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Using coefficient of variation (CV) for GCaMP6 'synchronised episode' spikes, good idea or not?
Using GCaMP6 we have recorded fluorescence activity of kisspeptin neurons that exhibit synchronised pulsatile firing activity. I measured the intervals between each episode, which are quite variable. However, I am unsure whether or not using the coefficient of variation to analyse their variability is a good idea (since most papers I read have applied it to individual neuronal firing to analyse variability between spike intervals but not to population spike activity). Also, do I need a minimum number of 'spikes' to use CV (since in my recordings there are only around 4-10 spikes in around 3 hours)?

You can use the CV with a small sample but of course, it may not have converged yet. But 4-10 spikes/ 3 hours does not sound right to me. You may need to reconsider the event detection algorithm you used to get these numbers and/or the quality of the recordings. Additionally, the CV metric is useful when there is considerable bursting activity and you do not expect to see much bursting with calcium imaging given the temporal dynamics of GCaMPs.


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At what rate does synaptogenesis occur in adults?
From many articles, I can find the rate of synaptogenesis at its highest: roughly 580,000/minute (weeks 6-23 after conception). However, I'm having trouble finding the rate with which it occurs in adults. I find articles stating that it is higher in areas like the hippocampus than other areas and depends on things like exercise and stimulation, but no numbers.
What is the rate of synaptogenesis in a adult brain?

I did not find the estimate in the cited document (perhaps you confused synaptogenesis with neurogenesis in p. 3?). Anyway, one would need to specify whether that refers to the whole brain or a brain region. I can only provide numbers for mice, if that's useful to you.

@vkehayas You are right, I did misread the neurogenesis reference on page 3.  The logic will still hold (we start with 0 synapses, and we have N after D days, so N/D synapses per day), but I'll have to adjust the numbers.  Mice numbers would be useful, especially hippocampus and whole brain numbers (from what I understand, the hippocampus  has very high rates of synapse creation compared to others, so that number and the whole brain number would provide useful bounds).

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How fast does activity affect synaptogenesis?
How long does it take for the increased activity due to a novel stimulus to cause an increase in synapse generation?
There are many studies which show that the number of synapses in the brain increases within 24 hours of doing a novel task, so I know the number is less than 24 hours. I'm interested in questions like "If I do yoga for an hour, will the later part of the hour benefit from synapse creation caused from earlier in the hour?" Obviously I don't know if yoga in particular would benefit from said synapses, but if synaptogenesis is not up-regulated in less than an hour, then I can certainly rule such an effect out.

Synaptogenesis at such a fine temporal resolution is currently still best studied in animal models and reduced preparations where the activity levels can be more precisely controlled and advanced imaging methods can be used to monitor morphological changes. A series of studies with relatively high temporal and spatial resolution have been carried out in vitro and in vivo with two-photon microscopy on dendritic spines, which are considered as a proxy for the existence of synapses, since ~98% of them contain one.
The fastest effect after stimulation is the enlargement of pre-existing  or newly-formed spines and their synapses, as fast as ~2 min (Matsuzaki et al. 2004, Harvey et al. 2007, Hill and Zito 2013). Next, immature structures (often called filopodia) are starting to form within the first ~15 min (Maletic-Savatic et al. 1999). It is not yet clear what percentage of those structures bear an actual synapse, however they certainly have the potential to obtain one. A more gradual increase in the number of spines that persist for several hours and are very likely to contain a synapse occurs in later stages, ~30 min after stimulation (Engert and Bonhoeffer, 1999; Nägerl et al., 2004, 2007). However, note that the overall spine density is almost never affected in vivo (Holtmaat and Svoboda 2009), which indicates that compensating mechanisms counter-balance any synaptogenesis, so you should not expect to see an overall increased number of synapses.

References
- Matsuzaki, M., Honkura, N., Ellis-Davies, G. C. R., & Kasai, H. (2004). Structural basis of long-term potentiation in single dendritic spines. Nature, 429(6993), 761–766. https://doi.org/10.1038/nature02617
- Harvey, C. D., & Svoboda, K. (2007). Locally dynamic synaptic learning rules in pyramidal neuron dendrites. Nature, 450(7173), 1195–1200. https://doi.org/10.1038/nature06416
- Hill, T. C., & Zito, K. (2013). LTP-Induced Long-Term Stabilization of Individual Nascent Dendritic Spines. Journal of Neuroscience, 33(2), 678–686. https://doi.org/10.1523/JNEUROSCI.1404-12.2013
- Maletic-Savatic, M., Malinow, R., & Svoboda, K. (1999). Rapid dendritic morphogenesis in CA1 hippocampal dendrites induced by synaptic activity. Science (New York, N.Y.), 283(5409), 1923–1927. https://doi.org/10.1126/science.283.5409.1923
- Engert, F., & Bonhoeffer, T. (1999). Dendritic spine changes associated with hippocampal long-term synaptic plasticity. Nature, 399(6731), 66–70. https://doi.org/10.1038/19978
- Nägerl, U. V., Eberhorn, N., Cambridge, S. B., & Bonhoeffer, T. (2004). Bidirectional Activity-Dependent Morphological Plasticity in Hippocampal Neurons. Neuron, 44(5), 759–767. https://doi.org/10.1016/j.neuron.2004.11.016
- Nagerl, U. V., Kostinger, G., Anderson, J. C., Martin, K. A. C., & Bonhoeffer, T. (2007). Protracted Synaptogenesis after Activity-Dependent Spinogenesis in Hippocampal Neurons. Journal of Neuroscience, 27(30), 8149–8156. https://doi.org/10.1523/JNEUROSCI.0511-07.2007
- Holtmaat, A., & Svoboda, K. (2009). Experience-dependent structural synaptic plasticity in the mammalian brain. Nature Reviews Neuroscience, 10(9), 647–658. https://doi.org/10.1038/nrn2699

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Modularity score comparison between different algorithms in network analysis
I used different algorithms for splitting my large gene network into different sub-networks using Cytoscape. I compared the modularity scores and decided that the algorithm with the best modularity score will be used for clustering the network.
My colleague came up with the argument that modularity scores can only be compared for different number of clusters being created by the same algorithm.
So, my question is if modularity scores can be used to compare between different algorithms or only in the case of the same algorithm producing different number of clusters.

If you don't get an answer here, you might do better to transfer your question (delete and repost) to SE Bioinformatics, which would seem more appropriate.

Since the goal of modularity estimation algorithms is to find the community structure that maximizes modularity, it is valid to compare different algorithms based on their modularity estimate. However, i) it is not the only consideration for choosing a community detection algorithm, and ii) the obtained modularity estimate will depend on the particular structure of each network, e.g. its number of nodes. For a principled comparison between several different algorithms, see Yang et al. (2016). Based on multiple criteria, they identify the multilevel (or Louvain) algorithm (Blondel et al. 2008) as the overall best choice.

References
- Yang, Zhao, René Algesheimer, and Claudio J. Tessone. “A Comparative Analysis of Community Detection Algorithms on Artificial Networks.” Scientific Reports 6, no. 1 (August 2016). https://doi.org/10.1038/srep30750.
- Blondel, Vincent D., Jean-Loup Guillaume, Renaud Lambiotte, and Etienne Lefebvre. “Fast Unfolding of Communities in Large Networks.” Journal of Statistical Mechanics: Theory and Experiment 2008, no. 10 (October 2008): P10008. https://doi.org/10.1088/1742-5468/2008/10/P10008.


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Which predator raises its tail to signal no threat?
A guy in a bar once told me that there is some animal which raises its tail when at a watering area in order to signal to the other animals that it's not going to attack. He told me this as an argument to justify humans eating other animals.
Is this true that some animals do this? If so which ones? Links to video evidence would be extra appreciated.
Cheers,
Steve

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What percentage of a cell's volume is occupied by protein?
I was looking at one of David Goodsell's illustrations of a cell:

And it seems to suggest a very crowded picture of the intracellular environment. Just how crowded are cytoplasms? What percentage of the volume is typically taken up by protein, water, and other major species?

According to this, that picture is probably pretty close.

What kind of cell? It would be best if you can specify a certain kind of cell, since protein content clearly varies between cells (eg a WT E. coli, vs one that is overexpressing a protein from a plasmid)

@MarchHo Pick whichever one you want.

I'm sure you're aware of this, but that picture is in no way an accurate representation of a real cell.

The tricky part is to define what is the volume of a biomolecule as it is a folded chain full of bumps and holes. Water is all around and in the folded structure and is actually important to keep the conformation of at least some of the proteins/RNA/DNA.
At the same time we know that 60% of your body in mass is water. Let's visualize that. Bio molecules have roughly the same weight per volume than water. Now add into the equation that a good third of the filled actually is water due to the structure holes, adsorption etc. You now have roughly:

% empty space = 60%-(40%/3)= 47%

To help think about it imagine a grid with roughly one cell out of two being filled. That looks pretty crowded to me. Then you of course have variations with blood and secretions on one side and bones on the other but you have the big picture.
For an example look at an electron microscopy picture of a striated muscle cell: http://histology.med.umich.edu/sites/default/files/muscleQ4.jpg. It looks pretty much like the half filled grid isn't it? Of course seeing individual molecules is hard but the white space correspond to mostly empty space with a couple of actine fibers. The dark corresponds to actine+myosine fibers: an extremely tight space. And we have roughly half of each :-)

According to the Molecular Biology of the Cell, (4th Ed), the cell is ~70% water, the remaining 30% of which is composed of macromolecules (proteins, nucleic acids, and carbohydrates). While this is just a single citation, there are lots of other sources in the literature that cite similar values.

I'm afraid this is a description of the mass percentage while the question was about the volume.

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Where does tracrRNA comes from?
I'm talking about CRISPR system. I know the crRNA is transcribed from the palindromic repeat and the "spacer" but I don't know where the tracrRNA comes from.

Usually the tracrRNA is a part of the CRISPR locus and is encoded in the the vicinity of the CRISPR array (e.g. upstream or downstream of the cas genes or the array).
http://www.genome-engineering.org/crispr/wp-content/uploads/2013/01/crispr_processing1.jpg


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What does metal-dependent mean?
I was reading about Cas1 and Cas2 and came across this excerpt:

...Cas2 was identified as a metal-dependent endoribonuclease that cleaves ssRNA or dsDNA...

What does metal-dependent mean in this context?

What is the source of this quote?

Here, http://www.cell.com/cell/fulltext/S0092-8674(15)01321-5 it's (the quote) at the beggining

It means that these enzymes need a metal ion as a co-factor for their function. This metal ion is typically bound somewhere near or in the active center and helps stabilizing transition states.
Without these metals, these enzymes cannot function properly, that's why chelating agents are used in protein or DNA preparations to inhibit their function.
References

Information available at cut rates: structure and mechanism of
ribonucleases.
The Role of Metals in Enzyme Activity


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How do parents give their offspring a chromosome?
Whenever an organism sexually reproduces, it gives its offspring one chromosome from each of its pairs of chromosomes. My questions are

Is this done randomly?
Is it uniformly random?
If so, what mechanism allows it to be random, considering that the laws of physics are deterministic?

(Note: I'm a little rusty on this subject, so if there are any errors in the question, feel free to correct them.)

Are the laws of physics deterministic? I think no one knows, currently.
In any event, yes, the segregation of homologous chromosomes during meiosis I is random: there is an equal probability for each chromosome of a homologous pair to segregate into a given gamete, and this is independent of other homologous pairs. This idea dates back to Mendel, who observed that the heritable “factors” (what we now know as genes) responsible for macroscopic phenotypes are inherited independently of one another (this is his Law of Independent Assortment). This isn’t actually true when considering linked genes, but is certainly true of chromosomes, as was described by Sutton in 1903:

...many points were discovered which strongly indicate that the position of the bivalent chromosomes in the equatorial plate of the reducing division is purely a matter of chance - that is, that any chromosome pair may lie with maternal or paternal chromatid indifferently toward either pole irrespective of the positions of other pairs...


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Can a gene be inactivated using CRISPR if it is not in the interspace of short palindromic repeats?
I have recently studied how CRISPR works but there is something that I do not understand at all. I have heard a lot of people claiming that with this method it is possible to modify any genome by inactivating, activating, removing or adding genes. However, as far as I have understood, DNA regions can only be modified if they are in the interspaces of short palindromic repeats. So, my question is whether a gene that is not in the interspace of short palindromic repeats can be modified or removed? And if it is possible to do so, how?

The CRISPR acronym was assigned when the system was discovered as a sort of bacterial immune system to kill viruses by storing parts of the viral DNA in the interspaced palindromic repeats. This was before CRISPR became a big deal for gene editing. But the name stuck. At least they didn't call it something like Sonic Hedgehog.

When people talk about genome editing with CRISPR, they are really talking about using CRISPR associated nucleases like Cas9 and Cpf1. These nucleases are useful since their sequence specificity is determined by a guide RNA and they can therefore be used to cut at specific sites in the genome. This actually has nothing to do with the repeats themselves.
See this answer for a brief overview of how genome editing with Cas9 works.


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Name of dsRNA (or dsDNA) where all strands are identical
What is the name of dsRNA (or DNA) where all component strands are identical (i.e. where the complex consists of multiple copies of the same ssRNA)?
Example: 2 identical ssRNAs forming a dsRNA
C C G C G G C G G
| | | | . | | | |
G G C G G C G C C

Furthermore, is there a different name for it depending on the degree of complementarity (full Watson-Crick complementarity vs. full complementarity with non-Watson-Crick basepairs vs. lower complementarity due to bulges etc)?
My thoughts
You probably wouldn't say "RNA homo n-mer" (for the example above "homo dimer/2-mer") since I assume that would be referring to a 2-nucleotide long ssRNA?
Can you use the terms dimer, trimer, tetramer, 5-mer, 6-mer etc in multiple ways; (a) referring to the binding of nucleotides to each other to form a polymer/n-mer of nucleotides i.e. polyribonucleic acid, and (b) to whole ssRNA or dsRNA binding to each other to form a "dimer"?
You also probably wouldn't refer to it as a "homo duplex" since that refers to  something related to chromosomal crossover.

Welcome to Biology.SE! A few comment to your questions: 1) dsRNA is very rare, afaik it only occurs almost exclusively in some viral genomes; unless you include self-basepairing in structural elemnts 2) As long as there is complete base pairing something like this would be a palindromic sequence, however that term is also used for short elements within a long DNA strand, and doesn't necessarily imply that actual DNA molecule is double stranded.

Such a nucleic acid sequence is described as a palindrome or palindromic.
Wikipedia has an entry for palindromic sequence in which it is defined as:

A palindromic sequence is a nucleic acid sequence on double-stranded DNA or RNA wherein reading 5′ (five-prime) to 3′ (three prime) forward on one strand matches the sequence reading 5′ to 3′ on the complementary strand with which it forms a double helix. This definition of palindrome thus depends on complementary strands being palindromic of each other.

It should be noted that this is a description (rather than a name) that is usually applied to segments of larger nucleic acid molecules or to synthetic constructs. I am not aware of a generic name for short dsRNA (or dsDNA) like the one in the question as they are not, to my knowledge, found in Nature and so there has been no reason to devise a name for them. Thus, there are no names for variants either. If you wish to write an article about such things you would need to invent your own terms, but keep well clear of ‘-mers’ (see use of e.g. tetramer).
The sequence presented in the question does not conform to the Wikipedia definition, above, as it has a central mismatch and is therefore not a perfect double-helix. However, as the use of the term palindrome for nucleic acids is a somewhat cavalier extension of the general use of the English word palindrome (an example of which is “ABLE WAS I ERE I SAW ELBA”), I would regard a further minor modification of the Wikipedia author’s definition as unexceptionable.

Note that the biological palindromic sequence does not quite match the general meaning of palindrome.  The DNA sequence is complementary to its reverse, whereas the normal palindrome is the same as its reverse.

@mgkrebbs — Yes. But I did note that, didn't I? I wrote "the use of the term palindrome for nucleic acids is an extension of the general meaning of the English word palindrome" and gave a reference to and example of the general meaning of the word, that can be compared to the example in the question for NAs and the reference I provided for that. However, it is worth emphasizing to those not familiar with Napoleonic English.

I don't agree that palindromic sequence is an extension of the normal word meaning of palindromic because it (in general) violates the one central meaning of palindrome, that its reverse is the same.  Since it completely throws out the core meaning and is in conflict with the normal meaning, it is not an extension but rather an alternative meaning.  (Palindromes of course have no known biological significance, unlike palindromic sequences.)

@mgkrebbs —  From a linguistic point of view the "use" of the word has certainly been "extended" — from a single string of characters to two strings having special properties in two-dimensions. Only if the 3' end of the first string is joined to the 5' end of the second string do you have a palindrome.in the original sense. I've tried a modification of my own in this spirit, but do suggest alternatives.

The specific sequence you have posted is not strictly a palindrome since the reverse complement of the top strand is not the same as the bottom strand. Although there is no central body making these definitions, a better term, in my opinion, would be inverted repeat, of which palindromes are a subset (inverted repeats with no intervening sequence). Of course, the final say would be its predominant usage in the literature (of which I am not overly familiar).
Furthermore, the specific sequence you have shown forms an internal loop, though there is no requirement that internal loops be formed from inverted repeats.

Yes. That's another way of looking at it.

…although the description "inverted repeat with intervening sequence" does not capture the mismatch of identical bases in the intervening sequence, which palindrome actually does.


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A missing endogenous retrovirus in humans, but present in gorillas and chimpanzees?
I have read an article about an endogenous retrovirus called PtERV1. It is present in gorillas and chimps, but is missing in humans (original study here).
According to the article, this retrovirus is very similar to HIV. And all of us (gorillas, chimps and humans) have a protein called TRIM5α to fight against PtERV1.
Nearly at the end of the article the author says: currently, there is no explenation for why the endogenous retrovirus (PtERV1) has never entered the human genome.
Is that a typo? Isn't a missing endogenous retrovirus just basic heredity? Especially because humans have the TRIM5α protein against PtERV1 just like gorillas and chimps, which indicate that we used to have it, but we lost it due to how heredity works.
Or did the author meant something deeper that the average user would not understand without a lot of pre-knowledge about genetics?

I think your question boils down to:
Why do modern chimpanzees contain endogenous PtERV1 whereas humans do not?
This is discussed in the original research article:
Kaiser SM, Malik HS, Emerman M. 2007. Restriction of an Extinct Retrovirus by the Human TRIM5α Antiviral Protein. Science 316(5832):1756-1758.
PtERV1 was active after the phylogenetic split of humans and chimpanzees, so any infection would be from separate events. In other words, the endogenous virus was not inherited from a common ancestor:

Comparison of individual PtERV1 proviruses in gorilla and chimpanzee genomes suggest that this virus was active 3 to 4 million years ago, after the separation of chimpanzee and human lineages.

They hypothesize that modern humans evolved from ancestors that were protected from PtERV1 by TRIM5α:

Although we cannot rule out the possibility that PtERV1 never infected human ancestors for other reasons, our data do suggest the possibility that TRIM5α was fixed in human populations because of its ability to confer protection against PtERV1 and that modern humans have descended from ancestors who resisted infection.

This does raise the question of why humans were not infected whereas chimpanzees were, despite both containing PtERV1 restricting TRIM5α. This seems to be out of the scope of your question, but they do talk about it in the article if you're interested.

Just to clarify, PtERV1 was not inherited to gorillas and chimps by their common ancestor. Gorillas and chimps got infected by PtERV1 separately. Correct?

@WatchHat Yes, that’s correct.


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What is the name for when genetic deviation results in an organism that doesn't work?
There is a word for this, and it's escaping me. I want to reaearch more papers on it, but I can't find them or what the word is called.
It's typically used in the context of fitness and evolution. If there is a dead individual, it doesn't have a fitness and the mutation is called _____. ?? ( in some models could be given a zero or neg inf)

Hum... it is quite unclear for the moment. All individual have a fitness. Their fitness can be zero though. I am not sure what you mean by "genetic deviation". Do you mean a mutation? Are you looking for an adjective that qualifies a type of mutation, like a "lethal mutation" or maybe "recessive/dominant lethal mutation"?

Or are you looking for the term 'deleterious'?

LETHAL. That is the word. They are lethals. Hahah thanks!!!

If you are referring to the mutation
I think the word you are looking for is lethal.
A lethal mutation is a mutation that causes the death of its carrier. Now there are recessive lethal and dominant lethal. For dominant lethal mutations, all heterozygotes are inviable. For recessive lethal, only double mutant homozygotes are inviable.
If you are referring to the individual
An individual that is not able to survive and reproduce is said to be inviable (I already used the term above). However, the reason for it is not necessarily genetic.

@GerardoFurtado Thanks, I attempted to clarify that lethal refers to the mutaiton. I also highlighted the use of the term inviable


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What is the most complex plant form?
At school we were told on scale of 0 through 1000 the animal kingdom ranges from amoeba the simplest/primitive being at 0, and Humans the most complex animals at 1000; what are the equivalent complexity species (?) in the plant kingdom? What is the least complex plant, and the most complex?

"Complexity" is a notoriously subjective and difficult-to-define term. Complexity differences between amoebas and vertebrates are hard to dispute, but amongst plants is a different story.

That whole thing of being more complex is non-sense, you can't say that for animals and you can't say that for plants either. It all depends on how you look at it. Average number of cells? Size of genome? Size of the proteome? Adaptability to different environments? Mental abilities? You can't place human on the top of any of them (maybe we could argue about if you define it as mental abilities but that doesn't sound right) and you can't place amoeba at the bottom either.
Also, if you look at a phylogenetic tree, an organism is also not more complex by the number of nodes it has behind them (I've seen people thinking this means more evolved and associate that with more complex).

The venus fly trap would certainly appear one of the most complex plants.
The plant almost 'bridges' a lifeform gap.


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What does it mean for Caenorhabditis species to be "pseudoparasitic"?
In this Wormbook chapter, Kiontke says that some Caenorhabditis species live "pseudoparasitically" on warm-blooded animals. What does it mean? What is a pseudoparasite? I understand a parasite to be in association with a host where the relationship is beneficial for the parasite and harmful for the host. How is pseudoparasitism defined?
I have found several definition:

Something in the blood that is mistaken for a parasite: not applicable to Ceanorhabditis as no Caenorhabditis has ever been found alive in blood
A false parasite; may be either a commensal or a temporary parasite (the latter is an organism accidentally ingested and surviving briefly in the intestine): could be this
an object or organism that resembles or is mistaken for a parasite: could be this
interpreted to be parasitic but not actually parasitic: could be this
This definition actually sounds like the definition of a parasite and only applies to invertebrates, so not applicable to Ceanorhabditis

In conclusion, I would say that some Caenorhabditis are pseudoparasitic of warm-blooded animals, which means they are commensal and cause no harm. However, I don't see the point of saying they are pseudoparasitic. I would rather just say commensal.

It might just be my opinion, but I think part of the issue approximates something like: The more you know about a subject, the pickier you become about how you would describe something. I remember this being true in undergrad calculus, when the professor would lay out a concept, but also hint that it's not the full picture because of more advanced concepts that they knew, and we couldn't know unless we pursued a PhD in Mathematics.

Why don’t you Email the authors themselves?  When I contacted Walter Sudhaus many years ago he was very helpful.


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Why does deamination in the lagging strand lead to an increase in the relative number of guanine and thymine to cytosine and adenine?
My question arose from this article on Wikipedia on the GC-skew in bacterial genomes: https://en.wikipedia.org/wiki/GC_skew
As far as I understood, the lagging strand (the template strand), during replication, is more often single stranded than the leading strand (template), so it is more prone to mutations like deamination. Therefore, on the lagging strand (here, the one being the template to the strand formed by Okazaki fragments), one should expect more Ts and fewer Cs. Conversely, the strand synthesised by Okazaki fragments should have an enrichment of As and a depletion of Gs. Why does the Wikipedia article mention a increase in the ratio of (G+T)/(C+A)? I would expect an increase in the ratio of (T)/(C). I don't get the link with Gs and As.

Please cite as a quotation the actual sentence(s) that mentions the (G+T)/(C+A) ratio. I cannot find it and without it your question is unclear. The article you mention is very dense — I have not been able to understand it merely by skimming it — and the impression I get is that it is not mainstream, but represents opinion rather than fact. You may be unaware that anyone can write articles for Wikipedia — the only quality control is readers.) I think your question would be better as “What causes the GC skew between strands” and cite this article as one explanation (which you don’t understand).

I'm voting to close this question as off-topic because the purpose of this list is to answer questions about biology, not to clarify the reasoning of scientific authors. In this case rephrasing the question so that it is focused on the possible causes of GC skew would be valid but not one in which the answer is assumed in the question.

wikipedia article has it exactly wrong. For reasons beyond comprehension people responsible for this article refuse attempts to correct this very confusing error. Lagging strand, not the leading strand, has the excess of Gs and shortage of Cs.
I'll use the occasion to edit it again, let's see how long this edit stands.

You may or may not be right but your answer is inadequate here because it is merely an assertion without argument or external support. You are wasting your time just editing a Wikipedia article when your edit is reverted. You need to engage in a discussion notifying others of your intended change and your arguments for it and asking why it was previously reverted. If you fail to get agreement, then I believe there are adjudication procedures. As here, you may be e convinced you are right but you have to convince others.

I think you are referring to this sentence from your wikipedia link:

There is a richness of guanine over cytosine and thymine over adenine in the leading strand and vice versa for the lagging strand.

Note that this is not saying (G+T) > (C+A). It is instead saying (G)>(C) and (T)>(A). I think that those are not the same as saying (G+T) > (C+A), though that is also true, probably?
So I think that there is no contradiction there- it is just, as you say, more Ts (relative to expected equality with As) and fewer Cs (relative to expected equality with Gs).
If I understand correctly, the importance of the GC skew, and the reason that it is interesting, is that it acts as a deviation from Chargaff's parity rules (as explained in the article). These rules state that for any given hunk of DNA, (G)~(C) and (T)~(A), which is the expected composition for (for example) double-stranded DNA, because of base-pairing.
Edit: for more information on Chargaff's rules, see this other question which I have (through pure coincidence) answered here. Note that the second parity "rule" is a statistical phenomenon, rather than a logically required rule. The wikipedia page on Chargaff's rules is also informative.
Hope that helps.

I don't understand the second parity rule of Chargaff: 'In other words, in each DNA strand the frequency of occurrence of T is equal to A and the frequency of occurrence of G is equal to C because the substitution rate is presumably equal.' Why should the numbers of Cs and Gs be equal on one strand? "It is instead saying (G)>(C) and (T)>(A)." Is that true in a single strand? In the template strand of the lagging strand?

see edit to answer linking to answer to question about parity rule.

Both of Chargaff’s rules were based on observation rather than logic. Indeed, it was because he was unable to rationalize his first ‘rule’ that Watson and Crick got the Nobel Prize for the structure of DNA and not him. It is also the reason to regard these ‘rules’ as no more than history.

@David is correct about Chargaff making descriptive observations, as is also stated in the linked answer. I'm not sure that I understand why these rules should be purely regarded as history when they remain a highly accurate (though merely statistical) portrait of DNA composition. I think there are a lot of arguments about why that Nobel happened the way it did, I'm not sure that I agree with that characterization but going into it would be rather off-topic here.

but isn't the second parity rule of Chargaff broken in bacteria? How could he analyse the nucleotide composition of a single strand?

Let me put it differently. I dislike the word ‘rule’ in this context because it implies some fundamental understood physical ‘law‘, and I dislike the two being associated as they are distinct in time and importance. A better word would be ‘observations’. The first set of observations were made on a limited subset of genomes and were not understood until the double-helical nature of DNA was established. They then became history — observations that were now explicable. The second set of observations are distinct and obscure. Associating them with the first set as another ‘rule‘ is unjustified.

@David- I can agree with that interpretation of 'rule', hence scare quotes. I think that further work has come closer to putting the second 'rule' on the same footing as the first, but it is fairly unintuitive.

The second parity rule is still holding in bacteria, in that the frequency of complementary nucleotide on a strand are highly correlated. I would say that deviations from the rule are larger in bacteria, for a variety of reasons (including the increased prevalence of GC skew). Note that in strict terms (e.g. A nts == T nts on a strand) probably no genome exactly matches Chargaff's second rule, due to sampling error etc. The wikipedia page on the rules has a lot more information if you are interested. But as David said we are getting quite off-topic relative to original question.

The problem with Chargaff's so-called second rule is that almost nobody has heard of it (that included me, who's been around a long time) and almost nobody seems interested in it (it is barely mentioned in the literature). I suspect that there must be a trivial explanation for the observation, such as recombination randomizing the position and direction of genes, which is what you find if you compare different bacterial genomes. So ultimately I cannot see that any deviation from this 'second rule' to be either interesting or important.


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Can someone identify this species from the pea family?
Can someone identify this species from the pea family? The plant was photographed in Morocco in spring. The location is south of Marrakesh at the foot of the high Atlas, in a dry riverbed.

From Tangier to Agadir passing by Asni in the atlas, you encounter quite a bit of ecological variation in Morocco. It could help to tell where in Morocco and/or what type of ecosystem, you found this plant in (esp. that we can't see the soil from the pictures)!

It would be good in general to have close up views of the flowers and fruits especially in many of these cases, rather than several holistic views.

Also, for Fabs/Legumes, it would be helpful to see a pic of a single compound leaf, picked off and put on a neutral background.

The plant appears to be Medicago arborea. Common names include moon trefoil, shrub medick, alfalfa arborea, and tree medick. It is a member of the pea family Fabiaceae. The species is characterized by the woody stems, the leaves (three), and compressed, coiled seed pods.  See further description in the links below.  It is a native of the Mediterranean basin and apparently becoming rare in nature.
http://botanyphoto.botanicalgarden.ubc.ca/2015/09/medicago-arborea/
https://en.wikipedia.org/wiki/Medicago_arborea


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Can onion consumption cause Heinz bodies in humans?
It was well attested that eating onions can cause the presence of Heinz bodies in the blood of cats, dogs, and other animals, due to the toxic effect of, apparently, thiosulfate, which denatures hemoglobin. Google scholar finds numerous articles corroborating this, but I'm having trouble finding relevant information for humans. Can eating raw onions cause the presence of Heinz bodies in humans at some dose?

May or may not be helpful: Humans have been eating onions, garlic, leeks, etc. (which are variably toxic in some animals) for centuries; cats, dogs and water buffalo (etc.) have not. OTOH, lots of people have onion intolerance. What is the basis for human onion/garlic intolerance? Searching for that question is more likely to get you helpful results than taking a stab in the dark with what's toxic for only some animals. (Not my down vote.)

Thanks @anongoodnurse. I have removed the reference to onion intolerance to keep the question more focused. I honestly can't imagine why anyone would downvote a perfectly valid question.

Humans are capable of breaking down a great number of toxins other animals have trouble with, it is an adaptation to eating cooked food. perhaps onion is one of them.


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Analysis of dynamic connectome data?
I have heard about existence of full brain connectome data of some worms or fishes. I have heard about GEVI - genetically engineered voltage indicators - that allow to see voltage data at subcellular level. My question is: are there available the mentioned data in processed form (approriate for simulation, mathematical analysis, modelling) and, possibly, are there available some analysis and modelling of them? I am searching materials for neural code that is used in brains and those data and analysis would be very helpful for me.
I am aware of enormous body of coarse resolution MRI imaging data. But my question specifically targets connectome/neuron/subneuron level full data and their analysis.

C. Elegans is the only species with a fully characterized connectome and I don't believe there's been much electrophysiological work done on them. The GEVIs are still being optimized and have their own share of issues particularly with signal resolution - distinguishing between subthreshold changes in membrane potential vs action potential. See the embedded paper. If anything, it will be awhile before the response properties of the neurons in C. elegans are characterized. However, I'm sure you could try modeling smaller circuits where the connectivity and neural properties of the neurons are known.

Actually, there seems to be quite a bit of data on C. Elegans. IIRC recently some spiking activity was detected, while earlier it was believed there's none.


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Techniques of molecular medicine/biology for aesthetic medicine?
Are there scientifically valid methods (possibly in the developmental stage) that can be used for aesthetic medicine. Usually surgical of physical therapies are used for aesthetic medicine, but actually all the problems of aesthetic appearance should be traceable to the genetic/epigenetic causes and that is why the molecular treatment at that level should be possible and optimal.
My question is can be considered also as a veterinary medicine question (aesthetics of pets) and that is why it is really a biology question.
https://journals.sagepub.com/doi/full/10.1177/2470289718787086 is the only more or less relevant article that I have managed to find.
Also CRISPR can be quite promising tool, but I have not managed to find scientific studies for aesthetic medicine of it.


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Can someone help me identify this Brazilian spider?
Does anyone know anything about the identification of this spider? Sorry, but it's the only image I have. It was shot at 2004, January 25th (summer), at 11:27 AM, in Cerrado biome at Minas Gerais state, Brazil. It was walking over a Paepalanthus inflorescence (Eriocaulaceae), probably waiting to prey on its pollinators. A small section of web can be seen raised to the left (where it apparently comes from another inflorescence), touches one of the small flowers, and then it's apparently still connected to the spider, in a pattern that reminds me of Salticidae, though I'm not sure. I think its size is around 1 cm. I doubt a specific identification will be possible, but family, superfamily, subfamily, anything will be fine.

Interesting!  See those long spines on the legs?  Only two groups of spiders (that come to mind, anyway) have that sort of arrangement:
Lynx Spiders (Family Oxyopidae) and Pirate Spiders (Family Mimetidae).
Lynx Spiders are wandering hunters, and the ones I'm familiar with tend to have a body shape more like the familiar Grass Spiders (longish, tear-drop shaped abdomen and hunters cephalothorax - roughly rectangular, and often very blocky at the face.
For instance:
https://bugguide.net/node/view/1965

https://bugguide.net/node/view/1489229/bgimage
So, your spider looks to be a South American Lynx Spider, which unfortunately I'm not at all knowledgeable about.
I'm going to discount Pirate Spiders as a possibility, even with the association there with a bit of web (Pirate Spiders invade other species' webs and kill the occupants), because they're much more 'orb-weaver'-like in their general body shape.  This one is so Lynx Spider-like that I am pretty confident that it is one of those.


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Can someone identify this Brazilian flower?
The photo was taken in january 2004, at Parque Estadual do Rio Preto (Black River State Park), in the Cerrado (savanna-like) of northeastern-central Minas Gerais, Brazil.
The plant was herbaceous/shrub, but maybe it was because of its tender age?


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Is there natural occurrence of induced pluripotency / expression of Yamanaka factors and what is the evolutionary explanation of that?
Is there natural biological processes in which the full (full reprogramming into pluripotent state) or partial (partial reprogramming, stopped before point-of-no-return, preserving the functional distinctiveness of the cell) induced pluripotency (https://en.wikipedia.org/wiki/Induced_pluripotent_stem_cell) and expression of Yamanaka factors occurrs? What is the evolutionary explanation of such rejuvenation factors? I would like to see the natural explanation otherwise it begs for the idea that the Universe is created with the human as the goal of it (anthropocentric hypothesis) and it is quite uneasy for me.
I guess, that natural reproduction processes can involve some kind of rejuvenation/induced pluripotency and they determined the existence of Yamanaka factors.

Regeneration of complex tissues like limbs is known in many animals. Salamander has been used as a model for limb regeneration. During regeneration, the cells at the amputation site de-differentiate to form what is known as a blastema which in turn differentiates to form different kinds of cells.
Christen et al. (2010) have found that de-differentiation in zebrafish involves upregulation of some of the Yamanaka factors.

We found that some of the pluripotency associated factors (oct4/pou5f1, sox2, c-myc, klf4, tert, sall4, zic3, dppa2/4 and fut1, a homologue of ssea1) were expressed before and during regeneration and that at least two of these factors (oct4, sox2) were also required for normal fin regeneration in the zebrafish. However these factors were not upregulated during regeneration as would be expected if blastema cells acquired pluripotency

There is evidence for the expression of the homologs of Sox-2, Klf4 and c-Myc in regenerating newt tissues as well (Maki et al., 2009)
Having said that, I would reiterate what Bryan Krause said in his answer: these factors are essential for the renewal and maintenance of embryonic stem cells. Some of these factors (especially Sox2) are also expressed in non-embryonic multipotent cells like neural stem cells (Seo et al., 2011; Sarkar and Hochedlinger, 2013; Zhang and Cui, 2014).
c-Myc is a proto-oncogene and is normally involved in cell proliferation in all actively dividing cells.

What is a pluripotent stem cell?
A pluripotent stem cell is a cell that can differentiate into any of the major tissue categories. Every animal exists as a collection of pluripotent stem cells at an early stage of development: if you are looking for an evolutionary purpose, that's where you should start, and the purpose is pretty obvious: you start as a single fertilized egg and end up as a complex collection of tissues, so at some point that one cell has to become a collection of tissues, and there is an intermediate step which is a pluripotent cell.
None of this has anything to do with induced pluripotency, however.
What makes a cell pluripotent?
The answer to this question isn't really all that unique to stem cells: all cell types are differentiated from others based on their expression of transcription factors. Transcription factors determine what proteins get produced (including other transcription factors), which in turn determines how a cell functions and what role it plays.
Pluripotent stem cells express pluripotent stem cell transcription factors. Yamanaka started with embryonic stem cells, and looked for transcription factors that were special to those cells.
What does it mean to make a pluripotent stem cell?
Given that the identity of a cell is based on the transcription factors it expresses, the way to make one cell type act like another cell type is to change those transcription factors. A cell is a pretty complicated environment: there are lots of different transcription factors and lots of other types of proteins, so it's possible that it wouldn't be feasible to reprogram a cell this way.
However, Yamanaka and colleagues tried to artificially make an adult cell produce those transcription factors observed in embryonic stem cells. Indeed, they found that if they used the right combination of transcription factors in the right environment, the cells started to behave like embryonic cells, and they could further make those cells differentiate into different tissue types. These transcription factors are the so-called Yamanaka factors.
Summary
An induced pluripotent stem cell is a cell that has been transformed to produce transcription factors that are found in embryonic cells. Transcription factors are what make different cell types different from each other, by controlling everything else that the cell produces. All of this machinery is ubiquitous in development, the only intervention that the humans are doing is to make a cell express genes it would normally only express if it was an embryonic cell.
All of this information is already present in the Wikipedia article you linked.

Takahashi K, Yamanaka S (2006). "Induction of pluripotent stem cells from mouse embryonic and adult fibroblast cultures by defined factors". Cell. 126 (4): 663–76.
Takahashi K, Tanabe K, Ohnuki M, Narita M, Ichisaka T, Tomoda K, Yamanaka S (2007). "Induction of pluripotent stem cells from adult human fibroblasts by defined factors". Cell. 131 (5): 861–72.
Yu J, Vodyanik MA, Smuga-Otto K, Antosiewicz-Bourget J, Frane JL, Tian S, Nie J, Jonsdottir GA, Ruotti V, Stewart R, Slukvin II, Thomson JA (2007). "Induced pluripotent stem cell lines derived from human somatic cells". Science. 318 (5858): 1917–20.


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Name/term for mechanisms by wich the relative size/number of cells of some tissue/organ are preserved
The cells of some organ or tissue are dividing and also dies (apoptosis). But this happens in somehow controlled manner so that the total size of the organ is approximately preserved or the total number of cells approximately stays the same. As far as I understand, this is somehow collective process, because cells in one side of the tissues should somehow coordinate the division/apoptosis processes with the cells of the far side. I have read in one book about cells, that such controlling mechanisms are purely undesrtood even today. Of course, such mechanisms work only approximately (or - to be more precise - they are more complex than just static preservation of the size/number), e.g. numberadipose cells can increase with time.
But anyway - my question is - what is the name/term for such controlling mechanisms and what are other important keywords/terms which I can use for searching more research papers about this theme?
I have specific interest in the control of those processes, e.g., with the aim to bound those processes for adipose cells and to encourage those processes for the muscle cell.
"cell cycle control" and Hippo-pathways mechanisms can be the answers, but I am still searching for the matter.

'Eutely' is the term used for organisms with a fixed number of somatic cells. I'm not aware of any term for sub-organismic structures.

Welcome to SE Biology. Answers here should be supported by some sort of external authority or verification so people can check if they are correct. I realize it is not difficult to look up the word you suggest, but it would be better if you could edit your answer to provide a link. The format is square brackets for the linked text and normal brackets for the link, with no spaces between (unlike my example to demonstrate): [Eutely] (https://simple.wikipedia.org/wiki/Eutely)

You are referring to organ “scaling” and “allometry”.

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

"what is the name/term for such controlling mechanisms and what are other important keywords/terms which I can use for searching more research papers about this theme?" The question asks for a search term. Judging an answer by length is like judging an airplane by weight.

I am not merely judging by length. The comment above is a standard statement for "insufficient explanation" that I just copy-pasted. Your answer could be better if you provided some explanation or references (or both).

Allometry is in my view a correct answer. I have no quarrel with that. I agree however that the answer is best expanded on a little bit. I don't think a good answer is one that is minimally sufficient, because they are not explanatory nor pedagogical. Scaling and allometry are not the same thing; it would be prudent to explain each, ideally with an example, or at least a link to a useful, practical page that works the explanation well. I also do not think that considering allometric relationships addresses the question completely; there is emphasis on the control aspect of organ size.


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How were we able to determine the age of the first cell?
I heard in episode 20 of Youtube channel CrashCourse's biology series that every living organism descended from a single microorganism 3.8 billion years old. I'm astonished by that figure. Even though it leaves a good 100 million years of wiggle room.
As a mathematician I happen to have a fair background in physics so I have been able to grasp the concept of carbon dating and a few other techniques, none of which seem to me to explain how this was determined. What trace could we possibly have of such an organism ? I can't imagine a team finding a fossilised cell and shouting "We've found the first cell !".
Might it have something to do with a well determined evolutionary rate conjectured to be constant and leading back to that particular time ?

I can't imagine a team finding a fossilised cell and shouting "We've found the first cell !"

Well... not the very first cell, but one old cell, yes!
Most of these very old fossils are microorganisms found in seafloor hydrothermal vent precipitates, in stromatolite or in very old sedimentary rocks typically in Greenland but also in eastern Canada. There were also very old fossils found in sandstone in Australia.

Might it have something to do with a well determined evolutionary rate conjectured to be constant and leading back to that particular time ?

No, that's now how we do. We just look for very old fossils. The reason we can't do such simple regression is three-fold.
As measure of 'evolutionary rate', we would typically use the substitution rate at neutral loci. The method is referred to as "molecular clock". The principle is easy (the stats and detailed implementation are a bit less easy). Consider a diploid population of size $N$. Each generation $2N\mu$ mutations are being created at a given locus, where $\mu$ is the mutation rate at this locus. If those mutations are neutral, then a fraction of $\frac{1}{2N}$ of these mutations are going to fix (fixing means reaching a frequency of 1 in the population). This result can be demontrate with a number of technics (incl. diffusion equations and branching processes) but I am not going to detail that now. This means that $2N\mu \frac{1}{2N} = \mu$ mutations will fix every generation in a population. If each substitutions occur at a new locus, then the number of substitutions accumulated over $t$ generations is $2t\mu$. For the substitution rate at neutral loci to scale with time we need constant mutation rate.

The assumption of constant mutation rate is very likely violated on such time interval.
For very distantly related lineages, substitutions won't always occur at new loci. There are tricks to deal with that but there's a point after which, all substitutions will occur at loci that have already received substitutions and there is no signal left to analyse.
We need two lineages to compare their number of substitutions but there is no reason to think that the oldest forms of life quickly separated in different lineages that would have survived until today

Was it really 3.8 billions years ago?
The date of 3.8 billions years ago that you got from CrashCourse (or that you may have read somewhere) is not as accurate as the Green brothers (authors of CrashCourse) may have made you think it is. There is much more than a 100 million years of wiggle room. The only think we can do is find a very old fossil of something that looked like a living thing, date it and claim that life is at least as old as this fossil is.
We think life appeared after the formation of the ocean (which happened 4.41 billions years ago), so any fossil older than that would be quite an extraordinary discovery. The earth was formed about 4.54 billions years ago, so of course we won't find any fossil older than that.
Papineau et al. (2017) is good read on very old fossil (and potential fossils) that we've found. From their abstract

Here we describe putative fossilized microorganisms that are at least 3,770 million and possibly 4,280 million years old in ferruginous sedimentary rocks, interpreted as seafloor-hydrothermal vent-related precipitates

You will notice that we don't quite know the exact date of when abiogenesis happened. I recommend you having a look at this paper if you want to learn more.

Once again, I am reminded of just how fast (geologically) that life happened after it became possible. I think that this is a good sign that even though planets move in and out of "habitable zones" and some stars have a violent early history, that there is still going to be a lot of life "out there" (at least microbiology).

This article [https://www.sciencedaily.com/releases/2006/07/060721090947.htm] provides a good overview of the kinds of evidence there is for extremely ancient rocks containing traces of once-living cells.  The other half of the question is how to determine when the rocks were formed, trapping those traces.  The answer to that part of the question is not carbon dating (because the half-life of carbon-14 is too short), but radiometric dating of a different sort.  [https://en.wikipedia.org/wiki/Radiometric_dating] does a good job of describing radiometric dating methods that work on the scale of a few billion years.


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EVOLUTION OF MAN QUESTION
I have a few questions concerning man's origins
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Man has 10  vital Organs and support systems. yes or no? Man needs all 10 of his vital Organs or he dies. yes or no?
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Either those 10 vital organs evolved together all at once, or they evolved separately.. yes or no?
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If they "Evolved" Separately they must have had an order of evolution. yes or no?
Can anyone provide a plausible order of evolution of vital organs from microbe to microbiologist? (TOE)
Stomach Skin Heart Lungs Brain Upper Intestine Liver Lower
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Intestine Pancreas Kidneys
which one(s) could have been the first, second, third etc..?
If UCA for all flora and fauna (Evolution) were to somehow be true, and If we slowly go back in time, Our "Ancestor(s)" would, at some point, have 9 Interdependent vital organs, then 8, then 7, then 6 5 4 3 2... Yes? or no?
A Microbe has ZERO interdependent interlocked VITAL Organs and their support systems. A Microbiologist has TEN interdependent. interlocked. VITAL Organs and their support systems.  Yes? or No?

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


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Why are low temperatures lethal?
Why can't we (human, or even unicellular organisms) withstand low (body) temperatures (5 - 25°C). I have a limited background in chemistry and biology, so this might be obvious, but not to me.
I know that low temperature reduce the speed of chemical reactions, so any creature cold enough should just perform slower? Or are there any other cold-induced effects that prevent certain reactions? (a reaction requiring more energy to happen, would still happen, but at a lesser rate, right?)
And, supposing a bacteria/virus/small&simple organism was subjected to low temperature (above freezing, but low enough to stop working), what would prevent this organism from booting up again when subjecting to "normal" temperature?

E. coli can be routinely placed in the fridge on agar plates at 4°C for over a month (personal experience) and remain viable.

See tardigrade: http://www.popularmechanics.com/space/a11137/secrets-of-the-water-bear-the-only-animal-that-can-survive-in-space-17069978/

@MarchHo They can also be frozen at -80 and revived …

Low temperatures change the speed of different chemical reactions, throwing delicately balanced systems out of balance. How resilient a creature is to temperature changes is largely a function of how complex it is, and how buffered it is against this kind of change.
Tardigrades as kmm mentioned essentially can't be killed by cold, surviving down to almost absolute zero (absolute zero ≈ minus 273.15°C). Most unicellular organisms can be frozen (especially if frozen quickly or cryoprotected with something like DMSO) and revived later without any change. Most strain libraries of bacteria are kept frozen for cost reasons. Even human cell cultures can be frozen and thawed, even though some of the cells will die. (If even 10% of your cells died you as a person would probably die, so freezing is off the table unless you are very clever indeed.)
Humans and most mammals are pretty sensitive to temperature changes, even though reptiles are not. Most fish are cold-blooded and are adapted to cope with the relatively cold temperatures, but the human heart is not well adapted to even relatively warm temperatures. The atria and the ventricles of the heart stop communicating below 27°C (80.6°F)or so, and below 20°C (68°F) the heart can stop beating entirely. Nerves are complex systems, and absent regulation systems in the nerves themselves to compensate for the changes in temperature, they can stop firing completely. A simple heart can run with less sophisticated orchestration, and is, therefore, more resistant to temperature change. A complicated heart involving the coordination of the atria and the ventricles to produce effective pumping action is affected much more strongly by the drop in temperature.
So, in general, more complicated implies more vulnerable to temperature changes. There are exceptions, however. Bears can hibernate and drop their core body temperatures without any ill-effects, so it's possible to adapt to. Fish deal very well with cold temperatures if exposed gradually, and some fish could live quite happily in a slushie, salinity notwithstanding.

In a very general way, you answer to the question. But reptiles aren't that much less complex than mammals (are they less complex at all?) and, as you mention, there are mammals that can hibernate. The question could be rephrased as "what are the adaptations that some animals have (bears, reptiles, fish etc) and others lack (mammals in general) that allow the core temperature of some organisms to drop without negative consequences?". I think there's still room for discussion.


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How many ATP molecules are formed?
What is the number of ATP molecules formed during the photosynthetic processes which consume 8 molecules of $\text{H}_2\text{O}$ due to noncyclic electron transport and subsequent photophosphorylation?
Assume that quinone cycle facilitates the transfer 4H+ to the lumen of thylakoid membrane for every two electrons passing through electron transport system and one ATP is formed for every 3H+ moving down the proton gradient by the mediation of F0F1-ATPase
MY ATTEMPT: In the lumen, due to hydrolysis 16 H+ are formed. Due to quinone cycle 32 H+ are taken from stroma and transferred to the lumen and NADP+ takes 48 H+ so in stroma there is deficiency of 80 and there are only 48 H+ in the lumen. If I assume that if there were initially hundred H+ on both sides then after non cyclic transport inside the lumen there are 148 H+ and in stroma there are 20 H+ so to have equilibrium then there should be 84 H+ on both side so total 64 H+ should travel then I am getting 64/3 ATP which is wrong. Where I am going wrong?
Screenshot of question paper

I had attempted but iam getting 64/3 ATP as answer which is wrong.

I have no knowledge in photophosphorylation, but isn't ATP synthase creates 3 ATP for every 10 H+? and so maybe it's 64/3.3 ATP

Sorry for the poor quality of the image, but its just as a reference for my answer.
You have made the question too complex. From the figure, we find that 1 H2O gives 2 H+ and 2 e-. 2 e-, through quinone cycle, provide 4 H+ i.e. total 6 H+ which form 6/3 = 2 ATP i.e.
1 H2O => 6 H+ => 2 ATP
Multiply this equation by 8 and you get:
8 H2O => 48 H+ => 16 ATP
So, 16 ATP should be the answer.
Reference:
Pradeep's: A textbook of Biology for Class XI, 2015, Vol. II, page IV/106

Let us continue this discussion in chat.

I threw an answer up, but according to my calculation, and ignoring ATP from NADPH, 16 ATP should be correct. I upvoted this.

@JM97 is it okay now?

@aayush Srivastav in your answer you are not considering the fact that reduction of NADP to NADPH is causing a deficiency of protons which effects the proton gradient

@JM97 I don't think that considering H+ gradient from NADP+ reduction is important because your question does not say to consider it (like the 4 H+ from Q cycle). Also, considering it is not only out of the scope of question (as said by @Kendall) but also it will always give a value in fraction.

So if we do not consider the role of NADP then only 40 protons must travel so only 40/3 ATP ARE GENERATED

I don't know whether its important to maintain H+ equilibrium inside & outside thylakoid. I have only studied that each proton delivered inside thylakoid builds up a proton gradient, so each of those protons should be removed from inside.

Think about this one: you have 100 H+ inside & outside. By splitting 2 H2O, you get 12 H+ more inside and 10 H+ less outside i.e. 112 inside and 90 outside. So, to have equilibrium there should be 101 H+ on each side i.e. 11 H+ should travel out, giving 11/3 ATP, which is obviously wrong as 4 ATP are actually produced.

That is the real question which I was really asking, WHY DONT WE APPLY PRICIPLES OF CHEMISTRY IN THIS PROCESS?

Now if that is your real question, then I think you should edit your question or ask another question which clearly states your problem, and maybe you will get better answers in chemistry SE (I'm just guessing).

I think we can look at it like this

Your noncyclic pathway liberates 4H+ from two water molecules. We're doing that because to get one O2, you've got to split 2H2O. This happens in photosystem II. So in the next step (you know, really broadly) the electrons are passed to cytochrome b6-f complex, where each electron allows it to pump 2H+ into the thylakoid space. Since we got 4e- from splitting 2H2O, from that we can get 8H+. So net H+ = 8 + 4 or 12H+/O2, or we can rewrite it as 4ATP/O2.
For 2H2O you also got 2NADPH, which can also be used to get ATP. I think it's 3ATP/NADPH, so you get  (6+4)ATP/2H2O and repeat four times:
8H2O = 40ATP
Ignoring NADPH oxidation:
8H2O = 16ATP

please see the z scheme given at Wikipedia yours is different , according to Wikipedia only 2e are needed for reduction of NADP to NADPH but according to yours 4e are reducing 2NADP, SO WHICH ONE IS CORRECT?

The reduction of NADP to NADPH requires two electrons per NADPH produced, diagram. So, either representation is correct, but I utilize 4e > 2NADPH because the light reactions don't just release radical oxygen, they release O2, hence I always begin with 2H2O. @JM97

why don't you consider the fact that reduction of NADP to NADPH also contributes to proton gradient

Because you specified noncyclic electron transport.

reconsidering it again from starting then 8 water molecules gives 16 protons and 16e then first inside thylakoid lumen there is an increase of 16H+ second quinone cycle facilitates transfer of 32H+ from stroma to lumen so there is decrease of proton of stroma and increase of protons in lumen. Third 16e will reduce only 8NADP to 8NADPH so there is decrease of only 8e on stroma. Overall:inside lumen +48 , in stroma -40 so to get equilibrium as per chemistry principles only 44H+ should pass therefore we get 44/3 ATP.

do you want to say that in non cyclic electron transport there is no role of reduction of NADP to NADPH in creating proton gradient? If I follow your assumption then also 48 H+ all will not be transferred only  40H+ will transport so that in equilibrium on both sides so that there will be 8H+ on both sides

The NADP does play a role in the proton gradient, but it's outside the scope of the textbook question. To be specific, though, the concentration of protons in the lumen is higher than the stroma. So you would expect more H+ in the lumen than the stroma.

As we know that for 4 H²O molecules one non cyclic electron transport occur which gives us 4H+ ions ..this 4H+ ions gives 2 ATP so 8H+ ions will gives us 4 ATP....so
Ans= 4ATP molecules /8H+ ions

ACCORDING TO ME THE ANSWER IS 24 ATP THAT IS BECAUSE
8H+ IS PRODUCE DE TO PHOTOLYSIS.
16 H+ WILL BE TRANSFERRED INTO LUMEN.
SO 8 ATP WILL BE PRODUCE BY ATPASE {TOTAL 24 H+]
4 NADPH2 WILL PRODUCE 12 ATP
4 ATP WILL BE RELEASED FROM ELECTRON WHILE MOVING IN PS1.
SO TOTAL 8+12+4 = 24 ATP.

First: Please don't write in all caps as this is seen as yelling. And then it would be nice to show some references.


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Do viruses compete with each other or even infect each other? (Virus vs Virus)

I have read on a few websites that there can be competition between
the viruses in a host for replication, nutrition etc. Do viruses fight against each other, i.e. are there viruses that infect or attack other viruses directly or indirectly?
If yes, can this property help in curing or limiting hazardous viruses such as HIV
using less hazardous viruses which can be cured and can compete with
these hazardous viruses?

Can you please link to your websites and maybe provide direct quotes or a clear description of what you mean by "fight"?

By fight I mean can one virus destroy the other one by some method such as decoding the RNA

From what I understand virus on virus action is not particularly common but it isn't unheard of.
Consider the Sputnik virophage which

reproduces in amoeba cells that are already infected by a certain helper virus; Sputnik uses the helper virus's machinery for reproduction and inhibits replication of the helper virus.

Also consider the Mavirus virophage, which

is a double stranded DNA virus that infects the marine phagotrophic flagellate Cafeteria roenbergensis in the presence of a second virus — Cafeteria roenbergensis virus. Mavirus can integrate into the genome of cells of C. roenbergensis, and thereby confer immunity to the population.

As a last example, consider the Organic Lake virophage, which

is a double stranded DNA virus that infects the marine phagotrophic flagellate Cafeteria roenbergensis in the presence of a second virus — Cafeteria roenbergensis virus. [...] [It] preys on Organic Lake phycodnaviruses, which in fact may rather belong to Mimiviridae than to Phycodnaviridae.

So yes, viruses do at least occasionally attack viruses and inhibit their infectious potential and grant a sort of immunity. I'm not aware of any applications of this in medicine for now but maybe somebody else can add something to this if they know.

As TG2 mentioned, some viruses may exploit the presence of an additional virus, but viruses generally don't infect other viruses (as in a smaller virus injecting its DNA into a larger virus) simply because they lack the built-in resources and protein-machinery to replicate other virus species.
Natural selection causes each virus strain to retain only the genes it needs to replicate itself, which means the chances of being able to replicate a rent virus inside a fundamentally different virus are effectively 0 for all practical purposes.
Additionally, there's no reason for viruses to infect other similar (by surface structure or content) viruses because in the case of an infection, the virus particles would quickly cannibalize each other, collectively thwarting themselves.


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Why do animals have fur and feathers?
Does it give them protections from harm?
Sphynx cats, being furless, can get hurt from thorns if they go through bushes
So I'm assuming it's more like defense from animals biting them.
A lion mane is attraction for females and protection on the neck since most predators go after the throat.
Why do only lions have manes for protection and not other cats like domestic cats?

Could you specify one question? Fur and feathers, or the lion mane?

Im justing asking the fur and feathers for animals gives them protection from predators simailr of lion Manes for their neck

short answer insulation.

you have to think this out for yourself Gian, read some stuff. It's mechanical and thermal.  you have to read a lot about evolution of fur and feathers, you'd learn a lot!!!

The nice thing about studying evolution is that questions like this can be answered with replicates of history. There are two groups of homeotherms; Birds, and mammals. Both these groups require an enormous amount of food to fuel this self-generated heat. Body heat is too expensive to throw away. So fir and feathers are convergent examples of insulation to keep this hard-won heat in. That there are many examples of feathered dinosaurs that could not fly implies that feathers were not originally for flying.

but whats the purpose can the fur and feathers also be protection from wounds from predators like the claws wont get to close to the skin

@Gian: Of course.  Evolution is not simple engineering, where something only does one thing.  For instance, a mammalian ancestor probably evolved fur for insulation.  Later, some species evolved it futher as protection (thick fur), camoflage, sexual adornment (the lion's mane), weaponry (rhinoceros horn), &c.  Birds went even further, evolving insulating feathers into flight structures & sexual adornments like the peacock's tail.

@Gian the technical term for what jamesqf is explaining is called exaptation.

...also... in the case of lions it looks like the evolution of the male's larger mane has been influenced by additional factors other than heat regulation, as described in this article: http://science.sciencemag.org/content/297/5585/1339

oh so fur is for tempter not protecting from claws from other animals like defense. in the flim Jungle Book Shere khan mention to Mogli he has no fur or others as fur was more of protection from predators. Mogli being human with out any defense of protection wouldnt survived from tiger claws and sharp fangs through his skin. If he was covered with fur he will be protected

@Gian: Much as I appreciate Kipling, he's not an authority on animal biology, at least in the rather egotistical voice of Shere Khan.  Fairly short fur isn't much protection against claws: just ask my dog :-)

I'm more up on hairs than feathers so I'll answer with respect to fur -
PFA Maderson in American Zoologist, 1972, suggests that mammalian hairs began as mechano-sensory organs and later gained sufficient density to function as insulation -

A chance mutation led to subsequent multiplication of the originally
  sparsely, but spatially arranged papillae, causing the induction of a
  sufficient density of "sensory hairs" to constitute an insulatory body
  covering.

This is a function which has not been lost - it may be a defining characteristic of mammalian hairs that they act, via follicular nerves, as sensory organs. In humans the density of follicular nerve supply is especially high, enough for W.Montagna, "Evolution of Human Skin", 1985, to liken them, regardless of size or location, to the dedicated feeler hairs - vibrissae - of related apes - which makes the sensory function the principle one most of the hairs on modern humans serve. As I suggest they probably are the principle function of hairs of other "hairless" species like Hippopotamus, Elephants, Mole Rats - which, like humans, are not actually hairless.
A whole range of functions besides sensory became possible once hairs evolved, including insulation, water shedding, protection from direct sunlight and physical abrasion, visual signalling/communications and dispersal of pheromones. Mammals managed to evolve and use them all. Manes in lions are probably signalling (of male sexual maturity and sexual fitness) rather than protective.


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Fatty acids into glucose
I have a question regarding the synthesis of glucose from fatty acids. In my book as well as in other posts on stackexchange, it states that fatty acids CANNOT be turned into glucose for the following reason:
Fatty acids are converted into acetyl-CoA, which cannot be reverted into pyruvate because humans do not have the enzyme, but some plants do. Therefore, fatty acids cannot be turned into glucose.
Glycerol however can be converted into glucose by gluconeogenesis.
However, fatty acids can be turned into acetone by ketogenesis and acetones CAN be converted into pyruvate and therefore also into glucose. So doesn't that mean that fatty acids can be turned into glucose?
Fatty acid -> acetyl-CoA -> acetone -> pyruvate -> glucose.
Ketogenesis happens during a carbohydrate deficiency (or diabetes mellitus). The brain is able to use ketones for energy, but preferably uses glucose, so I'd assume some ketones are converted to glucose as well?

This question has already been asked and answered on this site. Please search previous questions. If you have a hypothesis about a reaction sequence, write out the reactions in full. That way you will discover the fallacy of your argument yourself. Arrows between compounds don’t cut it.

As stated in the original comment, I have looked at other posts on Stackexchange and I have also presented the answers that I found. Yet I haven't seen anyone say anything about the conversion of fatty acids into glucose via acetone.
@user1136: It isn't really about net synthesis of glucose, the question is: are fatty acids able to be converted into glucose? If acetone can be converted into glucose and fatty acids into acetone, then isn't the conclusion that fatty acids can be converted into glucose via ketogenesis? I am not talking about fatty acids into to acetyl-CoA to glucose

Fatty acid chains are used to form acetyl-CoA molecules. Two acetyl-CoA molecules condense to form 1 molecule of acetoacetic acid. Part of acetoacetic molecules are converted into acetone & beta-hydroxybutyrate.
If fatty acids can be converted into glucose, then isn't the book and the posts wrong? They state that fatty acids can't be converted into glucose because acetyl-CoA into pyruvate isn't possible, but the conversion via acetone should be possible?

I don't know the exact chemistry behind it, but when I look up reactions of the conversion I find the following: acetone -> acetol -> methylgloxal -> pyruvate -> glucose, so maybe this explains how acetone is converted into pyruvate?

I don't believe that there is significant conversion of ketone bodies to glucose in starvation. There is no evidence that the methylglyoxal pathway is used in normal animals, and indeed methylglyoxal is highly toxic. Experiments in 1984 feeding rats with high concentrations of acetone (which is only produced from ketone bodies by non-enzymic reactions) fail to convince.


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What are the names of these plants?
I found these plants in my backyard in South Florida. What are they?

Please only ask one question per post. Remove one of the species from the post and open a new question for it. Additionally, we ask that more details be provided for species ID including size of specimens and more accurate locaiton (Florida has various habitats, so it'll be useful to others in the future to know where you saw these plants). Please add more details.

failure to follow my previous advice will likely result in your question becoming closed and going unanswered. Please put a bit more effort into your post(s) to avoid this scenario. We want to help, but we need you to cooperate too. Thanks!

I just figured out how to edit it. Sorry for the inconvenience

The main plant in the photo (with the larger leaves) is called Virginia creeper. The botanical name is Parthenocissus quinquefolia.   The leaves are very distinctive in leaf groups of 5 to 7 leaflets.  It is an aggressive woodland vine in the grape family Vitaceae.
Links:
https://en.wikipedia.org/wiki/Parthenocissus_quinquefolia
https://plants.usda.gov/core/profile?symbol=paqu2


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Deuteranopia confusion lines
For people with protanopia (absence of "red" cones), confusion lines look like this (which is quite intuitive for me)

Analogous picture for tritanopia (absence of "blue" cones)

But picture for deuteranopia is quite different. Confusion lines are
  intersecting at one point. But this is not a point nearby green color,
  it is opposite. Why?

I have a conjecture.
Let me remind you about RGB. There is a three-dimensional space (coordinates are RGB coordinates). There is a cone in this space which corresponds to all colors which we can possibly see. Then we consider a section of this cone by a plane. And this is your RGB diagram.
I think that people have chosen a random plane. There is a line for excitation of green cones only. And this the plane intersected negative part of the line. If we chose this plane more carefully, this the picture for green confusion lines would be similar to red and blue.
A friend of mine says that that choice of this plane is not random. It is a plane of constant brightness.
He even conjectured that "green" cone cells are activated not when they absorb green light, but when there is no green color at all.

Is this plane indeed random?

For more details look up here

Is this plane indeed random?

Answer : I don't think so.
HUMAN CONE RESPONSE
Let's take a look back at human cone response curve.
This is cone response curve for normal people :

But picture for deuteranopia is quite different. Confusion lines are intersecting at one point. But this is not a point nearby green color, it is opposite. Why?

In case for Deuteranopes, let's take a look at their cone response :

As you can see Deuteranopes have their green cone sensitivity shifted very close towards red.
This also why Protanopia and Deuteranopia is what we know as Red-Green color blindness, where they have difficulty in distinguishing shades of red from shades of green since its cones sensitivity is very close to each other (almost similar).
So for deuteranopia, why the intersecting point is it not green ? Well, despite the actual missing cone is green, its sensitivity is shifted towards red. Also, this "intersecting point" is called copunctal point.
CONFUSION LINE :
Now about confusion line, indeed each cones in our eyes is sensitive to each RGB primary (even though it's a little bit misleading). And yes, RGB color space is in 3-dimensional. But confusion line is mapped based on chromaticty diagram from CIE 1931, not RGB. Some specific transformation and normalization method need to be performed to convert 3-dimensional RGB into 2-dimensional chromaticity diagram.
As we know before, Protans and Deutans have their cone sensitivity close to each other, thus their copunctal point (point where the fundamental color is missing, point where all the lines converge) is also close to each other.
Here's the copunctal points (1) for all dichromats :
COPUNCTAL POINT     x         y
Protan             0.747     0.253
Deutan             1.080    -0.800
Tritan             0.171     0.000

CIE is quite tricky, they can have negative value as well (RGB can't have negative value). This copunctal point is very important since it's the fundamental information of the missing wavelength from colorblind, and this missing wavelength is converted into CIE colorspace and then mapped into the diagram. So, even though the deuteranopes confusion lines looks a bit confusing, it is the correct mapping from actual missing point in wavelength.
(1) Wyszecki & Stiles, Color Science (2nd ed.), 1982, Table 1 (5.14.2) p. 464


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Has there even been a clinical study where healthy volunteers consented to be infected with a pathogen?
I am curious if there has ever been a (modern) clinical study where a healthy volunteer was purposefully infected with a pathogen in order to test the effectiveness of a therapeutic or preventative measure (like a vaccine)?
If not, would the FDA allow for ethical exceptions in cases where there is an extreme case of urgency (like in a pandemic)?
Obviously these would be willing volunteers who signed waivers, etc. So Nazi experimentation, the Tuskegee trial, and other studies without total consent from the participants wouldn't qualify here.
Edit: Self-experimentation wouldn't qualify here either because the bioethics of self-experimentation are different than testing on others.

What counts as "modern"? There is a long history of self-experimentation by medical researchers many of which would seem to fit your criteria ...

Why is this question being downvoted? Is this stackexchange not appropriate for questions on medical and biological history?

@BryanKrause I was going to contribute that very example as answer, but then I realized it doesn't strictly answer the question. The victims of the Tuskegee Experiment were not deliberately infected with syphillis, rather their existing cases of syphillis were deliberately left untreated, and the diagnosis was concealed from them,  "to study the course of the disease". Appallingly unethical, but not quite relevant to this specific question.

@Charles Ah good point, I got that detail wrong. I think I'm confusing it with a separate unethical experiment.

Is 1900 considered modern? Yellow fever, in Cuba, and not just one volunteer, but a whole group.

This is a great biological question! It asks a lot about how empirical science is done in the field of modern biology. I'm glad we encourage such questions from curious people who want to learn more.

One can't easily separate ethics from how biology is done, as much as some people have tried. (Though I suppose some have made bioethics into a separate and successful media career, so it can be done in that way.)
In addition to the comment-answer about the Tuskegee Study, Nazi doctors in Germany performed experiments without consent, which included infecting concentration camp prisoners with the bacteria that cause tuberculosis.
Your question is about volunteerism, however, and the victims of the United States and Nazi Germany did not give full — or any — consent to experimentation.
In this week's issue of Nature, there is a news article which interviews bioethicist Nir Eyal about a recent preprint, of which he is a primary author.
In this interview and in the preprint, your very question about coronavirus vaccine research, specifically, is discussed, as it concerns the matters of consent, ethics, and safety of doing accelerated biological research about this virus in a time of emergency.
In answer to your first question about modern clinical studies, Dr. Eyal notes:

Are there any precedents for infecting healthy people with a pathogen?
We do human-challenge studies for less deadly diseases quite frequently. For example, for influenza, typhoid, cholera and malaria. There are some historical precedents for exposure to very deadly viruses. The thing that demarcates the design that we propose from some of these historical instances is that we feel there is a way to make these trials surprisingly safe.

As an example, there was a challenge trial for malaria performed in 2012. Healthy individuals were bitten by mosquitoes carrying the malaria parasite and then treated with antimalarial therapies.
Clinical trials are done under the aegis of government agencies with review and approval processes, some of which are described on the FDA web site. IRBs or Institutional Review Boards provide oversight:

Under FDA regulations, an IRB is an appropriately constituted group that has been formally designated to review and monitor biomedical research involving human subjects. In accordance with FDA regulations, an IRB has the authority to approve, require modifications in (to secure approval), or disapprove research. This group review serves an important role in the protection of the rights and welfare of human research subjects.

History does guide us to worry about the ethical issues surrounding medical trials, especially under exploitative regimes that leave people to fend for themselves during a time of global crisis:

Do you worry that countries with authoritarian governments could conduct such studies on vulnerable groups, such as prisoners or members of persecuted minorities?
We would only recommend conducting the studies in an ethical fashion, with fully informed consent. Vaccine makers want to sell their product to other countries. They want to publish their scientific articles in prestigious journals and there would be many obstacles if their trial doesn’t adhere to widely accepted standards.

But in the modern age, in non-corrupt regimes, science does aim, for the most part, to do the right thing, and there are methods and regulatory mechanisms in place to try to enforce societal standards that move us past the days of Tuskegee and Nazi concentration camps.

Challenge trials! Terrific answer, thank you!

This is routinely done with the common cold for all sorts of purposes, including chasing after the mythical cure.

Another example for norovirus, which I imagine was a very unpleasant study to take part in.  In this case it wasn't even to evaluate a treatment, but just to determine the infectious dose.  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3952671/

As far as I remember, in the book "Microbe Hunters" by Paul de Kruif, there is a description of a vaccination trial for a deadly desease with a whole group of volunteers, not just one volunteer (done in Cuba? Early 20th century?). It was in one of the last chapters. Chapters. "...and the human cases—those brave souls in Cuba that met miserable fates in the name of science."

OK, I found it: "In May 1900, Major Reed ... The board conducted many of its dramatic series of experiments at Camp Lazear ... The risky but fruitful research work was done with human volunteers, including some of the medical personnel"

"...they learned how to stop the spread of yellow fever by finally ceasing animal experiments and testing the vaccines on humans instead."

From the preprint, it appears that the key point in whether or not such studies are ethical is if they propose an increased risk to participants. It is not yet clear if social isolation and curfew will contain SARS-CoV-2, so I am not sure if at this moment the argument can be made that most volunteers will be affected at some point in time and as such they are not facing an increased risk. Regarding the recent malaria study, this was only conducted with existing treatment of malaria. To this date, no trial of Covid-19 treatment delivered convincing evidence of effectiveness. Furthermore,

[cont’d] the Case Fatality Rate of Malaria is much lower than the apparent CFR of Covid-19, so the overall risk in the malaria setting is substantially lower than that in a proposed SARS-CoV-2 study. Even in the 20-45 year old group, case fatality rate of SARS-CoV-2 appears to be around 0.2 which means 2 of 1000 infected will die. // Dr. Eyal outlines circumstances under which a SARS-CoV-2 human challenge trial would be ethical, but I do not think we have reached these circumstances yet.

The Tuskegee Study is a bit out-of-place here, because it doesn't actually meet any of the criteria in the question: not the "purposefully infected with a pathogen" criterion, not the "in order to test the effectiveness of a therapeutic or preventative measure", etc. Rather, the subjects were already-infected men, and the study studied their untreated syphilis. (That's why it was so monstrous: the study continued for decades after syphilis was curable, but they just -- didn't. They didn't even warn the men not to infect their wives, etc.)

I discovered a book while working in a library entitled Inhumane Medicine or Inhumane Science or something, that discussed much of the Nazi efforts to produce medicine by using POWs. One passage I recall talked in great detail about the methods they used to incubate Typhus in prisoners and how to maintain the disease sustainably within that population. It was fascinating and terrifying.

Yes, Dr Barry Marshall self administered Helicobacter pylori to investigate whether it causes stomach ulcers. He won a Nobel Prize for it.
https://en.wikipedia.org/wiki/Barry_Marshall

All the time!
For example Flucamp does research on influenza, rhinovirus and (non-SARS) coronaviruses, that involves deliberate infection of paid volunteers.

When the trial starts, we only inoculate them with a weak cold or flu virus so the body can fight this off without a high level of risk, before monitoring the disease cycle as they go from healthy to sick to healthy again in our bespoke medical research facility.

Science Magazine notes that such trials are on the rise as we learn ways to weaken a pathogen before introducing it to a human subject.

Today, people are being deliberately infected with malaria, influenza, shigella, dengue, norovirus, tuberculosis, rhinovirus, Escherichia coli, typhoid, giardia, and campylobacter.

Julius Wagner-Jauregg, an Austrian psychiatrist, while investigating fever to cure forms of insanity (pyrotherapy), infected his patients with malaria. This triggered an immune response that cured neurosyphilis. He was given the Nobel Prize in Medicine in 1927.
Sources:

Tsay, Cynthia J. "Julius Wagner-Jauregg and the legacy of malarial therapy for the treatment of general paresis of the insane." The Yale journal of biology and medicine 86, no. 2 (2013): 245.
Julius Wagner Jauregg. In Wikipedia. Retrieved from https://en.wikipedia.org/wiki/Julius_Wagner-Jauregg

Welcome to Biology.SE! This looks like a reasonable answer and it's great that you provide supporting references. However, please include the complete reference information since links can break. One easy way to get that information is to search for the paper on Google Scholar and click on the ‟ symbol to get reference information. This is a good example of how to format references. Thank you!

Operation Whitecoat, a research program run by the US Army, used enlisted men who had registered as conscientious objectors and volunteered for the program. The research investigated defenses against possible biological weapons, testing vaccines and antibiotics on these volunteers.
https://en.wikipedia.org/wiki/Operation_Whitecoat

From the Wikipedia page about the British Common Cold Research Unit, which operated from 1946 to 1989:

Thirty volunteers were required every fortnight during trial periods. The unit advertised in newspapers and magazines for volunteers, who were paid a small amount. A stay at the unit was presented in these advertisements as an unusual holiday opportunity. The volunteers were infected with preparations of cold viruses and typically stayed for ten days.


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What percentage of RNA splicing happens during transcription?
Splicing can happen either during transcription, or directly afterwards.
I am reading about single-cell RNA seq, and according to this paper, they observed that 15–25% of reads contained unspliced intronic sequences.
Now assuming that the majority of reads from RNA seq will come from RNA that has finished being transcribed...
Does this suggest that 75-85% of all genes are spliced during transcription? In other words, are 80% of our genes fully mature (spliced) immediately following transcription?

I don't think it will be possible to give a conclusive answer to this question, because a) it's a matter of active research and b) the rate / percentage of transcripts that are fully spliced co-transcriptionaly is almost certainly not constant but will depend on a lot of factors & regulatory mechanisms.
Another important detail is that this analysis / paper is based on mRNA sequencing, which uses oligo-dT primers to enrich for polyadenylated mRNA molecules. However, oligo-dT primers can also bind to stretches of A's inside of RNA molecules (this process is called internal priming) and since such stretches are more common in introns compared to exons this may contribute to the abundance of intronic reads in mRNA sequencing data (I don't have a good literature source for this specific case, but it's a known 'issue' for sure).
Maybe some of these reviews are also helpful (not sure if all are freely available):

Splicing and transcription rates in living cells
Environmental influences on RNA processing
Co-transcriptional spliceosome assembly and function


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How does one confirm the discovery of a new species of plant/animal
Hearing from the National Geographic and the news about the discoveries of new species of plants/animals, I was wondering how can a person confirm when they have actually discovered a new species of plant or animal?
How can they identify with enough certainty that it is not one of the species that has been previously discovered (out of the umpteen varieties of species)? Is there some kind of official/international database of species for plants/animals they typically look up to to confirm it? Also, how is the process of naming of a new species decided and why does it end up being a Latin name?

Basically, you have to examine as much of the relevant 'material' (preserved museum specimens) of the proposed new species and its closest relatives, and compare the diagnostic characters of your proposed new species versus those of its presumed closest relatives to confirm it is actually distinct. For example, with snakes (my field), we use counts of head and body scales, relative distances between features, relative length of tail, hemipene morphology, and even colouration, to determine species.
When combined with genetic evidence of monophyly of the new species and adequate divergence from closest relatives, it becomes a very robust species description.
Finally, names can be accepted or rejected by the ICZN based on existing names for proposed species, though it's a very confusing mess for most groups. I'd recommend checking out their website for more in-depth guidelines

Tried searching a sample  "Galleria mellonella" in ICNZ in the search bar but didn't find anything there

or are there other mayor international organizations that list the Latin names of plants / animals?

these will be relevent https://biology.stackexchange.com/questions/52990/where-can-i-get-a-file-list-of-the-common-and-scientific-names-of-species and https://biology.stackexchange.com/questions/14059/is-there-a-downloadable-list-of-all-species-along-with-their-traditional-classif Tree of Life web project is decent.


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Help with preparing Congo Red TSA
So I want to make Congo Red TSA. My instructor gave some hints but I still have some questions:

I start by making two stock solutions: 20 mg/ml of congo red and coomassie in two different falcon tubes. To prepare 30 ml of each, would I dissolve 600 mg in sterile water?
The final concentation in a 500 ml TSA solution needs to be 40 μl/mL of CR and 20 μg/mL of coomassie. How do I calculate the amount of solution needed for the TSA?

1) Yes, that's correct.
2) This is just a simple matter of applying the equation $C_1V_1=C_2V_2$. For congo red:

$C_1=20\frac{mg}{mL}$
$C_2=0.04\frac{mg}{mL}$
$V_2=500\ mL$

I'm sure you and a calculator can figure the rest out.