Reconstruction of wildlife distribution based on poorly-sampled data cross-posted to Signal Processing, Cross Validated, and World Building Stack Exchange

Hi, I thought I'd also put this here in case there are any field biologists with ideas on the matter.

Problem: After reading a series of fantasy novels, I noticed that the biosphere in that world made no sense. To clarify, this is a world where despite magical occurrences, the world itself is almost entirely non-magical. 'Alternate history magical realism,' perhaps. i.e., unlike, for example, Harry Potter, in which almost all plant and animal species mentioned are fictitious and magical, this series uses real flora and fauna. This allows me to extract information about the fictional world's environment based on the distribution of these animals, by assuming that similar animals will live in similar climates on Earth and in the fictional world.

Ignoring the likelihood that the original author did not put enough thought into worldbuilding to make this a necessarily reasonable endeavor, my idea for how to proceed was as follows:

As maps exist of the fictional world, and the path of the characters can be plotted, I hoped to mark every mention of a specific plant or animal in the text, along with the location of the characters when it occurred, and from this reconstruct a plausible distribution for each species. I've created a theoretical example (in photoshop), for illustration:

where the red dotted line represents the paths of various characters, the orange, green, and blue splotches represent the true distribution of the species; the stars, triangles, and circles represent the locations at which a species is mentioned; and the brown, green, and blue lines represent the reconstructed contours of the distribution.

Is there a method to do such a reconstruction? It sounds a bit like a Monte Carlo analysis, but I figured I should check... (It also sounds rather like the magical programs detective shows use to plot serial killers' locations)

Note: It should be clear from the problem statement that just because a species is not mentioned at a specific location does not mean that it does not exist there. i.e., a sample at a specific location returning only 'A' - 'Bill and Jeff saw a lemur.' - does not exclude the possibility of 'B' and 'C' also at that location, but not sampled. Just because the text may specifically say that Bill and Jeff saw a lemur, and doesn't mention any other flora or fauna doesn't mean we should assume that they are in a universe devoid of anything but the occasional lemur.

Final Thoughts: Ideally, the analysis method would further:

take into account the coverage of the paths, and not assume that (in
the example above) nothing exists in Mexico or northern Canada, just
because there are no samples taken there. Remember that samples can
only be taken along paths.
take into account edges, in this case coastlines. If A, B, and C are
land animals, it does not make sense that a reconstruction of their
distribution would include water, even if their range surrounds a
lake or something.

Sorry for the long-winded explanation. Any thoughts?

The problem of how to infer species distributions from scattered species occurrences is common in ecology, and there exists a number of methods to construct distribution maps. As a start, you should have a look at Species Distribution Models (SDMs) using regressions models or Maxent, and the paper by Elith et al (2009) is a good starting point and a standard reference. SDMs using maxent is now a common approach, which integrates species occurrences as point data along with environmental layers (e.g. temperature, moisture and topography) to predict species distribution maps, and this can also include absence data or "pseudo-absence" data (randomly sampled data from a region of interest). The maxent software is described and can be downloaded here: http://www.cs.princeton.edu/~schapire/maxent/
A common criticism against distributions produced by Maxent is however that they ignore e.g. species interactions, and they only considers the species occurences and the environmental variables that has been included in the model.

In your "Note", you touch upon the issue of detectability, which is an important issue that has received much attention recently. The problem is largest when you only have presence data, and to have real presence/absence data is preferable. Even if you don't have real absenses (the species has been searched for but not found), an estimate of sampling effort in different areas is still very useful, since this means that you can at least evaluate whether absenses is due to "real" absense or lack of sampling. In your case, the movement paths of characters could be used as a measure of spatial "sampling effort". The main issue with detectability in studies of distribution of species trends is if there is trends or bias in detectability, which means that apparent changes over time or patterns in distribution might be due to differences in detectability and not real differences between areas or over time. This could for instance be the case if observers are more likely to spot a species in one type of habitat (open savannah) then in another type of habitat (closed forest). Useful starting points for issues of detectability are Dorazio (2014) (technical though) and Kery et al (2010).


Does the most common definition of "allele" include a change in phenotype? I'm prepping an activity for my biology students on cystic fibrosis. There are about 2000 different mutations of the CFTR gene that cause CF. Since the final phenotype is pretty much the same, can I still claim that all these mutations represent different alleles?

I like to point out that genes tend to have more than two alleles - it's something that students really struggle with. But if every allele needs to have a different phenotype based on the standard definition, then this isn't ideal.

Thanks for the help.

Yes, allele is an alternative form of the same gene which can be produced through any variations/mutations of a gene, such as deletion, segmental duplications, inversions, insertions through transposons, even a SNP or point mutation (http://en.wikipedia.org/wiki/Allele) and as correctly stated many alleles do not produce any observable/discernable phenotypic variation. A gene can have many alleles in a given population, but do not confuse allele with gene homologues (which I suspect what you were alluding to above in the second paragraph), which are similar versions of a gene such as RIN1, RIN2 and RIN3 (http://homepage.usask.ca/~ctl271/857/def_homolog.shtml).


Genetics independent assortment? As indicated in this question, what do you think is is the best explanation for the observed progeny, is it because distance between genes affects recombination frequency? My main concern is question b).

Any help would be greatly appreciated thanks in advance!!

Until now, it looks good. When you are looking at basic mendelian gene linkage problems like these and you find out that the chi square analysis rejects your hypothesis, it means that there is linkage. In that case, you should have a case where your two recombinant genotypes have an approximately equal number of progeny and your two parental genotypes also have an approximately equal number of progeny. In your case, 220 is about 230, and 270 is about 280.

(source: k12.ny.us)
This image is just like your problem. I want you to imagine that b+ and b represent A and a in your problem and that vg+ and vg represent B and b in your problem, respectively. You start out with an AaBb crossed with an aabb. On the gametes line, it lists all of the possible gametes of this cross. On the line where it describes testcross offspring, we see a situation very similar to yours. In this case, AaBb = 965, aabb = 944, Aabb = 206, and aaBb = 185. We have our two pairs: AaBb/aabb and Aabb/aaBb. Sound familiar?
The recombinant offspring are defined as the offspring that do not have a genotype of either parents. The reason this is important is because you need a crossover to get a recombinant. The closer two alleles are together on the same chromosome, the harder it is to get one of the alleles to cross over without the other one crossing over with it.
Let's clarify. This means that if the alleles are closer, you get less crossovers. All recombinant exist because of a crossover. Therefore, the closer two alleles are, the less recombinants you get.
Quick note: the formula for the distance two alleles are from each other is expressed by this formula:
100(recombinant frequency) / (total offspring) = distance apart.
This is consistant with everything we have said, because as recombinant frequency decreases, distance apart decreases as well.
Another way to explain it: on the gametes, AB and ab really like to stay together, as they are LINKED. It is very difficult to separate them. That is why there are more AaBb and aabb; they only require the gametes AB and ab.
Apply the formula to find out how far they are apart. I think you can figure out the rest from here. I want you to try and answer the question.
Hope this helped! :)


White blood: cells concentration Anyone knows of a table with average concentration that can be found in  white blood?

Something like:

Neutrophils - 80%
Mast cells - ?%
Dendritic cells - ?%
B cells - ?%
Helper T cells - ?%
Killer T cells - ?%
Natural killers - ?%
Others - (whatever is left)
(the sum should be 100%, of course :))

Also: are helper T cells and killer T cells visually different? I can only find pictures of T cells, but not of each. I am also unable to find pictures of natural killers. - Thank you!

Here are some figures from Cellular and Molecular Immunology, 8th Edition:

Hopefully they're helpful in some way.


Relationship between bacteria size and temperature? I'm, doing a research in a TOC (total organic carbon) degradation in a BAC (biologically active carbon) filter for the grey-water treatment. Recently, I started to wonder if there is a relation between bacteria size and temperature. If anyone know any research paper or did a research by himself/herself where such relation has been checked, it would be of a great help.

Thanks in advance.

There is a negative correlation between growth temperature and genome size for prokaryotes, which may be driven by selection for smaller cell size overall in warmer environments. Sabath et al., 2013 provide a good discussion:

  Smaller cells tend to have smaller genomes in both prokaryotes and unicellular eukaryotes (Shuter et al. 1983; Lynch 2007), for reasons that are not fully understood (but see Dill et al. 2011). This correlation suggests that cell and genome size are functionally related, such that an evolutionary change in one would induce an evolutionary change in the other. Previous studies have hypothesized that reduction in cell size could be advantageous, either to optimize surface-to-volume ratio for uptake of scarce nutrients (Dufresne et al. 2005; Giovannoni et al. 2005; Moya et al. 2009), or to decrease predation by bacterivores or bacteriophages (Yooseph et al. 2010). Similarly, we speculate that bacteria adapted to high temperature could be subject to selection favoring smaller cell size, which also requires smaller genome size—regardless of gene content.


Identification of this humpbacked, brown, clawed insect climbing up my wall? I noticed several of these guys outside, all in a vertical position clinging to a wall. I didn't come to them too closely, but my immediate reaction was that they are scorpions.

I thought that maybe it's a curled-up scorpion, or maybe there's some kind of particular scorpion that is this circular in shape? These are probably silly conclusions, but I'm not an expert in this field. I would really appreciate the insight of a professional!

thanks very much.

That's the exoskeleton (shed outer shell) of a young cicada, left behind when it emerged as an adult and (we can imagine) flew off somewhere to sing, and find a mate.

This article on EarthSky has a nice description of the big cicada hatch this summer (2013), and also a great picture of an adult cicada emerging from the exoskeleton. However, this article and other recent news about cicadas mostly deals with the Eastern US genus Magicicada, and it's likely that in Arizona you're seeing a different genus (that is, a different type of cicada).

You'd probably have to find an adult in order to identify exactly what genus and species of cicada you've got. Alternatively, you could listen for their songs – this site has examples of calls from many Western US species, including the Apache Cicada Diceroprocta apache, which seems to be a common cicada in your area.


Plastid and mitochondria I am not a biologist, so please bear with me for this basic question. Although I tried googling, I am confused.

What is the difference between plastids, chloroplasts and mitochondria?
Are there any plant sequence databases for each of them (plastid, chloroplast and mitochondria)?
Can we separate chloroplast, mitochondria, plastid sequences from whole genome assemblies?

What is difference between plastid, chloroplast and mitochondira?

Plastid is a general term for an organelle which consists of Chloroplasts, Chromoplasts, Leukoplasts/Amyloplasts and Apicoplasts.

Chloroplasts (Chloro = green) are involved in photosynthesis; they express Chlorophylls and have the thylakoid structures which are involved in the electron transport chain that results in ATP formation during the light reactions of photosynthesis. As it is obvious chloroplasts are found in the green parts of the plants such as leaves. Chloroplasts also have the enzymes of biosynthetic pathways involved in carbon fixation.

Chromoplasts (Chromo = colored) express more of other pigments and less of chlorophyll. Neither do they have thylakoid structures. Therefore they are not involved in photosynthesis. When fruits ripen, the chloroplasts differentiate to chromoplasts. Flowers also contain a lot of chromoplasts.

Leukoplasts (Leuko = white) do not have any pigments and usually carry out biosynthetic processes. When they store starch they are called amyloplasts.

Apicoplasts are found in parasites like plasmodia (causes malaria) and are vital for their survival. The Apicoplast is involved in biosynthetic pathways but the precise importance of it remains unknown.

The mitochondrion is a very different organelle and has a different evolutionary origin. Mitochondria, like Chloroplasts, produce ATP from an electron transport chain but use chemical substrates (NADH, flavin etc) rather than light as a source of initial energy. Mitochondria are thought to be an outcome of an endosymbiosis between an ancestral eukaryotic cell and an $\alpha$-proteobacterium. Chloroplasts, on the other hand have descended from a Cyanobacterial endosymbiont. Therefore the structure of mitochondria is very different from that of chloroplasts.

Chromoplasts, leukoplasts, amyloplasts and apicoplasts have lost the photosynthetic ability. Similarly, there are variants of mitochondria which use different electron acceptors (other than oxygen) and some are just incapable of ATP synthesis.

  Are there any plant sequence database for each of them (plastid,
  chloroplast and mitochondira)?

Chloroplast genome database: {link}

I don't know of a separate plant mitochondrial database but you can see this resource called MitBASE.

NCBI also has the organellar DNA sequences.

  Can we separate as chloroplast, mitochondria, platid sequence from
  whole genome assembly?

Usually the organellar genomes will assemble as separate contigs when you sequence from the whole cell DNA prep. By homology it is possible to say if the contig is a mitochondrial or chloroplast DNA. But the best way would be to experimentally isolate the organelles and sequence their DNA.


Promoter in the lac operon Here is the question:

Suppose an experimenter becomes proficient with a technique that allows her to move DNA sequences within a prokaryotic genome. If she moves the promoter for the lac operon to the region between the beta galactosidas gene and the permease gene which of the following would be likely?

Here is the answer:

Beta galactosidase will be produced.

My question to you is: why is this so? I have no idea where this conclusion came from.
Thanks.

Since @biogirl has given an answer, I'll add my opinion:

β-galactosidase would be expressed but the permease and transacetylase would not.

The operator lies adjacent to/slightly overlaps the promoter, upstream of the lacZ gene. Binding of the repressor to the operator blocks the promoter, and induction of theoperon involves the repressor leaving the operator unoccupied. If you precisely excised the operator and transplanted it between the lacZ and lacY genes then I think the promoter would be constitutively expressed leading to β-galactosidase synthesis, but the operator would block the polymerase from transcribing the permease gene. In this view the operator would be acting more like a terminator.

Then, if an inducer was added it would relieve the effect of the transplanted operator and the downstream genes would be transcribed. It's even possible that this experiment has been done sometime in the last three decades.

added later:

The OP has now edited the question in such a way as to make my answer, and the answer from @biogirl, nonsensical. The original wording referred to moving "the lac operon" not "the lac promoter", hence my question in a comment asking "operon" or "operator"?

I'll leave my answer here, but this question is now so compromised that I advise everyone to just forget about it.


A plant in my aquarium seems to be growing small plants under its leaves, what's going on? In my aquarium I have this plant. I think it's a kind of swordplant. I've loosely attached it to a large piece of driftwood in the hope that it will grow itself on there, I saw that they had done the same in the petstore.

Now recently other plants have started to grow from under its leaves. I've tried to take a picture of it, these are the biggest ones but there are smaller ones on other leaves:

The plant seems to be doing pretty well, I added some iron and fertiliser to the water. The aquarium is positioned so that it catches a bit of direct sunlight late in the day and tons of indirect sunlight almost all day. It also houses shrimps and two apple snails.

My question: What are these small leaves? Is the plant procreating or does are these some kind of parasitical plants of another species?

From what I see ,it does look like some kind of Echinodorus ( Amazon sword). They do propagate by stems with new plants. They prefer to have roots in substrate.


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!

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.


How are atoms in benzopyridines and benzopurines numbered? I am well-aware of the numbering system used for the traditional bases, as seen below.

My question is how are the atoms in the size-expanded bases seen in xDNA and xRNA numbered?

This is a question of chemical nomenclature and the principle source for this is the IUPAC (IUBMB in case of biological molecules; but not in this case). You can find all hetero-ring nomenclature references on the IUPAC web site:

http://www.acdlabs.com/iupac/nomenclature/

http://www.acdlabs.com/iupac/nomenclature/79/r79_702.htm

(I'm skipping the actual naming step)

Numbering is actually done according to
http://www.acdlabs.com/iupac/nomenclature/79/r79_72.htm

That means, if you take the skeleton without hetero atoms, you start

  in a clockwise direction commencing with the carbon atom not engaged
  in ring-fusion in the most counter-clockwise position of the uppermost
  ring, or if there is a choice, of the uppermost ring farthest to the
  right, and omitting atoms common to two or more rings.

Now, if there are more than one possibility due to symmetry, you chose the numbering that gives the heteros the smallest possible numbers (this means your purines would be actually wrongly numbered if they weren't an exception---see the List of retained names).

So, we have finally in dxC and dxT the start at the lower nitrogen, going anti-clockwise (the other N at 3, methyl at 6, ribose at 8), and in dxA and dxG similarly the start at the lower right N, going anti-clockwise with other Ns at 3, 6, and 8, and ribose at 8, as well.


Does the Petri dish lid orientation on workbench affect aseptic technique? When examining an incubated plate, it is rather clear that holding the plate in one hand and the lid in another is best for aseptic technique, or simply resting the lid on the plate as shown below.

However, I can't seem to find an answer for what to do with your Petri dish lid when doing manipulations like plating. It's pretty obvious that the above practice is, well, practically impossible.

Thus, I always went under the assumption that when placing the Petri dish lid on the workspace, the orientation of the lid did not particularly affect risk of contamination, assuming that you're technique is indeed aseptic (ethanoled workbench, Bunsen burner, etc). However, discussing with collegues has resulted in mixed answers. Some say it doesn't matter, some say the lid should be facing up, some say down.

When doing manipulations like plating, is there a common practice for exactly how to place your Petri dish lid?

DISCLAIMER: I am a computational biologist and haven't touched a Petri dish since I was an undergraduate biology student.

I would expect that the best thing to do would be to place the lid face down.
When placed so on the bench, it is only the tip of the lid that comes into contact with your (presumably sterile-ish) bench. If you place it face up, the interior of the lid will come into contact with the air of the lab. Despite the presence of the bunsen, I would expect that to gather more contamination.

Since the lid is larger than the dish itself, the lip of the lid never touches the dish. Therefore, if the lip of the lid touches the bench and becomes contaminated that is not a big problem since that contamination should be blocked from spreading to the actual culture. If, on the other hand, the lid were placed face up, the interior of the lid (which hangs just above your culture when closed) will have come into contact with possibly contaminated air and could then cause contaminants to drop onto your culture.


What equipment is needed to perform simple plant electrophysiology? What is the minimum needed equipment to perform simple plant electrophysiology? I am looking for some simple experiments that I could run at home for learning. Ideally, I would transfer the skills to stud neuroscience later on (the skills could be related to operating a microscope, doing recordings with microelectrodes, signal processing, statistics, etc). How expensive this would be?

Electrophysiology on plant cells means single-cell recordings, as there are no gross compound action potentials.  As you correctly say, this means micro-electrodes; this in turn means computerized manipulation of the pipettes, a decent microscope, signal amplifier, recording software, stimulator slash voltage/current control, Faraday cage, analysis software (Matlab), and not unimportantly a vibration-free workbench (whole departments have moved house due to micrometer vibrations in the building). I guess you should think anywhere between 10k - 100k (dollars, euros whatever) as a reasonable estimate.

A student internship would be advisable finance-wise, but especially because single cell recordings, and electrophysiological skills in general, are relatively difficult to master.


Why are the bodies of the Risso's dolphin covered in scratches? Risso's dolphin in wild population seem to obtain scratches with aging. What is causing them and what do they mean?

[ From Jefferson et al. 2015, Marine Mammals of the World, 2nd edition, p 212: "At sea, the best identification characteristic is the coloration and scarring. Adult Risso's dolphins range from dark gray to nearly white, but are typically covered with white scratches, spots, and blotches. Many of these are thought to result from the beacks and suckers of squid, their major prey, but others may be caused by the teeth of other Risso's dolphins. If fact, this species is the most heavily-scarred of all the dolphins." ]


Can in the case of multiple sclerosis (MS), a too high osmotic pressure in the nerve, lead to a high intracellular concentration of potassium? Can in the case of multiple sclerosis (MS),
a too high osmotic pressure in the nerve,
lead to a high intracellular concentration of potassium,
and also lead to 'pumping up' of nerve cells,
which then due to the strongly increased internal pressure,
the insulating myelin sheath can be pressed broken,
resulting in a lesion,
or a strong reduced transmission of stimuli ?

If that were to happen,
one can expect in cerebrospinal fluid,
cytokines, which are normally also a component of the nerve cell contents,
and that it wrongly can be interpreted,
as inflammatory reaction to a potential autoimmune disease.

Is there research of this ?

Firstly, demyelination has got nothing to do with membrane integrity of the neuron. Demyelination causes the current to "leak" through the ion-channels and thus causing loss of signal.

There is an old article which reports a study on membrane integrity of RBCs of MS patients but there seems to be no connection.

It has been proven that neurons do secrete some cytokines such as IFNgamma but the signaling is mostly para/auto-crine and I dont think the cytokines will accumulate in CSF.

MS is identified by the presence of anti-myelin antibodies, which might be the exact biomarker for the disease. A general neuroinflammation is not concluded as MS.

So to answer your final question

  Is there research of this ?

There is none that exactly talks about neuron membrane dynamics in MS. The most parsimonious assumption is that there is no effect, but any hypothesis has to be proven. It might be experimentally difficult to address this question and how to design the experiment for this study would be an interesting question.


Inoculation vs. vaccination Is there any actual difference between inoculation and vaccination or are these terms interchangeable?

In case the difference exists, would it be correct to say that inoculation is purposefully infecting a person with a pathogen in a controlled way, even when the person is already infected, to induce immunity while vaccination is administering dead or weakened pathogens to a healthy person as a preventive measure to check future infections?

Also, would it be correct to say that vaccination is an advanced form of inoculation?

Both are forms of immunisation.

Inoculation is exactly that. A live organism is introduced in a controlled way, so as to minimise the risk of infection, and is essentially the same process followed by many people in history.  It is inherently risky.

Vaccination is introducing a weakened version of the pathogen, so that the immune response is triggered and the body is prepared to fight the actual pathogen if necessary. This was pioneered by Edward Jenner, wherein he noticed that cowpox (related to smallpox) immunised the milkmaids against smallpox.


What is this brown spider with black and white stripes? (Atlanta, Georgia) Location: Atlanta, Georgia

Spider mostly brown, with black and white stripes. Would fit on a teaspoon.  Ran quickly but not very far when I tried to catch it.

Click to zoom in the pictures below:

It resembles Dolomedes tenebrosus, commonly called the Dark Fishing Spider, and it belongs to the family Pisauridae.

Image Source: Bug Guide

Males are generally thinner in profile than the females, which is well depicted below.

Image Source: Spiders.Us

Based on the pictures provided, you seem to have captured a male Dolomedes tenebrosus.


How and why are cells irradiated in human-rodent hybrid cell biology? When human-rodent hybrids are made the amount of human chromosome in the hybrid can be reduced by irradiation. Why and how exactly is this irradiation step performed?

Human cells are irradiated with X rays (to fragment the DNA) and then fused with rodent cells. This is useful for mapping because closely linked markers are more likely to appear in the same hybrid: there is a lower probability of radiation induced breakage between the markers because they are close together.


Has there ever been an attempt to create nutritionally tailored food for adult human consumption? For all domestic animals, and for all animals kept in laboratory, complete and precise composition of perfect food is figured out (cat food, dog food, cattle, rats, laboratory monkeys and apes) -- which contains precise composition of carbs, fats, proteins, aminoacids, minerals and vitamins. Everything is known. Convenient dry cat/dog food contains exactly that. Animals are healthy on this food.

The composition is also known for human babies. This is manufactured as "baby formula". Everything baby's organism needs to be healthy (and to grow).

How let's take human adults.

Was ever attempt made to create "dry human 'dog-food'"? This sounds stupid, but there are emergency situation in which such food can come very useful.

So my question is, is there anything special in human biology that prevents creation of complete "dry human food" that contains everything our organism needs to be healthy ?

Or it was created but tasted so disgusting that nobody would eat it ?

Or it actually exist somewhere ? Just curious.

Yes.  Rob Rhinehart has developed what he refers to as "a food substitute intended to supply all of a human body's daily nutritional needs, made from powdered starch, rice protein, olive oil, and raw chemical powders" which he calls Soylent.
It was developed and tested largely in 2013, crowdfunded late 2013, and is expected to start shipping in 2014. Tests of at least 30 days with no other food intake have been performed, though this is being marketed as a food and not a medical aid of any sort, so does not require FDA testing.
Even if this didn't exist, there are numerous "complete" human diet foods meant for medical use.  These are mentioned in an article about soylent:

Jay Mirtallo is a professor of pharmacy at Ohio State and the immediate past president of American Society for Parental Enteral Nutrition, which focuses on the science and practice of providing food to patients through both intravenous injections and feeding tubes. His main concern with Rhinehart's plan is that he's making the concoction himself, rather than buying it from reputable suppliers.
"He basically made medical food," Mirtallo says. "If he wanted to switch to a liquid diet, those are already available."
Indeed they are. Companies like Abbott Nutrition and NestléHealthScience sell dozens of medical food products, intended to be used by patients under medical supervision and administered intravenously, orally, or through an incision in the stomach.
"They’re very complex products, in terms of making sure you get them in a form that’s palatable but that stays in a form that’s bioavailable to the body," Mirtallo says. "Some of the products are very difficult to get into a liquid form and may lose their potency when they do that, or could interact with other substances that keep them from being absorbed completely."

Rob appears to be attempting to make a consumer version, and so far reports are positive.
But even if you don't trust Rob's mixture, there are countless medically complete nutritional foods that are FDA approved, though not generally available at the supermarket.


Histidine aromaticity I understand that the imidazole ring in histidine is aromatic. I also realize that it retains it's aromaticity when protonated.
I am wondering why it is not mentioned at all in basic text books such as Lehninger? Also, across the web there are a number of places claiming that histidine isn't aromatic in all cases.
Another reason I am a little confused is, if protonation doesn't harm the aromatic nature, then why is histidine such a weak base?
Am I missing something?

This is one of my favorite charts demonstrating the complexity of amino acid properties:

http://www.jalview.org/help/html/misc/aaproperties.html

Histidine is probably the most complicated amino acid in this regard (just compare how many circles it falls into).  But don't undersell Cysteine and Methionine; those sulfurs exhibit some surprising behavior, especially when coordinated properly.  Cysteine of course forming disulfide bonds, Methionine occasionally functioning as a methyl-transferase.

Biochemistry text books make some over simplifications because presenting the full messiness of these classifications is pretty confusing. Lehninger itself is the worst about this (and especially when presenting math).  Voet and Voet is probably the most reliable about presenting this complexity. I still think Lehninger is a better teaching textbook overall (I was first taught Biochemistry from the 3rd edition), but I also recall spending a week being confused about a topic before someone pointed me at V&V and I realized Lehninger was oversimplified to the point of being wrong, in that case.


Reference sequence for defining single nucleotide polymorphisms Single nucleotide polymorphism (SNP) or genetic variation in general, by definition are relative to a reference sequence. When we talk about databases of SNP as in ("dbSNP—Database for Single Nucleotide Polymorphisms and Other Classes of Minor Genetic Variation", or "A map of human genome sequence variation containing 1.42 million single nucleotide polymorphisms" -- titles of well known research papers), what is the reference genome? Similarly for defining a "SNP Map/Profile" of a person (in medical genomics), what is the reference genome sequence? Is there a de facto reference, or is it context dependent? There is a sentence "Scientists are trying to identify all the different SNPs in the human genome" at http://www.cancer.gov/cancertopics/understandingcancer/geneticvariation/page36 -
what is the reference genome here?

I don't see your point. If we take e.g. the definition from Wikipedia:

SNP "is a DNA sequence variation occurring when a Single Nucleotide ... in the genome ... differs between members of a biological species or paired chromosomes",

there is no place for reference genome. SNP is just a variable position with (commonly) two alternatives in individuals of the same species. In whole-genome sequencing projects some SNPs can be discovered (namely those which are in heterozygous state), but definitely not all.

One can investigate SNPs and/or use them as genetic markers irrespective of the availability of the reference genome. That's the way one does it for non-model organisms - e.g. utilizing RAD Seq: you discover SNPs simultaneously with genotyping.


How exactly does symbolic language for apes work? I'm talking about the panels with lots of colored symbols on them you sometimes see in documentaries and the like. Apes point at the symbols in a specific order and in this way can communicate with humans.

I already googled around a lot, but wasn't able to find any detailed explanation on how exactly the language works (meaning of all the symbols, grammatical structure of the language and so on). It might just be because I don't know what words to use for my search, so can anyone with more expertise in the field point me in the right direction?

The best article I found was this one. In it it says among other things that:

Kanzi, an unusually intelligent Bonobo chimp trained at Georgia State
University, was remarkable in that he learned to use around 200
symbols on a portable electronic symbol board, a computer with buttons
in the shape of absolute arbitrary symbols rather than manual signs.
More interestingly, Kanzi learned how to use this board while watching
his foster mother, Matata, being taught by traditional reinforcement
methods. So Kanzi did learn how to use arbitrary symbols without being
taught, although he did observe direct reinforcement of each symbol
during the process and the symbols were taught one at the time.
The
evidence for the mastery of syntax is not so convincing. While
chimpanzees can learn to order their symbols to get what they want, it
is not clear that they have mastered syntax. The reason is that when
they initiate communication, even adult chimps often abandon the order
they have learned and phrases such as, "Fight mad Austin," a famous
utterance of Kanzi's friend Panbinisha. Here the order doesn't seem to
matter. Apparently Panbinisha was trying to express, "there was a
fight at Austin's and someone (Austin?) was mad". It is interesting
that even human children simply don't make such errors once language
acquisition begins, and certainly adult speakers would never utter
such strings. Notice it lacks any morphemes (-ing, at, I, she, -ed),
the hallmarks of grammar.

The trainer of Kanzi has published some materials but I do not know if they are available free online. You could probably send her an email and ask. The article goes on to state:

The maximum number of lexeme symbols (simple nouns, verbs, and
adjectives) is interesting, too. The brightest chimpanzees master
fewer than 200 of these symbols by adulthood. Human children know
about 50 by the time they are 18 months old, when they begin learning
nouns, verbs, and adjectives at the rate of about 5 per day. So the
maximum achievement in symbol acquisition among other primates is more
than matched by human children before the onset of language
acquisition. In fact, the type of phrases spoken by chimpanzees and
gorillas also resemble those spoken by children before they acquire
their first language: "give orange" or "give Bobby orange" (without
the pronoun me) are common expressions of children before the onset of
language learning around the age of two.
The results suggest that
while chimpanzees and gorillas are far more intelligent than anyone
had imagined during the first half of this century, they are not
capable of human language. Rather, they have a primitive version of
the semantic ability children use before that explosion of
language-learning around the age of two.

At least according to that article there is not much of a grammatical structure at all. The apes does not so much care about the order of the words either, even if the can learn a certain order, especially if they get something to eat if they do it right.


Can you help me identifying this spider? I took this picture in Ohrid, Macedonia, it is the first time I see this kind of spider here.

This spider was 2-3 cm long and was outside in urban building.

I tried to identify it by your photo via Seek app and the result is "cross orbweaver / Araneus diadematus

The result seems true when it's compared to description in this site

For comparision see this image:


Maternal immunity without prenatal vaccination? It is recognized that antibodies from the mother provide a level of protection to infants. This is why mothers are often advised to get vaccinated when they're pregnant. However, does the vaccine have to be given during pregnancy or would a vaccine taken as a child-teenager, if still effective as an adult, function the same way?

I'll try to give an example to clarify. Suppose a person is fully vaccinated against Whooping Cough, at least based on the current schedule, but does not receive a pre-natal vaccination. Is it reasonable to suppose that if the vaccine is still effective and is causing the body to produce antibodies, that these maternal antibodies would be passed on such that the infant would still receive some protection that it would not receive had the mother not received the childhood vaccinations?

Further Detail
I am interested in this question because it could influence studies which look at rates of infection/cases in infants, in order to measure the effectiveness of cocooning. These studies assume that because these children are too young to be vaccinated, the vaccine cannot be influencing their susceptibility, except through cocooning. But if childhood vaccination results in a high enough IgG levels, that might not be the case, and so this result should be considered in such studies as this one.

tl;dr

If a woman was vaccinated when she was a child, will she be able to provide passive immunity to her children?

It depends on the vaccine. Generally, if the mother still has high levels of protective IgG  during the third trimester (especially if it's type 1 or 4), those antibodies will cross the placenta and provide passive immunity to the newborn. In whooping cough, though, good levels of newborn IgG require vaccination in the third trimester.
Maternal immunizations
Immunizations are given to adult women prior to conception, while pregnant, and after delivery to protect the mother from infection, protect the fetus from infection, protect the fetus from congenital anomalies associated with maternal infection, and to protect the newborn from infection through passive immunity and through decreased exposure to infected contacts. The exact recommendations differ for different vaccines and different levels of maternal risk. From the same recommendation, you can see that some vaccines are recommended only if maternal antibody titers are negative and some are recommended regardless of maternal antibody titers or prior immunization.
Passive immunity of the newborn
IgG undergoes active transport from the maternal circulation to the fetal circulation across the placenta.

The reference linked above is an excellent review of transplacental antibody transfer and the science that underpins maternal immunization recommendations for passive immunization of the newborn (especially in the case of whooping cough). Key points here include:

Newborn IgG levels correlate with maternal IgG levels (i.e., the active transport mechanism isn't saturated in most cases). This suggests that low IgG for a particular antigen in the mother will result in low IgG for that same antigen in the newborn.

Antibody transport begins as early as week 14, but both the total transport and the rate of transport increases over the length of the pregnancy. This suggests an hypothetical optimum time for an intervention that would temporarily boost the level of any antibody.

Pertussis example
Whooping Cough, or pertussis, the illness caused by Bordetella pertussis, an encapsulated bacteria, is quite dangerous in the newborn. A few years ago recommendations for vaccination against pertussis were updated to immunization in the third trimester, regardless of the mothers prior immunization status. This recommendation is based, in part, on the understanding of transplacental transfer of IgG described in the article I linked in the earlier section, and in part on data on the association between timing of maternal immunization and fetal, all in the context of increased pertussis case rates.
Shortly after these recommendations were updated, additional, more thorough data confirmed this recommendation, though it suggested a slightly narrower window for the ideal time of Tdap administration (from 27-36 weeks to 27-30 weeks).
An aside re: the relationship between passive immunity of the newborn and childhood immunizations
Passive immunity from antibodies transferred to the fetus during pregnancy declines pretty sharply after birth. By 8 months the maternal IgG contribution is effectively gone. This is passive immunity because only the products of B-cells (the antibodies) are transferred. Immunization of the child, on the other hand, provides active immunity, because they develop the capacity to produce their own antibodies. I'd refer you to the allergy and immunology chapter of Bernstein and Shelov's Pediatrics for Medical Students, a surprisingly good general reference.
How should we interpret the linked article in the OP
This article is a comment on a very interesting study in baboons. It doesn't present any new data, but does comment on epidemiological data from a natural Swedish cohort between the discontinuation of whole-cellular pertussis vaccine 1979 and introduction of acellular pertussis in 1996. They reference this data through a misinterpretation of yet another study that analyzed infection rates between 1986 and 2007. The misinterpretation is as follows:

The (1996) drop was pronounced in infants too young to be vaccinated (Fig. 1A), itself a clear indication of herd immunity.

This is incorrect. That figure represents the decrease in infection rates for infants under 1 year of age at the point when vaccine was re-introduced. This included infants who were vaccinated (at 3 and 5 months).
The data before the re-introduction of vaccine, e.g., in 1995, though, does provide a good natural experiment for the epidemiology of pertussis in a non-immunized and immunization remote population. It had been 16 years since the use of whole-cell pertussis and you can clearly see the waning immunity in the population incidence as a whole. If you are really interested in digging into these questions, this cohort is a good place to start. Sweden is very good at collecting important data, so it may be out there.


How did a plant evolve to know there were animals alive that would eat it's fruit when it decided to produce this fruit? How did plants come to "know" there were animals alive that would eat it's fruit when it first produced this fruit?

The plant does not "know" there are animals. It is just that plants, that accidentally evolved (due to mutations) a fruit that attracts animals (which can spread its seeds etc.) had an advantage over plants that did not have them. The disadvantaged plants just became extinct after a while. And you must be aware that the first fruits were rather "pre-fruits", but already a selective advantage to their bearers.


Why do mammals rarely have eyespots? An eyespot is a marking to mimic the eyes. Many examples of eyespots can be found in fish, reptiles (including birds), and insects. Recently Radford 2020 has shown that artificial eyespots can reduce predations in cattle. However, apart from cats (tigers and servals), mammals, especially herbivores, rarely have this trait.
Why does mammals rarely have eyespots?

A lot of mammals do have eyespots. Specifically "mid-guild" predators such as raccoons, coatimundis, ringtails, foxes, raccoon dogs, many opossums, skunks, red pandas, civets, etc. It's thought to be an anti-predator defense, with the eyespots or face mask being places further back on the head. A predator might mistake these eyespots for its actual eyes, and because they're placed further back they create the optical illusion that the animal's head belongs to a much larger animal than it actually does.

This is a photo of the gray four-eyed opossum (Philander opossum). It's called "four-eyed" because of the two eye spots it has just above it's eyes. It's thought that the position of these spots mimics the position of the eyes on a much larger predator, so if a predator like a raccoon or a coyote sees the opossum they'll mistake it for a much larger predator and they'll leave it alone.


What is a Singleton Variant I'm reading a paper that on a population genetics study where they sequence a number of genomes. The study states that 101 Singleton Variants per individual where found. What does Singleton mean?

A singleton in mathematics is a set with one element.

They are likely referring to variants found in only one individual in their pool. It's possible there are other uses of the word singleton but given the context I think it is most likely.


Do the eggs for larger litters come from the same meiosis events, or different ones? There are some species of animals that give birth to more than one pup at a time. In these species, are the fertilized eggs all from one or a limited group of meiosis processes, or are they from different ones?

To illustrate the idea, take for example a case where some animal ends up with seven offspring in a litter. Do the original eggs come from different meiosis events?

Meiosis   Meiosis   Meiosis   Meiosis   Meiosis   Meiosis   Meiosis
   |         |         |         |         |         |         |
   V         V         V         V         V         V         V
   1         2         3         4         5         6         7

Or from a smaller set of events?

  Meiosis     Meiosis
 / |  | \     |  |  |
V  V  V  V    V  V  V
1  2  3  4    5  6  7

I am aware that, at least in mammals, that egg cells are actually produced long before they are used, and pooled for later use:

Meiosis  Meiosis  Meiosis
   \\\\    ||||    ////
    VVVV   VVVV   VVVV
    =====Egg Pool======
    |  |  |  |  |  |  |
    V  V  V  V  V  V  V
    1  2  3  4  5  6  7

I do not have any idea how this would work for other types of life though, like birds, reptiles, or fish. How does it work for those sorts of life?

I am mainly interested in this to understand how the mother's chromosomes are represented in the offspring. Are all of her chromosomes guaranteed to be represented in at least one offspring?

I'm not sure about the ubiquity of this but, in many animals, each primary oocyte that undergoes oogenesis only produces one mature egg. The other products of meiosis are polar bodies, which are not fertilised. These cells often degenerate but can sometimes play supportive roles in embryogenesis.

To answer your question, each mature egg is necessarily from a different meiosis event and so it is not guaranteed that all of the mother's chromosomes are represented in her offspring.


Has Colony Collapse Disorder (or its equivalent) been noted in other species? Colony Collapse Disorder is a well studied phenomenon relating to the decline of bee populations - has this disorder, or its equivalent, been observed in other colony-based species?

In some ways tangent to what you are asking, but many cases of classical Allée effects (i.e. a positive relationship between population growth rate and population size, see Allée & Bowen, 1932, Drake & Kramer, 2011) should be relevant, especially after your clarification in the comments.

One famous, early example of species collapse and extinction in a colony living species is the Passenger pigeon. This was an extremely common North American bird, estimated to 3-5 billion individuals, and maybe the most numerous bird species on the planet. It was heavily hunted during the 19th century (mainly by netting), which coupled to deforestation of nesting grounds led to a population crash. One of the main reasons for the rapid collapse was probably that the species was a colony nester and depended on large flocks for courtship/reproductive behaviour. This also meant that conservation measures failed when the critical situation was noticed (although hunting bans/restrictions was also weakly enforced). The few remaining wild individuals failed to breed and artificial breeding attempts also failed. The last individual died in 1914 at Cincinnati Zoological Garden (extinct in the wild from ~1900). For more information on the Passenger pigeon extinction see the wikpedia page and Encyclopedia Smithsonian.

I hope you find this example useful, even though the collapse was initiated from hunting. There are many more examples of Allée effects in colony living species that describe similar effects, but maybe not as strikingly as the Passeger pigeon case. There is a fairly recent book "Allee Effects in Ecology and Conservation" (Courchamp et al, 2008), which might be of interest to you.


What's the worst that can happen from eating too many spicy peppers? Can you die? Some peppers, such as the habanero or Carolina reaper are extremely spicy, and when eaten in larger amounts than one is accustomed to, can cause some discomfort.

I've also heard anecdotes claiming that pepper spray, if applied with sufficient intensity, can cause death.

What if you were to eat as many spicy peppers as possible, despite the noxious taste? Is it possible to commit suicide in this way (and what would the cause of death)? Would you faint from excessive mouth pain? Would uncontrollable vomiting prevent you from consuming further peppers?

The more "dangerous" properties of spicy peppers are chiefly due to capsaicin.
Sigma-Aldrich sells purified capsaicin, for which they provide safety information, including an MSDS. Most of it is the usual, unsurprising set of warnings about irritation to eyes and the respiratory system. However, there are LD50 numbers:

LD50 Oral - rat - male - 161.2 mg/kg
LD50 Oral - rat - female - 148.1 mg/kg
LD50 Dermal - mouse - >512 mg/kg

From this, we can conclude that one would have to eat quite a bit of capsaicin to die. If lethality in humans is exactly the same as rat (which it probably isn't),  a 70 kg human would need to consume about 11 g of capsaicin to reach similar levels of lethality.
The Carolina Reaper, one of the hottest known peppers, averages about 1.6 million on the Scoville scale. Capsaicin amount is related to Scoville heat units, so we can make an imprecise conversion from one to the other.
Using values given in 2 publications (Nwokem 2010 and Al Othman 2011) we can observe the following trend:

So on average, about $6.25 \cdot 10^{-5}$ mg/g capsaicin per SHU. With this, we get $(1.6 \cdot 10^5) \cdot (6.25 \cdot 10^{-5}) = 10$ mg/g, or 1% capsaicin for dry Carolina Reapers. To eat the equivalent of 11 g of capsaicin in peppers, you would have to eat 1.1 kg of dry peppers - which should be a couple of dozen.
So, I think we can conclude that it is relatively "feasible" to consume a dangerously large amount of capsaicin by eating very spicy peppers. However, there are numerous caveats with my reasoning:

Human LD50 and rat LD50 are not necessarily the same.
Toxicity is not necessarily linearly related to body weight.
Peppers have compounds besides capsaicin that contribute to hotness.
It would be very difficult to eat such a large amount of spicy peppers, and various involuntary reflexes would interfere. Even if one were force fed the peppers, I imagine the body would attempt to vomit it up - which brings up the question of how the toxicologists even managed to feed several milligrams of capsaicin to rats to measure the LD50.


Current state of direct RNA sequencing I had a colleague ask me recently whether mRNAs could be sequenced directly. I found this Nature paper[1] published by Helicos in 2009, in which they describe their developments in the area. It's been several years since this was published, and yet RNAseq and most other transcriptomic analysis is still done by first reverse transcribing RNA into complementary DNA.

What is the current state of RNA sequencing? Has Helicos failed to deliver on their technology? Have any other platforms risen to the challenge (or attempted to do so)? Or is the technology successfully in production and still simply overshadowed by the wide adoption of traditional cDNA-based sequencing methods?

Ozsolak F, Platt AR, Jones DR, Reifenberger JG, Sass LE, McInerney P, Thompson JF,  Bowers J, Jarosz M, Milos PM. 2009. Direct RNA sequencing. Nature, 461, 814-818, doi:10.1038/nature08390.

Helicos stopped shipping reagents around 2010-2011, as they couldn't compete with Illumina. For now it seems that reverse transcription -> Illumina-sequenced cDNA is so much cheaper than any other option, that's the method that is dominant.

Oxford Nanopore has discussed direct RNA profiling, but unfortunately their first product still hasn't shipped (for DNA or otherwise), and they haven't even released data, it may be a little while longer.


Getting xyz co-ordinates from a .map file (CCP4 format) in VMD I have a .map file which contains x-ray crystallography data of a bacteriophage. The format of the file is CCP4. I can open the file using VMD. However, I am unable to get the xyz co-ordinates. It shows the following error when I click on the option of saving data in xyz format:

`No timesteps selected; trajectory file will not be written.'

It is a big file of 64MB.

The file I am referring to may be downloaded at:
ftp://ftp.ebi.ac.uk/pub/databases/emdb/structures/EMD-1086/map/emd_1086.map.gz

Can't we save xyz co-ordinates for CCP4 files? Or is it possible to extract any other form of data?

I am new to VMD and these formats.
Any help would be appreciated.

Just Download and Install: CCP4: Software for Macromolecular Crystallography


How does a cell distinguish left from right? Although the human body is mostly left-right symmetrical, it consistently has asymetries. The heart is consistently slightly to the left side of the body. The liver is consistently on the right side.

This is quite perplexing when we consider that the human body has developed from a single cell. It seems like a single cell is mostly left-right symmetrical. A single cell could be oriented any which way in the womb, and it is unclear how the developing body would "know" which way is left or right.

So, how is it that the body develops the clear assymetry. Can anyone explain this interesting phenomenon in layman's terms?

Developing symmetry is is just a matter of Homeotic genes creating axial patterning, genes that produce a chemical gradient across a cell or group of cells. This is how developing organisms orient individual cells, up, down, left, right, anterior, posterior, medial, lateral, are all just gradients of different chemicals, the cells can detect the difference in concentration one one side or the other to orient itself. Most of these start getting produced when the embryo is only around a few cells so there is not much room for ambiguity.  Later more homeotic genes are added to create gradients for things like segments and limbs. Note polarity is often exhibited in a single cell, even in single celled organisms, this is a chemical gradient that orients the inside of the cell, this can easily be turned into orientation of dividing cells.

As for why things move away form this symmetry that's easy, evolution can mostly only work with what it has, evolution is about good enough not perfection.  Often good enough creates a kluge, a rube goldberg type solution then descendants then get stuck with. The earliest vertebrate ancestor pikaia is completely symmetrical even down to the gut,  A fish is nearly perfectly symmetrical, with the only deviation being to increase the length of the gut without increasing the length of the fish, which would waste a lot of material The solution is to coil and pack the intestines instead of having a straight line. This does not just happen in vertebrates you can see these solutions again and again in mollusk, insects, and even echinoderms, keeping the body compact while making the gut longer means asymmetry. As Some organisms progressed further and further away form the "fish" body plan alteration would result in asymmetry. Lungs for instance force a big asymmetry because you are taking what was a simple one way path into two divided systems, blood now has to return to the heart twice before making a complete circuit. More energetic animals specialize even further abandoning or partitioning part of the circulatory system to close off these two parts entirely so they can have high pressure blood flow without exploding their lungs. Now asymmetry is not a bad thing limbs and sense organs stay symmetrical because there is a stronger evolutionary pressure to keep them symmetric, moving with asymmetric limbs wastes a lot of energy (try running with only one shoe on).

Image sources.


What areas of the brain are involved in doing arithmetic operations? Do neuroscientists already know what areas of the brain are involved in mental calculations? Has any fruitful research been done on that or not yet? Do you think that if we understand what areas of our brain are responsible for doing arithmetical tasks we may one day have the ability to improve someone's calculation skills by non-invasive methods?

This is a part answer to your question.

According to "Arithmetic processing in the brain shaped by cultures" (Tang, 2006), the parts of the brain that are activated while doing arithmetic is to an extent, governed by culture, in the article, the authors assert:

  Using
  functional MRI, we demonstrated a differential cortical representation
  of numbers between native Chinese and English speakers.
  Contrasting to native English speakers, who largely employ a
  language process that relies on the left perisylvian cortices for
  mental calculation such as a simple addition task, native Chinese
  speakers, instead, engage a visuo-premotor association network
  for the same task. Whereas in both groups the inferior parietal
  cortex was activated by a task for numerical quantity comparison.

(The article also includes fMRI imagery examples).

It also seems that recognition of simple arithmetic starts at an early age, according to "Infant brains detect arithmetic errors" (Berger et al. 2006).


Where can I find DNA decryption research? What is the name of the science that studies the mathematics of DNA?

Where can I learn about maths, statistics, types of code, numbers, patterns and graphs for genes and information found in DNA?

I can think of several possible terms for what you could mean (with my interpretation of what people in those fields do):

Computational biology (the study of biological topics using computation)
Bioinformatics (the study of biological topics using computation)
Mathematical biology (the study of biological topics using mathematics)
Sequence analysis (the study of patterns in nucleotide [DNA] and protein sequences)
Genomics (the study of genomes or more generally large quantities of nucleotide sequence)

These all bleed into each other and doubtless other people have different interpretations.

There has been a ton of work in these areas, so they probably cover what you mean, but without some more concrete examples it's a little hard to say which is most appropriate.

As an aside, "DNA decryption" will be interpreted by most people in light of attempts to encode non-biological data in DNA and then decode it (see e.g. george church's stunts). However, based on what you say I think this is not really what you are interested in.

If you are looking for the technical literature for such fields, you could see the following journals, which are some of the better-known peer-reviewed journals focusing on these areas:

Bioinformatics
PLOS Computational Biology
Genome Research
BMC Bioinformatics
Molecular Biology and Evolution


Is this a plant or a fungus? It was soft and covered in flies. My guess is fungi.

Location: South Florida.

Identified Species: Clathrus ruber

  Scientific classification

  Kingdom:  Fungi

  Division: Basidiomycota

  Class:    Agaricomycetes

  Order:    Phallales

  Family:   Phallaceae

  Genus:    Clathrus

  Species:  C. ruber

Source:
http://en.wikipedia.org/wiki/Clathrus_ruber


What prevents backflow of blood from right atrium to vena cava during atrial systole Vena cava is valve less. So,  during atrial systole what prevents backflow of blood to them?

Pressure differences. Atrial contractions are much more gentle than ventricular ones, and in normal circulation the venous pressure in the vena cava often stays higher than the right atrium, even during atrial systole. If the pressure in the atrium does rise above the vena cava pressure at the peak of systole, there can be some backflow, although it is slight and brief in normal physiology.

The major veins are typically somewhat distended so they are constantly pushing blood into the right atrium. Blood continues to flow from the veins into the right atrium and from the right atrium into the right ventricle throughout ventricular diastole, including during most of atrial systole.

References:

Anderson, R. M. (1993). The gross physiology of the cardiovascular system. Robert M. Anderson.

Wexler, L., Bergel, D. H., Gabe, I. T., Makin, G. S., & Mills, C. J. (1968). Velocity of blood flow in normal human venae cavae. Circulation Research, 23(3), 349-359.


Does the oxygen concentration equilibrate between red blood cells in the liver sinusoids? In the sinusoids of the liver, venous blood from the hepatic portal system mixes with arterial blood from the hepatic arteries.

Do oxygen molecules move between oxygenated RBCs and non-oxygenated RBCs, so that the partial oxygen saturation of the blood in the sinusoids reflect partial saturation of the RBCs? Or do RBCs retain their initial oxygen saturation, so that the partial saturation of the blood in the sinusoids reflects a mixture of saturated and unsaturated RBCs?

The oxygen saturation (in lungs) and desaturation (in target organs) takes place via diffusion along the concentration gradient (i.e. partial pressure for gases). Therefore as long as RBCs from two different sources and having different partial pressure of oxygen mix up, the oxygen level starts to equilibrate between these cells.

But diffusion as a passive mechanism is not very fast and can take some time. So the only possibility for the second variant (there is a mixture of two types of RBCs) is if the mixture exists for very short time in liver sinusoids, so that the blood leaves them without really mixing completely up.

This is not true, at least in some animal models the blood within the liver seems to reach equilibrium very quickly and its resulting partial pressure can be influenced by adjusting the blood flow from different sources (using vasoactive substances injected directly, as in the referenced paper).


Determining net charge of amino acid at given pH I am trying to calculate the net charge on an amino acid, but I seem to be doing it wrong. The question I am trying to answer is "In a pH 7.0 buffer, what will be the charge of Methionine?" We are referred to a table that gives us the following information:
$$\pu{p}K{_\pu{a\mathrm{1},\ce{COO-}}}=2.28$$
$$\pu{p}K{_\pu{a\mathrm{2},\ce{NH3+}}} = 9.21$$
$$\pu{pI = 5.74}$$
From what I understand, if pH > pI, (which it is here), the amino acid should have a negative charge because even though the pH is high enough to deprotonate all the carboxyl ends and not enough to deprotonate all the amino ends, since it is higher than the pI some of the amino ends have been deprotonated (in addition to all the carboxyl ends).
Yet my answer book says that the net charge would be zero! Are 5.74 and 7.0 "close enough" that we can consider net charge to be zero still? If so, what is the standard permissible 'fuzzy' range? If not, then what is going on here?

You are right in your reasoning: at any pH for any titratable group, there is a distribution between the protonated and deprotonated species. We can calculate this distribution and therefore the average charge of the species with the Henderson-Hasselbalch equation:

$$\mathrm{pH = pKa + log\left(\frac{[B]}{[A]}\right)}$$

Or, rearranged:

$$\mathrm{\frac{[B]}{[A]} = 10^{pH - pKa}}$$

Where A is the conjugate acid and B is the conjugate base. For carboxyls and primary amines, this can also be written as $\ce{\frac{[COO-]}{[COOH]}}$ and $\ce{\frac{[NH2]}{[NH3+]}}$, respectively. As a simple example, if the pH was 2.28, the ratio between the protonated and deprotonated form of the carboxyl group (pKa = 2.28) would be $\ce{\frac{COO-}{COOH} = 10^0 = 1}$. This means $\ce{[COO-] = [COOH]}$ and the average charge of the carboxyl is thus -0.5.

Now, for cases where $\mathrm{pH \neq pKa}$, we need to determine the mole fraction, $\chi$, for each charged species. Given that $\mathrm{\frac{[B]}{[A]} = \frac{\chi_B}{\chi_A}}$ and $\ce{\chi_A + \chi_B = 1}$, we can derive these equations:

$$\mathrm{\chi_{COO^-} = \frac{1}{1 + 10^{pKa - pH}}}$$
$$\mathrm{\chi_{NH_3^+} = \frac{1}{1 + 10^{pH - pKa}}}$$

Plugging in the numbers, we get:

$$\mathrm{\chi_{COO^-} \approx 0.999981}$$

$$\mathrm{\chi_{NH_3^+} \approx 0.993872}$$

To state it another way, ~99.9981% of the carboxyl groups are in the deprotonated (negative) state and ~99.3872% of the amino groups are in the protonated (positive) state. The average charge of methionine at pH 7 is simply the sum of these mole fractions, accounting for the charge of each species, and is approximately equal to -0.006109. I assume your textbook is rounding.

You can plot these functions to see how charge varies with pH:


Why Only DNA can Contain Hereditary Material? Well I'm well aware that it is proven that DNA contains  genetic material via transformation and Hershey-Chase Experiment of T2 bacteriophage. Still I was wondering what is the reason only DNA contains it and not protein or RNA.
What I've learned is that DNA is the most stable of all these molecules and it has the ability to replicate itself.
Other than this I can't find any solid answere.
Thanks!

I think any discussion of this question can benefit from a historical perspective. For a long time, it was in fact believed that proteins was the hereditary material. The Nature Scitable page on the discovery of DNA (1) starts with the following passage:

  In the first half of the twentieth century, Gregor Mendel's principles
  of genetic inheritance became widely accepted, but the chemical nature
  of the hereditary material remained unknown. Scientists did know that
  genes were located on chromosomes and that chromosomes consisted of
  DNA and proteins. At the time, however, proteins seemed to be a better
  choice for the genetic material, because chemical analyses had shown
  that proteins are more varied than DNA in their chemical composition,
  as well as in their physical properties.

While perhaps easy to dismiss in hindsight, it is possible to understand the reasoning of the day. The "central dogma" of molecular biology, that genetic information flows from DNA to RNA to proteins was only described later, and explained how the production of complex proteins consisting of 20-odd amino acids can be directed by a polymer consisting of only four nucleotides. This allows great complexity and variety in phenotypes while maintaining simplicity of the genetic material. The central dogma also facilitates the seperation of the use (through protein expression) and storage (as DNA) of genetic material.

As Watson and Crick noted in their famous paper, the double helix of DNA, when discovered, immediately suggested how the genetic material could be elegantly copied. While the more complex structure of proteins would likely require a more complex copying mechanism, the specification of amino acids through three-nucleotide codons in DNA allows the regularity of the DNA material to be retained for easy replication while allowing complex proteins to be produced.

However, even though DNA is the primary genetic material today, the situation may have been different at the time life first appeared. According to the RNA world hypothesis, RNA may have been the original genetic material and that DNA is a variation of RNA, not the other way around as it is commonly seen.

For a fuller historical perspective, I recommend the book "What is Life?" by Erwin Schrödinger, which was written before the discovery of DNA as the genetic material.


Is it mostly true that predators or parasites traverse wider spatial areas than their prey or hosts? Does it tend to be true that as you go up the food chain, the species tend to cover wider areas?  I am basically asking whether a population's prey varies spatially more than a population's predators and parasites, which would vary more temporally: the predators and parasites to which a population is exposed tends to be the same across the population but the prey vary more spatially because the prey tend to traverse smaller areas.  I would think this were true, since predators have larger body sizes and my thinking is that species with larger body sizes tend to travel farther and parasites may locate on multiple hosts, which collectively carry them farther than any single host.  This is my inference, but I do not even know what to type into Google Scholar in order to check this.

The ability of prey to find refuge in predator-free habitats is a fundamental hypothesis for predator-prey stability. The availablility of predator-free patches allows the prey metapopulation to maintain positive population growth in some patches, despite being decimated by predators in other patches. If the predators are far superior dispersers, they would eat all the prey, possibly driving the prey—and themselves—extinct.

That being said, it's difficult to make generalizations about spatial food webs. In nature, prey, predator, and parasite populations persist due to a multitude of factors, including the spatial configuration of suitable habitats, their dispersal rates, interactions with competitors and mutualists, etc. For example, in a system where carnivores hunt herbivores, sure, the predator may disperse across the landscape, hunting across more than one herbivore metapopulation; in other systems, such as those that may be more spatiotemporally variable (e.g., prone to disturbance and local extinctions), the ability of the prey to disperse faster than the predator could be a crucial aspect of predator-prey stability.

Some theoretical resources include: Comins et al. 1992, Holt 2002,
Amarasekare 2008.

A foundational experiment is that of Huffaker, who dispersed mites on oranges: Huffaker 1958. Also, take a look at work on host-phage interactions: Schrag and Mittler 1996.

For Google Scholar searches, try various combinations of the following words: spatial, host, parasite, predator, prey, stability, coexistence, food web.


Does loud music affect hearing and balance? From many sources I understand that strong disturbances can destroy hair cells in the cochlea.

Does the sound damage always counts simply as the number of decibels recieved by the ear? E.g., if you listen to music in the train and you have to play it louder to hear it clearly?
Is therefore a one-shot of noise less damaging? I.e., hair cells are not as disturbed?
How long would you have to listen to the 120 dB music to lose your hearing? What is the healthy limit per day (how fast do the hair cells recover)?
Could it also affect your balance (since it is managed by the same organ)?

First off, there are many flavors of decibels, as it is a relative measure. For the sake of clarity I assume you are talking dB sound pressure level, or dB SPL, which is a unit of sound pressure relative to a standard sound pressure of 20 µPa and widely used.

The damaging effects depend on the sound pressure received by the ear. Whether this is a compound signal or a single source doesn't matter. Like whether you crash your car against a wall at 80 mph, or head's on against a truck both travelling at 40 mph - it doesn't really matter. It's the mechanical energy transferred to the hair cells that counts.
A one-shot noise... I don't really understand what you're aiming at, but as said above, it's the raw sound pressure that counts. Further, prolonged exposure is definitely more damaging than a short exposure. However, when the sound pressure is strong enough, e.g. a bomb blast which lasts just a fraction of a second, hearing can still be permanently lost provided the sound level is high enough.
According to the Ear Center of Greensboro, a rule of thumb is that the maximal safe exposure to sound of 100 dB is half an hour, and for every added 5 dB that time is cut in half. Thus, for 120 db that would add up to 7.5 minutes before permanent damage occurs. The safe loudness limit per day has primarily been established in terms of maximum sound levels for occupational exposures (i.e., sound exposure for 5 days per week, 8 hours per day). Likely it is dependent on where you live, but here in Australia, the Government has set the safe occupational limit to 85 dBA. The dB(A) is a weighted unit of loudness that is corrected for the hearing sensitivity of the human ear.
The labyrinth of the inner ear is a system of interconnected chambers and canals. The fluids in the cochlea (responsible for hearing) and vestibular system (responsible for balance) are indeed interconnected (fig. 1).

Fig. 1. The ear (upper panel) and structures of the inner ear (lower panel). Source: Washington University.

However, sounds enter the inner ear via the tympanic membrane that connects with low impedance to the cochlea, but there is no direct connection to the vestibular system. Hence, only very loud sounds may affect balance, but that are likely accompanied by mechanical blasts that will physically damage the delicate inner ear structures. Loud music of 120 dB will not damage the vestibulum.


Left and Right Handedness Today I found out that the gene for being Left-handed is dominant while Right-handed is recessive. I personally am left handed and so is my father. My mothers father is also left handed and I was wondering whether or not I am homozygous or heterozygous for the left handed gene. Is there any way to determine this without getting genetic testing or by actually having kids? Thanks.
Source: My science teacher

I'm afraid your science teacher is wrong. Handedness is a complex trait. It is not determined by a single gene, and can't be described as being dominant or recessive. Handedness does apparently have a genetic component, but many other factors are involved as well. See the Wikipedia article on handedness:

  Handedness displays a complex inheritance pattern. For example, if
  both parents of a child are left-handed, there is a 26% chance of that
  child being left-handed. A large study of twins from 25,732
  families by Medland et al. (2006) has indicated that the heritability
  of handedness is roughly 24%.

  To date, two theoretical single gene models have been proposed to
  explain the patterns of inheritance of handedness, the first by Marian
  Annett of the University of Leicester and the second by Professor
  Chris McManus of UCL.

  However, the growing weight of evidence from linkage and genome-wide
  association studies suggests that genetic variance in handedness
  cannot be explained by a single genetic
  locus. From these studies McManus et
  al. now conclude that handedness is polygenic and estimate that at
  least 40 loci contribute to determining this trait.

What may be confusing is that the preferred hand is often called the dominant hand, but that usage of the work 'dominant' is unconnected to the concept of dominance in genetics.


Scoring matrices (BLOSUM & PAM) in BLAST and other sequence-comparison programs The Wikipedia page on BLAST states that:

  The scores are created by comparing the word in the list in step 2* with all the 3-letter words. By using the scoring matrix (substitution matrix) to score the comparison of each residue pair, there are 203 possible match scores for a 3-letter word. For example, the score obtained by comparing PQG with PEG and PQA is 15 and 12, respectively with the BLOSUM62 weighting scheme.

I do not understand how they got a score of 15 for PQG v. PEG. What is a scoring matrix, how is it computed, and how is it used?

Step 2 on that page is Make a k-letter word list of the query sequence: “Take k=3 for example, we list the words of length 3 in the query protein sequence (k is usually 11 for a DNA sequence) sequentially, until the last letter of the query sequence is included”.

The two most common families of scoring matrices are BLOSUM and PAM. Each of them has a score for every possible alignment combination between the 20 standard amino acids1. They both do more or less the same job but have been derived using different approaches.
BLOSUM matrices

(image taken from Wikipedia)
The BLOSUM matrices are built from actual alignments between very conserved regions of protein families. The score for a given pair of amino acids aligning with each other is the log-odds score measuring how often this particular alignment is found and how often it would be expected to be found by chance:
$$ S_{ij} = \left ( \frac{1}{\lambda} \right ) \left ( \frac{p_{ij}}{q_i * q_j} \right )$$
Where $p_{ij}$ is the probability of finding the two amino acids $i$ and $j$ aligned to each other in a homologous sequence and $q_i$ and $q_j$ the background probability of finding the amino acids $i$ and $j$ in any protein sequence. The $\lambda$ is a scaling factor set to ensure that the matrix contains easily computable integer values.
In simple words, the BLOSUM matrices give you a score based on how often the alignment you observe in your sequences is found in alignments of similar sequences.
There are several BLOSUM matrices which have been computed using proteins of more or less sequence similarity. The most commonly used one is BLOSUM62 which was built using alignments between proteins of $\ge 62\%$ sequence identity. This is a nice middle ground and will do for most cases. If you are comparing proteins that are very closely related, you might want to use a matrix based on more similar sequences such as BLOSUM90 (built from sequences with $\ge 90\%$ sequence sequence identity) and for less conserved proteins, you might use something like BLOSUM45 ($\ge45\%$ sequence identity).
PAM matrices
The PAM matrices are built using a different approach. First, a global alignment (as opposed to the local ones used in BLOSUM) of of a set of sequences sharing 85% sequence identity is computed. Next, a score for the alignment of all possible pairs of amino acids is calculated based on its observed frequency in the aligned proteins. Then, the scores are extrapolated to alignments of different sequence similarity using mathematical tools. The PAM matrices assume a model of protein evolution and score the alignments based on that model.
The PAM-I matrix is the only one that was actually built from real alignments. The rest were obtained by  multiplying PAM-I by itself N times. In PAM, unlike in BLOSUM, the higher numbers correspond to greater evolutionary distances between proteins.

With all that in mind, the scoring matrices are used by BLAST to calculate the score of the alignment. You can think of this score as the sum of the scores of each individual pair of aligned amino acids in your BLAST result.
Useful references:

http://statgen.ncsu.edu/st590a/notes/76_ST590A_100509.pdf
https://en.wikipedia.org/wiki/Point_accepted_mutation
https://en.wikipedia.org/wiki/BLOSUM
http://www.ncbi.nlm.nih.gov/pubmed/21356840

1The non-standard amino acids Selenocysteine and Pyrrolysine are not included in any matrix I know of, probably because they are too rare for any reasonable conclusion to be drawn from statistic analyses.


level of organisation of proteins Is there any disulphide bond in a quaternary structured protein?
If yes, please provide examples.
In tertiary structured proteins, what is(are) the most important characteristic(s)  of tertiary structured proteins?
a) globular in shape
b) have both alpha helix and beta sheet
or, is there any characteristic that I do not mention?

Interesting protein structure trivia question!

Disulfide bonds form more or less spontaneously when two sulfhydryl groups from cysteines are close enough to each other in the proper orientation in a reducing environment.  So given this, its possible for them to exist, even though in most cases the distance between the cysteines in a disufide bridge is small and intra-domain.

Inter-domain disulfide bonds are rare.  The most common example is that some immunoglobulin domains in antibodies have an intrachain disulfide bridge.  I also found reference to one in a starch synthetase from rice.

In tertiary structure, the overall shape is an important one.  Globular shapes are the most common, but elongated protein folds, triangular folds,  rings, disk-like structures made out of wedges are popular examples of how protein structures can do amazing things when selection requires them to.


What is "theae folium"? I wanted to buy black tea at a pharmacy and the pharmacist told me that russian tea is actually black tea so I bought it instead.It's made out of theae folium leaves and for some reason I can't find anything about that plant on the internet and I know that black tea is made out of camelia sinensis leaves, not theae folium.Can anyone tell me what is this plant and is it really russian tea (i found somewhere that russian tea is made from a different plant) and what is this "Russian" tea good for?

Judging by this image in wikipedia, I would say Theae folium is another name (probably a name in another language) for Camellia sinensis


Why doesn't the rest of the body have something like the "blood-brain" barrier to protect itself from pathogens? According to Wikipedia:

  "The blood–brain barrier acts very effectively to protect the brain from most pathogens".

This is because the pathogens cannot pass through the tight junctions of the endothelial cells lining the inside of the blood vessels delivering blood to the brain through BBB.

But if so, why don't tissues/organs in the rest of the body employ the same barrier, and thus avoid pathogens from ever entering those tissues/organs through the bloodstream?

There can be many reasons to why BBB-like barrier is not present in all the capillaries of the body. Let's talk about them one at a time.

Source

Blood-brain barrier has its own side effects. Some major side effects are cerebral edema (accumulation of excess water in the extracellular space of the brain, which can result when hypoxia causes the blood–brain barrier to open) and (possibly) Epilepsy. See this wikipedia article:

  Several clinical and experimental data have implicated the failure of blood–brain barrier function in triggering chronic or acute seizures. Some studies implicate the interactions between a common blood protein (albumin) and astrocytes. These findings suggest that acute seizures are a predictable consequence of disruption of the BBB by either artificial or inflammatory mechanisms.

Another problem is that BBB doesn't allow passage of drugs, diagnostic and therapeutic agents through it. Again, see this article:

  Overcoming the difficulty of delivering therapeutic agents to specific regions of the brain presents a major challenge to treatment of most brain disorders. In its neuroprotective role, the blood–brain barrier functions to hinder the delivery of many potentially important diagnostic and therapeutic agents to the brain. Therapeutic molecules and antibodies that might otherwise be effective in diagnosis and therapy do not cross the BBB in adequate amounts.

Now, if you want to know why the body doesn't have BBB-like barrier (not exactly BBB), then there are three parts of the answer.

These kinds of barriers are highly specialized for a particular organ or organ system, which may not be useful for another organ/organ system. Also, creating specialized barriers for all the parts of the body will take a lot of energy, cells and even more time to develop completely. Possibly, in the evolutionary course, body preferred to have phagocytic cells circulating in the body instead of having specialized barriers throughout the body.
These barriers might not be a total solution for immunity or restriction of pathogens. See this part:

  It is believed that latent HIV can cross the blood–brain barrier inside circulating monocytes in the bloodstream ("Trojan horse theory") within the first 14 days of infection. Once inside, these monocytes become activated and are transformed into macrophages. Activated macrophages release virions into the brain tissue proximate to brain microvessels. These viral particles likely attract the attention of sentinel brain microglia and perivascular macrophages initiating an inflammatory cascade that may cause a series of intracellular signaling in brain microvascular endothelial cells and damage the functional and structural integrity of the BBB. This inflammation is HIV encephalitis (HIVE).

Also, it is not necessary that those pathogens would infect only those tissues to which they reach via bloodstream. Pathogens like HIV cause infection in the blood cells. See this image from here:

  Once a person is infected with HIV, the virus begins to attack and destroy the CD4 cells of the immune system. CD4 cells are a type of white blood cell that play a major role in protecting the body from infection. HIV uses the machinery of the CD4 cells to multiply (make copies of itself) and spread throughout the body. This process, which includes seven steps or stages, is called the HIV life cycle.

Similar barriers are already present in many parts of the body. For example- Blood-Ocular Barrier, Blood-Testis Barrier, Blood-Thymus Barrier, etc. They may also have some loopholes. For example, see this article-

  Possible consequences of blood-thymus barrier failure are trophoblast-specific or tumor-specific antigens penetrate into the thymus, deletion or anergy of antigen-specific clones and acquired thymic tolerance induction.


PCR markers for C57B6 Do you know any primers that can be used to genotype mice and check if they are still C57B6? I'm concerned about genetic drift in my colony. I bought a breeding pair 3 years ago and expanded. I wanna make sure my animals still retain genetic markers of c57b6. Thanks

Jackson Labs offers a service for this for what looks like a reasonable price. I have no experience with the service other than general good feelings about Jackson.

We have a unique selection of mouse single nucleotide polymorphism (SNPs) panels useful for a diverse set of mouse research applications.
Applications of SNP scanning services

Development of congenic mouse lines
Confirmation of C57BL/6 substrain background

[...]
Available custom designed SNP panels specifically tailored for your needs
The right panel for your needs - $179/sample
[...]
C57BL/6 substrain characterization panel distinguishes between C57BL/6J (B6J) and C57BL/6N (B6N) or C57BL/6NTac (B6NTac) genetic backgrounds

--GENOME SCANNING SERVICE
Edit to include some points raised in comments:

"These panels [i.e. the ones Jackson labs offers, noted above] seem to be intended for comparing between known strains, like when you make a transgenic strain and are in the process of backcrossing. It would not be as useful for monitoring drift, or for comparing an unknown C57BL-derived line to a standard one." – Bryan Krause
Any mouse colony will diverge from other colonies, especially if there are relatively few founders.

The identification of two CNVs in the small portion of the genome screened demonstrates that individual mice of highly inbred strains are not isogenic and suggests other CNVs may be segregating within C57BL/6J as well as other carefully maintained inbred strains.

--Genomic copy number and expression variation within the C57BL/6J inbred mouse strain

At the very least, intermittent back-crossing to a mouse from a different source is recommended.

With time, isolation and a little spontaneous genetic drift, a founder pair can produce a new substrain in as little as three generations (something to bear in mind if you're breeding mice in-house without “refreshing” the gene pool with an intermittent backcross to a bona fide C57BL/6J ... Clearly, substrains of C57BL/6 (and other inbred strains) are not all the same.

--All (C57BL/6) Mice are not Created Equal

Simply buying new mice as needed, from the same (reliable and standard) source each time, gives you a better chance of consistency, since a large breeder is less likely to see on-going founder effects.

If you have a solid reason for keeping your own colony, talking to the experts at Jackson Labs would be a good starting point; presumably monitoring strain consistency is something they think about as an ongoing issue, and they can give better advice than we can.


How many areas are there in Brodmann map? I read Wikipedia claiming 52.
I heard that this can be extended to 54.
I see there is no limit of having more areas - just better understanding of the neuroblast migration and fibroblast too, probably.
How is this newer classification of Brodmann map done?

I am no expert on the topic, but according to an article published on the centenary of his study, it states that the microscopical structure and classification of these areas are in parallel to the evolutionary distinction between old and new cortical subdivisions. So as and when new subdivisions are deduced (based on its function, cytoarchitecture or the structure and organisation of cells) the map can be extended to include them. There was no upper limit to the number of divisions set in any article I read so it would be nice if you could provide some reference to where it says that the extension can be done to 54. If you are interested, you could have a look at the map published by Constantin von Economo in 1925.


Is intelligence (or mental ability) genetically transferred (inherited characteristic) from the parent to the offspring or is it an acquired trait? The question is simple- whether our mental ability i.e. ability to acquire and store knowledge and comprehend and analyse the stored bits, an inherited trait (i.e. genetically transmitted from the parent to the offspring) or is it an acquired trait (depends on environmental, social factors)?

P.S. - Please attach the link of any reference/research (if any) with your answer.

Standard IQ test are often considered the best proxy for intelligence. Studies show IQ heritability varying between 0.5 (ref) and 0.8 (ref).

TO make sense of these numbers, you will need to understand the concept of heritability. You can find info on this important concept in the post Why is a heritability coefficient not an index of how “genetic” something is?. Other posts also offer an intro to this concept (see this, this, this or this post). You can also simply have a look at wiki. You might want for example to be able to understand the equation $H_N^2=\frac{V_A}{V_P}$ without further explanations.

The H2DB database may interest you as well and of course the wiki page on heritability of IQ


What is this brown insect with a large wingspan? I found this dead creature on my window last night and spent hours looking for something that could explain what this is. I was unable to inspect it in person though, because opening the window would make the creature fall down.

It is roughly three inches in length and has a wingspan of five inches. I found it in the UK in August.

Here are some pictures:

It is a moth from the Sphingidae family (hawk moths). They are generally large, robust and often have lobed wings (like the one in your pictures). I'm not closely familiar with this group of insects, and not with species found in the UK, but the individual you observed is very similar to e.g. Laothoe populi (Poplar hawk moth), which is also found in the UK.

(Laothoe populi, picture from Wikipedia)


What is the name of the bird which feeds on penguin blood and meat in Tristan island? I just watched a National Geographic documentary "Unseen Islands: Atlantic Arks" and there was some thing strange in Tristan island. Some small bird which changed its diet to feed on the blood and meat of the penguins on this island.

I want to know more about this bird - or its name so I can search it - and if there are other examples of this behavior of changing diets.

You almost certainly mean the Tristan Thrush, Turdus eremita, which is endemic to Tristan da Cunha. The species is considered to be an opportunistic omnivorous scavenger, but their diet includes the eggs and chicks of many seabird species, as well as the adults of some smaller seabird species.

The Wikipedia page for the species mentions that Tristan Thrush has been recorded drinking penguin blood, citing a BBC documentary which I don't have access to. Five species of penguin have been recorded on Tristan da Cunha, but only the Northern Rockhopper Penguin breeds there (the others are rare visitors to the island). Given the nature of penguin colonies (i.e., densely-packed, and with abundant chicks as well as occasional sick adults), there would be many opportunities for an opportunistic omnivorous scavenger to eat penguin blood, chicks, eggs, or carrion.