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Does all of life on Earth use the same DNA compounds for all species?
If an organism on Earth has got DNA, would it always have C,T,G,A?

I have left school 16 years ago and this question is not homework related. I had no idea how to approach googling this question. I like SE a lot and the answer I got here is great.

If an organism on Earth has got DNA, would it always have C,T,G,A?

Yes! All three domains of life (Archaea, Bacteria and Eukaryota) as well as all DNA viruses use these four same nucleotides.
Genetic code variations
There are however slight variations in the genetic code. In other words, there are variation in the meaning of a sequence of nucleotides and the corresponding protein sequence. See Alternative_genetic_codes.
RNA based life
There are also viruses (which you may and may not want to consider alive) that use RNA (and hence U instead of T) instead of DNA. See RNA virus.

Yes, there are no variations on this. There are 3 domains of life; Archaea, Bacteria and Eukaryota. All use these identical nucleotides. All use all four of them, and this is one of many lines of evidence for the single origin of life on Earth.

No, you can check out non-canonical bases on Wikipedia. I believe that most organisms, including E. coli and Homo sapiens have base modifications. In E. coli, the base modifications help them identify phage DNA and destroy it using restriction enzymes. In humans, many base modifications exist. A prominent modification, methylcytosine, can influence the state of chromatin and hence the expression of genes. Wikipedia mentions more obscure cases, e.g. a phage that has 2,6-diaminopurines instead of adenines.
I think that one should clarify the nomenclature in each context. I would envisage two cases:

a simplified case where base modifications are not considered, here methylcytosine = cytosine, methyladenine = adenine
a stricter case where modifications are considered, here methylC does not equal cytosine

Our simplified view of the reality of nucleotidic bases can be justified and explained by the limitations of current sequencing methods. It is impossible, as far as I know, for Illumina sequencers to differentiate modified from unmodified bases. Even sequencers like PacBio's Sequel or Oxford Nanopore's MinION that can detect modified bases can do so only at very high coverages and with some errors.

Methylation does not make nucleotides not "ACTG". I don't believe that was the question. AGCTs are in everything.

@KarlKjer, well I don't know the exact definition of 'ACTG'. That's a bit vague and it would be clearer to say 'adenine, cytosine, guanine, thymine' bases.


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How is the gradient in density gradient centrifugation made?
From the literature I read, I came to understand the following. Please correct me if wrong.

In CsCl gradient centrifugation, the gradient is achieved by centrifuging the CsCl solution at high rpm, which causes the heavy Cs ions to distribute unevenly throughout the solution, due to sheer centrifugal force.
In Sucrose gradient, solutions of decreasing concentrations of sucrose are layered one over the other slowly.

Why can't we achieve the sucrose gradient by simply centrifuging it like in the CsCl gradient?

Sucrose gradient separations are an example of a rate-zonal centrifugation technique (fair technical document on centirfugation separations). The idea is you layer lighter sucrose solutions on top of one another, for example, 35% at the bottom of the tube (the most dense zone) and 15% at the top band (the least dense zone). There might be 5 or 6 layers. You then layer the sample, which may contain cell lysate, at the very top.
This method is done on a centrifuge, and the idea is that in order to penetrate down to a more dense layer, the component of the lysate must exceed the density of the preceeding sucrose layer. Quite literally the dense components are pushing down through the sucrose layers. The method is suitable for organelles and proteins. The layering must be done deliberately and carefully, however, because the sucrose layers and sample will easily mix if they're disturbed. The same concept applies to ficol density gradient separations: If there's no density of solution below the sample for it to pass through, there's no separation.
On the other hand, the CsCl method is an example of an isopycnic centrifugation suitable for the separation of nucleic acids, see the above mentioned reference. This is because the DNA migrates to where the denisty of the DNA equals the density of the gradient, referred to as the neutral buoyancy or isopycnic point.

Thanks for the answer. But, if you have a solution of sucrose of a particular concentration and you centrifuge it at high rpm, would it be enough to form the density gradient like the CsCl, or is it necessary to layer solutions of varied concentrations and then centrifuge? Why exactly do we need solutions of different concentration unlike CsCl method where we use just one solution of CsCl of a specific concentration?

It's necessary to layer the sample on top of the sucrose solution. In the CsCl method the sample is in suspension and works on a different principle. If you suspend your sample in the sucrose solution, you won't accomplish anything. For example, if you want really dense things like organelles, you could put a single dense layer of sucrose under the sample and spin that, but you'd only obtain one fraction: The constituents with the highest density.

The principle behind the sucrose gradient is denser things push down from layer to layer until they're no longer dense enough to get through and end up as a band somewhere along the gradient, or pellet completely to the bottom.

So, if you mix them together and then spin, everything will just pellet to the bottom and you get no separation.

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By definition, will some children always be stunted?
I had a question about stunting i.e. height-for-age. The WHO defines at as any child whose height-for-age is 2 standard deviations below the median height-for-age.
Given this definition, wouldn't there always be stunted children? I must have misunderstood the definition because this seems like one of those challenges that needs to be "fixed" but my current understanding means its sort of unfixable.
Any insight is appreciated.

I'm voting to close this question as off-topic because it seems like its asking more about statistical/mathematical distributions vs biology.

You are correct, that under that definition; unless there were no variation (which would be impossible), there would always be individuals that fall below 2 standard deviations. However, "stunted" under this definition would not be a problem if variation was extremely low. So yes, it would be unfixable by definition, but if variation fell, then the "problem" would be fixed, because it would no longer be a problem.

I disagree with the last sentence. No matter what the actual distribution, there will always been extreme observations.

Karl Kjer: Many thanks for your answer! I think it encapsulates the trouble I am having with this but I think you may be pointing to an answer. Perhaps what WHO need to do is to add to the definition suggesting an SD cutoff after which this stops being relevant. That is, if the spread is much lower and most of the world's population are more tightly centered around a mean, then stunting stops being relevant as a public health challenge.

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How can i confirm that the given pedigree chart is of an autosomal dominant trait?

This image is from the NCERT textbook. In diagram A, which represents an autosomal dominant trait, I found out that autosomal recessive inheritance also satisfies the pedigree. Yet, the NCERT text book states that it is a dominant trait. How can that be? Is it because the dominant trait is more probable here? If so, how is that it is more probable in this case?

Sure, both are possible here!
Your book probably makes an implicit assumption of low frequency for the "red allele".
Assuming, "red" means "disease", it is quite standard to assume that the "red allele" is at low frequency in the population. If this is the case, then it is unlikely that partners of the members of the main family being represented in the tree carry this allele. It is therefore quite standard to assume that partners does not carry the "red allele". If this assumption is made, then recessive autosomal cannot explain the observed tree.

Both are possible here, as Remi.b stated.
It could be autosomal dominant, assuming that the first male in the pedigree is heterozygous for that trait (assuming that "red" means the trait). Since he is heterozygous, and the female is homozygous recessive, there is a 2:2 chance of their children getting that trait or not, which is actually shown!
So if the male is heterozygous recessive for autosomal dominant, and passed it on to 2 of his children, then those children that received that trait are also heterozgous, resulting in the person with that phenotype from the F2 generation.
Also the trait could be seen as autosomal recessive, as you had said, if the females in the parent generation and F1 are carriers.

how about X-linked dominant trait? It is also possible for this pedigree. So, how can is test which is more probable, autosomal dominant or X linked dominant?

If it was sex-linked dominant, the other female offspring would also be seen as having it.


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Is there a simple way to generate sets of sequences that re-capitulate the topology of pre-defined phylogenetic tree
I would like to generate ensembles of N sequences in such a way that the phylogenetic trees obtained from my ensembles (e.g., by neighbor joining) have the same (or nearly the same) topology as a specified "real" tree obtained from an alignment of N proteins.
My starting point would be an empirically determined amino acid substitution matrix. The matrix would be used to generate a "random" sequence representing the root of my simulated tree. The root sequence would then be evolved, "split", and its products evolved, iteratively until N sequences are generated. Somehow, the topology of the "real" tree would be used to guide the branching process.
This problem arises in determining the significance of correlations between mutations at different sites in a protein (specifically, the "mutual information" measure). One would like to determine the contribution of "pure phylogenetic" correlations to the mutual information for a given alignment of proteins.
The answer to my question seems connected to the "parametric bootstrap procedure" commonly used in phylogeny reconstruction. In fact, the reference below seems to use this procedure to generate the ensembles I describe above. However, their procedure is not explained in detail. This makes me think that there may be a simple answer to my question.
reference :
"Separation of phylogenetic and functional associations in biological sequences by using the parametric bootstrap"
K. R. Wollenberg and W. R. Atchley (2000) PNAS 97, 3288–3291

Yes, what you are looking for seems to be an alignment simulator, which is quite commonly used in phylogenetics. Given a phylogenetic tree and a substitution model, you can use for instance INDELible or DAWG to simulate the extant sequences (N sequences at the tips). These programs can also simulate the indel process (gaps), which means your final sequences won't have, by default, the same length -- but you can change the settings to exclude insertions/deletions.
There is no absolute guarantee that the tree estimated from the simulated sequences will follow the "true" one (used to simulate the sequences), but they should be close enough if:

you don't simulate gaps
the branch lengths are not too short
the sequences are large enough

Thanks Leo. I scanned through the INDELible paper and this seems to be exactly what I was looking for (e.g., calls for an equilibrated root node and a newick tree as input).


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What is a good biochemistry reference for reading papers about metabolic pathways associated with human disease?
I studied first and second year biology at university about 15 years ago, taking courses in cell biology, comparative physiology, microbiology, and human cell biology. I also took the supporting courses in organic chemistry, but I have never taken a formal biochemistry class.
Recently, a family member developed a rare cancer and we have been reading through journal papers in nutrition and medicine while trying to understand how diet plays a role. These make extensive reference to specific metabolic pathways in human cells -- some I am familiar with, but many which I am not. In all cases though, my cursory education in the pathways of metabolism and cell function feels inadequate.
So, what are some comprehensive biochemistry texts that can be used as a reference for reading papers in the nutritional and medical sciences?
I would prefer not to use a "concepts" book as one might find in a light version of a course. I am not a shy reader and am not daunted by the prospect of using a more comprehensive book as a learning vehicle, nor of having to do further backtracking to the world of organic chemistry when I encounter a class of molecules that deserves attention.
Lastly, I'm on a bit of a budget too. If you know of a book with a long lineage that is likely to be offered cheaply in previous editions, it would be of tremendous value.


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What are the total number of alleles for a single trait?
Humans receive a copy of gene from both parents and each gene has an alternative form called allele. Does every person possess two genes and four alleles for a single trait?

To fully answer your question it would take an entire course of molecular genetics and quantitative genetics. I will be only very brief and will let you seek for more information on your own.
Basics of molecular genetics
You are confounding gene copy and allele. As we are diploid, we have two copies (I am ignoring here sexual chromosomes and mtDNA) of every locus. This is true for genes too. We have two copies of each genes. Now, we may or may not have the same allele at these two copies. If we have the same allele at both copes, we are homozygous, otherwise we are heterozygous at this locus.

You might want to have a look at the post Do men and women have the same number of genes?

Now, each chromosome is made of two sister chromatids (although this number varies depending upon the stage of life cycle). The sequences at the two sister chromatids are exactly the same, so you can't have different alleles at two sister chromatids.

You might want to have a look at the post What is the relationship between DNA molecules and the chromosomes?

Basics of quantitative genetics
Of course, a single phenotypic trait is not necessarily mapped out by a single locus. There are usually plenty of loci involved (see Quantitative Trait Loci, epistasis and eventually pleiotropy). There is also other source of phenotypic variance than genetic variance such as environmental variance for example.

You might want to have a look at the post Why is a heritability coefficient not an index of how “genetic” something is?

Ok ,but I can't get your point .As there are two copies of one gene each from father and mother and we have an allele for every gene copy so, combining these we got two genes and four alleles .?Can we?

We receive one copy of every locus (or gene as you seem to get stuck with this term) from each parent. If these two copies differ, then we have two different alleles (heterozygous), otherwise we have only one type of allele (homozygous). In some life stage of the cell cycle, each chromosome is made of two identical chromatids. When this is the case, there are 4 copies of the gene but never more than two different alleles.
You really seem to use the term "allele" when "gene copy" should be used. Think of an allele as a pokemon card. When you ask someone "do you have Pikachu?", you're not asking whether the person has the exact same card that the one that is in your deck of cards. Alleles are the same! So even if you have 2 copies of a given locus (that is two pokemon cards), you might or might not have two different alleles.
You also use the term "gene" where it would be more correct (or more general) to say "locus". You should check out the definition of locus.

Ok ,but I can't get your point .As there are two copies of one gene each from father and mother and we have an allele for every gene copy so, combining these we got two genes and four alleles .?Can we?

@RabikJohn See edit

By two copies of gene you mean that there is a pair of alleles which we receive from our parents?Like in pea plant diploid cells have a pair of alleles for each gene Rr Yy or Tt?

I just insist to use the term gene copy and not allele because the two gene copies we receive might be the same allele. I feel like I am repeating the same thing over and over. I am sorry if it does not help.

Genes are sequences of DNA that do specific things (typically, that get encoded into proteins).
Chromosomes are long DNA strands that contain, well, DNA, and some sequences of that DNA are genes.
Those genes occur in specific places along the chromosome, just like the word "genes" occurs in specific places in this sentence (second and fourteenth word, namely), and if you copy-pasted this sentence they would be in the same places in the copy. This means two ways of recognizing the same gene in two copies of a chromosome are its sequence (which might not be identical if there are copying errors, but will be very close), and its location in the chromosome.
There is a bit of an ambiguity there; sometimes we use the word "gene" to refer to a literal sequence of DNA that forms a gene, but sometimes it refers to the more abstract concept of the same sequences that occur at the same locus in different people and do the same thing.
It's a bit like people can talk about "a Harry Potter book" and refer to the literal paper-and-ink book on their shelf, or they could be talking about the abstract stories in the Harry Potter series.
If you see a DNA sequence with ATCG and it's labeled as a "gene", it would be the first one. If people talk about "we've found the gene for Parkinson's", "how do we recognize the same gene in two copies of the chromosome", it will typically be the second one. And because the sequences aren't always identical you can have similar sequences of DNA, in the same place, that do basically the same thing, so they're "the same gene" in the abstract sense, but they do it differently from each other. Those can be thought of as variants of one another, and those variants are called "alleles".
In the Harry Potter analogy, alleles are like which of the six Harry Potter books we're talking about. So if you have two Harry Potter books in your library, The Philosopher's Stone and The Prisoner of Azkaban, you wouldn't count it up and say you have four books: the two Harry Potter books, and The Philosopher's Stone, and The Prisoner of Azkaban. You would understand that "Harry Potter books" is a general term that refers to a certain kind of books, that have enough in common that they can be considered "the same" in the sense of all being one series, and that this specific kind of books comes in six variants. You can't have "a Harry Potter book" that isn't also one of the six specific Harry Potter books that exist (I bet there are more now but let's ignore that for the analogy).
Also, if a person has on their bookshelf two copies of The Prisoner of Azkaban, do they have one Harry Potter book, or two Harry Potter books? It depends on whether we are talking in an abstract or a concrete sense. They have two literal paper-and-ink books on their shelf, but they have only one Harry Potter story.
Similarly, every person has two copies of a gene, i.e. a certain DNA sequence at a specific place, or "locus", on the chromosome, and if we're talking about literal DNA sequences we'd say they have two genes, but if we're talking about the more abstract concept we wouldn't say that. Usually when people talk about genes they're talking in the abstract sense, and thus talking about different sequences at different places on one chromosome, not copies of the same sequences in different chromosomes. Kind of like if someone asked you how many book series you own, you wouldn't count your paperback and hardcover copies of the same Harry Potter books as two series.
So to answer your question "Does everybody possess two genes" -> yes, for one sense of the word "gene", but it's not necessarily the one you meant.
As for the alleles, just like your two HP books aren't four just because they also have a specific title, people don't have four alleles because they have two copies of a gene and those copies are each a specific kind of that gene. People have one or two alleles, depending on whether the two copies they have for that locus are the same allele or two different ones.
By the way, it is not true that every gene has one variant called an allele (or, put in a better way, that every gene comes in two variants). Some genes don't vary much at all between people, so there's only one allele for the human race and everyone has the same one, while others have tons of alleles. But every person will only have one or two of those alleles, unless they have more than two chromosomes.

Thanks,I think I got it know .Are you trying to say that we have two copies of genes on every locus(of homologous chromosomes) but one gene can have homozygous allele or heterozygous allele so at one locus we can only have one allele so combining alleles of both locus we came up with just two alleles for two copies of genes ?

You are phrasing things in an unusual way so it's hard to tell! You say "two copies of a gene in every locus" as if "locus" is the abstract concept of a place on a chromosome, but then say "both locus" as if talking of the literal place on each copy of the chromosome. We have only one gene at each literal place on the chromosome where that gene is (just like you can have only one first word in a sentence), and because there are two copies of the chromosome that means two copies of the gene for each locus (where locus=abstract concept "that place on chromosome 2 where gene A is found").

@RabikJohn Also, a gene "having homozygous or heterozygous allele" is strange phrasing because "heterozygous"/"homozygous" isn't about the gene. Like a sock in a drawer isn't "matched" or "mismatched"; it's a person wearing a pair of socks, and them being the same or not, that makes that pair matched or mismatched for this person. A gene has alleles, i.e. variant forms it exists in. People have two copies of the gene, each in one of those variant forms. If the two copies are the same variant(allele) the person is homozygous for that gene; if the two copies are different, they are heterozygous.

I confused you because I was confused myself about itI don't know what does actually mean to have two copies of genes on homologous chromosomes? I always think it might be like that one locus on mothers chromosome will have a gene and father's chromosome will have the same gene on same locus but with different alleles and when they combine to form homologous chromosomes then we will have two copies of genes for every locus  but I can never understand how does two homologous chromosomes with two different alleles (as ithink they have) express a single trait ?

@RabikJohn The way genes express traits is very complicated, and not really about chromosomes. Chromosomes are about packaging the DNA so that it can be duplicated in reproduction. Outside of reproduction DNA is transcribed into proteins, which do everything in the body. This transcription has several intermediate steps, which can involve "amplifying" genes (making many copies to make more proteins), silencing them, etc. So what it means to have two alleles depends on the genes and traits involved. Sometimes if you have two alleles means you have two types of a certain protein.

If we  have more than two alleles for a single trait then the protein product produced depends on both alleles or an intermediate protein product is formed ?And can you tell me something about location of genes on homologous chromosomes?

@RabikJohn With "more than two alleles for a single trait" do you mean "more than two genes" (i.e. the trait is affected by many sequences at many places on one or more chromosomes; any of these sequences can have variants that are different or not on the homologous chromosome)? Because again, no human has more than two alleles of a gene, unless they have more than two copies of a chromosome. If you are heterozygous for a gene I think the typical case is for both proteins to be produced; for example the sickle-cell gene, heterozygous carriers have both normal and abnormal red blood cells.

Yes ,by more than two alleles I mean two genes,As there can be only two alleles for a single trait so these two alleles can be different on homologous chromosomes as( I think you are saying) then these two "alleles" are present on "homologous chromosomes" I mean to say one gene is present on one chromosome out of homologous chromosomes or an allele is present ?


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What kind of lichen is it?
I found that in a monastery garden in Czech Republic this winter. I tried to search it on the internet but unfortunately I didn't find it.

I'm pretty sure that it is a cup lichen from the genus Cladonia. A probable species is Cladonia pyxidata, which is relatively common across Europe. My lichen knowlegde is rusty though, and Cladonia is rather species rich with several species that are relatively similar.

(C. pyxidata, pic from http://fungi.myspecies.info/taxonomy/term/4557/media)

Cladonia is right for sure. Pyxidata I doubt. Impossible to be sure from a picture anyway.

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Can polystyrene sulfonate bind calcium or sodium in the gut? How?
Polystyrene sulfonate is used as a potassium binder to treat hyperkalemia in traumatic rhabdomyolysis, acute and chronic kidney disease. It is listed as an ion-exchange resin that can also remove sodium or calcium from solution, but is also available in sodium salt or calcium salt form. How might this work?

Are you talking about Sodium Polystyrene Sulphonate (a.k.a SPS)?
If yes, then ...
Quoting from Chaitman, Dixit and Bridgeman (2016)

Synthetic cation-exchange resins are insoluble polymers resembling a crystalline lattice. When placed in a solvent, this structure swells, allowing the exchange of ions between the reactive group on the resin (in the case of SPS, sodium) and ions dissolved in the solvent.

However, other cations like sodium and calcium ions can bind too.
As SPS moves through the intestine, sodium ions are released and exchanged for potassium ions.

References
Chaitman M, Dixit D, Bridgeman MB. Potassium-Binding Agents for the Clinical Management of Hyperkalemia. Pharmacy and Therapeutics. 2016;41(1):43-50.

Welcome to Biology SE! Please clearly attribute the sources you used if you are quoting from somewhere else. Your sentence starting "Synthetic cation exchange...in the solvent" appears to be taken verbatim from https://www.ptcommunity.com/journal/article/full/2016/1/43/potassium-binding-agents-clinical-management-hyperkalemia.

I am really sorry! I am pretty new to this!
Well it is from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4699486/


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Twins reproducing with each other ( just hypothetical)
If 2 twins (look exactly the same and also the genes which control their morphology, behaviour etc. are same and present at the same locus) produce an offspring , will their offspring be exact copy of their parents ?
Sorry . I know its not moral.

Aside from the fact that identical twins have the same gender and thus cannot reproduce, even if we ignored that issue the offspring would not necessarily be identical to their parents, because people are diploid (have two copies of each gene) and meiosis shuffles genes up somewhat. So for example if the twins are heterozygous for a gene (their two copies are different), with one copy being allele A and the other b, their offspring could be Ab (like their parents), or AA or bb (unlike their parents).
If the twins are monozygous for every gene then their children would indeed be genetically identical to their parents, stray mutations aside. That's what happens with some laboratory animals, that are inbred to the point they are pretty much all genetically identical, and they are monozygous for almost everything.

...and inbred individuals may suffer from inbreeding depression. There are several potential reasons for such inbreeding depression including the fact that deleterious alleles tend to be slightly recessive (see Evolution of dominance of alleles)

Monozygotic twins won't be able to reproduce (naturally), because they are of the same sex. Dizygotic twins may or may not be of the same sex, just as regular siblings; genetically speaking, they are just siblings, not twins, so this case is out of the scope of your question.

@SaraswatiSharma If you consider this answer answered your question, you can click on the checkmark next to the answer to mark the post as being answered.


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Did Darwin explain why he believed that domestic dogs descend from several distinct species of ancestor?
Charles Darwin begins his book Origin of the Species (1859), in which he argues that species evolve as a result of variations caused by natural selection, with a chapter about variations that have occurred not naturally but under domestication. There he writes

I may, without here entering on any details, state that, from
  geographical and other considerations, I think it highly probable that
  our domestic dogs have descended from several wild species.

The ancestry of the subspecies Canis lupus familiaris is a controversial topic, but I have not found any papers which argue that it descends from several wild species. When the view is that the subspecies descends from two separately domesticated strands of ancestral wolf - East Eurasian and West Eurasian - the strands are not, as far as I am aware, referred to as separate species, but even if they were, two is not "several".
I appreciate that in a book on natural selection Darwin does not wish to spend more than a chapter on selection under domestication, but does he explain elsewhere his detailed reasons for his conclusion?

"Does (Darwin) explain elsewhere his detailed reasons for his conclusion?"
Yes. After Origin of the Species, he wrote a whole book, The Variation of Animals and Plants under Domestication (1868), which begins with Chapter 1.I on "Domestic Dogs and Cats".
He writes that "we shall probably never be able to ascertain their origin with certainty" and then gives detailed sources for both sides of the argument. It's Pallas against De Blainville.

Firstly, the great difference between the several breeds; but this
  will appear of comparatively little weight, after we shall have seen
  how great are the differences between the several races of various
  domesticated animals which certainly have descended from a single
  parent-form. Secondly, the more important fact, that, at the most
  anciently known historical periods, several breeds of the dog existed,
  very unlike each other, and closely resembling or identical with
  breeds still alive (...)
(A)t a period between four and five thousand years
  ago, various breeds, viz. pariah dogs, greyhounds, common hounds,
  mastiffs, house-dogs, lapdogs, and turnspits, existed, more or less
  closely resembling our present breeds (...)
As long as man was believed to have existed on this earth only about
  6000 years, this fact of the great diversity of the breeds at so early
  a period was an argument of much weight that they had proceeded from
  several wild sources, for there would not have been sufficient time
  for their divergence and modification. But now that we know, from the
  discovery of flint tools embedded with the remains of extinct animals
  in districts which have since undergone great geographical changes,
  that man has existed for an incomparably longer period, and bearing in
  mind that the most barbarous nations possess domestic dogs, the
  argument from insufficient time falls away greatly in value (...)
The existence of a single race, remarkably constant in form during the
  whole Neolithic period, is an interesting fact in contrast with what
  we see of the changes which the races underwent during the period of
  the successive Egyptian monuments, and in contrast with our existing
  dogs. The character of this animal during the Neolithic period, as
  given by Rutimeyer, supports De Blainville's view that our varieties
  have descended from an unknown and extinct form.

At this point it's not looking good for Pallas. But Darwin continues:

(W)e should not forget that we know nothing with respect to the
  antiquity of man in the warmer parts of the world. The succession of
  the different kinds of dogs in Switzerland and Denmark is thought to
  be due to the immigration of conquering tribes bringing with them
  their dogs; and this view accords with the belief that different wild
  canine animals were domesticated in different regions (...)
The main argument in favour of the several breeds of the dog being the
  descendants of distinct wild stocks, is their resemblance in various
  countries to distinct species still existing there.

Moreover,

(s)everal canine species evince no strong repugnance or
  inability to breed under confinement; and the incapacity to breed
  under confinement is one of the commonest bars to domestication.
  Lastly, savages set the highest value (...) on dogs: even half-tamed
  animals are highly useful to
  them: the Indians of North America cross their half-wild dogs with
  wolves, and thus render them even wilder than before, but bolder: the
  savages of Guiana catch and partially tame and use the whelps of two
  wild species of Canis, as do the savages of Australia those of the
  wild Dingo. Mr. Philip King informs me that he once trained a wild
  Dingo puppy to drive cattle, and found it very useful. From these
  several considerations we see that there is no difficulty in believing
  that man might have domesticated various canine species in different
  countries. It would indeed have been a strange fact if one species
  alone had been domesticated throughout the world (...)
If any wild canine species had distinctly exhibited the tan-coloured
  spots over the eyes, it might have been argued that this was the
  parent-form of nearly all our domestic races. But after looking at
  many coloured plates, and through the whole collection of skins in the
  British Museum, I can find no species thus marked. It is no doubt
  possible that some extinct species was thus coloured (...)
The belief that our dogs are descended from wolves, jackals, South
  American Canidae, and other species, suggests a far more important
  difficulty. These animals in their undomesticated state, judging from
  a widely-spread analogy, would have been in some degree sterile if
  intercrossed; and such sterility will be admitted as almost certain by
  all those who believe that the lessened fertility of crossed forms is
  an infallible criterion of specific distinctness. Anyhow these animals
  keep distinct in the countries which they inhabit in common. On the
  other hand, all domestic dogs, which are here supposed to be descended
  from several distinct species, are, as far as is known, mutually
  fertile together (...)
Pallas assumes (...) that a long course of domestication eliminates that
  sterility which the parent-species would have exhibited if only lately
  captured; no distinct facts are recorded in support of this
  hypothesis; but the evidence seems to me so strong (independently of
  the evidence derived from other domesticated animals) in favour of our
  domestic dogs having descended from several wild stocks, that I am
  inclined to admit the truth of this hypothesis.
There is another and closely allied difficulty consequent on the
  doctrine of the descent of our domestic dogs from several wild
  species, namely, that they do not seem to be perfectly fertile with
  their supposed parents. But the experiment has not been quite fairly
  tried; the Hungarian dog, for instance, which in external appearance
  so closely resembles the European wolf, ought to be crossed with this
  wolf: and the pariah dogs of India with Indian wolves and jackals; and
  so in other cases. That the sterility is very slight between certain
  dogs and wolves and other Canidae is shown by savages taking the
  trouble to cross them.

Concluding:

Notwithstanding the difficulties in regard to fertility given in the
  last two paragraphs, when we reflect on the inherent improbability of
  man having domesticated throughout the world one single species alone
  of so widely distributed, so easily tamed, and so useful a group as
  the Canidae; when we reflect on the extreme antiquity of the different
  breeds; and especially when we reflect on the close similarity, both
  in external structure and habits, between the domestic dogs of various
  countries and the wild species still inhabiting these same countries,
  the balance of evidence is strongly in favour of the multiple origin
  of our dogs.

In short the main support for multispecific origin is that different breeds of the domestic dog, differing from each other in many physical respects, are very ancient and they are similar to wild species in the same geographical areas.

It seems that this was based on arguments in 1780 by Pyotr Simon Pallas that most domestic animals had descended from two or more aboriginal species that had since become mixed by interbreeding. Here's a brief summary in a letter Darwin wrote to Charles Lyell:

The doctrine of Pallas applied to our domestic breeds, we will say to Dogs, is as follows. He believes that man tamed a wolf in one country, the jackall in another, the fox in another & so on with other species. He does not suppose that these wild species were more variable than others. He hypothetically supposes that when long domesticated they lose their tendency to sterility when crossed with the other domesticated species; & by their crossing when domesticated he believes that all our domestic races have originated. He or his followers further believe that the crossing gives as a tendency to new characters to arise, & this is not a little hypothetical. The whole doctrine is very hypothetical. Yet I certainly believe (but cannot here give reasons) that the American domestic dogs have descended from at least 3 or 4 aboriginally distinct species, & that European dogs probably from several other species. There truly is, as you say, “an uncomfortable vague-ness” in whole doctrine.

--Letter to Charles Lyell, 25 October 1859
Lyell argues with Darwin on this in several letters, e.g. here and here.
Another letter shows a little more of his thinking:

By my theory, all dogs, wolves, foxes, jackalls, &c. have descended from some one very ancient species. The passage you allude to refers only to the amount of modification which our domestic dogs have undergone under domestication. I do not believe that the whole amount of difference in domestic dogs has been produced under domestication, but that part of difference is due to their having descended from several wild species. It is a distinct question whether these wild species have descended from one aboriginal stock as I believe has been the case.

--Letter to Caroline Sarah Wedgwood, after 21 November 1859
I don't know anything about Pallas, and as far as a cursory search shows me, he didn't write in English, so I can't say more about Pallas's reasoning. It seems that Darwin's argument for multiple origins boiled down to his gut feeling that dogs are too variable to have originated from a single species, but he readily admits that this isn't a strong argument, and seems reluctant to strongly defend it.

Thanks for this. "(Pallas's) whole doctrine is very hypothetical. Yet I certainly believe (but cannot here give reasons) (...)" leaves it open as to whether he thought he had a strong intellectual argument or was going by gut feeling. I wonder what his personal involvement was with dogs. It's known he studied and bred pigeons, became very knowledgeable about their variation, and discussed them with expert breeders

"I most heartily subscribe to what you say about the qualities of Dogs: I have one whom I love with all my heart." --Darwin, to unknown recipient

I wonder what the "rather old book" was that Darwin's unknown correspondent had referred to.


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Why can we sniff so much?
What was the point for us humans (or other mammals) to develop such a strong sense of smell? Depending on the source, we can distingiush from 10.000 to even trillions of smells. But how was the ability to sniff "artificial" smells (e.g. paint or burning rubber) being useful to our ancestors?

While the question combines a few points, an answer may be far from trivial (e.g.: when also considering the recent reduction in some animals such as humans, https://en.wikipedia.org/wiki/Evolution_of_olfaction#The_Olfaction_Tradeoff  , or considering the ancient non-olfactory role of olfactory receptors within early mammalian embryogenesis found by Dejosez et al. Science 2013, http://science.sciencemag.org/content/341/6153/1511 )

Smell samples the chemical composition of the environment, the groups of molecules you are sampling in those examples still exist in nature. It is like asking why being able to taste pizza would evolve, it doesn't, not by itself anyway, it is the inevitable result of being able to taste the things and conditions that make up pizza, carbohydrates, proteins, fats, oils, acids, bases, salts, etc. things that would be important for our ancestors to be able to detect.
With paint you are smelling volatile organic compounds, and many are important biological and/or hazard markers, some are related to rotting meat, others to infection, others to food sources, and others to natural toxic water sources. With burning rubber you have many different smell depending on the rubber, but in each case you are smelling a burning organic polymer which releases organic compounds which again would exist in nature.


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How long does it take for DNA to degrade
Can i still use 3-4 years old bacterial DNA template for my PCR? They were kept in -20 all this while. Will the DNA degrade?

Degradation of DNA is gradual, but continuous, even in the freezer. However, they can sequence DNA from ancient animals in permafrost, or Neanderthal teeth. Fresh is always best, but there is no reason not to try PCR on your samples.

Yes, 3-4 years at -20ºC should be fine. I have never had any problem with plasmids stored this long (or even longer). Shorter and linear DNA fragments might be a bit less stable.

Not only can one sequence DNA from permafrost, but it can remain sufficiently intact to produce a living plant after 30,000 years.


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Please Help Identify These Bugs
I live in KwaZulu-Natal, South Africa, and the only indoor bugs I've experienced issues with are fleas, as I have two cats (and a big garden). This morning, however, I put on a fleece top that had been lying around somewhere, got a lift to the store, and returned to suddenly feel a crawling sensation. I lifted up my shirt to find these tiny bugs crawling all over my upper body. I did some Googling, went upstairs and carefully observed my bedding and bed, however, the only evidence I found was a few newborn fleas / flea larvae (which I intend to deal with today). I should also mention that a flock of wild Egyptian Geese have been raising five goslings in my yard, and they get very close to me when I'm walking outside at times. My house is also not carpeted, it has oregon pine floors throughout. I tried to take a photo of the critters, however, they're very tiny and move very quickly, so it was difficult to get a clear shot. Any advice would be greatly appreciated.

How do they differ from the fleas you have?

They aren't fleas. The fleas look like fleas and jump around. These are very tiny, appear to look quite different to fleas, and crawl only. I did some Googling, and the closet thing I have found that looks similar is Book Lice.

Definitely look like book lice (psocoptera) to me. We already have a handful of quesions regarding these: see here, here, and here

Yes, this is a book louse (order Psocoptera). They feed on all kinds of organic matter, and are very common. Fun fact - they are called "book lice" because they are often associated with old books, feeding on the organic glues in the bindings. (they are also called bark lice - I'm sure you'd know why).


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How should I interpret for example AA result, when SNPedia only has CC/CT/TT listed?
I don't know how to properly formulate this question because I'm new to this, so please edit this if you can...
For example when I would check SNPedia for rs gene, it would have listed CC/CT/TT genes, but my result says AA, so how should I interpret this? I assume it has not been tested, but I want to know for sure, because I have encountered this numerous times already...

You'll need to learn about DNA strand orientation: https://www.snpedia.com/index.php/Orientation

Ah! Thank you! I'm just a beginner at these things. :)


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Laemmli-SDS-PAGE problems
I did Laemmli-SDS-PAGE for my Ammonium sulphate precipitate but I had very weak band and have very weird part at the end of gel. Please help me to solve that problem. Thanks

Did you remove the ammonium sulfate by dialysis or similar?

No, I did not. I precipitated by AS and used PBS to dissolve, added buffer and loaded on gel

Your gel looks just fine to me. It simply indicates that your ammonium sulfate precipitate contains massive amounts of this small protein at the bottom (whatever this is). The upper bands look fine, the amount loaded is appropriate: they are not overloaded like the bottom one, but not too faint either. The fact that your first and last lanes look a bit smeary is because of the massive amount of the small protein (lanes do look smeary when overloaded this much). The bottom band is definitely really some protein, and not a staining artifact; I have seen this shape before with purified proteins overloaded on SDS-PAGE.
One thing you could do, assuming you still have enough of these samples, is to run a complementary gel with 100 times less material. Dilute by a factor of 1/100 in 1X Laemmli denaturation buffer, and load a new gel with the same volume as for this one. You won't see the upper bands anymore, but you will have a much cleaner bottom band that you will hopefully be able to assign an apparent molecular weight to (or even cut out for mass spec identification; wear gloves and use clean tools if you do that, otherwise they will mostly detect keratin from your skin).
Assuming the point of this gel was to check the outcome of ammonium sulfate precipitation used as a purification step, well obviously it didn't work well to separate all these bands, and you might need to repeat and try different concentrations. But if the bottom band is the one you are trying to purify, then you were successful (the top bands represent less than 10% contamination, I would say by eyeball estimation). If you're interested in one of the top bands, then it clearly didn't work.
Is one of these lanes the supernatant? If so, you also have massive amounts of the small protein there (it's in every lane). Such a high enrichment looks suspicious: could that be purified lysozyme that you added during the purification procedure to help break down bacterial cell wall? (assuming you're trying to purify a protein over-expressed in E. coli).

Thanks you for your respond. I would like to determine the molecular weight of the bottom band, because when I overlaid the half of gel with pathogens, the place of inhibition zone is the bottom of the gel (the second lane, beside ladder) . I will try to dilute the buffer as you suggest. Thanks

OK, so if you're interested in the bottom band you can definitely dilute (I suggested by 1/100, but you might need to try a few different dilution factors until you get a reasonable band). You can also use a denser gel, to make this band migrate slower (in this gel, it looks like this band is in the migration front). What was the percentage of this gel? Also, if the answer helped you, please mark it as accepted. :-)

Hi, I tried to dilute it to several different dilutions but it was not different as before, I did not get a reasonable band. The percentage of this gel is 4- 20%. I think maybe the size of this compound is smaller 11KDa (because I used Color Protein Standard marker, 11-245 KDa) or this compound is not protein, like lipid


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How can autoimmunity be selective?
Vitiligo is a skin disorder where the pigment disappears. More on Wikipedia. This is believed to be caused by autoimmunity and has made me interested in autoimmunity in general.  I am still very much a layman, however.
One of the characteristics of vitiligo is that it is uneven. Some patches of skin look normal, others are completely albino-like.
If the immune system has decided that skin pigment is an enemy, why doesn't it destroy all the skin pigment?
I understand that little is known about vitiligo, so I will accept answers describing similar effects in other autoimmune disorders.

Your supposition is incorrect, the immune system does not destroy pigment


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How has the theory of evolution changed over time?
I learned at school and in the documentaries like everybody that (to summarize) molluscs evolved into fishes then reptiles then mammals then humans.
Does the theory still make the same claim ? or does neo darwinism only defends speciation where for example all camelidae are related and all felidae are related, but both aren't related.
If not, why the famous evolution trees never identify any of the supposed common ancestors ?

Comments are not for extended discussion; this conversation has been moved to chat.

How has the theory of evolution changed over time?

It improved quite a bit. To put things in perspective; today most of evolutionary biology is about evolutionary genetics while at Darwin time (On the Origin Of Species was published in 1859), we really had no idea about DNA (the basic structure of DNA was only discovered in the 1950s).
A number of the original claims were found to be wrong though (or off-topic). We've added much more than we've removed though!

I learned at school and in the documentaries like everybody that (to summarize) molluscs evolved into fishes then reptiles then mammals then humans.
  Does the theory still make the same claim ?

This claim is not correct (and has never been) or at least is very misleading. I hope your teacher did not really tell you that!

or does neo darwinism only defends speciation where for example all camelidae are related and all felidae are related, but both aren't related

Nope, this would be even more wrong!
Among all extant species today, none are ancestors of others. They all share a common ancestor though. The common ancestor between a lynx and cat lived more recently than the common ancestor between a lynx and an oak tree.
Also, the claim put an emphasis on humans, which sounds like you viewing some kind of goal to evolution or eventually some kind of 'improvement' where humans would be the best or something like that. That notion of good or better is not just wrong, it is off-topic in any scientific discussion.
Some of the clades you mention contain other mentioned clade (for example, humans are mammals), however 1) fish is not a clade (not monophyletic, see this post for an intro to phylogeny) 2) ancestors of mammals have never been mollusc 3) note that the term reptile you use can take two different definitions; a popular meaning and a rigorous scientific meaning (which we use called Reptilia) (have a look at the post If dinosaurs could have feathers, would they still be reptiles?). In any case, no ancestors of mammals were reptiles (although mammals are Reptiliomorphia).

If not, why the famous evolution trees never identify any of the supposed common ancestors ?

I don't really understand this question.
We are able to date pretty well the common ancestors of most lineage of interest through molecular tools. We have a lot of fossil records which, when dated, match our finding with molecular tools. Note that the one most recent common ancestor between two lineages is a single individual (although recombination makes this point more complicated but I won't talk about that here). Of course, we probably never have a fossil of this single individual, but we often have fossils of individuals that are quite closely related to this individual.

You seem to have an extremely biased view of the theory of evolution. I am sorry if your teacher taught you so wrong. The best for you is to simply start with an intro course such as Evo101 for example. Evo101 is short, very introductory and easy to read.

There's also a problem with "famous evolution trees", in that we don't know what the OP considers "famous".  Lots do show common ancestors, though it's hard to show millions of species on a piece of paper.  Here's one site (of many) that attempts to do it: http://www.onezoom.org/  And another: http://www.sciencemag.org/sites/default/files/styles/article_main_large/public/images/sn-treeoflife.jpg?itok=AXS5irW-

@user2534 Comments are not for extended discussion. Asking for evidence of speciation has nothing to do with the main point of the post to start with. You should have a look at this post and probably this one too.

Comments are not for extended discussion; this conversation has been moved to chat.


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What are the applications of predicting the structure of proteins?
Protein molecules are very important as they are used for catalyzing almost all the chemical reactions in the cell, regulation of gene activity and provide cellular structure.
However, in predicting the structure of protein I haven't been able to find many use cases. In the omicsonline I was able to find a paper on Computational Methods for Protein Structure Prediction and Its Application in Drug Design:

Most modern drug discovery projects start with protein target identification and verification to obtain a verified drug target. For structure-based drug design the three-dimensional structure of the protein needs to be determined experimentally by using either x-ray crystallography or nuclear magnetic resonance (NMR) spectroscopy.

Therefore, since proteins are vital for maintaining the body are there any other use causes for predicting the structure?

Just off the top of my head, protein structure is very important for determining how proteins interact, for example determining molecular pathways or viral capsid structures. Knowing the structure of a protein can help scientists better understand what it does and how it does it. By looking at protein structures, scientists can determine exactly how a different allele for a gene causes changes in an organism's phenotype at a biochemical level. Predicting sites within a protein's structure that have an enzymatic function allows scientists to predict how various factors effect it's function. Differences in temperature or pH can have an effect on protein structure as well, and understanding how a proteins changes based on pH or temperature changes can help scientists determine how a protein functions in its specific environment.

To answer your question specifically in the context of drug design: it would of course be great if we could rely on protein structure prediction for drug design, but structure prediction is still not completely accurate. Drug design projects are expensive, so it is often wiser to spend the money on experimental structure determination first, because it will provide a more reliable basis for structure-guided drug design (the alternative would be to spend the money on more failed attempts at designing a good drug, because these attempts are guided by an inaccurate predicted structure).
Also, experimental structure determination is valuable for prediction, because it increases the library of known structures for homology modeling.

protein structure prediction is still in its infancy hence the lack of examples, the benefits are immense however, in proteins structure = function, and as you said proteins catalyze or make up nearly everything in body. We can find out the structure unreliably but predicting the structure would allow us to build proteins to order becasue predicting the structure from sequence means predicting protein folding, which is in many way the holy grail of modern biology. Being able to do it reliably and with more complex proteins would allow us to construct proteins to performs specific tasks instead of hoping to stumble across one that does it then just copying it.


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What is the difference between how motor function is controlled in cerebrum vs frontal lobe?
At least according to wikipedia, the frontal lobe houses the primary motor cortex, but in a different article about the cerebellum, it says the cerebellum controls motor function. So, do both parts control voluntary movement at once? What's the difference in the roles these two parts play in movement?
https://en.wikipedia.org/wiki/Cerebellum
https://en.wikipedia.org/wiki/Frontal_lobe

The motor cortex, basal ganglia, and cerebellum all contribute to motor control.
Cortex stores movement memory, basal ganglia is responsible for "chunking", or segmenting the memory, and cerebellum compares cortex memory and current movement to correct for errors and to update perception of movement. So to answer your question they all control different components/processes of learned movements at the same time and in conjunction.


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Ratio of oxygen produced / consumed by plants
Related questions:
How long can a plant generate oxygen from its own carbon dioxide, produced during nighttime?
Are plants actual oxygen factories?
But the actual question I'm interested in is:
What is the ratio of oxygen produced during the day vs. consumed at night.
Even ballpark numbers are sufficient, as this came up in a conversation about a Mars colony game where a tree produced 2 units of oxygen during the day and consumed 1 at night (with the game-night being half the length of a game-day because...reasons). Colonists would then need about 1 to 1.5 oxygen per full day/night cycle.
My friend and I were like "this ratio does not sound right" and haven't been able to find any any decent numbers to back up our opinion...or refute it.
Obviously the chemical reactions involved are mirrors of each other, and the output depends on the amount of light, and so forth...But wouldn't trees just be...less active at night in order to conserve energy, while more active during the day?

define plant, the answer is vastly different for cacti, trees, grass, or algae.

@John Given the context of what my friend and I were discussing: Trees. If you want more specific than that, I don't honestly care, pick one.

well it depends on what your colony is using, algae is the best at producing oxygen, about 1.9grams per cubic meter of algae , https://www.sciencedirect.com/science/article/pii/0043135488901054

@John 1.92g is a net value. For all I know it could produce 1g per hour of daylight and consume 0.84g per hour of nighttime for a ratio of 1.2:1. Or it might be that it produces 0.2g per hour of sunlight and consumes 0.04g per hour of night for a ratio of 5:1, that's the number I'm interested in.

This quoestion may help you , https://biology.stackexchange.com/questions/58238/how-much-oxygen-does-a-plant-use-up-at-night

@John Hmm. So that does make it seem like half (2:1) is the right number. The paper linked in the answer is about something else, but that statement is part of the conclusion.


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The 4-chambered heart
Birds and humans have a four chambered heart. All animals having 4-chambered hearts are warm-blooded.
Why are crocodiles an exception? Why are they cold-blooded even though they have a 4-chambered heart?

https://news.ucsc.edu/2014/12/crocodile-genomes.html

So, the slow evolving genome is the reason...

The short answer is crocodiles may be secondarily cold blooded, but the long answer is warm blooded and cold blooded is not a binary condition but a spectrum.
It has to do with how much heat you generate with your own tissue as all organisms generate some heat and gain some from the environment when they can. on one end you have extreme ectotherms (some insects) at the other extreme endotherms (such as arctic mammals) and a huge range between them covering nearly every level of metabolic activty. The ancestors of crocodiles (Crocodylomorpha) were terriestial and highly active and was thus likely near the warm blooded end of the spectrum and thus with a four chambered heart. They actually look like what you would get if you tried to turn a crocodile into a wolf.  But it is believed that as the line that led to modern crocodiles adapted more for an aquatic environment they switched back to a more ancestral metabolism. Although  I should mention crocodiles and esspecally alligators are capable of producing considerable metabolic heat and activity even for prolonged period, more than other "reptiles", comparable to slowest metabolism mammals. they kep many anatomical adaptation to a higher metabolism as they also aid in diving and still benefit their higher metabolisms.

https://www.livescience.com/51162-dinosaurs-warm-blooded-growth-rates.html interestingly enough there's some evidence that dinosaurs may have been in the middle of the spectrum

If by in the middle you mean the same as mammals. Also growth rings have been shown to be really poor indicators as they can be caused by all kinds of things.


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need to identify species of this Leaf-footed bug?
I found this bug in Pune/India. I checked many species of leaf-footed bugs, but none of them is matching this one. It was about 3cm long. It was not showing any movement.

looks similar to some Leptoglossus species -- not sure if that genus is in India or not...

I think you are right, can you identify species?? @theforestecologist


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What are the small lumps in the mouth of the fish, and what is its function?

Today I was performing a fish head dissection to investigate the gas exchange process in biology. Then when I opened the mouth I noticed these small hard structures at the base, I assume they may be a form of teeth that allows the fish to grind hard shells of invertebrates and plant matter. Yet I was curious as to why some fish have this and others don't and what exactly it's function is. Also if you have a name I would highly appreciate it as I can label it in my lab book. Thank you so much for your time.

Yes those are teeth and some have them and some do not for the same reason some have sharp teeth wile others have flat scrapper teeth, it depends on their diet.
this kind of teeth are called molariform, and are used for crushing shellfish more than anything else. This slide show will help you, https://www.ru.ac.za/media/rhodesuniversity/content/ichthyology/documents/Anatomy%20Lecture%207.pdf


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Endomembrane system
I learned that the endomembrane system includes the nuclear membrane, ER, the golgi, lysosome, endosomes etc. But why doesn't it include the mitochondria and the chloroplast?

Another clue in favour of the Endosymbiotic theory? For instance Mitochondria having both in inner and an outer membrane.

Small vesicules continuously bud from the ER membrane and fuse into the Golgi, and this vesicule trafficking is also involved in adjusting the cytoplasmic membrane's composition and extent. This is a defining feature of the endomembrane system.
The membranes of chloroplasts and mitochondria are not involved in this vesicule trafficking, which is why they are not considered part of the endomembrane system (even though they "have membranes" and "are inside the cell", which is the etymology of the term "endomembrane").


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What does the "G" and "V" in penicillin V and penicillin G stand for?
I've been looking for a convincing explanation for the designation penicillin G and V. The answers I've found includes G as in "gold standard" and "V" as in "viscus" but they're not sourced and not especially credible explanations.

The first discovered penicillins were designated I, II, III in Britain and F, G, X in America. I can't find what the letters stand for. Could it be that, as they were determining the composition of natural penicillin (which originally referred to the Penicillium culture supernatant), they designated compounds alphabetically and these letters happened to correspond to penicillins?

Penicillin V is synthetic and, according to this book, was named V for vertraulich (German for confidential).


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Evolution of the (phenotypic) facial features of the indigenous people of (west/central) Africa
I am not even remotely an expert in this field; I just got curious, so help me.
First of all, let us remove all human sentimental attributes from this question (such as connotations of scientific racism or emotional reactions thereof) and ask it from a purely scientific point of view. The typical facial feature of a West/Central African person (the so-called broad African type) exhibits a wide nose, a lack of nasal bridge projection (similar to many Asian noses) and a prognathous skull shape that resembles more closely to our ancestor Homo Heidelbergensis than many other indigenous phenotypes from other parts of the world do.
I agree that this claim sounds anecdotal, and is certainly not true of all Africans (for example, Ethiopians), but one cannot dismiss it simply on grounds of ethical policing. I cannot help but notice that many of my African friends remind me of our shared ancestry (with no disrespect meant whatsoever), as is clear from the photographs below, one of a supposed Homo Heidelbergensis and one of a random African Homo Sapiens of today.

My question is the following. What is the reason behind this seeming resemblance? Is this appearance an illusion and possibly a construct of a prejudiced mind, or does this have a valid scientific answer? For example, are most Africans closer to our ancestors than the rest of humanity is? How does evolution answer this question?
Thank you for your help.

Note that I had never heard of the expression "broad african type" and could not find much reference to this term when googling. But anyway, I'm happy to use it to refer to a particular set of typical facial features.

What is the reason behind this seeming resemblance?

Note that the Homo Heidelbergensis image is not a picture (obviously) and much of what is being depicted was open to artistic interpretation. It is possible that some of the feature you are thinking of are not real. Have a look at the post In reconstructions, how are various shapes of facial features determined from skull only?.
You list several phenotypic traits and it would be too broad of a question if you were expecting an explanation about the evolution of each of these traits. I will just pick one classic trait; the nose.
One of the role of the nose is too even up the temperature of the air that we're inhaling. As such, the shape of the nose is under differential selection pressures depending on the environment. So if the nose of Homo Heidelbergensis looked alike (assuming it really looked like on the facial reconstruction) today's "broad African type", it is probably because of shared environment. Note however that nose shape vary a lot among african lineages and also among non-african lineages. You might want to have a look at this popular article.
A big point of ressemblance is the skin color that you don't talk about. Have a look at the posts Why do we assume that the first humans were dark-skinned? and How did some humans evolve to be white? to learn more about skin color

Is this appearance an illusion and possibly a construct of a prejudiced mind, or does this have a valid scientific answer?

First, see my above point about facial reconstruction.
H. Heidelbergensis lived in Africa and in this resepct shared an environment that is like the environment that modern african are encountering that what modern Han Chinese are encountering. In this respect, we could expect some ressemblance.

For example, are most Africans closer to our ancestors than the rest of humanity is?

No, they're not and they cannot be. The MRCA of all humans today is more recent than the MRCA between any human and H. Heidelbergensis. You should have a look at this intro to phylogeny to understand a little bit better how different lineages relate evolutionarily speaking.

Thank you for this wonderful answer. Could you also briefly comment on why a prognathous mouth is better suited in central Africa? Thank you again!

I never meant that all features that one would identified with the so-called "broad African type" are adaptive. I said some might be and went on talking about skin and nose. I don't know if prognathous jaws would be in any way adaptive and I don't know if H. Heidelbergensis (and other hominids that lived in Africa) had such jaws. I can't think of a hypothesis for why they would be adaptive either.

Prognathous mouth is believed to be related to diet during childhood not anything genetic. It is the norm and the underdeveloped jaw we see in industrial populations is due to living off of soft processed foods their entire lives. Wisdom teeth issues are linked to this as well.


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Oxygen balence from growing plants for food
I had thought photosynthesis and respiration where pretty much Oxygen and Carbon neutral per calorie.
http://news.mit.edu/2014/technical-feasibility-mars-one-1014

If, as the project plans, crops are cultivated within the settlers’ habitat, Do found that they would produce unsafe levels of oxygen that would exceed fire safety thresholds, requiring continuous introduction of nitrogen to reduce the oxygen level.

Says that a closed system of plants grown to provide calories for human will end up with more oxygen.
Where does the imbalance come from? Where does the extra Carbon go?

If oxygen and respiration were carbon and oxygen neutral, there wouldn't be free oxygen at all. Plants would just respire all the oxygen they produce.
The extra carbon goes into the plants themselves. It isn't just what they use for energy, it is also what they are made of.
See also this question:
Are plants really oxygen neutral?
Plants are oxygen neutral when we take into account the decomposition of the plant, i.e. take the long-term view where the carbon making up the plant gets back to being CO2.

I though the free oxygen was accounted for by oil and living things, I guess it also needs to include all the decomposing things. So there is expected to be more oxygen in soil than poop, and even if you burn the stalks the ash is out of circulation for a while, that makes sense.

Well, in the context of that other question living things = decomposing things... By "decomposition of the plant" we mean that if the carbon in the plant ended up back as CO2 (which happens via decomposition processes, which includes "being eaten and the carbon being part of another organism for awhile"). In practice life is self-perpetuating, so all the carbon doesn't end up in the atmosphere; there is always a certain amount stored in things that haven't decomposed yet, like living organisms and fossilized dead organisms (including oil and coal).


text:
Do tRNAs that recognize multiple codons have any preference for one over another?
What are the effects of the different binding strength/affinity between the synonymous codons corresponding to a single tRNA ?

Your question could do with clarification. You ask a specific question in your title, but you need to spell out what you mean by "preference" in the body of the question. Asking if literature exists, is not a scientific question of any sort, and appears to be concerned with something different, more in the realm of chemistry. Nor do you give us any indication of what you have found out for yourself on this topic. See  the help on "how do I ask a good question". Nevertheless, I have given you an answer.

I have now edited your question to a form that is more acceptable to SE Biology.

There is an extensive literature on synonymous codons and their usage in different organisms. I shall assume that the question concerns relationship between strength of codon–anticodon interaction and the efficiency (speed in this case) of translation.

It is not disputed (I am aware of few experiments on this) that the strength of codon–anticodon interaction depends on the number of hydrogen bonds made.
It was predicted that for optimal rate of translation one needs a balance between association and dissociation of the codon–anticodon pair. Hence weak interactions (all AU) — which would disfavour association — or strong interactions (all GC)  — which would disfavour dissociation — would not allow a rate of protein synthesis as fast as that for intermediate interactions (mixed AU,GC).
This appeared to be borne out
in the codon usage patterns of rapidly growing organisms such as Escherichia coli, something subsequently confirmed by more extensive studies. To be precise, the more highly expressed proteins (e.g. ribosomal proteins) were encoded by mRNAs containing the intermediate  codon–anticodon interactions predicted to allow rapid translation. In contrast, poorly expressed proteins (e.g. repressors) were encoded my mRNAs predicted to produce slower translation.
One should be aware, however, that there are other factors that influence the codon usage in different organisms, and that these can overide the effect of codon–anticodon interaction strength.


text:
Does anyone know what are these birds?
Never saw them before, they appeared suddenly , the day my father died.
Place is Serbia in Europe.
Does anyone know what are these birds?

Looks like European Starlings (Sturnus vulgaris).  They are often seen in large numbers and are native to most of Europe, including Serbia.  They were introduced to North America (Central Park, New York City) as a project to introduce species of birds from works of Shakespeare and are now widespread.

Source: https://www.allaboutbirds.org/guide/European_Starling/id


text:
How does antibody structure relate to function?
I know that antibodies have 2 binding sites (as Y shape) so they can bind to 2 pathogens for agglutination. They have a hinge, heavy and light chains, constant and variable sections on these chains.
But how do these structures (and any obvious structures I have missed) relate to the function of antibodies?

This is a broad basic question that is well covered on numerous sites on the internet as well as standard texts that an be read on NCBI bookshelf. If you read the help on "how to ask a good question" you will see that you are expected to explore such sources first. Try a search for antibody structure and function or consult Ch 33 of Berg et al.


text:
A reliable source of Cas9?
I live in Egypt, and I do want to perform CRISPR-Cas9 genome modification, but there are no reliable sources of Cas9. I can order some Cas9 online from the US, but not much. So... my question is, is there any way I can replicate a small amount of Cas9 to get a bigger amount? Or maybe extract some from S. Pyogens? I've been searching about this for quite some time, so any support would be really appreciated.
Note: I'm not really the "Biology" guy, so please tell me if I sound ridiculous.

You could get a synthetic gene for Cas9 and overexpress it heterologously.

I'm more curious why you are planning to do some genome modification while not being the biology guy...

I might be wrong but I'd guess it'll probably be more expensive to figure out how to produce the compounds you need than to just buy them (esp. if you're not a "biology guy").

Well.. I can't exactly tell you what I'm working on because I signed an NDA, but what I can tell you is that I'm a programmer and I want to create bacteria that can pass information through controllable electrical connections(interfaced with a microcontroller).

@None Hi, would be interesting to discuss more on your project


text:
Seeing new colours with new photoreceptors
If we developed new "eyes" that could see "non-visible spectrum colours" and connected them to our brains, would our brain be capable of identifying and interpreting those new colours? Is our brain hardwired to only de-encode information about RGB using our SML cones?
How is color information transmitted from the eye to the brain?
Our brain receives the information as an FM signal, but does that mean a different "carrier frequency" is used in the FM will the brain detect and interpret this new colour?
Cerebral activity during exposure to non - visible light
We lack the ability to see colours outside of the visible-spectrum due to a lack of photoreceptors.
https://www.quora.com/Why-cant-we-think-of-a-new-colour-Is-it-really-impossible-to-think-of-any-colour-that-doesnt-exist-right-now-Is-the-light-spectrum-the-only-possible-source-for-new-colours-or-might-there-be-something-else Note that this link states we can "imagine" new colours in a pseudo kinda way.
The two points I found online providing information about my question: Yes adding new photoreceptors/sensors to our eyes could be a way to see new colours and yes sending a different signal would seem to be the way to interpret a new "colour". But those answers only partly apply to whether it's actually possible and only narrowly approach this question.

"new eyes" = synthetically designed or robotic. I'm aware that the modulation of another animal's eye's wouldn't fit the bill and therefore we can't reliably transplant eyes from other creators to boost our vision capabilities. (e.g. Mantis Shrimp eyes would certainly be incompatible and require special vision processing capabilities http://phenomena.nationalgeographic.com/2014/07/03/natures-most-amazing-eyes-just-got-a-bit-weirder/ )

Each human optic nerve contains between 770,000 and 1.7 million nerve fibers, So it will be beyond human grasp to swap eyes in the near future, genetic eye and optic fiber development has to happen in the womb. Eye grafts require some kind of neural nanotechnology which is probably multiple generations away.
If you replace a human photoreceptor with another color, the result is: un-demonstrated/unknown.
Genetically engineered photoreceptor color swap (swap UV and blue)  which sends impulses to the same optic nerves as the previous color, may, and probably would work fine.
If you switch one eye to CMY and keep the other as RGB, it should have a usable result.
If you switch both eyes to CMY it's fine too, we would expect that there would be a fair vision perception, perhaps equivalent to RGB in clarity.
If you design a fetus with 4-5 photoreceptors and let it develop normally, It would have an unknown result. Perhaps the baby would have augmented vision, perhaps troubled. It's not know and many scientists would love to know the result.
I'd wager that a human with 4-5-6 colors of photoreceptors can be genetically engineered to see, within our lifetime.

Awesome, I believe that there is a man or woman who's been given a robotic eye (about 3 years ago) and it was very blurry and low saturation but the same colours as our SML receive. I just did a quick google and found about 5 links to different events claiming to be the first transplant and one really neat one to combat ARMD. I think that with Crispr being our modern DNA modifier would could eventually learn enough about DNA to design improved sight. But back to the question, yes certainly would be fascinating to know the outcome of "extra" or "new" colours.

@Tmanok If I get the reference correctly that was a photoreceptor chip grafted to the retina.

There be tetrachromatic humans already. https://web.archive.org/web/20120214002707/http://www.klab.caltech.edu/cns186/papers/Jameson01.pdf

Awesome John thanks for sharing!
@Ratchet Freak, yes there was a transplant of an entire bionic eye in colorado 2015, another in the UK but different operation and then a neat one for ARMD (AMD is the generally more accepted term) where they grafted an electrode array connected to a pair of glasses with a camera. I'm sure there have been more but when you read "first, first, first, first" all during different years it makes you think "first time using this method? Your title is misleading and earns a skepticism award".

Humans probably couldn't use UV photoreceptors, a study found that all animals that can see UV's, birds and some mammals, have eyes smaller than 5-7mm. https://io9.gizmodo.com/want-ultraviolet-vision-youre-going-to-need-smaller-ey-1468759573

There are two issues associated with "seeing extra colors". One is seeing parts of the light spectrum we currently do not see; for example, seeing ultraviolet or infrared light. Another is discriminating between different combinations of wavelengths, and perceiving more colors than we actually do.
Our color vision is based on three different receptors who are sensitive to different wavelengths; the brain infers color from the differences between how those receptors are activated. This allows to tell some combinations of wavelengths from others, but not all: we can tell red light from blue light, because the first excites the red-detecting cells a lot more than the two others and the second excites the blue-detecting cells a lot more than the two others, but we cannot tell yellow light from a combination of red and green light, because in both of those cases we have the red and green cells excited the same and the blue cells not as much. This is why our color vision is "three-dimensional", i.e. all colors can be generated from three basic ones.
Somebody who instead of a blue receptor had an ultraviolet receptor, would be able to perceive more wavelengths than we do, but they would probably see more or less the same colors - "ultraviolet" would be "blue" to them. There may be differences because the kind of combinations they ran into would be different - for example because they'd have a wider range between the "green" and "ultraviolet" sensors than we have between "green" and "blue", maybe more of the world would look cyan than it does to us.
To see additional colors, the same way that ordinary trichromat humans see more colors than color-blind people, and be able to discriminate between more combinations of wavelengths than we do now, we would need extra receptors. And that's where the questions arise of whether the brain would be able to handle the extra colors, or whether the optic nerve would transmit it as its own channel.
As it happens there are cases in humans where they have four different color receptors. The main case happens because the genes for some color receptors (red/green) are on the X chromosome, and in women one of their two X chromosome is inactivated in each cell, but which it is is random - meaning that if they have two slightly different versions of that receptor on their two chromosomes, some cells in the retina will have one and others the other - making two different color receptors in their eyes where other people have one.
It appears that most women with this conditions do not see more colors than others, which could be because the two receptors don't vary enough. But it appears that some rare cases do have better abilities to discriminate colors and a richer color experience, which suggests that human tetrachromacy is possible and already exists in a few rare individuals.
See also:
https://en.wikipedia.org/wiki/Tetrachromacy#Humans
https://theneurosphere.com/2015/12/17/the-mystery-of-tetrachromacy-if-12-of-women-have-four-cone-types-in-their-eyes-why-do-so-few-of-them-actually-see-more-colours/
https://theness.com/neurologicablog/index.php/tetrachromacy-in-humans/
https://www.researchgate.net/profile/Zoltan_Jakab/publication/254932347_Looking_for_potential_indicators_of_human_tetrachromacy/links/546c88c80cf2c4819f216fa5/Looking-for-potential-indicators-of-human-tetrachromacy.pdf
https://arxiv.org/abs/1703.04392
Enhancing human color vision by breaking binocular redundancy (this isn't about the abovementioned cases of tetrachromacy, but of people trying to induce tetrachromacy by stimulating the two eyes differently)
This paper gives a good general overview of color vision in the animal kingdom, and debunks some misconceptions (such that animals with a zillion color receptors see a bazillion more colors than we do - they actually process color very differently and the number of color receptors they have is related to that).
https://www.sciencedirect.com/science/article/pii/S0960982214013013
Another overview of human color vision:
https://www.imbs.uci.edu/colorcoglab/4-9.pdf
Human Potential for Tetrachromacy

Hi Rozenn, this makes perfect sense after having read about Mantis Shrimp perceiving very specific wavelengths of UV, although researchers have no idea why they have this innate need to see those wavelengths it can be assumed that they're related to something in their habitat and the fact that they filter out non-essential colours leads me to think that they are blocking out sun refraction underwater. Who knows, but do you'd think having photoreceptors that do not overlap with each other in the UV spectrum would be very odd- binary colour hue but with variable saturation in fact.


text:
What can pass through the intestinal membranes?
As I understand it, most substances need help to pass through the walls of the intestines.
For example, in hepatic recirculation (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2781307/) bile salts are grabbed and transported across the intestinal membranes by particular polypeptides.
Is there a summary of the sorts of things that can be transported across intestinal membranes? For example, hormones, stearates, lipids, etc. What general classes of molecules can pass the membrane and what cannot?
I am not looking for an exact answer, but a general characterization of major classes of organic molecules and their ability to pass through intestinal membranes into the body.

Your title says abdominal wall, which to me suggests outer muscular layers and/or parietal peritoneam, but your question seems to relate more to the inner epithelial gut tube lining or maybe the visceral peritoneal layers. Could you clarify what layer(s) you specifically are interested in.

Virtually all nutrients from food can be absorbed into blood through the lining of small intestine and colon.
What can be absorbed in the small intestine:

Water
Simple sugars (monosaccharides): glucose, fructose, galactose...
Amino acids and small peptides (dipeptides, tripeptides)
Free fatty acids, monoglycerides and cholesterol
Minerals: sodium, potassium, iron, etc.
Vitamins
Nucleic acids
Alcohol
Various other substances from food (polyphenols, sulfate, oxalate, caffeine, preservatives...)
Bile acids
Steroid hormones, such as cortisol, aldosterone and sex hormones (JCEM)
Drugs
Various toxins

What can be absorbed in the colon:

Water
Short-chain fatty acids (from bacterial fermentation of dietary fiber and sugar alcohols)
Sodium, potassium and some other electrolytes

What cannot be absorbed in the intestine:

Polysaccharides (such as starch), oligosaccharides, disaccharides
Dietary fiber (soluble fiber can be fermented and the resulting substances can be absorbed in the colon)
Whole proteins and big peptides
Triglycerides, diglycerides
Peptide hormones, such as insulin, glucagon, calcitonin, prolactin, growth hormone and parathyroid hormone (Cambridge Core)

Sources:

Lumenlearning (type of transport for all main nutrients)
Best Practice & Research: Clinical Gastroenterology (detailed description with carriers involved)

This table from Ganong's medical physiology will help you get your answer.

I hope it helps.

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


text:
Why placental progesterone suppressed or drop before onset of labour?
As we know during pregnancy predominant hormone is progesterone which is at early pregnancy about first 3-4 months produce by corpus luteum  of pregnancy together with estrogen after that placenta can make its own progesterone with estrogen till birth but for initiation of labour estrogen go up and progesterone should go down because it prevents uterine contraction. Does anyone know mechanism of suppressing of progesterone and rising of estrogen before onset of labour ?
In other word mechanism of initiation of labour ?

Pregnenolone -the precursor of progesterone is principally converted to estradiol instead of progesterone.Thus the oestrogen:progesterone ratio increases prior to parturition.

Fetal cortisol stimulates activity of placental 17 α hydroxylase/17, 20 lyase (CYP 17) enzyme, which catalyzes the conversion of pregnenolone to estradiol.

Confinement of the foetus in the uterus stimulates the stress responses.

Stress leads to a rise in foetalACTH. The rise in ACTH causes production of cortisol from the foetal adrenal glands. The rise in foetal cortisol leads to an increased oestrogen:progesterone ratio by upregulating aromatase enzymes, which convert androgens to oestrogens. Cortisol also reduces progesterone production.


text:
Why do nerve gas victims have chronic neurological issues?
The article on Wikipedia says the following:

The effects of nerve agents are long lasting and increase with continued exposure. Survivors of nerve agent poisoning almost invariably suffer chronic neurological damage and related psychiatric effects.

Unfortunately, the original paper seems to be paywalled. Why does this happen? Is it because it takes a long time to replenish the acetylcholinesterase inhibited by the nerve agent?
Here is the link to the original paper.

I will have a look at it in the next days.

I would like to add a bit to Chris' answer. While it is true that the underlying mechanism of the long lasting effects of nerve gas has not been established, several hypotheses exist (reworded from Jokanovic et al, 2010):

Long lasting effects could be derived from withdrawal of nerve gas after repeated low-level exposure or acute exposure. This means that the synapses are degraded or even the neurons die because of the constant excitation caused by the nerve gas.
Nerve gas may affect neuropeptide metabolism through the release of endogenous opiates and/or through interactions with yet unidentified receptors
London et al. (2005) reported that exposure to nerve gas may cause serotonin disturbances in the central nervous system, which are implicated in depression and suicide in humans.

Most of the nerve agents (and quite a number of commercially used pesticides) fall into the class of organophosphates (OP). Their mechanism of action is the inhibition of the acetylcholin esterase which leads to the build-up of acetylcholine in the body and thus a permanent activation of mucarinic and nicotinic acetylcholine receptors.
Irreversible inhibitors of AChE may lead to muscular paralysis, convulsions, bronchial constriction, and death by asphyxiation - and organophosphates can act as these. See here for some more information.
According to reference 1, four different toxic effects can be differentiated:  The cholinergic syndrome, the intermediate syndrome, organophosphate-induced delayed polyneuropathy (OPIDP) and chronic organophosphate-induced neuropsychiatric disorder (COPIND).
The cholinergic syndrome is happening in the acute phase of the OP poisoning and can be explained by the inhibition of the acetylcholin esterase.
All quotes are from reference 1:

In cases of human poisoning, general acute symptoms of peripheral
  nicotinic and muscarinic intoxication are clearly apparent.
  These symptoms include miosis
  (unreactive to light); sweating, rhinorrhea, lacrimation, and
  salivation; abdominal cramps and other gastrointestinal symptoms;
  respiratory difficulties and cough; dyspnea, constriction sensation in
  the chest, wheezing; twitching of facial muscles and tongue, tremors,
  and fasciculations; bradycardia and ECG changes, pallor, and cyanosis;
  anorexia, nausea, vomiting, diarrhea, and involuntary urination and
  defecation. These signs and symptoms are accompanied by central
  effects such as dizziness, tremulousness, and confusion; ataxia;
  headache, fatigability, and paresthesia. Finally, seizures,
  convulsions, twitching, coma, and respiratory failure may also occur.
  If the subject survives the first day of poisoning, personality
  changes, mood swings, aggressive events and psychotic episodes
  including schizoid reactions, paranoid delusions, and exacerbations of
  preexisting psychiatric problems may also ensue.

The intermediate syndrome happens after the acute phase, around 7,7% of the patients develop it.

The term Intermediate Syndrome (IMS) was first described by Senanayake
  and Karalliedde (1987) because it appeared in the interval between the
  end of the cholinergic crisis and the onset of OPIDP. Following
  exposure to various OP pesticides, clinical manifestations of IMS
  typically occur within 24–96 h, and affect patients without
  fasciculation or other cholinergic signs. The reported incidence of
  IMS ranges from 7.7% to as high as 84% (Shailesh et al., 1994).
  Although IMS is well recognized as a disorder of neuromuscular
  junctions, its exact etiology, incidence, and risk factors are not
  clearly understood. IMS generally occurs among patients with prolonged
  and severe inhibition of AChE, although not every patient with severe
  AChE inhibition develops IMS. Other risk factors of IMS include
  delayed metabolism of OP pesticides due to toxicokinetic factors or
  impaired organ function, severity of poisoning, elevated muscle
  enzymes, plus adequate or late oxime therapy. IMS has been linked with
  exposure to specific OP pesticides displaying the dimethyl phosphate
  moiety (e.g. fenthion, dimethoate, monocrotophos, dichlorvos,
  methylparathion) but has also developed after exposure to parathion
  (ethyl phosphate) and methamidophos (phosphoramidate; De Bleecker et
  al., 1993; Yang and Deng, 2007).

The organophosphate-induced delayed polyneuropathy (OPIDP) cones later and has been connected to the phosphorylation and subsequent ageing of the neuropathy target esterase by the OP (see reference 1 and 3).

OPIDP is relatively rare neurodegenerative disorder in humans that is
  characterized by loss of function and ataxia of distal parts of
  sensory and motor axons in peripheral nerves and ascending and
  descending tracts of spinal cord. The early neurological symptoms
  usually are sharp, cramp-like pains in the calves, tingling in the
  feet and hands followed by distal numbness and paresthesia. Pain and
  weakness in muscles spread rapidly and patients become unsteady and
  unable to keep their balance. Progressive leg weakness occurs,
  together with depression of tendon reflexes. Symptoms may also appear
  in the arms and forearms. Sensory loss may be mild. Muscle tonus of
  the limbs gradually increase and spasticity appears in the lower
  limbs. Physical examination reveals distal symmetrical and mainly
  motor polyneuropathy, with wasting and flaccid weakness of distal limb
  muscles, especially in the lower limbs. In severe OPIDP quadriplegia
  with foot and wrist drop were observed as well as mild pyramidal signs
  (Lotti, 1992). There may be some functional recovery in less severe
  cases with more distal involvement and sparing of spinal cord axons,
  but pyramidal and other signs of central neurological involvement may
  become more evident with time. The recovery affects only sensory
  nerves, while motor neurons may permanently lose function as indicated
  by Morgan (1982) who described the lack of improvement over 47 years
  in 11 patients poisoned with TOCP.

The chronic organophosphate-induced neuropsychiatric disorder (COPIND) happens to persons with a chronic exposure to OP and is most likely caused by permanent damages to the central nervous system (CNS), but the real cause is not known yet.

The most common symptoms of COPIND include cognitive deficit
  (impairment in memory, concentration and learning, problems with
  attention, information processing, eye-hand coordination and reaction
  time), mood change (anxiety, depression, psychotic symptoms, emotional
  lability), chronic fatigue, autonomic dysfunction, peripheral
  neuropathy and extrapyramidal symptoms such as dystonia, resting
  tremor, bradikynesia, postural instability and rigidity of face
  muscles

References

Neurotoxic effects in patients poisoned with organophosphorus
pesticides
Long-term health effects of nerve agents and mustard
Neuropathy target esterase (NTE) and organophosphorus-induced
delayed polyneuropathy (OPIDP): recent advances

While I feel that Thawn's addition provides a better answer for my original question, I really appreciate your answer too. That was an interesting read, thank you!