text:
Are the number of base pairs in a given chromosome same between different individuals?
This is a basic question but I couldn't find an answer through a web search; hopefully this is the right place to ask. Is the number of base pairs in a
particular chromosome the same in all individuals? For example if I take an
X-chromosome from two random humans would I count exactly 155,270,560
base pairs in both cases? or are there mutations that would make one longer than the other? If they're not exactly the same, what's the range in length variation?

Not only is it not the same in two different individuals. It's not the same in one individual (over their lifespan or two different cells at any given point). https://en.wikipedia.org/wiki/Telomere  Also see https://en.wikipedia.org/wiki/Insertion_(genetics) and https://en.wikipedia.org/wiki/Deletion_(genetics).

@Adam make an answer out of that

If anyone would like to use my comment to formulate an answer (or improve on the existing answer please feel free). I don't really have the time right now to put together a well referenced answer I would be happy with.

@ Adam, I will add it.

Welcome to Biology.SE.

if I take an X-chromosome from two random humans would I count exactly 155,270,560 base pairs in both cases

No, you would probably not find the exact same number of base pairs because mutations do no only change one nucleotide to another (what we call a substitution) but sometimes add or delete few (or sometimes many) nucleotides.
note, btw that you don't need to take two different individuals, you can just consider the two X chromosomes of a female (or any other pair of chromsom in any gender) and find this difference in the length of chromosomes.

what's the range in length variation?

Good question (+1)!
Telomere issue
Before I start, I want to make clear that I consider the length of those chromosomes at the moment of conception. Chromosomes will vary in length during the lifetime due to telomere reduction. I will not consider this in the following calculations. Also, some mutations directly introduce (or delete) a large number of nucleotides (transposable elements for example), I am not considering those mutations here, assuming they are rare in comparison to to single insertions and single deletions (this assumption might not hold!). So please really take the following with a grain of salt.
Let's make some messy calculations
In classical theoretical population genetics, we tend to consider mostly substitutions. But I can maybe try to make some extrapolation out of this work if you allow me to make some strong assumptions, use poor estimates of actual true values and using some non-rigorous mathematics! This is going to be ugly and not extremely trustful $\ddot \smile $.
Not explaining why this is true (it is a result coming from Coalescent Theory), the expected number of pairwise differences between two neutral sequences for a diploid population is $E[\pi] = 4\cdot N\cdot \mu$ (quite an impressively simple result), where $N$ is the population size (assuming panmictic population) and $\mu$ is the mutation rate for the whole sequence. Assuming a constant per site mutation rate of $\mu_s = 10^{-9}$. Knowing the length of the sequence of interest (chromosom X) $L ≈ 1.55 \cdot 10^8 $, the mutation rate for the whole sequence is $\mu = L\cdot \mu_s = 0.155$. Let's consider a population size of $N = 5 \cdot 10^7$ (the equations assume a panmictic population so I just took some value that felt more or less reasonable to me much smaller than the actual worldwide population size). Therefore the total number of substitutions should be $E[\pi] = 4 \cdot 5 \cdot 10^7 \cdot 0.155 ≈ 10^7$.
Now, let's assume that only a fraction of $\frac{1}{100}$ of the mutations bring variation in the number of nucleotides, we might want consider the value $\frac{1}{100} \cdot 10^7 = 10^3$. And because a mutation that deletes a nucleotide from a long sequence will rather diminish the number of variant in sequence length that increasing it, let's say that will divide this number by 10!... so I'd say that two typical X chromosome would differ in length by about 100 nucleotides.
I am sure that with some work one can come up with more rigorous calculations and a more accurate expectation. Intuitively, the result of 100 nucleotides doesn't sound totally crazy (it is not 1 nor 10^6 at least).
Also, one could probably use available sequence data to estimate this value.

In some sense yes but it is kinda misleading the way you put it. Mutations can bring variations in the length of chromosomes. Then, within the lifetime of an individual chromosome length varies a lot becuase at every mitosis, chromsomes can shorten (you'll need to read about chromosoomal replicate, telomeres, DNA strands direction, Okasaki fragments to understand why). So one such mechanisms explain variation as a function of the age of the two individual you sample while the other mechanism in independent of age and explain variation in the length of chromosomes that are present in the egg.

Thanks for the explanation. So it seems there are (at least) two different mechanisms that can change the length of a chromosome :  (1) telomere reduction and (2) random base pair deletion (is addition also possible?). From what I read so far the first involves removing parts of a repetitive sequence of bases at the ends of the chromosomes. This seems like a more deterministic process than the second. I think the calculations you made account for the second type. If correct (100 out 155 million) the range is  pretty small.

I calculated the expected difference in length between 2 chromsomes sampled at random from eggs (without considering telomere shrinkage during lifetime, which would force us to consider the distribution of age, the distribution of the number of mitosis given age and the expected telomere shrinkage at each mitosis). The expected total range of length in a given population is necessarily greater that the expected pairwise difference in length....maybe 10 or 100 times as much I'd say intuitively.

Also please, again, don't take those numbers too seriously as the calculations are not really rigorous. I was happy to see that I ended up with a value that felt intuitive to me.

There are also transposable elements that can change loci in a genome. In various microbes, they can take up or remove plasmids. Retroviruses can incorporate their DNA into their hosts.

I understand these are really back of the envelope type calculations; but
still they're useful enough to guide the next level of detail. A next step
for me is to learn how these variations are accounted for when creating,
updating, and processing databases of chromosomes.

It's usually easier for
me to learn something if I have a concrete problem with real data to work
with. If I pick a single short chromosome from a simple organism and I just
want to do some simple statistical analysis on the variations of that chromosomes;
What would be a good introduction material on how to access an openly available
database and do some simple calculations.

You should open a new post for your new question and check an answer if your question in this post has been answered (or just don't check anything if your question hasn't been answered yet). I am not quite sure what exactly is your question but if you haven't yet, you might want to first follow a course of bioinformatics.

"find this difference in the length of chromosomes."  That was never shown before because we only got gapless genome in January 2022. How does crossingover work then? As for telomeres... Just consider stem cells only.

You would never count 155,270,560 bp in X chromosome. 7 years ago gapless (status complete) human genome did not exist, this is from GRCh37.p13. That is info about genome that had fake gaps inserted. But in January 2022 we finally got all genome (Y chromosome too) and perfect number is 154,259,566. All other numbers for other chromosomes are in wikipedia taken from here. https://www.ncbi.nlm.nih.gov/assembly/GCA_009914755.4
P.S. You literally did not know the basic of it. 155,270,560 is a number with inserted fake gaps, you can see it here: https://www.ncbi.nlm.nih.gov/grc/human/data?asm=GRCh37.p13 The number you wanted was on tab Ungapped lengths, at the time it was 151,100,560. So that means at the time of GRCh37.p13 some of it was not known.

Are there mutations that would make one longer than the other? If they're not exactly the same, what's the range in length variation?
As pointed out in the other answers, there can be mutations that change the length of the DNA between individuals and even single cells of the same tissue.
There are different processes that can change the genome length. The most common ones are:

micro-indels (insertion and deletions) or sometimes just simply indels: Small changes (1-50nt) [1]. Usually happen during imperfect DNA repair via Non-Homologous End Joining post a double-strand break.
Copy number variation (CNV): bigger variations that generally happen due to deletions and duplications of DNA segments >50bp.
Transposon expansion
Chromosomal translocations

We can ignore microindels and chromosomal translocations for the moment because the former impart only a small change to the genome size and the latter are usually rare and in most cases, are extremely deleterious.
With a stringent mapping, CNVs are known to cause 4.8% variation in the size of the human genome [2]. It is to be noted that this information does not account for the frequency of the changes; this is just a sort of maximum limit. It can also be noted that deletions have a greater contribution to variation compared to insertions.
LINE-1 retrotransposons are known to be quite active in the human genome. They accounts for ~17% of the human genome and are one of the major sources of inter-individual variation [3]. They are especially noted for promoting somatic heterogeneity in differentiating neurons [4]. Since LINEs expand by copy-pasting, their activity is correlated with increase in genome size. Transposon activity is generally suppressed in germ cells by a class of small non-coding RNAs called piRNAs [5].
I haven't found an article that exactly describes the variance in the genome size due to LINE-1 or other transposable elements. I'll add a reference if I find one.

Interesting numbers. If one mechanism alone (CNVs) can cause 4.8% variation in length and some claim "in terms of DNA sequence all humans are 99.5% similar to any other humans" (https://en.wikipedia.org/wiki/Human_genetic_variation) then either some very loose definitions are being used or these variations have odd statistics –

@secretlyfamous Note that CNVs need not disrupt homology i.e. "similarity" between two genomes. When we talk about similarity we generally refer to sequence homology. And the statistics presented are for the upper-bound of the length of CNV regions. The variation is therefore an upper-bound and not the standard deviation.

thanks for the explanation. It's a little hard for me to accept that (unrestricted) insertion/deletion does not change homology; but I'll save the details for a future question.

@secretlyfamous imagine duplications, it just creates an extra copy of the genomic region which would again be homologous to the reference. There is a chance of homozygous deletions too. Another point to be noted is that when people say that the genome is 99% similar (or even when comparison between different species is made; for e.g. chimpanzee and human genomes are 95%(?) similar) then the non-transcribed (intergenic) regions are not considered.

authors: Валерий Заподовников


text:
Why do tattoos persist if body cells are regularly renewed?
I am not quite sure if it is true, but I read somewhere that within 7 years all the body's cells are replaced with new ones. I am not quite sure if it is cells or atoms.
If it is then why do tattoos persist for so long? If the cells which were impregnated with the dye have been replaced, then why do the tattoos still remain?

That's not true - some cells turn over quite quickly, others take months or years, others never replicate.

It's a damn pity that that's not how it works, wouldn't have minded getting a tattoo if I knew it would fade in 5 years time and have disappeared entirely in another 10.

Smarter Every Day explained this quite well on their YouTube channel.

First, tattoo pigment isn't injected into cells. If you were to puncture a cell with something the size of a tattoo needle, it would die - full stop. Many cells are destroyed in the process though, mostly by tearing, which initiates the wound healing process.
So what actually happens is the particles lodge in between the cells of the dermis (the layer below the epidermis, or outer layer of skin) and new cells crowd around it as damaged cells are replaced.
Since the particles in good tattoo ink are too big to be carried off by macrophages, they just sit there. That doesn't stop them from trying, though. Macrophages take up the pigment but are unable to escape with their garbage. Fibroblasts envelope the particles, both intracellularly and within the extracellular matrix they generate. At the end of a fibroblast's life, its contents are taken up by the same process - still too big to remove.
Smaller particles will be carried off by macrophages capable of both consuming the particles and migrating into the lyphatic system, which is why some ink fades more than other kinds. Ink composed of fine particles would be expected to fade severely. New tattoos are also sharper because some of the ink that was injected is lodged in the epidermis, which is the layer that grows out and is shed over time.
In this biopsy of a tattooed mouse, you can see how the epidermis has carried some of the pigment out of the skin while much of the dermal layer's pigment has been either removed lymphatically or enveloped:

Source: Tattooing of skin results in transportation and light-induced decomposition of tattoo pigments--a first quantification in vivo using a mouse model.
Thus, over time the pigment will be moved around a bit by this cellular activity, in fact deeper into the dermal layer on the whole.
The intent of using laser light to remove tattoos is to break those particles down into smaller pieces burst any cells containing them - again initiating the wound healing process. However, unlike in previous cases, when macrophages reach the site they can now sweep the remaining particles away to the lymph nodes.

Sources

General - Tattoos and tattooing. Part II: Gross pathology, histopathology, medical complications, and applications.
Process - Cutaneous Wound Healing

Secondary sources:

Fate of tattoo pigments in skin (pdf)
How Laser Tattoo Removal Works - Smarter Every Day

It would be great if you could add citations because this does not sound quite intuitive. For instance, when you mention particle size and clearance from dermis has a connection, then add a reference for that. Also, you should add some reference for the particle size distribution of the tattoo ink. Most tattoo pigments are composed of metal salts, there is also a possibility of leaching (I am not sure how it does not happen. There are some reports on diffusion of tattoo pigment though)

Additionally, it is very strange to phrase the sentence "puncture a cell with a tattoo needle" when the tattoo needle's tip is hundreds of times larger than a cell.

Destin produced a quite nice video that could be used as a reference for this answer. https://www.youtube.com/watch?v=D0B7F5UbTOQ

-1 See my comment to March Ho's answer: the majority of the ink seems to be intracellular, albeit after a certain time. In any case, all the articles that I've read say there is no ink in the epidermis.

@WYSIWYG Metal salt leaching would be interesting, but I think some of those issues might be better answered in a separate question. Some of that information is available in the sources I have added.

@MarchHo Some people aren't familiar with the relative sizes of cells and needles, so I thought that would be important to mention.

Contrary to the other answer posted, this paper shows via microscope images that the tattoo ink is in fact absorbed into cells, and forms small intracellular round granules.

Electron microscopy of untreated tattoos revealed membrane-bound
  pigment granules, predominantly within fibroblasts and macrophages,
  and occasionally in mast cells. These granules contained pigment
  particles.

Images a, c and e are images of toluidine blue stained cells, while images b, d and f are images of unstained cells showing the tattoo pigments.
Images a and b are prior to the laser treatment, c and d directly after the treatment, and e and f 90 days post treatment with the laser.
The reason why the tattoo marks persist is not because the pigments are deposited extracellularly, but that they are deposited intracellularly.
The pigments form intracellular granules that are not broken down, and therefore in the absence of external forces such as a laser, the pigments will remain there for long periods of time.
This paper (thanks to biozic) also describes the tattoo ink being persistently found intracellularly instead of extracellularly.

Biopsies obtained from tattoos 1, 2, 3, and 40 years old differed only
  in the types of ink used. All the ink particles were found to be
  located in dermal cells. The epidermis was completely devoid of
  pigment particles. The basement membrane was continuous at the
  epidermal-dermal junction. Ink particles were found throughout the
  upper dermis but all were within the boundary of a cell membrane.

According to this TED video (which unfortunately does not state its primary sources), the fibroblasts that contain these engulfed ink particles are themselves taken up by newer fibroblasts when they die, therefore the ink particles remain in the dermis and are not removed by cellular renewal.

Several other articles confirm that the majority of ink particle are intracellular (mainly in fibroblasts and macrophage) after the skin healing process is done [http://dx.doi.org/10.1111/j.1365-4362.1987.tb00590.x]. But, according to these articles, pigments are not deposited into cells: they end up there after a complex and time-consuming process.

@biozic Can you point out where in the article does it say that pigments are not deposited into cells? The 24 hour post tattoo result clearly describes intracellular tattoo ink deposits.

Do these cells persist for a long time? Mast cells release their granules when stimulated and macrophages are chemotactic (can move around). Only fibroblasts seem static but even they can undergo apoptosis. So as the OP asked, what would happen when these cells die/move and are replaced by new cells?

@WYSIWYG See the video citation. I was unable to find a better primary source.

@MarchHo What I wanted to say is that ink particles aren't specifically deposited into cells. According to the article, when they looked at a 24h-aged tattoo, "Homogenization of the epidermis, the epidermal-dermal junction, and the upper portion of the dermis was almost complete". "Both epidermal and inflammatory cells had ink particles in their respective cytoplasms [...] Ink particles were also found in the enlarged intercellular spaces".

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What is the percentage of people living in England in 1500 AD whose lineage is still alive?
This sounds a bit random, but it stems from a lecture in statistical genetics which I attended a while ago. We were shown a population lineage graph from which it was clear that most lineages eventually go extinct. The further you go in to the past, the smaller the percentage of the individuals living at that time whose lineage is still alive today. This probably makes sense in the context of evolution.
So I am curious about the speed of that process in human populations. I am aware that this speed, quite possibly, varies over time and geographically. Are there any estimates about that speed in European populations? To be more specific, I would take England at 1500 AD as a starting point. What is the percentage of the people living in England at that time whose lineage still exists?
EDIT
I am very grateful to @Richard Erickson for the reference to the Galton-Watson process. It is really fascinating that +70% of all known Chinese family names have become extinct. It would be really interesting to know more about the speed of the process of extinction - in particular in European populations.

It totally depends. This is difficult to answer based on just calculations because unless you have exact data for the population dynamics of the region. This is mostly an issue of bookkeeping (census). The further you go in the past the smaller was the percentage of the individuals living at that time whose lineage is still alive.: not necessarily true; imagine population bottlenecks.

@WYSIWYG Out of curiosity: how do bottlenecks change this? The percentage still seems a largely monotonous, if not continuous, function.

Assuming arguendo that a bottleneck killed all except 10 people in the population in 1500, right after your 1500 sample was taken. The percentage of people who still have their lineages extant today would be greatly reduced.

@Nick birth and death are stochastic processes and though the mean behaviour may seem monotonous, there are always fluctuations. Let us assume that there was only one couple left after a mass extinction process. All the subsequent generations would be their descendants. Similarly, during a bottleneck a few individuals give rise to the entire population. Now, if you take generation-0 and any later generation-Y, compared to some generation-X and generation-Y (X<Y) then there the lineage would be intact for the former. Plus there are other factors such as fitness of the starter population.

@March Ho The percentage of the people living at a time point before the bottleneck who have a living lineage would still be lower than for the generations afterwards. I know that a scenario can be constructed in which this is not strictly true but, generally, the rule holds for realistic bottlenecks - at least in species with birth rate not much greater than those of humans. However this point is a bit tangential to what I asked.

Interesting question +1. One can calculate such things using Coalescent Theory but the issue is that it assumes constant effective population size which is obviously very wrong for England. The Coalescence should have very long branches, much longer than expected from constant effective population size. I don't think there is an analytical method for dealing with growing population size. Also, the descendents went through several bottlenecks and rapid expansion so it definitely is not an easy case. I don't think that theory can help here, one will need to analyze data to answer this question.

Check out Galton-Watson branching process models. They area closely related topic that focus on the probability of an individual surname going extinct.

In reaction to @WYSIWYG's comment: The further you go in the past the smaller was the percentage of the individuals living at that time whose lineage is still alive is very likely to be true but not necessarily indeed. However, The further you go in the past the smaller (or equal) was the number of individuals living at that time whose lineage is still alive is always true.

Here is a partial answer that also expands upon a previous comment:
Between 1900 and 2013, 20,000 English surnames had gone extinct according to the Daily Mail's summary of research on surnames. This is a partial answer because it only tells us how many names are gone and is from the wrong time period.
To completely answer your question, I suspect you need to conduct primary research. I would suggest the following broad steps:

Gain access to the data needed to answer your question. British Census records only appear to available from 1841 to 1911 so you most likely need to sample old names (e.g., graveyard based studies).
Use the data to parameterize a statistical model such as a Galton-Watson branching process models.

I doubt the answer to your question can quickly be found unless somebody has already done it. Although, if done well, it could probably be a masters' thesis. However, before embarking on such a project, I would suggest doing a good literature search to make sure it has not been done before.
Note: If anybody finds the answer, please feel free to take content from my answer and include it yours.

Thanks. Daily Mails seems to refer (though not providing a direct link) to research done by ancestry.co.uk. I haven't checked that site yet but it would be another port of call. The thing is that family names are a sort of proxy variable. There was a lot of emigration from the UK. Also, people adjusted the spelling sometimes. More importantly, females traditionally took over the family name of their husband (so their own family name may become extinct while their lineage may continue). The emergence of double-barrelled family can also affect the stats.

You're welcome. I know this data would be hard to come by. An academic researcher might be able to get it from ancestry.com or ancestry.co.uk. I know Google shares information with academics. Otherwise, it might also be machine learning exercise in reading in old church records or something like that. Good luck with the question though!

I realize there it would be a lot easier if only a subgroup of the population is taken into account - the nobelty. I presume good records exist. The question is how to get them.

@Nick, good point. Check out out Galton's work. He was afraid of the "good" aristocratic names going extinct.

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text:
Career progression through biosafety levels?
Does a career in infectious disease typically progress through biosafety levels, or do people select one and specialize their training in procedures specific to those hazards?
That is, say Dr. Kliener wants to work on TB (BSL3). Does he first on have to work on MRSA (BSL2), which he has no interest in, just to build up experience? Or could he simply learn everything there is to know about TB and BSL3 lab procedure, don hairnet and gown, and get to work with someone who has experience under those conditions?

As far as I know, the higher biosafet levels (3 and 4) need a special training. For the BSL 2 labs I have worked in, you need a proper training (technician or any relevant study as biology, biochemistry and so on) so you know how to act and behave in the lab. And of course you need some introduction (rules and safety for the lab).

BSL 2 access requires a 1-2 day course, which is training generally offered by the institution.

I have found that BSL2 access tends to not be highly regulated. Some of the BSL2 labs I have worked in did not even require 1-2 days of training, while others did. In any case, the current policy at my current institution is that BSL3 access is denied to anyone who does not possess an undergraduate degree, and those with it must apply for and take a course.

There is major jump in the risk to researchers between BSL-2 and BSL-3. BSL-2 laboratories are very common in part because potentially infectious viral vectors are commonly used in molecular biology.

My short answer would be no, careers of people who study pathogens requiring biosafety training are not focused biosafety level.
More broadly, the people I know who study infections diseases are not motivated by the biosafety levels of their infections organisms. Rather, they are motivated by biological questions and their research that often require higher biosafty for their labs.
For example, the researchers featured in a recent (July 2015) National Geographic do not study Ebola because they want to work on a BSL-4 level virus. Rather they want to about learn about the disease from both a basic science and applied human heath perspective.
Your hypothetical Dr. Kliener would not work his way up the biosafety chain as a conscious. Let's say a young Mr. Kliener always wanted to study human health. He probably would have started doing research in a BSL-2 facility as an undergrad research assistant (See BSL-2 requirements here. As a grad student, he might have worked at a BSL-3 lab if he choose a good program while spending years focusing on a specific pathogen or system. By the time he became because a PI, he would have needed to find a BSL-3 facility for his research. He worked his way up, but not because he wanted to study dangerous pathogens. Rather his research question guided his path.
Other career tracks could end up using a BSL-3 facility, but not necessarily need the stop at a BSL-2 facility. For example, a hypothetical Dr. Fish may have started off loving the outdoors. She studied limnology as an undergrad and grad student and did not step foot inside a lab. However, when she began working as biologists for a state conservation agency, a novel fish virus emerged. She now is tasked with studying it. Her agency trained her to work in a BSL-3 lab so she could culture fish with their virologists.

Here's a nice little walk-through by the CDC on Biosafety levels. Biosafety level reflects that potential risk microbes used (or potentially present in the case of human tissue samples) in the laboratory present to researchers. http://www.cdc.gov/training/QuickLearns/biosafety/
BSL-1 is for very low-risk organisms, like non-pathogenic E-coli. You can work with these guys on an open bench with minimal protection gear and be at little to no risk of disease.
BSL-2 is for low-risk organisms, like Staphylococcus, where risk of infection is low and/or infection is not likely cause serious consequences to researcher well-being. (Some dangerous blood-borne diseases can be worked with at BSL-2, because the additional pre-cautions do not impact transmission, which would only be likely to occur after a needle-stick or similar inoculation with infectious material).
BSL-3+ Labs are much less common, have much stricter requirements on facility structure and security and on researcher's protective equipment and procedures.
BSL-3 is for dangerous microbes that can be transmitted by aerosols, such as Tuberculosis.
BSL-4 facilities are rare, require expensive training and equipment and are used for deadly, exotic microbes, like Ebola.


text:
Is it "easier" for researchers to detect evolutionary ancestry than distance in the evolutionary tree?
I'm a researcher in another field who has wandered into a problem with applications to biology.  I hope to sell my results by making the following statement:

Given two species X and Y, it is "easier" for biologists to decide whether or not X is an evolutionary ancestor of Y, than it is for them to determine the distance between X and Y in the (unknown) evolutionary tree.

Question 1: Is this statement true in any meaningful sense?  Is it cheaper, less time-consuming, or more accurate to measure ancestry than to measure distance?  Or are the two tasks roughly the same?
Question 2: A reference request - what papers/textbooks could I read/cite to back up this statement?
Thank you!

In short, extant species are not ancestors of one another because, even if they are sister taxa, each has its own separate evolutionary history since they diverged. So, no to question 1.

Do you consider both X and Y to be extant species, or could X be a fossil? It might not make a difference theoretically (see the comment from @kmm), but in practice fossil species are sometimes viewed as representatives of ancestor species to extant species (or to more recent fossil species).

If you take two modern species (let's denote them with A and B) you can't really say that A is an ancestor of B or vice-versa, but you can say that they are related to some extent, that is they have a common ancestor that lived X years ago. But then all eukaryotes are believed to have a common ancestor that lived an eon ago. Hence the notion of phylogenetic relatedness  is relative by definition. That means that all species are related, but when you take a bunch of them you can try to reconstruct the order of speciation. This can be achieved by calculating distances (e.g. genetic sequence distances, morphological distances) and applying an evolutionary model. A brief summary is that you NEED to have a sort of distance to investigate ancestry in the first place and then you clearly NEED more than 2 species for your phylogenetic constructs to make any sense.
Since I find that your statement makes little sense, obviously I can't find a reference to bake your words. But I can give you an exhaustive list of good phylogenetics textbooks for your erudition.
EDIT
I believe that one thing is worth a remark. In fact it is easier to correctly reconstruct the order of speciation events than it is to precisely estimate any sort of evolutionary distance, because the distances we have are models. Simply put they approximate the number of evolutionary events that have happened since the last common ancestor of some species (or better to say the last common set of genomic and/or phenotypic traits, because speciation is a lot more than simple trait-wise divergence). From this point of view you might say that it's easier to estimate ancestry than it is to estimate distance, but then you will be over-simplifying things to such an extent, that you will drop the fact that there is no way you can speak about ancestry without having some distance estimations in the first place. The precision of distance estimations is a separate topic. So your statement will make a lot more sense if you modify it accordingly.

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text:
History: Do evolutionary and ecological processes occur at the same timescales?
Classically, it was thought that evolutionary processes occurred at a much slower pace than demographic/ecological processes. Nobody, ever thought about incorporating both processes into the same model as they were assumed to occur at different time scales. We slowly came to realize that this way of thinking is quite wrong and many demographic/ecological changes (demographic expansion for example) directly affect evolutionary processes and even more important that evolutionary processes can directly influence demographic/ecological processes. I take for example Kirkpatrick and Barton (1996) who investigated how dispersal load (fitness decrease due to maladaptive alleles brought to local populations by dispersal) affect the "evolution" of the species range limits.
Who (what) are the main authors (articles) that allowed for this switch in our viewpoint about the interrelations between evolution and demographic/ecological processes?

Dennis Chitty might have been an important author to establish the viewpoint that evolutionary processes can influence the probability of survival of a population. However, I know a little bit about his work only because he was professor at my department (way before I even arrived in the department) and he might therefore not be the most important author of all.

This doesn't directly answer your question but my current research is on building models that combine ecological and evolutionary processes. Thompson (1998) is one of the earliest papers to talk about rapid evolution on ecological time-scales. And also a recent paper highlighting the interactions was Schoener (2011).
Perhaps reading through these two papers and looking at their references will give you a better idea of when the shift in thought started.

Thanks a lot Sanalphatau (and welcome to Biology.SE). The Thompson (1998) paper will probably help indeed. +1


text:
Is our genome decaying (see "Genetic Entropy"), and, if so, is this evidence for our genome being "young"?
In the book Genetic Entropy & the Mystery of the Genome the author says that the genome cannot be old because the genome is "decaying". Decay is a very subjective term, but in this case he means that the fitness of humans is going down not up. Is it true that our genome is decaying over time, and that the fitness of humans is decreasing? Here is a quote from the book, that might explain his argument:

Kondrashov, an evolutionist who is an expert on this subject, has advised me that virtually all the human geneticists he knows agree that man is degenerating genetically. The most definitive findings were published in 2010 in the Proceedings of the National Academy of Science by Lynch.4 That paper indicates human fitness is declining at 3–5% per generation.There is really no debate on current human genetic degeneration.

Perhaps this more shines more enlightenment in my question. This idea of human fitness going "down" is my main concern. Essentially, in his book he claims that because we are going "down" (meaning fitness is declining) not "up" (whatever that means) our genome must therefore be young. If I understand the issue correctly, mutations "create new information" by creating different proteins or leading to an abnormal protein products. However, I thought that the force of natural selection should be strong enough to get a rid of those genes that are so and so responsible for our fitness declining.
Sanford, John C., and John R. Baumgardner. Genetic Entropy & the Mystery of the Genome. Waterloo, NY: FMS Publications, 2008. Print.
Feel free to point me to similar questions that may been helpful or are similar to this one.

You need to be more specific with what you are referring to with the "the genome is decaying" statement. "Decay" is also a very subjective/value-laden description of a genetic process, and you should specify exactly what process you are interested in. Is it just "random mutations" -> "genetic dissimilarity over time" (~genetic distance), or something else?  At the moment, it is really hard to understand exactly what you are asking about, and therefore hard to formulate a relevant answer.

@Lucian - I suggest you edit this as much as needed to make it acceptable as a clear question, or let someone else do this for you. You won't get your question answered if you get it closed first. Avoid personal claims like, "I have read extensively on evolutionary biology." You may well have read a few books, but if the books are written from a Creationist point of view, you have not read extensively. That's a bit like claiming you've read a lot about astrophysics because you've read every one of Ken Ham's books. A good answer follows from a good question. Help us to help you.

I think this question has been completely changed, to the point that neither of the answers to it make any sense.

@MarchHo I still think the core aspects of your answer is relevant though, to the last part of the question (you might need to reframe it a bit though).

The question makes more sense now, I removed my down vote. Good job for improving over your original post!

The book you quote is not peer-reviewed; assertions like these are not scientific, they are just the author's opinions: "Kondrashov, an evolutionist who is an expert on this subject, has advised me that virtually all the human geneticists he knows agree that man is degenerating genetically." I would encourage you to distinguish between replicable observations ("facts") vs. rumors, anecdotes, and hearsay.

@mdperry As the OP mentioned, they are not familiar with the discipline of evolutionary biology. Therefore it is not justified on out part to expect them to discern between a bad reference and good ones. We should point the right references to them. The question is clear now and is on-topic.

@WYSIWYG Did you ever consider that this OP could be trolling? Cutting and pasting excerpts from a creationist for one's Biology SE posts could be considered inflammatory.  If the OP is genuinely curious then helping them to evaluate the literature in a field, and pointing out weak vs. strong arguments is demonstrating the epistemology of the scientific approach. If we just spoon feed them I fear we will end up with a generation of scientists who rely on others instead of reasoning answers for themselves.

@mdperry I apologize if that was ever the image I projected. I was advised to not use personal statements like "Ive read about evo bio", I am no evolutionary biologist. I am a double major in geology and chemistry with interest in planetary science. I am very interested in knowing the mechanism by which the non living chemicals formed the first living thing. I am not an evolutionary biology, in my original question i've stated the reason why I wanted to know, but I removed it. I felt that I was being lied to when this was brought up from creationist all the time.

This question is also addressed in this post. You can have a look there, too.

@WYSIWYG yes someone earlier pointed out to a very similar question. I managed to get answers to questions that I did not even know how to ask yet.

If I understand the question correctly, you are asking why random mutations (most of the non-silent ones are deleterious) cannot create information and improve the overall fitness of the organism.
This is a common creationist statement, and has been shown to be incorrect in many different ways. The best way this can be shown to be false is by simply applying natural selection.
E. coli has a beneficial mutation rate of $10^{-5}$ per genome-generation (source) and a detrimental mutation rate of $2×10^{-4}$ per genome-generation (source).
Therefore, at first glance, the claim that the "genome is deteriorating" appears plausible. However, natural selection quickly acts on these mutants with deleterious mutations due to their low fitness. Therefore, the deleterious mutations are removed from the gene pool and are replaced with their beneficial counterparts instead.
If we define "information" as beneficial adaptations to the environment, random mutations themselves do not directly create the information. It is the application of natural selection that allows the fitness of the organism to increase despite the presence of random mutations.

I have two concerns with this answer: 1) How did you do to infer that the OP was interested in the ratio of beneficial over deleterious mutations? 2) you said random mutations themselves do not directly create the information. I can see you are trying to use the OP's words (which is great in general) but it end up sounding quite weird. Definitely, mutations create genetic variance (and therefore increase information or decrease Shannon entropy) while directional selection reduces genetic variance (decrease information).

Of course, it is the combined effect of those two things that allow for adaptation. It is also wrong to say atural selection that allows the fitness of the organism to increase despite the presence of random mutations as it seems like mutations are bad and NS is good which is wrong.

@Remi.b - Selective pressure is shown to select out the beneficial mutations. That's how evolution works.

I am well aware of the basics of evolutionary biology. Mutations increase genetic variance (and therefore shannon's definition of information) by introducing new variants in the population. Natural selection decreases genetic variance (by selecting out deleterious variants) and it therefore decreases information. This is the very basics of evolutionary biology. The term "information" seems to be slightly loaded as being "a good thing" but under the standard mathematical definition the above answer is partially wrong

I agree with @Remi.b Information content is basically a log likelihood function of the entropy. MarchHo, I think you mean information in the sense of functional repertoire of genes, but such a terminology may be misleading. You should clarify it.

The book in question is more of an informational pamphlet than a scholarly monograph. The sort of thing that you might find someone handing out on a street corner. The sophistication of composition is at about the second year UG level. The problem I have with this post is that the term "Genetic Entropy" has no clear sense, and may mean different things to different people. The notion seems to approximate: "The Shannon-entropy of the human genomic sequence". Shannon-entropy measures information content in bits, in contrast to thermodynamic entropy which uses energy units to measure disorder.

@Remi.b should I delete this question?, I thought it was silly to ask the question we are having discussion about this and I had no way of defending natural selection, as like I stated I am only familiar with genomic research. In the book a lot of analogies are used to make the reader understand. the author is a 25+ year Cornell University professor, so he is not just some guy. The argument he poses is used very commonly from creationist I come around ( I am heavily surrounded by creationist views) and really it is an eye opener to me how passionate creationist are about "debunking evolution"

Well, the question is unclear (I hope I managed to make clear why this is the case in my now deleted answer/comment). The question ended up being closed as unclear. You can delete if you want but you don't need to as it is closed anyway. However, as you checked @MarchHo's answer, it seems like he managed to give you a helpful answer (and so other might see something helpful in MarchHo's answer). So maybe just keep it like this. I am just hoping that the error/misleading information in the last paragraph will be corrected by March Ho. Thank you Lucian09474

@Remi.b You make a good point on defining information in terms of Shannon entropy, I think I have a misconception here, will update the question once I figure out what is wrong.

@Lucian09474 You cannot delete posts with upvoted answers. The question is okay if you clarify it. It is fine if you do not know a certain concept and ask a question about it. However, your question should be specific and should have a clear statement.

@Remi.b I think the answer makes sense if "information" is not defined in the sense of Shannon entropy, since the "information" as defined by the question clearly has nothing to do with it.

To my knowledge there is no other commonly accepted definition of information than the one suggested by Shannon. I don't mind using another definition but the definition should then be written down (which is currently not the case neither in the question nor in your answer).

Kolmogorov information is also commonly used - most kinds of mutations other than substitutions (such as duplications, be they internal tandem or whole-gene or genome) automatically increase the Kolmogorov information content because the strings that represent genome sequences have to be made of more bits to describe them.
Any mutation also increases the Kolmogorov information content of the gene pool.

The book makes the argument that the human population with access to modern medicines is at a point where natural selection is less fierce and allows carrying more of the deleterious genes into the next generation than ever before. This argument cannot be countered by referencing E.coli, since we are in a different evolutionary situation. I completely disagree with the findings of the book, but this answer does not provide a satisfying retort for me.

Regarding the reference to Lynch, actually reading this paper is illuminating (http://www.pnas.org/content/107/3/961.full). What Lynch is saying with regards to degeneration is that he and others feel that modern technological advances may relax selection pressures, thus allowing the survival and reproduction of many who would otherwise be selected against, increasing the rate of mildly deleterious mutations in the human population.
Sandford willfully misreads this in order to inject his creationist/intelligent design mythology (Man's creation by god, the fall, no evolution, but rather decay from god's perfection, etc). However, this is definitively NOT what Lynch and other biologists are suggesting. Decay is a loaded word. The genome is constantly changing from generation to generation on an individual basis. Selection simply eliminates overtly deleterious mutations.
Lynch is suggesting a sort-of technological doomsday, where human success at subverting selection ultimately lead to an unsustainable mutational burden and the collapse/extinct of humanity. Differences in selection pressure affect what genomes are propagated onward. Previously deleterious mutations that can be survived in our current environment are seen some malign decay, but this is how selection works. As the environment changes (including technological changes), selection pressures changes. If selection pressures revert, such persons will once again be selected against. An overly dramatic shift in selection pressure (such as collapse of society, or other forms of massive environmental change) could indeed kill us off, but this is true of any species and is in no way unique to humans.

Are you suggesting that Prof. Sandford's assertion, quoted above "There is really no debate on current human genetic degeneration." is not actually supported by the reference that he cites?

Well, I think he's being intentionally misleading, especially in his word choice. This is probably related to a typical (sometimes intentional) creationist misunderstanding of evolutionary processes. If there were some ideal human genome, then most mutations, increasing our divergence from this ideal, could reasonably be seen as degeneration.
Evolutionarily speaking, there is no ideal genome, only those that are more or less well-suited to their current environment. He's postulating a non-existent absolute where there are only relative differences.

A small addition to what March Ho has mentioned in their answer.

Fitness is not absolute; it is dependent on the present environment. Fitness has no meaning when the selection factor is not defined.
You can consider a commonplace example: Can you, by just looking at an individual say how fit they are (of course I am not talking about those who are clearly ill, obese or malnutritioned)? Unless you assess their performance in a task you cannot really say how fit they are. Same goes with evolution.
Now consider another hypothetical example. You would be aware of the fact that the sickle cell trait (mutant haemoglobin) provides immunity against malaria. If your task is some kind of physical exercise then obviously the sickle cell trait is deleterious. However, if there is a malaria pandemic then the sickle cell trait would provide a great survival advantage and therefore these individuals would be deemed fit under these conditions.
It is to be understood that evolution does not work towards "improvisation" of species. Just because we assume that a certain trait is advantageous for an organism, it is not necessary that it would evolve. Have a look at this post.

Also, as a deleterious allele spreads through the population, it can eliminate carriers from the population at an increased rate, meaning that non-carriers have an advantage and the mean fitness of the population consequently goes up. Sanford's main flaw is the treatment of relative fitness as absolute.
Also, the whole mutational meltdown from decay stuff is only a problem in small populations, where deleterious alleles can be fixed that much more rapidly. To extrapolate this to organisms with large population sizes or to hold it as a general truth of evolution is iffy.

Well, you've already mentioned Alexei Kondrashov. Here's his talk  (in russian unfortunately): http://www.youtube.com/watch?v=YsgO8JTN7KE
To summarize it:
Yes, that decay is happening and at a pretty catastrophic rate. As of 2012, he estimated the rate of IQ decay (and fitness decay is somewhere close) to be within the range of 1% and 10% per generation. The former is ok according to him, cause "in 100 generations we'll surely be swept away by a nuclear war between big-endians and little-endians". The latter will be unfortunate, cause in 10 generations we'll "fall prey to our own stupidity". He speaks of stupidity because our brain is the most transcriptionally complex structure in our organism, thus it suffers from genetic damage sooner than anything else.
(It's worth noting here that AFAIK, one of Kondrashov's children has Down syndrome; another one, Fedor, is a remarkable geneticist as well, focused on epistasis.)
Those estimations are supported by the following molecular data: no matter the age of the mother, she gives 15 new single-nucleotide mutations on average to her offspring. Father gives about 10 mutations per each year of his life after reaching puberty, historically 70 on average. Out of those mutations most are neutral or silent (due to genetic code degeneracy), but on average ~1 out of 70 leads to a change in aminoacid sequence of some protein, usually harmful.
Here are 2 papers: decay of cognitive indicators of children with parent's age: http://journals.plos.org/plosmedicine/article?id=10.1371/journal.pmed.1000040
Another link from Kondrashov: drosophila simulation of middle-class neighborhood (MCN) population, where each family has exactly 2 children, son and daughter, and no natural selection pressure is applied: such population rapidly deteriorates with fitness in wilderness decreasing by 2% per generation: http://www.ncbi.nlm.nih.gov/pubmed/9371795.
Kondrashov says that after several generations you can hear the difference between MCN drosophila and wild-type - wild-type is much more noisy and active.
He also mentions that frequency of autism, diagnosed in the US has increased 5-fold since 1950.

It appears to me you are using a nonstandard definition of fitness. Fitness is simply the expected number of offspring, given a genotype, for a carrier with that genotype. Cognitive indicators et cetera don't necessarily correlate with the ability to reproduce, and unless they did there are no real implications for fitness.

@AnkurChakravarthy True. In fact, I'm mixing here the data about IQ and about fitness. They say that average non-silent aminoacid substitution in a protein decreases fitness (expected # of children) of organism by 1%, so 2-3% per generation, when fathers are ~30 year old on average seems to be a correct estimation.


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What is the basis for the determining sex from position of adult pelvis?
I've read that a person with enough knowledge of anatomy can tell the difference between a "woman" who is a slim man that is very good with makeup and an actual woman.
They usually claim to be able to tell the difference between the two by certain things like digit ratios and pelvic position. Is there any basis to these claims? The one I'm specifically interested in is the "position of the pelvis", as that is the most recent example of the claim I've seen. This is a direct quote from a  novel that I'm reading.
EDIT: it looks like I phrased the question badly. As anongoodnurse stated, I'd like to know if there's any basis for telling if a living person is a man or a woman by looking at them.
An example is if you dress up a slim man with a feminine looking face, get a make up artist to make the face look like a very attractive woman, and put that man in a little black dress, would a person knowledgeable about human anatomy, for example a GP MD, OBGYN, mortician, or Sherlock Holmes (kidding), is there any basis for that person to be able to say: "nope, that's a dude".

"Position of the pelvis" is pretty vague, but there are very clear differences in pelvic morphology between females and males. This sexual dimorphism looks like:

Female pelves are wider and flatter, which I think you could tell from surface anatomy. Of course if you could palpate, then you could tell for sure.

I think the OP is asking about the difference by looking at living people. Can you tell all this by looking? "I think you could tell from surface anatomy." How? If you had a good look at the surface anatomy, you'd see a penis, and wouldn't need to palpate.

@anongoodnurse thank you, that's exactly it. I googled the question and the information i got would be useful for an archaeologist or a pathologist, but not really some random knowledgeable genius to spot some spy cross dressing as a woman to fool the world.

@ton.yeung It's something I think would have to be determined with an experiment designed specifically to answer that question, but I couldn't find any.


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What is a functional screen?
I was going through this paper, but did not understand a term.
What is the meaning of functional screen?
(I am not a biology student, I don't understand much, and a small simple explanation would be enough)

From the abstract of the linked article (Guttman, 2002):

We used an in vivo genetic screen to identify 13 effectors [...]. Although sharing little overall homology, the amino-terminal regions of these effectors had strikingly similar amino acid compositions.

And from the body:

The screen relied on the type III secretion signal and the endogenous promoter of the hop gene and was thus highly specific.

Hence, the authors search and identify proteins with a secretory signal under the regulation of a hop promoter. A functional screen in this paper refers to the analysis of protein samples to detect the presence of proteins with a particular function.


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Could fingerprints potentially be changed using a gene gun?
Not to confuse with your "DNA fingerprint"  I've read surgery is readily used to not just remove but even to change people's prints through employing very small grafts between opposing hands.
About 5 years ago a Chinese group identified SMARCAD1 as a key player in the development of fingerprints. this was  discovered by generating gene expression profiles of people with a very rare condition called adermatoglyphia. These people have  no finger prints.
A gene gun, which uses micropartical bombardment is a technique that propels microscopic particles of heavy metals, coated with the gene of interest, "deep" into tissues.
If you were to alter the genetics of the epidermal stem cells, you could potentially permanently change the tissue that arises from those stem cells. Could this in principle work if over expression of SMARCAD1 resulted in remodeling of the prints or has other more important genes been shown since to be involved?
Do any model organisms have fingerprints, or a version thereof?
I know I'm fishing here, lots of questions. I thought it was an interesting topic and wanted to see what people here had to say.

People cannot change their fingerprints. It is possible to temporarily remove enough of the pattern to make the fingerprint useless for identification, but nothing more. Note that today, the fingerprint isn't the only evidence. Palm prints, especially the hypothenar eminence, is just as valuable. Even leather gloves can leave scientifically acceptable evidence in the form of skin prints.

@anongoodnurse you take your opposing thumbs, and perform 100 or so micro skin grafts between each thumb. If the graft takes, your going to perminantly alter your print. As I said this technique is already well described. Here's one example. http://www.csee.wvu.edu/~ross/pubs/FengJainRoss_AlteredFingerprint_TechReport09.pdf

@anongoodnurse I'm not asking about the surgery, what I'm referring to here is inducing local genetic changes of the  epithelium to eventually alter the print, we know there is a genetic component to finger print development. . Micropartical bombardment is a way of introducing foreign DNA into cells by propelling microscopic particles of heavy metals coated with the exogenous gene. During development differences in gene expression are what make tissues different. I think it's reasonable to assume that the cells under the ridges are genetically different from the found between the ridges.

A real gun would change your fingerprints much more efficiently.

Chimpanzees have fingerprints.  Next all you have to do is find the homologue of SMARCAD1 and let the animal testing begin!  But actually I doubt it will work.  This website goes into some depth and links some additional sources that show fingerprints are developed in the womb and are fully set by 6 months of gestation.
It seems likely that SMARCAD1 may have to do with having fingerprints or not, but not likely that it has anything to do with their composition.  It would be difficult for one gene to have enough variation to provide 6 billion variations in output.  You could hypothesize that it's a combinatorial output from other genes as well, but the studies linked above focus more on environmental interaction as the cause of variation.
I would guess that the patterns are set and no amount of gene therapy is going to change your fingerprints.  The simplest experiment would be to knockout the above gene in an adult for some period of time and see if the fingerprints fade.

More like 60 billion variations, since every fingerprint on every finger is different.  Once you realize that fingerprints differ on the same person from finger to finger...it's pretty easy to see that the exact pattern on each finger can't be genetically determined.


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How do single-celled predators chase other cells?
From my understanding, single celled organisms have been seen avoiding, and chasing, potential food or other organisms.
How do they accomplish this? They do not have eyes or ears or a nervous system. My understanding is that chemical reactions are involved somehow.
How do single-celled predators chase other cells? What happens on a chemical level?
Edit:To help keep a more constrained question, the single-celled organism I am considering is Paramecium

This is actually a very broad question. Chemotaxis (the response to changes in a chemical in the environment) is only one of the "taxis". If you could refine this, say by singling out one single celled predator, I think it would be a less broad question.

@anongoodnurse I am trying to find a common predatory Ciliate that does the behavior that I have described - is Paramecium a good example?

Yes, paramecium is a good example.

it is always useful to show work you've done yourself to answer the question.

@aaaaaa my work so far is essentially google searches leading to links which fail to answer the question. All I can find is definitions of "single-celled organisms", "paramecium", or broad explanations of the digestive system.

It could be I just don't know the correct terms to search for, if this is readily available information

Detection of and movement according to a gradient of a chemical species is a strategy that single cells use to track a target across space. There are very many strategies of movement depending on the cell and its environment, but a common problem that while cells can sense the concentration of chemicals, they cannot sense its gradient (the direction in which it increases) because they are of too small a size to rely on the difference of concentration on one side and the other. Howard Berg and his co-workers have discovered a mechanism that allows single cells to move toward increasing concentration zones by a combination of concentration sampling and movement. See his webpage, http://www.rowland.harvard.edu/labs/bacteria/projects/track.php


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Protein folding, extra dimensions and bio-mathematics
One metaphor that I have found to explain how proteins fold so quickly to a native shape is that of the blind golfer.
I have made a video to illustrate this metaphor. This shows how the shape of a slope can determine precisely where individual elements will end up.
The video represents many zero-dimensional points each following its own one-dimensional path down a three-dimensional slope to end up in a two-dimensional arrangement. Or almost: the one-dimensional paths are curves in three-dimensional space, the final resting surface is not flat, and one marble sits on top of three others.) The movement takes place through the fourth dimension of time.
Proteins form three-dimensional shapes, so the "slope" that their components slide down must be in an extra dimension.
Atoms have been observed to jump through a crystal lattice, without any indication that, in travelling from their start point to their end point, they pass through the three-dimensional space that we can observe. Is it conceivable that the component parts of a protein move through an extra dimension as the protein "folds"?
There are very simple protein chains whose native folded shape is well known. Is there any data available to suggest what path the different molecules in the protein follow during the folding process? Or do they appear to "jump"?
I imagine that it would be possible to create a mathematical model in n-dimensions to describe the simplest "slope" that the protein molecules could follow as the protein collapses into its native state.
What mathematical work is currently being done in this area?

What are you asking about precisely - like now it looks too broad - there's like 100 thousand know structures. You also don't get that PES is mathematical construct - these slopes simply describe energy and there's one dimension on degree of freedom

PES = "protein expression signatures"? Sure, there are lots of things I don't get. I do understand that that "the map is not the terrain", however closely a mathematical construct appears to model reality. Precisely, I'm asking if there have been attempts to generate n-dimensional shapes which can describe the movement of individual molecules in a protein as it folds, in the same way that my video shows a 3D shape that defines the movement of a set of virtual marbles so that the end up always in the same position.

There are really two question nuclei in here. One about quantum tunneling in protein folding, and another one about free energy surfaces and trajectories on them. They're related and both interesting, but definitely distinct.

Short Answer

What mathematical work is currently being done in this area?

A... lot?
Longer Answer
The "n-dimensional slope" thing that you're talking about shows up in the modern theory of protein dynamics as the "landscapes" concept. There's no truly standardized form for the theory, so it goes by many names. Try googling folding funnel, energy landscape, probability landscape, free energy surface, etc.
adendum
Oh, and also the current consensus is that the "quantum leap"-style effects that you were talking a little bit about don't play a large role in folding, at least in the initial stages. The current thinking is that most (not all!) of the dynamics of protein folding can be modeled using classical physics. Quantum effects can't come into play until the atoms of a protein are closely smooshed together (ie after the initial "collapse" phase of protein folding has finished).

Thanks for your rapid answer. From skimming the first articles that come on a Google search for folding funnel protein, it looks as if the mathematics that is used is mostly concerned with describing the release of energy, not with the topology of the "funnel" itself. The diagrams I see look more like artist's impressions than calculated projections onto a 2D screen. Are their names of people you can suggest, who are dealing specifically with the topology of these funnels?


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Are there any auto-immune diseases caused by T cells not detaching from antigen presenting cells (APCs)?
By not detaching I'm referring to after they have formed an immunological synapse, if they don't ever detach.


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Are Protocadherin Gamma Cluster transcripts considered separate genes?
The PDCH@ cluster of genes share exons and are therefore isoforms of each other.  However, they are considered separate genes, by both HUGO and Ensembl.
A "gene" is defined as "a locus of co-transcribed exons" (Venter 2001), and this locus clearly fits that definition with no ambiguity. So why are these transcripts considered separate genes?

What is your question exactly?

The question is, why are these transcripts considered separate genes?

Thanks, I slightly modified the question to improve clarity. Feel free to roll back. You may want to add a link to Venter, 2001 too. And transcripts are not genes.

Related: http://biology.stackexchange.com/questions/31766/can-intron-become-exon-in-alternative-splicing/

I would say they are considered different genes because each isoform is under the control of its own promoter.

Having multiple promoters doesn't mean isoforms are different genes.  E.g., http://www.pnas.org/content/97/5/2291.full


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Is dysharmonia an actual disease or something only Oliver Sacks believes in?
In his book Musicophilia, Oliver Sacks discusses a case involving a woman named Rachel Y. who lost the ability to process harmony in a car accident. He then explains how this lead to simultanagnosia. He terms this loss of harmony "dysharmonia."
Is dysharmonia an actual medical condition or is this something Sacks just believes but has no real evidence for? My google fu didn't yield anything besides his book.  If it is legit, which regions of the brain are damaged and why are those regions in particular thought to induce dysharmonia?
Click here to read the case.

This might be better suited to [skeptics.se], I'm not sure...

Never used Skeptics so I can't really say if I agree or disagree. If it is, that's fine. I'll let others weigh in and if it is mods can migrate it.

Check out their welcome to new users post to learn about the site and how it works. You don't necessarily need to have the mods migrate it, you could just post the question there, possibly with some edits to satisfy their question criteria.


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Will salting the ground kill insects and spiders?
I want to kill the insects and spiders living in my egress using something non-toxic to humans, dogs. I was thinking copious amounts of salt would kill earth dwelling bugs and what appears to be ground spiders with funnel like webs. The insects seem to be majorly silverfish. I am in Missoula Montana.

I think the bugs are coming from the egress. Here's an internet photo similar to my egress. The ground at the bottom is the area in question.

Not sure what the spiders will do, but salt is toxic for plants. In my place at least (Western Europe), usage of salt would kill the native plants and leave the ground to nettle.

The ground in question is in the egress. I want to stop the whole basement window food chain.

I have had some success with boric acid against an infestation in my bathroom.

Dusting the area with a diatomaceous earth based insecticide ought to do the trick, while being essentially non-toxic. If you want to prevent plant growth there too then of course salt the earth.
See Efficacy of modified diatomaceous earth on different cockroach species (Orthoptera, Blattellidae) and silverfish (Thysanura, Lepismatidae)

As soon as I dumped diatomacous earth on my 5 egress windows, hundreds of millipedes, centipedes, spiders, silverfish, beetles, hornets came up out of the ground and the surrounding grass. Before that was 50lbs of salt, which didn't bother anybody. All the basement windows are beautiful white wastelands. THX @jzx :D

Hahaha, happy to be of service!


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What are the exact differences between stereocilia and microvilli?
This is a question in an old exam of Histology. I tried to answer the question, and I've made many searching attempts, but without resulting in any fixed/exact information. In some articles on the web, I've read the stereocilia and microvilli have both actin core, and this website states that stereocilia doesn't have actin filaments! I'm just feeling lost at this point. And now, I'm just searching for an exact answer for that question.
Note : It may be a super easy question for you. So please note that I'm a novice self-learner at Histology.

Both are actin based.

Is this information come from a trusted resource ?

Haha well I don't know… do you trust me?

http://www.uniprot.org/locations/SL-0293 and http://www.uniprot.org/locations/SL-0302

Thanks. But I still need to know the differences between them.

Stereocilia are basically modified microvilli. They are much longer than microvilli, and lack the villin protein.
According to Ross histology textbook, they both contain actin filaments.

Microvilli are found in locations where their function is related to absorption and secretion, for example, in the intestine. Stereocilia have more or less the same function but are rare. Although both have an actin core, there are significant cytoskeletal differences in stereocilia. These include the presence of fimbrin and the absence of villin, and so on.
References:

https://www.researchgate.net/publication/318305308_Difference_Between_Cilia_and_Microvilli
https://www.biologydiscussion.com/difference/difference-among-cilia-stereo-cilia-and-microvilli-animal-tissue
https://pubmed.ncbi.nlm.nih.gov/8731041/


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Thinking quickly causes elevated mood
I read this article: http://www.sciencedaily.com/releases/2006/09/060926171045.htm
It says, "When people are made to think quickly, they report feeling happier as a result. They also say they are more energetic, more creative, more powerful, and more self-assured. In short, they reported a whole set of experiences associated with being "manic."
"The results of our experiment suggest the intriguing possibility that even during moments when people feel stuck having depressed thoughts, interventions that accelerate the speed of such thoughts may serve to boost feelings of positive affect and energy."
Is there any biological basis for these claims or could the results be self-reporting biasness?

The original paper can be read here: Manic Thinking: Independent Effects of Thought Speed and Thought Content
on Mood


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Endothermy in different species
Birds and mammals are both endothermic, meaning they metabolically generate the heat they need to keep their body within a certain temperature ranger.
But birds are closer relatives to reptiles than they are to mammals, and reptiles are not endothermic. Thus birds and mammals developed endothermy independently; and here is the question:
How does thermal regulation differ in birds and mammals?

This question is not too broad and deserves no close votes for that reason in my opinion.

This is in between a comment and an answer...
Notes

reptiles can have several definitions. Some of them causing birds to be a reptile.
You probably meant "evolved" instead of "developed".
Thermoregulation is performed by a set of different mechanisms and it is plausible that your question would be considered as too broad. Note however that I am NOT a physiologist and might overestimate the scope of the question.

Similitudes between birds and mammals
From wikipedia (here)

In cold environments, birds and mammals employ the following adaptations and strategies to minimize heat loss:

Using small smooth muscles (arrector pili in mammals), which are attached to feather or hair shafts; this distorts the surface of the skin making feather/hair shaft stand erect (called goose bumps or pimples) which slows the movement of air across the skin and minimizes heat loss.
Increasing body size to more easily maintain core body temperature (warm-blooded animals in cold climates tend to be larger than similar species in warmer climates (see Bergmann's Rule))
Having the ability to store energy as fat for metabolism
Have shortened extremities
Have countercurrent blood flow in extremities - this is where the warm arterial blood travelling to the limb passes the cooler venous blood from the limb and heat is exchanged warming the venous blood and cooling the arterial (e.g., Arctic wolf[3] or penguins[4][5])

In warm environments, birds and mammals employ the following adaptations and strategies to maximize heat loss:
Behavioural adaptations like living in burrows during the day and being nocturnal

Evaporative cooling by perspiration and panting
Storing fat reserves in one place (e.g., camel's hump) to avoid its insulating effect
Elongated, often vascularized extremities to conduct body heat to the air


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Mouse Colony Software
I am looking for a good mouse colony census program that tracks the mice we have in the lab, breeding success of breeders, lineages, multiple user access, etc. Jackson labs has a program that does this but is is cumbersome and a bit pricey (softmouse is also an option, though a pricey one). I figured that since colony management is so pervasive there must be a good piece of software to deal with this, but have mostly been out of luck. It would also be great if it is currently supported software that isn't outdated and free or sold at a relatively cheap price. Thanks.

check this out: http://e-mouselab.com

When you mean track the mice, you mean like mice movement?

And what counts as cheap?

Here is a list of programs that could work:

E-mouse Lab: http://e-mouselab.com, seems like the best fit for your requirements.
ZooEasy: http://standalone.zooeasy.com/en/pedigree-software/breeding-mice/breeders/index.html, Cheaper, good for breeding and pedigrees.
LabGuru: http://www.labguru.com, seems very professional and great for mice specimens as well.
MouseHouseApp: http://www.mousehouseapp.com, This is an iPhone and iPad app, so this would be good in the lab, but it depends on whether or not you have an iOS device.

Also, from what I found, Jackson Labs actually offers free mouse colony management programs. It does seem like it is cumbersome, but also a great program.
I will add more when I get time.


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What motivates birds to make birdsong?
I was pondering the question "Why do humans make music?" and on an intuitive level, my answer was "because of the feelings it evokes of course!"
But I then wondered, what about songbirds? Does a songbird have a feeling that compels it to make songs? I know there are plenty of instances of birds dancing and singing (at least, some call it that), but what motives does a songbird have to make birdsong?  How does this compare to the emotions and motives humans feel?

Why do bird sing?
The main reason, male bird sing to attract mates (often, only males sing). Birds may also sing to communicate to their peers. For example a song can mean "This is my territory, you'd better not approach!". There are other reasons birds can sing (although I think I cited the two most important ones); you'll find much more information if you just google why do birds sing?, there are plenty of very accessible online articles on the subject. Here is one such article that you may like reading
Talking about emotions is always difficult due to the absence of a good definition of what an emotion is. But anyway... yes, if females are attracted to the mates that sing well, it probably (depending on your definition) means it cause them to feel some emotions (sexual excitement for example).
Evolution of music in birds and humans
Bird song to attract mate (sexual selection). Humans, on the other hand, have evolved music production for different reasons (or at least this is what we think). The field of evolutionary musicology is a field in the junction between evolutionary psychology and biomusicology. In evolutionary musicology (and in evolutionary psychology) empirical testing is very complicated and therefore, today we can only think and make hypotheses but we can't test them. So always take with a grain of salt what you read in those fields.

+1 As a side note, like AliceD you are good at formatting. I'd give an extra +1 for style if I could. I also did not know biomusicology was a thing! Very interesting. I will have to read my songbird books and consider what you say about emotions. Maybe I should look more carefully at how they define the term.


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What was the first gene(s) found to code for ncRNA
I could not find a source that states what the first gene found to code for ncRNA was. Someone told me, however, it was a gene that coded for either rRNA or tRNA. To this point in time I have had no other confirmation that this is true.

The first eukaryotic genes cloned were the 18S and 28S rRNA genes from the frog X. laevis as described here: http://www.genome.gov/25520303
And yes, they are definitely ncRNA genes.

I don't think you answered my question. I asked what the first gene or genes found to code for ncRNA were. Not the first genes cloned.

I don't think you read my answer; the first eukaryotic genes cloned actually were ncRNA genes.


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How is atrophied muscle different than normal muscle in a chemical or biological way?
I am a writer with a question for a story I'm working on. In it, the character suffers from muscle atrophy due to spinal damage. So that I can portray this accurately, what would cause this type of wasting? I'm hoping there is a chemical or biological difference between atrophied and regular muscle.

Unfortunately, this will be a very broad question related to the cause of the atrophy. Causes include (But by no means are nowhere limited to) - Disuse, neuropathy, injury, guillan-barre, polio, osteoarthritis, rheumatoid arthritis, burns, ALS, alcohol and so on. Each of these will have different effects. Is there a way to narrow this down, or is this a general article on regular tissue versus affected tissue?

I am writing a fiction piece. The character has spinal damage and the muscles are atrophying due to paralysis.

I edited your question to reflect this, if you think this completely changes the question you want to ask, notify me and I can roll it back. Although, either way this may belong more on biology.se.


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Is there a good site or software to see if a primer pair spans an exon junction?
I am going to perform some RT-qPCR tests to validate an experiment.
I'm currently in the process of ordering primers, and I would like to get them from the Harvard Primer Bank since these have been validated before.
However, I would like to get primer pairs that span an exon junction (i.e., one primer on one exon, the other primer on another exon.)
Currently, I have to do a lot of steps to figure this out, since the Primer Bank only gives the positions of the primers on the CDS, and not on the entire mRNA molecule.
Does anyone have a quick way to check on which exons the primers belong?
Thank you!
Is there a good site or software to see if a primer pair spans an exon junction?

If there is a such a site, I have never encountered it. Since you say you have the genomic coordinates for each primer it seems to me like all you need is a list of the genomic coordinates of every transcribed exon in the human genome. Assuming that is correct then you are in luck because such lists do exist in the form of a GFF3 file. You should be able to obtain a comprehensive annotated GFF3 file of the human genome from the EnsEMBL website. It is possible that the UCSC browser has a similar file (except in their '.bed' format) but I  am less familiar with the contents of that site.


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Testing CO₂ for cell culture
I'm am refurbishing some old CO2 incubators. I would like to test the precision of the CO2 sensor. There is a sample port on this incubator.
What sorts of  methods are commonly used to measure CO2 in these incubators?
Strangely, the manufacturer of the incubator makes no recommendations.
I need to be able to report the measurement as a percentage.

I would presume calibrating it with a known gas concentrations is what they do at the factory. In my lab, the calibration is done by the servicing company.

Chemistry SE might be able to come up with a simple way get some known concentrations.

Found this:
http://www.mybacharach.com/fyrite-gas-analyzers.htm
Probably what I need


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Did not understand a small excerpt from a research paper
Was going through this paper, among multiple things that i did not understand, I came across this part:

Each amino acid residue of a single
  window was encoded into a unitary bit string of length 20, where a
  bit was set (value = 1) if its position in the string corresponds to the position of the amino acid residue and zero otherwise

Did not understand this line. Someone please explain what position they are talking about

The paper's description is poor, but they seem to be describing an encoding where each of 20 possible amino acids are associated with a position within a string of 20 bits, e.g. alanine with offset 0, cysteine with offset 1, etc.  With that representation, one amino acid residue within a window is encoded by a string of 20 bits, 19 of them being 0 and the other a 1; the single 1 bit occurring in the place corresponding to the residue.
This interpretation is supported by the paper's citation of  Qian N, Sejnowski TJ (1998) "Predicting the secondary structure of globular
proteins using neural network models." J Mol Biol 202: 865–884.  Qian's paper says:

Each group has 21 units, each unit representing 1 of the amino acids (or spacer). For a local encoding of the input sequence, 1 and only 1 input unit in each group, corresponding to the appropriate amino acid at each position, is given a value 1, and the rest are set to 0.

+1 good answer although do not agree with "The paper's description is poor" part. The sentence quoted in the OP's question seems confusing but reading the entire paragraph in the paper puts things into context nicely.

@ddiez, I did not mean to imply the paper was poor (or the surrounding paragraph), but that the quoted sentence did a poor job of describing the representation, which was essentially the sentence's only job. The surrounding paragraph I don't think makes up for that, although it does provide necessary context.  The problem is that nowhere does it convey that there is a defined bit position within the bit string for each kind of amino acid.  It says "corresponds to the position of the amino acid residue" where it would be better ...

(cont'd) if it said something like "is the one defined for that type of amino acid".  Once one understands the bit-for-residue-type representation, one might be able read the sentence as communicating something like that, but if one has not yet thought of that approach, the sentence does not put the idea across well (IMO).


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GO term for orthologous gene IDs
I have a list of orthologous gene IDs from the first supplementary file in here.
The gene IDs are of the following type:
EOG6STSR2
EOG60ZRJB
EOG6SBFJ2
EOG6P5KX3
EOG6B5PRW

I want to do the GO term analysis for these IDs. I tried mapping them to FlyBase IDs from OrthoDB and then using DAVID. But many of the orthologous IDs are not getting mapped to the FlyBase ones so I'm not getting proper results.
Is it possible to get the GO term analysis done directly for the orthologous gene IDs without mapping them to the FlyBase IDs?

You mean the .bed files in the study?

Yes. I got the orthologous gene IDs from the fourth column of the bed file.

I have a solution for accurate ID conversion but it makes use of a small script (that you'll have to write). The idea is quite simple and the implementation is easy. Would that be fine or you just want an existing reliable ID converter?

I'm comfortable with writing a script. I had written one initially which took the file from OrthoDB, extracted the lines with DMEL as Organism ad then mapped the IDs in the given file.


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Can Biting Insects Detect Specific Places On A Host Body?
I'm gonna make a presumptive statement: It -seems- as though I get bitten by mosquitos and other biting insects in -exactly- the same places over and over. I mean within a few mm. Is that true?
If true, that implies that insects have a mechanism to detect certain preferred spots in order to get blood or whatever they want. (Location of blood vessels? Sweat glands?)
And if that is so, what -is- that mechanism? What are they going for? And how does this detection work?
IOW: How do they know to bite me exactly on the side of my right knee over and over and over... but never on other spots?

Lice, for example, live on the (hair of the) head, which seems specific. Some other insects bite where the skin is accessible, and that can just depends on our clothing habits.

There are at least two sources that influence patterns of behavior: the individual that is doing the biting, and the individual that is being bitten.
The example of lice in one of the comments is a good example.  Three categories of lice that get on humans are: head lice, body lice, and pubic lice.  They are related species (possibly the same species in some cases - https://www.insidescience.org/content/are-head-and-body-lice-same-species/550), but each type has their own preference for habitat and feeding.  There are all kinds of reasons for a species to have a preference, and some stick to those preferences quite strongly.
As for your mosquitoes, their absolute preferences are still not known but blood seeking insects do have their senses attuned to clues such as carbon dioxide and heat (that help identify potential hosts) as well smells and other influences on their senses.  There might be something special about the side of your right knee as far as mosquito senses go, but not every individual in a species sees, smells, hears, etc. the same way.  My brother has a gene that makes broccoli taste very bitter, but I am fortunate to not have those taste buds.  Color blindness is another example of differences in perception, but even without being color blind, what you see as red is probably not how someone else sees red due to natural variations in the patterns of sensory cells in the eye.  For a consistent pattern of behavior from the mosquitoes, in spite of individual differences we still need to consider another source of variation that might lead to this mosquito preference: the host.
If the variation of individual mosquitoes is trumped by a consistent pattern of predation, perhaps the mediating factor is the host.  Your knee could have a special smell, or other sensory flag that attracts mosquitoes.  There are efforts to understand how a mosquito's perception directs who gets bitten: http://www.scientificamerican.com/video/future-repellents-mess-with-mosquit2013-12-23/ .  Not enough is known yet about the preferences of mosquitoes to say for sure what makes your knee so good.  There is also a chance that your knee is not special to the mosquito because it appears the most appetizing.
Host behavior is another possible influence.  The knee is just far enough away from the reach of your hands.  Conscious or absentminded grooming would both be limited at that distance.  The knee may also be better than an ankle or a foot, because of what is worn or because the knee moves less than the lower leg during walking and other movements.  If you are bitten on the lateral (outside) side of your knee, this would add evidence to this hypothesis of your movement influencing mosquito behavior, because the inside of your knee more frequently brushes against the other leg.  The frequency of the inside of the knee being a safe place for a meal is much lower.
As for why it's the right knee rather than the left, there is  possibility that that is also a reflection of you, rather than the pests.  Humans display preferences in dominance for both hands and feet.  One side of your body may be selected more often than another because of you being right- or left-handed, or right- or left-footed.  This could affect grooming habits (how you swat at the bugs), how your cross your legs, which side you carry items or lean against other objects which might brush against the body, influence how well you spray yourself with bug repellent or who knows what else.  (Just for curiosity's sake, ¿are you right-handed or are you left-handed?)
In short: There's a lot of evidence to collect before we could come to a definitive answer.  There are a lot of possibilities, including that your knee may not be the tastiest spot, but rather a relatively safe spot for dinner.
For more unempirical thoughts on the relationship of insects to the lower limbs, please see: http://fishboyridesagain.blogspot.com/2005/11/bugs-and-trousers.html


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How much penicillinase is needed to deactivate 125mg of amoxicillin?
How much penicillinase is needed to deactivate 125mg of amoxicillin?
Penicillinase in penase concentrate from CPC.
20,000 Levy Units/ml/min
I need IU of 125 mg of amoxicillin.
Please note that the problem is with finding the right parameters for amoxicillin, not penicillin G.
My goal is to test an amoxicillin product (i.e. it contains more than just amoxicillin) so the overall problem is more complex, I wanted to keep the question focused.
I would like to know the minimal amount of penase needed to deactivate 125mg of amoxicillin (that's the amount of amoxicillin in the product) in a reasonable amount of time, say 5 minutes. I want the minimal amount of penase because I am not sure what is its influence on bacterial growth, I am going to test that separately. Maybe I am going wrong about the whole problem?
I think that this paper could be helpful in general: Microbiological Applications of the Inactivation of Antibiotics and Other Antimicrobial Agents but it's behind a paywall and I can't access it at the moment. So far, I failed to find any other useful resources.

This question cannot be answered without a time factor. Assuming no enzyme degradation, theoretically a single enzyme molecule can do it given enough time.

Well, you could be a chap and answer the question, instead of downvoting, including factoring in the time factor - it would be just one abstraction higher than a simple number and also more valuable and informative.

This is not a homework question! It even doesn't fit the homework policy. The first two points are off the table immediately. The last point, "A question that addresses a basic biology concept that may seem trivial to biology professionals" is obviously invalid too since it seems none of you are able to answer the question for amoxicillin as opposed to penicillin G.

@jkbkot You should also show some basic effort. Levy Unit is not a standard enzyme activity metric. As it seems it is used only in case of Penase. Add some of your calculation on how much penicillinase is would deactivate an equal amount of penicillin. From your question it seems you are asking others to do your calculation. The edit was useful but I suggest that you add some more details.

@WYSIWYG I agree I should have added more details from the beginning, sorry about that. I'll add more of my own research a bit later in the day, thanks.

@jkbkot Moreover, there are several types of penicillinases which would ahve different activities. I don't think CPC has mentioned the composition of their product. I am afraid you would have to do an assay to determine the activity. There are no research papers (from my quick search) also that compare activities of a given penicillinase against different penicillins. Plus, the time factor is necessary. Amoxicillin can eventually degrade spontaneously as well.

@WYSIWYG thanks, that also helps - I spent quite a bit of time going through research papers myself and haven't found any useful references. Maybe one behind a paywall, unfortunately inaccessible to me at the moment. I'll update the answer

I still think this question shows an appalling lack of effort. If you had truly replicated TomD's results as above, you should have posted them in the question to begin with, so they know you have already done it and not spent their time doing your calculations for you. Also see this Meta answer for my opinion on this topic. Many members of the community vote to close questions for being homework if they are poorly researched and show no effort.

@MarchHo yes, I should have included a bit more information which I already admitted and said sorry. Also, sorry but appalling is too strong of a word and just adds more evidence to the hostility of this community. The question as it stands now is fine and it is also thanks to the effort of the helpful comments (which yours were not). If we are being pedants then everyone should have paid a lot more attention to the fact the question was about amoxicillin instead of assuming the poster is an idiot.

As March Ho has pointed out, we could do with a bit more information on this one.
I am going to attempt the calculation for penicillin G, and the necessary information seems to be available.

From here, A Levy Unit (LU) is the amount of penicillinase that inactivates 593 IU (International Units) of Sodium Penicillin G  per minute at 25°C and pH 7.0
From here and here, the specific activity of penicillin G is about 1667 Units/mg
I am assuming your concentrate is 20,000 Levy Units/ml (not 20,000 Levy Units/ml/min, which does not make sense to me)
Therefore 1 Levy Unit will inactivate (593/1667)mg, or 0.356 mg, of penicillin G per minute, pH 7.0 and 25oC
2.81 Levy Units will inactivate 1 mg penicillin G under identical conditions
351 Units will theoretically inactivate 125 mg penicillin G in 1 min under the conditions stated.
Your concentrate is 20000 Units/ml, or 20 Units per microliter.  So you will need (351/20) microlitres, or about 17.5 ul.
This assumes that the enzyme continues at a constant rate given by the specific activity right until the end.  This might not necessarily be the case, as one would expect the rate to slow down as the substrate concentration falls below Km.  Personally, I would use at least a 10-fold excess. 176ul - Seems a lot?

Please feel free to provide further information, or to edit the answer in any way you feel is necessary

Thanks for the answer! It helps me to realize that 1) I seem to understand how to compute this myself, I actually did it for penicillin G and got the same result as you 2) the real problem is that there seems to be no IU definition for amoxicillin, or at least I'm failing to find it so I'm not sure how much penase is needed. I am actually figuring out a way to test amoxicillin - maybe I could ask about that directly too? I need to double check pharmacopoeia first though...

Now I see they say that for other penicillins one should use 20 times more penase. Is there no more specific information available?