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Evolution of the energy generating system in mitochondria
Both yeast and humans have mitochondria. Given that yeast have a much shorter time between generation I would expect evolution to have had more time to optimize mitochondria of yeast.
The main function of mitochondria in yeast is essentially similar to that in human cells.
Is their efficiency roughly the same or did the stronger evolutionary pressure allow yeast to evolve much better mitochondria? Is there empirical research about mitochondria that studies the difference between the mitochondria of different species that includes metrics of their efficiency?

Please express your concept of efficiency in precise chemical/thermodynamical terms. Without this your question is unclear and is likely to be removed as such. I would be interested what examples you can cite in support of your apparent assumption that generation time favours yeast evolution over that of man. Enzymes with greater turnover numbers, for example?

@David : I don't believe that it makes sense to specify a specific way to measure efficiency in a question like this. If someone did research into this question they chose their own metric. Formulating this question in a way that rules out particular metrics makes no sense.

@David : The idea that evolution is a process that's faster then time between generation was a basic idea I learned in my bioinformatics classes in university. I don't see why it should have be justified in order to ask a question.

If you don't define your terms we can't discuss your question sensibly. I have suggested a particular form of efficiency, which is not restricted to mitochondria, enzyme turnover number. You could define it as ATP produced per pyruvate molecule and I can answer that. 2. My immediate response is that I don't necessarily buy this "basic idea". I might argue that the time for evolution of mammals has been sufficient to "optimize" their mitochondria. Therefore you need to formulate the idea precisely, citing a reference in support, if possible, in order to rebut this default counter-argument.

If you have numbers about enzyme turnover numbers or about ATP produced per pyruvate molecule to argue that the time for the evolution of mammals has been sufficient to optimize their mitochandria I am happy to hear that argument as an answer to my questions.

Before I provide a sort of answer to this question, could you indicate what you know about mitochondria? Do you know what their prime function is and its biochemistry? Do you know how they are believed to have originated?

Yes, I do have taken a biochemistry courses in my bioinformatics studies.

ANSWER SUMMARY
The criterion of efficiency of mitochondria is taken as the yield of ATP per carbohydrate molecule oxidized using the electron transport chain and oxidative phosphorylation. Experimental values for this are similar for yeast and humans, whereas theoretical values derived from differences in the structures of the ATP synthases actually imply a higher yield for mammalian mitochondria.
It is argued that it is not surprising that the difference in generation times did not produce the result expected by the poster. First, the period after the separation of eukaryotes from prokaryotes is no longer than the period between the origin of eukaryotes and that of the aerobic bacteria from which their mitochondria arose. Second, the stage would have been reached when there were mechanistic limitations on further increases in efficiency of this complex system. If the differences between mammalian and yeast bacterial ATP synthases is real (and an even ‘worse’ yield for bacteria, that have an even shorter generation time), this suggests that the main evolutionary pressure on this system varies between organisms, rather than being simply to maximize the yield of ATP.
ANSWER ELABORATION
Criterion of efficiency
The main function of mitochondria is to use molecular oxygen to oxidize NADH and FADH2 via the electron transport chain and oxidative phosphorylation to produce ATP. A suitable and generally accepted measure of efficiency — reminiscent of that applied to man-made mechanical devices — would be the percentage of the energy of this oxidation that is converted to ATP (rather than being released as heat). Any reader not familiar with the biochemistry of this system is advised to read the footnote* before proceeding further.
Is there any difference?
The traditional way in which the yield of ATP in oxidative phosphorylation has been measured is by the P/O ratio (the ratio of ATP produced to oxygen consumed). Results obtained over the years have varied becauase of technical problems — see review by Hinkle (2005). As summarized more recently (2010) by SJ Ferguson,  the historical controversy was not about differences between species — they were no indications of differences even between bacteria (the precursors of mitochondria, performing oxidative phosphorylation in their intermembrane space) — but merely about the true value of the P/O ratio.
As Ferguson goes on to say, the gradual elucidation of the structure of the ATP synthase and the elucidation of its mechanism led to a believe that deductions from this were a more reliable indication of the stoichiometry than the experimental measurements. Specifically, a 360˚ rotation of the F0 component of the ATP synthase could be seen to result in the synthesis of one molecule of ATP, and that this required on hydrogen ion bound to each of its c subunits (see diagram from Wikipedia article, below).

He describes the results with yeast as follows:

X-ray crystallography of yeast ATP synthase revealed a ring of c subunits attached to F1 even in the absence of other subunits of the F0 sector (9). This work not only suggested that a and b were not interdigitated with c but also revealed the surprising stoichiometry of c10. The C-terminal helix of the hairpin c subunit is at the outside of the ring and contains an essential aspartate or glutamate residue. This residue is believed to pick up an H+ and rotate away from an interaction with the α subunit. Thus, 10 protons should drive a 360° rotation of the c ring, which is structurally connected to γ, giving synthesis of 3 ATPs as γ rotates through 360° within F1; the H+/ATP ratio would be 10/3 = 3.3. The P/O ratio for NADH would be 10/(3.3 + 1) = 10/4.3 ≈ 2.3, thus moving below the range of values directly determined.

It was assumed that ATP synthases other than yeast would also have 10 c subunits, but, surprisingly, although bacterial ATP synthases also have 10 subunits, the bovine (and other vertebrate) one has only 8, suggesting a higher P/O ratio than yeast — greater, not poorer, efficiency.
Mitochondrial evolution in context
Whatever the actual P/O ratios in different aerobes, the more rapidly-dividing species do not show a clear increase in efficiency in this respect. I suggest that in this respect the evolutionary timescale shown below (adapted from The Cell: A Molecular Approach) should be considered.

What is clear is that the time for an improvement in efficiency of energy production to occur between the divergence of yeast and animals (A) is much less than that between the time at which mitochondria were acquired from bacteria by the first aerobic eukaryote (B–A). Note also the long period the system had to evolve in the aerobic bacterium that gave rise to mitochondria (C–B). My argument is that by the time of appearance of mitochondria, the system had time to evolve to the optimum that mechanistic considerations would allow. Otherwise one would have expected those bacteria to further evolve a system much superior to yeast or mammals in the C–B timescale.
Other aspects of the evolution of the mitochondrial energy generating system
It should be noted that there have been changes in the mitochondrial energy generating system over evolutionary time. For example, in the cytochrome oxidase system the same set of core subunits are found in prokaryotes and eukaryotes. However additional subunits have been acquired in primates. Rather than being concerned with the catalytic efficiency of the system, these additional subunits are thought to be concerned with regulation.
Better systems to study the effect of division time on evolution of eukaryotic ‘efficiency’?
Because mitochondria had probably reached optimal mechanistic efficiency in energy generation when they were acquired, they do not appear to be a good choice for studies of the type the poster envisages. Perhaps he might do better with something related to nuclei, which are not present in bacteria. However there are problems of interpretation. For example, if it were found  that some aspect of the DNA replication machinery in yeast allowed this process to proceed faster than that in mammals, could one conclude that this was due to the shorter generation time of yeast? No! One could equally argue (and it would seem to me more likely) that the lower generation time resulted from an evolutionary pressure for faster DNA replication, a pressure that does not exist in the more slowly dividing mammals.
FOOTNOTE *
ATP in mitochondria (and the inner membrane of aerobic bacteria) is synthesized from ADP using the free energy released by the oxidation of the reduced cofactors, NADH and FADH2 (produced from the oxidation of particular carbohydrates), by molecular oxygen. The mechanism of this, rather than involving simple coupled chemical reactions, involves the movement of hydrogen ions across a membrane in which there is a concentration gradient (strictly through a proton motive force, to which membrane charge also contributes) using an ATP synthase, a molecular machine, the structure of which clearly indicates the stoichiometry of input hydrogen ions to ATP synthesized. The hydrogen ion gradient results from three stages in the electron transport chain (complexes I, III and IV) where a hydrogen ion is translocated into the inner mitochondrial intermembrane space. This is described in standard text books of biochemistry such as Berg et al..

How do you know that perfection was reached back then? It's an empiric question and you aren't refering to any empirical work that made any attempts at measuring.

@Christian — OK. I had assumed a little greater knowledge about the ETC. I'll add a footnote in a day or two explaining things in detail. While waiting for the coup de grace you might do something to clarify your question (or your mind). How about an evolutionary diagram with a time scale showing 1. The time between the origin of life and the origin of aerobic bacteria. 2. The time between the origin of aerobic bacteria and the origin of eukaryotes with mitochondria. 3. When  short-generation time eukaryotes, such as yeast diverged from longer-generation ones that gave rise to mammals.

My question is pretty clear. I want actual empirical evidence about the differences between mitochondria of different taxons. Given that this doesn't seems to be clear enough (I'm used for Skeptics.stackexchange, that empiric evidence is a default for a decent answer), I added the desire for empiric evidence explicitly. You haven't provided any empirical evidence but only argued that you don't think that any difference exist based on theoretical arguments.

@Christian — The wait is over. I have completely rewritten my answer following the discovery of the data about the number of c subunits in yeast and bovine. The two-page Ferguson review is a must-read in relation to this.


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Bottleneck effect
Is it true that animals that faced a severe bottleneck will have genetic deficiency for a long time? Does it mean they will all look the same for a long time?

A population bottleneck (see also founder effect), by definition is an event of sudden reduction of genetic diversity due to a sudden reduction in population size. Of course, such reduction of genetic diversity is not restricted to animals (unlike you seem to suggest) but to any population of living creatures.
Given that part of the phenotypic variance is caused by genetic variance, it means that after a bottleneck, phenotypic variance will be lower after the bottleneck than before the bottleneck indeed. However, a bottleneck might be coupled with a environmental change which could change the genetic variance in itself and the above might not be true anymore (see this post for an introduction to quantitative genetics).
Because, deleterious alleles tend to be recessive, a reduction in genetic diversity often causes a reduction in mean fitness. In humans, cases of founder effects have been shown to be associated with an increase in recessive genetic disease such as observed in Quebecois or in Amish.
The time needed to restore the genetic diversity very much depend upon the exact demography at play, as well as the mutation rate and selection coefficients. As a rule of thumb that many population geneticists use in numerical simulations; if $N$ is the population size at equilibrium (after bottleneck), then $10 \cdot N$ generations is enough to restore a good genetic diversity.

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Do squirrels and blue jays play a role in oak tree distribution?
White oak (Quercas alba) acorns have lower tannin levels than red oak (Quercas rubra) acorns, therefore animals tend to eat the white oak acorns before red oak acorns.  Animals such as squirrels and blue jays will often catch red oak acorns for later consumption when the tannin levels have lessened or when food sources are scarce.  Since red oak acorns are more likely to be hauled off, cached, and forgotten about wouldn't this cause red oaks to be more widely dispersed than white oaks?  By this I mean that white oak trees would be spaced closer together than red oaks.
Source 1: https://www.allianceforthebay.org/2017/09/the-complicated-relationship-between-acorns-and-animals/
Source 2: https://link.springer.com/chapter/10.1007/978-1-4419-0378-5_6?no-access=true

I just checked recovery rates from articles, they cited losses of 75, 40, 80 percent. Squirrels and many species of birds that cache foods. any loss rate higher than 3 percent would mean that every squirrel grows at least 3-10 trees far away from the parent tree every year.

I remember hearing a loss rate in the 70 percent range years ago.  I'm not having much luck finding squirrel population data, but the best I could find is ~50/acre in an urban setting from this site.  There is also a q&a site with an answer of 3 squirrels for every human world wide - no reference cited though.  Terms like widespread and abundant are used often.

In case anybody is curious this paper seems to answer this question.

The obvious conclusion to follow from these summaries is that acorns
  of RO have a significant dispersal advantage. RO acorns are dispersed
  greater distances from their sources, cached more often in a wide
  variety of environments, and even show the ability, under some
  circumstances, to escape partial predation. Acorns of WO, in contrast,
  should show short dispersal distances and may be in fact adapted for
  rapid germination near or under parent trees.

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What is the nesting period of the European Turtle Dove in middle to southern Italy?
While the breeding period to the north, in Switzerland, seems to be early May until early July, and I have not found any information for the Naples area.
Also, are they likely to nest a second time?

Yes they are likely to breed a second time, and sometimes three times. It mostly depends on the complex graph of nourishment that they can come by to breed up to three times in a year.
They have higher chances of breeding 2-3 times in Naples than in Switzerland according to this document: http://www.birds.kz/v2taxon.php?l=en&s=289
The mean first egg date is May the 18th in the UK, and if you compare the average temperature for London and Naples at that time, spring is about 30 days earlier in Naples, and the birds can migrate there from Africa first, so the mean first egg date in Naples is between the 18th of April and 18th May. They probably start nesting very soon after they arrive.
It depends how good the harvests are and how disruptive the industrial farming is on their migratory path that year, while the nesting time was measured for may in the UK one year, a satellite tracking of a turtle dove placed it's arrival in the UK in June another year.
The result is an erratic timing from April to June in Italy.
http://www.avibirds.com/migration/Turtle-Dove.jpg

That Kazakhstan link is interesting because it shows they CAN breed multiple times, but of course it doesn't tell us if it happens in Italy. The climate differs to much between those.

And secondly, bird migration doesn't have to work like that. That the temperature is 30 days earlier in Naples, doesn't mean they arrive there 30 days earlier. They might all start together. Flying from Italy to the UK takes only a day or perhaps a few.

Italy's springtime and fall are 2-3 months longer and more verdant than the UK's I expect they can breed 2 times at least there on a good year.

Oh, I expect they can, but that doesn't mean they DO. Streptopelia decaocto, a close relative, breeds 6 times or more and even in winter in Holland and the UK.

I was reading references that say " The most important ultimate
factor affecting on the timing of the breeding season of most
birds is the food supply, either for the laying female, or for
feeding the young" so I'm just saying that winter dormancy is much earlier and later southern Europe, because I used to check birds eggs in the woods in mid May, which is a lot colder and stiller than italy and france are in mid April. one month earlier, like april 18th, is a very coherent assumption, and more than one brood is a very likely possibility.

I think it would be difficult to answer except people living around or visiting frequently the Naples region as the bird distribution covers the whole central Europe during summer time.
Then my answer will focus more on the italian part.
One interesting reading would be this document from the European Commission.
Disclaimer: this document refers to biological aspects of the turtle dove, but the main topic is the pressure of the hunt on that bird.
In page 10 they mention that:

Stable populations are found in central Europe: Italy, Austria, The Czech Republic and Slovenia (BirdLife International 2004a).

Page 14 table shows the period of migration and breeding countries (EU 25 only).
And in page 17, they shows that probably between 200'000 to 400'000 breedings pairs are present in the whole Italy (Estimation by Birdlife International)
Here are some refrences:

Breeding and distribution at IUCN
Distribution at avibase

As you can see the distribution os quite large and the figures of estimated breeding pairs very large.
You can also check the observations (not only breeding) with that avibase link.
For the probability to nest the same place, I would say it's possible as in general the birds can go to the same place as the previous year but I cannot say more if the European Turtle Dove have a different behaviour or not. If they have a quiet place where there are no disturbance (Hunting, human activities) or predators, they would probably come back to the same place.

Although you have gathered a lot of info, you have not answered the question: what is the breeding period in Italy and do they nest more than once (in a single year).

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Varied Carpet Beetle Larvae
I keep finding what I'm 99% sure are carpet beetle larvae on my walls, of all places. Yet when I look around and search thoroughly, I cannot find any signs of an(y) adult Beetle(s). Why/how is this happening and if it's not a carpet beetle larvae, then what is it?

Maybe attach a photo of one to this question?  That would help with the second part.

The eggs of carpet beetles would be exceedingly small. What makes you so sure? Also, seeing eggs of an insect, but not finding the adults would not be unusual at all.

I saw dozens of carpet beetle larvae in an old home I live in for more than a decade but never did I once see the adults. It can happen. See here for a visual.

Related: What kind of insect can this be?..., Can anyone help confirm this tiny insect larvae?, Bug Identification: Is this small tubular, black bug...,
How to protect my mounted insects..., What is the name of the critter depicted..., What small insect is this?, What bug is this...


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Type of plant cell that builds a secondary wall in between two primary walls?
I read that there is this type of pattern in cell wall synthesys. What is the type of cell that does that and in what kind of scenario?

Secondary cell walls are found in many plant cells especially ones used in for structural functions, such as the lignified cell walls in xylem such as in wood. This occurs in a mature plant cell, where the cell constructs a second wall between the primary cell wall and the plasma cell membrane, which is made up of strong cross-linked cellulose microfibrils, which are then lignified.

The secondary cell wall adds additional support to the cell, enabling it to carry out effective structural functions in the plant such as transportation of water and mineral ions in xylem from the roots to the leaves.
Occasionally, there is a tertiary cell wall located on the inner side of the secondary cell wall adjacent to the plasma cell membrane. This is usually very thin and is made up mainly of xylan with a small ratio of cellulose (unlike the primary and secondary cell walls which are mainly cellulose). It can be found in the xylem tracheids (usually found in the wood) of gymnosperms (e.g. conifers, ginkos). As for purpose, again, it strengthens the cell even more and sometimes contains nutrients ready to pass through the membrane into the cell.

It's totally off topic sorry. My question is really simple and precise.


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How are viruses isolated?
I read several different articles about virology, including the Wikipedia article on viruses and none of them explain how a virus is isolated. Some talk of injecting a virus into a chicken egg, but this does not isolate the virus, it just reproduces it.
If a researcher filters the particles in a serum to get those of a particular size, it proves nothing, because every creature has many thousands of different viruses in their blood, so any sample filtered by size will potentially have hundreds of different viruses in it, all the same size range. How can they possibly be separated?

Fairly relevant publication.

I eventually figured out the answer to this question after reading some introductory textbooks on virology.
Though, as another answer states, there are many different possible techniques to isolate a virus, there is one basic approach that can be considered the standard method.
The key pre-condition is that you must know or suspect the type of cell which the virus uses to reproduce. Most viruses use only a single cell, or perhaps two different kinds of cells at most, to reproduce. There are about 200 different kinds of cells in the human body.
Once you know (or suspect) the cell type, the next step is to obtain a culture of that cell so that you can grow that cell type indefinitely, an immortal culture.
Next, the researcher samples a subject thought to harbor the virus (or viruses) of interest in the area where there might be infected cells. The sample is purified by filtration and/or centrifuge to remove bacteria, cells and other organisms so that only viruses remain. The sample is then diluted to various degrees and each stage of the dilution is used to innoculate a different cell culture. If successful, then a plaque will appear on or in one or more of the cultures after a number of days where the virus is multiplying. That section of the culture can then be taken out and the plaque will hopefully contain a single virus of a single genetic type, which is called an isolate. The isolate can then be further studied.

This answer is misleading as concerns cell types for culture. Rather than choosing the differentiated cell type the virus infects and attempt to immortalise it — a lengthy and specialist process — you see if you can infect established immortalized cell lines — not necessarily human (remember they initially used eggs). Your remarks about tissue specificity reflect a misunderstanding. Tissue specificity reflects the mode of delivery of the virus. For infection in vitro this has been circumvented and all that is required is the receptors the virus uses, which will be present on many cell types.

Apologia
This answer was prepared in response to a previous question about Measles virus, but the question was removed for reasons I am not party to but which I can guess. As I spent some time on it I thought I’d post it in reply to this question. It is specific for measles virus, although there are obviously aspects that apply to other viruses, and deals with characterization as well as isolation. I am not a virologist (although I have done some biochemical work on pig herpes virus) so the it was is based solely on my reading of the papers cited and of Field’s Virology. I welcome suggestions for corrections or additions. It may seem to some that the question does not justify an answer of this detail. However it may also be of interest to young contemporary students and researchers who may have difficulty in envisaging the technological limitations of post-war experimental science.
Original Isolation and Characterization
The Edmonston strain of measles virus was isolated in 1954 by Enders and Peebles from the blood of a child with measles, David Edmonston. Before this scientists had found that an agent which was small enough to pass through filters that retained bacteria (i.e. possibly a virus) could cause measles when inoculated into monkeys and could be passaged in eggs containing developing chick embryos — the best method available until then. What Enders and Peebles managed to do was to maintain the virus in cells growing in tissue culture (a far more convenient host experimentally) — initially primary human kidney cells, and then monolayer cultures of chick embryo cells.
They used light microscopy to detect the changes in the cells that demonstrated that they were infected (the original paper contains many photographs of the cytopathogenic effects on infected cells). They could passage the virus by inoculating uninfected cells with infected cells, and they also isolated some virus from the cells by breaking open the cells and using the technique of centrifugation to separate the (larger) virus particles from the soluble cell contents and debris. (Subsequently much improved purification procedures were developed, resulting in preparations suitable for electron microscopy.)
One of the main techniques for characterizing viruses at this time was immunology. Thus, they found that the tissue culture fluid reacted with the antibodies in serum from measles patients by the complement fixation test, showing that it contained measles antigen. Previously they had showed that the cytopathogenicity of their preparations was neutralized by such antibody-containing serum.
Their paper ends with a summary of the evidence that what they isolated was the viral agent responsible for measles, and the further evidence needed for conclusive proof.
Subsequent characterization
The subsequent 60 years saw a steady improvement in analytical method, so that characterization did not rely solely on observation of cell pathology and immunology (the methodological repertoire of which also developed immeasurably). Electron microscopy in the 60s allowed cellular infection to be followed in greater detail and, after improvements in purification, the structure of the virus itself to be observed. The nucleic acid, protein and lipid envelope components could also be analysed with such purified virus.
The emerging techniques included gel electrophoresis of proteins (to determine their size and relative abundance, and to effect small-scale preparations). Larger scale purification of the virus proteins was possible with purified preparations, allowing  amino acid sequencing, especially of the most abundant proteins (e.g. the nucleocapsid protein, N),  and cDNA cloning and sequencing technology led to the sequencing of the whole Edmonston virus genome by Bellini et al. in 1985. This latter resulted in a much greater understanding of the gene expression of the virus, and provided tools such as specific oligonucleotide probes for various genes and antibody reagents to detect specific proteins.
Comment on Poster’s specific questions
The crux of the argument in the question would seem to be:

“If a researcher filters the particles in a serum…any sample filtered by size will potentially have hundreds of different viruses in it, all the same size range…”

The above addresses this only implicitly. To be explicit:

Using either the serum from patients infected with a specific virus, virus passaged in eggs or viruses grown in cell culture one is massively increasing the proportion of that virus to any contaminants.
It is not easy to grow viruses in cell culture. Therefore when conditions are found for one virus they are unlikely to be optimal for other (low-level) contaminants. Thus the actual passage in culture removes viral contaminants. The purification problem becomes one of separation from cell debris.

Modern Methods of Purifying Measles Virus
Below is a summary flow chart taken from the article Manufacture of Measles Viruses by Langfield et al..

One of the key methods in this proces, Tangential Flow Filtration, is also known as Cross-Flow Filtration and is described in this Wikipedia article.

There are many ways. In many cases especially traditionally viruses of interest were either the only virus present, or overwhelmingly more abundant than other types, so simple dilution will end up with a single virus type. Differential growth can help; many viruses have very specific growth requirements and if you only offer a particular cell type (or an egg -- most viruses do not grow in eggs!) it's not unlikely that only a single virus will grow out. Those are probably the most common and simple approaches -- dilution, or attempted growth with many different cell types/conditions followed by dilution. If they don't work, it becomes a lot tricker. Complexities in Isolation and Purification of Multiple Viruses from Mixed Viral Infections: Viral Interference, Persistence and Exclusion (pointed out by @CMosychuk in comments) reviews some approaches.


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How are neuromodulator receptors distributed?
Irrespective of where, when and how neuromodulators are released, eventually they are detected by some receptors in the membrane of a target neuron (typically G protein–coupled receptors)
Neurotransmitter receptors are typically distributed on the dendrite and the soma of a neuron (and only occasionally on the axon):

at excitatory synapses (more distal)
at inhibibitory synapses (more proximal)

Does this rule of thumb also hold for neuromodulator receptors:

excitatory → more distal
inhibitory → more proximal

And are they clustered (like ligand-gated ion channels at synapses)?

There is a basic misunderstanding here: neurohormones are nothing more than hormones released by a neuron. Have a look here: https://biology.stackexchange.com/q/67048/24284

Thanks for the hint, I'll rephrase the question accordingly.

Do you have evidence that excitatory synapses/receptors are overall more distally distributed than inhibitory synapses? What is certainly true is that there are very few excitatory synapses on the soma. But at least when considering input densities, further out from the soma excitatory and inhibitory input densities are of roughly the same magnitude in the cortex: doi.org/10.3389/fnana.2016.00124. What you suggest, although unlikely, may still be right, but I can't think of any evidence from the top of my head. As for neuromodulator synapses/receptors, they are probably even less well studied.

Now that you ask me: no, I have no evidence, it's just a vague impression I gained: that inhibition - for regulatory (damping) purposes - occurs preferrably near the soma. For "calculatory" (finer tuned) purposes (concurring with excitatory synapses on an equal footing) it may occur also more distally.

Now think of neuromodulators performing more regulatory tasks (slow, unpronounced), even though not necessarily damping. Nearer to the soma they might perform these tasks more efficiently.


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If during exercise the affinity of oxygen for haemoglobin is decreased, what are the general consequences for tissues?
During exercise more respiration occurs, and hence more oxygen is required.
So the oxygen dissocation curve is shifted to the right.
So at a given Oxygen partial pressure, the haemoglobin is less saturated with oxygen, i.e. haemoglobin has less affinity for oxygen.
What is confusing me is that the role of haemoglobin is to move oxygen around the body, so if it has a lower affinity for oxygen, won’t it compromise this function? Even though more oxygen is released, doesn't the haemoglobin have to carry it to all the tissues in the body? So how is this change in affinity of benefit if it reduces the oxygen subsequently available for other tissues?

Search this list for h(a)emoglobin. This sort of question has been asked before. And while you are about it, tell us what effort you made to answer this question yourself. It is well described in numerous places on the web.

I have done a google search but could only find information stating that when we need oxygen, the curve shifts to the right and Hb % Sat decreased.
What I want to know (and could not find on the web or here) is that if the point of Hb is to move oxygen around the body, wouldn't a decreased Hb affinity for oxygen reduce the oxygen parts of our body get? So wouldn't a right shift  in one way 1) make it easier for the body to absorb oxygen but in another way 2) stop Hb transporting oxygen to parts of the body that need oxygen. I.e. wouldn't these two things work against each other.
Thanks.

I have tightened up your question, spelling haemoglobin in full (avoid abbreviations for clarity and indexing, especially in titles). I have also tried to answer your question. I think it is useful to have the curve in front of you, but I could have just said that it is not a zero-sum game, but even if it were, one can change the distribution of resources without starving those with lower priority.

The only part of the body with a major effect on O2 Sat/affinity is in the muscles, where the ph is decreased. The rest of the body will be relatively unaffected, and compensatory mechanisms kick in.

It may help to consider the diagram below which shows the percentage saturation of haemoglobin with oxygen (and hence how much it takes up or releases) at the different partial pressures in different tissues. (The actual pattern — and values — depends, of course, on the blood flow to different tissues.)

In general, the curves show that at the high oxygen pressure of the lungs haemoglobin is near saturated with oxygen — Hb takes O2 up —, whereas at the lower oxygen pressure in the peripheral tissues the saturation is less — Hb releases some O2. So in normal circumstances oxygen will be gradually released to tissues as it circulates through the body. The oxygen pressure in the tissues is acting as the control valve for release.
In cases where there is a vastly increased demand for oxygen, this normal control is insufficient. The hydrogen ions in the acids produced by respiration (carbon dioxide and perhaps lactate) act as an additional control as they cause the oxygen dissociation curve of haemoglobin to change e.g. from 1 to 2 in the diagram. (The molecular mechanism of this is understood, but that is not the question.) Hence at the same oxygen pressure, more oxygen is released (cf. the percentage saturation at 1 and 2).
Does this harm tissues other than the ones producing the acid? They obviously have lower priority, but you can see there is still oxygen left at 2, and physiological mechanisms (faster heart beat etc.) will increase the blood flow in general. So it is wrong to think of this as ‘all or nothing’, but as part as a general response which alters the balance towards the tissues in greatest need.


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Functional role of voltage-gated potassium channels
Having better learned here how action potential creation works in some detail, I'd like to pin down the functional role of voltage-gated potassium channels: they mainly shorten the time it takes the neuron to get back to rest potential. Without potassium channels, the sodium ions that entered the neuron through a sodium channel would slowly diffuse away (electrotonically) and the sodium potassium pumps reset the potential. With potassium channels, this process is drastically accelerated (by quickly moving positively charged ions out of the neuron in situ). Without potassium channels, an action potential would be created nevertheless by the sodium channels alone, i.e. a peak of 40mV would be generated (equally fast!), but it would decay much slower, not yielding a pronounced peak.

Would you agree that this is a correct description of the main
  "purpose" of potassium channels involved in producing action
  potentials?

In any case, potassium channels seem to  work equally well when their "closing" potential would not be -80mV, but e.g. -70mV, i.e. the resting potential. But because it's -80mV the potassium channels produce an afterhyperpolarization. My second question is:

Does afterhyperpolarization play a ("positive") functional role,
  too, or is it just unavoidable? If so: Which "negative" and
  undesirable effects might it have? (In some respects it might
  have been better, if there was no afterhyperpolarization.)

The meaning of reversal potential
Ion channels do not themselves have reversal potentials except for via a weighted average of the ions that they conduct. The reversal potential for a given ion is given by the Nernst equation and besides physical constants is a function only of the relative concentrations of ions inside and outside the cell.
The equilibrium potential of the whole cell is given by the Goldman equation, which is similar to the Nernst equation but covers any number of ions. Note that you can also calculate a "reversal potential" for a channel using the Goldman equation by considering all the ions that a given channel will conduct.
The reason that a cell's equilibrium potential at rest is not equal to the potassium reversal potential is because cells are not permeable only to potassium at rest; although potassium dominates, there is some conductance to other ions, which depolarizes the cell slightly.
There is no way for a potassium-selective channel to have a reversal potential any different from the potassium reversal potential, unless it were to be permeable to other ions as well.
What would happen if there were no potassium channels?
If there were no potassium channels at all, cells would rest near 0 mV, give or take a few mV. The "leak" channels that allow cells to rest at a negative potential are primarily potassium channels. However, it seems like your question is mostly directed towards voltage-gated potassium channels.
What would happen if there were no voltage-gated potassium channels?
As you suggest, cells would repolarize much more slowly. However, your question still has inaccuracies.
1) This repolarization would not be from sodium diffusing away, it would be from potassium leaving the cell through leak channels.
2) The sodium-potassium ATPase is not directly responsible for the membrane potential or for repolarization in an action potential. Ion concentrations change very little during an action potential. The thing that changes is the permeability to different ions. The sodium-potassium ATPase is important, however, for maintaining the relative inside concentrations of sodium and potassium ions over the long term.
In addition, as you also suggest, there would be no afterhyperpolarization.
Is there a purpose to the afterhyperpolarization? Is it just unavoidable?
There is somewhat of a purpose. Although the afterhyperpolarization isn't strictly necessary to get action potentials to fire, there are some hyperpolarization-activated channels in some cells, and in all cells the hyperpolarization facilitates the removal of the inactivation block of sodium channels. In general words, it serves as a bit of a 'reset signal' beyond mere repolarization.
However, the afterhyperpolarization is also pretty much unavoidable without a very fine-tuned engineering of the repolarization process (you would need to rapidly close potassium channels as they approached rest, which would also slow down the return to rest).

Overall, this material would be well-covered in an introductory neuroscience textbook. My personal recommendation is Purves:
Purves, D., Augustine, G. J., Fitzpatrick, D., Hall, W. C., LaMantia, A. S., McNamara, J. O., & White, L. E. (2014). Neuroscience, 2008. De Boeck, Sinauer, Sunderland, Mass.
(any other edition is fine, too, and there a lot of other good alternatives as well)

Thanks a lot for this - once again - great answer! You say: "repolarization would not be from sodium diffusing away". Not at all? Or only to a (much?) lesser extent than potassium leaking?

(Yes, you are right, I was mainly interested in voltage-gated potassium channels, I should have made this explicit. On the other side: I wouldn't have learnt about the important functional role of potassium leak channels!)

@HansStricker The net diffusion of sodium across the membrane will (almost) always be sodium coming in, because the reversal potential of sodium is greater than the membrane potential of the cell. The Nernst equation is your friend. Only if the membrane potential is raised higher than the reversal potential for sodium could sodium net flow out. This is plausible if calcium currents push the membrane potential to a high voltage, but this would be a very minor amount and would reverse as soon as the cell was back to the sodium reversal potential.

Ah, once again, I've not been clear enough! I meant diffusion not across but parallel to the membrane.

@HansStricker Since you'd like to emphasize your question on voltage gated potassium channels, you are mainly talking about action potentials; in the context of an action potential, you have sodium coming in all throughout the cell. There could be some flow into the dendrites, but the flow of sodium into the dendrites is going to depolarize them (and many dendrites also have active sodium conductances) unless there is leak of potassium out of the dendrites: you have to cross the membrane eventually. :)

No, I believe not to talk only about action potentials, but also about electrotonic potentials as described at minute 2:00 in the video I linked to. Wandering electrotonic potentials seem to be responsible for the propagation of action potentials (at least in the video). They wander passively, by diffusion and electrostatic repulsion. And they might be enough to degrade the initial peak slowly.

@HansStricker Your question stated: "Would you agree that this is a correct description of the main "purpose" of potassium channels involved in producing action potentials?" and also "Does afterhyperpolarization play a ("positive") functional role, too, or is it just unavoidable?" - both are referring to action potentials, and yet now you say you don't mean just action potentials. I think you might have some confusion here and it would be helpful if you made more clear what you are actually asking and make sure you are making your questions specific.

I find your critique a little bit unfair. Electrotonic transport of sodium ions occurs already during action potential creation and cannot be completetly separated from it. I ask - among other things - how electrotonic (horizontal, parallel) and potassium-channel based (vertical, across membrane) transport of positively charged ions compare and compete. And I cannot see any severe confusion in my mind - and to be honest, not even in my question.

Please do some more reading: if you cannot tell that you are asking about 8 different things at once, you are not sufficiently understanding what you are studying. Note how many different things I had to address in my answer to cover your original question, and now you are bringing in addition concepts in the comments. You seem to be trying to learn by coming up with hypotheses for how things work and then proposing them here rather than learning the basic concepts first. Please get an actual textbook and don't rely only on Khan academy.

Sorry for insisting, but you still said nothing explicit about the effect of sodium ions which just came in through a sodium channel wandering/diffusing away from the site, in both directions (to soma/dendrites and down the axon). This effect does exist inarguably, but it might be much smaller than others (i.e. compared to potassium ions diffusing away through leak channels). Could you please confirm?

Yet another point: Meanwhile I am quite sure that if there were (hypothetically) only sodium ions and channels (and no potassium ions and channels at all), the action potential - once created - would never go away, not even slowly, because why should the probability of sodium channels being open ever decrease again significantly once it reached a maximum (giving rise to maximal voltage) - given that ion channels "have no memory about the duration of their own state" (@Jojo)?

I have to correct myself: the sodium channels would remain maximally open only when there were (hypothetically) no inactivation gates (described by variable $h$). In the presence of inactivation gates - closing at maximal voltage - $m$ would oscillate slightly around its maximal value.

As theorized about here, there might be another "purpose" of voltage-gated potassium channels: They give spreading action potentials - especially in myelinated axons - the form of wandering decaying pulses (compared to a stationary peak at the site of creation, that simply decays, nevertheless giving rise to a rise of the potential at distant sites).
What this shaping is good for – per se – is another question. Why is it per se better that the potential arrives at the next trigger zone as a pulse: the ion channels there won't see a difference, will they? They are unaware of whether potassium channels were present or not at the first trigger zone, they will experience roughly the same (rise of) potential after roughly the same time.
Well, as a pulse (which fades out as it faded it) the signal is shorter, otherwise it lasts longer, making temporal fine tuning harder.

I don't understand what you are suggesting here, and your link in reference is simply to another answer by yourself.

Sorry for that, I'll try to explain - and visualize - it in more detail.I guess it's not nonsense - and maybe even common knowledge - but hard to explain in a few words.

Sorry, I could also be more explicit in my criticism. What is a "wandering decaying pulse"? That doesn't sound at all like what an action potential is, so I don't understand how voltage gated potassium channels could be conveying a property that action potentials don't have.


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Why are dogs so selective about choosing a spot to defecate?
Anybody who walks a dog knows that dogs are normally selective about choosing a spot to defecate. They sniff around for a long time, while I just want to be on my way.
I understand about marking territory with urine. Is it the same with feces?

As a dog owner, I personally don't find dogs so complicated to please for pooping spot. They sure investigate the ground for good peeing spots though.

Well then your experience is very different from mine, which was the reason for the question.

By your own admission the OP is primarily opinion based, thus, I VTC.

I don't see where I admitted that Charles. Perhaps you could clarify. That was absolutely not an opinion-based question, and I have no doubt it has a research-based answer.

@Charles and Remi.b, while dogs do certainly have different personalities, being picky about the spot where to defecate (not only to urinate) and spinning around before doing so are very common behaviours (not the exception), and well documented.

@KarlKjer You mention your experience in a comment, which may be interpreted as your question being based solely off your experiences alone [with a household dog], instead of literature/observations within the field. Also, your title is somewhat loaded by using the term "fussy"; perhaps a more neutral word that should he used is selective. All of this, of course, is my own opinion/perspective. Please correct me if I'm wrong/you disagree on any accounts.

@GerardoFurtado IMO, the OP comes off as opinionated and subjective. I'm not debating that dogs do or don't perform these behaviors, but instead, I have an issue with the manner in which the OP contextualized and supported their claims & question.

@Charles Indeed, on a second read, I agree with you. I edited the question changing the wording a little bit, trying to make it less opinionated/more neutral.

I can't say that I've ever noticed this, but it seems possible that what the OP observes might happen when the dog is walked (quite possibly on a leash) in a peopled/built up environment, and therefore is related to house training?  Whereas my dogs, and my friends, generally run off leash while we're hiking or riding in wilder places, and don't seem to be at all choosy/

Marking territory with faeces
Despite urine being the most common way for dogs to mark territory, they also can use faeces to do so. Not only the faeces have a unique scent for the dogs, but, most importantly, it contains secretions from the anal glands, which are very important in dog communication. In fact, when you see two dogs sniffing each other "behinds", they are smelling the other dog's anal glands secretion.
So, being selective about the place to defecate is indeed an expected behaviour in dogs.
Magnetic sensitivity in dogs
However, if you are specifically talking about the dog spinning around after it — more or less — decided where to defecate (which makes the dog seem like it had not yet decided if it is going to defecate or not) one factor that plays an important role is that dogs like to eliminate with their bodies aligned to the North-South axis.
According to Hart et al. (2013):

Dogs preferred to excrete (sic) with the body being aligned along the North–South axis under calm Earth's Magnetic Field (MF) conditions. This directional behavior was abolished under unstable MF. The best predictor of the behavioral switch was the rate of change in declination, i.e., polar orientation of the MF.

So, the dog has to spin some times until it finds the desirable orientation, which explains the behaviour.
It's worth mentioning that the interesting aspect of this research is not the fact that it explains why dogs spin around before eliminating, but the fact that it shows that dogs have magnetoreception!
Still according to Hart et al. (2013):

It is for the first time that (a) magnetic sensitivity was proved in dogs, (b) a measurable, predictable behavioral reaction upon natural MF fluctuations could be unambiguously proven in a mammal, and (c) high sensitivity to small changes in polarity, rather than in intensity, of MF was identified as biologically meaningful.

Source: Hart, V., Nováková, P., Malkemper, E., Begall, S., Hanzal, V., Ježek, M., Kušta, T., Němcová, V., Adámková, J., Benediktová, K., Červený, J. and Burda, H. (2013). Dogs are sensitive to small variations of the Earth’s magnetic field. Frontiers in Zoology, 10(1), p.80.

And what would be the reason to defecate aligned to the N-S axis?

Well, that's a very interesting question, which will need a lot of research to be answered. Since this paper is quite new, I doubt any other team have already studied the reason of that alignment.

My dog is defective. Given a choice, he poops facing east, which is almost all the time. My girls are smarter. They don't obey any inner magnetic nonsense. They just find a spot that feels right to them and do their business, And I pick it up, which makes me a desecrater in their sight. Foolish human.


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How to produce correct epithet of a species named in the honor of a person?
I want to name a new diatom species in the honor of Prof. Vodyanitskiy. What will be the species epithet: "vodyanitskiya", or other? Are there any rules that regulates how the end of such epithets is changed?

The correct form of the specific epithet depends on the generic name (masculine, feminine, and neuter generic names will each require the corresponding, grammatically correct, form of the specific epithet), and on the type of the specific epithet itself:
Thalassiosira bradburyi is named after J.P. Bradbury. Thalassiosira hendeyi is named after N. I. Hendey. The letter "i" is added to the person's last name in both cases. Hence, Thalassiosira species named after V. A. Vodyanitskiy should be, in my opinion, Thalassiosira vodyanitskiyi.

If I'll honor the species name to Vodyanitskiy, what is grammatically correct specific epithet?

The form of the epithet depends on the generic name, viz. my answer. What is the generic name of the newly proposed species?

Thalassiosira - the genus of diatoms.

Thalassiosira bradburyi is named after J.P. Bradbury. Thalassiosira hendeyi is named after N. I. Hendey. The letter "i" is added to the person's last name in both cases. Hence, Thalassiosira species named after V. A. Vodyanitskiy should be, in my opinion, Thalassiosira vodyanitskiyi.

Very nice. If you put this comment in your answer, I'll accept it.

@user1615266: My original answer was only partly correct, because the form of the specific epithet depends also on the type of the epithet itself. i edited my answer and included my previous comment in it.

You should check the article 60 of ICN: http://www.iapt-taxon.org/nomen/main.php?page=art60
See in particular Recommendation 60C about specific epithet, and in the specific case, the rule 60C.1 (specific epithet derived from a person name).

You can use the genitive case (as Plant of Vodyanitskiy) as in rule (a), which is independent of generic name, so  if the professor is male: X. vodyanitskiyi, and she is female: X. vodyanitskiyae.
or as adjective (so inflected according the genera), in rule (c): X. vodyanitskiyana, X. vodyanitskiyanus, X. vodyanitskiyanum

Note: there are other rules to have a valid published name, and it is recommended to explain why you choose such name. In additional to the ICN code, there is the companion book: The code decoded. A user's guide to the International Code of Nomenclature for algae, fungi, and plants(Regnum Vegetabile 155), by Nicolas Turland


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What kind of insect is this? (seen in Goma, Democratic Republic of the Congo)
We recently (in November) saw this insect in Goma, DRC.
I would appreciate help identifying it.

Common name is "Giant Water bug". These are hemipterans, in the family Belostomatidae. Images can be found here: https://bugguide.net/node/view/12796

Also, it's best practice to add another image of your species to confirm that you are talking about the same species. -1

Except for distinctively marked species, with insects, species identification often requires expert microscopic examination. Photo ID to species is generally impossible.

While I would absolutely agree with the other comments that you should elaborate and provide photos to allow your answer to be assessed, I'd certainly agree with this. I'd also explain in your answer that 'giant water bug' is the common name for the entire family, and therefore that while identification to species level may be impossible from the information provided, it's still correct to identify it as a giant water bug.

This answer still requires some elaboration to gain my upvote (and presumably upvotes from others as well).

@Bryan Krause. You must be into vertebrates. This is as close as you can get with photos of insects.

Tell us why you think that family, give information in your answer rather than a link, etc etc. I never asked you to give a specific species. Your answer as is does not meet the standards of the site.

I guess it might have something to do with the way this completely unique and unmistakable family looks. I did not take DNA samples from it, but I am as confident of my identification as I would be in calling a giraffe a mammal.

Karl, you've established yourself as an insect expert here, and your point about species-level IDing is understood and respected by many of us who frequent ID posts. However, I agree with @Bryan that your post (& others) could be improved by providing more detail (e.g., clues you used, characteristics (and sources/keys) the OP could use to ID to species, life histories, etc.) and/or a photo (even if it clearly states that it's just an example species from the genus/family). This post would qualify as a comment if the link died, but could serve as a great teaching aid with a bit more detail! :)

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


text:
why do sodium channels close with excessive extracellular potassium ions in cardiac myocytes?
When there is an excessive concentration of potassium ions outside cardiac myocytes, the membrane potential surely goes up. I would have thought that this would make it easier for the membrane potential to go up past the threshold level, opening sodium ion channels and causing an action potential like at a synapse.
However, I understand that as the high concentration of extracellular potassium ions actually deactivates voltage gated sodium ion channels as opposed to opening them. Why does this happen?
Sorry if this question is pretty basic. We haven't covered anything nearly as complicated at school, especially not about cardiac cells.
Thanks for answering!

Short Answer
Depolarization block keeps sodium channels in a different state where they aren't available to open.
Longer Answer
The answer here applies equally to cardiac myocytes and neurons, and has to do with the gating properties of sodium channels (calcium channels have some similar behavior, which is also important).
Voltage-gated sodium channels at rest are pretty much all in a 'closed' state. The probability of a channel switching to an 'open' state increases with increasing voltage. However, those channels don't simply stay open indefinitely: they transition to third, 'inactivated' state. 'Inactivated' channels can't reopen. This helps keep sodium-mediated excitation brief and saves a lot of metabolic energy versus 'forcing' a cell to repolarize by only overwhelming the sodium conductance with potassium conductance.
Channels will stay in the inactivated state if the membrane remains depolarized. The probability of a channel switching from 'inactivated' to 'closed' (and therefore 'ready to open') increases with decreasing voltage. If a cell does not repolarize sufficiently, many sodium channels will stay in the 'inactivated' state. Further, channels that do switch to the 'closed' state could open, but not in synchrony. The eventual result is an equilibrium with a mix of sodium channels in open, closed, and inactivated states. There aren't enough 'closed' channels around to switch to open, there aren't enough 'open' channels to depolarize the membrane more, and as 'inactivated' channels switch to 'closed' there are other channels switching from 'open' to 'inactivated'.
This whole condition is referred to as 'depolarization block.'
Here's a helpful review on voltage-gated sodium channels that contains information covering what I discussed in my answer:
Catterall, W. A. (2000). From ionic currents to molecular mechanisms: the structure and function of voltage-gated sodium channels. Neuron, 26(1), 13-25.
You can also find lots more information in textbooks and elsewhere if you look for the term 'depolarization block.' Note also that I have simplified the gating transitions for voltage-gated sodium channels for the purpose of this answer, so some sources might explain a more complicated system; the general principles still apply to the question, though.


text:
What organelles are in an onion cell?
I was wondering what organelles are in an onion cell, because, based on the labs we are doing in my biology class, I only saw a nucleus and cell wall. My friends and brother say there are all the organelles that you would find in a typical plant cell, but I can't find any evidence anywhere. I need to create a model and it's due in a week.

what magnifivation was used to see it

OK, so the first thing you always do when recreating a cell microscope slide (like drawing or modelling the cell) is that you only draw or model what you see. In your case, this would just be the nucleus, the cell membrane and the cell wall.
To answer your question, onion cells (you usually use epithelial cells for this experiment) are ‘normal’ cells with all of the ‘normal’ organelles: nucleus, cytoplasm, cell wall and membrane, mitochondria, ribosomes, rough and smooth endoplasmic reticulum, centrioles, Golgi body and vacuoles. You cannot see most of these as they appear translucent as well as being too small to see under the light microscope. You need an electron microscope to view these. Note: chloroplasts are not present in an onion cell as it is not a photosynthesising cell.
This is a typical onion cell slide with labels:


text:
what snake is this and is it venomous?
Found on my house on Khao Yai, Thailand

Looks like a common wolf snake, or house snake (Lycodon capucinus). Here another picture. I think they are not dangerous, but be sure to take precautions (I might have guessed wrong from just your photos).

I'm not sure about that; it seems too blue, and it looks like the rear of the head on this one is wider.

what could it be then?

It's a Lycodon for sure. One of the characters that helps when differentiating from other similar snakes is that the head is quite prominently separated from the neck. Also the nape band is quite common in many, but not all, Lycodon sp. I can't comment on whether it's indeed L. capucinus or another Lycodon species though.


text:
Can there be multiple EPSPs with constant current injection to a neuron?
I am performing a current clamp experiment and measuring the change in membrane potential of a neuron with different current injections. A constant current of 50pA is injected to the neuron for 100ms. The current is not enough to cross the threshold for the neuron so there are no action potentials. But will the neuron have multiple EPSPs in this setup?

If you stimulate the soma you shouldn't get any EPSPs except for spontaneous but they'd have to be larger than the membrane depolarization you induced. You expect to see a step increase in membrane voltage.


text:
How do firing patterns arise from the activity of many ion channels?
In his answer to another question, Bryan Krause says:

Ion channels don't exhibit any firing patterns: neurons exhibit
  firing patterns that depend on all the channels present [...].

I understand it this way: The observable and measureable firing pattern1 of the neuron (created at the trigger zone) is the linear superposition of tiny "firing patterns2" of all the (voltage-gated) ion channels at the trigger zone, which in turn depend on the probabilities of opening and closing which are the same for all ion channels of the same type and obey some Hodgkin–Huxley-like law. These probabilities correspond directly to the shape of firing pattern1.
The rhythm with which each single sodium channel opens and closes ("firing pattern2") doesn't have to mimick firing pattern1 exactly, only roughly and probabilistically: the open-close-ticks must occur near to the spikes of  firing pattern1, but not exactly and not at every spike. And some complete outliers are allowed. The rest is superposition.
Seeing things this way, indiviudual ion channels do exhibit "firing patterns2", but these may look quite different than firing pattern1 (although not completely).

Is this kind of reasoning correct?

If so: Can the following conclusion be drawn: The time scale of a firing pattern1 depends on the number of ion channels at the trigger zone? This might be seen when looking at the rise time of a single action potential: If there is only one sodium channel, rise time will be larger, if there are many, it will be smaller. Is this correlation strictly linear?

Typically the activities of the ion channels are not called firing patterns as in neuroscience we refer to "firing" when we mean the elicitation of action potentials (spikes) but yes: Whenever an AP was fired a sufficient amount of sodium channels had to be open and therefore I thing your reasoning is correct. In other terms what you are saying is that the effective channel conductances change during an action potential.
On your conclusion: In the regime of natural parameters the time scale of firing pattern 1 mostly depends on the time constants of the voltage gated ion channels and not so much on the absolute number of channels (especially if all the conductances would scale equally).
In the world of Hodgin-Huxley like coupled- and nonlinear-dynamical systems the voltage does not scale strictly linear with increasing the participating max. conductances. The interplay of max. conductance and temporal gating dynamics resulting in the effective conductance itself depends on the voltage and there are nonlinearities. So the correlation between the number of channels and the AP rise time is not expected to be strictly linear.
See the figure for a little example: I tested my reasoning by increasing the max. conductance for the sodium channel of a simple HH model and checked the max. steepness of the voltage (normalized by peak voltage).
Hope that answers your question(s).

+1. Simulations are always appreciated! I've formatted your figure to remove the white space on the top but feel free to roll-back to the previous version if you don't like the result.

I like this answer, but I think it's a bit too forgiving of the misconceptions in the original question. The original question seems to presume that firing frequencies in neurons come from the open and closing times of ion channels, which is not accurate, or at least not accurate in the sense of how an ion channel physiologist/biophysicist would use those terms: channels flutter open and closed at much much higher rates.

Searching briefly, this page has a good depiction of the difference between single channel openings versus populations of channels: http://nerve.bsd.uchicago.edu/med98b.htm

Thanks for the edit, vkehayas. Yes, I fully agree Bryan! It took me some while to translate the question into a way I am used too discuss such issues. After reformulating my comments in that direction again and again I decided too just remove the paragraph completely and to give more like a minimal and "forgiving" answer but yes, you are right.

Thanks to all for your efforts (in trying to understand my question and giving helpful answers and comments). Especially thanks to you, @BryanKrause, for the link which gives me a better background.What I am still missing is a picture of single channel's "being open patterns". And why not relate these to firing patterns?

@HansStricker The link I shared has exactly that. See Figures 10, 11, 12 for example, or Figure 15. You'll see the channels more or less just flutter back and forth at a given depolarization. These flutters happen much much faster than action potentials. Action potentials arise from a whole bunch of channels randomly fluttering, and overall conductances through certain channel types are from an average of the number of channels open (i.e., their open probability), not all channels of one type are open at the same time.

@BryanKrause: Maybe you can understand how hard it can be to see the "forest (= the firing pattern) for the trees (= the open patterns)" - both conceptually and experimentally.What I still cannot see: Is there a refractory period of approx. 2 milliseconds for single ion channels or only for the neuron as a whole?

@BryanKrause: Just for the record: I did not suggest, that "all channels of one type are open at the same time". But they must be open somehow synchronized (= not too far away from the "beat"), otherwise no observable action potential would arise.

@HansStricker I don't see a reason why there should be a refractory period for an ion channel as conformational changes of proteins are purely stochastic processes driven by physical forces that act quasi-instantaneously and there are no saturation effects. It is just biased flickering between two or more favoured conformations (local minima in the proteins energy landscape).

Wikipedia explains refractory periods at the level of ion channels. What's wrong with that?

@HansStricker Voltage gated sodium channel inactivation is one of the contributing factors to refractory periods, but it is not the only contributing factor. Ion channels do not "fire" - it makes no sense to talk about "firing patterns" of an ion channel. The voltage gated sodium channels of cells with all sorts of firing patterns have the same inactivation kinetics, the differences in firing patterns are due to other differences. Also the 'synchronization' of voltage gated sodium channels opening is because of positive feedback from changes in membrane potential, not gating time.

@BryanKrause: I can not bring together the following: You say "channels flutter open and closed at much much higher rates" (than neurons fire). You say "channel inactivation is one of the contributing factors to refractory periods" (which is in the range of milliseconds). Wikipedia says; "Inactivation of ion channels occurs within milliseconds after opening." How does this fit together with "fluttering at much higher rates"?

You are mixing two different things: One is the probabilistic fluttering between open and closed states of the channels which you can imagine as a binary process (Bernoulli, short time scale) and the other on top is a slowly varying process dependent on the systems state (things like the voltage). The latter shapes the expectation value of the fast process over time. The quote from Wikipedia just states that the expectation value of the fast process goes down within miliseconds (which is slow in comparison). Hope that helps

Reading at Wikipedia: "This creates a current caused by the flow of ions through the channel. Shortly after opening, the channel is blocked by the peptide ball." This sounds (in my ears) as if it happened by an automatic and necessary inner mechanism of the channel. But you say "no, it happens by a contingent outer mechanism", right?

Yes! The ion concentration affects all the channels but the single channel has no memory about the duration of its own state. The net effect of ions flown through all channels (or wherever else, i.e. current clamp) in the proximity combined change the potential and give rise to an inactivation of single channels through  conformational switches.

So the flow of ions  through a single ion channel (and the resulting change in voltage) would not be enough to inactivate it - but it participates. Now I got it!

Let me summarize what I believe to have learned from Jojo's and Bryan's comments in form of a visualization: The red curve is the probability governing the open and closed state of an ion channel (as a function of time - we see two spikes) The dotted patterns below show 50 ion channels fluttering between open (black) and closed (white) states, according to the probability of being open. The thin black curve is a smeared out average of the first ion channel being open (showing two slight elevations, i.e. on a coarser time scale some kind of "firing pattern" – please forgive me, Bryan). The fat black curve is the smeared out average of all ion channels. The blue curve is the number of channels being open at a given point in time which is somehow proportional to the conductance, current, and/or voltage being measured. Noise is large due to the small number (25) of ion channels.

For 200 ion channels and overlaying the 200 patterns, it would look like this:

Find a higher resolution picture here.
See two related biological scenarios here and here.


text:
Why marker and control are loaded in the beginning or ending lane of the gel?
I have seen gel images in several literature. Almost in all, markers and controls are loaded in the  extreme lanes (before 1st sample or after last sample) of the gel. I am just curious, is there any reason or logic to do so? Is there any problem if I load it in the middle lanes, in between my samples

Control or marker?

No important reason. It is for esthetics, and also for ease of description in figure legends. One could argue that it might be confusing to have the markers or the control in the middle, but since the relative locations of these wells would be recorded, it does not matter where you put them. In publication, it would be easier to say, for example, "The control is in the far right lane, and the ladder is in the far left lane" Rather than saying, for example "Third from the left".


text:
Why is the body cooled during cardiac surgery?
When undergoing cardiac surgery, the heart is disconnected from the blood circulation and blood is passed through a heart-lung machine and cooled so that the body temperature of the patient is reduced.
I understand that this would slow down metabolic processes but how exactly does slowing down these processes benefit the patient?
Thanks for answering!

As you mention, hypothermia is routinely induced during cardiac surgery. There is a blog post including a photo of a heart being cooled with ice chips here: https://www.heart-valve-surgery.com/heart-surgery-blog/2010/10/17/ice-cardioplegia-open-heart-surgery/

The primary therapeutic benefit of deliberate hypothermia was long thought to be, as you say, the slowing-down metabolic processes, which reduces the amount of oxygen needed by the brain and other vital organs (source). Cooling the blood during open heart surgery therefore allows the operation to be performed more slowly (2-4 hours).
However, according to this open-access article on the benefits of therapeutic hypothermia for cardiac surgery:

the widely held notion that hypothermia protects because lower
  temperatures slow metabolism is not completely accurate. Recent
  research has shown that hypothermia can alter a plethora of cell death
  and cell survival pathways including gene regulation resulting in the
  inhibition of apoptosis and inflammation and the up-regulation of
  anti-apoptotic or trophic factors.

So basically it does slow down the metabolic processes but it also reduces inflammation and cell death.
After surgery, rewarming needs to be done slowly to maximise the chances of recovery (source).

Does the lowered amount of oxygen used by organs other than the heart really matter? Surely they have a good supply of oxygen due to the heart-lung machine.


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Are microRNAs transcribed from the same DNA strand as their parent messenger RNAs?
I am new to micro RNAs. I have been trying to find the answer to the question if microRNAs are transcribed from the same DNA strand as the messenger RNAs encoded by the encompassing gene?
From the scientific articles I have read so far, I infer that it is the same strand. If so, does the transcription of microRNA and mRNA occur simultaneously?
Finally, does the strand from which the microRNA is transcribed have any implications for its interaction with its mRNA target?

What do you mean by "the same gene as mRNAs"? What scientific article makes you think that? Try searching for microRNA promoters, e.g. In Drosophila.

@David What I meant was if the miRNA is created from the complementary DNA strand from where the mRNA is created.

The following bear on the question of the relationship of the transcription of microRNAs to that of the pre-mRNAs of protein-coding genes:

Some microRNAs (termed ‘intergenic’) do not reside in a protein-coding gene (e.g. Drosophila mir-31a). Here the question does not arise.

Many (although not all) of those that do reside within a protein-coding gene are found exclusively in introns (termed ‘intronic’) — e.g. mir-11 and mir-998 in Drosophila gene E2f1.

For those microRNAs that reside in a parent gene, the direction of transcription is generally, although not exclusively, the same as that of the transcript (ca. 70%, according to this review).
The question arises whether the intronic microRNAs are generated from the spliced introns of transcripts of their parent genes. One of many papers which consider this is by Ramalingam et al. (2014). It appears that in some cases this may be so, but in other cases this appears to be ruled out by a disparity between the expression profiles of parent genes and microRNAs, and between different microRNAs encoded in the same intron.
The co-directionality or otherwise of transcription of ‘parent’ mRNA and microRNA has no implications for the interaction of microRNAs with their, often numerous, ‘target’ mRNAs. This is because (1) there is no genetic relationship between parent mRNA and target mRNAs — the parent mRNA, lacking the intron that gave rise to the microRNA, is not the target; (2) the hairpin loop of the microRNA precursor (imperfect though it may be) in effect represents both strands, from which may be generated either the 5ʹ portion, the 3ʹ portion, or both, depending on the microRNA. The miRBase site contains information on relative abundance of 5ʹ- or 3ʹ-fragments for individual microRNAs, and the microrna.org resource lists potential target mRNAs.

Thank you, David. That is really what I was looking for. By the way, even if a miRNA is not from the same DNA strand, it can form the miRNA-mRNA complex right?

I have added a line to your question to include this concern, and have addressed it in my answer, which I have modified somewhat to improve it. The Ramalingam paper may be of interest.

That is very helpful. Thank you very much once again.


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Has any flying creature evolved into a sea creature?
I am talking about a creature that has evolved true flight.
Has any such creature evolved into a sea creature, that permanently dwells on water (like fully aquatic fish) and doesn't come out? According to the theory of evolution, many sea creatures of the deep past evolved into land animals and some of them went a step further, evolving flight. I am talking about the reverse process, excluding semi-aquatic or semi-terrestrial animals.

Penguins are as close as you'll get, I think. But they too must come on land.

Clarification of the question
The following feedbacks from the OP are his comments below

By creature of course I denote animals
I meant animals that can fly (not glide) and control their flight
By sea creature I mean those animals that either breathe in water with gills (e.g. fish) or the ones that have to surface to breathe (e.g. whales).

Answer
Water beetles are the perfect example.

They live underwater, some of them very rarely (if ever) surface as they capture air under their abdomen and can breathe it for a long time while underwater. Just like dragonflies, butterflies, flies, bees, ants, bugs and many others, beetles are Pterygota and therefore have flying ancestors.

Answer before clarification
It all depends what you mean by "sea creature" and "flying" as well as by you mean by "semi-aquatic" and "semi-terrestrial" and also what you mean by "creature".
Here are examples of eventual interest to you.

Birds that are good swimmers, including those that can't fly anymore such as many penguins. No birds can breathe the air dissolved in the water though.

Insects that evolved a larval stage in the water while the ancestors are fully terrestrial. I don't think any insect can breathe under water however several species can carry quite a lot of air with them underwater (such as water beetles) or many just stick their butt out of the water to breathe (like culex mosquito larvae).

It is unclear whether by the use of the term "creature", but if you accept examples from non-animal forms of life, you'll find examples of seed dispersal through water while ancestors used air, you'll find plenty of examples of parasites too.

If by "creature", you meant "animal" and by "flying", you meant high level of control flight and by "sea creature", you meant animal able to breath air dissolved in the water, then I personally can't think of an example of a flying animal evolving into a sea animal.
None of these examples are as pleasant for you as an example of a big flying bird evolving gills that now live in deep sea though but unfortunately, I can't think of such case.
For fun, you might want to have a look at the post How many times did terrestrial life emerge from the ocean?

Your usage of the term "creatures" as well as the phrase "according to evolution theory" and also the phrase "many sea creatures of the deep past" make it feel like you don't have much knowledge in biodiversity, evolution and evolutionary time scale. You might want to get some intro knowledge on the subject. Understanding Evolution by UC Berkeley is a very introductory and pretty short free online course on evolutionary biology if you are interested in.

Oh, I understand. I wanted to be as specific as possible. I meant animals that can fly (not glide) and control their flight and where they go (like birds do). By semi-aquatic I meant that comes out of water to land as part of its life, and by semi-terrestrial that comes to water as part of its life. By creature of course I denote animals.

And what did you mean by "sea creature"? As the question is now restricted to animals, you maybe meant "breathing the air dissolved in the water"? If this is the question, as explained above, I can't think of any example then (but I might be wrong).

By sea creature I mean those animals that either breathe in water with gills (e.g. fish) or the ones that have to surface to breathe (e.g. whales). Both categories stay in water and don't come to land. Sorry about my mistake, by semi-<> I mean that spends a part of its life either on land or water.

@Dominic See edit following your feedbacks

Birds can't do it because they lay eggs that need warmth. If penguins could bear live young or lay self rearing eggs, they and other birds could become fully marine.

Sorry I couldn't find any species that dwells underwater all its life and never comes out for an extended time (but only for a little to make a bubble or something). I may not have looked much enough, there may be such species.


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Why is the skin of European bog bodies brown?
What causes this? Is it to do with decay or is it to do with substances within the bog dying the skin?

The anaerobic decomposition of moss produces tannins in the peat.

The bog water interacts with the acids in the moss and produce tannin
  and other chemicals that preserve the bodies that fall or are cast
  into the bog; hence the numerous well-preserved bog bodies.
  http://www.digitalmedievalist.com/opinionated-celtic-faqs/bog-bodies/

The tannins tan the bodies just like tanning leather; the color of the bodies darken and the tanning action also preserves them.


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Inexpensive way to determine mass of tiny seeds?
My niece is doing a science project and she wants to weigh various seeds, determine their volume and density. She tried using my kitchen scale, but it is not sensitive enough.
I've suggested weighing 100 seeds then dividing to get an average weight, but she (she's 11) wants to weigh each one. I don't want to get in the way too much. I don't mind buying a scale, or other simple equipment as long as it isn't expensive.  Is there any way to do this inexpensively?

A pharmacy is a public business, and they should have a scale sensitive enough to weigh seeds.  They will have to let you in back to use it of course.  If you show up with her and she has the seeds and she asks the manager nicely, they might let you back and help you use it.  I would show up rather than call; if you show up you will see the manager / pharmacist but if you call you will not talk to the manager.
If this works she needs to be sure to credit the pharmacy in her project!
I recommend she weigh several seeds of each type - they might vary.
Your 100 seed idea is a better one, I think.  I understand your sentiment.

You did not ask about volume but this could be done with a graduated cylinder.  Put some water in it up to, say, 5 ml.  Then drop in a seed.  How much farther does the water level rise?  That is the volume of the seed.


text:
Overexpression by integration of an additional copy vs promoter exchange
In Becker et al (2011), the authors increase the expression of several genes through different methods. For some genes (e.g., lysA, ddh), they achieve overexpression by integrating an additional copy of the gene and its flanking regions. On the other hand, for other genes (e.g., lysC, dapB, fbp, and the tkt operon) they take another approach and instead replace the native promoter with a strong constitutive promoter (Psod or Petfu).
Is there an advantage of one technique over the other? Why was one technique preferred over the other one for certain genes?

Modifying promoters can give finer, more targeted control of expression than changing copy numbers. In the paper you referenced, for the ddh gene, it sounds like they just wanted to boost production of that protein, so making a second copy made sense. But with some of the other genes, they wanted to alter metabolite fluxes through a more complex pathway. Copying a whole operon would not achieve this, because then you would just get two pathways doing the exact same thing. But even copying the one or two genes in the operon that you want to investigate might change their relation to the other genes in the operon. Bacterial operons are generally organized such that the genes for the transcriptional regulators are located adjacent to the genes they regulate. This proximity is necessary for the proper functioning of the operon, and if you copy a gene, depending on where you put the copy, it may not function as it usually does. In these cases, it's better to mess with the promoters because you can leave the organization of the operon largely intact.


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Unsure about definition of "n" and "C" values in mitosis
I am preparing for a Biology exam and I'm reviewing the "n" and "C" notation used in mitosis.
My professor said that when the cell replicates its DNA in S phase of mitosis, we get twice the "amount" (C) of DNA, but we still have the same "number" of chromosomes.
Does this mean that if the replicated chromosomes were to "split apart" from their centromeres, we would have a 4n cell (so a cell with 4 sets of chromosomes)?
At the same time, my intuitive response sort of says, "well, they're replicated, so they're exactly the same, so you'd technically have 2 sets, not 4 right?".

I don’t know what the professor inferred exactly in class. Our somatic cell consists of two set of chromosomes that one set is maternal, and the other is paternal. In other words, human somatic cell has diploid number of chromosomes (2n). However, mature ovum and sperm are haploid number of chromosomes (n). The fertilization combines these two haploids into one diploid.
Somatic cell is always diploid throughout mitosis, but the amount of DNA is duplicated during interphase, especially in S phase. The amount of DNA may be represented as “C” for better understanding. The number of chromosome and the amount of DNA are 2n/2c in G1 phase during interphase. The number of chromosome and the amount of DNA are changed into 2n/4c in S phase. The amount of DNA is separated exactly half into two daughter cells in mitosis. The number of chromosome and the amount of DNA come back to 2n/2c after mitosis.

While I've not heard of the "C" notation previously, "n" is common notation that indicates the ploidy of a cell. The "n" refers to the number of unique chromosomes within a cell. Eukaryotic cells are generally diploid, or 2n. The multiplying number - "2" in the diploid case - refers to the number of versions of each unique chromosome. For example, humans are diploids (2n). We have 23 unique chromosomes (22 regular chromosomes and 1 sex chromosome), but we have 2 variants of each chromosome to give us a total of 2*23 = 46 chromosomes.
Prior to S phase, diploid cells contain 2n content (maybe "content" refers to "C" notation?) of DNA. During S phase the cell duplicates its DNA content generating 2 sets of 2n chromosomes (2 copies of 46 chromosomes for a total of 92 chromosomes in the human case). You are correct in that it is 2 sets of 2n rather than 4n, since the convention would indicate 4n as a tetraploid (many types of plants are in fact tetraploid, https://en.wikipedia.org/wiki/Polyploid).
At the end of the mitotic cell cycle, cell division functions to separate the 2 sets of 2n chromosomes into two distinct cells, each containing 2n chromosomes. If all 4 chromosomes separated from each other and the cell was able to divide into quarters rather than halves, that would yield 4 1n cells. This latter idea is what occurs in meiosis.

For human male, XY are unique chromosomes, that doesn't imply n=24 instead oh 23. Edit your definition please.

I appreciate the point regarding X and Y chromosomes being different relative to each other. They do, however, fall under the same generalized heading of "sex chromosomes", which are a unique subgroup of chromosomes that manifest themselves in different ways in different species (mammalian sex chromosomes versus Drosophila sex chromosomes versus C. elegans sex chromosomes versus ZW system of sex chromosomes). For this reason a more generalized reference to sex chromosomes is appropriate, though I will make edits given the explicit example of humans being used.

See https://en.wikipedia.org/wiki/Sex-determination_system for an overview of sex determination


text:
Misunderstanding about nucleotide biosynthesis
Some months ago, I asked what was a phosphoester bond, because I didn't really understand the following picture and explanations provided in the "Molecular biology of the gene" from Watson, Baker, Bell and al. (7th edition).

The explanation is the following:

We can think of how the base is joined to 2'-deoxyribose by imagining the removal of a molecule of water between the hydroxyl on the 1' carbon of the sugar and the base to form a glycosidic bond (Fig. 4-2). The sugar and base alone are called a nucleoside. Likewise, we can imagine linking the phosphate to 2'-deoxyribose by removing a water molecule from between the phosphate and the hydroxyl on the 5' carbon to make a 5' phosphomonoester. Adding a phosphate (or more than one phosphate) to a nucleoside creates a nucleotide.
Thus, by making a glycosidic bond between the base and the sugar, and by making a phosphoester bond between the sugar and the phosphoric acid, we have created a nucleotide.

What I didn't understand months ago was, to resume, "why is the bond between the phosphate group and the 2'-deoxyribose called a phosphoester bond since the phosphoester bond (which is, by definition, a P-O bond) already exists before the bonding between the phosphate group and the sugar?"
While this question is still bothering me (I was not entirely satisfied with the answers I got back then, because the synthesis of a single strand of DNA is something which is probably different from the synthesis of nucleotides themselves), the question I'm asking myself right now is: "why do general biology books always talk about condensation reactions, while this article and this book do not mention it in the biosynthesis pathways of nucleotides?"
What I mean is: it seems like the biosynthesis of nucleotides is far more complicated than just being two condensation reactions. Furthermore, when I look at the 10th step of this picture (which comes from the article I mentioned above), I see a condensation reaction at the end of the pathway, but it does not occur where the book from Watson and al. suggests it should:

So, after months of wondering and researchs about all this, my final question about this is, as mentioned above:
Why do biology books always mention condensation reactions while, apparently, it doesn't have a lot to do with the manner in which the nucleotides are synthesized?

I'm voting to close this question as off-topic because this list is about biology, not the motives of authors of texts, which in any case can only be a matter of speculation.

A condensation reaction is defined on Wikipedia as

a reaction in which two molecules or moieties, often functional
  groups, combine to form a larger molecule, together with the loss of a
  small molecule. Possible small molecules that are lost include water,
  acetic acid, hydrogen chloride, or methanol, but most commonly in
  biological reactions it is water.

It doesn't say anything about the number of steps required to reach the final compound, nor about the type of bonds formed. Following this definition, the nucleotide synthesis occurs via condensation reactions.

Thanks a lot for your answer. However, it still does not explain why the book from Watson and al. talk about the loss of two water molecules, and it doesn't explain either why that same book explains the synthesis of nucleotides in such a simplistic way, while it is apparently way more complicated than just a phosphoester and a glycosidic bond...

It is a simplification but it is correct. You start with 3 molecules, you end up with one via 2 condensation reactions and you lose 2 H2O in total. What is the problem? the schematic is pretty straightforward.

If it is really what happens, then there is no problem anymore. The last thing that is still bothering me is that phosphoester bond thing.


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Do leaves grow larger by adding cells at the centre or at the edge?
I'm writing a paper on wrinkling of plant leaves. For biological and physical background information, I would like to know whether leaves grow by adding cells at the edge, at the center or in a completely different way. Since I need to confirm any information I get, please do not write opinions or guesses. It would be great if someone could find a reliable source with link since all my researches didn't lead to a good answer to this question.
Thanks in advance!

Welcome to Biology SE! Homework questions are off-topic on Biology unless you have shown your attempt at an answer. For more information see our homework policy.

Hello, I think you misunderstood my request. I'm currently writing my bachelor thesis in physics and thought that some biological context in the introduction would be nice. Since I do not understand most of the literature in biology, I would be glad if someone could explain in easy words how plant leaves grow. If my question is still inappropriate, feel free to close or delete.

i am not a plant biologist to give a full-scale answer, but, generally, the cells at the tip and edges of a leaf are the oldest, whereas the cells at the base of the leaf are the youngest. In many, but not all plants, leaves grow from basal leaf meristem, a tissue containing plant stem cells that divide and differentiate into leave cells.

Plant leaves develop from leaf primordium or meristem tissue (this tissue has special properties that allow it to continue dividing to make more more cells, i.e. stem cells - not stem cells like cells in the stem but the technical term 'stem cells). Because of the hormone balances to maintain this division property the meristem tissue will remain close to the stem or branch of the plant at the base of the leaf whilst the new cells added to the leaf slowly move outwards.
https://www.sciencedirect.com/science/article/pii/S1369526616300929


text:
Is it possible to graft plants from different families?
For example, I have some Eastern Hemlock rootstock (Pinaceae), and want to graft a scion from Dawn Redwood (Cupressaceae) onto it. Is this possible? Is anything like this possible?

Not knowledgeable in this area, but I note the Dawn Redwood is deciduous and the Hemlock, like most conifers, is not.  Since deciduous plants commonly store reserves over the winter in their roots, an evergreen rootstock may not be compatible with a Dawn Redwood scion.

It makes me think of a french artisan who sells trees with 20-40 individual heirloom grafts on a single tree, which all flower and fruit throughout the summer. all apples, apricots, compatible trees. i found fig on mulberry, both moracea family.

No. Exceptions are always possible, but it would be a noteworthy.
I just find this notes in: https://courses.cit.cornell.edu/hort494/mg/specific.grafting/compatibility.html

Interfamilial
Although there are a few reports of short-term graft union formation between distantly related (interfamilial) herbaceous species, there are no confirmed reports of interfamilial grafts between woody perennials.
One extremely curious report of natural interfamilial graft compatibility which must be considered unconfirmed, and even unlikely, was the observation of La Rue (1934) [...]