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Why, specifically, does each generation, on average, improve upon the design of the species rather than degrade it?
In every non-life example I can envision, a copy of a copy is always a degraded or less pure version of the original unless some outside influence acts to correct the copy back toward the ideal represented by the original. Photocopies get blurrier with each generation. Casts from a mold are distorted from the original from which the mold was made. In fact, each cast degrades the mold itself. When data is copied on computers or across networks, parity checks verify that no mistakes were made, but even then, every long once in a while, combinations of errors can cause a false positive in a parity check. So given enough time, the copies would degrade.
In eukaryotes, new individual organisms always begin as a zygote, so in all kingdoms, reproduction boils down to the genesis of a single cell. This involves correctly building the DNA as well as all of the other complex architecture of the cell. Why doesn't this cell degrade like every other example I can think of? In fact, cells are capable of such perfect reproduction that the system generally supports the introduction of additional randomness in order to promote the possibility of productive change. I can think of some probable contributing factors that make this work, but I must be missing something. I can't imagine that this model would actually work the way it does - so well in fact that the design actually improves over time. What am I missing or underestimating?
Contributing Factors (I guess):
Perfect Building Blocks: Cellular development follows a pattern at every level, and ultimately operates all the way down to the molecular level. At that level, nearly all building blocks are identical. Life is built of stable atoms, not something like plutonium, and in the rare event that an atom does change, the result is simply a different kind of atom, which still tends toward a stable form in the long term. Because the structures of life are ultimately made of stable components that are plentiful everywhere in the environment, the essential structures being copied are precise and can be copied precisely. Photocopies and casts are not precise to the molecular level, so copying them is more approximate by nature. Digital data propagation, however, is a very similar process. Bits are also theoretically perfect building blocks.
Fitness Correction: When mistakes do degrade the reproduction process, rather than maintaining or randomly improving upon it, there is a correction mechanism that removes the defects from the process. Those defects do not survive to reproduce. This evolutionary process acts to keep the reproductive pattern focused back upon a theoretical ideal which is independent of a specific physical form to be copied. This seems like the most essential element of the explanation, because it is ultimately only through progression that digression can be avoided, but it is also the part that seems the most dubious. Astronomical quantities of defects would have to be produced before developing just one advantageous feature. I would expect living creatures to be 99% defective with only 1% surviving to breed. I would expect 99.9% of zygotes to expire without being born or sprouting from seed. I would expect all sexual organs (ovaries, testes, stamen, etc.), if not the majority of the whole body, to be mostly dead cells, with just a few successes surviving to fertilization. I would expect 99.9% of the genome to be experimental, almost completely unusable liability to the species. Essentially, I would expect premature death to far outweigh successful life everywhere and at all times. And even so, I would still expect evolution to be even slower than it has been.
Mutation Management Mechanisms: I understand that there are mechanisms in reproduction that decrease the likelihood of mutation in more established and stable parts of the genome compared with sections that are more open for discussion - epigenetic structures, HOX genes, etc. Portions of all genomes have been established and functional for hundreds of millions of years, so I gather that there are mechanisms for protecting them (I suspect probably far more than we have yet discovered).
Note: The numbers I present are fuzzy and are based not on calculations but on general impressions I get of the magnitude of the numbers involved and the relative rareness of useful mutations. Is there any place where this kind of calculation has been performed with more realistic approximations of probabilities?

This question is based on a false assumption. Degradation has been observed in many organisms, and it depends on the specific conditions of evolution. Do a web search for "genome degradation" if you want more info.

They don't, there are a lot more failures than successes.

copies are always degraded, crystal lattices and many other self catalysing reactions  would beg to differ. Also "degradation" in your usages equals mutation which we observe quite a lot of.

You have clearly given this a lot of thought. Unfortunately, as @adam.r said, you are laboring under certain misapprehensions. The quick answer is that each generation does not "improve" on the last. That is a common misconception. In a bit more detail:

First of all, your copying metaphor is a bad one. There was no "perfect original", I expand on this theme at length in my answer here but, briefly, all species are constantly changing. They are not moving away from a platonic ideal of the perfect species (or towards it for that matter), they are simply changing in response to the world around them. What's 'good' today is not necessarily 'good' tomorrow.
Your copy machine metaphor does hold for changes from one generation to the next though. Copying DNA is fraught with errors. There is a huge cellular machinery in place whose only job is to catch and correct those errors. Nevertheless, many get through and result in diversity that can then be selected for or against through the process of natural selection. So, the copies do actually degrade. That, in fact, is the very basis of how evolution works.
Another important point is that most changes are neutral. They have absolutely no effect one way or the other. There are many reasons for this but the main ones are

The vast majority of DNA does not actually code for protein. What it does do is an area of active research but minor changes in sequences that don't code for protein are extremely unlikely to cause a change in phenotype.
Almost all of the information necessary to produce a viable organism is in the genes, and genes represent a very small (~5% in human for example) percentage of the genome. Changes that affect the fitness of an individual are almost invariably found in the coding sequences of genes. This means that of the ~30 billion possible sites for mutation in any given cell, 95% of them (even less actually since only exons count and they're ~2%) will not cause a phenotypic effect.
The genetic code is redundant. Basically, DNA is "read" in "words" of three "letters", the codons. Since there are 4 bases in the genome (A,C,T and G) this means there are 64 possible codons. Each codon specifies a particular amino acid (the building blocks of proteins) and a given sequence of codons will result in a specific sequence of amino acids. However, there are only 22 amino acids, many of which are specified by the same codon:

As you can see in the image above, in most cases, changing the third letter of the codon does not affect the amino acid that will be specified. This means that even for those mutations (changes) that occur in the coding region of genes, the chances are relatively high that they won't actually result in any phenotypic change. If you change the genetic code but the changed codon still codes for the same amino acid there will be no change in phenotype.

As for your contributing factors:

Perfect Building Blocks: Nope, sorry this one is wrong. First of all there is no such thing as a minor change that involves changing an atom. Any change that happens at the atomic level is huge by definition. That kind of thing happens a the hearts of stars and in nuclear reactors. The chemical reactions in our body involve changing molecules not atoms.
There is no such thing as a minor change really, if you replace one atom in a molecule by another, you are significantly changing the properties of that molecule (this is less true for large, complex macromolecules where some changes can indeed be minor). If you were to change, for example, a single atom in normal table salt ($NaCl$) from sodium to hydrogen, you would get $HCl$, hydrochloric acid and not something you want to put in your soup.
There are no perfect building blocks, in biology nothing is perfect, that only happens in math.
Also, the organism does not follow the same pattern from the organismal to the cellular to the molecular (never mind atomic) level. In fact, there are very different organizational principles at play at the different levels and the way that cells are organized (see here for example) has nothing to do with the way that a cell's contents are organized.
Stability is overrated. In fact, our bodies contain loads of unstable (reactive) chemicals, oxygen being chief among them. By definition, chemical reactions involve changing molecules (not atoms, but we don't deal with that level, biological effects tend to be at the molecular, not atomic level). All reactions that go on in the factory that is your body involve the changing of one molecule into another.
Fitness Correction: Actually, at the cellular level, the corrections try to faithfully reproduce the template they are copying from. When a cell copies itself, it will also copy its DNA. It does so by using its own DNA as a template. There is no "theoretical ideal", the cell has no information about the genome of its parent, only its own. As I mentioned above, there are various corrective mechanisms whose job it is to spot errors and correct them. They have no way of knowing whether a given change will be beneficial or harmful to the individual, as far as these processes are concerned, any change is bad and should be corrected. The only thing they do is try to make a daughter cell's genome identical to the parent cell's.
When a change makes it past the cellular level, then it can be selected for or against based on whether it makes the individual carrying it more or less likely to reproduce. This, however, is not a directed process. It just happens. If a mutation makes a male blue whale stronger, it is more likely to be the one that catches up with the racing female and so more likely to reproduce. There is no direction other than the selective process itself. There is no one around comparing new individuals to an ideal and selecting accordingly. If you're better at reproducing than your peers, your genes will be selected.
Actually, many many gametes are discarded. Many cells die. You just don't know about it because they die before you can see them. So deleterious (very bad) changes do occur.
"I would expect 99.9% of the genome to be experimental, almost completely unusable liability to the species." In a way this is true. Despite recent findings, 98% of the human genome does not directly affect the phenotype. It is only the 2% that represents the protein coding parts of genes that has a direct effect on fitness. In fact, in the human genome specifically, there is a short sequence that does not code for any protein and does not (directly, though there are various theories about this) affect our phenotype, that has been making copies of itself and propagating in our genome for generations. Today, this sequence (Alu) represents ~10% of the human genome, that's twice as much as all our genes together!
Mutation Management Mechanisms: The basic protection mechanism you mention in your question is quite simply death. Mutations that render housekeeping genes (like the HOX cluster) inactive kill the organism that carries them. That does not mean they don't occur, it simply means that when they occur, we don't see them because the individual carrying the mutation is dead (see point 3).

Almost ten years later, I just realised that a core part of your answer — “most changes are neutral” — is pretty shaky. What you’re describing there is Kimura’s Neutral Theory, which was  controversial as soon as it was first voiced, and has over the past decades seen sustained attacks from contradicting evidence. I believe it’s fair to say that it is, these days, a strict minority view.

@KonradRudolph I don't claim to be an expert or even remotely knowledgeable about the details of Kimura's theory, but wasn't that focusing on coding sequences? All I am saying here is that the vast majority of mutations will not cause a phenotypic effect and that isn't remotely controversial. Am I missing something?

I'm likewise no expert but neutral theory has definitely be applied to non-coding parts of the genome. Anyway, it concerns fixation of alleles in a population, not mere singular occurrence in an individual. This might be compatible with what you wrote.

@KonradRudolph yes, all I am saying here is that most mutations are unlikely to result in any changes detectable at the phenotypic level. Nothing to do with fixation, just a simple fact about how the genome is organized and how the vast majority of it doesn't code for protein so the rest, even assuming regulatory function, is far less sensitive to mutation.

I’ll add a slightly different perspective, although terdon’s answer already contains the relevant facts.
The thing that makes DNA endure in the face of imperfect copying is that, like computer storage, it’s digital. The relevant property of digital data here is that individual pieces of information aren’t given on a scale, they’re drawn from a strongly limited number of possible alternative values. That property allows error correction to take place: if possible values were continuous, error correction fundamentally wouldn’t work.
This gives the appearance of error-less copying. In reality it’s anything but, same as with computer storage and data transfer. Nevertheless, as you’ve noted, errors will accumulate, even with an error correction mechanism in place. And even though most of these errors have no influence on the outcome (due to downstream effects like the degeneracy of the genetic code), many more are detrimental than are positive. In direct contradiction of this we can see that species (but not individuals!) improve their adaptation in each generation.
Why? Because evolution. More specifically, because natural selection acts in a purifying manner to rid the gene pool of defects. This is a fundamental part of Darwin’s and Wallace’s argument. Less adapted individuals have an (ever so slightly) reduced chance at reproducing, and therefore prevent detrimental changes in the gene pool from accumulating.


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Comparing Shine Dalgarno scores, creating a distribution
I am in the process of creating a poster for the phage that I recently annotated. The phage is an A4 and the portion of the poster I am working on is analyzing the data that we have collected. I have an excel sheet that has all the Shine Dalgarno scores for each gene that we annotated and decided was the best. Using mathematica I tallied all the data into a table and this is what I got (The x value of the list shows the score, the y value shows the amount of genes that had this score):
How can I create a distribution from this data? Would I need to use a Histogram, a plot, or some other graphic to represent the data?
Biologically speaking, can we make any observations about the genome from these scores?

you can use histogram to plot this data but I am not sure what your scores mean. In the end your figure should convey some relevant information..

me either - this print out is highly idiomatic to the software you are using...

Please give us the data in text form so we can work with it. It would be relatively simple to produce a histogram using R for example but I'm not about to copy it by hand.

{{441., 6}, {168., 1}, {378., 3}, {483., 8}, {462., 4}, {336.,
4}, {143., 1}, {587., 1}, {504., 4}, {819., 1}, {468., 1}, {567.,
5}, {351., 1}, {294., 3}, {399., 2}, {438., 1}, {588., 2}, {299.,
2}, {525., 3}, {426., 1}, {390., 1}, {609., 4}, {225., 1}, {693.,
2}, {420., 5}, {357., 2}, {672., 2}, {231., 1}, {315., 2}, {455.,
1}, {252., 1}, {273., 1}, {364., 1}, {300., 2}, {546., 1}}

I know what Shine-Dalgarno sequences are, but what are Shine-Dalgarno scores and how did you determine them?

I would expect to see if every gene has a strong SDS, and that every strong SDS is in a gene (and if not, an explanation of why).
Mathematically, that can be calculated using Fisher's Exact Test (since I don't see any p-values for your scores).
You should also provide a diagram of the genome showing coding sequences or genes, and mark each SDS on it.

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Deducing synaptic strength from electron micrographs?
There are several promising techniques for connectomics based on iterative sectioning and imaging of tissue with scanning electron microscopes (e.g. FIB-SEM and ATUM)
By looking at such micrographs, one can identify synapses:

Is there any way to measure synaptic strength using these types of techniques?

i guess you cant determine synaptic strength by just detecting synapses.. perhaps by labeling the receptors you might be able to say something using confocal.. there are some studies like that

Thank you @WYSIWYG. Would you mind pointing me to some of those papers?

I am sorry.. I don't know of papers. I just heard them in some talk.. i shall look up and get back..

@WYSIWYG: I would be extremely wary of using such approach... you should really combine it with some ephys.

@nico: totally agree on that.. i just said that there are some studies which check protein activity at the synapses using labelled proteins. It is not absolute.. Btw i still need to find reference for it.

First of all, definitions. By synaptic strength let's understand ability of post-synapse to elicit current flow/depolarization in response to neurotransmitter appearance in the synapse. How can NT appear? By release from pre-synapse or through uncaging (optical activation of "caged", or inactive NT).
Second, post-synapse contain all sort of stuff, but main sources of current/depolarization are ionotropic receptors of NTs, e.g. NMDA-R or AMPA-R. This molecules are not just floating ion membrane but attached to extensive scaffolding just below of the membrane. Scaffolding includes actin, and more importantly PSD95 (in case of excitatory synapses).
I work in vivo and don't do any EM. But in vivo issue of observing molecules is that you can't label sensitive proteins without disturbing function. Some things are just too delicate to be labeled with fusing GFP.
PSD95 has been used for in vivo labeling with GFP. One paper I will point you to, is this knock-in work in mice: Live Imaging of Endogenous PSD-95 Using ENABLED: A Conditional Strategy to Fluorescently Label Endogenous Proteins, J Neurosc. 2014
This is the figure that shows strong correlation between brightness of synapse (aka number of PSD95 molecules) and current that occurs in cell body when authors uncaged glutamate at different synapses.

Figure description
Now, how does that relates to your image? PSD stands for "post-synaptic density" protein, because in EM synapse is very dark. I don't know links, but I would assume some correlation between brightness of synapse in EM and its strength.

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How can I describe running a solution four times through a chromatography unit (in an instruction)?
I'm translating a document from Russian:

The mean retention time for the first four injections of RNase should be (40.8± 2) min. If the mean RT is beyond this range, adjust the gradient system (change the content of acetonitrile within the 20% - 32% range) and chromatograph the RNase solution four times.

I'm aware that we don't use chromatograph as a verb in English usually, but we do use it in Russian this way. What would be the generic English expression for this, usable in a procedure description? I know that we have the word run but this might be too colloquial for an official paper.

I'm voting to close this question as off-topic because it is about language and not biology.

@terdon -  it's about terminology used in biotech, as pointed out by one of the tags. Had I asked it on ELL SE, it would have been voted for closure as off-topic too, or the replies would have been not very professional.

I feel it is more about the use of a specific word and not jargon. I just don't think this sort of question is on topic here since it isn't really about biology but about English. By the way, have a look at yesterday's chat transcript, we did find a few examples of its being used as a verb. Personally, I would say and run the RNAse solution through the chromatographer four times, but this isn't really my field.

@terdon - I see. I decided to bring it out from the chat area to help out (possibly) some fellow translators, web surfers etc.

Sure, and only one user so far feels it is off topic. I need to get another 3 to agree with me, and perhaps I'm alone in my opinion. Also, argh, typo in my previous comment. I meant . . .  run through the chromatograph, not chromatographer.

"Pass", "transit", "process"

I would say simply:

repeat the chromatography four times

or less formal, but quite acceptable:

re-run the column (or whatever it is) four times

This puts the emphasis on the process.
But I’m not exactly sure what’s happening. You have four injections of RNAase. If they are not right are you repeating each once or what? If the former, then it would be:

repeat the chromatography (or re-run the column) for each sample

It sounds to me as written that the intention is to attain accuracy via averaging a set of four runs, and if target value not attained, make adjustment and repeat another set of four runs until mean is within desired range. Perhaps state as "... then repeat another set of four runs.  Repeat as needed until the desired mean retention time is achieved."

@N2ition — Could be. But your use of "runs" suggests that is the most natural term to employ.

I would continue to use inject to describe loading samples into the liquid chromatography system and replace

chromatograph the RNAase solution four times.

with

inject the RNAase solution another four times.

Thank you! Will inject always imply ..and record the chromatogram in this context?

I think one can do better than this. The emphasis shouldn't be on injection but on repeating the process of chromatography.


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Meaning of "pure" in "pure plant DNA" (horizontally transferred to bacteria in soil conditions)
The abstract of Transformation of Acinetobacter baylyi in non-sterile soil using recombinant plant nuclear DNA, by Simpson et al., 2007:

To provide estimates of horizontal gene transfer from transgenic crops to indigenous soil bacteria, transformation frequencies were obtained for naturally transformable Acinetobacter baylyi BD413 using a chromosomally integrated plant transgene. The transgene comprised sequences for two phenotypic markers: kanamycin resistance (npt II) and green fluorescent protein (gfp), expressed from their own bacterial promoters. Recipient bacteria carried a copy of these two genes, with deletions in their 3'-termini abolishing the marker activity, these genes were integrated into a 16S rRNA gene in the bacterial chromosomal genome or carried on a broad host range plasmid. Successful recombination between the plant transgene and the bacterial genome resulted in restoration of the markers, allowing detection through antibiotic selection and fluorescence. Transformation parameters of increasing complexity, without any enrichment steps, were used to approach the field conditions, while still obtaining measurable transformation frequencies. In pure culture filter experiments, transformation was detected using ground, chopped and whole leaves, as well as whole sterile seedlings, and ground roots. In sterile soil microcosms, transformation was detected using pure plant DNA (3.6 × 10-8 transformants per recipient) and ground leaves (2.5 × 10-11). Transformation was also detected for the first time in non-sterile soil using pure plant DNA (5.5 × 10-11). Since the same constructs were used throughout, these data allow predictions of even more complex environmental systems where measurable frequencies are not easily obtainable.

What is the meaning of pure plant DNA? That the transferred DNA was in the form of purified DNA solution dripped onto soil, as opposed to some ground leaves whose cells included donor DNA (and some of these cells were crushed while being grounded and thus shed some DNA material onto soil)?
Was it done in order to promote transformation?


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What is the function of cystine, cysteine, and cysteine protease?
I am not a biologist, and I have a probably dumb biological question. For some purpose, I need to understand the function of the CTNS gene, and here is the definition of it:
"This gene encodes a seven-transmembrane domain protein that functions to transport cystine out of lysosomes.
I did not know what cystine is, and when I checked Wikipedia, I see that "Cystine is the oxidized dimer form of the amino acid cysteine."
What I understand is lysosomes digest a bigger peptide, and cystine is created as a result, and it is taken out of lysosomes by the enzyme produced thanks to the gene CTNS. My question is, where does cystine go and what is it used for after leaving lysosomes? And is it ever broken further into monomers of cysteine?
I also read about a term "cysteine protease". What is its relation to cystine?

I'm not sure as to what level of detail I should answer this question, but I will try to give you as much information as I can that I think will be relevant to.. whatever it is you are doing.
Cysteine proteases
Are a class of enzymes that degrade proteins, and utilise cysteine-residues as part of their catalytic mechanism.
Cystine
Is, as you said, a cysteine-dimer.. Which basically means two cysteines stuck together.
These are often formed in the intermediate steps of a cysteine protease's catalytic mechanism.
But also, during protein degradation within the lysosome, cystine can be released as a free molecule. When this happens, it will be transported in to the cytoplasm, to be processed via anabolic pathways into various products, such as glutathione (an antioxidant).

So, basically, the function of your seven-transmembrane (7TM) transporter protein is:
To make accessible to the cell, the digested products of proteins (or, amino acids).

Cystine is an amino acid. Cysteine is also an amino acid. These can all be used by a cell to create new molecules, such as proteins, or antioxidants, or vitamins or cofactors, etc., so many things. And can indeed be broken down in to cysteine.
The function of the CTNS gene, is to provide the cell with the genetic information used to synthesise the 7TM-transporter protein.

Thank you very much for the reply. Two followup questions: 1) When you say "To make accessible to the cell, the digested products of proteins (or, amino acids)", you mean specifically cysteine (or cystine), right? Other aminoacids are made accessible to the cell by other transporters? 2) When you say "Cysteine proteases are a class of enzymes that degrade proteins", do you mean "degrade any protein", or are specific type of proteins degraded by specific enzymes?

Based on the structure of cystine, I would guess that this particular transporter is quite specific to cystine.. But I honestly am not sure. Sorry, I usually try to do some research before answering questions on here since I do not actually know a whole lot about all of the questions that I answer.. but since it didn't appear that this would be needed of me, I did not do this before answering this time.

Cystein proteases are enzymes that degrade proteins. A good example of this would be papain - which comes from papaya. Often used as a meat tenderiser. And, also found in pineapple juice - if you were to take a steak and put a few drops of pineapple juice on it, and then leave it for a while, you would come back to find the steak a gooey mess of "mush".. for lack of a better term.

Thanks! One more dumb question: If cystein proteases degrade any protein, why is there a specific "cysteine" in the name, given cysteine is a specific aminoacid? Sorry that those may look like random questions, but they are in fact not. There is a paper titled "Cysteine protease inhibitors effectively reduce in vivo levels of brain beta-amyloid related to Alzheimer's disease", and I am trying to make clear the potential relation of cysteine and amyloid beta in my mind.

Well, as I said, "Cysteine proteases ... utilise cysteine-residues as part of their catalytic mechanism." Proteases are proteins! =D And proteins are made up of amino-acid-residues.. So basically, the cysteine residues are the amino acids within the protease that are responsible for catalysis. Another way to say this is: "Cysteine proteases utilize cysteine as their catalytic residues".....Does this make more sense?

And.. ohhh! I wish you had posted the paper title before I went off rambling. I think I've read this paper before, I would have related my answer to better suit this. (Do this next time). I assumed the reason you had said "For some purpose" was due to confidentiality-agreement reasons.

OMG, this is too complicated for a computer scientist! :) But yes, it makes more sense now. I was thinking that when cysteine proteases are used to break down the protein, then the product is cystine, but now I understand that this is not the case at all. The product of breakdown can be any aminoacid which would be used further for cell's purposes.

Let us continue this discussion in chat.

The cytosol is maintained as a reducing environment and so disulfides are readily broken. The resulting cysteine can then be metabolised in a number of pathways:


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Confusion about the brain regions - temporal cortex, hippocampus and and white matter
I am a computer scientist working with brain data. I have some data from different brain regions, and the regions are called temporal cortex, parietal cortex, hippocampus and forebrain white matter. I want to show those regions on a brain image in a presentation.
The problem is, when I search the brain images online, I cannot find the regions my data mentions. The regions in the search results are usually called "lobe" rather than "cortex". And when I search for "forebrain white matter", the results are usually about "cerebral white matter". I am totally confused. Here are a few questions:

Are "cortex" and "lobe" the same thing? Or does cortex means gray matter while lobe contains both gray and white matter?
Does hippocampus contain gray and white matter? Or does it reside in the inner side of the temporal lobe, meaning it is in the white matter part of the temporal lobe?
Are "forebrain" and "cerebrum" the same thing?
Why is hippocampus considered part of the temporal lobe although it has the long side of it outside of the temporal lobe?

Cortex, in general, means the outer part of an organ. The opposite of cortex is medulla.

"Lobe" refers to a section of the cerebral cortex, which is the outer part of the cerebrum. The cerebrum contains several structures, but the one that most people care about is the cerebral cortex, which is the 2-4 mm thick layer on the surface of the cerebrum. The cerebral cortex (or "cortex") is divided into several lobes, e.g. temporal lobe, occipital lobe. So, cortex and lobe are not the same thing, as the lobes subdivisions of the cortex as a whole. (See https://en.wikipedia.org/wiki/Cerebral_cortex)
The hippocampus is a region of the cortex in the temporal lobe. Therefore, it consists of gray matter. However, it is connected to several other structures by white matter (e.g. the fornix), and these structures are related to the hippocampus. (See https://en.wikipedia.org/wiki/Hippocampus#Anatomy)
Forebrain refers to the cerebrum as well as other structures, such as the thalamus and hypothalamus. The forebrain is defined as the telencephalon (which is basically the cerebrum) and the diencephalon (which contains the thalamus and hypothalamus). (See https://en.wikipedia.org/wiki/Forebrain and https://en.wikipedia.org/wiki/Diencephalon)
I don't know what you mean by the temporal cortex having "the long side of it outside the temporal lobe", but the temporal cortex and temporal lobe are basically the same thing.

Sorry, I had a typo in the 4th question. It should say "hippocampus". Corrected.

So, then, although "cortex" and "lobe" are different things, what my data means by "temporal cortex" is probably the same as "temporal lobe"?

I did not know temporal cortex consists of gray matter. So, temporal lobe thickness is 2-4 mm since it is part of the cortex. How about the gray matter thickness?

@user5054 the cerebral cortex is composed of the gray matter; so thickness would be the same. However, cortex is not equivalent to gray matter. In the spinal cord, the organization is reversed (outer part is white matter). The term, "gray matter", IMO has relatively little significance nowadays because we can see the anatomy of the brain at a much higher resolution. So, while the organization does matter, the terms - gray/white matter per se convey little information.


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Phospholipid Bilayer structural reversal
What would happen if the phospholipids in the phospholipid bi-layer were reversed, the fatty acid tails now facing outwards and the phosphate heads facing inwards? I'm assuming this will not affect the protein channels, but perhaps the loss of cholesterol in the structure of the bi-layer. Would this then mean that the fluid mosaic model no longer holds?

Why should protein channels not be affected ? Even if they are not reversed, environment around them will change which will have a disastrous effect.

I guess that it true, but the point here is to make the inference in the bi-layer structure after the reversal. What would it's characteristics be, and how would it's functions be altered?

DO you mean to ask that if we assume nothing in the proteins change(eventhough that isn't realistic), what will be the impact of reversal of the bilayer ?

For a start, let's just not consider the protein channels unless absolutely necessary.

its easy to do this by the way -just mix the lipids into oil

This would have quite dramatic consequences. The layers are ordered in the way they are, because of their polarity. In the way they are ordered, the hydrophobic tails are inside and directed towards each other, the hydrophilic heads are orientated to the outside and inside. Since both sides of the membrane are surrounded by aqueous solutions, this is necessary to allow a contact between solution and cell membrane and to allow an exchange of molecules between them. If the layers would be oriented the other way, this contact and exchange wouldn't be possible. Proteins channels in the membrane wouldn't be possible as well, since the intermembrane domains are composed preferrably of amino acids with hydrophobic sidechains, while the domains on the outside of the membrane contain more hydrophilic amino acids.
A turn like this would need a completely different composition of life - meaning it couldn't be based on water like it is.

Your answer is sufficient to an extent, @Chris, it implying that the fluid mosaic model is made no longer possible. However, I do not understand why the phosphate heads point outwards while the fatty acid tails point inwards if there was to be diffusion of lipids into the cell. It is conventionally known that lipids dissolve into the phospholipid bi-layer, but how would this be possible as there are phosphate 'heads' present? Imagine a lipid wanting to diffuse into the cell, how will it pass through the phospholipid bi-layer if the phosphate heads are hydrophilic in the first place?

You have to think about how fats (or fatty acids) travel through the blood stream: As small droplets (or micelles) which are organized in the same way: Hydrophilic part outside, hydrophobic part inside. They can fuse with membranes (or are actively taken up) and can so be transported to the cells.

Can you explain how fatty acids travel through the bloodstream or provide a source where I can read further on this matter? Are you referring to 'blood lipids'?

A nice source is the Wikipedia article on blood lipids.

I may have misheard previously that lipids "dissolve" into the membrane. Is it sufficient to say that they fit through the gaps in the Phospholipid bi-layer, therefore not repelled by the phosphates? Do protein channels come into affect this process at any stage?

The lipids travel in form of complexes with proteins which can then dock to the cells via special receptors (the interaction between Apolipoprotein E and the LDL receptor would be such an example). This can lead to the take-up of the lipids by the cell (for example for further break-down) or also into the membrane (for example for cholesterols).

Someone has thought this was a very good question and performed an MD simulation on spontaneous bilayer assembly. There, lipids start in random orientations. The ordered bilayers we know and love spontaneously assemble in under 100ns.
So if the lipids were jumbled up (or even reversed), the would probably reform fairly quickly. I wouldn't imagine that it would do the cell much good though...

If the layer is opposite,then there wont be any cytoplasmic liquid(cytosol) inside the cell, as tail is Hydrophobic.If there is no cytosol,then no function of the cell.Even it becomes difficult to pass substances through the cell when layer is different.

Do you have any source for your answer ?

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Why mosquito bite is confined to a certain shape?
I think this problem should be asked in a physiology forum rather than biology@ stackex but I'll give it a try.
So my question is simple - why a mosquito bite is usually confined to a certain shape (shape = red area) and not just disappearing continuously? Can our body cells tolerate some level of antigens without changing color from that?

Question of physiology are very welcome to our site! There is even a often used tag for that. It is totally on-topic.

Some biological processes have a threshold response (or a steep hill equation). Perhaps that's what's happing here.

What you're referring to as a mosquito bite is actually the "wheal" (red swollen bump in the skin) that forms from an immune system reaction to antigens (foreign molecules) in the saliva of the mosquito that it leaves behind inside the bite.  It's not technically a toxin, just something that causes an immune reaction.
It's also not an infection, it's inflammation.  Infection might set in if the skin is scratched open and bacteria move in.
The reason it's red is that immune cells release cytokines (like histamine and that cause cause edema that leads to swelling, heat, itching, etc - and recruit other cells to do the same.
The cytokines that act locally have a range of effect, especially histamine.  The degree of immune reaction determines the size of the wheal and how long it lasts.  Scratching it contributes to irritation and can prolong resolution.  Scratching it open can lead to infection.

You are totally right but still haven't answered the question I asked. Why the red swollen bump in the skin in confined to just a certain area and not continuously decaying?

I see your point that some wheals tend to have patterns (the most iconic one being the bullseye lesion of tick bites associated with lyme's disease). Demarcation of borders differs between individuals as well - not everyone has the same reaction to bites.  In this image: http://www.visualphotos.com/photo/1x8722914/skin_allergy_caused_by_mosquito_bites_049286.jpg  you'll see the most common presentation of a mosquito bite wheal.  The edges are not well demarcated; rather, there is a fade-away of erythema.  This is as I mentioned largely a result of the limited range of inflammatory cytokines.


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Difference between intervertebral and vertebral foramina
In the human spine, what is the difference between intervertebral and vertebral foramina? Is it just a matter of perspective and do they refer to the same thing or are they different?

They are actually different.

(source: emory.edu)
INTERVERTEBRAL FORAMINA is actually spaces between adjacent vertebrae which gives passage for spinal nerves to exit.
Whereas, VERTEBRAL FORAMINA forms vertebral canal.
Source:
Organization of the Nervous System: An introduction for students in the Human Anatomy Course


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Why does looking at bright light trigger sneezing in some people?
Why does looking at bright light trigger sneezing in some people?
Are there any recent studies that have found a cause for this Photic sneeze reflex? The Wikipedia article only references studies pertaining to the effect, stating that the cause is unknown. The article also states that "the condition affects 18–35% of the population", which seems to be quite a large percentage.
What could have lead to the development and persistence of such a genetic trait in humans? Are there any evolutionary advantages to this?

In high school biology, we had to read a book called "Survival of the Sickest". In this book, the idea is presented that this reflex evolved during humankind's "caveman" days. The author presented the anthropological induction that after spending periods of time in a dark, dank cave, mold spores begin to accumulate on the human body and inside immediate and open orifices. The nose, being moist, open, and pulling air in, would then be prime nesting ground for mold. Some claim, then, that humans evolved this reflex as a way of clearing the nose of mold and other impurities upon exiting a cave and entering the brightly lit outside world.

This trait might be correlated to other traits not necessarily be or ever been under selection. I think the first step would be to understand the mechanism behind this connection and whether people from different population have the same rate of appearance of this trait (e.g. in northern population should be  more frequent)...

I agree, but the question was regarding why we evolved this trait, not how the body does it. And that's anthropology; we take the most likely and feasible conclusion from a sea of other likely conclusions. I just wanted to add a new dimension to the existing responses. You know, providing another path in which people can direct their research. Regarding correlating rates of expression and geolocation, I don't think northern populations would inherently show more expression, and I believe the author introduced some evidence of this type, but I cannot recall and I no longer have the book.


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Does leaving land alone actually help nature conservation?
I like nature conservation - the idea of creating protected areas where nature lives on its own and wilderness is "created" like that. Is is possible to raise the natural value of land only by leaving it on its own - I mean in the way that humans do not touch the land in any way (buildings, roads etc.)?
I know about some "private" protected areas in Europe, where NGOs thought this piece of land should be protected but the authorities failed to do so, so they bought the land and took care of it themselves (restricted public access to help conservation, removed invasive species etc.)
I wonder what does it take to correctly protect an area - is it OK to leave the land alone and never touch it again or is it necessary to take care of it somehow. I mean things like invasive species (I can imagine the normal "unprotected" nature is full of them) like various types of grass, invasive animals etc. I can imagine this may be largely location dependent (some parts of the world are more influenced by humans than others). My location is the Czech Republic.

I think the concept of a 'correct' wilderness is unclear. There are some landscapes which have been suddenly 'left alone' by humans, and a meaningful answer could consider the general ecological trends of being 'left alone' in this way. Examples include the landscape around the Chernobyl, or abandoned farms. But then the question would be 'in the absence of deliberate conservation interventions, what measurable ecological benefits (e.g., changes in invasive-species populations) arise from simply leaving land alone?' Would you be happy to edit your question into that form?

Your question seems to ask exactly the same so what is the reason for rephrasement?

It removes the reference to a 'correct' wilderness. There is no such thing: natural areas may be managed towards specific goals, like maintaining the number of species present in the area, providing habitat for a key high-value species, or protecting key ecosystem services such as water retention. None of these are 'correct', but each outcome is measurable, and a 'desired' outcome can be defined in each case.

Rephrased to "raise the natural value of land" - is that better?

This may be a better fit in [gardening.se]

I'll give you an example, because this question is pretty case specific. In Delhi, my hometown, they kept areas of the forest, the 'Sanjay Van' free from construction and people and only very recently started cleaning it up. As a result, an invasive variety of the Acacia tree (known locally as keekar) more or less took over the forest and has basically wreaked havoc on the wildlife.
I think better than just letting Nature take it's course, humans should help get abandoned areas back to a sustainable point, where it can integrate with the wildlife, but again, it depends on each area.

According to Peterkin, there are three types of naturalness - past natural (the way it was before humans), future natural (the way it would be if humans left it alone), and present natural (the way it would be now if humans had never touched it). How best to conserve a site will depend on what type of naturalness you want to achieve. There's no rational argument to prove any one type is "better" than any other in the long term, but many conservationists take a safe approach and adopt the strategy with the least risk of extinction (this being the only result one cannot undo), it would be a mistake though to presume that this strategy was definitely the best, it's just in some environments we can't afford to find out.

The German Green Belt see here
I give you a another example. The green line in Germany. This is are are where the German Wall was (you know east and west Germany) This area was untouched by humans for 40 years. And now it is a protected area, because now its one of the last places for a lot of animals and plants to live.


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Stomach sagittal section
Can anyone please tell me where is exactly the stomach in this image?

This is a sagittal section from the University of Michigan Visible Human Browsers.

Thank you.

Given that this is a mid sagittal image showing the right hand side of the body, the stomach isn't really in full view.  It could possibly be the black structure immediately inferior to the liver in the centre of the image

@RoryM Thank you for your answer! I added 2 more photos, can you please tell me if we have a better view of the stomach,and if yes where is it? Thank you again!

@The.Blue.Shrimp the second picture seems to be further right, while the horizontal lumen underneath the liver in the third one might be the pylorus.

The below structure circled in green clearly is part of the stomach antrum. The location is correct, and the mucosal folds are characteristic. Kerckring valves of the small intestine and semilunar folds of the colon both look different.


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What are the main challenges for developing imaging techniques for cellular-scale structures?
Small disclaimer: I'm not a biologist, so I'll try my best to write a high-quality, objective question, but please forgive me if it doesn't turn out as expected.
Imaging technologies such as MRI and CT Scans are used routinely to inspect anatomical structures inside the body of alive patients, and, as such, are powerful diagnostic tools. A typical MRI machine will produce volumetric images with a voxel width of 1,000,000 nm. This is more than sufficient to identify a broad class of issues, such as tumors and aneurysms. Yet, given that a human cell has about 10 nm in diameter, that resolution is 5 orders of magnitude below what would be required to image individual cells in vivo. As such, MRI, and the like, can't be used to diagnose macular degeneration or hearing loss by imaging the damaged retinal or inner ear tissues, for example, and thus rely on less precise exams, such as hearing tests. At the same time, in vitro, technologies such as electron microscopy are capable of imaging individual structures inside cells, and are, thus, capable of reaching resolutions that are impossible for live patients. If we had some hypothetical imaging technique capable of inspecting individual cells, it would enable a wide range of conclusive diagnosis for conditions that, currently, are still hard to track.
My question is: why is there such a gap, and how far we are from developing technologies capable of imaging cellular-scale structures inside the body? For example, would it be possible to create a nano-MRI machine capable of imaging someone's organ of corti, or individual retinal ganglion cells? If so, what are the relevant advancements in this direction? If not, what are the physical or practical limits that make it impossible?

I think the question would be better focused on just MRI, and possibly a better fit over at Physics. It doesn't make much sense to compare MRI, which images through tissue using magnetic fields, to something like electron microscopy that requires you to slice into something and apply super carcinogenic chemicals to increase contrast. They're not in the same realm of approaches.

https://physics.stackexchange.com/questions/621545/why-does-mri-magnetic-resonance-imaging-have-high-contrast-and-spatial-resolut https://physics.stackexchange.com/questions/111770/how-specifically-does-an-mri-machine-build-an-image-from-received-radio-waves

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References for historical momentum in asexual species definitions
For sexually reproducing organisms, the scope of a species is somewhat fixed by reproductive compatibility.
However, this all collapses for organisms that exclusively reproduce asexually.
Here, my impression is that historical momentum is the primary driving factor of species scopes, i.e.:
Clades continue to stay on the species level to maintain continuity, while they would be categorised with a higher or lower rank if clades had to be taxonomically ranked from scratch without respect to history.
For example, the species of Escherichia coli and Pseudomonas aeruginosa have been discovered (and thus have been made species) very early and now comprise a diversity of subspecies.
In particular, the genus of Shigella appears to considerably overlap with E. coli or is even thought to be a subspecies of it.
I am here looking for references supporting (or refuting) my impression, for example:

Has this ever been prominently noted?
Are there any instances of species being split on account of being “too large” (as opposed to other miscategorisations)?

Background: Why I care
As long as the taxonomy is phyletic, what does it matter at what level clades are ranked?
Right now, this affects me in several ways (assuming that my impression is correct):

The common way to present the composition of an ecological community is showing the abundances on a fixed taxonomic level.
For example: “Our community contained 80 % Pseudomonas, 15 % Escherichia, and 5 % Bacillus.” and analogous graphical representations.
Of course, I can deviate from this (e.g., by listing lower ranks for diverse clades), but then I have to justify it – and here the desired reference might help.

If differing subspecies of a “big” species are present in an ecological community, this may lead to a superficial underestimation of the community’s diversity.
Mind superficial:
I am aware that this does not affect any good quantification of diversity.
However, it does affect superficial diversity as estimated from representations such as that mentioned in the previous point, and the resulting discrepancies between objective and subjective diversity often demand an explanation.

Biosafety classifications are often determined on the species level, in particular, if the subspecies is unknown.
For example, even though P. aeruginosa lives on our skins, it automatically gets classified as risky on account of some black-sheep subspecies.

One issue is that I don't know what you mean by "historical momentum". Do you mean, when humans found the organisms in question?

@MaximilianPress: I mean, e.g., that E. coli continues to be a species only because of its history as opposed to what would be a more balanced taxonomy given our current knowledge.

Right- I talk about that specifically a little, below. I would then ask a different question: are species definitions themselves only still around because of historical momentum? Somewhat related: it might be helpful to read / learn more about classification, here is a video from Joe Felsenstein, old warhorse of computational phylogenetics, discussing this question (starts ~8 minutes): https://www.youtube.com/watch?v=PcD15i7yzJ8

are species definitions themselves only still around because of historical momentum? – To some extent sure, but then there is some merit to having a rough idea of how diverse a clade is by its level. Anyway, this is something I cannot change.

Our exchange has served to confuse me further regarding your question. Is your argument, basically, that E. coli is more diverse than a species first described yesterday because the type strain for E. coli was described first and it has therefore undergone more evolution since then? (That doesn't make any sense to me, but I'm having trouble understanding any other meaning.)

@MaximilianPress: E. coli is more diverse than a species first described yesterday because the type strain for E. coli was described first – Yes, though the reason is not evolution, but rather things like: 1) The definition of E. coli had to be expanded to maintain monophyly in light of new insights. 2) New insights on the properties of E. coli or strains thereof. 3) The definition of E. coli is overly broad by modern standards either due to new insights on what aspects matter for bacteria or general changes of standard as to how narrow a species should be.

I'm going to delete my answer because it doesn't seem to be helpful here. Based on our exchange, I remain puzzled about how the presentation of results at a fixed taxonomic level is methodologically enforced compared to the (to me) clearly superior phylogenetic method, there is a bunch of literature on this as we've discussed. Potentially editing the question would clarify this.

@MaximilianPress: The presentation of community composition is not methodologically enforced, because it is not about methods or quantification, but about presentation. Just to be very clear, I am talking about things like “Our community contained 80 % Pseduomonas, 15 % Escherichia, and 5 % Bacillus.” and graphical representations of similar information. I have no idea how I can make things much clearer, but am open to suggestions.

"Our community contained 80 % Pseduomonas, 15 % Escherichia, and 5 % Bacillus.” and graphical representations of similar information." I think that this is a much clearer statement of what you anticipate needing (or expect people to want from you) than I am getting from the question. I think that in your question you could take such a statement and then talk about what you think is wrong with it, and what kind of statement you would prefer to make instead. And also, to be very explicit about how it interacts with history (where I think I get confused). Also, asexuality seems irrelevant to me?

@MaximilianPress: Edited. Asexuality is relevant, because for sexual organisms species levels get readjusted based on insights on reproductive compatibility AFAIK. While this is not perfect either, it regulates the scope of species to at least some extent.

FWIW I think the question is clear, it's just hard to find the sorts of sources requested, especially reliable ones. It's more the thing that people talk about at a conference rather than writing papers on. I suspect you might find some discussion in an article arguing for a change but I've gone through several of these now and not found anything to quite back this up.

I have tried to ask a similar question from a rather different prospective: basically, whether taxonomic categories can eb defined by differentiating between quantitative and qualitative evolutionary changes.


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Relative Property of Alleles
If there are three different alleles to a gene, is it possible that the first is dominant to the second, but recessive to the third?

Sure it is!
When we say that an allele is dominant on another what we really mean is that the phenotype obtained from that specific mutation of the gene somehow "masks" the phenotype of the other.
The easiest example would be that of pigment. A gene X could code for an enzyme which produces a red pigment. A mutation in X could result in a allelic variant x coding for a non-functional enzyme that does not produce pigment. In this case X will be dominant on x, as in the presence of both the pigment will still be produced (because you will have half functional and half non-functional enzyme molecules).
Things can, however be slightly complicated.
For instance, if the allele R codes gives a red pigment and r gives a white pigment Rr could give pink. This is called incomplete dominance.
On the other hand you could have co-dominance, where WW is white, ww is black and Ww is black and white.
The example you are asking for is called serial dominance and the "classical" example given is that of the rabbit coat color where you have for alleles with a dominance hierarchy like:
c+ > cch > ch > c
c+ gives a fully functional enzyme, called tyrosinase
c gives a non-functional enzyme, resulting in an albino phenotype
cch (chincilla phenotype) and ch (hymalayan phenotype) give partly functional enzyme (interestingly, the latter gives a temperature sensitive fur color).
In reality the rabbit coat genetics is even more complex, see this documents (PDF) for a more complete list of all the various loci and possible alleles involved.


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What would cause E. coli to change from filamentous growth to normal growth?
In my lab we've observed a phenomenon in which a culture of E. coli is found to shift from normal rod growth to filamentous growth and then back to normal rod growth again several times over the course of 400 hours. This was shown by an OD600 graph which oscillates from high values (~5) to low (~0.5) (the culture was also viewed directly).
The shift to filamentous growth is usually associated with an SOS response in E. coli and this makes sense (the media is M9 supplemented with 0.2% casamino acid and 0.1mM thiamine hydrochloride), however we don't know why it switches back from filamentous to normal growth.
Has anyone observed a similar phenomenon? Does anyone have any suggestions why this might be happening?

How exactly is the culture maintained over the 400 h period? Are there any periodic events?

Expression of sfiA (sulA) causes filamentation during the SOS response, so presumably sfiA is induced, as part of SOS, in response to some sort of DNA damage. Once the DNA damage is repaired the SOS genes, including sfiA, will be repressed again and normal growth will resume.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2902570/
In addition to the other answer(s), E. coli has been shown to have filamentous spikes even under controlled conditions. This is not the same situation as it sounds like you have a non synchronized culture in which this happens, but it could be related.

I found that E. coli exposed to predators such as amoeba changes completely from normal form to filaments (on agar) that look wound up like spaghetti but are not only longer but significantly wider. In this form the predator can't attack E. coli and it lives among the amoeba for extended periods. It does not look like a simple point mutation to me, which merely disables cell from cell dissociation.
So I have now two types of E.coli, opaque whitish looking filmaentous colonies and the normal more translucent colonies. In one case the filamentous form turned back to the normal form after repeated transfers on predator free plates.
So the question here could be: which is the E. coli that lives in the real world out there in soil water and biofilms?
Ralf Cord-Ruwisch Aug 2014

When you add a citation, can you either provide a link to the PubMed (or the journal) or provide a complete citation including journal, volume, year, issue and page number. This makes it easier for people to actually find them.


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One Gene and many proteins
Imagine a gene with  $n$ exons and $m$ introns. How many proteins are possible from that gene? Would all the proteins be isoforms?

Is this a homework question or a assignment? If so, please tag it accordingly and tell us what you have done to solve this.

This question cannot be answered in its current form. How many of the exons contain a valid START codon? How many exons are in UTRs? How many actually code for protein and don't contain in-frame STOP codons? Please [edit] and make it more specific.

I might be wrong, but aren't numbers $n$ and $m$ are connected as $n=m+1$?
Answer seems to be combinatorial: how many combinations of $n$ objects can be assembled under certain restrictions? Namely, how many isoforms certain gene can have.
Restrictions include: how many exon-intron junctions on codon (or precisely between codons), how many exons are actually contain protein-coding sequence of mRNA (some exons are coding untranslated region, 3'- or 5'-UTR, for example), how certain gene processes alternative splicing.
So, as you can see, answer will highly depend on sequence of given gene. As far as I know, maximum number of isoforms is limited by 5, even though there are genes with hundreds of exons.


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What's behind the amazing colour combinations in pests & insects?
What's behind the amazing colour combinations in pests & insects ? Do this colour combination signals any character/ poison of the pest/insect ?

What pest? Which insect? Bright colors often indicate poisonous animals but you'll need to be much more specific for us to be able to answer you.

Or that's what they want you to think...

@Oreotrephes sneaky buggers :).

Why Close vote? I think, its answerable!!


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Why is fructose not glucose the main energy source of sperm?
The seminal fluid contains fructose as the main energy source for the sperm and not glucose.

Why is fructose and not glucose the primary energy source for these
  sperm, since glucose is the preferred energy source for most other
  tissues?

I am not sure this is a very reliable source but it does seem logical.

@biogirl Not all answers there are reliable, but this one seems to be genuine. But you never can tell without a good reference.

i am not very sure about this but perhaps since glucose is preferred source for other cells, fructose is allotted to sperm so that other cells dont compete for it.. totally a wild guess because I dont know of any other reason.

FYI : Seminal vesicle is the only place in the body where fructose is secreted.

I have been searching this for a while and I got something of an answer, which I am posting below.
There are primarily two advantages of using the polyol pathway and aldose reductase to produce fructose from glucose via sorbitol:-
1) Quoting the book here,

Seminal fluid contains up to 11 mmol/L (200 mg/dl) of free fructose.
  It is the major energy source for the sperm cells in their
  all-important race for the ovum. The advantage of fructose over
  glucose may be that many bacteria, which compete with the sperm cells
  for the available nutrient, prefer glucose to other energy sources.

Thus, to avoid other competitive bacteria and cells from utilising the energy source of sperm, fructose is used as the energy source since the bacteria prefer glucose.
2)Another reason is that the metabolism of sorbitol into fructose is energetically efficient way (no ATP required) as compared to glycolytic conversion of glucose into fructose(G$\rightarrow$G6P$\rightarrow$F6P$\rightarrow$F). Tapping the polyol pathway is energetically preferred to metabolizing fructose produced during glycolysis.This is only to show the possible evolution of the polyol pathway once the advantage of using fructose as the energy source was established. It does not explain why the fructose was advantageuos but just that if it was advantageous, the semen-producers would develop the currently existing machinery to produce fructose as the exclusive source of energy.
Hence, sperms (seminal secretion) contains fructose as the primary energy source and not glucose.

Neither of these arguments make sense to me. Firstly, if there was an advantage to using fructose amongst bacteria that might encounter semen then they would evolve to exploit the niche. I note that E. coli for example will quite happily use fructose as C source. On the second point, I don't see how the fact that you can make fructose from glucose without using ATP is an argument against just using glucose in the first place. In any case I think that arguments from energetic efficiency are rarely convincing.

@AlanBoyd The second argument is only to show the possible evolution of the polyol pathway once the advantage of using fructose as the energy source was established. It does not explain why the fructose was advantageuos but just that if it was advantageous, the semen-producers would develop the currently existing machinery to produce fructose as the exclusive source of energy.

@AlanBoyd The first argument, though not substantial in its claims, is the only one I could come up with. If you do know an alternative argument, I would be most happy to consider it and accept it as an answer.

I admit that I have not come up with an answer, but it seems to me that maybe there is something else about fructose that makes it a better choice. Maybe it has some function, other than as a C source, in the fluid. It may be relevant that it is much more soluble than glucose, although the concentration that you quote is way below the solubility limit for either sugar.

If glucose was used in place of fructose it would get used up very quickly as it has a high glycemic index but fructose has low glycemic index and gets used up slowly by the spermatozoa so that they can survive for many days (upto 3) in the females body for successful fertilization.

Thank you for your contribution. Your answer could benefit from some references. Please [edit] to add citations to reliable sources that support the assertions made here. Un-sourced material may be disputed or deleted.


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Strongest muscle of Human Body
Which is the strongest muscle of human body ?
Confusion b/w Masseter muscle (Muscle of Jaw) and Tongue and Muscle of Heart and Muscle of Uterus.

What do you mean by strongest? The one that can apply the highest force or the one that has the greatest endurance?

First internet search result gives you everything you may be interested in, and looks reasonably reliable: http://www.loc.gov/rr/scitech/mysteries/muscles.html

You'll be interested in THIS Wikipedia article. It really depends on how you define "strongest" (Newtons, Wattage, Newtons per Kilogram, etc.). Here are a few relevant excerpts from the article:

In ordinary parlance, muscular "strength" usually refers to the ability to exert a force on an external object—for example, lifting a weight. By this definition, the masseter or jaw muscle is the strongest. The 1992 Guinness Book of Records records the achievement of a bite strength of 4,337 N (975 lbf) for 2 seconds. What distinguishes the masseter is not anything special about the muscle itself, but its advantage in working against a much shorter lever arm than other muscles.
If "strength" refers to the force exerted by the muscle itself, e.g., on the place where it inserts into a bone, then the strongest muscles are those with the largest cross-sectional area. This is because the tension exerted by an individual skeletal muscle fiber does not vary much. Each fiber can exert a force on the order of 0.3 micronewton. By this definition, the strongest muscle of the body is usually said to be the quadriceps femoris or the gluteus maximus.
The heart has a claim to being the muscle that performs the largest quantity of physical work in the course of a lifetime. Estimates of the power output of the human heart range from 1 to 5 watts.[14] This is much less than the maximum power output of other muscles; for example, the quadriceps can produce over 100 watts, but only for a few minutes. The heart does its work continuously over an entire lifetime without pause, and thus does "outwork" other muscles. An output of one watt continuously for eighty years yields a total work output of two and a half gigajoules.


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How is instinct carried from one generation to another?
How can non-structural information, specifically instinct (a fixed pattern of behavior that an organism reverts to as a response to certain stimuli), be passed on from generation to generation (such as an unborn baby's instinct to begin inhaling and exhaling amniotic fluid while still in the mother's womb to "practice" breathing, a sea turtle's inclination to enter the sea after hatching, etc.)?
Does DNA have anything to do with it? I can't imagine what else it could be, considering that the genome is the only thing an organism passes on to it's progeny.

This stuff is hard-wired into either the organism's nervous system, or endocrine signalling pathways (e.g., hormones), or possibly a combination of those two mechanisms.  In that sense, yes it is encoded in the genome, but not in a language that we can understand or interpret yet. Also, don't overlook all of the macromolecules that the female provides to the developing egg during oogenesis, your mother gave you lots of things besides a copy of her genome--you just don't have any of those macromolecules left now--but you wouldn't be here without them.

and also epigenetic factors, just look on recent Nature paper, memory can be transferred without change in genetic code per se: http://www.nature.com/news/fearful-memories-haunt-mouse-descendants-1.14272

Please try adding some explanation along with citations for how instincts are hard-wired. What you are essentially talking about is the physiological mechanism whereas the actual question appears to be about the genetic basis.


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How do I find the number of child terms associated with a specific GO term?
I am trying to figure out how to find the number of child terms associated with a specific Gene Ontology (GO) term using QuickGO, without just counting the amount of terms in a list. For example when I want to find the number of child terms associated with the GO term 'heart development'.
I could just click on the tab 'Child Terms' and count, but what if it would be a very long list, how can I find the correct amount?
I assume there is some way to do this by going to Protein Annotation and applying a filter, but I do not know how to do this.

Any help?

Does it need to be done using QuickGO? Would you be open to downloading the ontology .obo file and parsing it? Do you only want direct child terms or all descendent terms (children, grandchildren etc)?

I am only looking for direct child terms. I would like to find a way to do it in QuickGo if possible, but I am interested in any other methods possible! :-)

I don't think it's possible to do this via QuickGO. You can, however, do it from GO's website, using their GOOSE tool. This offers an interface to the GO SQL database and lets you run queries. It also offers example searches, one of which ("Find descendants of the node 'nucleus'") can easily be modified to return what you are asking for:
SELECT COUNT(*)
FROM
 term
 INNER JOIN graph_path ON (term.id=graph_path.term1_id)
 INNER JOIN term AS descendant ON (descendant.id=graph_path.term2_id)
WHERE term.name='heart development' AND distance = 1 ;

In the query above, I modified the example and changed 'nucleus' to 'heart development' (GO:0007507) and changed distance <> 0 to distance = 1 to make it list only direct descendants. Finally, I also changed SELECT DISTINCT descendant.acc, descendant.name, descendant.term_type to simply SELECT COUNT(*) since all we are interested in is the number of descendants. If you also want their names, leave the SELECT line as is. That will show both the list of names and the total in the output.
The modified query shows us that this term has 30 descendants:

When I also tried running this query in HeidiSQL in UCSC MySQL (database 'go') I found 22 results instead. Any idea why?

@Wolgast different ontology versions presumably. Or a completely different SQL schema. The ontology files are not static, They change quite a bit and quite often. What you need is the number found in the specific ontology file you happen to be using. Don't assume that different online versions will give you the same result.

GOOSE is now deprecated :-(


text:
What determines the efficiency of electron production in photosynthetic bacteria?
Is there a specific gene involved, perhaps? Would one be able to genetically engineer a bacterium to oxidize water and generate electrons quicker? I am speaking about this biological problem in terms of an application to solar cells.
Edit: I am not inquiring to the existence of a gene responsible for photosynthesis, I am inquiring as to why some exoelectrogenic bacteria can produce electrons in electron transport more efficiently than others. Is there a reason for this that can be traced to a certain gene that makes certain exoelectrogens superior to others?

Electrons aren't actually generated during photosynthesis. Instead, they are excited (brought to a higher energy state) when they absorb light. The decay back to the original energy state is coupled to chemical reactions, which is how the cell uses the light to make compounds that would otherwise be unfavorable.

Nothing. Electron transfer (not production) has been found to be about 100% efficient and involving quantum phenomena.

Are you looking for a physics-based answer? The main reason kind of boils down to the fact that the structures of the photosystems affect the physics in such a way that the efficiency is greatly increased. Also, it must be noted that the dynamics are different in plants compared to photosynthetic bacteria. The energy transfer mechanisms are slightly different.

You may or may not consider this an actual answer to your entire question, but it's interesting nonetheless.
A physicist friend of mine did some work recently modelling the quantum dynamics of photosynthetic complexes, and their coupling constants for passing energy throughout the photosystem. His results showed that, (and I believe this is in agreement with the literature), that photosynthetic systems are actually about as efficient as it is possible to be (not only this, but they are the most efficient energetic systems known to man I believe - over something like ~90% efficient).
If you begin altering positions of chromophores and so on, the photosystems exhibit remarkable robustness and you get a more or less logistic decay in efficiency (i.e. removing one or 2 chromophores results in marginal reductions in efficiency, more still in considerably more severe debilitation, until ultimately it's efficiency is markedly lessened, but further manipulation has a plateau in efficacy reduction).
Much of the work that's been done on the quantum biology of photosystems has concerned the FMO Complex (Fenna-Matthews-Olson) which is a simplified model system from photosynthetic algae - you might find more detailed answers to your queries by reading up in this area.
As for discrepancies seen in photosynthetic effectiveness bought about genetically, there are theories that suggest that the organisms are actually protecting themselves. E.g. to avoid over-production of ROS species. I can't offer you much in the way of a well evidenced case for this though, it's just a conversation I had with a post-doc at work recently, who completed his PhD on photosynthetic cyanobacteria.
EDIT Here's one of the papers about optimality in the FMO:
http://aip.scitation.org/doi/pdf/10.1063/1.4930110

May I know who this post-doc is? I have been researching this field for quite some time, and I am pretty interested in the modeling of the system, in particular the FMO complex

The guy who did the FMO complex modelling was a fellow PhD student - Lewis Baker. There is some information at his university page here. I'm sure he wouldn't mind you getting in touch directly. http://www2.warwick.ac.uk/fac/sci/moac/people/students/2013/lewis_baker/msc_year/mp3/

@Joe Healey's answer is great, but I would like to expand on the subject, having done a thorough literature review on the subject before.
Before we do that, I would like to clear up some misunderstandings that you seem to have about the electron transfer.
Just like @stords said, electrons aren't generated during photosynthesis. Where it comes from is from the oxidation of water mediated by the reaction center. The reaction center is part of the photosystem,  which contains all the light-dependent parts of the reactions. The oxidation is performed by the oxygen-evolving complex. This process of oxidation isn't very well understood. However, most photosynthetic bacteria contain similar complexes. Note that green sulfur bacteria doesn't use H2O for oxidation, but instead H2S.
Reaction center
Now, in the light-dependent reactions, we have what's known as a light-harvesting complex, which contains many pigments that absorb light and get excited. The pigments then transfer the energy to the reaction center, which also gets the electrons from the oxidation. So when the energy from the antenna reaches the reaction center, the energy excites the electron to a higher energy level. This higher energy electron is transferred to the electron transport chain, where it reduces various electron acceptors, and while doing so, using the energy released to pump electrons to make a proton gradient. This proton gradient is used to make ATP. Even in bacteria, the process is very similar. The exact details can be read here
Excitation efficiency
Now, answering your question, what really determines the efficiency of the electron transfer is actually the energy transfer occurring in the light-harvesting complex (LHC). Now, different organisms have different mechanisms, but all scientists agree that there is some quantum mechanics behind this. In the following discussion, I will be referring to the dynamics of the FMO complex, the antenna complex found the green sulfur bacteria, and commonly used to study the quantum mechanical interactions of energy transfer.
Now when we have this transfer of energy from one pigment molecule (chlorophyll in plants, bacteriochlorophyll a in green sullfur bacteria), we call it an exciton. This exciton is a quantum mechanical state. Now, in quantum mechanics, there is a concept called superposition. Basically, superposition means that a single quantum mechanical state is composed of multiple states. In the case of the light-harvesting complex, when we say that the exciton is in a superposition, what this means is that the energy can travel in all possible pathways from a pigment to reaction center, and when the best pathway is found, the interactions in the complex causes the state to collapse into the best state. This is how the transfer of energy occurs in less than 1 ns!
This dynamics is very complicated, and very surprising, since this quantum mechanical dynamics is occurring in an open system. Typically, it is very hard to observe quantum mechanical dynamics because of something known as decoherence. This is when a mixed (superposition) state collapses into one state. However, interestingly, the complex uses this decoherence to collapse into the best path for the exciton to reach the reaction center.
This field is very interesting. If you have any questions, please leave a comment. I am a little rusty on this subject, but I am very interested in this subject. If you want to see more examples of quantum mechanics in biology, look up "quantum biology". Quantum biology is a new field studying the intersection of quantum mechanics and biology.
References:

https://en.wikipedia.org/wiki/Light-dependent_reactions
http://rsif.royalsocietypublishing.org/content/11/92/20130901
https://en.wikipedia.org/wiki/Fenna-Matthews-Olson_complex

Vibrational-electronic coupling: Vos et al. is most likely, but some have suggested quantum entanglement which would be great if photosynthetic organisms grew at cryogenic temperatures.

We're looking for long answers that provide some explanation and context. Please don't just give a one-line answer; explain why your answer is right, ideally with citations. Answers that don't include explanations may be removed.


text:
What are the functions of magnetic bacteria?
I'm trying to understand why are bacteria "equipped" with magnetosomes ("intracellular organelles in magnetotactic bacteria that allow them to sense and align themselves along a magnetic field") and why and for what do they need such organelles.

You can find a detailed discussion of this topic here.
Magnetic bacteria contain chains of magnetic crystals (magnetite or greigite) which cause the cells to be oriented in a magnetic field.
It was originally proposed that magnetic bacteria use their magnetosomes to ensure that they swim downwards into the sediment (everywhere on earth, except at the equator, these lines of force have a downward component vector.) However, the current view is more complex than this: magnetic bacteria are microaerophilic and occur in stratified aquatic environments (i.e. ones where there are zones of oxygen concentration at different depths). In this view the magnetic "sense" is not a true taxis, but rather is used to keep the cells oriented in the magnetic field while they adjust their position by sensing oxygen (aerotaxis). As you may be aware, the standard way that Gram-negative bacteria operate is to perform a biassed random walk in three dimensions. The alignment of cells with the magetic field will reduce the dimensionality of the movement, which is more efficient.


text:
Do cockroaches lay eggs in human flesh when they "bite"?
Recently, I discovered a "bite" by a cockroach, and not only is the "bitten" area red and swallowing, and more specifically, it have a big hole in that area, but when I clean it with hydrogen peroxide solution, something is happening, that is, a yellowish/greenish thing comes out from the holes from each infecting area.
Do cockroaches lay eggs in human flesh when they "bite", and much more importantly, would hydroxide solution kill the eggs and parasites inside those of those holes?

I assume you mean peroxide solution (hydrogen peroxide); not hydroxide (e.g. sodium hydroxide, a strong base).

@NickT - Wow, how do you know?

Because hydroxide solutions are not usually for-sale unless you're looking in the plumbing aisle.

Whilst asking if cockroaches embed eggs in their bites is fine, I'm a little concerned that asking if hydrogen peroxide that I'm putting into the cockroach bite that I sustained is really on the edge of asking for medical advice, which is off topic.

No, cockroaches do not lay eggs into human flesh. You most likely received an infection of some sort from the bug, or it wasn't a cockroach.

the yellow/green liquid is probably pus


text:
Do humans emit more carbon through respiration or defecation?
Where does most of the carbon we ingest go? I understand that a large amount is exhaled as carbon dioxide, but what percent is defecated (and theoretically deposited in the ground)?

not sure why the question got downvotes, but realised 'excretion' probably wasn't the right word, so changed it to 'defecation' to be more clear - pooping or breathing, where does most of the carbon we ingest go?

You should use the term "bodily waste" or something else. The answer depends on the icountry, chaing the ratio by 100%, individual's diet and exercise habits in the sense of calories, and if you mean carbon which is converted to CO2 and methane after digestion. you can rephrase it as "do humans use more calories than they waste after digestion" .... rich countries eat nearly twice as many calories as they use, and other countries use 1 to 1.5 times as many... consider that average daily calories breathed out is about 2000:  https://en.wikipedia.org/wiki/List_of_countries_by_food_energy_intake

note that hot countries also have different characteristics.

The short answer
In a comparison between exhaled and faecal carbon, exhaled carbon wins.

The long answer
Warning: Assumptions, approximations and averages ahead.
Calculating faecal carbon excretion
The average human being produces about $29 \text{ g}$ faeces (dry weight) per day, the major component of which is bacteria [1]. For now, neglect variations with fibre and other dietary components. Also, assume that all of it is bacteria.
Now, carbon makes up about $50 \%$ of bacterial dry weight [2]. Thus daily carbon excretion in faeces is about $15 \text{ g}$.
Calculating carbon exhalation
An adult human being breathes about $20$ times a minute [3]. Each breath has a volume of about $500 \text{ mL}$ [4]. Thus the exhaled volume per day is $20 \times 60 \times 24 \times 500 \text{ mL} = 1.44 \times 10^7 \text{ mL}$.
Exhaled air is about $4 \%$ carbon dioxide [5]. The density of carbon dioxide at $37 \  ^{\circ} \text{C}$ and $1  \text{ bar}$ is $1.713 \text{ kg m}^{-3} = 1.713 \times 10 ^{-3} \text { g mL}^{-1}$ [6].
Hence, the mass of carbon dioxide exhaled per day is $0.04 \times \left(1.44 \times 10^7 \right) \times \left(1.713 \times 10^{-3} \right) \text{ g} \approx 987 \text{ g}$.
And since $\text{CO}_2$ is $\frac{12}{44}$ carbon, the mass of carbon exhaled per day comes out to be $\frac{12}{44} \times 987 \text{ g} = 269 \text{ g}$, which is at least an order of magnitude greater than the figure we got for faecal carbon.
References

Rose C, Parker A, Jefferson B, Cartmell E. The characterization of feces and urine: a review of the literature to inform advanced treatment technology. Crit Rev Environ Sci Technol. 2015 Sep 2;45(17):1827-1879. https://doi.org/10.1080/10643389.2014.1000761.

Lawford H, Rousseau J. Studies on nutrient requirements and cost-effective supplements for ethanol production by recombinant E. coli. Appl. Biochem. Biotechnol. 1996 Mar 1;57-58(1):307-326. https://doi.org/10.1007/BF02941710.

Hooker EA, O'Brien DJ, Danzl DF, Barefoot JA, Brown JE. Respiratory rates in emergency department patients. J Emerg Med. 1989;7(2):129‐132. https://doi.org/10.1016/0736-4679(89)90257-6.

https://en.m.wikipedia.org/wiki/Tidal_volume

https://www.bbc.co.uk/bitesize/guides/z9hycdm/revision/3

https://www.engineeringtoolbox.com/carbon-dioxide-density-specific-weight-temperature-pressure-d_2018.html

I didn’t like the question — who cares? But the answer is exemplary.

Sorry you didn't like the question, David. However, Adhish gave a very clear and simple answer, so the question can't have been that bad! Thankyou Adhish, that was great.

I also had no idea that bacteria make up the majority of faecal dry weight, that is fascinating


text:
Is there a known efficiency rate for CO2 capture from ambient air in photosynthesising plants?
When humans take in air to their lungs, we capture about 5% of the total quantity of the air as oxygen (which in turn equals about 24% of the available oxygen in the air)
Is there an equivalent rate for plants when photosynthesising (or a rate for any one specific plant?). I.e. if a plant had a given amount of air pass through their stomata, what percentage of the available CO2 is used by the chloroplasts?

Stomata should be compared to human alveoli, not the lungs. Also the lungs are pumps with heavy circulation whereas the plant heomoglobin is passive. The oxygen will tend to be carried by a metabolite whereas the CO2 can diffuse straight into the transportation medium, and the exchange depends on the gaseous gradient near the internal stomata surface.

I understand that trying to compare leaves/stomata to lungs/alveoli is problematic. However, I guess it would be possible to measure the amount of air that passes through a plant organism in a given period of time, and to measure the CO2 levels before and after in a sealed environment, and calculate from there? I guess there must be a lot more variables given it is a passive process in a non-homeostatic environment (like the lungs are) - but I maybe an efficiency range would still be possible?

I've started towards a way to figure it out - 1 litre of CO2 weighs 1.964g at NTP, and the amount of CO2 in one litre of air is about 0.04%. So one litre of NTP air contains 0.0007856g of CO2.

An adult tree (yes, very generic!) can take in about 21kg of CO2 per year, or 21,000 grams. 21000 / 0.0007856 = 26731160. So an adult tree must process at least 26 million litres of air a year (and that is assuming it is being 100% efficient!). Please let me know if I have done my calculations right


text:
How long to breathe (the equivalent of) all of the atmosphere?
I have done some rough calculations of how long it might take humanity: approx 80,000 years (that's taking Earth's population as 7.5 billion, 11,000 litres a day of breathing, the weight of 1 litre of air at sea level at 1.225 grams, and the total weight of the atmosphere at 5140 trillion tonnes)
Please let me know if my calculations are massively out!
My question for you is admittedly much more complicated to answer - how long would it take all animal species combined to breathe the equivalent sum total weight of the atmosphere? and how long would it take all life combined (also including the weight of air of respiration in plants, fungi, algae, etc)?

Volume is probably not the best way to think about respiration for most of life on Earth, as it only really applies to animals with lungs (a small proportion of earth's biomass). Instead, it would make more sense to think about rates of respiration in terms of oxygen demands. With that in mind, an average human needs around 0.85 kg of oxygen per day (according to NASA). So, the annual oxygen needs of the human population would found by multiplying 0.85 kg/person/day by 365.25 days/year and 7.5 billion people to get ~2.3e+12 kg of oxygen per year.
For a crude estimate of how long it would take to use up our atmosphere's oxygen at that rate, we could simply divide the total capacity of oxygen in the atmosphere (~1.4e+18 kg) by the annual oxygen demand of the current human population (2.3e+12 kg), to get a rough estimate of 600,000 years for Earth's current population to use up all of Earth's current atmospheric oxygen (note that both calculations require some pretty dubious assumptions, but the problem already seems to start that way if I'm reading it right).
For an even cruder estimate of all life on earth, we can again take the Atmospheric Oxygen capacity (~1.4e+18 kg) and divide by the annual oxygen flux from atmosphere to biosphere (~3.0e+14 kg) to get around ~4700 years. (note that this assumes no flux from the biosphere back into the atmosphere, and also assumes that lithospheric flux is negligible.)
If you want to go further and calculate how long it would take for just animals to use up an atmosphere worth of oxygen, you could start by looking at how Earth's biomass is distributed, and make some more assumptions about the oxygen demand of other animals compared to humans following this same idea that I've used above.
Capacity and Flux estimates came (via wikipedia) from (Walker JC (1980) "The Oxygen Cycle". The Natural Environment and the Biogeochemical Cycles), but there are probably more up-to-date estimates available somewhere. The general idea would be the same.

Thankyou for the answer @MikeyC, those numbers from the oxygen cycle wiki page are really interesting too. Our initial figures are closer than they seem... as I was calculating the total amount of air that passes in and out of our lungs, only approx. 5% of which is taken in as oxygen... which should make my number 20 times less than yours, not 10 times less, so I will check that when it comes to doing the math more thoroughly....

I've started towards a way to figure out an answer - 1 litre of CO2 weighs 1.964g at NTP, and the amount of CO2 in one litre of air is about 0.04%. So one litre of NTP air contains 0.0007856g of CO2.

An adult tree (yes, very generic!) can take in about 21kg of CO2 per year, or 21,000 grams. 21000 / 0.0007856 = 26731160. So an adult tree must process at least 26 million litres of air a year (and that is assuming it is being 100% efficient, which it won't be... humans take up about 5% of available oxygen that they breathe, not sure what the rate is for stomata...)

There are an estimated 3 trillion trees on Earth. 3 trillion x 26 million = 8.1*10^19 litres .... however, I now realise I had the atmosphere in the units of tonnes, not litres...

... So that would be 9.92 x 10^19 grams of air, or 9.92 x 10^13 tonnes of air. Which is about 100 trillion tonnes of air, if I have understood the conversions right

If we take a totally wild guess of 10% for the efficiency of CO2 uptake of the air in the stomata of trees, that would bring the figure to 1000 trillion tonnes. That would mean it would only take 5 years for all the trees on Earth to filter the equivalent of the whole atmosphere!


text:
Is the minicolumn the unit of the neocortex?
There are many arguments for what the unit of the neocortex is. "Columns" seem to be the standard, but what exactly those are is extremely contradictory between individuals, cortical regions, and species. Often times, when a column is referred to, it's actually a functional column without any anatomical borders (such as Hubel and Wiesels ocular dominance columns). Sometimes, the "column" is semi anatomical, such as the rat barrel cortex. Other times, these functional columns are confabulated into anatomical units, without any evidence for a border.
So my question is, could Mountcastle's "minicolumns" be the actual anatomical unit of the cortex? I've heard arguments that they are mere developmental relics. But they seem like the only reliable and consistent unit in the cortex.

I am skipping the background information (I will amend my question later) for now.
So, what is known about minicolumn?

The term was coined by Ramon y Cajal who saw narrow stripes, running from white matter to the surface (reference) in his preparation with Nissl staining.
The hypothesis about minicolumns to be anatomical units was proposed by Mountcastle in 1957, known as "columnar hypothesis" in neuroscience (reference).
It has been shown that minicolumns grow from progenitor cells within the embryo (reference), and don't require brain functions to emerge.
Minicolumns  contain neurons within multiple layers of the cortex (reference).
One of the latest review on the topic (Buxhoeveden & Casanova, 2001) contains 121 references to experimental papers on this topic.

I wouldn't say that these columns are developmental relic, for there is a known heterogenity among these structures (like hypercolumns, macrocolumns and segregates) and it is rather improbable that all these types are relics.
So, as long as we stick to the term "anatomical unit", I see no problems why columns (with all possible types and sizes of them) should not be it.

Thanks for the reply! Unfortunately it succumbs to the terminology confusion I mention in the question. The columns of Ramon y Cajal were the "minicolumns" of Mountcastle. Mountcastle's "column" was described as a bundle of minicolumns fused with dense horizontal projections., But evidence for actual anatomical borders on these "columns" is lacking. Same for ocular dominance columns, hypercolumns, macrocolumns, etc... Specifically, I am curious if the minicolumns, not columns, are developmental relics. In other words, is there evidence that minicolumns carry distinct functional significance?

@Preece I will amend my answer soon to address your question, sorry for a delay!


text:
Why do drugs which are hormones have long half-life?
Hormones normally have short half-life.
How is it possible that they have long-life in drugs?

Can you give a specific example? Water soluble hormones differ from non-soluble in their half life. Also, many drugs contain modified hormones (e.g. insuline analogs).

All I can say with the limited question is that steroid hormones can be very long lived - most others will degrade relatively quickly.

The question is a bit vague, but in general a drug formulation is made of the active principle plus a series of other non-active compounds call excipients.
Excipients have multiple roles such as:

They act as fillers to add volume to the drug. Often only very small amounts of the active compound are present in each pill/capsule/etc. and it would be complicated for the patient to handle these very small amounts.
They act as binders to keep everything together and avoid the pill to crumble.
They can modify the pharmacokinetics of the active principle by speeding up or slowing down its release.

(there are many more resons to add excipients, see the relevant Wikipedia page for a longer list)
This last point is what you are looking for. If the hormone (or any other molecule, it doesn't really matter) is complexed with excipients it will be released in the blood or metabolized slower/faster depending on the specific molecules/formulations/mode of administration.

@leonardo: that is a good point. The example of insulin is interesting as insulin has an half-life of ~5 minutes, but the commercial insulin formulations have a whole range of duration, even up to 24h. http://www.diabetesguidelines.com/health/dwk/pro/guidelines/ispad/09_02.asp