text:
Why is the ribonucleoside derived from thymine, 5-Methyluridine, abbreviated m5U and not T?
The wikipedia article about Nucleosides presents a table in which there are three columns — Base, Ribonucleoside and Deoxyribonucleoside — and structures, names and abbreviations for the nucleosides corresponding to the five bases, adenine, guanine, thymine, uracil and cytosine.
The abbreviation pattern for the deoxyribonucleosides is quite regular — they are all termed dN, where N is the first letter of the name of the base and ‘d’ indicates ‘deoxy’ (i.e. dA, dG, dT, dU, dC).
In the case of ribonucleosides, apart from one exception, the pattern is similar — they are all termed N, where N is the first letter of the name of the base (i.e. A, G, U, C). The exception is the ribonucleoside related to the base, thymine, which is not abbreviated T — as one might expect, but as m5U, from its name 5-methyluridine.

What is the reason for this? Why does the abbreviation for ribonucleoside derived from thymine deviate from that for the other bases?
Do people distinguish between m5U and U when referring to RNA, or is the letter U used for both?

I have simplified your question and removed the reference to alphabet. We are just talking about abbreviations, which by their very nature are imprecise, but arise over time because they are convenient.  We are not talking about God creating animals and giving them all names. Think about it in relation to your knowledge of DNA and RNA.

The m5U isn't a common constituent of RNA, regardless of the nomenclature, and so this notation does not explain why uracil is used in RNA - the answer you linked at the beginning of your post already contains the best explanation for that along with the explanation for why thymidine is found in DNA: simply, it started out as uracil and replacement machinery to deal with thymidine RNA never evolved.

The question that is open, is not why is uracil used in RNA. The question is why is m5U/T not used in RNA? I will change my question to only focusing on the nomenclature.

Because it's a different base. You could ask why isn't a uracil used that is methylated at any other point, as well, it's a different compound, it wouldn't "fit" in the transcription/translation machinery.

@David I'm getting a bit confused about what the actual question the OP has here; after I re-read the latest comment the OP says "the question is..." what you changed the title to be, but then after that says "I will change my question to only focusing on the nomenclature" which is exactly the opposite. I think we need some clarification or this should probably be closed as unclear.

You say your question is why is T not used in RNA, and not primarily about abbreviations. You certainly fooled me! I have changed the title to reflect this. Have I understood you correctly? If so the question needs revising to say that. And please stop talking about alphabets. I can help you with this (and answer that question). If this is not your question please clarify. Do you understand the roles of the different RNAs in protein synthesis? Are you worried about the fact that the base thymine (5-methyl uracil) is found in some RNA? Do you know where it is found? What books have you read?

@BryanKrause Sorry, am away and was working on my phone so things got messed up. My comment above should clarify things I hope. The problem is the question is more a stream of consciousness submerging what appears to be the major concern expressed in his comment.

@David No worries, I think we are more or less on the same page of being a bit uncertain about OP's intentions while trying to sort things out. If the new title is indeed what the OP wants answered, then it is a pretty clear duplicate of this question.

@BryanKrause It may appear to be a duplicate, but the poster is right in saying all the answers answer a different question — why T not U in DNA. So I think we should persist and, eventually andif appropriate make two distinct questions, perhaps by editing the previous one.

@David Why did you change the title? I will change it back. The title perfectly fits the question. Just leave it like this. It is the first question that needs to be answered before it makes sens for me to asks "why is m5U/T not used in RNA". I would then open a new question. And why are you using words like "you fooled me"?

I changed the title because you said in a comment "The question that is open, is not why is uracil used in RNA. The question is why is m5U/T not used in RNA?". I know something about the subject and will be able to help you if I know what your question is. I asked you specific questitions to help clarify this and you ignored them. I repeat, is your question about biology — why one base is used in RNA, whereas another is used in DNA — or about nomenclature  — why in the rare cases in which thymine occurs in RNA it is described more specifically? "You fooled me", was as the question was unclear.

@David. Sorry for the confusion. I meant that in link "The question is why is m5U/T not used in RNA?" is still open. But before I will ask this question in a "new thread" I want to get  certainty about the nomenclature. So this question is only about the nomenclature.

I have been away and working on my phone. I did not look at the link to the Wikipedia article on nucleosides, partly because of the screen size, and partly because it is a rule that questions must stand alone and not depend on someone having to go to another site. I now see what you are talking about. I will edit your question to reflect this and then give an answer. I will remove your reference to the lack of occurrence of T in RNA as it is not relevant. Until the title of the existing question is modified I suggest it is better not to ask a new one as it will be flagged as a duplicate.

I have given notice of my intention to change the title of the old question on the employment of U in RNA. I'll give it 24 hours and then attempt to change it.

From the standpoint of modern molecular biology, one can say that the table in the Wikipedia article would be better if — in the first instance at least — it left blank the entries for the ribonucleoside corresponding to the base thymine and the deoxyribonucleotide corresponding to the base uracil. This is because the thymine ribonucleoside is not a normal constituent of RNA, and the uracil deoxyribonucleoside is not a constituent of DNA.
It would also be more honest if the article explained that the abbreviations used in DNA and RNA databases employ the single letter to represent a deoxyribonucleoside monophosphate residue or a ribonucleoside monophosphate residue, as the case may be, and that only the chemist or student of nucleotide metabolism is likely to be concerned with the abbreviations presented.
It is in metabolism (for which these were named) that the abbreviations make sense. ATP is adenosine triphosphate, so the ‘A’ has to represent the nucleoside, adenosine, and dTTP, deoxy-thymidine triphosphate, is the metabolite that is a DNA precursor used by DNA polymerase. The reason that dU justifies inclusion is that dUMP exists in cells — as a precursor of dTMP (which is then converted to dTTP).
So finally to your Q1 about 5-methyluridine. The answer is that, as far as I am aware, this does not occur in cells as the free nucleoside or the free related base or nucleotide. It can only be considered as occuring at a particular positions in certain transfer RNAs (and ribosomal RNAs) where it is produced by the enzymic modification of the uracil ring by a 5-methyluridine methyltransferase. So in the metabolic era, before the detailed chemical analysis of minor bases in structural RNAs, there was never any reason for biochemists to refer to 5-methyluridine and consider its abbreviation.
You may or may not be aware that there are many minor bases of this type in different tRNAs, all produced by enzymic modification of the four bases occuring in an initial RNA transcript synthesised by RNA polymerase. There are over half a dozen different modifications of uracil, so it was far more meaningful for the scientists working on them to distinguish them with abbreviations that indicated their chemistry, rather than assigning arbitrary single letters to them. The fact that one could logically employ T as an abbreviation for 5-methyluridine would have been of no practical use, and, because of the association of thymine with DNA, could well have led to confusion. Hence, the committee standardizing nomenclature would have been faced with a fait accompli. In such circumstances realism prevails over idealism. (And in any case the names of the bases are a mess — how many students have been confused by adenine/adenosine but cytosine/cytidine.)
Regarding your second question: people don’t talk very much about m5U and U, but when they do they naturally distinguish between them because they are different molecules. Specifically, the databases for tRNA structures will distinguish clearly the different modified bases.

I think this sentence is unfortunate: "So finally to your Q1 about 5-methyluridine. The answer is that, as far as I am aware, this does not exist as such in cells, and only occurs at a particular position in certain tRNAs".
tRNA occurs in cells, ergo m5U occurs in cells. I read here, that it also appears in rRNA.

"Your second question doesn’t seem to make sense..." It is a simple question and you provided a clear good answer for it: "the databases for tRNA structures will distinguish clearly the different modified bases." No need to be more verbose as necessary.

@newandlost Ok about the second question. I'll remove the remark.

@newandlost — Regarding m5U and its occurrence in cells, I'll rephrase the sentence when I have a moment. The "as such" was meant to imply that there is no free ribonucleoside, m5U, or the related base, or any related nucleotide mono-, di- or tri- phosphate in cells. So these molecules are never encountered within cells, and for biologists (rather than chemists) are not discussed and naming is of little concern.m5U can only be considered as part of some tRNAs (and rRNAs) where it is the base that is of interest (rather than the nucleoside or nucleotide residues) as that is what is modified.

@newandlost — I've made the changes now. I could also add references to the discovery history of the identification of m5U in tRNA and rRNA, and examples of how it is designated in databases, if you really think this would be useful.

Good answer. Just a minor point --- RNA can also be broken down to the constituent ribonucleotides, as part of continuous RNA turnover. Wouldn't that release free 5-methyluridine then? (in very small amounts)

@Roland — It certainly must do initially, although it may be rapidly degraded as it is unlikely to be recognized by salvage pathway enzymes.


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Why are peas in mendelian genetics different?
In mendelian experiment, yellow seeds were seen to be dominant over green seeds. The peas I've seen are generally green and not yellow. Did he use a different variety of pea plant ?
The other trait that was seen was white or grey seed coat where grey is dominant over white.
Why are these results not consistent with the peas found in pea pods ?

If I had to guess, they were varieties of pea plants that we aren't accustomed to dealing with.

The yellow colour of pea seeds is a rare trait and is found in many parts of the world ,China and Fiji islands for example. It's not usually found in Indian market though.(Wikipedia)

@SanjuktaGhosh I think that's what OP is looking for, and you should submit it as an answer!

@Gaurav Probably Remi got it right, OP has confounded the concept of dominance with one of high frequency.

You are confounding the concept of dominance with the one of high frequency. The dominant phenotype might be at lower frequency than the recessive phenotype.
Dominance

Dominance in genetics is a relationship between alleles of one gene, in which the effect on phenotype of one allele masks the contribution of a second allele at the same locus

Trait frequency
Let's imagine a case where A is dominance and a recessive. Let, $f$ be the frequency of A alleles in the population. The frequency of individuals that have the dominant phenotype is the frequency of AA individuals plus the frequency of Aa individuals. Under Hard-Weinberg assumptions, the frequency of individuals having the dominant phenotype is therefore
$$f^2 + 2 f (1-f)$$
The frequency of individuals having the recessive phenotype is $(1-f)^2$.
If
$$f^2 + 2 f (1-f) < (1-f)^2$$
reorganizing the in-equation yield to
$$f < 1 - \frac{1}{\sqrt{2}}$$
So under the condition that $f < 1 - \frac{1}{\sqrt{2}}$, the dominant phenotype is present at lower frequency than the recessive phenotype.
If the calculations were unclear to you, then you should have a look at the wikipedia article of Hardy-Weinberg principle.

@AnamikaGhosh As you have not reacted yet, I suppose I may fail to answer your question. If there is anything unclear, feel free to comment on it.

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Why do large neurotransmitters travel faster down the axon?
I understand that with large neurotransmitters, like neuropeptides, the precursor neurotransmitter and the enzymes are produced in the soma and quickly travel down the axon to be modified in the axon terminal.
With the small molecule transmitters, the enzymes are made in the soma and then transported slowly down the terminal to the terminal where they synthesize the small transmitters.
Why is it that the precursors and enzymes for large neurotransmitters travel fast down the axon, whereas the enzymes for the small transmitters travel slowly? Is there a specific reason?

is their a molecular weight for "small" and "large" transmitters that you can reference? Can you add a general reference that talks about this question?

@VanceLAlbaugh I edited the question a big to what I assume the OP was getting at, and already included some clarification in my answer. Textbooks often distinguish two major categories of neurotransmitters: small molecules vs. peptides.

I presume you are referring to fast versus slow axoplasmic transport.
I presume by "small neurotransmitters," you are referring to "small molecule" neurotransmitters like GABA, glutamate, acetylcholine, and the catecholamines like dopamine.
For the "large" neurotransmitters, I assume you are referring to peptides.
(for a quick reference on these two categories you can see this book blurb)
Although local protein synthesis is possible outside the soma, particularly in dendrites, and there is even evidence for protein synthesis in axons, including neurotransmitter peptides, most protein synthesis still seems to occur in the vicinity of the nucleus, at the soma. Synthesis anywhere else means you need to transport the mRNAs and translation machinery instead, since the mRNA needs to be made at the nucleus. Even the "large" neurotransmitters, which are peptides, need to be synthesized just like bigger proteins.
Back to axoplasmic transport... There are two main mechanisms for moving things down the axon. The faster version of this transport is really for the transport of vesicles. To transport a neurotransmitter peptide in this fashion, you fill a vesicle full of the peptide and send it on its way along the microtubules via kinesin and dynein motors.
Larger, non-membrane bound proteins, however, are often not transported in vesicles, but by the slower transport mechanism. Note that this transport is still pretty fast, way faster than simple diffusion, it just isn't as fast as the "fast" transport. The exact mechanisms of slow transport are still an active area of research and not fully understood.
To get back to your question, "is there a specific reason?" The reason isn't so much about the speed, but about the mechanism of transport. Small peptides and membrane-bound proteins move in vesicles via fast transport. Large proteins not bound in membranes move via slow transport. The enzymes that synthesize the small neurotransmitters fall into this latter category. Importantly, although the neurotransmitters may be small, the enzymes themselves can be big, at least certainly bigger than the small peptides that are equivalent to the "large" neurotransmitters.

Absolutely fantastic answer. Thank you so much for this! Thanks to the links as well haha, I understand everything about the answer I was looking for. Thanks again.

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Can some prokaryotic cells be larger than eukaryotic cells?
Can the sizes overlap in some bacterial species? My science teacher claims so. My research says the opposite. Can someone confirm?

Overlap not even uncommon. Compare this Anabaena (Cyanobacteria) image and Chlorella (green alga) image. Many of the eukaryotic planktonic algae overlaps with size of cyanobacteria.

You should really unaccept the answer by Radek Martinez and change it to Remi.b's answer. The former is both unhelpful and simply not correct, while the latter gives specific examples of its point.

Prasinophytes are the smallest known eukaryotes. They are around 0.5 µm in diameter.
Thiomargarita namibiensis is the largest known prokaryote. They are around 100-300 µm in diameter.
So, yes some prokaryotes are much larger (up to about 500 times larger) than some eukaryotes.

To add to it, Pandoravirus, a virus, is about 1 µm by 0.5 µm. So not only can some prokaryotes be larger than some eukaryotes, some viruses are larger than some eukaryotes.


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Does X-inactivation lead to expression of sex-linked recessive disorders in half of carrier females' cells?
If one of the two X chromosomes in female mammals is randomly inactivated (i.e. becomes a Barr body) in each cell, shouldn't half of all cells in a female who is a carrier for an X-linked recessive disorder (say, Duchenne muscular dystrophy) express the disorder?

Similar question to: http://biology.stackexchange.com/questions/31635/in-human-females-one-x-chromosome-is-inactivated-forming-barr-body-then-how-exa

Yes and No... You are correct that X-Chromosome Inactivation will randomly inactivate the good X-chromosome (i.e. the one NOT carrying the mutation/disease) half of the time. However, this doesn't always seem to be associated with a disease phenotype. It likely depends on the gene and other factors, like the gene allele's function, to determine whether there is a disease phenotype that manifests with inactivation. Check out this paper that looked at Duchenne muscular dystrophy in females that is available freely on PubMed.


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Basic understanding of cell cycle (mitosis) phase
Update

This is for a diploid cell (2n).
At G1, cell growth before the DNA is duplicated.
At S, DNA replicated. Chromosomes doubled!
At G2, cell growth
Then Mitosis; Prophase, Metaphase, Anaphase, Telophase, Cytokinesis
Could anyone explain if the chart is correct or incorrect?

Closevoters: please read the actual text of the close reason. The OP here has clearly shown their attempt at an answer.

I agree with @terdon, this might be not the greatest question but there is no reason to close it.

can you explain what mlcl means?

Further one chromosome does not contain the whole genome just a chuck of it (however sometimes a whole genome can be on one chromsoome in the case of simple life forms such as bacteria) can you please specify  the organism you are talking about?

Mlcl= Molecule. and idk what organism is. It wasnt specify. Initial chromosome number was 6 (which i believe 2n=6).

how do you count the number of genome copies?

All chromosomes form the genome (https://research.cip.cgiar.org/confluence/display/potatogene/What+is+DNA,+a+gene,+a+chromosome+and+a+genome) ps you can tag me next time so I will get a notification (using: @Rick Beeloo)

@RickBeeloo Thank you so much for the link. It was definitely helpful. So since chromosome has 6 according to my question, then number of genome copies would be 6 in G1 phase. I know number of chromosomes increase in anaphase (# of chromosomes would be 12 in anaphase). I'd like to know if im on the right track.

The total set of chromosomes (in this case thus 6) is the genome (maybe the answer to this question will help you: http://biology.stackexchange.com/questions/24126/do-human-cells-contain-only-one-copy-of-the-genome and read the comments) so 6 chromosomes is 1 genome copy and 12 chromosomes are 2 genomes copies (only for mitosis then)

@RickBeeloo i have updated my answer. I think i get what you're saying. i see that in this case, only in anaphase the number of genome copies would be 2 since there is 12 chromosomes if 2n=6. On other cases, number of genome copies would be only 1 since there is 6 chromosomes in G1,G2,Metaphase, and after cytokinesis. Correct?

I think your chromosomes and genome numbers are correct now (you can look a this great explanation about human chromsomes during mitosis http://datbootcamp.com/biology-strategy/chromosome-and-chromatid-numbers-during-mitosis-and-meiosis/ ) I'm not sure what you mean with number of DNA molecules?

You might want to clarify that "DNA molecule" here refers to the entire double helix, with both strands. Since the strands are not covalently bound to each other, some would say that the double helix is made up of two molecules, one for each strand.

# DNA molecules
A chromosome can have either 1 DNA molecule or 2, this depends upon what stage the cell is at that moment. It actually might help to know what chromatids are:

A chromatid (Greek khrōmat- 'color' + -id) is one copy of a newly
  copied chromosome which is still joined to the original copy by a
  single centromere. (wiki)

This means that the number of chromatids is directly related to the number of DNA molecuels.

Before replication, one chromosome is composed of one DNA molecule.
  Following replication, each chromosome is composed of two DNA
  molecules; in other words, DNA replication itself increases the amount
  of DNA but does not increase the number of chromosomes.(wiki)

We can now add another row which indicates the DNA molecules, chromatids are directly related to the number of DNA molecules thus from left to right:
 46        92         92        46

These are the basics, now in some more detail about mitosis:

So based on the number of chromatids and your chromosome number you can figure out the nubmer of chormatids and thus the number of DNA molecules:
Thus before replication (G1) = 6, then after S phase (G2) = 12, then metaphase = 12 and after cytokinesis = 6. Just as in your table so that part is correct!

# of chromosomes
You can read these from the table, however I think it's important to understand what is happening. In simple words chromatids and chromosomes are related in this sense:

It is only when sister chromatids separate – a step signaling that
  anaphase has begun – that each chromatid is considered a separate,
  individual chromosome (source)

The phase in which the chromatids seperate is called anaphase, so after this seperation:

we consider the previoulsy chromatids as chromosomes. Thus anaphase and telophase contain the double number of chromosomes as the amount you started with. However anaphase and telophase are not mentioned in your table. So let's go back to the phases in your table. During metphase the chromatids are still connected to each other, meaning that we consider them as one chromosome (the same is true for G1 and G2, because we did not seperate anything). So that part of you table is correct too.

# genome copies

The human genome is the complete set of nucleic acid sequence for
  humans (Homo sapiens), encoded as DNA within the 23 chromosome pairs
  in cell nuclei and in a small DNA molecule found within individual
  mitochondria.(wiki)

However read this question and the answers,  some say 1 genome per cell and some say two genomes per cell, this confuses me too so I'm not sure about this one, however based on the wiki it would say that 2n = one genome, which would make sense because the two pair of chromosomes are not equal and when saying you have two genomes per cell you are actually counting mitochondrial DNA twice.

I think the number of genome copies is correct on my chart. What do you think?

I think it is @Chris


text:
Does one memory cell take part in different memories?
Does one memory cell take part in different memories? For example, both in the visual memory of a bird and a monkey?

According to engram theory: Yes.
However, you need more than one cell to encode a memory engram.
The idea is that the combination of cells encodes the memory, not the cells themselves.
I am most familiar with the hippocampus, in which cells participating in the encoding of "concepts" like Jennifer Aniston, Bill Clinton or the Sydney Opera House have been found in humans Quiroga et al. (2008)


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Why we utilize dextro glucose and levo amino acids?
Our body only digest dextro(Right handed) glucose and levo(Left handed) proteins and can't digest Levo glucose and dextro proteins. Why?
Our body synthesis levo proteins. What is the reason?

Because of different proteins taking care of each.

Great question - AliceD is correct that our enzymes exhibit stereospecificity for each, but there is also another vital reason why humans utilize D-glucose and L-amino acids... will post as an answer

I am not clear what your question is. Are you asking why only one stereoisomer is used in each case, or are you asking why it is D-sugars and L-amino acids (rather than D-amino acids)?

Our body digests only certain type of enantiomers like L amino acid and D sugars because enzymes are specific for their substrates stereochemistry meaning they will only recognize a particular enantiomer.So I hope this answers to your first question.
Now, why we only see L amino acids and D sugars, there is some interesting hypothesis listed in this article.Here is the link
http://guava.physics.uiuc.edu/~nigel/courses/569/Essays_Fall2006/files/Rajan.pdf
I am adding some answers I found from research gate here, which includes
1)I think the prevalence of L-amino acids in biological systems is a quirk of our evolutionary history; there's no reason D-amino acids wouldn't work chemically, but once early life forms started building proteins out of L-amino acids, L-amino acids became abundant an it became selectively advantageous to use L-amino acids because then you could use the amino acids you obtained by eating someone else. It's a matter of compatibility; if you use D-amino acids, you have to build them all from scratch, because you're not going to find them in your environment. As long as you use L-amino acids, you don't even need to maintain the de novo synthetic pathways; you can just eat something that has those pathways (hence the 'essential' dietary amino acids).
2)There are a couple of reasons for biological homochirality.
One, our galaxy has a chiral spin and a magnetic orientation, which causes cosmic dust particles to polarize starlight as circularly polarized in one direction only. This circularly polarized light degrades D enantiomers of amino acids more than L enantiomers, and this effect is clear when analyzing the amino acids found on comets and meteors. This explains why, at least in the milky way, L enantiomers are preferred.
Two, although gravity, electromagnetism, and the strong nuclear force are achiral, the weak nuclear force (radioactive decay) is chiral. During beta decay, the emitted electrons preferentially favor one kind of spin. That's right, the parity of the universe is not conserved in nuclear decay. These chiral electrons once again preferentially degrade D amino acids vs. L amino acids.
Thus due to the chirality of sunlight and the chirality of nuclear radiation, L amino acids are the more stable enantiomers and therefore are favored for abiogenesis.
3) Morozov, L. 1979. Mirror symmetry breaking in biochemical evolution. Origins Life Evol Biosphere 9: 187-217
But I think we have D amino acids also, as this paper says https://www.hindawi.com/journals/scientifica/2016/6494621/
Hope this helps!


text:
What causes the cardiac ventricular pressure change during the isovolumetric part of the cardiac cycle ?
Why does the cardiac ventricular pressure change during isovolumetric contraction and relaxation. The volume ( both valves are closed)  is constant, Does Boyle's Law not apply?  P1V1= P2V2 at constant temperature.

Remember - during isovolumetric contraction and isovolumetric relaxation that the wall tension and thus pressure within the ventricle is changing, despite no changes in volume. Can you add some more to your question to show that you've given more of a research effort? Like add an illustration or graph of what you're thinking? It would definitely improve the quality of your question.

Boyle's law doesn't apply to all fluids: only gasses, not liquids. Liquids like blood are (mostly) incompressible, so their volume does not change substantially when you add pressure.
During isovolumetric contraction, the ventricular walls are pushing in on the blood contained in the ventricle, causing the increase in pressure, but there is not yet sufficient pressure to force the blood out the pulmonary/aortic valve.
Source:
Hillegass, E. (2016). Essentials of cardiopulmonary physical therapy. Elsevier Health Sciences.

The pressure increase in Ventricle is due to the depolarization of Ventricle myocardial cells I.e. the continued action potential through the ventricle noted as QRS wave in ECG.
This makes the ventricles contract and hence the pressure increases without changing the volume of the blood as all the valves during isovolumetric contraction are closed.


text:
How did the nucleus of eukaryotic cells evolve?
What is/are the most popular theory/theories on how the nucleus evolved?
I know mitochondria came from alpha-proteobacteria, chloroplasts from cyanobacteria and that eukaryotes evolved directly from archaea, but what about the nucleus?

Devos et al. 2014 will be of interest as well as wikipedia > Nucleus#evolution.

I hope these papers by Wilson and Dawson (2011) and Devos et al. (2014) will help you.
In summary these two review provide evidence for the following statements:

The nuclear pore complex is well conserved with some regions of divergence.
The nuclear lamina appears quite variable between major supergroups.
Centrosomes are ancient structures but exhibit a complex evolutionary history.
There is evidence for prokaryotic ancestors of some nuclear components.
Analysis of divergent organisms is essential to fully understand nuclear biology and its origins.

But this is not an answer to the question. The poster is clearly asking for theories on the origin of the nucleus (he makes comparison with the origin of mitochondria) but your ‘summary’ of the papers does no more than say “there is evidence fro prokaryotic ancestors of some nuclear components”. Answers need to be self-contained and provide information in response to the question.


text:
Why metacarpus is considered hand proper?
This textbook states

The hand (or manus) consists of the following parts: (a) wrist or carpus, (b) hand proper (or metacarpus), and (c) digits (thumb and fingers).

How could I justify why are digits not considered as hand proper? Hand is a prehensile organ and digits are of primary importance for prehension. So then how could metacarpus be considered as hand proper?

Proper in this instance means the main body of the hand, the part that has no other identifier. the fingers and wrist have other terms to identify them, the hand proper does not. If I say the the hand you are not sure whether I mean the hand as a whole or that part in particular so it is called the hand proper. Its an old usage of the word, but that is common in anatomy text.
From webster it is the 6th definition. Proper: strictly limited to a specified thing, place, or idea

If you define a hand as a prehensile organ, try grasping an object with just your fingers(digits). Try that action without your thumb.
You cannot make a firm grasp of anything without using your metacarpus. Most people don't hold thing using just their fingers. In effect your prehensile organ known as the hand is incomplete is you include only fingers. The metacarpus are involved in the grasping action.
Finally what amounts to a hand has already been defined. So metacarpus is considered part of the structure that we call a "hand".

But why the adjective "proper"?

There is possibility to grasp objects only with fingers but it's impossible to grasp objects only with metacarpus. So why is it still considered as hand proper?


text:
Do we know the physical-nature of "senses" or qualia?
We have a peculiar property/ phenomenon called  having 'sense' or qualia, also sometimes called as consciousness.
Such as, if we see a red flower; we perceive a particular colour, "red". That is an example of sense.
Now scientists could tell, what was the wavelength of red light, which group of cone-cells responded, what group of nerve-fibres were sent message to which part of brain; and how the informations are being computed in brain, what gene-expression-pathways are working. They can describe the chemical reactions and other molecular interactions, even molecular-orbitals taking part.
But could science yet tell; what was that "red"? and why it was not perceived-as blue but was perceived-as red? Similarly, hot, cold, pain, tickle, joy, fear, hunger... whatever we "sense" in our mind; what are they made up of? Are they simply flow of information? doesn't seem.  Could chemical-reactions make-up sense? or what else they could be?

To avoid the answer from being too-broad; I can simplify it in following  alternatives:

qualia does not exist. It is just a myth.
qualia exists, but it is nothing more than information and computation.
qualia exists, but we do not know its nature.
qualia exists, we know its nature, and that is more than information and computation.

Which one is true on present scenario?

I'd post this as a comment rather than a question as I do not know categorically. I'm pretty sure the answer is 'No'. That said, the real argument I think is similar to that of free will. Few people are seriously arguing that we AREN'T conscious, but rather whether we have 'consciousness' or rather something that is an illusion of consciousness - we know what it feels like, but thats all we can really say.

@JoeHealey Don't know how you could think it... do you NOT feel any 'pain' when a nail get pricked in your feet?

Sure, but you cannot know whether your perceived sense of consciousness or an actual 'consciousness' is responsible for you detecting that stimulus. That's pretty much my point, you can't disentangle those 2 concepts. Really the only counter argument I think you could make is that those 2 distinctions are pretty semantic, and functionally it doesn't matter. If you consider lower organisms, 'pain' is a pretty conserved feature, but at what point do you decide an organism is not 'aware' of the pain? i.e. where does the line between what we consider consciousness and not begin to blur?

Yeah it's tricky in the character limit of comments. Give me a few minutes and I'll try to distill my ideas in to an actual answer - but it will still just be my opinion. I have a feeling this question might be a bit subjective, but maybe someone has more reliable sources.

I meant your phrase "perceived sense of consciousness or an actual 'consciousness' is " is not clear to me. "Sense" (such as red, blue, green, cold, hot etc) and "consciousness" are same thing in semantic (grammatical) difference. That is NOT my point. Did you mean entangle of "Feeling Pain" and the biochemical "Information" of injury?

I don't think it is subjective or opinion-based. It is clear that we have ability to get "sense". And it seems strange how some bit of information would work as red, green, do, re, mi or cold or hot. For me it must be something more than "informations". Might be those thinking consciousness does not exist; are actually missing the point.

I would disagree with you that the different between "sense" and "consciousness" is only semantic. We very definitely understand sensory mechanisms. For example, we understand HOW we see/perceive "red". What we don't understand is what the 'concept of red' is. To me, that is the difference between 'sense' and 'consciousness'.

Let us continue this discussion in chat.

I'm voting to close this question as off-topic because this is a CogSci question. Migration is not advised though as the site is already crammed with like minded questions. I advise OP to go to that site, refine the question and see what can be made of it.

@Christiaan Why it is off-topic here, and what are the possible duplicates you think?

@Christiaan is it due to because "You should only ask practical, answerable questions" here ? however still I think it is a scientific question though it is unsolved mystery to us yet. So our question database should contain one. As well one possible duplicate I could find there (http://cogsci.stackexchange.com/questions/15667/can-a-sufficiently-complex-ann-simulate-consciousness) , is closed

As well that cogsci question is not an exact duplicate.

I'll try my best to give you my answer. But I maintain that this is still somewhat subjective.

Firstly, I think the short answer to your question as stated:

Do we know the physical-nature of “consciousness”?

Is no.
I would personally say that our notion of 'sense' - that is, our ability to perceive stimuli, is not the same as consciousness (whatever "consciousness" means at this point). To me, and I think many others, the concept of 'consciousness' is simply being self-aware.
Science understands most if not all sensory pathways very well in terms of the electro-chemical and/or mechanical pathways involved.
To pick from your 4 options:

Consciousness does not exist. It is just a myth.
Consciousness    exists, but it is nothing more than information and computation.
Consciousness exists, but we do not know its nature.
Consciousness    exists, we know its nature, and that is more than information and    computation.

I think we can rule out 1 - we know we have something that we call consciousness - else we wouldn't be having this conversation!
We can certainly rule out 4 as well because we also wouldn't be having this discussion if it's nature was understood by now! :)
My own opinion steers me toward 3. Though I think understanding it might actually be impossible.

To run with your example of perceiving the colour red, I concur that we understand the physical processes that have occurred to enable us to see, and understand that we saw, red.
However...this puts me in mind of a kind of brain-teaser people sometimes mention: how do I know that what I consider to be red, is the same thing you consider to be red. Now, I don't personally think there's much to this, as colour is a physical property, but it does raise the possibility that the 'concept of red' is not immutable between individuals.
Some more food for thought is whether we actually possess a consciousness. By which I mean, it is an extant, natural phenomenon, like energy for instance, and you either have it or you don't. The alternative is similar to the debate about free will vs. the illusion of free will (I personally fall on the side of thinking the latter). That is to say, do we merely have the illusion of consciousness?
Taking the discussion from the comments about pain and expanding further; just because I feel pain, I do not believe equates to consciousness. How far down the evolutionary tree do you have to travel before you would decide a creature has no 'consciousness'. Sure, we probably agree dogs are conscious, but are they self-aware? Do they exist any further than to satisfy their biological needs? Even if we say yes... how much further do you need to go? Are sharks self-aware? Are hag-fish or nematodes self aware? And yet, we know that all these organisms are capable of sensing pain. So it's clear that simple sensing pain is not enough.
The last thing I recall reading about the basis of consciousness (and the closest thing I think we have to an answer as to what the physical basis of consciousness is) is that it is an emergent property of a complex system like our brain. The degree of 'inter-connectedness' in our brains is what makes us intelligent (not just size), and current thinking is that it's the density and number of networks inside the brain that is key.

"Sure, we probably agree dogs are conscious, but are they self-aware?"  I did not meant self-awareness or existential intellegence. So, should on OP I use only the term "Sense" instead of "Consciousness"? As well, term "sense" too have 2 meanings. When we tell about "red", "green", "sweet", "salty" etc as sense; it indicates certain entities/ features in our "mind", which we can not deal "from outside". Whereas when we tell "electronic sensor" or even ligand sensing; we simply indicate information detection.

Hmm.. perhaps I'm misinterpreting your meaning. Is what you describe as 'sense' (e.g. "To have a sense of.."), what is more properly known as "quale" (pl. "Qualia")?  https://en.wikipedia.org/wiki/Qualia

Thank you for your effort. It is NOT a terminology question, but seeking nature of a phenomenon which is existent yet at a grey zone in science and under high debate.

Sure, I know you aren't asking what the term is. I was trying to estabilsh wether qualia is what you were referring to when you say 'sense'. I'm just trying to establish what we both mean :)

I did not knew the term quale.  However doesn't seem to me "the density and number of networks inside the brain that is key". If complexity is the cause of sense, I have to say a supercomputer with artificial intelligence posses sense. It seems to me, the phenomenon of sense is exclusively found in living things.

That is the basis of machine learning/artificial intelligence though. The interconnectedness of layers of ANNs is exactly what makes them powerful, when combined with reinforcement. Furthermore, if you compare a supercomputer running the largest neural network you could manage, the number of interconnections would likely still be several orders of magnitude smaller than the trillions of connections/synapses in a human brain.

Let us continue this discussion in chat.

Let us continue this discussion in chat.

Oops no so many chat-rooms being created. Actual one is here

Based on logic, I would go with 3. The qualia (or 'senses' at its most colloquial meaning),  exists. But we do not know its nature.
But the problem with dealing it experimentally, because qualia are

private; that is, all interpersonal comparisons of qualia are systematically impossible.

, as mentioned by wikipedia in a description by Daniel Dennett ,  though  it is not clear to me any difference in his terms ineffable and private in the 4-point description cited on wikipedia.
It is not possible for us to conclude about whether a dog or bacteria or robot or stone or even another person do have any qualia or not.

However to me it does not seem it could be interpreted as only an emergent property. If we keep up the complication of an AI network, why the codes will once start to feel some "red" or "green" or "hot" or "cold" or something like that.

It doesn't seem at present we could do anything with it (but if we tell it does not exist, then it would be a denial to a truth. In fact even if it is accepted as an "illusion", then we have to accept, "that-illusion" exists.) . However, may be in far future we would be able to decipher it; as Dalton shown us the first atom, or Bequerel the first radioactivity, or Mendel for the first time that we have 'something to do' with the phenotypic expressions of living creatures !


text:
Need clarification on Coalescent with Recombination
I've been reading about recombination with coalescent. The link to that file is as follows:
http://www.stats.ox.ac.uk/__data/assets/pdf_file/0008/4688/Reading_for_Recombination.pdf
I get the part where it says (page 142) that the rate of a coalescence event is k(k-1)/2 and the rate of recombination is kp/2. The image they have on the same page shows the intensity of coalescence and recombination. But I don't quite understand how those have been calculated. I mean the first event is a recombination event and not a coalescence event. I know they are using the rate formula I've mentioned above but I don't understand what sequences they are considering. If someone can give me a detailed answer I would really appreciate that.
I've attached the image as-well incase you don't want to read the pdf :)

Can you provide citation for the now-broken link?


text:
What is the difference between these two depictions of chromosome?

I understand that this is a single chromatid, but would this be considered a chromosome? Also before mitosis, the chromosomes appear as single chromatids but during interphase they replicate to form sister chromatids which are attached by a centromere and are also collectively known as a chromosome.
I do not understand the difference between the two of them. Are they both to be termed chromosomes?

Here is the thing, chromosome refers to a lot of different things ( however, all are coiled up DNA).
Let me explain step by step.
You have DNA, it has a diameter of 2nm, it is coiled with histone proteins and make 10-11nm fiber. This is what we refer to as the chromatin fiber(Beads on a string). At this point we are in interphase where too much coiling is not required because a lot of transcription, replication going on. At the S phase of the interphase, DNA replication takes place and sister chromatids are formed or do they? The answer is yes and no. The thing is even though DNA has replicated and coiled upto certain extent, we dont call the replicated dna as sister chromatids because we only consider them to be sister chromatids when we can clearly see them as separated threads connected at centromere during the M Phase.
So, to put it in simple words, you have the sister chromatids formed (during the S phase) long before you are actually calling them as sister chromatids, you just wait for them to condense further and when you can finally see them as distinguishable threads you call them as sister chromatids.
Now, your real question can be answered. You have posted two chromosomes, one green and the other is red, red has two chromatids connected at centromere. Lets start with the red chromosome. The red one is the metaphase chromosome. Try to remember cell cycle. You have your DNA replicated by the S phase of interphase, then comes G2 and then M Phase starts with prophase, at this point your chromatin fiber gradually starts getting condensed and by the end of prophase, your 10nm coiled DNA (Chromatin fiber) ends up coiled to 700nm fiber but remember, you have two 10nm fibers connected at centromere after the S phase but they were so thin that you could not distinguish the two threads separately, now you can because they coiled in a very organized manner and now you have two 700nm fibers attached at the centromere, this is the maximum condensation achieved and as this final condensed version is observed at the metaphase it is named metaphase chromosome.
So, the red one is definitely a chromosome. What about the green one? That too is a chromosome. the green one is formed at the next step of cell cycle that is anaphase. Here the two sister chromatids split at the centromere and move towards the opposite poles of the cell as  new chromosome. but wait, haven't I called them sister chromatids throughout the answer and suddenly calling them chromosomes? Yes, the previously called sister chromatids are called as  individual chromosomes the moment they are separated from each other at anaphase.
So in summary, the thread like structure that you see in interphase are coiled DNA(Not called chromosomes), chromosomes are also coiled dna but the difference is that these are way more coiled. The red one is metaphase chromosome (1400nm) with two sister chromatids(700+700=1400). The green one is also chromosome but these are actually sister chromatids that got separated at anaphase(only 700nm), you can call them as daughter chromosomes
I hope this helps

Before S-phase the nucleus has two copies of each chromosomal DNA, e.g. a pair of Chr-1 DNA molecule.
During S-phase each DNA molecule replicates and after condensation ends up forming a chromosome(dyad) with two chromatids (sister chromatids). At metaphase a cell has 46 dyads (considering mitosis/Meiosis-I).
This dyad then separates at the centromere in Anaphase and the two chromatids move towards two opposite poles. On reaching the poles they are called chromosomes.

The word for such chromosome is dyad, but it is relatively less in use I would say.


text:
What are some uses of oxidative/reductive power inside cells?
I know respiration and photosynthesis are based on oxidation and reduction, and the formation of NADH and NADPH in them is very important for many cell processes. I know that NADPH, for example, is used in the CBB cycle to fix carbon. However where else are oxidation and reduction reactions needed in cells? I can think of an example for oxidation: getting rid of toxic products. For example, alcohol dehydrogenase in the liver oxidises alcohol to acetaldehyde. However I can't think of much else, and i'm especially stuck on ehy reductive power is useful in cells.

This topic is quite broad, excluding energetic metabolism, there are still many reactions that use redox equivalents, whether NADH, NADPH, or FADH. Here are some paradigmatic illustrations.
Xenobiotic metabolism

Oxydation of substrate : as you mentioned, alcohol to aldehyde to carboxylic acid. Generate reducing power. (The alkane oxydation shown below occurs in bacteria)

Mono-oxygenation : hydroxylation of a substrate with $O_2$, with the other oxygen atom reduced to water. This proceeds as follow with CYP450 enzymes :

Regeneration of oxided gluthatione

Anabolic metabolism
Basically every time there is a need to create/remove a double bond, or move from carbonyl to aldehyde to alcohol and back, redox equivalent are used.

Fatty acid elongation : as this proceeds with acetyl-CoA as carbon source, intuitively one sees the need to reduce the carbonyl to obtain an alkane chain.

HMG-CoA Reductase (HMGCoAR) catalyses the commited step in cholesterol synthesis.

Synthesis of prostaglandins from arachidonic acid. (More generally, any lipidic mediator)

There are many, many more examples. You may want to check out the Wikipedia page for NADH, NADPH, FADH, or the list of enzyme that use them (1, 2, 3)
All illustrations from Biochemical Pathways, G. Michal & D. Schomburg, 2nd edition, Wiley


text:
NADH generated by glycolysis must be oxidized back to NAD+ in order for glycolysis to continue. What three positive pathways exist for this to occur?
I know where NAD+ is reduced to NADH but don't have the slightest clue as to three pathways where NADH is oxidized to NAD+.
If you could give me some guidance that would be great!


text:
Does a gene code for protein molecules or a DNA codes for protein molecules?
To my understanding, a gene consists of a unique sequence of nucleotides that codes for a polypeptide or an RNA molecule. In my textbook, it is stated that DNA codes for protein molecules.
So I thought, a gene only code for 1 protein molecule or 1 RNA molecule
However, DNA can code for a number of protein molecules or RNA molecules, as a gene is a stretch of DNA.
Is my understanding correct?

Your understanding is correct in that DNA encodes RNA, and this is a one-to-one relationship generally (although there are exceptions, see link below).  However, a given RNA can encode myriad proteins via translation.  This is because of different translation start sites and splicing of RNA.  You can read about this relationship between DNA/RNA/protein (the 'central dogma' of molecular biology), here:
https://en.wikipedia.org/wiki/Central_dogma_of_molecular_biology
But in the title of the quesiton you also ask about whether a gene or DNA encodes protein.  A gene is comprised of DNA; if someone talks about a gene, this just means a transcribed sequence, i.e. a region of DNA that is made into RNA.  Whether or not this is then translated does not impact its definition as a gene.  If it is transcribed, you could call it a 'protein-coding gene', otherwise you can call it a 'non-coding gene'.


text:
What type of immersion oil should I buy?
I have an old Nikon Alphaphot microscope that came with a 100x oil immersion objective, but no manual. I've seen plenty of sources that explain that you need to place a drop of oil between the slide and objective, but when I went to order immersion oil I discovered that there are several different types. There's Type A, Type B (apparently similar to Type A but more viscous), and a number of specialty types. My plan is to use the microscope for projects like looking at blood cells, pond water, and other high school science project-type investigations?
Which type of immersion oil is right for all around, general purpose use?

For the best image (where you lose the fewest photons and get less refraction), you want the immersion oil to have a refractive index as close to the refractive index of the coverslip you intend to use.  In my experience, this is not much of a consideration on the oil-side, but rather on the coverslip-side.
There is little difference between type A and B oil, although for other types of oil see here.  If I were you, I would just use some type A.
For a lesson on the impact of immersion oil on optics, see this Zeiss website (similar sites for Nikon and other scope manufacturers exist too I'm sure!)


text:
Why does capsaicin irritate mammals and also kill fungi? Are the two related?
From this article I heard about a study (search "Tewksbury") which concluded that chilies make capsaicin to discourage mammals from eating their seeds, since grinding by mammals' molars render the seeds unable to germinate. Birds, on the other hand, don't break open the seeds and spread the plants far and wide.
But, they also reference a different theory: capsaicin evolved to defend against a certain kind of fungi that infected pepper plants.
My question is: why does the same chemical do these two things? It seems like quite a coincidence, unless capsaicin has some general destructive properties. But Wikipedia's explanation talks about how capsaicin artificially stimulates a certain receptor in our mouths -- which sounds totally unrelated to fungi.

Recent study has shown that capsaicin indeed has antimicrobial properties. For example, see this article:

Two pungent compounds found in Capsicum species (capsaicin and dihydrocapsaicin) were also tested for their anti-microbial effects. The plain and heated extracts were found to exhibit varying degrees of inhibition against Bacillus cereus, Bacillus subtilis, Clostridium sporogenes, Clostridium tetani, and Streptococcus pyogenes.

In one of the attempts to study its mechanism, a study on yeasts suggested that it works in following ways:

Detoxification of capsaicin by a PDR-type ABC
superfamily of multi-drug resistance transporters
Osmotic stress response and damages in membrane
structure caused by the capsaicin treatment
Genotoxicity of capsaicin to yeast cells
The effects of the deletions of the genes those were
induced by the capsaicin treatment
Mechanism of capsaicin in the growth inhbition to
yeast cells:
The DNA microarray analysis of antimicrobial
mechanism of capsaicin shows that capsaicin induced
an osmotic stress element, the key genes for membrane biosynthesis, and the PDR network and repressed the genes for ribosomal components
and cellular growth. The growth characteristics of
deletion strains suggest that PDR5 is important for
the resistance to capsaicin. These observations that
the PDR network may pump out capsaicin from cells
are the first findings. The contribution of the PDR
network also suggests that capsaicin enters to the
cells and capsaicin functions as a toxic substance to
the yeast cells. This toxicity is possibly to the
mebrane structure and/or as osmotic stress.
Full article (PDF) here.

Though in mammals, its mechanism of action is quite different; it acts on ion channels to give a burning sensation. See this article:

The burning and painful sensations associated with capsaicin result from its chemical interaction with sensory neurons. Capsaicin, as a member of the vanilloid family, binds to a receptor called the vanilloid receptor subtype 1 (TRPV1). TRPV1, which can also be stimulated with heat, protons and physical abrasion, permits cations to pass through the cell membrane when activated. The resulting depolarization of the neuron stimulates it to signal the brain. By binding to the TRPV1 receptor, the capsaicin molecule produces similar sensations to those of excessive heat or abrasive damage, explaining why the spiciness of capsaicin is described as a burning sensation.

However, it is toxic for mammals too. Capsaicin is a highly irritant material requiring proper protective goggles, respirators, and proper hazardous material-handling procedures. Capsaicin takes effect upon skin contact (irritant, sensitizer), eye contact (irritant), ingestion, and inhalation (lung irritant, lung sensitizer). The LD50 in mice is 47.2 mg/kg.
Though its mechanisms are different, it performs quite similar functions: protecting the plant from predators and infections i.e. a defense system.
It seems like quite a coincidence, unless capsaicin has some general destructive properties.
It is neither a coincidence nor capsaicin has general destructive properties. In fact, capsaicin is being used as an analgesic too. See this article:

Capsaicin is a chili pepper extract with analgesic properties. Capsaicin is a neuropeptide releasing agent selective for primary sensory peripheral neurons. Used topically, capsaicin aids in controlling peripheral nerve pain. This agent has been used experimentally to manipulate substance P and other tachykinins. In addition, capsaicin may be useful in controlling chemotherapy- and radiotherapy-induced mucositis.

Its mode of action is, seemingly, somewhat similar. See this:

The mechanism of action of topical capsaicin has been ascribed to depletion of substance P. However, experimental and clinical studies show that depletion of substance P from
  nociceptors is only a correlate of capsaicin treatment and has little, if any, causative role in pain relief. Rather, topical capsaicin acts in the skin to attenuate cutaneous hypersensitivity and reduce pain by a process best described as ‘defunctionalization’ of nociceptor fibres. Defunctionalization is due to a number of effects that include temporary loss of membrane potential, inability to transport neurotrophic factors leading to altered phenotype, and reversible retraction of epidermal and dermal nerve fibre terminals. Peripheral neuropathic hypersensitivity is mediated by diverse mechanisms, including altered expression of the
  capsaicin receptor TRPV1 or other key ion channels in affected or intact adjacent peripheral nociceptive nerve fibres, aberrant re-innervation, and collateral sprouting, all of which are
  defunctionalized by topical capsaicin. Evidence suggests that the utility of topical capsaicin may extend beyond painful peripheral neuropathies.

(P.S. substance P is a neuropeptide, a potent vasodilator & iniates expression of almost all known cytokines.)
Pay attention to the last line 'utility of topical capsaicin may extendbeyond painful peripheral neuropathies.' i.e. capsaicin may have more effects on body than known!

So why does the same substance have these different mechanisms of action in different organisms? Is this common in biology?

It is so because of structural complexity of compounds. Many compounds out there and in here are similar in structure; this is the cause of side-effects of drugs, it is the cause of competitive inhibition of enzymes, and so on. It is not very common, but no surprise if we keep finding more such cases.

Capsaicin binds to an ion channel that is fairly well-conserved across metazoa and fungi.  Influencing the activity of an ion channel can have a seemingly small impact on us (e.g. spicy food 'taste') but for a colony of fungus, such activity can cause the individual cells to stop dividing or migrating in a certain direction (fundamentally changing their behavior).  In other words, capsaicin can be lethal or at least make living difficult!  For more information about these channels and the specific mode of action of capsaicin in mammals, see David Julius' lab website.

Interesting, and thanks for the link. Since I don't have a biology background, what is an ion channel and what functions does it perform? Would it be correct or approximately correct to say "Yes, capsaicin does have 'general destructive properties', the property being that it binds to this ion channel which is important in a lot of life forms" ?

see metroplex's tome-like response below.  'destructive' is inaccurate; it's not destructive to birds apparently, and it's not destructive to the plants that produce the compound.


text:
Division of proteins
This textbook states

Proteins determined by a single gene may divide to form different proteins with various physiological actions.

First how do proteins divide? Second if it's just fragmentation then what is this process called? Third since my textbook doesn't explain it could anyone explain with an example of how different parts of original protein( considering that protein has divided by fragmentation) perform different physiological actions?

This is not a very helpful passage, I agree.  Some proteins are cleaved by other proteins (a protein that cuts another protein is called a protease).  Other proteins cleave themselves.  Otherwise, proteins are quite stable and don't just fragment wily-nily.
In the case of the first group (proteases acting on other proteins) the coagulation cascade may be a good place to start for you.  Precursor proteins in this pathway are converted to active enzymes by a chain reaction of protein 'division' and other protein modification.  This page has other interesting cases of this process, such as in food digestion, which may be what you're looking for.
Some of the second group are self-cleaving such that an intervening sequence is removed, and the ends are pasted back together.  (This is analogous to how introns are spliced from messenger RNA and the exons are spliced together.)  Such intervening protein sequences are called 'inteins'; the removal of one intein can generate one functional protein, so this isn't protein division.    However, some viruses encode self-cleaving regions that will split the mother protein into two or more pieces.  A famous example of this process, now used widely in biotechnology, is the 2A peptide, which is used to 'split' a single transgenenically-expressed protein into 2 (For instance if you want to express a protein and a marker such as GFP simultaneously, you could employ the 2A peptide to link these together.)
The first group may be of more interest to you because of the known role of these proteases in human health.  Also, in your question it sounds like you also may be referring to random 'fragmentation' of proteins, which is not currently known to be an important contributor to protein breakdown in the human body, even in the stomach.  Enzymes such as pepsin are responsible for digesting proteins.

Good mind reading! The use of the word ‘divide’ here makes it clear the author of the book knows little or nothing about this subject. Not too suprising in  a book on physiology. The questioner should be warned.

I don't have access to the textbook, but my first thought is that the author is talking about gene duplication during evolution. If a gene duplicates, the two copies may end up diverging, creating two similar but slightly specialized proteins that fulfill different functions.Wikipedia
I agree that the sentence is not well written, whatever the intended meaning. Some context may be helpful.

I don't think that's the case. It mentions "proteins determined by a single gene", as in different isoforms produced by alternative splicing. In addition, it could be referring to certain polypeptides such as PTH, which is cleaved into two smaller fragments.


text:
Staying underwater: would mutual rebreathing help?
If two people want to stay underwater for as long as possible, could they last longer if they exchange breaths in turns (ie: through a simple tube or mouth-to-mouth) than if they simply hold their breaths alone?
Would there be any dangers in doing this somewhat regularly?

Theoretically:
I'm going to assume that in your scenario, both individuals took a deep breath of regular air before submerging themselves, as this changes quite a lot (you'll see why in a second). Regular air on Earth as you probably know is made up of 78% Nitrogen, 21% Oxygen, and other trace elements like CO2 and ArgonColumbia University. What we care about is oxygen, as this is what our body can't function without.
The air we exhale is approximately 14-16% oxygen [2], which is a significant decrease, but is still very breathable. If we choose 15% as the exhaled percentage and 21% as the inhaled percentage, the percentage decrease is approximately 29%. Thus, with each breath taken by the other individual the amount of oxygen in the shared air decreases drastically. Another problem is the dilemma of CO2, which is exhaled at a 5% percentage increase. I would imagine the two people wouldn't make it more than a minute before the oxygen level in the shared air is too little to be absorbed and the CO2 makes them both lightheaded to the point where they faint and forget about the tube altogether.
If both individuals had breathed in pure 100% oxygen it would delay their impending deaths but it wouldn't prevent it. I love doing this sort of stuff and could calculate the difference in time between both before the air is unbreathable but...
Practically:
It wouldn't work. It may sound like something that would work but think about it this way: the very first breath one of them takes it literally sucking the air out of the other's lungs. No matter how much one tries to synchronize breathing in and out with the other -  based on lung size, lung volume, diaphragm surface area and many other factors - one's breathing in simply cannot equal the other's breathing out. One of them would eventually breathe in too much, leaving the other choking and gasping for air, leading to a tug-of-war of air, that unless they resurface will lead to both of them drowning.
[2]:
P.S.Dhami; G.Chopra; H.N. Shrivastava (2015). A Textbook of Biology. Jalandhar, Punjab: Pradeep Publications. pp. V/101.

Another method: Since CO2 production rates are higher when breathing from a tube (compared to both people holding their breaths), both people would run out of air faster.


text:
Why babies cry after they are born?
Well I have noticed that almost all of the babies cry after birth, but some of them (1 to 1,000,000? births) don't cry. So, we have:

Why is this happening (the cry after birth)?
Also why animals babies don't cry when they are born, but human babies cry? I have noticed that many mammals such as giraffes or chimps don't cry at all (The chimp only makes it's ordinary sounds).
Are there any special genes that humans have and animals not?

Lots of baby animals "cry" after they are born, everything from puppies to calves often vocalize when born

Crying keeps lungs dry by increasing alveolar air pressure, which otherwise is fatal.

I don't know if you have ever witnessed one, but childbirth is a rather extreme and violent expierence, were the child is pushed through something that is a bit to small for its head. That alone would be reason enough to cry. And crying has indeed a function for the lungs, as explained by JM97

Mouse pups chirp to communicate with their dame. However most of the they make are at frequencies far higher than a human ear can hear.

Having delivered at least a hundred babies, I guarantee you that your statistic is wrong. As long as the baby is breathing, the fluid in the lungs will be resorbed. Still, usually they are cold and wet and under bright lights when delivered. The more you mitigate this harsh new environment, the more peaceful the birth can be. Some babies don't cry at all. If everything else is ok (color, muscle tone, heart rate, etc.), it's no biggie.

So, you believe that they cry because of that change?

Just saw a water delivery, and the baby spoke briefly to say hi, he didn't cry. https://www.youtube.com/watch?v=U2AIRNxTFjk Depends how tight the bird is too. sometimes it's only like going down a airplane escalator for the baby.

Babies start crying when they realize that they have been born in Hell (of sensual perceptions).

I'm answering this question (mostly) based on prior knowledge.
Inside the womb, the foetus relies on the mother for oxygen i.e. it receives oxygen from the mother's bloodstream via the umbilical cord.  A foetus doesn't use its lungs for breathing inside the womb. Ever.
Besides, lungs of a foetus are considered fully matured no earlier than the 36th week of pregnancy. (Though there are exceptions to this)

During fetal life the baby's lungs are filled with fluid and they do not perform any respiratory functions. [1]

At birth, the baby is forced to breath on its own for the first time. Hence, the baby cries - or more precisely - gasps for air.
This 'cry' of the baby is actually a strong respiratory effort, thereby aiding the baby in its first breath. This is also why newborns don't produce tears on their first cry. Because it's not really a cry, it's a gasp for air.
Now the reason why such a considerable effort is required for the newborn to breathe is because:
A) Lungs are being used for the first time, and
B) The lungs of a foetus are filled with amniotic fluid when it's inside the womb. Effort is needed to push this fluid out from the lungs after birth.
I'm not aware if there's any genetics involved in this. I don't think there is.
Source: [1] http://www.thehindu.com/todays-paper/tp-features/tp-sci-tech-and-agri/babys-first-cry/article2267767.ece

I don't disagree with answers that talk about lung function. But a scream would do the same thing. About whether humans are unique, in terms of care they are among the most helpless of animals. Crying in babies is a form of communication that calls the parents into action when care is needed. In the first moments of life in the light and air, besides the shock of being squeezed through an opening so small that the skull is squeezed into a different shape (ouch), an infant urgently needs care.

This water  baby delivery did not cry, it practically only spoke. https://www.youtube.com/watch?v=U2AIRNxTFjk


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Gorgonopsid--What's In a Name?

The Gorgon--a terrifying, monstrous female with hairs made of live snakes and a stare so horrifying that it would literally turn you to stone.

The Gorgonopsid--a predatory protomammal that hunted down its prey via saber-like teeth.
Herein lies the problem.  The gorgonopsid looks nothing even remotely like a snake, nor is it likely that it could stare down its own prey into a statue.  So why call this family of predatory protomammals "gorgonopsids", anyway?

If I had to guess, it is because the skull of this animal must have horrified early paleontologist of the 1890s. This was an animal that had a skull that was both reptilian and mammalian. Some kind of horrid in between animal. Neither mammal nor reptile. In the era before the evolution theory was accepted...this animal looked like a defiance to the order of God's creations. There were fish, amphibians, reptiles, birds and mammals. The five kingdoms of animal life. There should not be such a beast, a half reptile, half mammal. Like the gorgon half beast, half human.

Gorgon (via Latin from Greek Gorgō, from gorgos meaning ‘terrible') + opsid (Ancient Greek ὄψις (ópsis) for "appearance”) (often referring to the face).

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


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Is Gorlin's sign hereditary?
"Gorlin's Sign" is the ability to touch the tip of the nose with the tongue.  It is present in half of people with Ehlers-Danlos syndrome, but is also present in a minority of people without that disorder: among them, both me and one of my sons.
Is it known whether this trait is hereditary?  If so, is it a simple genetic trait (e.g., is it sex-linked, Mendelian)?

Can you please link to your source when you state It is present in half of people with Ehlers-Danlos syndrome, but is also present in a minority of people without that disorder? This source may be a good starting point to try to answer your question.

@Remi.b - I just added source of that statement (Wikipedia).


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Is there anyone discovered new drugs by actively create mutations in drug-producing organism?
Recently I was reading about drug discovery.
As far as I know, there are currently 2 sources of creating new compounds by:

Screening from natural sources.
Synthesizing by add/remove/replace-ing the functional groups of a known compound using chemical processes.

On the other hand, molecular pharming is the process of producing drugs by integrating the drug-encoding genes into bacterial (typically E. coli) genome.
I came up with the idea that if we create mutations in these drug-producing colonies, by UV light for example, eventually by chance we can obtain some new compounds once the mutations occur in the drug-encoding region or related genes.
I want to search in the previous studies for those who has come up with this idea already, I tried with several keywords and there's no luck.
I would want to ask is this idea practically possible? How high is the chance of having new compounds compare to screening natural sources and chemical systhesis? And if someone has already done this study, can you please provide me some references on this matter?

Would you consider the idea of site-directed mutagenesis for creating mutations?

It could be site-directed mutagenesis or any kind of random mutation when exposed to stress. But the product is unknown. Because the use of known mutant strain is not the idea at all.

I'd say this is possible, but not really practical. Mutating genes by UV light is not that hard, it's just the screening for the (new) compounds that makes it difficult. You would probably be better of creating diversity using established chemical methods.
Usually UV mutagenesis is done for whole organisms, but some people probably also tried this for single genes (even though they'd hit the whole genome). This is the easy part; you could get an enormous amount of diversity with very little work. Even though mutations that change enzymatic products are probably much more rare than mutations that change substrate specificity or product chirality, people find those mutations (example from the top of my head: p450 hydroxylation patterns, although they probably used targeted mutagenesis).
Determining if a specific compound is produced by an organism is also not very hard. You break all the cells, put the solution on a column and check with your favorite analytical method whether or not your compound is in there. Checking for new compounds is much harder. You need better analytical methods such as MS/MS as you don't have analytical standards, and the adapted molecule might not even be detectable with the analytical method you used for the starting molecule. We are very good at detecting needles in haystacks, but determining if there is a needle, a stick, or maybe a piece of hay from another species in the haystack is much harder. You'd already have to predict what kind of altered molecules you expect to find.
When you have successfully done all this, you have identified a single new molecule. Nowadays, people use libraries with >100,000 compounds to screen against their disease protein of interest.
The idea of mutating enzymes to produce new products is not that strange, people work on this, publish, find a lot of interesting things and we learn a lot about enzymes. As an approach for drug discovery this approach is just not high-throughput enough.

Indeed, small molecule and secondary metabolite detection has been, and often still is done through both random and rational mutagenesis. UV light is one option, but often it's easier to use slightly more aggressive methods such as ethanemethanosulphate (EMS) exposure.
Streptomyces for example, the model organism for secondary metabolite production has been subjected to all manner of mutagenesis methods throughout the years (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3472513/).
A random mutagenesis approach used frequently these days is genetic rather than chemical, and uses the mobile elements transposons for random insertions. (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3416362/)
Much secondary metabolite production these days is done via modification of Non-Ribosomal Peptide Synthase clusters (NRPS). These clusters exhibit something called the 'colinearity rule' (http://www.sciencedirect.com/science/article/pii/S1074552110000499) whereby, the 'modules' that make up the protein complex, play 'pass the parcel' with the growing seconday metabolite, with each module subsequently adding a new moiety - like a conveyor belt. It's possible to therefore predict the molecule an NRPS will make just from the modules and mutations you see within it, whether produced randomly or rationally.
However, it's often the case that we understand the myriad of secondary metabolite molecules that an organism is capable of producing so poorly, that simply screening the wildtype organism turns up hundreds of thousands of molecules before you even need to consider modifications.

I think your sources point more towards mutagenesis to produce more of a certain molecule, not towards producing completely new molecules.

I hadn't interpreted the OPs question in that manner, but on rereading I guess that's possibly what he meant. In that case I would say random mutagenesis to produce totally novel compounds is functionally impossible. On average, mutations are neutral, and of those that aren't they're more frequently deleterious than advantageous so you'd need an extremely long time frame and a selection pressure to generate mutations that would stick to be able to produce a brand new molecule. It's simply not feasible to start from scratch.


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Why we aren't making Darwin's theory a Law
I was wandering about darwin's theory which is controversial theory and there are no enough evidence to prove it right or falsify it, since I'm a biology student so i studied basic way of a hypothesis going to be a law ,the last thing to be a law is theory...am i right?
Hmmm if yes then it's been about more than 130 years since darwin died and there is still no response to his theory?why this taking so long? Are we supporting Darwin because if we don't then we gonna recreate our basic embryology and evolution? If no then why we aren't making it a scientific law?

We have Newton's laws and Theory of relativity, but we still don't have Einstein's laws. I personally think it isn't a law because we cannot practically prove it yet.

Sorry i didn't got your point...Do you mean that the theory of relativity is also pending?

Yes. Theory of relatility is controversial. It needs some more modifications to be completed, as well as Darwin's theory.

Yes it needs but darwin's theory is based on fossil records and till date we have found fossils of a million years ago dino but not the fossils of humans completely even about 30%

In my opinion, Darwinian theory is like a naive approach, a kind of "-ism" to explain evolution. We also have Lamarck's theory, Kimura's theory and a lot of modern adjustments. None of these are able to fully explain the high diversity of the nature. Maybe we can never prove it, maybe eventually we might be able to prove it, but for now there is not enough evidence and too many opposite critics to make it a law.

I'm voting to close this question as off-topic because the definitions of terms such as hypothesis, evidence, theory, law, axiome belong to the field of philosophy of science. You should give it a try at Philosophy.SE.

Despite being a subject of philosophy, we already have a post that answer your question here. The post could as well be close as a duplicate.

Tho H. Ho is very obviously wrong! I would love to be able to down vote his comments! The theory of evolution (often called "modern evolutionary synthesis") is a theory. A theory is a a set of hypoteses extremely strongly supported by evidences. There is nothing controversial about the theory of evolution, just like there is nothing controversial about the theory of gravity. None of these theories will ever become laws because a law is just something different from a theory (not something better).

Thank you for your helpful clarification, except your love to voting down my wrong opinion couldn't make anything better.

Possible duplicate of How do we know that humans and chimpanzees evolved from a common ape ancestor?

To me, this is mainly a semantic issue (scientific theory vs scientific law, especially in lack of a clear definition of a scientific 'law'), and therefore opinion-based.  As @Remi.b writes, the Q is a bettet fit for philosophy-SE, but too vague for that site as well.

@ThoH.Ho I hope you did not take it with too much offense. If you just google hypothesis, evidence, theory, law you'll get many websites that make short intro to the semantic of these terms. These definitions are a matter of philosophy of science (a very interesting field of philosophy IMO).

Don't tell me you came here from zakir naik! ;)

@polisetty why? What he have done to you?

Scientific Laws differ from Scientific Theories in that Laws do not posit a mechanism or explanation of phenomena. Scientific Laws are merely distillations of the results of repeated observation. As such, a law is limited in applicability to circumstances resembling those already observed, and may be found false when extrapolated.
Examples are like
Ohm's law only applies to linear networks, Newton's law of universal gravitation only applies in weak gravitational fields, the early laws of aerodynamics such as Bernoulli's principle do not apply in case of compressible flow such as occurs in transonic and supersonic flight, Hooke's law only applies to strain below the elastic limit, etc. These laws remain useful, but only under the conditions where they apply. Such laws do not explain how and why they work.
https://en.wikipedia.org/wiki/Scientific_law
Darwin's Theory of Evolution in contrast contains both observation, and a proposes an explanation of the phenomena of species formation.


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Mapping ATC codes to names (Computational Pharmacology)
From Wikipedia:

The Anatomical Therapeutic Chemical (ATC) Classification System is used for the classification of active ingredients of drugs according to the organ or system on which they act and their therapeutic, pharmacological and chemical properties. It is controlled by the World Health Organization Collaborating Centre for Drug Statistics Methodology (WHOCC)

The WHOCC Website has a manual search. But I'm looking for an automated way to map ATC Codes to their names. I'm currently interested in mapping third-level ATC codes. For example:

N03A → ANTIEPILEPTICS
C03B → LOW-CEILING DIURETICS, EXCL. THIAZIDES

In addition to third-level codes, an ideal solution would map codes of any level to their name. After lot's of Googling, I've yet to find a dataset (such as a JSON or TSV file) that contains both ATC codes and their names.
Fingers crossed I don't have to write a web scraper.

You can download their database and parse your list. It seems to be not free (they take ~200 Euros). I would say that it is not really worth 200 euros. You can automate the search by appending the search term to the address https://www.whocc.no/atc_ddd_index/?code=N03. Anyway, this is not a biological question in a strict sense and would be put on hold.

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

Thanks @WYSIWYG—sorry I overlooked the Order page. I wasn't expecting the United Nations to sell access to data that's part of essential biomedical infrastructure.

After some more intense Googling, I found a TSV that did the job:

versioned blob link

You can access the file as raw text with the URL https://raw.githubusercontent.com/OHDSI/Vocabulary-v4.5/661804cf3c17add61b02e2e83e477f48acb011d5/21-ATC/atc_code.txt.
Thanks OMOP Standardized Vocabularies V4.5 for making this file available on GitHub!
This file was last updated on Aug 24, 2014 and is not actively maintained. It would be much more preferable if WHOCC hosted their datasets in a machine readable format. Furthermore, WHOCC should openly license to their content.
I'll keep this question open in case anyone knows of a better solution.


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Can there be forced evolution
Can we force a species to evolve through a mixture of natural and artificial selection in a closed environment?

Maybe pose a more specific scenario and we can suggest whether this would be feasible experimentally.  Purely artificial selection, as was used to generate basically all of the food we eat, for example, is definitely a form of forced evolution but it happened in a somewhat-poorly controlled environment (a farm over a long period of time, in the case of plant or animal breeding).

Exactly what are you asking? Artificial selection clearly exists, as does the combined effects of natural and artificial selection. How does "forced evolution" different from this?

I don't think this question shows much research effort on the part of the OP. The OP acknowledges the existence of Artificial Selection so has even answered their own query surely?

Selection (whether natural or artificial) is one of the force causing evolution. So yes, artificial selection is one way to 'force' evolution to happen in a specific way. One could select trees for bigger fruits or dogs for longer fur for example. One cannot force "Natural Selection", as "forced natural selection" is defined as "artificial selection".
You might want to have a look at an intro to evolutionary biology such as Understanding Evolution by UC Berkeley for example

In addition to what others have replied, perhaps what you're referring to is speciation, i.e. can you force a species to evolve into a new one that is a distinct species from the original one? I'd say yes, but if you wanted to be quick about it then you'd have to choose an organism with a very short generation time, subject them to different selective pressures than the original population are subjected to and prevent the two populations from mixing and interbreeding. I guess you could say a new species had evolved when they can no longer produce viable offspring with the original population. Might take a while though. In fact maybe this would work better/be quicker with an asexual organism but it would be more difficult to identify the point at which a new species had evolved.

Yes, we can. One example is pushing bacteria to evolve antibiotic resistance by putting them under artificial selective pressure, i.e. adding antibiotics in the medium.
You can find it here http://gizmodo.com/watch-as-bacteria-evolve-antibiotic-resistance-in-a-gig-1786389688


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Which algorithm to find the evolutionary relation of 5 sequences?
After Multiple Sequence Alignment (MSA), data sets are produced on which models of evolution are used. I've seen in books that if there is strong similarity between the sequences then Maximum Parsimony (MP) is used, if that is low then Minimum evolution, and if there is very weak similarity then Distance based Method is used. However, all of these have their own cons.
Since character based methods are more reliable (as book), Can these methods be used even when there is low sequence similarity?
Are there any algorithm that builds the precise tree model without considering similarity of the sequences?

How do you measure sequence similarity? What book do you refer to?

Multiple sequence alignment ? D W Mount, bioinformatics sequence and genome analysis..

If you work with protein coding sequence and on the DNA level their to divergent, then it is better to use the amino acid sequence for alignment and phylogenetic reconstruction.
Better sampling can also help you, for this you can check the online databases with BLAST to find similar sequences that would fill the gap.
The problem with sequences with low sequence similarity is that it is difficult to identify homologous positions/characters and all alignment based methods rely on the assumption that the aligned positions are homologous.
Finally, there are alignment-free algorithms as well. (https://en.wikipedia.org/wiki/Alignment-free_sequence_analysis)
In general about algorithms for phylogenetics:
Nowadays, journals usually require you to run maximum likelihood (ML) analysis or Bayesian analysis. Both of these methods are referred to as model based. The most common programs used for these are RAxML (ML) and MrBayes (Bayesian). Another common software is MEGA (Molecular Evolutionary Genetics Analysis), which can run different tree building algorithms.
Usually, for quick reference maximum parsimony or neighbour-joining trees are good. For publication a maximum likelihood tree is very useful, since it returns a single best tree. While Bayesian analysis and maximum parsimony return a collection of trees.
It is also helpful different algorithms and if all return similar trees than you can be more sure about the relationships.

Can you add sources to allow users to background read on your answer? Could you tell us the benefits of the methods described in terms of the question? Of now, it seems more like a general comment than an answer

I added a bit more targeted part to the answer. I don't exactly know of reference for what I wrote in the general part. It is what I hear from colleagues and see in current publications.


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Do I need primers if ordering from a DNA synthesis provider
Do I need to design / synthesize primers for PCR if I am ordering from a DNA synthesis company and they are providing free cloning into my preferred vector backbone? Any good reason to order primers as well?

It really depend on what you need to do with the plasmid you are ordering. Can you specify it?

Only if you intend to subsequently amplify the DNA you've ordered. I tend to never fully trust anything I don't confirm myself so primers to sequence the insert in the construct they give you might not be a bad idea either.


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What is a starter cell?
I am reading the paper Cooperative Subnetworks of Molecularly Similar
Interneurons in Mouse Neocortex and a term "starter cell" apears there (page 6):

This yielded tissue sections where SOM or
  VIP starter cells carry both nucleus-localized GFP and cytoplasmic mCherry

Does anyone know what a starter cell is?
(I couldn't find it on the web)

Nice question - this terminology isn't referring to a special type of cell or anything, but to a peculiarity of the technique they are using.
They are labeling a subset of cells with rabies virus; rabies then travels in retrograde fashion to presynaptic cells, and labels those as well.
The "starter cells" are those initially infected cells, where the tracing "starts." This reference more explicitly states this terminology, and talks about the technique extensively, I would strongly recommend it for helping to understand the paper you are reading.

I understand now.... I will also read the article you reffer to. Thank you for your clarification!


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What is the 'fallacy' in simple segregation rules in reference to polyploidy?
I was reading a paper Why polyploidy is rarer in animals than in plants’: myths and mechanisms, Mable 2004 where I found this sentence.

Stebbins (1950) suggested that autopolyploids were probably more frequent than often considered because of the ‘fallacy’ that simple segregation rules (i.e. auto- polyploids showing multivalent associations and allopolyploids showing bivalent associations) can be used to distinguish modes of origin.

What does it mean? I know that autopolyploidy is where the chromosome sets are from the same species and it is the other way for allopolyploidy. What do segregation rules mean here and what is the fallacy?

@Richard Smith-Unna Could you please answer?


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How to design internal primers?
I have sequences of the Cytochrome c oxidase I (COI) from several populations of Peringia ulvae (Mollusca; Gastropoda; Littorinimorpha; Hydrobiidae). I need additional COI sequences from a specific population. When using the same primers and PCR protocol as for the other populations, I do not get any PCR product for the specific population. My PI suggested me to design internal COI primers for Peringia ulvae. How can I do that? Should I use the COI sequences from the other populations?

You could try simply ordering a degenerate version of the primers you have. If possible, try aligning the sequences for many known COI alleles from your organism and see which bases in particular are variant. If the sequence is conserved, keep that base, if it is variable, add a degenerate/random nucleotide in to your primer order. The mix of primers you get back will then have every possible variant for a given position, and that might help you to get amplification.

Try to lower the annealing temperature of your PCR. If there are few mismatches between the DNA sequences of the different populations you may be able to amplify them all with the same primer set by making your annealing less stringent. One question, are the primer annealing inside the coding sequence of COI or on the flanking region?

@alec_djinn How can I know where the primers are annealing?

@JustineVandendorpe do you know the sequence of the primers? If so, then just use BLAST to understand where they anneal.

@alec_djinn I know the sequences and ran a BLAST. Thanks a lot!

If you are not getting amplification, there are multiple things to visit before you want to design internal primers. You should try troubleshooting your PCR reactions before designing and ordering internal primers. If you are doing the PCRs wrong, it is likely you will run into the same problems again with internal primers.
There are excellent guides to trouble shooting PCRs - Just a google search "Trouble-shooting PCRs" should give you a lot of material to go through. This is from NEB, but there are several others, each manufacturer having their own, so you could refer to one of whose reagents you are using.
Primers generally give good reads from the 5' end for about 600-700 bp and after that the quality of base calling deteriorates, so if your target amplicon is above 1500bp or so, you would need internal primers because the 'external' primers would give you good sequences for only 1400 bp or so (600-700 bp from both directions, for fwd and rev primers). So internal primers can be used to sequence the regions that cannot be reached by the main (external) forward and reverse primers. The published papers from where you are using the external primers will most likely have the internal primers if CO1 is long enough to require internal primers.
Otherwise, you would need to align the existing sequences from the other populations, and look through regions of the alignment that are conserved which could act as potential priming sites. There are other issues to be taken care of before you can consider a 'conserved region' a 'priming site' and go ahead and order primers. Again there are excellent primer design tutorials available, just a google search away.
Let me know if any parts of the answer are not clear, or sound like jargon and I will do my best to simplify it for you. However, I would strongly suggest troubleshooting the PCR first - for e.g. trying a gradient PCR to find the optimal annealing temperature.

Thank you very much for your answer. I am also using the reagents from NEB so I had a look at their Tm Calculator. With the parameters I entered, I got a warning message saying: "Tm difference is greater than the recommended limit of 5 °C." Do you know how can I solve that?

Hi, what is the annealing temperature that you are using in your PCR and what is the Tm for your primers?
Also, do you have something like Nanodrop readings of your DNA samples? Do you know their concentration? If the concentrations are too high/too low, PCRs will be inhibited.

I am using an annealing temperature of 52 °C. The Tm suggested for my forward and reverse primers are 49 °C and 59 °C, respectively. The DNA concentration of my samples ranges from 0 to 870 ng/µl.

870 is WAY too high. Generally 25-100ng of DNA is recommended in the reaction mixture.