucky to have incurred a genetic mutation which survived. Cells have protective measures against cancer. So a cancer cell which has survived has very likely multiple mutations (e.g. 3 mutations in a same cell is unlikely than 1 mutation in a single cell). Also this 5% of smokers has a subset of mutation not caused by smoking + random mutations.

Where did you read that statistic? It does not appear in the article you link.

Consider that only 16.666% of Russian Roulette https://en.wikipedia.org/wiki/Russian_roulette players die on the first round :-)

Cigarette smokers are most certainly prone to cancer. See Cecil Medicine, Chapter 183, on the epidemiology of cancer, exposure to tobacco is the most important environmental risk factor for cancer development, at least in the US:

Exposure to tobacco is the single largest cause of cancer in the United States... All forms of tobacco can cause cancer. Cigarette smoking causes cancer of the lip, oral cavity, nasal cavity, paranasal sinuses, pharynx (nasal, oral, and hypopharnyx), larynx, lung, esophagus (squamous cell and adenocarcinoma), stomach, colorectum, pancreas, liver, kidney (adenocarcinoma and renal pelvis), urinary bladder, uterine cervix, and myeloid leukemia.

Cancer may be identified or the cause of death in fewer smokers than might be expected, though, because smoking is an even greater risk factor for cardiovascular disease, and death due to cardiovascular disease.
Cancer is an unlikely phenomenon in an individual cell, but becomes  more likely at the organism level, and even more likely over time. Though tobacco may be the most important environmental risk factor for cancer, age is actually a stronger predictor of cancer (see again, Cecil Chapter 183. Autopsy studies give us a quite remarkable example, this one shows incidental prostate cancer in nearly 60% of men over 80 who died from other causes. That figure is not out of the ordinary. Live long enough and you are likely to develop cancer.
Death due to heart disease may account for the lower than expected rates of cancer diagnoses and deaths in smokers. Nothing prevents cancer as well as dying from something else. And as discussed in the blog in the Washington Post you linked to, up to 2/3 of smokers die from smoking related causes

+1 for "Nothing prevents cancer as well as dying from something else"

I've edited the question and removed the 5% part :-)

@user73023 thanks! I took it out of my answer as well.


text:
Is this an Eastern Banjo Frog?
[

I found this little guy in my orchid on the upstairs balcony. I live at Sanctuary Point which is on the south coast NSW

You should probably add more precise size indications, as well as the country and the meaning of "NSW" (my first guess would have been "North-South-West", but it doesn't really make sense...).

Funny, after some guessing work, it seems that you are in New South Wales, a region of Australia. I first assumed that people forgetting to indicate their country were from the United States...

Ok....a few more details. I live in Australia, in the state of New South Wales on the east coast. The climate is warm temperate, the area is semi rural and my house is built on a 100 year flood plain. The frog was about 60 mm long and 45 mm wide with darker brown markings down it's back. Hope this info helps!

I've just added a photo which shows the frog's back.


text:
Expected bands in polyacrylamide gel
I have something in my notes that doesn't seem right.
If I use restriction enzymes on a PCR product how many bands should I see provided I know the restriction enzimes will cut the DNA? If I use two restriction enzymes I expect two cuts then then gel should show three bands. Then, if I use just one enzyme and I know the enzyme will cut just once, then should I expect two bands? According to my notes one band is expected.

If your restriction enzyme only targets a single site on the DNA sequence then it will split each DNA strand into two fragments. If the restriction enzyme cuts every strand then you will see those two fragments. Note that if the two fragments have the same length they could appear as a single band when separated using gel electrophoresis.
If the enzyme doesn't cut everything the uncut DNA will also be present. This is why you should always separate some uncut DNA in the gel electrophoresis.


text:
What animal does this skull belong to?
This skull was found in Greece, about 40 years ago, possibly in the island of Euboea (there is uncertainty about the area it was found).

The length from nose to the end of horns is 67 cm. The skull's length without the horns is 42 cm. Just for reference, the floor tiles in the pictures have a side of 33cm.
What could this animal be? It does not have to be native to Greece, even though a native animal would be more probable.
Update:
The size of the skull points to an animal larger than a goat. It looks more like an antelope, a gazelle, or even a deer.  Only deers are native to Greece, however the horns look nothing like deer.
I believe the horns are the key to unlock this mystery.

Lichtenstein hartebeest possibly a female looking how thin the horn base is

Its definitely a bovid, most likely an african antelope specifically a Hartebeest or Alcelaphus buselaphus . There are several sub-species but those horns are a dead giveaway. The the horn do vary a bit by sub-species. The Neumann's or Tora hartebeest might be your best bet but I can't be 100% sure. They are all popular hunting trophies since forever and are even kept in some european game reserves so it is not that hard to find there skulls in private hands. Search "hartebeest skull" and you'll find a million of them so you can try for a more exact match.

There is limited information using only the bones and horns. But I suspect that is a Kri-kri or Cretan goat based on the reported location and the features of the horns.
Greece is trying to standardize its goat pedigrees by further classifying them based on regional names and features. This could be more specifically a Skopelos goat but I doubt it based on the horns being so short. As you report the length of the horns to be 25cm that puts a lot of evidence as this being a  Cephalonia/Kefalonia/Kefallonia goat depending on how you want to spell it. These Cephalonia goats have an average horn length of 25cm.

Thank you for your answer (+1). My impression is that this animal is too large to be a goat. It looks more like an antelope or gazelle. Moreover, the horns do not match the ones I see in pictures of kri-kris or other types of greek goats.

Yeah they are quite thick


text:
Are gametes determined by the sex of an organism?
In the Wikipedia article for biological sex, I read the following sentence.

"The gametes produced by an organism are determined by its sex:..."

However, is it not through the gametes produced by an organism that "sex" is defined? Should this sentence be the other way around?

Please clarify, do you mean the type of gametes produced (i.e. eggs and sperm) are determined by the sex?

related: What's the difference between male and female?

Short version of the above link; sex is often determined by chomosomal makeup, but it can also be determined by other factors (e.g. environmental cues or sequential hermaphroditism). Sexes are defined in terms of Anisogamy (different-sized gametes).

The gametes produced by an organism are determined by the organism's sex - Thus, that statement from Wikipedia appears correct to me. In the case of humans, males have two different sex chromosomes. Thus, males produce gametes with either a Y-chromosome or an X-chromosome (XY). Female humans also have two sex chromosomes, but they are two different X chromosomes (XX). Thus, when females produce gametes they have a single copy of one of the X chromosomes in each gamete. In most cases, a fertilized embryo results and is either XX or XY - in the case of males the embryo gets the Y from Dad and the other sex chromosome is one of the two X's from Mom. In the case of a female the embryo gets the X chromosome from Dad and one of the two X's from Mom.

Here is an image describing what I said above with a link to the page to read more:

Here is a link from a basic genetics course from Dr. Young in the UK that has a more in-depth explanation.
Here is a link to another article from Nature Education that help explain how this works in humans as well as some other organisms that are slightly different.

No. You are confused. There are different types of chromosomal sex determination. If one sex is heterogametic (an example of one system like this are mammals, which have an X and a Y chromosome) then the sexual phenotype (male versus female) is determined by the presence (or absence) of the Y chromosome. If you have a Y you will develop testes,and the androgens produced by the testes will direct all of your secondary sexual characteristics to develop the male fates.
In the absence of a Y chromosome the default developmental pathway of the somatic gonads is to form ovaries. The ovaries produce estrogen which will direct all of your secondary sexual
characteristics to develop female fates.
Gametes are either sperm or eggs.  Early after fertilization some of the embryonic cells get sequestered away to form the primordial germ cells (PGCs). Later on these cells will mature in the somatic gonad to form the germline, giving rise to more sperm (or eggs).  These germline cells have no effect on the sex or gender of a mammal.  In some animals (like model organisms that can be subjected to genetic screens) you can isolate sexually transformed mutants where, for example  the XX animals develop as males and produce sperm, and the XY animals develop as females and produce oocytes.  There are other possible mutant situations as well where the male sex produces oocytes,  and the female sex produces sperm.

you're interpreting the question differently - the sex of the organism determines the gametes - males produce haploid sperm with either an X or Y sex chromosome, females produce ova that have one of two of the X chromosomes. I agree with you though - the way the sex is determined is not by the necessary presence of a particular chromosome though.

It looks like we need clarification from the person asking the question

In mammals carrying a strong loss-of-function mutation in the TDF (testis determining factor) gene, which is the only gene directly required for sex determination on the Y chromosome, both the XX and the XY individuals develop as fertile females. No TDF = no testes, no testes = no androgens, no androgens = default female developmental pathway. This shows that the Y is necessary for male fates. IF: you create an XX transgenic mouse carrying the TDF gene, THEN: it will develop as a fertile XX male. This shows that TDF (SRY or sry) is sufficient for male fates.

I agree with you - though the most common condition is that the sex of the organism determines the gametes – you're talking about a very rare type of anomaly - how rare is a strong loss of function mutation in the TDF?

We may me be addressing different sections of the original poster's query. I do not object to the edited title. My comments are replying to the body of the question: ". . . is it not through the gametes produced by an organism that 'sex' is defined?" To this I posted an answer that starts "No. You are confused." My gametes in no way influence or affect my sex or gender. The primary signals for mammalian sex determination are, as far as I know, chromosomal. It is the zygotic chromosomes that dictate and control the development of the embryos somatic and germline sex.


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What is the actual function of HDLs and CETP?
I know that HDLs collect cholesterol from peripheral tissues and transport it back to the liver using SRB1 - Reverse cholesterol transport and dumping it in bile. So the tissue is producing some extra cholesterol (why would it? apart from some atherosclerotic condition) and our HDL gets it back to the liver.
This is a bit fine. But then there is CETP which is giving back the cholesterol to VLDLs.
So is it not confusing that our HDL took the excess cholesterol from the tissues only to give it back via VLDL?
So my questions -
Q1 - Why would a tissue have extra cholesterol?(when excellent feedback mechanisms exist - eg. SREBP SCAP INSIG path). Does the HDL pathway make sense only when there is some atherosclerosis?
Q2. Reverse Cholesterol transport refers to the SRB1 part only or SRB1 + CETP combined?
Q3. What is the rationale behind handing over the cholesterol back to VLDLs by CETPs? I know that considerable LDLs get back to the liver too but isnt just SRB1 pathway just fine? Why is it so important to equilibriate your lipid content across lipoproteins? I understand this is the mechanism how torectrapib works but presence of CETP in the body signifies that it must have some ulterior motive, right?
please help :)

this question has a VERY large focus - you probably could have posted each of the 3 subquestions as individual posts... might be hard to get someone to tackle the whole thing - but I bet eventually someone will

Split it into 3 questions :) Do you know of any other forum which caters to medical students' doubts? Just asking.. What to do of questions which don't find an answer!


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Is diabetes mellitus a sex-linked disease?
There are two types of diabetes mellitus.
a. Type 1 diabetes mellitus
b. Type 2 diabetes melliuts
Is either of them a sex linked disease? Can either one be inherited? My book says, "this disease is transmitted as a recessive genetic characteristic." What does this mean?

You seem to be confusing inheritance with being sex linked. The two are not related. While sex linked characteristics are indeed inheritable, not all (or even most) inheritable traits are sex linked. As for what a recessive characteristic is, have a look here (the first hit when you search for "recessive genetic characteristic" in Google.

Is either of them a sex linked disease? Can either one be inherited? My book says, "this disease is transmitted as a recessive genetic characteristic." What does this mean?

Neither are sex-linked. Type 1 can be directly inherited (in a non-Mendelian fashion), but Type 2 genetic factors mostly increase risks. "Recessive genetic traits" are traits that only express themselves when ONLY the recessive alleles are present in the organism (a dominant allele, if present, will 'overpower' recessive one).
Longer info:
Diabetes mellitus Type 1 (Juvenile Diabetes) is inherited, but it is autosomal with complex dominant/recessive rules:

Type 1 diabetes is a polygenic disease, meaning many different genes contribute to its onset. Depending on locus or combination of loci, it can be dominant, recessive, or somewhere in between.

That results in some interesting, albeit complex, expressions:

The risk of a child developing type 1 diabetes is about 10% if the father has it, about 10% if a sibling has it, about 4% if the mother has type 1 diabetes and was aged 25 or younger when the child was born, and about 1% if the mother was over 25 years old when the child was born.

Diabetes mellitus Type 2 does have genetic components, but the vast majority merely increase the risk of developing Type 2 Diabetes. Environmental factors play a large role in Type 2.

Excess body fat is associated with 30% of cases in those of Chinese and Japanese descent, 60-80% of cases in those of European and African descent, and 100% of Pima Indians and Pacific Islanders.

Fascinating and complex indeed! So even though there are different risk factors for Type 1 based on mother or father having it, you still wouldn't term it "sex-linked"?

@Oreotrephes: sex-linked just means that it depends on some gene present on the sexual chromosomes (chromosomes X and Y), so that it is not passed equally in the progeny (e.g. a gene on the Y chromosome will not influence females, who are XX). I would also like to add that epigenetics plays a very important role in the development of diabetes.

I understood from your explanation that type 1 is inherited but the defective gene is on autosome not on sex chromosome. But didn't understand what you said about type 2. Does the same explanation goes for type 2?

Actually the genetic component of type 2 diabetes is much higher than type 1. See this link http://www.diabetes.co.uk/diabetes-and-genetics.html

@Snipergirl - That doesn't contradict what I said. The genetic components of Type II increase risk of getting the disease, with the development left up to environmental factors. You can directly inherit Type 1 regardless of environmental factors. At least, as far as I'm aware.

@MuhammadRafique - The genetic components for Type II would be mostly autosomal, though if I recall correctly it's development is more prevalent in women so there may be some sex-linked genetic factors, but I have not read anything directly stating that.

@MCM the way in which your answer is worded is somewhat misleading; the comparisons between type 1 & 2 are not comparing the same thing (you don't list the absolute or relative risk of 1st gen relatives of type 2 diabetics for example, but you do for type 1)


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How is adrenaline (also known as "epinephrine") a ligand?
I keep reading that adrenaline is a ligand, however, from what I understand a ligand is a molecule or ion which donates a pair of electrons to a central transition metal ion in a complex. If this is the correct definition of a "ligand", then how can adrenaline be a ligand?

In biology, ligands are chemicals that attach to receptors on cell membranes, stimulating a cellular response. You’re using the definition of a ligand in chemistry. :)

@lightweaver - that's sufficient for an answer when you include a link to the respective definitions.

The definition of "ligand" in the question, "a molecule or ion which donates a pair of electrons to a central transition metal ion in a complex" is clearly a more technical 'chemistry-type' of definition. Ligands in biology and medicine can be all sorts of molecules, though most of the time we think of them as molecules that bind to a particular receptor. Those receptors can be ion channels, enzymes, transmembrane receptors at the cell surface or within the cell in an organelle, nuclear proteins that control expression of genes in the cell nucleus (i.e. transcription factors), etc...the list could go on and on... In fact, more recently we have come to appreciate that compounds like bile acids - that were previously thought to be important only in fat absorption in the gastrointestinal/digestive tract - are also ligands for receptors that control gene transcription ("Farnesoid X Receptor") as well as increase energy expenditure in brown adipose tissue and skeletal muscle (through receptors like the "TGR5" receptor).
But... back to the question...
If a molecule binds to a receptor, then it's a ligand for that receptor. The ligand doesn't have to donate any electrons specifically to a transition metal. Most of the time in medicine/biology the binding of a specific ligand to its receptor is a reversible process that is dependent on the concentration of the ligand and the availability of the receptor (among other things). The specificity of ligand for the receptor is due to chemical factors like hydrogen bonding, electrostatic interactions (like positive charges attracting negative charges), as well as other chemical interactions beyond the scope of this question. As you can see from the picture below, the hydroxy groups (-OH) that are part of the serine residues on the receptor are hydrogen bonding with the hydroxy groups on the epinephrine molecule itself. Moreover, the carboxy group (-COOH) on the aspartate residue is binding to the positively charged amino (NH3+) on the epinephrine molecule.


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If so many different hormones/molecules work by activating adenylyl cyclase, how do they have different effects?
It seems that many hormones and molecules work by activating adenylyl cyclase to convert $\text{ATP}$ to $\text{cAMP}$, such as adrenaline and glucagon. Both of these seem to bind to $\text G$ protein receptors, cause an alpha subunit to dissociate and bind to adenyly cyclase to activate it, and then adenylyl cyclase forms $\text{cAMP}$. If so many molecules work in the same way, how can they have different effects?
My guess is that perhaps they may have different molecules inside which respond differently to elevated levels of $\text{cAMP}$? I presume both cells affected by adrenaline and by glucagon have the protein kinase which, when activated by $\text{cAMP}$, is able to activate glycogen phosphorylase to break down glycogen, as both adrenaline and glucagon increase blood sugar levels. Perhaps liver cells have more of the glycogen phosphorylase enzyme for a greater rate of breakdown of glycogen?
But then when I consider the heart, adrenaline increases heart rate but glucagon does not. If they have the same mechanism of action, how can this discrepancy arise? Could it perhaps be that adrenaline increases heart rate not by acting in the heart cells but in the medulla oblongata to increase the heart rate? But then again I come to the problem of why glucagon does not have the same effect. In this case I could hazard a guess that the glucagon molecule is too large to pass across the blood brain barrier.
But this is just one example of a possible problem in how two different molecules use the same mechanism. Although I cannot find a link now, I think I remember that long term potential ion to for new memories involves activation of adenyl cyclase. If that is so, it doesnt make much sense becaus adrenaline certainly doesn't help in the formation of new memories!
EDIT: I have just also read that insulin works by activating cAMP in hepatocytes/muscle cells, however it also seems that glucagon works by activating cAMP in the same cells! Two directly opposing effects using the same mechanism in the same cells- I'm very confused now!

Slightly different shapes mean that they will bind to slightly different receptors. The receptors will be the first step in a cascade, at it is what happens after. There are a lot of other reasons, like tissue specific chromatin structure can effect the genes that are available for transcription, etc. Your question may be a little too broad to provide a good answer. If you could compare and contrast one example of a hormone induced signaling pathway to another and ask why the specific results of one might be different from the other, then that might allow for a more specific answer.

I think this is a good conceptual question. It does seem perplexing from many cell biology books that a number of dinstinct signals with different meanings all go appear to go through the same "node" --- why don't they get mixed up?

@21joanna12 sounds like you found an error in your textbook because insulin does not increase the amount of cAMP in the cell (it suppresses it) and antagonizes the increase stimulated by glucagon.

@21joanna12 in reference to the question above - adrenaline (i.e. epinephrine) increases heart rate through actions on the pacemaker cells of the heart - there are no glucagon receptors on the pacemaker cells (this is why there is no response to glucagon in those cardiac myocytes).

@Roland A lot of cartoon representations in textbooks happen to be generalized in a way you can look at many possibilities (sometimes even the entire known pathway) in the same image much like this. In reality, we know the response depends largely on the downstream interactions that are actually available, and if we know those, we can produce an image more similar to this one.

@VanceLAlbaugh I approved your edit, but I am not 100% sure that I agree that this is essentially a question about metabolism, so I am not 100% sure that I agree that it should be tagged as such. Technically almost any process that the cell undertakes is metabolism, but I am not sure that we should add it to every question related to cellular function.

@AMR Point taken – if you want to remove the metabolism tag I guess I'm fine with that but I think the other text edits are necessary for grammar clarification, etc. thanks!

@VanceLAlbaugh I am going to raise as a meta question and see what is said. The edit review didn't show any text edits. Are you sure those were not approved in a previous edit of the question?

@AMR yes I think you're right – I think I was thinking of the edits on the answer not the question

@21joanna12 - does that answer below clarify your question? If so, check it as the answer so we can move on... if not, are you still confused?

How can hormones/molecules have different effects if they all work through cAMP? The short answer is that receptor expression on cell types is highly specific, and only if a cell has a particular receptor will it respond to a particular hormone. Thus two different hormones can have different biologic effects because the cells that contain those receptors are highly specific. Overall it is the presence of specific cellular receptors that determines the specificity of hormones and their effects.
A little more in depth of an answer... This is a classic concept from graduate physiology and was a real step forward in our understanding of hormone action in the 1950s/1960s. Earl Sutherland, who received the Nobel Prize in 1971 in Physiology or Medicine for this work, was on the faculty at Case Western Reserve University (and later at Vanderbilt University). Dr. Sutherland was studying the actions of hormones that were involved in glycogen metabolism (i.e. glycogen synthesis and glycogen breakdown). These classic studies identified a substance, now recognized as cyclic AMP (cAMP), whose intracellular concentration was increased in liver cells that were treated with hormones that stimulated glycogen breakdown. Conversely, cAMP was decreased by hormones or other conditions that were associated with glycogen synthesis. Most interestingly, it was identified that different hormones that either increased or decreased glycogen synthesis/breakdown had similar effects on the intracellular concentrations of cAMP (e.g. epinephrine, glucagon). This suggested that somehow cAMP was a common signaling molecule (or "second messenger") that transmitted the extracellular hormonal signal to the inside of the cell to have a biochemical effect (in this case stimulating glycogen breakdown).
In the case of Sutherland's studies, the increased concentration of cAMP stimulated the activity of Protein Kinase A (PKA), and the lack thereof decreased PKA activity and allowed the actions of protein phosphatases to predominate. For example, when glucagon binds its receptor on hepatocytes (liver cells), that receptor is coupled to an intracellular enzyme ($G_S$) that is activated and then can activate an enzyme called adenylyl cyclase, which increases synthesis of cAMP from ATP. The increase in cAMP then binds to PKA and phosphorylates the glycogen synthesis enzymes and breakdown enzymes. When the glycogen synthetic enzymes are phosphorylated by PKA they are inactive and, conversely, when the breakdown enzymes are phosphorylated they are active. Thus, glycogen receptor activation leads to activation of the glycogen breakdown machinery and inhibition of the glycogen synthetic machinery. This makes sense physiologically if you think about it - glycogen acts to increase hepatic glycogen breakdown and increase hepatic release of glucose into the circulation.
In brief, once Sutherland's group demonstrated the importance of cAMP as a second messenger protein within the cell, other groups began realizing that many other hormones led to changes in intracellular cAMP but each had there own effects. The differences in these effects were determined by the cell type that the hormone was acting on and whether or not that receptor was coupled to a particular second messenger system. Thus, you could have any number of receptors on the cell surface that are available to bind extracellular ligands (e.g. hormones, nutrients, drugs). However, each of these different hormones can be "coupled" or linked to different types of intracellular "second messenger" processes to transmit a signal. There are many types of second messengers that help transmit extracellular signals to the inside of the cell.
As you mention in the question, cAMP is a common second messenger system for a variety of different cell types. However, those different cell types have different receptors that are coupled to cAMP. Thus, hormones can have different effects depending on the tissues that express the receptors. For example, the glucagon receptor is expressed on hepatocytes which increases $G_S$ activity and thus cAMP, leading to glycogen breakdown and increased hepatic glucose production. Similarly, the $\beta_2$ adrenergic receptor that binds epinephrine/norepinephrine on smooth muscle is also coupled to $G_S$ which increases cAMP and leads to smooth muscle relaxation. These very different hormones have different biologic effects in different tissues, even though the effects are both driven by cAMP-dependent mechanisms. Briefly stated, it is the receptors that are present on a cell, that determine the response of a particular cell to that hormone.
This is graphically shown in the image below from this medical biochemistry link in adipose tissue - though the same concept is true for liver cells. Glucagon signals through its receptor to increase adenylyl cyclase, cAMP and then PKA activity, while insulin inhibits that activation by increasing the activity of PDE (a phosphodiesterase) that works on breaking down cAMP and subsequently keeping PKA in its inactive form.


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What is the P in LogP?
How does this value actually get calculated?
Logarithms are usually written as
log(base 10) of x
So what is the 'P' equivalent of 'base 10'? I know it stands for octanol/water, but what does that actually mean in a computational context?
I've found many explanations of LogP online, but they usually just say the same thing, which is what LogP is used for. How does one actually calculate it?
Sorry if this is a ridiculously simple question. Bridging the gap between chemistry and math is not my strong suit.

If it's a bridge between Physics and Chemistry than either of those SE sites may be better than Bio.

If the base isn't specified it is usually assumed to be base 10. So you could write it as log10(P). see https://en.wikipedia.org/wiki/Partition_coefficient

Would be much easier to show a particular example.

It means the following:
$$\log P = \log(P) = \log_{10}(P) = \log_{10} \left(\frac{C_{\mathrm{octanol}}}{C_{\mathrm{water}}} \right) $$
With $C_{\mathrm{octanol}}$ being the concentration of the solute in 1-octanol and $C_{\mathrm{water}}$ the concentration of the solute in water.

$C_\text{water}$ is not concentration of water but the concentration of the solute in water. Similarly for octanol.


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Average Nucleus size of human skeletal muscle cell
I’ve been struggling the last couple of days to find reliable data on the average nucleus size of a human skeletal muscle cell. If I deduce it from pictures it should be in the range of 20 micrometers long and 3 micrometers in diameter but I need reliable data and a proper source.
Could anyone help me with this?

Welcome to Biology.SE! You may find it beneficial to take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!

The average "length" for normal human myonuclei is 11.75 µm according to the abstract for:
Watkins, S. C., & Culien, M. J. (1988). A quantitative study of myonuclear and satellite cell nuclear size in Duchenne's muscular dystrophy, polymyositis and normal human skeletal muscle. The Anatomical Record, 222(1), 6-11.
If you can get access to this paper it should have more information for you.

If I am correct, the myoblast are combined into myocytes. Do you think I can assume that the nuclei stay the same size?

Sorry — I messed up. The results were for myonuclei in myocytes (I have no idea what I was thinking when I wrote myoblasts). Now corrected.


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What is the mechanism of cytokine release syndrome in CAR T cells?
CAR T cell administration results in cytokine release syndrome (CRS). But what is the mechanism that induces the CRS in CART therapy? Also, what factors correlate with CRS severity? CAR structure? Or tumor burden?

CRS in CAR T therapy is likely the result of hyperactivation of a large number of immune cells, either by antigen-specific/co-stimulatory activation (T cells) or by non-specific activation due to significantly elevated pro-inflammatory cytokines. CRS is the most prevalent adverse effect following CAR T infusion, but does not always happen. These two reviews provide a lot of detail, and reference many primary studies, but I will summarize briefly below:
1) http://www.nature.com/articles/mto201611
2) http://www.bloodjournal.org/content/124/2/188?sso-checked=true
In patients with CRS, it manifests clinically whenever maximal activation of the infused T cells occurs. From ref 1,
"In the setting of early CAR T-cell trials utilizing “first-generation” constructs (without costimulatory signaling elements), insufficient T-cell proliferation/cytokine production and lack of antitumor response were noted.30 The addition of costimulatory signaling in second-generation CAR design (CD28 or 41BB) translated to improved T-cell activation/expansion, cytokine production, and most notably dramatic antitumor responses in patients with hematologic malignancies.3,31,32"
So the 2nd-gen CAR design leads to better antitumor responses, but can also cause an intense burst of cytokine release that sets off a sort of 'chain reaction' wherein many other native immune cells also begin to massively release cytokines. One of the key pathogenic cytokines in this cascade appears to be IL6. From ref 2,
"Emerging evidence implicates IL-6 as a central mediator of toxicity in CRS...[]... IL-6R is cell associated on macrophages, neutrophils, hepatocytes, and some T cells..[]... High levels of IL-6, present in the context of CRS, likely initiates a proinflammatory IL-6-mediated signaling cascade"
and from ref 1,
"As an effective alternative IL-6 receptor (IL-6R) blockade with the Food and Drug Administration-approved mAb, tocilizumab has demonstrated near-immediate reversal of CRS.3,35 Investigators are now determining the effect of IL-6R blockade on CAR T-cell proliferation, persistence, and most importantly, antitumor effect. Despite this unknown, the use of IL-6R blockade has generally been accepted as front-line treatment for sCRS following CAR T-cell infusion.23,31,36"
Finally, it does appear that tumor burden has been correlated with CRS severity, presumably because of the higher antigen load available to activate the CAR T cells. From ref 1 and 2, respectively,
" It has been demonstrated that the degree of CRS severity is dictated by disease burden at the time of infusion as patients with high tumor burden experience a more sCRS.3,31,32"
"In recent reports of CRS following adoptive T-cell therapy for cancer,10,14,8,28 the incidence and severity of the syndrome also appears greater when patients have large tumor burdens, presumably because this leads higher levels of T-cell activation."
Hope this helps. Clearly there is a long way to go in terms of predicting and managing these adverse events.


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Do we vaccinate sick people?
As I understand, vaccination helps the human body to create antibodies and stimulate immune system to react against specific antigens. If someone gets sick, do vaccines help to stimulate immune system? If so, do we vaccine sick people for some specific disease?

This at the moment could be construed as being quite broad. An example of a post exposure vaccine would be rabies. Source from WHO. There are likely many more examples.

@James Your comment is quite good and may be developped and promoted to an answer. It provides keywords ("post exposure vaccine") and example to answer the question.

Yes. Sick people are occasionally administered vaccines. But you need to keep in mind the mechanism of action of vaccines.
Broadly speaking, there are two types of vaccines.
Active immunization works by exposing the immune system of an individual with a pathogen (be it organism or derived proteins, etc). This type of immunization results in development of adaptive immunity in the individual, with long lasting effect; but it can days or weeks to fully develop.
On the contrary, passive immunization works by directly administering protective agents (antibody, etc). This will provide the individual with almost immediate protection; but will not lead to development of adaptive immunity, and thus will be short-lived.
You may find this wikipedia article informative.

Hi at welcome to Bio.SE! This is a good answer and overviews vaccines neatly, however you've glossed over the core of your answer to the question. Could you provide some examples of situations where sick people have been administered vaccines?

HI James. Thank you. A common example is a tetanus vaccine. I believe if people are thought to have a potential exposure, as in an accident, etc and do not remember whether they are up-to-date with their vaccination, they will get passive immunization for immediate but temporary protection. Other examples are small-pox, chicken-pox, hepatitis A & B. There is a more comprehensive list under "FDA licensed immunoglobulins" on this wiki page.

Are you sure passive immunization is vaccination?

The only case I can think about is postexposure vaccination against rabies.
As rabies virus proliferates unnoticed by the immune system, immediate vaccination after exposure is one of possible treatments (and the first one successfuly used).


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In what two ways is ATP used in coupled reactions?
I already have down "A coupled reaction is when leftover energy from a reaction fuels a reaction that needs more energy. ATP can break apart to transform into something new and use the energy created by breaking a bond to fuel a reaction in need of more energy" I think that is one use but I am not sure and I still need another

A coupled reaction is where a catabolic reaction drives an anabolic reaction, usually with ATP as an intermediary. The energy released from the first reaction allows for the formation of ATP from ADP and P. The second reaction is then driven by the hydrolysis (breakdown) of ATP, which releases energy.

So the answer to your question is: In a coupled reaction, ATP is first used to store energy from a catabolic reaction and then used to release energy for an anabolic reaction.

Another use of ATP is phosphorylation of different substrates including proteins.