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The sex of the offspring of twins?
Given identical twin males, Michael and Douglas, Douglas and his wife have four children, all of whom are girls.  Michael and his wife have only one child, a boy, and are expecting another. What are the chances it will be another boy? If Michael and his wife have more children, what are the chances they will all be boys? Is there any support/evidence for, or a study about, one twin of an identical pair will have children all of the same sex and the other twin will have children all of the same (or opposite) sex?

Personal medical questions aren't allowed here, but you can easily edit it to make it not personal. The gender of your children is determined by chance.

This is NOT a PERSONAL medical question, rather a question regarding research of identical twins and their offspring.  Gender is not determined "by chance", as chance is defined as "a possibility of something happening,fortuitous, accidental".  There is no accident in the gender of a child.

@MichaelPrice in this context chance refers to the fact that something happens without observable cause, not that is accidental. Gender is defined by chance determined by the probability of an ovule being fertilized by an spermatozoid carrying an X or Y chromosome. Different fertilization events (i.e. for each child) happen independently of one another. I am not aware of any research proving gender bias, yet I am not an expert in that field.

I know what you're asking, you should just remove the details about you, your wife and your brother. It might seem trivial, but that is the policy of the site. Anyways, a male's sperm is equally divided into gametes carrying an X chromosome and gametes carrying a Y chromosome. The gender of a child is determined by which sex chromosome is inherited from the father (since the mother only passes on X). So the gender of the child is determined by which sperm fertilizes the egg out of how ever many hundreds of millions. That's where chance comes into play.

@canadianer Afaik it is not just about chance, there is some regulation about the gender, for example after wars the boy/girl ratio is not 1:1. However I never investigated this, so it is maybe just an urban legend...

Note: This is based on literature searches I've done a while ago out of general curiosity. I'm in no way an expert on human reproduction.

If I understand you correctly you are basically asking if there are any evidence for sex biases in offspring between families, that has a heritable genetic basis. This has been an active research topic for a long time and there are a number of proposed mechanisms for how this can be achieved. Historical data sometimes shows deviations in sex ratios over time, e.g. in 20th centrury Europe after WWI and WWII (see data in Gellatly, 2009). There are also other reported/hypothesized deviations in sex ratio e.g. trends in sex ratio due to paternal age (e.g. Jacobsen et al, 1999), sex biases of offspring due to earlier insemination in the menstrual cycle, and the child rank. However, from what I've seen, the evidence hasn't been conclusive and different studies point in different directions.
As Irving et al (1999) point out, possible mechanisms for sex ratio biases can be:

deviations in X/Y-ratio of sperm
selection of sperm within the female reproductive tract
biases in implantation success and/or survival for embryos of different sex

Most evidence seems to point against explanation one, see tests in e.g. Irving et al (1999) and Graffelman et al (1999). Graffelman et al (1999) also tests for an effect of male age, but do not find support for this idea.
Another interesting study is Curtsinger et al (1983), which tries to look at vertical population transmission of sex ratio variation in Japan. They conclude that there is a marginally significant effect on the paternal side, which would support the idea that sex biases might run in families.

An analysis of vertical transmission of sex-ratio modifying factors that excludes effects of birth order in both the parental and offspring generations has detected a marginally significant paternal effect.

However, they also conclude that the genetic variability in sex ratio is very small, if there is one. This study also does not find support for effects of e.g. paternal age or child birth order.
Gellatly (2009) provides a model of how an autocorrelation in sex ratio between generations could be explaned (while still having a stable population-level sex ratio), using an autosomal gene modifying male sex ratio. Note thought that this is a proposed model, and not empirical evidence. However, Gellatly (2009) also use genealogical/pedigree data from North America and Europe to show that there is an heritable component in the human sex ratio (an association between sex ratio in F1 and F2 generations). However, from what I can see the evidence is weak, and the models only explains 0.5% of the variance in the data. The introduction to this paper also has a useful overview of the subject with more references you might want to check out.
All in all, my perception is that there are some evidence that certain sexes can be overrepresented in families, which could potentially mean that the sex ratio in the offspring of a twin brother can contain information on the probablility that his brother will have a son or daughter. However, to me, the evidence is far from conclusive and the estimated effects seem rather weak. So as a null hypothesis, you should definately go for a 50/50 chance of a son/daughter, irrespectively of what the sex ratio of the twin brother is.
As for the general calculation of probabilities of different scenarios, you just use the product of probabilities and sometimes summation of birth orders. For instance (if assuming 50/50 sex ratio), the probability of having three sons is $0.5^3= 12.5\%$ (births: MMM) and the probability of having 2 sons and one daughter is $3*0.5^3= 37.5\%$ (births: FMM, MFM or MMF, i.e. three ways to achieve this scenario out of eight).

I heard of a theory, that X chromosome is heavier than Y, so it is more likely that the child will be boy. But I guess there are many other theories in the topic...

The question you're asking is essentially a version of an old riddle:

If you flip a coin ten times and it comes up heads each time, what are
the odds that the coin will
come up heads when you flip it for an eleventh time?

And of course the answer is that the odds are fifty-fifty. You could instead argue that 10 heads in a row is evidence that the coin is weighted somehow, and the way you would deal with that is by flipping that same coin 1000 more times, or (somewhat less reassuringly) by finding 100 coins identical to your first one and then flipping them each 10 times.
It's the same thing with children's genders. For every family with 6 girls there are hundreds more families with more mixed genders. The only effect known to skew the male-female sex ratio at birth significantly is wide scale sex-selective abortion (it tends to reduce the number of females).

While I agree with you in a practical sense, your answer is assuming that the sex ratio is 50/50 for all couples/populations and that variation in sex ratio lacks a heritable component, which is an open empirical question. Heritable variation in sex ratio is known in many non-human animals.


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Is there a notion of RMSD for two different molecules?
The (least) Root Mean Square Deviation is used for comparing different conformations of the same molecule. However one may be interested in comparing the conformations of two different molecules e.g. two proteins of different backbone lengths. So is there any method for comparing conformations different molecules such as a generalized RMDS?

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Do residue sequence numbers in PDB files correspond to the positions in the backbone?
In other words if two residues have sequence numbers, say, 20 and 21 then are they next to each other in the backbone? If no (or not necessarily) then is there any way to find consecutive residues from a PDB file?

The residue numbering convention in the PDB is more-or-less entirely up to the depositor of the structure. While generally speaking sequential numbers are next to each other, there is no guarantee of that fact.
For example, the PDB allows for what are called "insertion codes", which are extra residues which interrupt the regular sequence progression. For example in the PDB entry 1IGY in between residues 52 and 53 on chain B is residue "52A". Normally, these insertion codes are used because the depositors want the numbering scheme to correspond with some external numbering standard, and there are extra residues (e.g. from affinity maturation) which would throw off this numbering.
Alternatively, the depositor might choose to mix up the numbering significantly. An example of this is the PDB entry 4OO9, which is the transmembrane domain of human mGlu5 with a lysozyme insertion to help crystallization. The mGlu5 is numbered from chain A from 568 to 832, but between residues 678 and 680 are residues 1002 to 1162, representing the inserted lysozyme. (So it goes 677, 678, 1002, ...)
Ultimately, the only reliable way to tell if two residues in the PDB which are sequential in numbering are actually sequential polymerically is to actually look at the coordinates and see if they're in a bonding configuration. There may be some information about "out-of-order" residue numbering in the header lines, but that's not always clear. Usually you have to deal with such situations on a case-by-case basis.

Thanks to @R.M. for the good description. I've also found a nice, detailed description with a few interesting examples here.

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Why is statistical mechanics relevant to RNA and protein folding?
This is a very naive question. As far as I understand the folding of a molecule is governed by the electromagnetic forces between its atoms and also between its atoms and the atoms in the surrounding environment (so basically a many body problem). So I don't understand how statistical mechanics, such as Boltzmann's law, come to play.
To my knowledge statistical mechanics and thermodynamics exist when we have an ensemble of particle such as in a liquid or a gas. So what is this ensemble for the RNA or protein folding problem?

There are too many possiblities. And it still would need supercomputers to calculate how a protein is folded. As well as it is still unkown how the complete mechanisms are working.... therefore statistics are necessary...

Consider a polypeptide, newly synthesized, prior to folding up into its 3-dimensional shape, or structure.  Each substituent amino acid, contributes to the unique sequence of the polymer, and each affects, in some small way, the number of different states that the polymer could be found in, at any given moment.  Given the constraints imposed by the length and geometry of the chemical bonds, there are some states the polymer cannot adopt, but there are many, many states that are potentially available, and each has a unique energy. Over time you can plot these energies yielding a distribution.

I’m no physicist, but your statement “To my knowledge statistical mechanics and thermodynamics exist when we have an ensemble of particle such as in a liquid or a gas” is surely incorrect. The problem of protein folding is one of thermodynamics — finding the structure of lowest free energy, and the path by which it is reached from a random coil.
One of the difficulties relating to the path is that of getting ‘stuck’ in a position in the energy landscape from which the protein cannot escape. This is called ‘frustration’ and there is apparently a quantitative treatment of ‘minimal frustration’ using the statistical mechanics of spin gasses. This is mentioned in a review by Onuchic and Wolynes, available on-line, which you will probably be able to understand better than I can.

If you want to relate statistical mechanics to RNA and protein folding, you're on the right track with ensembles. Macromolecules are very dynamic and exist in many physical states. These macrostates are what are described by David on an energy landscape. The macrostates can be further broken down into microstates which are closely related movements of the macrostates. It depends how specific you want to get when describing your system. Statistics come into play when describing the populations of the macromolecule in its different macrostates. Typically, the macrostate with the most favorable energy conformation is the most populated.

You seem to have confused two different ways of discussing a thing with two different things. Electromechanics always applies, whether talking about liquids or gases or what have you. All molecules are subject to electromagnetic forces. And all matter has populations of molecules, which we can talk about with statistical mechanics. In statistical mechanics we abstract away some of the details of electromechanics and treat them statistically, just like how in economics we abstract away some of the details of individual psychology. So both apply, in every case. The problem is that RNA folding is a particularly tricky physical system, so abstracting it away is with statistical mechanics is far harder than it would be for say, a noble gas.

Indeed, statistical mechanics is applicable to the systems with many degrees of freedom (typically of the order of the Avogadro constant, $N_A\sim 10^{23}$). Gases, liquids, and solids routinely fill this definition, as they consist of huge numbers of atoms or molecules, each of which has at least three degrees of freedom (for molecules we also need incorporate their rotation and elastic movement).
There are two ways how statistical mechanics can be applied to proteins (see, e.g., the discussion in the book by Doi):

one may consider a solution containing a macroscopic (i.e. $\sim N_A$) number of polymer molecules
one may consider a single polymer molecule as a statistical ensemble, because a polimer with many links can adopt huge number of configurations and therefore satisfies most of the criteria necessary for applying statistical phsyics. This is specially true for polymers with $10^5-10^6$ links, but provides useful guidelines for relatively short protein molecules, with typical lengths of a few hundreds od amino-acids.

As an example we may consider protein folding (see, e.g., this question): a protein would fold spontaneously even in a vacuum, and even if the forces between its parts were non-existent. The reason is entropy: a chain of molecules can adopt billions of configurations in space, of which the stretched configurations would form only a small fraction. Statistical physics tells us that all these configurations are equiprobable, and we therefore are likely (what practically amounts to certainty) to find protein in a folded configuration. (This equiprobable state is referred to as maximal entropy or maximum of an appropriate thermodynamic potential, if we are not dealing with a closed system.)
Adding interactions between protein links and between the protein and the solvent molecules makes the problem even more amenable to statistical physics analysis (although now one may have to deal with folding-unfolding phase transition).

References

M. Doi, Introduction to polymer physics
K. Huang, Lectures on statistical physics and protein folding

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What is a group of tortoises called?
This post at Mental Floss stated that a group of tortoises is called a 'Creep'. I had never heard of that before, and in trying to find the references for the name, I was surprised that I couldn't actually find anything.
Wikipedia showed no results in either of their lists for animal names.

http://en.wikipedia.org/wiki/List_of_animal_names
http://en.wikipedia.org/wiki/List_of_English_terms_of_venery,_by_animal

Neither did the Northern Prairie Wildlife Research Center: http://www.npwrc.usgs.gov/about/faqs/animals/names.htm
The closest I found was that a group of turtles is called a nest or a bale.
Is there an actual source for what a group of tortoises is called?

How big of a group do they say a creep is?

@rhill45 They didn't say anything about the size of the group, just what the (supposed) name is.

@rhill45 I asked this to my new friend at The Tortoise Group, and he replied: I thought that a group was any collection of more than one. So even though there are words for two (pair, brace, duo, couple, etc.) it would still officially qualify as a group!

Creep is correct. I sent an email asking this question to The Tortoise Group, which is a non-profit organization whose mission statement is:

Improving the lives of wild and desert tortoises through education.

The Executive Director replied:

It's a bale for turtles and a creep for tortoises. I am sure they could have come up with a better name!

If you have additional questions, there's a wealth of scientific information on their website.

Okay but where does the word come from? The OP isn't asking for someone to validate the claim but explain the origins since it isn't common or listed on many sites. Read the last sentence of the OP it asks for a source not a validation. He has already learned that creep is a word used to define this.

I apologize if I missed the point of the question. I emailed the same source asking specifically for the origin of the name, and will let you know if/when he replies.

Maybe for the etymology part of the question, this related question on a related SE site could help: http://english.stackexchange.com/questions/21336/a-murder-of-crows

I received this from The Tortoise Group: "That's a good question. I think with all those collective nouns, it's difficult to find out exactly when the term was first used, or how or why.  All I know is that it was used because tortoises creep slowly. Sorry I couldn't help with this one!"

What I found was that creep is a collective noun. The professor Peter Trudgill uses the word in a chapter about collective nouns and the example is of tortoises. I don't know what book to tell you to look in though. He is professor of sociolinguistics. From a search on collective nouns for animals, turtles, and reptiles, I only found turtles having the following collective nouns: bale, nest, turn, dole.
My guess is then that Peter Trudgill made up the word and some people have adopted it or it is primarily an English (England) word.

collective noun list two

I believe I found the source. In Geology, a creep is defined as a slow moving mass. By borrowing the word creep from Geology, one can accurately describe a group of tortoises.

Creep

I have worked in various parts of the world in sales of engineering equipment, but have always been involved in animal conservation, especially for turtles and tortoises.
One of my previous employers, now an engineering company was originally purveyor of turtle meat to HM Queen Victoria. They provided the Green Turtle Soup entrée  for Queen Victoria's Coronation Banquet, and for the Royal Family in general up to H.M. Queen Elizabeth II, who also had green turtle soup at her coronation banquet. It was not on ration points. The company had the royal warrant.
I'm afraid the general terms for tortoise and turtle in English come from the meat trade.
A "creep" originated in the Galapagos, where the tortoises were hunted often to extinction, by sailing ships crews, whaling or other, and even HMS Beagle.
Once on board a creep became a bale, also the usual description for sea turtles caught by nets, and stored, like their land cousins in tightly bound nets. There was a number of individuals and weight for a bale. There was a market standard for different species - say 4 Leatherbacks per bale, 6 Green per bale. Green turtles were favoured as they had tasty meat but did not expire quickly.
If the animals were caught by bill hook or harpoon they were put in a 'drag bale', thus injured they would be the first consumed by the crew. Those captured at sea or on land put in nets were "bales" (uninjured) when landed. Galapagos Tortoise may be one per bale.
There were markets all over the world; in London, it was Billingsgate for the meat, and for the shell it was Lower Thames Street. Turtles were delivered live to restaurants. Generally, the voyage and the occasional wash with water had purged them. Shell and meat would then be subdivided with other terminology, depending on the quality of species meat and shell.
Obviously, there are many other terms for chelonian meat and shell in other languages - florid descriptions in China and French/Creole on the East Coast of America for the Diamond Back Terrapin and the alligator and common snapping turtle, for instance.
I obtained this information from an old employee of the former employer's green turtle soup restaurant at a company dinner in London. No, we did not have turtle soup, and I did not kill him. He was a really nice guy and a war hero with the London Scottish Regiment. For the shell business, I know something from another of my employers. We were involved in trading heavy equipment to the former Soviet Union. Our offices were next to the dreadful fur trade warehouses on Lower Thames Street, which was next to the Turtle Shell Exchange (this may not be the correct title of the market).
My point is that our naturalist forbears took collective nouns, in this case, from general parlance. They were generally scientists. Conservationists came later. I think the collective noun was thus applied outside the tortoise/turtle trade to all species by English speakers.

can you add some external references to back up the claims in your answer? we generally like to see references for nearly all information so that other individuals can read more/further on the topic - thanks

http://www.britishcheloniagroup.org.uk/testudo/v2/v2n5darwin

https://www.theguardian.com/books/2004/jul/31/featuresreviews.guardianreview7


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Plasmid addiction system in high-copy number plasmids
Are there high-copy number plasmids that utilize a plasmid-addiction system?

According to the review by Kroll J, Klinter S, Schneider C, Voß I, Steinbüchel A. Plasmid addiction systems: perspectives and applications in biotechnology. Microbial biotechnology. 2010;3(6):634-657. doi:10.1111/j.1751-7915.2010.00170.x., there are high-copy-number Plasmid Addiction Systems (PAS), "specifically the addiction system depending on plasmid‐borne ORT utilizing the lac repressor."

The lac repressor protein (LacI) binds to the lac operator (lacO) and therefore represses the expression of the kanamycin resistance gene. When IPTG is available as an inducer, LacI is titrated by lacO, and the E. coli cells were able to grow in media containing kanamycin due to expression of the corresponding resistance gene. The same result was obtained when high‐copy‐number plasmids harbouring lacO were used for ORT. In this case the plasmid was stably maintained over 72 generations (Williams et al., 1998).

ORT = operator repressor titration
ORT is one of the three main groups of PAS.


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Is there a reproductive barrier between Khoisan and other humans?
I have heard in an ethnology lecture that more or less all human ethnicities interbreed without a barrier (rate of reproduction of fertile offspring) except the Khoisan + any other human ethnicities, where fertile offspring is less likely than when other humans interbreed (as a an anecdotic side note, there are rumors about Zulu men who prefer Khoisan women as second or third spouse in order not to produce too many kids). My question is if some can confirm or falsify this (any literature coverage)?

Check the book "Genetic Nature/Culture: Anthropology and Science Beyond the Two-Culture Divide" edited by Alan H. Goodman, Deborah Heath, M. Susan Lindee. Page 205 states that that is a myth started by geneticist F Lenz of Gottingen that has been disproven.

Oh dear, which (FL) on top is a very dubious source, thank you for clarifying this!


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Where happens MHCII coordination to a self-peptide, and what happens if the bond would be irreversible?
MHC-II proteins are presenting antigens on the surface of cells with lysosomal activities where they eventually might get transported off by some T-cell receptor-anti-gens, as far as I understand (pls apologise and correct me if I am wrong). I would be interested in two questions regarding this specific immuno-cascade reaction.

It appears that in cases self-pepties are bound to the MHC-II proteins (say HLA-DP2) when they are at the surface already. Where do such self-peptides come from? Do they come from inside the endosomal active cell or could they also come from "outside" from where the T-cell comes?
What would happen if (for some reason)
a) the self-peptide binds "irreversibly" to the MHC-II?
b) the self peptide binds irreversibly to the MHC-II and at the same time is structurally significantly distorted (e.g. if there is something, like a heavy metal bound in-between the MHC-II and the self-peptide)?

(I apologise for the case I got some terminology wrong or some basic concepts, I am no specialist in bio-chemistry.)

It appears that in cases self-pepties are bound to the MHC-II proteins (say HLA-DP2) when they are at the surface already. Where do such self-peptides come from?

Class II MHC molecules are capable of presenting any peptide of appropriate length, regardless of where it came from. Contents in a phagolysosome will contain both self and non-self peptides.

Do they come from inside the endosomal active cell

Some do, yes. While many proteins are degraded by the proteosome, some are actively imported into a lysosome and degraded there. This is termed chaperone-mediated autophagy. Full organelles may also be brought into the lysosome through "regular" autophagy.

or could they also come from "outside" from where the T-cell comes?

This is the case as well. Any ingested material from the outside could contain cellular debris, protein agglutinations, or foreign organisms. Peptides from all of these sources can be presented at the cell surface.

What would happen if (for some reason) a) the self-peptide binds "irreversibly" to the MHC-II?

According to this study, MHC II molecules are recycled, and their turnover is carefully regulated. There is no need for the bound peptide to dissociate during antigen presentation, so likely problems would occur when MHC II turnover is disrupted.

the self peptide binds irreversibly to the MHC-II and at the same time is structurally significantly distorted (e.g. if there is something, like a heavy metal bound in-between the MHC-II and the self-peptide)?

If the MHC itself is structurally distorted, it will not be recognized by any other cells. Remember that, during T cell selection, the cells must be able to recognize the MHC itself with a low affinity. T cells which bind strongly to the MHC itself undergo death by negative selection, whereas those which do not recognize the MHC at all undergo death by neglect. As a significant structural change would result in either an excessive affinity, or no affinity, no T cells capable of recognizing the complex would be present.

Thank you very much, that answers all but the last part. What I meant was what would happen if the self-peptide is distorted by the complexation. As far as I understand, there is (must be) some regulation against developing an immuno-response against self-peptides. But the question would be what would most likely happen if the self peptide is so strongly distorted, that it is no longer recognisable as a self-peptide. Does this make sense? In case what would happen?

"Class II MHC molecules are capable of presenting any peptide of appropriate length"  Just to clarify this, MHC molecules are not capable of presenting any peptide, but rather present a subset of peptides that have the required sequence determinants that allow binding in the MHC groove. Often there are key 'anchor' residues in the peptide that bind to hydrophobic pockets on the floor of the MHC binding groove. You are right in saying that it doesn't matter where the peptide came from though.


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Identify plant from genus *Solanum*
This spring we have recieved from a local Botanical garden in Southern Germany a pack of seeds with the label "surprise". We could grow one plant from the seeds, the seeds looked like "pepper" = Paprika Capsicum annuum seeds. The plant got about 50 cm high and bore one fruit of 5 cm length including the trunk. The leaf in the picture has 10 cm total length. It has a very rough backside but not really hairy one. Also the upper side feels rough but there are no hairs. Also some yellow flower can be seen.
Initially I thought it is some capsicum so I cut it but was surprised when I saw the thick pulp. The skin is also quite strong and like very soft leather. It has a nice sweetish taste and some remembrance of lemon in taste but also some exotic "veggie" note. What could that plant be?
After searching the web my idea was that it could be Solanum sessiliflorum DUNAL, that is Amazonian tomato or "cocona". But I am not sure at all. Any hints appreciated!

If I were you I would probably ask the garden :)

Yes, I had already that thought as well ;-)


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How to differentiate between Bombus lapidarius and Bombus wurfleini?
I am observing frequently different bumble bees in my garden (Austria prealpine-alpine region). One of them that I frequently saw is all black with red-orange abdomen (tail). From a very simple schematic poster I found I had concluded it would be Bombus lapidarius, but now reading a bit more on bumble bees I find it could as well be B. wurfleini. My question is now what would be the most obvious/simple way to discern between the two species?


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What is meant by [protein name]+/- (ie "Myod+" and "Myod-")
I have read a paper where this notation for protein names is used:

Myod+ and Myod-

(or another example, Myog+, Myog-).
What does this indicate?  In the paper I'm reading, and some brief googling, it seems that Myog is itself a protein, and not that there are two kinds called Myog+ and Myog-.
Examples are here (the one I'm reading) (Figure 6c), or here (page 3, pdf page (journal page 958)).

The paper you linked is not open-access, so many people won't be able to help you. However, as a common convention, ProtX+ and ProtX- typically refer to cells, tissues, or individuals that either express or don't express a particular Protein X.

Oh okay, that makes sense.  Thank you.  Sorry I didn't realize it wasn't open source.  It looks like the second one is available though (if I open in incognito, I can access)

To expand on @MattDMo , italicized names indicate genes, with the + or – being used to describe either genome or cell with or without an active copy of the gene and thus able to make the protein, the name of which may or may not be the unitalicized form of the gene. (Many genes are named for the phenotype they convey or some other reason when they are discovered before the protein product has been identified.)

@David or.......

@MattDMo either of those could make a concise answer. Probably not a lot of reference needed for an answer like this; one example might be nice but not really necessary.

@MattDMo — Do you want to follow up Bryan’s suggestion?

@David I did...

@MattDMo — Good.

The Stem Cell Reports paper linked in the question is open-access, so anyone can download it freely. Unfortunately the Nature paper is not.
There are two different abbreviation conventions being used in the open paper – MyoD+/MyoD- and MyoD+/MyoD-. The italicized version indicates the genotype of the cell, tissue, or individual being referenced, so for example MyoD- indicates the MyoD knockout they made. This convention is very widely used to refer to genes or mRNA.
Examples where the gene name is not italicized refer to the protein product of that particular gene and its presence or absence. So, MyoD+ cells express the wild-type protein, while MyoD- cells do not. This convention is also very widely used to refer to the presence or absence of the indicated protein.

Are there rules on the site against me sharing the part of the figure I am talking about (that is not open access)?

@user8243 it may be copyright infringement, but I'm not a lawyer.

I think my smaller question doesn't require it.  Reading through the methods, it seems all of their cells are from embryo sample, and no genes were explicitly knocked out.  Then here, does the minus indicate that no expression was observed?  Seems like it follows from your answer, but wanted to check

@user8243 the minus can either be used to describe a KO ("no expression is expected"), or to describe the results of an assay where expression is actually tested, such as immunofluorescence or Western blotting.


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What kind of bug is this on my curtain?
These bugs are frequently found hanging on a curtain next to my window.

This is a carpet beetle, although identifying the exact species is difficult. Compare for example the varied carpet beetle, Anthrenus verbasci:

from https://en.wikipedia.org/wiki/Varied_carpet_beetle#/media/File:Dermestidae_-_Anthrenus_verbasci.JPG

To add to @AL's answer.
This is a beetle of the Dermestidae family. These are a failry diverse group of beetles with a variety of names based on what they are most commonly found eating. Some of the species are specialist eaters of decaying animals. As you have found this one inside it is likely that you have one of the species known as Carpet Beetles. I would go so far as saying that what you have here is a member of the Anthrenus genus. To quote the Colorado Edu site I linked for carpet beetles:

The smallest dermestid beetles found in homes are in the genus Anthrenus. These are typically about 2-3 mm long and have a round body form. Adults have colorful body patterning produced by scales of yellow, browns and white. The larvae are spiny, with a body that is slightly narrower at the head end, which is often tipped with a small tuft of hairs. Species that occur within homes in Colorado, in approximate order, are the varied carpet beetle (Anthrenus verbasci), furniture carpet beetle (Anthrenus flavipes), and common carpet beetle (Anthrenus scrophulariae).

Carpet beetles are common destructive pests eating a wide range of items from clothes (cotton, silk, wool) to dust. If you have these in your house, expect to find holes in some of your less-used clothes, especially if they are stored in dark places.
The larvae are covered in hairs and look like small caterpillars. You may find them crawling along the floor in a quick humping sort of motion, much faster than a caterpillar/inchworm action.
You can control them with regular flysprays, but it is best to get an exerminator in to kill off the infestation and spot-control from there.


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How do the hair cells of the inner ear contribute to most of the hypercapnic respiratory response?
https://www.sciencedirect.com/science/article/abs/pii/S0306452210015253
Mice with damaged ears exhibited a significantly suppressed respiratory response to carbon dioxide.
From the study:

The mean respiratory frequency of control mice increased in response to CO2 by more than 100 breaths per minute, an increase of approximately 40–60% over their baseline values. In contrast, the ear-damaged experimental mean values increased by only 2–11%

Question: How do the inner ear hair cells contribute to most of the hypercapnic respiratory response?

Welcome Sarah. There's a related question, though the link may not seem immediately apparent. ;)

I don't know. Does anyone know? Did you try to find an answer? How? Please edit your question to include your research.


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How well does the radius of a tree correlate with its age?
I'm looking for a cheap non-invasive ways to approximate the age of a tree (a birch). Measuring the radius pops up in the mind as the first alternative. How would one do that? Measure at multiple defined heights?
I'm hoping that I could get some kind of confidence interval for the approximation, so that the data could be used in a scientific publication.
Or is there any reliable DIY radiocarbon dating technique?

I'd take a look here: http://www.arborilogical.com/tree-articles/how-to-age-a-tree/

It's going to depend very strongly on species.  I have some cottonwoods which I know were planted in the mid-60s, and which are about 4 feet thick at the base.  (Some of the annual growth rings are almost an inch wide.)  OTOH, some of the mountain mahogany I have for firewood is much older, yet only around 6 inches thick.

Radiocarbon dating won't work. For a start the tree needs to be dead, which since you're not using the rings I'm assuming it isn't. Also the atomic testing in the 20th century completely messed up the level of C14 in the atmosphere, so radiocarbon dating can't be used for anything that didn't die 70 years ago or more.

@RobMackinnon But it looks like the C-14 from bombs has been utilized in other tests. And as far as OP's original question goes, C-14 dating would not be a cheap way to do it, and you couldn't do it yourself. The uncertainty in the measurements also means that C-14 is only good for approximate age, and may be off by around 100 years, which is a lot compared to the lifespan of most trees. Dating based on bomb carbon might actually be better for recent objects.

The radius of tree is not a good measure of the tree age, the most efficient technique to know the age of a tree is with dendrochronological methods, this is the less invasive technique. However, knowing very well the dynamics of growth of each species you can infer the age, check out this study:
Jan Lukaszkiewicz and Marek Kosmala. 2008. Determining the Age of Streetside Trees with Diameter at Breast Height-based Multifactorial Model (note this is a direct link to a pdf)

A tried and true method is to measure the diameter of the tree (which plays into your radius idea). Measurements are taken at "breast height" (~4.3ft, 1.3m from the ground). You can purchase a 'diameter tape' or 'girth tape' which consists of pre-calculated measurements, this way you will not have to measure circumference and derive diameter from this measurement. Breast height has been a consistent standard measurement over time, despite where a tree may begin to buttress, or flare out at the base. Below is an image detailing atypical tree measurements.

This does not deal with age correlations at all, and does not answer the question.

Can you add references to your answer and change it in a way it actually answers the question?

authors: Абырвалг Шарикофф


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Do we posses technology to rebuild sequenced DNA?
Is there existing technology that would allow to rebuild DNA molecule from a digital file storing sequenced DNA?
If not, does there at least exist theory explaining how such device could be built?

This question is quite broad. Also see this: https://en.wikipedia.org/wiki/Artificial_gene_synthesis

Yes, in fact synthesizing short stretches of DNA and RNA is available through several commercial services. However this limited to tiny DNA fragments (say 120 base pairs or so). Longer sequences require custom laboratory work.

Making long sequences is possible too. The J. Craig Venter instistute synthesized an entire bacterial genome.

@user137 While it's true that long sequences can be made, this most often requires 'manual' stitching of several smaller fragments. However, current technology can already generate fragments of a few 1000bp (see e.g. here)

Thousands of base pairs is trivially possible with current technology - it's an off-the-shelf order from many companies. Tens of thousands becomes tricky. More importantly, although the question doesn't specifically ask this, this could not be used to re-create extinct animals (other than perhaps bacteria) because among other things epigenetic information would be missing.


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A good textbook on GMO
I am interested in learning about GMO. The topic is so wrapped in controversy, that it's hard to find a good book that introduces the basic concepts involved. I went through various university websites, but couldn't find any lecture notes on the topic. I don't know, is it too broad a topic? Is there even a book called Introduction to GMO? Maybe that's the problem.
I am interested in a book that tells you about how gene manipulation is done. How do biology students get introduced to this concept? I hope the question is not too general.

To be honest I don't remember being introduced to this at all in the classroom. I remember 1 lab in genetics where we transformed E. coli with GFP. Everything else I had to learn in the lab doing research at the undergraduate and graduate level.

@user137 Hmm, that would be a little troublesome. There must be some book that consolidates all the basic knowledge on the topic. For example, if I want to learn about Quantum Mechanics, I go look for an introductory text. Am I making a wrong analogy?

Welcome to Biology S.E.! If you need additional assistance, please visit The Help Center.

This is something that is being introduced to me in high school biology; although there hasn't been a major emphasis on it.

@PandaBear I think part of the issue is that so much of genetically manipulating an organism is technique based, and the best way to teach a technique is in the lab. The other part may be that GMOs in the wild are so new that we don't have much good research to write textbooks with yet.

@user137 Oh ok. I didn't think about it that way. That exlains why my search for lecture notes was futile.

I too had difficulty finding any textbooks or notes that focused solely on genetic engineering. However, after some rather intense looking, I did come across several textbooks that may be helpful. I wasn't sure how basic of a text you were looking for but I'm hoping college level is okay because that is all I have been able to find.
The first book was An Introduction to Genetic Engineering by Dr. Desmond S.T. Nicholl.
Another was Principals of Gene Manipulation and Genomics by Sandy B. Primrose.
If you need a more basic biology text for reference, I would recommend Miller & Levine Biology by Prentice Hall (Pearson Prentice Hall). Also, you could do a quick-study on genetics on Khan Academy - Crash Course: Biology and Ecology.
I hope this information was helpful for you!

I'll go the library and check these books out, see if I understand them. Yes, I do need to brush up my knowledge of basic biology.

Before going into the trouble of reading a textbook on GMOs, ask yourself if you truly understand what the "controversy" is all about? I'll restrain the following comment to GMO crops (as I strongly feel it is in that area that the hysteria whipped up by a public that is poorly educated in science harms society the most).
The public perception often seems to be fall somewhere in between these two extremes: "crazy scientists insert genes from jellyfish into [crop], making a jelly-[crop]-fish...which is just weird/wrong and must therefore be opposed" or "evil big corporation inserts bad genes into plants, which can then escape into the wild, transmit their bad genes into all other plants, and unleash..."...err...zombie plants?
However, I would suggest that a lot of people are blissfully unaware that MOST of our cash crops have been heavily genetically modified, through millenia of domestication, hybridisation and selection.
For example, durum wheat (commonly used in making semolina and pasta) is an artificial wheat crop, created sometime around 9000 years ago by farmers who crossed two different species of grass crops and selected for a hybrid polyploid plant that had favourable characteristics.
The modern maize plant is another artificial organism created many millenia ago by mesoamericans through hybridization and artifical selection, two of the traditional genetic modification tools available to early farmers.
The apple is a hybrid plant created through crossing of two different species of plants....again done at the dawn of civilization.
I suspect most people who are vehemently opposed to GMO technology are ignorant of the history of farming, let alone the science behind GMO.
===============================
Anyway, to answer your question, the "concepts" behind gene manipulation are very basic molecular biology techniques, applied in this context at improving the biochemistry of the organism. Therefore, a good place to start would be a basic textbook such as "Molecular Biology of the Cell" by Alberts or something akin. But a basic botanical textbook on crops would be just as beneficial, in my humble opinion.

I mentioned controversy, because whenever I type the word GMO in google, I get overwhelmed by the amount of conflicting information on the topic of safety of GMO. I am not interested in that aspect. Nor in the politics involved. I just want to learn the subject because I feel like I am interested in it.

Fair enough, but my point is that there shouldn't be any controversy about a subject matter that we have been engaging in, and benefitting from, for millenia....


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Purple caterpillar found in Peru rainforest
Caterpillar fron Peru rainforest with purple body and orange or reddish tips. From Manu National Park

That's a very striking caterpillar. Unfortunately a lot of caterpillars in those regions haven't been matched to an adult butterfly, so it might be very difficult to get an answer.


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Is it impossible for some female songbirds to sing?
I have read that in northern hemispheres, most female songbirds can't sing (for example, the Blackbird). Things are different in tropical regions. Birdsong is for males in some species; it is utilized to defend territories and/or attract other females.
While it seems impossible that female songbirds can't perform complex songs, can it be possible for captive birds?
I have read some reports that females are able to sing after being injected with testosterone. But the interesting question is whether females can be trained to sing without testosterone injections or other interventions?
There is an article showing that for one songbird species it is possible to produce female birdsong without testosterone injection (while older research claimed, females sang only when treated with this hormone): https://www.newscientist.com/article/2151727-female-birds-that-used-to-be-silent-are-now-singing-like-males/
There are dissertations about birdsong and sexual hormones: https://research.vu.nl/ws/portalfiles/portal/42186406/complete+dissertation.pdf
And here it is reported that female songbirds sang after getting testosterone: https://journals.sagepub.com/doi/abs/10.3181/00379727-41-10631?journalCode=ebma

It's usually helpful for people trying to answer the question if you include some links to the places where you have found these ideas. Thanks.

Here is an example link: https://www.newscientist.com/article/2151727-female-birds-that-used-to-be-silent-are-now-singing-like-males/

Great, could you edit your question and link it in the relevant part?


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Cut plasmids with unknown sequence only once
Is there a way to linearize plasmids in a sequence-independent manner?
The circular plasmid should be cut ideally only once. It does not matter where. But as soon as it is linearized, it should not be cut any more.
We are talking about plasmids up to about 20kb.

Do you have any information on your plasmid?

The method should not be dependent on the host/origin or on any other characteristics. It should work for bacterial plasmids, constructs, etc. So basically as long it is circular double stranded DNA the approach should work.

When you write "it does not matter where", does that mean it can cut in the insert of a recombinant, or is it necessary that the cut be in the plasmid vector itself?

@David Yes, it can cut the insert as well. It really does not matter where in the plasmid.

Ok. Well, I think my answer is ok. If it had to cut the plasmid you might have to engineer a DNAase attached to a protein that specifically binds to the origin of replication or the like — a major undertaking if it doesn’t already exist.

I was going to write a facetious comment asking if the poster believed in fairies, but I restrained myself. Why? 1. because it would not have been nice, 2. because it occurred to me that there was a hack you might be able to use to do this:

Let Nature do the work for you.

Long, long ago, I used to do DNA cloning myself, and so I frequently ran plasmids on agarose gels. I have lost most of the photos, but I happened to contribute a chapter to a text book in which I presented an example, so I reproduce a photo below:

What this shows is that in practice (at least they way I did it) a plasmid preparation does not consist of just a single band representing supercoils of the double-stranded closed circular DNA. Typically, and to varying degrees, there are two more species produced by shearing (or perhaps slight nuclease contamination) — relaxed nicked circles and doubly-nicked linear species.
The linear species would appear to be what the poster wants. (He doesn’t say what he intends to do with it, so I can't be sure.) If so, the band in the gel could be cut out, placed in a dialysis bag in suitable solution, and subjected to an electric field, when the DNA will be removed from the gel into solution by electrophoresis. (I can’t remember the details of the latter. I used to do it routinely, so it should be well documented on the Internet, and there may well be modern, more efficient ways of retrieving DNA from agarose gels.)
But if you wish to improve on Nature…
The proportion of linear species in the gel above is relatively low, so one might wish to go one better. In fact my original thought was to use low concentrations of DNAase calibrated to produce just the two cuts that would generate linear species, before I realized that there was probably no need to go to the trouble of calibration as plasmids contained nicked linear species already. There are many commercially available non-specific endonucleases such as bovine DNAase I that I imagine one could use. I am not quite sure how one would terminate the reaction and inactivate the DNAase. Heat perhaps; one could check how this is done in other procedures like footprinting.
It is possible that the nicking is caused by physical shearing, in which case one could perhaps vortex the plasmid to increase this instead of using DNAase.
The general idea of calibration to obtain the ‘right’ incomplete reaction is seen in the chain-termination method of DNA sequencing, for example. Any incomplete reaction will always give a range of species, of course.


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How long does foreign DNA stay intact in human blood?
How aggressively is foreign DNA in blood targeted and degraded by the human body?
I am asking because we have a metagenomics project where we want to detect parasite DNA in the human blood. The process from DNA extraction to sequencing to bioinformatic analysis is not a problem for us. But the question is if we can expect some signal in the data.

This paper may be useful https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3728338/

The De Vlaminck Lab has extensively studied the origins of circulating cell-free DNA (cfDNA) in human plasma and its utility in detecting infections and organ injury.1,2  Concerning your question of parasite DNA detection and parsing signal from noise, I don't think you'll find a better resource than their 2020 publication in Microbiome.3
If the (uncited) claims on their website are to be believed, cfDNA from all sources is cleared within one hour after release into the blood.

Our research pursues technologies and applications of cell-free DNA in infectious and immune-related disease. The great promise of cfDNA in diagnostic medicine derives from i) its abundance: 10-100 billion molecules of cell-free DNA can be isolated from just 1 mL of plasma. The combined DNA sequence of these molecules is sufficient to cover the human genome 1,000 to 10,000 fold. ii) Its origin: cell-free DNA is derived from dead cells and comprises rich information about cells in the blood and any vascularized tissue that can be accessed noninvasively. iii) Its short lifetime: cell-free DNA is cleared from the blood within 60 minutes. Cell-free DNA therefore provides a very dynamic window into health.

References

Burnham P, Kim MS, Agbor-Enoh S, Luikart H, Valantine HA, Khush KK, De Vlaminck I. Single-stranded DNA library preparation uncovers the origin and diversity of ultrashort cell-free DNA in plasma. Sci Rep. 2016 Jun 14;6:27859.
Cheng AP, Burnham P, Lee JR, Cheng MP, Suthanthiran M, Dadhania D, De Vlaminck I. A cell-free DNA metagenomic sequencing assay that integrates the host injury response to infection. Proc Natl Acad Sci U S A. 2019 Sep 10;116(37):18738-18744.
Burnham P, Gomez-Lopez N, Heyang M, Cheng AP, Lenz JS, Dadhania DM, Lee JR, Suthanthiran M, Romero R, De Vlaminck I. Separating the signal from the noise in metagenomic cell-free DNA sequencing. Microbiome. 2020 Feb 11;8(1):18.

But things like NIFT work because the foreign DNA is being constantly renewed.  Presumably non-human parasite DNA would be as well.

Thanks much! How would you inhibit the degradation of the cfDNA? EDTA and cooling? Cooling what temp?


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How do fish communicate?
Fish, as far as I know (of course there may be exceptions), don't have any vocal organs, despite the fact they are proven to be social. So how do they manage to communicate with each other? On land, organisms like the honey-bee have their "tail-wagging dance" and ants have pheromones, so what about fish?

There are a variety of fish species that produce sounds, including many species of Bocaccio (i.e. rockfish). This article is a great resource for learning more about 'fish choruses', a phenomenon where many fishes produce noise during dawn/dusk hours, much like the dawn chorus we're more familiar with for birds.
One of the most famous examples of fish vocalizations is probably the plainfin midshipman fish (listen here!). In this case, the hum is used to attract females for mating.
As for how these sounds are produced, this interview with a scientist at Scripps Institution of Oceanography says
"Fish make sounds by oscillating their swim bladder, or by rubbing the bones where their fins attach to the body, similar to how crickets make sound by rubbing their legs".

You should also check out Dr. Rodney Rountree's website. It looks old but has lots of useful information about fish sounds.  http://www.fishecology.org/soniferous/soniferous.htm

Fish also produce sounds; the difference is that they are put in different positions by the body to sound. The sound produced by fish is about 20Hz and therefore is difficult for humans to hear. However, these sounds can be recorded and reproduced using instruments.
Of course, some fish also rely purely on action to exchange sounds. Some fish use ultrasonic communication, similar to dolphins (although dolphins are not fish).
Some fish transfer information by changing body colour. These fish are usually located in the tropical shallow water. Some fish pass through the water with their fins flapping to communicate courtship information. A few, mostly deep-sea fish, release pheromones.

What do you mean by " they are put in different positions by body to sound"? Also, it would be really great, if you can provide any reference to substaniate your answer>>>

means thier  "tail-wagging dance" will make some noise

can you provide any reference to substantiate your answer???

Please provide some sources for the information you have in your answer.

I second MZiegenhorn's answer and Xavier Mouy's comment that a variety of fish species produce sounds, and I'll shamelessly refer you to our new website FishSounds for an inventory of published research (updated up to the end of 2020 - 2021 update coming soon) on fish sound production, and some example sound clips.
Fishes don't have vocal chords, but they can produce sounds in a variety of ways. In Ingrid Katz's words: "Fishes are known to produce sounds using five mechanisms: 1) swimbladder pulsations, 2) stridulation, 3) hydrodynamic movements, 4) substrate, body and tendon vibration, 5) air release. "
Regarding yazhuo's answer about fish sound production mechanisms, you can check Eric Parmentier's work, such as for example this book chapter:
Parmentier, E. and R. Diogo (2006). Evolutionary trends of swimbladder sound mechanisms in some teleost fishes. Communication in Fishes. F. Ladich, S. P. Collin, P. Moller and B. Kappor. Enfield, NH, Science Publishers: 43-68.
Now that I mention a book chapter, the entire book would be an excellent source to answer the original question, if you are up for the reading.


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Expected variant allele frequency of mutation present on 2 out of 3 copies of a 70% purity cancer sample
I am reading Nik-Zainal et al., 2012.
In such paper, (for sample PD4120a - a 188-fold depth ER+ breast cancer tumor), it is stated that:

The sample has 70% tumor purity.
The genome has one triploid chromosomal region.

The final point I don't understand is why "mutations occurring on the triploid chromosomal region before duplication would be present on two of three copies - with an expected variant allele fraction of ~55%."
If I correctly understood VAF calculation, such mutations should have expected VAF of $2/3 p$, where p is the purity. Therefore, $0.7*2/3=46.7\%$.
Why is this different from the reported expected VAF?

Migrated from Bioinformatics SE at author request

I'm sorry I did not read the article. But in the case that it is only the tumor which has the duplicated chromosomal region, I think you will have an increased contribution of the mutation relative to the normal. I'll try to illustrate with an example:
Let's say the total sampled number of cells is 100. Tumor purity makes it 30 normal cells and 70 tumor cells.
30 normal cells contributes 2 normal copies: 60
70 tumor cells contributes 1 normal copy and 2 mutated copies: 70 and 140
If we calculate the expected frequency of the somatic mutation we get:
140 / (60 + 70 + 140) = ~ 52%
Still not 55! But it's the best guess I have.

Thank you, this does indeed make sense. I will see if anyone else has a closer results + explanation.


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Why is DNA antiparallel? Can it be parallel?
My biology textbook mentions that DNA is antiparallel and it got me wondering - can DNA be parallel? What would happen if it was parallel? Could DNA still replicate correctly?

Interestingly the answer is yes. The problem with parallel strands is that the DNA is not pairing in the known way it does when it is combined anti-parallel (or Watson-Crick-pairs).
I have found different images illustrating the problems:

Both images are from this blog post (originally from a publication cited there which is not available online). Both pictures show a distorted DNA structure.
This article ("NMR structure of a parallel-stranded DNA duplex at atomic resolution") shows a more schematic solution of this problem by showing the single pairings. C and G cannot build up 3 hydrogen bonds as they do this in the Watson-Crick-pairing.

The antiparallel DNA duplexes are stabilized by Watson–Crick base pairing, while other schemes are possible for parallel duplexes. (A) Watson–Crick G:C base pair, (B) Hoogsteen G:C+ base pair, (C) Donohue G:C base pair, (D) Watson–Crick A:T base pair, (E) Hoogsteen A:T base pair, (F) Donohue A:T base pair and (G) C:C+ base pair.
Subfigure A and D show the Watson-Crick-pairs, the others come from parallel bindings.
This changes in structure disrupts the function of the DNA (which for example depends on the reverse strand for proof reading). Enzymes which replicate, transcribe, repair etc. DNA will not work on this changed structure, as their function depends on the structural features of the DNA.

here is an interesting paper about parallel double stranded RNA with A-A base pairing. This requires ammonium chloride though.

Wow. Thank you. that was more than I was hoping for. Thank you for adding all of the details.

I think one interesting possibility is that using PARALLEL construction it's very hard to make 'interesting' structures. This isn't important for DNA itself, but is critical for RNA molecules now... and even more so historically in the 'RNA world'. Consider: if making a structure using ANTIPARALLEL pairing, all the nucleic acid needs to do is 'turn around' 180 degrees (known as a 'hairpin' turn) before being able to pair with itself (i.e. form starting structure). This is well illustrated by tRNA
http://www.wiley.com/legacy/college/boyer/0470003790/structure/tRNA/trna_intro.htm
Now--try to draw a tRNA-like structure using PARALLEL pairing--a strand must go through a FULL 360-degree turn before being able to self-pair. This is wasteful and perhaps even impossible without lots of added sequence. Since most folks accept that the beginnings of life were RNA or RNA-like molecules that were both functional (which requires meaningful shapes) as well as 'coding' (DNA or RNA sequence), if shapes were overly convoluted or could not form, life cannot start.
This would be an evolutionary, as opposed to structural, argument against parallel structures.

Seems like an interesting hypothesis. Can you add references for the second part of your answer?

There is another issue here which is more biological.  In general, the enzymes that replicate and "read" DNA run in one direction along the single strand of DNA that they are operating on.  The fact that the other strand of DNA is running in the opposite direction makes it impossible for these enzymes to jump from one strand to the other and ensures that they are operating on the proper information to do their job.  If the DNA strands were parallel, the enzymes would be likely to attach at a locus and then randomly read information from either strand, and the information produced would be gobbldygook.  So while it is chemically possible to have parallel DNA, a biological system that was based on parallel DNA would be at a big competitive disadvantage and so if they ever arose, they were probably driven extinct by the systems we now see that use anti-parallel DNA.

welcome to bio. Could you add your sources?


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Are there any bacteria that could be used as food?
Bacteria are found everywhere. They can also grow on various substrates. Are there any bacteria that can be used as a food source? For example mix x with water and add some of these bacteria. These then either turn x into something nutritious or can be consumed themself. Are there any potential candidates? Bonus points if the substrate bacteria use to grow is abundant.

I think the catch might be nutritional density. Remember what happens when bacteria get too concentrated in brewing: They die out like in brewing alcohol.

Does yogurt count? Beer? Other fermented foods?

I was rather thinking about something abundant but not nutritious themself.Are there any examples with wood / cellulose?

https://en.wikipedia.org/wiki/List_of_microorganisms_used_in_food_and_beverage_preparation

@DKNguyen The die-off in uncontrolled beer fermentation is due to the alcohol produced by Saccharomyces cerevisiae, which is a yeast, not a bacteria.

One more fermented probiotic product https://en.wikipedia.org/wiki/Kombucha Though whether it is actually beneficial, is unknown, there are different opinions on that.

The best example of bacteria-as-food is the genus Arthrospira, which is a kind of cyanobacteria whose edible biomass is known as spirulina.

I didn't realize algae were classified as bacteria.

@DKNguyen Somewhat confusingly, cyanobacteria are both known as "blue-green algae" and also not really considered algae. Algae in general as a term is highly non-specific.

If consuming spirulina, note that spirulina can be easily contaminated with other algae's toxins, and that spirulina should be avoided as a vitamin B12 source as its B12 bioavailability is questionable.

From the comments:

I was rather thinking about something abundant but not nutritious themself. Are there any examples with wood / cellulose?

In fact, the traditional Filipino food called nata (examples of which include nata de coco and nata de piña) are basically cellulosic pellicles of the bacterium Komagataeibacter xylinus, produced by culturing the bacterium in the appropriate medium (coconut water for the former, and pineapple juice for the latter).
(This resembles the SCOBY that is used in making kombucha.)

While not used as a food per se, bacteria are used in production of many foods, and you eat masses of them when consuming the product. At a guess; in the 10's of millions per bite is my estimate.
One type that is commonly used in several sorts of foods are the Lactobacilli. These are commonly used to generate sour products, through their fermentation of sugars into lactic acid. They are used extensively in yogurt production (Lactobacillus acidophilus usually), as well as other fermented diary products (cheese, kefir, cream cheese, sour cream, etc.) sourdough breads, production of fermented pickles such as sauerkraut and kimchi.
In some cases, such as kimchi and sourdough, these are often the natural lactobacilli and other bacteria and yeasts that are on the material used to make the product, so no added culture. In the case of sourdough, the fermentation can also be a result of yeasts in addition to the lactobacilli.
Similarly, acetic acid bacteria (Acetobacteraceae) are used in the production of vinegars, though in most cases these are filtered out before selling, so you don't generally consume them.

Apart from the classical microbial food processes, there is also a more recent approach captured under the term "single cell protein" (https://en.wikipedia.org/wiki/Single-cell_protein). Basically microorganisms are grown on a suitable substrate, and the protein that makes up their cells is used as food. Typically it would be either a food supplement or used in animal feed.
Regarding bacteria, it's most interesting to look into autotrophs, which can fix carbon from CO2 with a source of energy, or methanotrophs, which grow on methane derived from natural gas or biogas.

Additionally, there are efforts to use methylotrophic (which eat methanol or methane) organisms as sources for protein. In the future this might be particularly interesting because methanol and methane can be produced renewably from CO2, water and renewable energy. See e.g. https://solarfoods.com/ (I'm not affiliated with them).

Basically all the mammals which eat a diet comprising hard-to-digest plants like grass, scrub, etc. use bacteria exactly like this. So cows, horses, deer, camels, goats, koalas, and so on. They either use foregut fermentation (like cows) or hindgut fermentation (like horses). In either case microbes, including bacteria, break down hard-to-digest carbohydrates like cellulose into easy-to-digest simple sugars.
For some foregut fermenters like ruminants (e.g. cattle), gut microbes (including bacteria) are also an important protein source--the cow gut is split up into multiple sections, the first section (the rumen) is a comfortable place for microbes to live and break down cellulose but some of the microbes end up traveling with the food into another section where the microbes themselves are also directly digested by the cow.
Even humans have some bacteria which do this in a limited fashion, just not as efficiently as grazing animals.
Bonus side note: This does not include panda bears. Panda bears eat specific parts of bamboo which are easy to digest and high in protein already and their digestion functions much more like that of a carnivore.


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Can the psychology of a person alter their immune system and health?
Can the psychology of a middle-aged person alter their immune health? I have read about the different types of linkage between nervous system and immune system.
Can someone outline the general facts about what is understood about this?

Can you provide some references for this?

I think you are referring to psychoneuroimmunology (http://en.wikipedia.org/wiki/Psychoneuroimmunology), which is an expanding field.

This paper should be helpful, effects of the placebo on immune response https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3504052/

I'm not sure what you mean by psychology exactly, but assuming you are referring to a persons mental state there is a known link between stress and immunity. This link occurs through neuro-endocrine pathways. The central nervous system and endocrine (hormonal) systems are linked through the hypothalamus, a key controller of hormone release in the central nervous system. In a state of stress our central nervous system reacts by increasing the release of hormones such as the steroid cortisol and catacholamines such as adrenaline (a.k.a epinephrine in USA).
We know that steroids have an effect of dampening down the immune system (in fact steroids are often used for this intentionally in the case of autoimmune conditions for example). Thus based on this we have a scenario where stress can lead to increase in cortisol (and other hormones) which in turn can have an effect on your immunity. The effect to which this impacts on your life is then further dependent on your psychology and social support.
More generally, the links between illness and psychology are integrated together in what is called the biopsychosocial model of illness. I suggest you look this up to gain a more in depth understanding of this complicated issue.

As a reference for stress causing inhibition of the immune system, here is a quote from Life: The Science of Biology (10th edition): "Within minutes of a stressful stimulus (one provoking fear or anger, for example), blood cortisol levels begin to rise. [...] Cortisol also inhibits the immune system (because dealing with the immediate stressor is more important than feeling sick, having allergic reactions, or healing wounds)."

Yes. It's called Psychoneuroimmunology Ziemssen & Kern 2007:

There is evidence for rich neural connections with
lymphoid tissue Steinman et al.(2004). Receptors for various neurotrans
mitters beyond acetylcholine and norepinephrine are
also present on lymphocytes. Whereas the parasympa
thetic neurotransmitter acetylcholine potently modu
lates several classical immune reactions via the vagus
nerve, the sympathetic nervous system can alter the
TH1/TH2 balance through stimulation of the beta-
adrenergic receptor for example Elenkov et al. 2000

In general: Personal well being (PWB) makes you healthier, Psychological Ill-Being (PIB) makes you unhealthier, here are some snippets of a review (Abdurachman & Herawati 2018):
Coping mechanisms improved the outcome of AIDS patients

Religious coping and social support as an effort towards PWB showed to boost the immune responses in people living with HIV/AIDS (Dalmida et al, 2013). They used CD4 + cell count to prove their findings. Then, the effort to PWB via religious coping was definitely associated with reduced psychological distress, increased health-related quality of life (HRQoL), and better medication adherence (8-item Morisky Medication Adherence). Dalmida et al, 2013

Weeks of Playing music shifts your immune system from inflammatory to anti-inflammatory

Researchers found an increased immune response through various indicators obtained through saliva samples such as: cortisol, cytokines and interleukin (IL) -4, IL-6, IL-17, tumor necrosis factor-alpha (TNF-α), and monocyte protein chemoattractant (MCP) -1 (Fancourt et al., 2016b). This study shows the psychological benefits of group drumming and shows the underlying biological effects, supporting the therapeutic potential for mental health.

One might think that this all comes down to happy = no stress. Since there is tons of research out there proving that
STRESS makes you unhealthy
Spinorial already mentioned the stress hormone cortisol and its effect on dampening the immune system. Here I wanna provide some more facts that I took from this review (Yaribeygi et al. 2017 doi: 10.17179/excli2017-480):
Stress makes your immune system to attack your guts
Stress can re-activate previous inflammation of your gastrointestinal system. It can get worse:

As a result, there is an increase in the permeability of cells and recruitment of T lymphocytes. Lymphocyte aggregation leads to the production of inflammatory markers, activates key pathways in the hypothalamus, and results in negative feedback due to CRH secretion, which ultimately results in the appearance of [gastrointestinal system] inflammatory diseases. [...] It has been suggested that even childhood stress can lead to these diseases in adulthood (Schwartz and Schwartz, 1983, found in Yaribeygi et al. 2017).

Stress stops the immune system from killing cancer

stress can decrease the activity of cytotoxic T lymphocytes and natural killer cells and lead to growth of malignant cells, genetic instability, and tumor expansion (Reiche et al. 2004 found in Yaribeygi et al. 2017)

Stress slowly kills you by damaging your blood vessels and heart
Most human deaths can be related to accumulated damages to the cardiovascular system (So stop worrying about immune system). The mechanism behind stress killing you seems to be fairly simple:

Stress can stimulate the autonomic sympathetic nervous system to increase vasoconstriction, which can mediate an increase in blood pressure, an increase in blood lipids, disorders in blood clotting, vascular changes, atherogenesis; all, of which, can cause cardiac arrhythmias and subsequent myocardial infarction

Stress Shortens Telomeres
I came across a paper when I was answering a question about telomeres. Mental stress shortens telomeres (Epel et al 2004). To understand how short telomeres affect the immune system, aging and health see Does Telomere length shortening cause our cells to stop functioning properly?


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How does spermaceti make a whale float?
In the biochemistry book I'm reading (Box 10-1, Lehninger Principles of Biochemistry), an example is given in whales of how spermaceti (a wax located in the whale head), when at sea level is a liquid, and allows the whale to float due to its buoyancy.
As the whale dives deeper, the wax turns into a solid (due to the colder temperatures), and hence this more dense wax is less buoyant and prevents the whale from floating back up due to the greater density of the seawater at these depths.
My limited understanding is that density effects buoyancy in so far as that the weight of the object displaces an equivalent weight of water. If the quantity of the water displaced is small enough that the surface area of the object isn't completely submerged, it can float.
Now with the whale example, considering the wax is fully enclosed by the head, how would this change in local density effect the buoyancy of the whale as a whole? The weight of the wax still remains the same (in so far as the example used in the book), the only thing that changes is its density inside the whale.
So with a constant weight, and only a variable local density enclosed by an object (the head) and limited to these conditions only (as this is all the example in the book uses), how is this possible?

It's volume, not weight that matters. I assume the solid wax takes up less space, and is therefore less buoyant.

So even if the volume of the head remains the same, this still holds? Ie: the local change in volume of the wax effects the overall buoyancy?

This page and its associated references seem to have your answer. It seems there are a number of hypotheses on the function of spermaceti, with buoyancy control being least likely.

@user4779 Your right that, with mass constant, the volume of water displaced by the head would have to change to affect buoyancy. Either the hand would have to shrink or water you have to be taken inside the organ.

@canadianer That makes sense, a change in volume of the head. Can I conclude the example in the book is misleading? I quote exactly: " When the temperature of the oil is lowered several degrees during
a deep dive, it congeals or crystallizes and becomes
denser. Thus the buoyancy of the whale changes to
match the density of seawater." Without any further specification of any other mechanisms involved, or any reference to volume.

@user4779 here's a different example. Say I have an airtight plastic bag filled with warm liquid wax. I toss it in cold water and it floats, because it's less dense than the water it's displacing. However, if I leave it there and the wax solidifies, it will become more dense (same weight, smaller volume) and may become either neutrally bouyant or it will sink, depending on the exact density change. This is what the example in your book was trying to get at, but apparently facts got in the way...

@MattDMo, interesting, that would explain it. Would this be due to a decrease in the surface area of the plastic bag, or is this irrelevant? For example if there was a large ship. Would putting all the cargo into one central spot versus spreading the cargo out, affect the buoyancy, where the surface area wouldn't change?

@user4779 The plastic bag is irrelevant, it's just there as a container for the liquid wax. Assume it is infinitely thin and infinitely flexible, with zero effect on the overall process. Buoyancy in water is directly related to the weight of the water that is displaced by an object - if the object weighs less than the weight of the water it displaces, it will float. Remember Archimedes - he was getting into his bath, and his body displaced the water, causing it to overflow the tub. That's what made him run down the street naked yelling "Eureka!" (Greek for "I have found it!"). Supposedly.

If you haven't already, try reading through this. It may help.

The important thing is that yes, the volume of the whale would have to decrease. This is quite normal for animals, every time you urinate, your body decreases its volume, it doesn't replace the urine with an equal volume of air. The surface area is not important in itself.

@MattDMo could you please share, how is this concept be applied to body functions? Clinical wise I found hydrotherapy.

@bonCodigo could you please clarify? What body functions are you talking about?

What version of Lehninger do you have? I just skimmed through section 10 (Lipids) of the 6th edition and found no mention of spermaceti.

This is for the 5th edition, page 347, part 10.1.

Buoyancy is controlled by "Archimedes' principle", as described in Britannica:

... any body completely or partially submerged in a fluid (gas or liquid) at rest is acted upon by an upward, or buoyant, force, the magnitude of which is equal to the weight of the fluid displaced by the body.

Here the weight is a force, not a mass, so the force that pushes an object is related to the density and volume of the object itself. In this context, considering the spermaceti, it's the temperature of the oil that matters, because it's going to change its density, thus the buoyancy force. However, the example you are referring to is a hypothesis on the spermaceti function developed by Clarke (1978). In summarizing, he stated that sperm whales are almost neutral at the surface, so they need to control their buoyancy in order to dive. So, it's possible they change the vascularization on the head (but also the blubber!) to change the density and descend or ascend.
Still, this remains a hypothesis that has not been confirmed nor rejected. Miller et al. (2004)  found data that don't support the theory proposed by Clarke, as the change in temperature and so density in the spermaceti should not be relevant for buoyancy during dives and sperm whales are not neutral at the surface; moreover, they actively swim while searching for food at the bottom, so they contrast the buoyancy force. A more studied and developed theory for the function of the spermaceti system (with the nasal apparatus) is that sound production and the change in density has a relevant role found for sound transmission.
Full references:

Clarke, M. R. (1978). Buoyancy control as a function of the spermaceti organ in the sperm whale. Journal of the Marine Biological Association of the United Kingdom, 58(1), 27-71;
Miller, P. J., Johnson, M. P., Tyack, P. L., & Terray, E. A. (2004). Swimming gaits, passive drag and buoyancy of diving sperm whales Physeter macrocephalus. Journal of Experimental Biology, 207(11), 1953-1967.

Hey all! It is good practice to provide full academic citations, as links can die.

Good suggestion! Thank you:)


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Expected number of SNPs in a sample of size `k`
Consider a Wright-Fisher population of constant size $N$. We sample $k$ haplotypes in this population. What is the expected number of SNPs?
I think the answer should be in Watterson (1975) but it looks like my institution does not pay for access to this journal.

Try using Sci-Hub.

Let $\theta = 4n\mu$, then $E(S) = \theta\sum\limits_{i=1}^{k-1}\frac{1}{i}$, assuming infinite sites model. This is indeed given by Watterson (1975).


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Do dingoes show wolf 'characteristics'?
I've read that Russians have been performing selective breeding on Red Foxes for about fifty years, aiming to make them tame. The wikipedia article says

The experiment was initiated by scientists who were interested in the
topic of domestication and the process by which wolves became tame
domesticated dogs. They saw some retention of juvenile traits by adult
dogs, both morphological ones, such as skulls that were unusually
broad for their length, and behavioral ones, such as whining, barking,
and submission.

I wonder, since dingoes are completely wild dogs that have only relatively recently split off from domesticated dogs, do they show more 'wolf-like' characteristics? That is, has their life in the wild selected against domestication genes?
Perhaps the best way to phrase the question is have dingoes gained more of the genes/traits that silver foxes lost in the Russian domestication experiment?

Just to clarify, by "wolf-like characteristic", I suppose you mean "characterstics that are shared with wolves but not with dogs", is that right?

Well, I suppose "not all dogs", since there may be kinds of dogs that have some of those traits. I guess "non-domesticate traits" might be a better phrase, but the whole subject seems tricky.

The question is interesting +1. To my knowledge, the level of domestication of Dingo's ancestors is debated. And when having a quick look at the wiki article it seems to be quite a mess indeed. I think one could draw quite a good answer from wiki>Dingo and its references.


text:
Why do all particles have the same influence on osmosis?
When people talk about osmosis, they say that when we add a mole of NaCl, then each its molecule gets dissolved into 2 separate particles and therefore we have 2osM/L solution.
But both Na & Cl are attached to molecules of water which means that those water molecules are not water anymore and they can't penetrate the membrane. Thus not only the presence of Na & Cl itself changes the concentration of water in solution, but also the number of water molecules taken by those particles.
Therefore if we put 1 particle that binds to 1 water molecule and 1 particle that binds to 5 water molecules - they change the water concentration differently.
Please somebody tell me where I'm wrong.

Just wanted to add that the kind of salt or solvent in the water does matter. The Chemical Activity of the ions or other soluates matter quite a bit.  For example osmosis can be caused by sugar, organic molecules fats as well as salts. Here, Chemical Activity is a general idea of the relative effect of different molecules on osmosis.
Different soluates can cause drastically different effects on osmosis.  e.g. see Table 1 in this reference.

You can see the importance of the number of molecules if you imagine a semipermeable membrane, on one side there is water, and on the other there is the salty water solution. Water molecules can pass the membrane but ions cannot. On the side of the solution, because Na and Cl are taking space and covering some parts of the membrane, the water molecules are "touching" the membrane less, so the flow of water molecules out from solution side is slower than the pure water side. This means that more water is flowing into the solution than out of it, slowly decreasing the concentration of the solution, until they reach an equilibrium when the flow of water to both sides is equal.
You are incorrect to say that the "water molecules are no longer water", because their interactions with the ions are intermolecular (ion-dipole), not intramolecular. Intermolecular interactions may slow down molecules, but since they do not lock the water molecules in place, they could still pass the membrane. Although, the concentration of solute is important in calculating osmotic pressure. The formula used when the contentration is low is different than if the concentration was high. For the formuals see Osmotic Pressure on Wikipedia.
The visualization with the membrane is my interpretation of Silberberg's explanation of osmotic pressure in Principles of Chemistry, page 412.

When you dissolve something in water, you build a solvation shell around this - so each ion (in the case of salts) gets surrounded by a number of water molecules. For more details read this Wikipedia article.
The concentration change in free water molecules is usually not taken into account since it can be neglected due to the vast number of "unbound" molecules. So if you have one litre of water, it contains approximately 56 moles of water molecules. If you dissolve 1 mole of sodium chloride in this water, and take in account that this takes quite some water to get solvated, there is ways more water available. So the water concentration is almost constant (especially when you work at physiological osmosis condition).

Okay, let's calculate this scenario: we add 1 mole of NaCl (~60g) into 56 moles of water. Each Cl atom binds to 6 atoms of water at average (according to wiki: http://en.wikipedia.org/wiki/Sodium_chloride). Let's suppose that Na takes up the same number of water molecules. Then 1 mole of salt takes 12 moles of water which doesn't look negligible to me. On practice the number will probably be lower because a single water molecule can be bound to both Na & Cl atoms which means that in highly concentrated solution 1 mole of NaCl will bind to 6 moles of water which is still not negligible.

It indeed sounds that its not neglectable. But you still have 80% of the water present. And: Water is a neutral molecule that can pass through the cell membrane, other dissolved substances cannot do this.


text:
Accuracy of a particular genetics test
Consider the question - Are genetic tests accurate?
I don't believe they are as the genes may not provide the complete information or maybe there are other genes responsible for a particular trait but they may not be known at the point when the test is conducted. This may not be the right answer though — I simply wish to understand from people here as to what they can say about the accuracy of these tests. If they are not accurate, can you explain why that is the case?

There are a lot of "genetics tests" you can do. Please describe more detailed, what kind of testing you mean, otherwise this question is too broad. (Accurate as in "Now we know 100% sure that...?" Of course not. Like all other tests you do on organisms. They are just too complex to be understood 100%)

Like the comment said this question is very broad but Im going to try and clear some things up for you. A "genetic test" is just simply a test that tells you whether or not you have a certain genotype. Yes, it is often times used to tell if a person has a disease or not, but that doesnt always have to be the case. I may just want to know, for example, if a mouse I have carriers a certain transgene. The reason why genetic tests are good at determining if someone has a disease is because many diseases are simple, or at least have a well-defined genotype. Sure, you can make a genetic test for a complex disease like obesity if you want, but no one does this because as you pointed out in your question there are sometimes more than one gene involved, so a genetic test for that would not be very good.
But for genetic tests of diseases of a known genotype, they are very accurate. Of course you have some false positives and false negatives. Look up the terms selectivity and sensitivity. If you have a sensitive test you will catch a lot of people with the disease but also many false positives. If you have a selective test you will not have many false positives but you may miss people who actually have the disease. Its a trade-off. Testing someone twice will clear things up usually.
And then there are cases where you have a disease with a known genotype but still have an inaccurate genetic test on rare occasions. Heres a paper about a disease known as Spinal Muscular Atrophy. There is a genetic test that works 95% of the time but sometimes it does not match up with the phenotype. In the paper they find a mutation that explains why the genetic test does not match the phenotype. Two things are interesting about the paper. One, the genetic test is not wrong, its just that the phenotype is not what you'd expect. And two, not all people who have a discordant genetic test have this mutation. So whats going on in these patients and why their test doesnt match their phenotype is anyone's guess.
The first point is especially important so I will repeat it. The genetic test was not wrong, the phenotype just did not match it as expected. Genotype and phenotype are not always correlated, and mistakes can happen when you assume they are.

@von-mises summed it up nicely enough, but you'll want to read the Wikipedia articles on heredity and heritability, in particular the latter.
Our genetic information can be informative, but it's not complete.  As you mention, there are lots of other factors that could and usually do come into play.  Often times there isn't just one gene, but rather many genes playing a role (these are called polygenic traits).  For example, see my answer to a question on hair color; there are dozens of simple changes that can affect the color of hair and eyes.  These complex traits are really hard to tease out!
Additionally, not everything is 100% from genes; the environment can also play a huge role. Often we talk about how heritable a gene or a trait is by giving a percent, meaning how much of is due to genes you inherit from your parents.  The heritability of IQ is an interesting read for an introduction to the concept. But this quantity is itself misleading, as it sometimes includes environmental variation, and it is only as good as the data you use to compute it.
So, what is the use of the genetic tests?  Well, for starters, ancestry is really interesting and useful for people.  Not just paternity or maternity (which is obviously accurate and widespread) but knowing where you are from.  23andMe can be informative, but you should know that their business model depends on getting genetic information for free from you.
There are, additionally, a number of traits that we've studied, or that do have strong genetic factors.  Sickle-cell disease is a classic example of something just from your genotype, whereas other things are less determinate; for example, the heritability of baldness is around 81%, and I know from my genome that I have a slightly lower chance of becoming bald.  There are other, more serious health risks that people would want to be tested for (BRCA for breast cancer, LRRK2 for Parkinson's, APOE for Alzheimer's) as well as inherited traits that are very genetically determined (like sickle-cell or Tay-Sachs).
In short, the genetic tests are very good at determining what the genotype is, which can be very useful for certain traits but completely useless for others.  The more we learn about what our genes do the more we learn how complicated the whole system is.  We are more than just our genes.


text:
Book Recommendations: GRE Subject Test In Biochemistry, Cell And Molecular Biology
There are probably a lot of really good answers that may vary significantly in terms of content.  I'm looking for a set of books that I can read in preparation for the GRE Subject Test In Biochemistry, Cell And Molecular Biology.  I have a Bachelors of Science degree, but never really studied any of the material on this exam (it's in a field which is not really related).  I'm interested in applying for a doctoral program in Biology, and would like to add something to my application so that it doesn't appear to come out of "left-field", as they say.  When I look at the questions from the sample exam in the link above, I can't tell whether they are introductory in scope or would require advanced study in particular areas.  Could somebody recommend a set of textbooks that would cover all of the ground for this test?  If one textbook exists which is sufficient, that would be wonderful, but I'm guessing that multiple texts will be required.  My goal is to learn the material necessary to do well on the exam as thoroughly as possible.
As an aside, I tried looking for study materials in online bookstores, but wasn't able to find anything that consistently got good reviews.  I don't think Princeton Review or Barron's have books on this subject, unless I overlooked something.  At any rate, I'm okay reading through a set of undergraduate university textbooks, but I really have no idea which ones would be good.

You can also try Lehninger Principles of Biochemistry. It covers all the topic except the part about cell motility and possibly, the 1-A-g ( I'm not too sure about it), but the book is for pretty advanced levels. I would not recommend it as a last minute reference book, but for thorough study it's great. Of course it's my personal opinion, so before you consider any book, I would rather advice you download a pdf copy of the same, to get a first hand experience.

Stryer's Biochemistry is a great book that pretty much covers all the requirements except those in A1 - Those are basic chemistry concepts which are not covered in Stryer. Any basic chemistry book will cover that. Make sure to verify, one-by-one, that all the test subjects are covered in Stryer. This answer is just a recommendation for a great Biochemistry book, not a guarantee for a one-shot success on the test.


text:
Cellulose acetate membrane filters vs. glass microfiber filters

At equivalent pore sizes and pressures, which exhibits faster flow rates, cellulose acetate membranes or glass microfiber filters?
I know cellulose acetate exhibits low protein binding, but what about glass microfibers? Would they be suitable when protein recovery is essential?

This might be relevant: how big are the proteins that you want to filter?

@GoodGravy ~270kDa

It would also depend on the pore densities and pressure resistance.
Silica is used for gel filtration chromatography to separate proteins. This can be achieved when proteins do not have affinity to silica, and most of proteins could be analyzed with silica gel. Silica and grass are similar materials. However, glass and silica have negative charges on the surface. Under low ionic strength condition, positive charged proteins or positive charged surface of proteins may bind to glass. Cellulose acetate does not have charge but it is hydrophilic.

Thanks for your answer. I have not been able to find any data on pressure resistance for the filters I'm looking at; do you know if it can be said as a general rule of thumb that glass microfibers typically exhibit faster flow rates than cellulose acetate membranes or vice versa? As in is one typically faster than the other or is it just a crap shoot without knowing the resistance?


text:
Blood pressure measurement
When measuring your blood pressure in your arm, when you hear the sound to measure the systolic, is that sound NOT the heartbeat?

what do you define by "heart beat"? The sound of the heart beating or the rate of the heart beating?

The sound in question is called the Korotkoff sound:

If the pressure is dropped to a level equal to that of the patient's
  systolic blood pressure, the first Korotkoff sound will be heard. As
  the pressure in the cuff is the same as the pressure produced by the
  heart, some blood will be able to pass through the upper arm when the
  pressure in the artery rises during systole. This blood flows in
  spurts as the pressure in the artery rises above the pressure in the
  cuff and then drops back down beyond the cuffed region, resulting in
  turbulence that produces an audible sound.

I'm glad you found that info. I wasn't sure if the question was asking about the sound of the heart or some artificial sound cuffs make.

@mattkaeo blood pressure + measurement = Korotkoff sounds, this what the question is about...