text:
Name of neurons affecting or being affected by a neuron?
This question is about terminology:

By which established and catchy terms are the sets of neurons with
  respect to a given neuron $N$ called which

directly affect $N$ synaptically
are directly affected by $N$ synaptically?

These terms came to my mind, but I am not sure which ones are most commonly used:

the presynaptic/postsynaptic neurons of $N$
the afferent/efferent neighbours of $N$
the afferents/efferents of $N$
the incoming/outgoing neurons of $N$
the neurons projecting on/to $N$ vs. the neurons projected on/to by $N$

Or is there no such established term, and anything goes, depending on the context?

At the simplest level, the terms 'pre-synaptic'/'post-synaptic' neurons should cover what you wish to describe.
'Afferent'/'efferent' are usually used to refer to axonal projections, usually between functionally distinct areas, or nerves. However, I wouldn't be too surprised if someone used these terms to refer to synaptically connected populations although I would consider it unusual. Simply, 'connected neurons' is also a term frequently used.

I will now go into a tangent to give you some background that should help you formulate an informed view about the vocabulary being used:
In areas that display a high degree of local connectivity, like the cerebral cortex and the hippocampus, any given neuron is connected with many different neurons. Hebb's theory of cell assemblies posits that a group of highly connected neurons may form over time in order to subsist a specific function. Given the high degree of connectivity, any given neuron will be able to participate in many different assemblies. It is often thought that these assemblies constitute the substrate of engrams, the physiological correlates of memory, at the level of the neuronal network. Hence, the concept of cell assemblies is prominent in our thinking about groups of synaptically connected neurons.
Setting aside the questions of the definition of the engram, recent efforts have claimed to identify engram cells under this or that experimental paradigm, although the connectivity of those cells has not been established. While we know that functionally similar neurons display a higher degree of connectivity and that groups of cells with correlated activity patterns can be formed by artifically-induced synchrony, the direct link between increased connectivity and behaviourally relevance has not been established.
On the other hand, only a handful of studies have directly measured the connectivity between more than two neurons (Song et al., Perin et al.), revealing the intricate properties of neuronal network structure. Depending on the level of description they may refer to distributed cell assemblies, synaptic clusters of neurons, $n$-vertex cliques, and motifs.
All this is to say that as soon as you start considering more than a pair of neurons, it makes little sense to talk about neurons that are exclusively connected with each other. As every neuron is connected to almost all other neurons in its immediate neighbourhood we often focus on the functional implications of their connectivity. Under this light, the concept of cell assemblies is central in modern neuroscience.

I added "directly" to modify "affect" in the original question.

Sorry for the inconvenience.

I think the only way to reasonably answer this question is to say: "read some papers and follow their conventions" - it's much too hard to develop an exhaustive description of how all of those terms are used without creating an answer that's much too broad. I'll give some comments, though:
Presynaptic/postsynaptic is most often used in the context of synaptic transmission/plasticity/etc where the subject is a synapse. You would not typically say presynaptic neurons to N when you are really just talking about a network from A to N.
Afferent/efferent 'neighbors' I have never heard used, won't claim it never is but it seems completely wrong to me.
As for afferents/efferents these refer to the fibers primarily. Those terms are most appropriate when you are talking about something like the spinal cord, where afferent projections head toward the CNS/brain and efferent projections head toward the periphery; in the brain I find them often confusing or incorrectly used. This is because the terms afferent and efferent don't actually refer to inputs and outputs, but rather to inward versus outward direction. Defining "direction" in the brain gets pretty ambiguous if you aren't talking specifically about primary sensory or motor areas.
Incoming/outgoing I rarely if ever hear.
In the context of "projecting" usually the noun form is used: projections, as in "thalamocortical projections" or "projections from V1 to V2." I'd say this is the least ambiguous/best terminology if you are talking about connections between different brain areas. Within a local brain area (i.e., a given nucleus or a region of neocortex) you would be less likely to use the term "projection" though it wouldn't necessarily be wrong.

But isn't the concept of "the set of neurons which directly affect neuron N synaptically" a very clear one, and would deserve a name? (And I did read more than just some papers, and didn't come up with a convention. Maybe because these sets aren't interesting and/or dealt with?)

It depends on context, but there's also no strict rules. If you are talking about just one cell in a computational fashion, you would probably just say "the inputs to cell X" but people would understand if you used some other terminology. I'd say this is typical of English in general, and maybe that gets carried over into scientific fields where English is the main lingua franca.

"Inputs to cell X" sounds good. Does "outputs from cell X" sounds good to you, too?

That's fine if you are talking about the outputs themselves; you could also use "targets of cell A" to describe the population that receives inputs from cell A.

You have to admit: terminology and wording is not very controlled and unequivocal in neurosciences.

.. which doesn't make life easier for the novices;-)

"Incoming/outgoing? I rarely if ever hear."
I found this wording here.

@BryanKrrause: Just to let you  know: I feel offended and censored by you and your actions (e.g. closing my questions without giving me good reasons and opportunities to react). I find it indiscriminating and would like to flag it - but I can't because you are a moderator.

@Hans-PeterStricker I explained to you why your last question was deleted in a comment on that question (cross-posting), including a link to the relevant discussion on Meta. If you prefer to delete your question at Psych&Neuro instead, ping me here and I'll undelete. I downvoted rather than closing your question so as to not unilaterally close it; the deletion is separate from my reason for downvoting. If you have issue with my actions you can post to Meta, or see https://meta.stackexchange.com/questions/28867/what-recourse-do-i-have-if-i-believe-a-moderator-has-abused-their-privileges

Cross-posting is not prohibited per se, is it? The distinction between Biology and Psych&Neuro is hard to make, and how can I consider it beforehand? Why is it bad to post the same question twice when it is not clear where to find the better audience? Why is it to be "punished"?

@Hans-PeterStricker Deleting a question doesn't "punish" anyone. Please read the meta I linked to you; I can link it again here: https://meta.stackexchange.com/questions/64068/is-cross-posting-a-question-on-multiple-stack-exchange-sites-permitted-if-the-qu I find it very rude to cross-post, because if a question is answered on one site, someone might still answer it on the other site despite it already having an answer. These sites have high bars for answers, and it often takes a lot of work to answer a question. It's rude to have someone take the time to answer an already-answered question.

Especially reference requests are not so hard to answer: If anyone knows a reference he/she just can give it. I deliberately did not ask for elaborate answers but just for a link. Personally, I cannot see anything rude in cross-posting reference requests. Finally and generally: What is bad with having two (independent) answers? Do you believe, every question can have only one correct answer?

@Hans-PeterStricker The problem is not having two independent answers, but having two independent questions that are the same question. In this case, the different answers end up in different places rather than the same place. Please please read the well-reasoned answers in the meta post I linked and don't make me rehash the entire discussion here, that's why I linked it for you.

But why not accept that there are questions that can equally well be posted at two SE sites? Why to force to ask them only at one site? Isn't it in turn a good opportunity to bridge gaps? (I understand your point better with respect to more or less eduacted SE sites like MathOverflow SE and Mathematics SE. But Biology and Psych&Neuro are on the same level.)

And be assured: Whenever I get an answer on one of the sites, I'll share it on the other - to the benefit of all!


text:
Recording policies in functional magnetic resonance imaging
Assume that the areas in a single-subject's brain that are involved in solving a task are supposed to be visualized with fMRI. The dynamics of the task solving process shall not matter (which areas are active first, which second?).

How, i.e. by which policy, are the data collected to give the final image?

I believe to have understood that data are collected per slices (of some millimeters thickness) and later postprocessed to give the final image.
For the sake of definiteness, let $T$ be the overall time it takes to complete the task (e.g. 10 seconds). Let $t$ be the time it takes to simultaneously take the BOLD data of one slice (e.g. 100 milliseconds). Let $N$ be the number of slices to be recorded (e.g. 20). Let $n$ be the minimal number of recordings of one slice that is necessary for statistical analysis ($n=?$). So there are $N n$ recordings of slices necessary which takes $N n t$ milliseconds, if only one slice could be recorded at once. If $T$ is too short, the experiment would have to be repeated $N n t/T$ times to get all of the required $N n$ slice recordings.
If $m$ slices could be recorded simultaneously, a single run of the experiment would suffice, when $m > N n t/T$.

In any case: In which order are the slices to be recorded chosen (in
  case they cannot be recorded all at once)?

Possible policies:

always from top to bottom (along the z-axis) in time $T$?
repeatedly from top to bottom in some time $T'=T/k < T$?
alternating between top-bottom and bottom-up in repeated experiments?
in a random order?
in an order informed by knowledge of the stages of the task (when different slices are primarly active at different times during the task)

Or is my picture of the recording process all too naive? Or is the question somehow meaningless (for reasons I do not see, but would like to learn about)?

@Remi.b I'm not a big fan of the question, but I strongly, strongly disagree that it belongs on Health.SE because 1) fMRI is used primarily as a research, not medical tool (it is not the same as "MRI" used for diagnostics), and 2) although this question oddly refers to "policies" which might imply healthcare, that isn't what it is asking at all.

@BryanKrause Ok, thanks for your light. I am retracting my close vote (and associated comment).

If I recall correctly, in BOLD fMRI an echo-planar imaging (EPI) sequence is typically used. In one example:

44 slices were acquired, every 3 seconds, 96 times in a row, leading
  to a total number of 4,224 images acquired in 4 minutes and 48
  seconds.

— https://www.imagilys.com/functional-MRI-fMRI/
You can read more about EPI here. I think you will find the zig-zag pattern in this link interesting. See also this link for a description of EPI.
fMRI is slow and has a low temporal resolution, because the hemodynamic repsonse of the blood is around 6 second long. This is perhaps a limiting factor for fMRI, which is why there is a limit to optimizing the sequences. However, one real impact of faster sequences is to capture head movement artifacts more accurately. Other sequences are used in anatomical MR imaging, such as FLAIR.

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Alpine flower identification — Italy/France
I have been using the internet to try to identify alpine flowers photographed in July 2007 on a shortish walk above Chianale (1800 m), in the Italian Valle Varaita (bordering the French maritime alps).
I have managed all except the blue/lilac one shown below. It looks a bit like a scabious or perhaps a knapweed, but neither seem to correspond properly. Anyone know?

Group of flowers

Close-up with triply split petals indicated by red arrows

Just added a close-up. Thought I had done so before, but there must have been a computer glitch somewhere as there is no edit record for deletion. Anyway, this shows why I am accepting the suggestion of Phyteuma orbiculare (for what my opinion is worth).

This is not Jasione montana, but Phyteuma orbiculare, another member of the family Campanulaceae. Except for the different flowers,
Jasione has no leaves on the upper part of the stem. This plant has. And these leaves are toothed and have a heart-shaped base, unlike Jasione.
And finally: Phyteuma is resticted to calcarious soils, whereas Jasione prefers non-calcarious soils.

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

Thanks. Looks more like it in one particular respect. That is the tips of the petals. In all the pics of Jasione I have found they seem lighter coloured and hardly split, whereas in my photo (you can see this if you zoom in) and this pic of Phyteuma (and others on-line) they are clearly split into three and curled back. I'll go back to my higher-res original and add to my question with a close-up later. This site has it in the appropriate Italian province of Cuneo (CN) at 1800 and 2500 m. Again, I'll wait before accepting.

@Always Confused Eh, no. Every purple stalk is a seperate flower and the tri-furcate things are the gynoecia. I don't know what this central thing is, it doesn't appear to be there in every flower. BTW: isn't this a new question?! :-)

I think the correct answer is @RHA's answer. I will leave my answer just for future reference and discussion.

Could it be Jasione montana?

Sheep's bit scabious, Jasione montana, is a low-growing plant in the Campanulaceae family found in rocky places and upland regions of Europe and western Asia. Other common names include blue bonnets, blue buttons, blue daisy, iron flower, sheep's scabious and sheep's bit.

Your flower's petals look a bit more "spiky" the Jasione montana though. As a kid (I grew up in Switzerland), I remember seeing bumblebees flying around these flowers. Have you seen any?

Thanks. Despite the difference in spikiness, it looks as if it could indeed be Jasione montane. Pity I didn't take a sharp close up, but it's my wife that's really interested in what species flowers are. I usually leave them out of photo-records, but even I find the profusion of flowers in alpine meadows stunning. I'll wait a couple of days before accepting to allow for other responses.

I think this is not Jasione, but Phyteuma, see my answer below. And about those bumblebees: could this have been a much larger blue plant: succisa pratensis? That plant I had in my garden and attracted loads of bumblebees.

I think you are correct. I will leave my post just for future reference but upvoted yours to bring it to the light.

I never answered about the bumblebees. Don't remember any. All I remember is the millions of insects that bit me, but that always happens when I'm walking as something in my sweat seems to attract them. (Same recently in California and Texas. Not a problem in Glasgow.)

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How optimal are the distances of voltage-gated ion channels on axons?
In both myelinated and not-myelinated axon segments ("axons" for short) there are theoretically maximal distances of voltage-gated ion channels beyond which propagation of the action potential would break down because the potential arriving at the next ion channel would be too weak to open it. (In myelinated axons it's about the distance between the nodes of Ranvier.)
In not-myelinated axons this distance is smaller, in myelinated axons it is greater.
Compared to these theoretically maximal distances there are the real distances between the ion channels (smaller for non-myelinated axons, greater for myelinated axons), resp. their mean distance along the axon.
My question is: How strongly do the real (mean) distances of ion channels deviate from the theoretically maximal ones? An axon with greater mean distance than the maximal one would not work very well, an axon with a significantly (and unnecessary) smaller mean distance would waste resources and would possibly produce distracting interferences.
Side question: What's "the" standard deviation of the mean distance of ion channels (nodes of Ranvier)? ("The" because there may be differences between types of neurons/axons.) Are there numbers available?

Cool question. I don't know if anybody looked into this. Keep in mind that the variability in the action potential and state of the axon will degrade the reliability if set exactly at the theoretical optimum assuming no such variability.

It is a cool question... but I don't think it's answerable.  We'd have to study a given neuron (potentially in a given species) with a given number of sodium channels per node, a given radius, etc... at which time you could do experiments and/or calculations.  If you fail to take these factors into consideration, each local "spike" will vary in how much it can effect the next node and the "maximum distance" will be subject to a large variation.  For example, in a larger neuron, the sodium has more space to diffuse cross-sectionally, leaving less sodium to diffuse laterally.

@rotaredom: I visited your profile and clicked "This user". Maybe you cannot (or at least did not try to) imagine what complicated psychological effects it may have for a user to surprisingly find him- or herself as someone else's hero. I would suggest not to play with this - it's somehow rude and cruel.

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Half-life and production rate of ion channels
There are "not millions, not a few hundred...somewhere in between (some tens of thousands)" of ion channels in a neuron.
Given the number of ion channels per neuron, knowing the  half-life of ion channels allows to calculate the production rate of ion channels, and vice versa.
I am looking for estimates of tpyical half-lifes of ion channels, somehow like this: "not years, not seconds... somewhere in between" but with better upper and lower bounds: months, weeks, .... minutes, hours.
Alternatively: estimates of production rates: "not thousands per second, not one per second ... somewhere in between".
[I know, that all numbers - number of ion channels, production rates, effective half-lifes - can change over time for a given neuron - this may have to do with long-term potentation. So I am talking about neurons in steady-state over a period in which no long-term potentation takes place. But I guess this won't change the rough estimates I asked for too much.]

The rate varies with channels and channel subunits, and you can also distinguish between membrane half-life and degradation half-life, because channels can be cycled bidirectionally between the plasma membrane and internal membranes like the ER. For many (most likely all??) channels these processes are under the control of phosphorylation and/or ubiquination.
For a rough estimate of magnitude though, the relevant time window is hours to days. I'll include a couple references below to support this time frame.
References

Bedford, F. K., Kittler, J. T., Muller, E., Thomas, P., Uren, J. M., Merlo, D., ... & Moss, S. J. (2001). GABAA receptor cell surface number and subunit stability are regulated by the ubiquitin-like protein Plic-1. Nature neuroscience, 4(9), 908-916.
Colley, B. S., Biju, K. C., Visegrady, A., Campbell, S., & Fadool, D. A. (2007). Neurotrophin B receptor kinase increases Kv subfamily member 1.3 (Kv1. 3) ion channel half-life and surface expression. Neuroscience, 144(2), 531-546.
Huh, K. H., & Wenthold, R. J. (1999). Turnover analysis of glutamate receptors identifies a rapidly degraded pool of the N-methyl-D-aspartate receptor subunit, NR1, in cultured cerebellar granule cells. Journal of Biological Chemistry, 274(1), 151-157.


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About which cells in the human body do we know most?
Are there model cells (in the sense of model organisms) in the human body (other than E.coli) about which is known most (with respect to structure, function, metabolism, gene expression, ...) and to which I can refer when asking questions about "typical cells" (which per se don't exist). The other way around:

About which cells (added: normal and mature) in the human body do we know most?

(Maybe there's a cell in the rat we know more about, but also know/believe that it is very similar to a human cell? Which one, then?)
Having asked this, I'd also like to know, about which neurons in the human brain is known most, e.g. about "pyramidal cells in cortical layer IV"?

Related question: Are all functions of a human cell known?

HeLa cells (from a cervical cancer) are probably the most studied human cells : https://en.wikipedia.org/wiki/HeLa.   Because these cells are cancerous and are "immortal" I don't know if any knowledge gained is that useful, so I'll post as a comment.

@VonBeche - The knowledge gained from study of HeLa cells is incalculable. Just one result - the polio vaccine - should give you an indication of their worth. However, it is not a normal human cell, so...

I would argue that HEK293 cells might be a contender against HeLa for the price of the most studied cells.

We know most about corneal epithelial cells because we see right through them.

@Gaurav: seriously or just joking?

@the put-on-hold voters: Is the extent of knowledge about a cell (type) really a matter of opinion?

I admit, an "extent of knowledge" might be hard to define and measure, but it doesn't seem impossible, does it?


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Do corresponding areas in the two hemispheres arise from the same stem cells?
After having asked this question about the connectivity between clonal cortical neurons, I'd like to know:

Do corresponding areas in the two hemispheres arise mainly from the same stem
  cells, such that these areas connect to each other more strongly than to others?

I answered this question, but I strongly advise you to do more research before asking some of the questions you are posing here. Ask yourself questions and look for answers like "where are the stem cells that give rise to neocortex located" and you will easily answer these questions. I think you are having a tendency to find one piece of information and try to connect it to too many other things without reading intervening information.

I'll try to take your advice.

No, they don't. The stem cells of each cortical hemisphere are located far from each other, in the subplate below the developing cortex.


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Distribution of the number of synapses per neuron
There is a mean number of synapses per neuron in the human brain which is not very well known, but is of order 10,000. (Some say, it's about 6,000, other say it's about 50,000.)

What is known about the distribution of the number of synapses - in a
  very rough sense?

The number is most certainly not distributed normally around one mean value of about 10,000 (because there are very different types of neurons).
More probable, there are some types of neurons with typical mean numbers of synapses (each distributed normally), which would give a distribution like this:

For the sake of simplicity I want to ask:

If we were to group numbers of synapses roughly into bins of powers of
  ten, how high would be the peaks, roughly?

You are correct, depending on the neuronal cell type or location in the brain (cerebellum versus a cortical layer for instance), the number of synapses will differ. I don't know if this has been systematically studied, cell type by cell type, region by region, so that the statistics you are looking for would be available... I imagine that work will be painstaking and difficult (particularly with the human brain) but the connectome project is making huge strides and is the likely source in the future for such information.

@LouisLeung: Do you accidently know a specific resource inside the connectome project which points into this direction?

The exquisite serial EM reconstruction of neurons with identifiable (and thus quantifiable) synapses has been demonstrated here: http://www.conte.harvard.edu/connectomics/. This paper at: https://www.ncbi.nlm.nih.gov/pubmed/26232230 has some synaptic statistics though it is volume- and not cell-specific which I believe is what you are after.


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Why are the neurites from hair cells to spiral ganglion cells called axons?
In Kandel's Principles of Neural Science I found the following figure which shows the innervation of the organ of Corti:

From the legend to this figure (30-10, p. 602):

"The great majority of afferent axons end on inner hair cells, each of
  which constitutes the sole terminus for an average of 10 axons.[...]
  Efferent innervation of inner hair cells is sparse."

BUT: The depicted axons that "innervate afferently" hair cells seem to go into the wrong direction (downwards, not upwards). What do the (red) bulbs touching the hair cells represent. I guess synapses, but which one is the presynaptic and which one is the postsynaptic neuron? (I guess: The hair cell is the presynaptic neuron - it's a sensory neuron! But then the neurites emanating from it would be afferent dendrites of the ganglion cells, not axons. I'm lost. Might it be the case that transport along these neurites is active - like in axons, not passive like in dendrites? Or are they called axons because they are myelinated? Or is it because in bipolar cells it is not distinguished between axon and dendrite?)
Question: Why are these neurites called axons?

In which respect? See here: Efferent nerve fibers. Anyway, it doesn't answer my question: Why are these neurites called axons?

I'll change the title and remove the introductory remark. Thanks for the hint!

@GerardoFurtado: Here I read that all neurons "have both afferent (incoming) and efferent (outgoing) connections". This conflicts a bit with what you say

I believe to understand now, thanks to @AliceD's answer to this question:
Why are Merkel cells innervated by an axon, and not a dendrite?

The axon seemingly emanating from the cell (hair or Merkel) is just by coincidence not a physiological part of the cell (hair or Merkel), but its functional axon. The tactile meniscus (in the case of the Merkel cell) plays the role of an "out-sourced" axon hillock of the cell (hair or Merkel) which possesses no axon hillock (and axon) on its own.

Please be fair and tell me what's wrong with this picture/answer.


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Cell differentiation by non-identical copies
There are in principle two ways that two cells with the same mother cell can differentiate/specialize/diverge:

Because they are not perfect identical copies (= different internal influencing factors). I explictly don't mean "non-identical on the DNA level", but on the level of other cellular components!
Because they are exposed to different external influencing factors (chemical, mechanical).

Can it be said, which of these two reasons of cell differentiation is the more common, frequent, resp. "important"? Or does it completely depend on the (type of mother) cell and some general circumstances?
If internal factors (= non-identical copies) are an important source of differentiation, I have two (optional) questions:

How does the mother cell manage to cleave into two non-identical copies in a rather fine-tuned and determinstic way? Or is any kind of asymmetry enough?
Which is the first cell (starting with the zygote) that cleaves into two non-indentical cells, different enough to give rise to differentiation? (From this answer I believe to have learned that this might happen already after 1-4 divisions.)

I found a partial answer to my and this question at Quora:
What regulates initial cell differentiation?
Ian Driver says:

In many organisms the initial cell has mRNA (or protein) partitioned
  in one half of the zygote.  One daughter cell inherits most of the
  mRNA or protein and goes on to activate or repress genes in that cell,
  but not in the other.  This has been visualized and well studied in C.
  elegans: Asymmetric cell division and axis formation in the
  embryo.

This question is kind of bad. There are common internal influencing factors that are unrelated to improper replication, most commonly:
Methylation. Addition of methyl groups to DNA regions inhibits RNA transcription from that region.
Imprinting. Can't recall exactly how this works but it's another mechanism for enabling/inactivating genes.
Histone structure (wrapping/unwrapping). DNA coiled tightly around histones is more unlikely to be transcribed.
External influencing factors include cell signaling, substrate detection, and large-scale endocrine signaling. Most important are growth factors and growth inhibitors (which let the cells know if they need to replicate quickly (repairing damage/large-scale growth) or slow down replication (overcrowding). Other external factors could include metabolism (produce these digestive enzymes when exposed to these foods) or endocrine signaling.
Non-identical copies at the DNA level (mutation) are thankfully relatively rare in practice, particularly among higher-order species with longer lifespans.

I didn't mean "non-identical on the DNA level" but on the level of cellular components - and just made this clear in the question. Is the question still bad, then?

confirmed your question is no longer bad.

Puh, I am relieved.


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Life cycle of proteins
I try to get a picture of the life cycle of a protein (considered as a specific molecule).
This is how I can imagine it:

After the cell is born a protein molecule is synthesized by gene expression for the very first time de novo. This happens at a specific point in time and in space, typically at an ribosome, which may be located anywhere inside the cell.
From the location of its generation (combination or recombination, see below) the protein travels to its final destination, e.g. as an ion channel in the cell membrane. (But possibly it was already synthesized very close to its point of use.) Or it just floats around in the cytosol. (Possibly, it gathers some other biomolecules around it.)
Whereever it arrives or not: the protein lives and works for some time.
Eventually, it gets damaged (= looses small functional units), but gets repaired in situ. Continue with 3.
Eventually, it gets marked by ubiquitin and destructed in a controlled manner. Continue with 7.
Eventually, it decays spontaneously (= splits into some larger fragments).
Its fragments are released (in case it was bound) and start again to float around in the cytosol.
Eventually, its (or other proteins') fragments are recombined (at specific points in time and in space, possibly at "re-factories" comparable to the ribosome-"factories"). Continue with 2.

Is this rough picture of the life-cycle of a protein essentially correct?
If so: What is known about the time ranges in which these processes take place? Especially: How long is the effective life and working time of typical proteins? Are there proteins that live and work only for minutes or hours, and others that live for months or years? (Specific examples are welcome!)

One missing aspect (for Eukaryotes) is that step 5 is actively promoted by tagging with ubiquitin (https://en.wikipedia.org/wiki/Ubiquitin). You might be interested in this post https://biology.stackexchange.com/questions/46274/is-there-selection-against-long-proteins-and-long-genes

Just today - after a heavy  autumn storm - I saw trees in a nearby park marked (by some red-white stripes) to be felled. Is this how ubiquitin works?

@HansStricker pretty much. Proteins tagged with ubiquitin (i.e. ubiquitinated) are recognized and degraded by proteasomes. Wikipedia wouls surely give some nice info about this :)

@gilleain: I added ubiquitinization in the question. Thanks for the hint.


text:
Are trees still carrying their leaves more likely to be felled by an autumn storm?
Is there evidence that trees still carrying their leaves are more likely to be felled by an autumn storm than trees already having lost their leaves?
At first sight this seems plausible (and might be easily verified statistically), but at second sight it seems mysterious, considering a) the weak forces that keep leaves attached to their branches (at least in autumn times), b) the flexibility of the branches, and c) the chaotic way in which they are shaken by a gust.
Anyway, after storm Xavier which passed Germany and Poland on the 5th and 6th of October, this was spread ("kolportiert") by the media and in private communication:

Is there a thorough biomechanical model which explains whether or why this is true or false, resp. to which extent?
I would suspect that in this model a) eigenfrequencies (of branches, limbs and stem) and b) resonance will play a role.
(This model would give an interesting analogy to the sudden generation of action potentials in neurons (corresponding to the breaking of a limb or stem) by spatio-temporarilly integrating the synaptic inputs (corresponding to the shaken leaves) on the dendritic tree [sic!]. Addendum: There's a great book that brings botanical and neuronal trees together: Giorgio A. Ascoli, Trees of the Brain, Roots of the Mind.)
(Note, that one short gust almost never will fell a tree. It must be a rather long gust, or an appropriately long and/or timed sequence of shorter gusts.)

Addendum: The way how fluttering ion channels (on a very short time scale - grey dots below) give rise to a rhythmic and possibly resonant temporal pattern (on a much longer time scale - red or blue line above) may be compared to the oscillations of the tree as a whole, whose "rhythm" (red) cannot be detected when looking at single leaves fluttering (grey):

See also here.

Most certainly, yes. Especially if that storm brings heavy winds (hurricanes, tornadoes) or ice/snow


text:
Misincorporation of dUTP into DNA?
Uracil, the RNA base, has been replaced in DNA by thymine, (which has the same base-pairing with guanine). However the synthesis of dTTP (more usually written TTP) requires dUTP:

To what extent is dUTP (mis)incorporated into DNA?

This question is an attempt to complete a set of questions on the base and sugar differences between DNA and RNA. I will answer it myself if no other answers are forthcoming.

I have provided and accepted my own answer to this question as it was posted as an attempt to complete a set of questions on the base and sugar differences between DNA and RNA. This should not stop anyone commenting on or criticising of the answer — I shall be happy to make improvements.

There follows an attempt to answer my own question, which I think is important to consider in the general context of postings on SE Biology concerning uracil and thymine in DNA and RNA synthesis.

There seems to be little misincorporation because of the low concentrations of dUTP in cells.

Any small amount of misincorporation can be handled by the DNA repair system that exists in cells.

I base statement 1 on the work of Grogan et al., published in Biochemistry 50, 618–627 (2011). They showed that in both mouse and human cell lines that the normal concentration of dUTP (and dUMP) was low. I assume that this must reflect cellular activities of dUTPase and thymidylate synthase being sufficiently high to remove dUTP and dUMP, respectively as they are formed. When thymidylate synthase activity was inhibited by anticancer drugs, these nucleotides built up, as expected.
In support of Statement 2 I refer to a separate earlier study in fission yeast by Seiple et al. in Nucleic Acids Research 34, 140–151 (2006). They used the drug, 5-fluorouracil, to inhibit thymidylate synthase and found that it caused misincorporation of uracil into DNA with concommitant cell damage. The role of the DNA repair system in mitigating this damage was shown using a mutant in the Ung1 gene, which encodes DNA glycosylase — here the cell toxicity was much higher.
Although there are some inconsistancies between the different systems used, and difficulties of interpretation.  I think that they provide general support for the two postulates. It would be useful if it were possible to locate kinetic data on the relevant enzymes to test my assumptions regarding the reason for the low dUTP concentration.


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How can rhodobacter possess a single 'PS-II' like reaction center?
I recently came across an information in my book Trueman's Elementary Biology ,  a popular text in India, that photosynthetic bacteria like Rhodobacter, Rhodopseudomonas etc. possess a single photosystem where the reaction center is PS-II like. Now how can PS-II work as a single unit? As far as I know, PS-I can operate singly in cyclic mode generating ATP only. But PS-II works in conjunction with PS-I to generate ATP, $\ce{O2} $ and $\ce{NADPH} + \ce{H^+} $. So how can PS-II work as a single unit in this case?

TL,DR: I think you've just swapped PS-I and PS-II.
Recall the differences between PS-I and PS-II.  Bear in mind that PS-I and PS-II were not so named because of the order they run in, but rather because of the order in which they were discovered.  PS-II comes before PS-I chronologically.
PS-II basically takes in water, breaks it down into $H+$, $\ce{O2} $, and a spare electron.  The hydrogen ions are sent inside the thylakoid space, creating a concentration gradient between the stroma and the thylakoid space.  Since the ions cannot cross the thylakoid membrane, they must have a transport channel of some sort.  This channel is known as an ATP synthase, and ATP is synthesized from ADP and a phosphate group using the energy created by the hydrogen ion moving down the concentration gradient.  You are then left with an O2 group in the stroma, and an electron in the ETC.
PS-I takes that electron and basically just boosts its energy to produce NADPH using the H+ ion sent out of the thylakoid space during ATP synthesis.
In other words, PS-I cannot take place without the H+ and the electron from PS-II.  However, if PS-II were to run alone, it would simply mean that somewhere along the way either the oxygen would bind back to the H+ and electron to form water, or else the electron and H+ would be used elsewhere in the cell.  Thus it would be PS-II running in cyclic mode producing ATP.

But I think u swapped b/w ps I and ps II. As I'm sure it is ps I which runs in cyclic mode.


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Why do some organelle (like ER and Golgi complex) cannot be seen under microscope during cell division?
I have recently read in a book that organelles like ER (endoplasmic reticulum) and Golgi Complex cannot be seen under a compound microscope during cell division. Why does this happen, and where do the organelles go during that time?

Could you cite which book you read this in?

In my textbook of 11 th grade.

By saying "disappear" I actually mean - cannot be seen under compound microscope, as under normal circumstances ER can be clearly seen.

Please include the title, year published, editors, edition, and publisher of any cited works if possible.

This is not my area of expertise at all, but here are some recent papers that might shed light on this: http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0117859, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2719565/, http://jcb.rupress.org/content/179/5/895

A cell when undergoes the process of cell division there are structures known as spindle fibres that are required to pull the chromosomes off to the poles of the cell so that it can be segregated into the cells properly while division. These spindle fibres are made of microtubules that are protein molecules constituting the cytoskeleton of a cell. Endoplasmic reticulum and Golgi apparatus are also providing a lot of support to the cells.
Also endoplasmic reticulum and Golgi apparatus are the sites where most of protein forms. While cell division these two organelles disintegrate so as to provide protein for microtubules formation, and so as to reduce support of the cell so the division of the cell is comparatively easier.
Also, during the cell division everything divides equally between the two daughter cells, so ER and Golgi bodies disintegrate so they can be equally divided into the two daughter cells.
Also, nuclear envelope is the continuation of the endoplasmic reticulum. Hence endoplasmic reticulum disintegrates with the nuclear envelope.
Here I have provided a set of possible reasons for your question.
You can refer Raven's biology for further information.

Could you please provide citations of your claims, which would help to enrich the answer. Also I don't get the point "While cell division these two organelles disintegrate so as to provide protein for microtubules formation" which you have said, as all the proteins required to run the division phase of the cell cycle are synthesized during the G1 phase so there is no need to disintegrate some organelles to provide that.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2814503/


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How can just random mutations explain mimicry?
I have been reading this article on drug resistance which explained that how random mutations in a bacterial colony can lead to development of drug resistance among some organisms in that colony.
A thought occurred to me that if mutations are just random (by random what I know (or think)  here is the number and time of a mutation occurring in an organism in a normal environment may not be fixed but random) events arising from copy errors during DNA replications then how come some animals in nature mimic their surroundings to save themselves from predators or catch prey?
Let's consider for the time being that an animal exhibiting mimicry have evolved through natural selection, after suffering a mutation in their DNA which made them well adapted to their environment, and also saved them from their predators. Now we know a fit organism, in the struggle for existence, produces offsprings which can withstand the adversities of the surroundings and thus increases in numbers. In this way we may assume that due to many such helpful mutations led to the evolution of a new species.
This may sound simple but it actually seems to me as an over simplification of the events that lead to the development of 'that' new species. First of all not all mutations are helpful. Some are lethal as well. Also mutations may often be silent due to the degeneracy of the genetic code and presence of introns in the eukaryote. But let us consider here that the mutation suffered by our test organism was neither silent nor harmful, that too leaves us with infinite number of mutation possibilities to get a favourable organism from an unfit (to the surrounding in which our test organism is struggling) parent generation. Thus I think nature may not test each and every kind of possibility to select the fit one because in that case the test organisms will be far too many in number. Also if we consider that the fit one emerged just by chance out of million other possibilities then its sure that it was either too lucky or there is some other factor except 'just' mutation which can explain mimicry. Thus can only general mutation explain mimicry or we need something more to explain it?

poss. duplicate: https://biology.stackexchange.com/q/66183/5198

Possible duplicate of Are mutations random?

@BryanKrause actually Remi b. added the question after I  asked this one, he added it as according to him many people get confused about the matter. Moreover I have actually asked 'if mutations are random then how can we  explain mimicry shown by organisms'.

@jyotiproy Duplicates don't have to be later than the original to be closed, and closing as duplicate is not meant to say "this is a bad question", it just means "this question is answered somewhere else." It would make more sense to point to that new Q&A rather than have this one be the example forever, because that one is more general and covers a common question here.

I was quite busy for the past few days, so I failed to frame the question I exactly had in mind. So today I took some time to correct it. Sorry for the inconvenience caused. Pls don't mind.

can anyone please help me to shorten this question. It has been occurring to me for weeks and I am desperate for an answer. I have asked this to my teachers too but failed to get a satisfactory answer.

@jyotiproy your issue is your question wanders all over and makes it really unclear why you think NS cannot explain mimicry, this makes the question unanswerable without explaining everything about evolution in detail which would be way too broad. Consider looking into the difference between selection which is random (enough) and selection which is the opposite of random.

@John I wanted to know that whether NS explains mimicry? If so then how can the random mutations be so perfect that it mimics another unrelated organism completely? Is it by chance or there is a controlling factor behind it?

Are mutations random?
I decided to open a new post (and directly attempt at answering it) as this claim is very common and a bit misleading. See Are mutations random?.
Your question does not need to be specific to species looking like their environment
You seem to not understand the basics of evolutionary biology. Your question is specific to why organisms look like their environment but what you should simply understand is the basics of evolution and selection.
You should definitely have a look at an intro course to evolutionary biology such as Understanding Evolution by UC Berkeley for more information.
How can there be such striking similarities between some organisms and their environment?
Natural selection is the (main) answer.
An important reason (but definitely not the only one) for why a population of organisms would evolve to look like their surroundings is camouflage. Camouflaged organisms can typically have a higher fitness in a population that suffers from visual predators.

I was quite busy for the past few days, so I failed to frame the question I exactly had in mind. So today I took some time to correct it. Sorry for the inconvenience caused. Pls don't mind.

/how come these animals (below) show such striking resemblance with their surroundings/
You are looking at the culmination of millions of generations of these insects.  The mutations are random, but only the helpful ones (of all the random ones) produce an advantage for the organism and so persist in the species.   If a random mutation caused an insect to look slightly more like its environment, that insect might do better at avoid predators or catching prey.   Thus it would be more likely to produce offspring which would also have its mutation.  Random mutations that caused an organism to look some other way would not confer any benefit as regards producing more offspring.
In each generation, if there is some random mutation that made the organism more similar to its environment, it could produce better fitness.  The end result, over thousands (even millions) of years, is an organism which looks very much like its environment.
Fitness is what drives evolution.  Read more at the link if you are interested.  The more offspring I have the more I pass along my DNA and the better my fitness is.  If I have a mutation that lets me have more offspring, that improves my genetic fitness.

In each generation, if there is some random mutation that made the organism more similar to its environment is wrong. Fitness is what drives evolution.  and The more offspring I have the more I pass along my DNA and the better my fitness is are misleading. Also, the overall phrasing is quite unusual

@Remi.b - do you mean by this that random mutations (which change the appearance of an organism) cannot increase fitness?

No, this is not what I meant. First sentence I quote, I mean that mutation are not directed toward increasing individuals fitness (it is the opposite). Second sentence I quote, I mean that there is much more to evolution than juste natural selection and third sentence I quote I mean that there is a reversal of the cause-consequence logic. I would add that the term random mutations does not mean much (see Are mutations random?)

I was quite busy for the past few days, so I failed to frame the question I exactly had in mind. So today I took some time to correct it. Sorry for the inconvenience caused. Pls don't mind.


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Bending your little finger without bending ring finger
It is possible to bend each finger without bending any other, except one for most people. It is more difficult for the ring finger, but when I try to bend my little finger independently my ring finger bends as well. I don't know if this is because of the muscle or  bone configuration, but I'm interested in the answer.

Is it possible to bend the little finger independently, and if so why is it so hard to do so?

I can bend all fingers individually and keep all other fingers straight at the same time. So... practice more. :-)

@AnoE lucky! I certainly can't

Yeah, I don't deny that - I just gave you an exception to the rule you assumed in your first sentence, "It is possible to bend each finger without bending any other, except one.". ;) To help you feel better, it requires quite some effort to do this kind of bending - the other fingers do want to come along unless I tell them in pretty clear terms that they shouldn't.

@Anoe edited to 'most people'. You're obviously an exception :P

Cheers for making me feel exceptional!

We just ran around our school campus surveying people about this out of interest and found that 20/47 (42.6%) can move independently. So in the minority, yes, rare, no! @AnoE

@Sirens wow, I had no idea so many could! I guess that may depend on for instance if it was like a musical school, and they’ve played piano, or perhaps at a certain age it gets easier. Very interesting though!

Oh, also, we did ask people who could bend if they played piano and only two who could bend said they could. One who played for six years but couldn’t was also very embarrassed

This does not have to be the case always, For example if you are a pianist you need all your finger to work independently.
OK, So coming to the main question.
In simple words, They are all interconnected. See the image [Source: Google Images]

They share flexor tendons (The flexor tendons allow you to bend your fingers) , If you try to move one, other is objected to come along.
Yes it is possible, As I mentioned before if you are a pianist, you don't have much choice. It is possible by little bit training.

@AlwaysConfused, it is like other areas where you can be more or less flexible (like doing the splits or whatever). I can bring all fingertips to the palm individually, but I also stretch my hands/lower arms etc. in all kinds of ways due to several kinds of sports where that is necessary.

The image that you have posted is the extensor group of muscles...change the image to the one showing the flexor group

Do you have a references that pianists can actually make their pinky and ring finger move 100% independently? I play piano and moving my pinky does influence my ring finger, but it is not at all an issue since they are independent enough. Playing the piano is essentially the same as typing on a computer keyboard, which all of us apparently can do fine, even with our pinky fingers.

To follow up on @biogirl's comment, an image like https://upload.wikimedia.org/wikipedia/commons/thumb/d/d1/Wrist_and_hand_deeper_palmar_dissection-en.svg/1000px-Wrist_and_hand_deeper_palmar_dissection-en.svg.png would also be clearer and easier to see!


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Are we naturally born right or left handed or ambidextrous?
Most of you here will be right or left handed. A few might be ambidextrous. But were we born that way?
I'm wondering if everyone was born ambidextrous, but as they grew up became more dependent on one hand, and that hand after more use now has stronger muscles, bones etc. Or were we naturally born with one hand stronger than the other?
I've heard somewhere that it has something to do with the brain, and which side which hemisphere is on. Not sure the validity of this statement. It's also been pointed out that chimps and apes show handedness, so this probably not just a human thing.
So, are we naturally born right or left handed? Or are we all born ambidextrous and does left or right handedness develops later?

Not sure what tags apply here...

well chimps and gorilla show handedness, take that for consideration.

Good question. I think the fact most people are right-handed suggests a genetic mechanism. Otherwise the choice should be random, and I would expect left/right to be equally common.  This article might be a starting point:  https://www.scientificamerican.com/article/why-are-more-people-right/

I think you are born left or right handed and I think the following experiment 'proves' it. In the Netherlands in the 1950s (and probably many other countries), left handedness was considered bad at schools they 'taught' children to be right handed. They all had to write with their right hand. It didn't help, left handed children remained left handed. Some still write with there right hand, but do everything else with their left hand.

tl;dr
Yes!
Is handedness determined before birth?
Without thinking of whether handedness is genetically or environmentally defined (see below), is handedness decided before birth?
Hepper et al. 1991 and DeVries et al. 2001 show that handedness can be inferred from from fetal position and hand usage. Typically, looking at what thumb is used for sucking is good indication of handedness.
Is handedness heritable?
The question

[A]re we naturally born right or left handed?

can sometimes be understood as

Is handedness genetically determined?

or in more concrete terms as

Is handedness heritable in humans?

If it is not obvious to you that this is your question, then you probably don't understand the concept of heritability! Then you should have a look at Why is a heritability coefficient not an index of how “genetic” something is? first and then come back here to read the results.
There have been a large number of studies on the question, unfortunately most of them were very small studies with small sample size. Medland et al. 2008 is pretty large scale twin study which report a heritability of 0.24.
In other words, yes handedness is heritable. To be more accurate, 24% of the total variance in handedness is explain by additive genetic variance. Yet again in other words.
The cooperation-competition hypothesis
On the evolution of the handedness in he human population you might want to hear about the cooperation-competition hypothesis. For that, you should have a look at this TED-ed video. As you watch this video, you'll probably be interested in reading the wikipedia article on frequency-dependent selection.
Thanks to @Mockingbird for pointing out to this video.

I understand heritability but that wasn't really my question. Sure, I get that you  an inherit the handedness of your parents, but as your answer shows, this doesn't happen very often. I'm asking whether or not we are born with the hand we use most often, or whether we aren't born with a particular handedness and it develops over time.

Ted-Ed has an interestjng video on this subject.

@BeastlyGerbil I understand. Please see edit.

Ah that's a lot better. Thanks. The hand used for sucking a thumb is a particularly interesting point...


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Relation between the number of children and maternal telomere lengths
I've read multiple papers with contradictory findings. Some suggests a strong negative effect by birth-giving on telomere lengths. Others disagree. However, none of them establishes causal relations in my humble opinion.
Which study is the most credible?

I think the first study should rather measure the change in average TL before and after rather than measuring just the after and comparing it to a control because the apparent difference could just be the variability we already normally have. The second study doesn't state how it was carried out. TL increases in dividing cells. For example, cancerous cells have longer telomeres.  It would be a good idea to look at hormones that control cell division and how pregnancy might affect their levels. It can also require multiple births to have a significant effect since pregnancies don't last much.

@user7777777 Cute analysis! So, none of them are very credible, statistically.


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What percentage of HIV cases are caused by each of the following pathways?
Most studies of STI focuses on sexual intercourses.  For example one study shows that approximately 70% of HIV is caused by male-male intercourse, and 20% is caused by heterosexual sexes.
However, I cannot find reliable data of the percentage of each of the possible pathways. For a list:

injection of addictive drugs
injection of drugs or blood for medical reasons
Sexual intercourse
non-penetrative sexual conducts (such as kissing)
Mother-child transmission
etc.

How do I find the data for the approximate percentage of cases that are caused by each the reasons above?
Note: the percentage data is calculated by the number of cases of one cause divided by the total cases. It can be an estimation, but it is different from the risk per exposure

It'll strongly depend on where you are in the world and which publications you are looking at as a consequence.

World data is the best but any data from the major countries (like G8, G20) would help!

Here's a start, from WHO/European Centre for Disease Control. From the report, for new infections in Europe not including the Russian Federation (or Belgium) in 2019:

50% heterosexual contact (not subdivided by penetrative/non-penetrative contact, but the latter will be a tiny fraction)
21% sex between men (ditto)
13% injecting drug use
0.7% mother-to-child transmission
0.2% "other" (nosocomial, transfusion or use of other blood products)
UNKNOWN 15%

See Table 8 in the full report for a country-by-country breakdown.
Note: these numbers (which are reported on p. 38 of the full report) are for the "WHO European Region", which includes lots of eastern European/former Soviet (including Central Asian) countries, where reporting (not necessarily actually infections!) is heavily skewed to heterosexual transmission (10 to 1). The figure below is for EU/EEA countries only.

Great to see an answer to this difficult question, so kudos! How does this answer square with the EU/EEA average pie chart puting sex between men at ~50% with heterosexual sex trailing by 6-7(?)%. I haven't read anything but the conclusion, but am curious from where your breakdown is obtained and if it's accurate. Is it based on sheer numbers? Is the pie chart not based on numbers?

I'm just quoting values from page 28 of the report. I didn't try to match up numbers between the report and the figure ... Conceivably the pie chart made a mistake in the legend/colour assignment?? Seems unlikely.  With more time, could look at Table 8 and see how the various country-level pie charts match up with the table ...

(Table 8 lists 9525 from sex between men, 8164 from heterosex, 955 from drug users, 167 from IVDU, so maybe I misunderstood the numbers on p. 28 ???)

@BenBolker I'm not finding the numbers you mention on page 28.

Oops, p. 38 ...

oops, discrepancies may be between "EU/EEA" and "WHO Western Region"

Ah, thanks. Yeah, that does seem to be the case.

There it is. Thanks!

Yes EU $\neq$ Europe


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Please help identify this plant
This plant/branch was part of a table decoration brought home from La Puente, CA, a week ago. It's been kept in a jar of water. I hope to:

Learn the name(s) of this plant.
Learn the correct morphology terms (not sure if I said that right) that apply to this plant/its leaves (e.g., about its shape, leaf base/tip/veins). I've looked at some leaf identification charts online but the ID'ing process is totally new to me so it's a little confusing.

Some notes about the accompanying images:

Images A and B --- The top leaf is kind of spiraled, and it has 3 "entire" leaf margins (they're smooth) and 3 surfaces. (Is there a morphology term that applies to the 3 surfaces?)

C, D, and E --- The leaf arrangement of the lowest 4 leaves seems to be "opposite" but then the other leaves above them seem to have an "alternate" or "alternate spiral" arrangement.

Here are the images:
Image A and B.

Images C, D, and E.

Regarding Image A: any chance that is 2 leaves that are flattened against each other as they emerge and unfold?

If your goal is to learn the basic parts of a generic vascular plant, this is a bad example.
As @BryanHanson's answer states, the wide, flat surfaces are cladodes, not leaves. The diagram included with the answer shows scale leaves, which can be seen in photos D & E; that means that the cladodes grew from the axillary buds of those scale leaves. Presence of an axiallary bud is normally the best clue to "is this a leaf?", but things get a bit confusing when the shoots take on this unusual morphology.

Since you mentioned it was a table decoration, I searched "florist greenery" and found images very similar to what you have.  Good chance it is from the genus Ruscus but you will have to compare your plant to online images to be sure.  Wikipedia on Ruscus.
Note that Wikipedia mentions that what appears to be leaves are not actually leaves, but cladodes, a type of hybrid tissue.  Wikipedia's entry summarizes a study on Ruscus aculeatus in particular (a molecular biology study, original here).
Looking at the paper linked above, Figure 2 (and others) show tiny "scale leaves" below each apparent leaf, and I think I can see these in your photos, but again, you will need to inspect more closely.

It does look like a Ruscus, they come from Eurasia, and he found  it in the Americas. Tell tale thing is the flower that comes in the middle of the underside of the leaves, so it's definitely a Ruscus variety.

@LifeInTheTrees the tiny white nub not quite mid-point on the underside of the "leaves" - is that a flower bud, or a dried up flower?

here is a bud... https://upload.wikimedia.org/wikipedia/commons/0/01/Ruscus_israeli.JPG and https://commons.wikimedia.org/wiki/File:Ruscus_israeli_cladode.JPG


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Identify this insect in Texas
Please help identify the insect in the attached picture.  It was found in the Dallas/Fort Worth area in Texas, today, April 18 2023.  It is about 0.25 inches long.
Update in response to comment:  It was found in the backyard of my house, in shallow soil that I had recently been digging in and re-grading.  The white background in the picture is a potting soil bag I flicked it onto to get a better look.

The thorax is all wrong for a juvenile cockroach as others have suggested. (A cockroach would have an enlarged prothorax covering the head, as well as plate-like meso-and meto-thoraxes). Also, the antennae are too short.
Instead...
Based on the size, location (soil), and body shape (especially indent at base of pornotum, apparent split between elytra seen at the right of your image, and the short filliform antennae), it is much more likely this is some species of ground beetle (Carabidae).

According to Wikipedia, "All carabids...have a groove on their fore leg tibiae bearing a comb of hairs used for cleaning their antennae." However, your image does not provide enough clarity to effectively check (though perhaps th right leg showing a spur associated with this groove?).

According to Wikipedia:

more than 40,000 species worldwide, around 2,000 of which are found in North America and 2,700 in Europe.[3] As of 2015, it is one of the 10 most species-rich animal families

As such, I do not intend to try to identify this to species.

Here is a key to Oregon species to demonstrate variability in morphology as well as to emphasize structures to emphasize when trying to ID to species level.

Although I do not believe this to be your species, I wanted to include an image of an example specimen for reference:

 Amber-colored Ground Beetle - Platynus brunneomarginatus. Photo  credit: Jim Moore (2018); Bugguide.net

Thanks @theforestecologist, that is great.  Eliminating roach as a possibility helps a lot.

Another possible difficulty with this specimen is the teneral appearance (I find it possible that the animal had only recently emerged from its pupa); the same animal seen a few hours (or more) later might be considerably darker.


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How is an extreme insulin overdose counteracted
I just watched this comedy skit that went -
Trainee: I just gave him 10 of insulin
Doctor: 10 what?
Trainee: 10cc
Doctor: * look of terror *
As a diabetic myself I know that 10cc or 1000u is an insane amount of insulin to have in one go. A 10ml vial (1000u) would usually last me over 2 weeks.
1000u in one go would most certainly be fata (if untreated) whether the patient was diabetic or not. Although individual insulin sensitivity varies greatly, I, personally, know that I would need around 1500g of sugar/glucose to counter that much insulin which I would've thought just isn't possible. What I'm wondering is, is there some other way that, assuming you're already in a hospital, they could counteract, filter out, or otherwise manage such a severe overdose? Or is IV glucose the only option?
I know glucagon injections can be use to treat severe hypoglycaemia but from my research the average person would no have enough stored glycogen. Please tell me if I'm wrong.

I'm not sure what you're worried about. The doctor is right there. I assume the trainee didn't give 10cc sq (that's a big bolus, and certainly too big for an sq dose.) So one can assume it was given IV. IV insulin only lasts a few minutes. A liter of D5&W (1000 x.05 =50g glucose) wide open and the crisis is averted. It's not momentary hypoglycemia that causes the worst outcomes; it's prolonged hypoglycemia. (I know a resident who mistakenly ordered IV instead of sq insulin. Nothing happened.) It is used, though, to treat DKA.

SQ insulin lasts for hours, a few to a lot depending on the type. A hefty dose of sq insulin without po intake can be, and has been, lethal.

@anongoodnurse so what youre saying is IV insulin is metabolised very quickly and even an large dose would be easily fixed?

Say someone did manage a 10cc sq overdose. How would you manage that?

See long explanation above. Just a lot longer observation period.


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Anticodon Translation Question

Could somebody please explain the answer for (c). I assumed that since transcription started at the bolded/underlined T/A base pair, the second codon would be UCU? Thanks!

Welcome to Biology StackExchange! Beware: Transcription and translation are two very different processes. Transcription indeed begins at the bold&underlined T/A, but translation begins at the start codon.

Hi! Thanks for your response. If it were to begin at the start codon, wouldn't the second codon be TTT and the anticodon would be AAA? Where does the answer, CCU come from?

This is a question best understood carefully and in parts. We know that transcription begins at the bolded AT pair, and that once transcription begins we are looking for a translation start codon (i.e., ATG).
From the transcription start, we have the sequence as follows:
5' TGCAGAGATGAGGAAAA...AGT 3'
Here is the start codon for translation:
5' TGCAGAGATGAGGAAAA...AGT 3'
If our start codon is there, then the next codon would be 5' AGG 3'. We know that an anticodon is the complement of the codon, so it would be 3' UCC 5'. However, we normally write sequences in the 5'to 3' direction, so that's how we get 5' CCU 3'.
I think another commenter was right in that you seem to be mixing up transcription and translation. The start codon refers to translation start, not transcription start. Make sure to slow down a bit and read the question, as it even gives you that information in part B ("give the first ten nucleotides of the transcript and box the start codon for translation").


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When to clean out a bee house?
I have a bee house which seems to be very popular...

I have noticed that a hole can become vacant and then filled again within half a day. Now, it's been up a few years and I don't necessarily pay that much attention to it. I suspect that some of the holes contain failed bees, so I would like to clean them out for new occupants, but I do not want to harm any that might be in there. The holes range in size from 2.5–6 mm in diameter.
How can I mark occupied holes without using anything that could be harmful? For example, I thought of using a marker pen on the material used to cap the holes, but might the solvent, even though it'd be a tiny amount, hurt the larvae?

I suspect that your best bet will be something non-toxic.
I would make a mark that is removable and not directly on the hole. Possibly something like beeswax to mark a circle around the hole or maybe even a pencil  mark might work. In the case of a pencil I would use graphite, not coloured unless specifically non-toxic. You might also be able to use a non-toxic water based paint-pen, such as is used by beekeepers to mark the queen.
I wouldn't put anything directly on the cap as you might put damaging pressure on the developing larva underneath or possibly occlude air-flow and cause death of the larva. Marking the cap could also transfer disease from one hole to another, which you obviously don't want to do.
Please take this advice with a grain of salt, I'm not an expert on this or even own a bee-house (though about to take up beekeeping as a family) and ask your local wildlife experts - seeing as you are in the UK, the Wildlife Trust might be a good place to start.

The idea with marking the cap itself was that when the bee emerges it will remove it, so if I see a mark still there after, say, three months, I would know to clean that particular hole. But a soft graphite pencil seems like a good idea—they appear to be using sand this year rather than the darker mud that's been used in previous years.


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Does the molecules in nerve cell membrane change 100% during the life of the nerve cell?
In their lifespan nerve cells do not divide and so they stay the same. They do get damaged sometimes and require some maintenance and change their axons a bit. They also require a lot of energy so they take in stuff and produce waste. This would in my opinion mean that the molecules in nerve cell membrane can change and that molecules do go in and out, but it does not imply that there is a process which changes the molecules in nerve cell membrane regularly. I have not been able to find information whether the molecules which make up the nerve cell's membrane change 100% during its life.
So does a nerve cell which can live 80 years change the molecules that make up the membrane regularly, so that in a long period of time almost every molecule in the membrane has changed? This would be an analogy about a human which replaces skin cells regularly.
In addition, I would be interested if nerve cells change replace other parts inside the membrane regularly in a molecule level.
In not long living cells, which divide I think that the molecules in the membrane have to change completely. If one cell divides into two, then the amount of membrane cannot be enough in neither of the cells so they need to take in stuff and grow the membrane. In this process even if the membrane may not be regularly replaced the dividing would cause the change eventually after a lot of dividing.

Hi Lauri, welcome :) maybe the genetic mutations accumulated over time due to environmental and physiological factors could make the 80 year old neuron express the wrong proteins for the membrane, or simply not produce them at all? A neurobiologist might appear and chip in at some point with a better idea.

@pawelekzzz Thank you! That is probably true. Changes in the neuron's gene could cause different proteins in the membrane and basically also to start the neuron to change the molecules in the membrane or stop replacing them. However, I don't see directly how this is relevant to my question. Or was your point that it could be at least theoretically possible that the molecules would change if there would be a certain genetic mutation?

I meant that at least the number of molecules related to membrane proteins that will
be regularly synthesized during the lifecycle of the neuron will be part of that percent. They will also change over time themselves (or entirely stop being expressed) after accumulating mutations that affect translational regulation.
Damage to membrane phospholipids measuring ~1 nm or less will be thermodynamically rearranged using existing phospholipids. Larger damage will be resealed through exo-endocytotic vesicle trafficking but those “lost” phospholipids will be recycled through a salvage pathway.


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Does the speed of muscle contraction within a single sarcomere differ between people?
Of course the number of muscle cells can be different person to person. But within a single sarcomere, are we all the same?
Would the frequency of the protein motor binding and release cycle different for each person? And if that is a constant, then do we all attain the same speed of muscle contraction?
If not, what causes the different speed?

In consideration of the fact that protein structure is encoded by your DNA, I would assume that it could be possible to have different muscle-contraction speeds that are dictated by the exact amino acid composition of a sarcomere. I don't know if the effects would be measurable or not. But I suppose it could be possible to have sarcomeres that are able to make stronger bonds than the sarcomeres of other people, thus having an increased reaction rate. And, as you said, release cycles might not be the same for each person which could also contribute.

@user1589188 if you talk about potential then initially yes, but considering the fact that muscle contraction is regulated chemically by the nervous system they would be different in different people even of the same age. Unless the portion of the  muscle fibre under consideration is damaged then they would show same frequency for requiring Ca+2 and ATP level. (Mutation in the DNA most likely lead to failure of proper binding)

Muscle contraction speed is also situation dependent-- varies with force and length even within an individual, even just by virtue of the sliding filament model... I'm not sure that the initial assumption that an individual sarcomere has a fixed speed is correct.


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Cancer and Evolution
Edit: just to clarify, I am asking what, if anything, the literature says can be gleaned about evolution by studying cancer, especially relating to how multicellularity evolved and the traits used to force cells under control of the organism.
Most of the original question details I had added were just my own thoughts on the topic.

Original question
Is there a sense in which cancer can be considered as a return to the unicellular "origin" of a cell?
It has always seemed to me like cancer is almost inevitable by the structure of the cell (its poor "design", essentially). The only thing standing in the way are the cellular controls: senescence/apoptosis (e.g. p53 pathway), immunosuppression (e.g. cytotoxic T lymphocytes), telomeres, etc...
So it seems like multi-cellularity did not evolve "ground-up", but was instead generated by slowly differentiating the functions of the various cells, while developing "top-down"controls against errant cellular behaviour.
Thus, cancer, which occurs when these protections fail, is in some sense merely a return to an ancient evolutionary root.
I suppose some arguments against this include the fact that modern cells are vastly different than their ancient ancestors (or even modern archaea/bacteria).
So the best we can perhaps say is that the core of the cell has been sufficiently preserved (ribosomes are still mostly RNA, are they not? :] ).
Further, it is hard to call some of the "micro-evolutions" of cancer (e.g. interleukin-8 production) as returns to primitive behaviour.
In these cases, I tend to see them as necessary occurrences to remove the "top-down" controls, rather than as integral to the destructive out-of-control growth characterizing oncogenesis.
But, debatably, perhaps not all of them are (e.g. extravasation in metastasis).
Obviously this seems very simplistic, but is there any literature thinking about it this way? Or directly debunking it?

Aside from anything else, your assumptions about multicellularity evolution seem off.  For example see The evolutionary-developmental origins of multicellularity (press-release version: From one cell to many: How did multicellularity evolve?)

While commending you for wishing to think about and discuss science, it has to be pointed out that this is question and answer site, not a discussion site. It is worthwhile reading the Help on What type of questions should I avoid asking to see why close votes are accumulating on your question. I would say it comes under the categoriy there of "there is no actual problem to be solved: “I’m curious if other people feel like I do.”" i.e. you are inviting discussion of an idea. Some other forum (Cynics?) may accommodate you.

@David I'm aware that this isn't a discussion site, which is why I asked specifically for literature. Thanks for your comment anyway though. I understand that the question is not exactly the cut-and-dry basic questions that this site seems to prefer. It may well be closed anyway, though I am not sure why it is so much worse than many of the other questions here....

Well, you seem to have changed your question and title now, and although I still think it's off-topic I'll leave things there. However I can't ignore the last sentence of your comment. Let me rephrase it: "Why pick on me officer? I wasn't the only one exceeding the speed limit. And some were going even faster."

Cancer and level of selection
Cancer results from the opposite action of different level of selection. There is selection on the population of multicellular individuals and there is selection on the population of cells within each multicellular individuals.
There is selection among cells within an individual for increase replication rate while there is selection among multicellular individuals in the population for controlled replication rate of their cells.
Major transitions
The passage from small unit of selection to bigger units is called a "major transition". Such transitions include the grouping of genes on chromosomes, the grouping of cells onto multicellular individuals, the grouping of multicellular individual onto colonies and, if there are several planets inhabiting life in the universe, then the grouping of life forms in every planet into a population of living planets. One can list other, more extreme or intermediate major transitions but there is quite a bit of debate on what really constitute a major transition.
Literature on the subject

[I]s there any literature thinking about it this way?

The keywords that will help search further information are group selection, kin selection, major transitions.
I recommend having a look at Major Transitions In Evolution by Maynard Smith and Szathmary and also The Major Transitions in Evolution Revisited by Calcott and Sterelny which is a book made of many small parts, each written by a different author on these same questions of level of selection.
You might eventually have a look at Evolutionary Dynamics: Exploring the Equations of Life  by Nowak as well.
These discussions of level of selection include discussion of what an individual is and what level is most important. The extremely popular and well written books by Dawkins will also bring you some light on the subject. Consider The extended phenotype for example.
For more book recommendations in evolutionary genetics, please have a look at Books on population or evolutionary genetics?.
If you like the sensation of thinking of the entire earth as an individual part of eventually a larger group of living planet, then you'll maybe enjoy having a physiological / ecological view of this living planet earth with Gaia by Lovelock


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3D Object Modelling in the Brain
Could somebody point out the neuroscience literature dedicated to the modelling of 3D objects in the human mind?
I'm interested in the brain regions, and particularly the details of the circuitry, involved in simulating/manipulating (or planning to manipulate) and/or recognizing 3D objects, or in relating them to the "2D" sensory information. Ultimately, my interest is quantitative, i.e. I'd be especially interested on more computational outlooks on the topic.
Edit: I am aware of the visual recognition pathway, which roughly speaking culminates with the inferior temporal gyrus (in the "what pathway"). However, some animals (not just humans) can simulate object properties (e.g. how will this plastic figurine warp if I bend it a certain way? What is that moving ballerina likely to look like in the next second?). This is more complex than object recognition alone.
Note: my question is asking for pointers to the foundational literature of this topic. I know it's somewhat broad, but I'm essentially asking where to start reading. Thanks! :)

@Charles Thanks for your comment. I was actually thinking about the modelling of the object, rather than something tied to a specific sense. For instance, the hippocampus and PPC both have multimodal sensory inputs, and encode something involving more than one sense. Although, if I had to choose a sense, I would say vision. I'll also edit to clarify a bit.

Is this the ability you are talking about?
https://en.wikipedia.org/wiki/Spatial_visualization_ability

@futurebird Yes, seemingly so. Though in writing my question I had more of a "simulation" view in mind, e.g. some notion of material properties must be involved when modelling the future.


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Is 7-nitroindazole neuroprotective against meth because it oxidizes peroxynitrate?
So 7-nitroindazole (7-NI) prevents methamphetamine (METH) induced neurotoxicity AND completely prevents meth induced dopamine depletion, but doesn't prevent meth induced hyperthermia. Strangely, a different study said that its possibly because of 7-NID's ability to prevent hyperthermia, (however it is important to note that this study did not test body temperature), yet all the other studies say the opposite, that 7-NI doesn't prevent meth induced hyperthermia.
Keep in mind that colder enviromental tempratures significantly attenuated METH-induced neurotoxicity
Could the reason as to why 7-NI prevents METH induced neurotoxicity and dopamine depletion simply be because it oxidizes dopamine oxidizer peroxynitrite noting that non-meth induced hyperthermia also cause neurotoxicity and produces peroxynitrite while showing the same neurotoxicity markers as METH induced neurotoxicity such as nitrotyrosine?


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What is methamphetamine's transport carrier across the BBB?
Which carrier protein allows methamphetamine to cross the blood brain barrier? I would assume it's SLC22 and possibly SCAMP1


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Why do palpitations happen when someone is nearing something rewarding?
When you are nearing something rewarding (IE: winning a prize, or winning a game), why do you experience tachycardia?
For example, if someone entered a raffle with the number 9284938, and the announcer was starting to announce 9..2..8..4, the closer the announcer gets when palpations would start to occur.
My guess this is something to do with dopamine since dopamine is a rewarding hormone and it gets metabolized directly into epinephrine, but I don't think I'm right.

Palpitations (irregular, extra heart beats) are different from tachycardia (an increased heart rate often accompanying excitement/fear, etc. It's cause is norepinephrine (also known as adrenaline in some countries.) There may also be dopamine in there somewhere, but the major effect is the rush you get from adrenal release of nor-epi.

@anongoodnurse Thanks! I edited the question.


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Can dopamine antagonists be used as dopamine upregulation?
Can dopamine antagonists such as Thorazine that are used to treat schizophrenia and bipolar be used to upregulate dopamine in the long term in healthy (non schizophrenic or bipolar) users to get a similar effect as a stimulant high without inducing neurotoxicity? Due to tolerance buildup of the dopamine blocker, my assumption is that it should result in dopamine upregulation when dopamine antagonist use is stopped.
As an example, in extremely high doses of methamphetamine, meth induces temporary schizophrenia (skin picking, crank bugs, paranoia, hallucinations, etc), and extremely similar, if not exact, effects to bipolar, which are the only two neurological diseases resulted from dopamine over-production and release. Over time, tolerance to meth builds up and it stops being effective, unless it is stopped for a period of time resulting in reverse-tolerance. Can this same dopamine downregulation effect be used in dopamine antagonists as dopamine upregulation, creating the same euphoric feeling resulted from meth use or bipolar hypomania if the dopamine antagonist is taken for a period of time then stopped?

Neurologically and physiologically in general the body is programmed to find it's state of homeostasis. Dopamine as a molecule within neurology can not in fact pass the Blood Brain Barrier in which is why the precursor L-Dopa is administered for deficiency. Regard to homeostasis in a non naturally deficient person, both down and or up regulation to find this balance over time can occur in which cessation is not a good idea without medical assistance as natural production may well have changed gene expression.

@kirill2485 - please be nice to people spending their time on your questions. The answer from Max was reverted to a comment by the mod team, explaining the reason it pops up again.

@kirill2485 - it's already clear that it's not an answer, because the post was converted to a comment. You wrote 'I already told you, this is NOT an answer...' - The capitals imply screaming, like 'oh my, not you again, dude, can't you read my question?'. You could say something along the lines of 'Thanks for the comment, but....'


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Would methamphetamine heal wounds, infections, and diseases?
Alright, so this sounds crazy but based on these research findings it is safe to assume that meth would allow wounds and diseases to heal faster by interleukin 6 . On the otherhand, using meth during illness would cause higher neurotoxicity due to extreme hyperthermia and fever.
Correct me if I'm wrong:
Firstly, dopamine increases interleukin 6 (IL-6) release and inhibits tumor necrosis factor release.
Interleukin-6 is the source of fevers and hyperthermia. Most importantly, IL-6 heals skin wounds. It's main goal is to regulate the immune system by raising and lowering temperature depending on if a person is sick or not. Raising body temperature will prevent a person from being sick and will make wounds heal faster, but will induce neurotoxicity, lowering it will prevent neurotoxicity but make someone vulnerable to infection. According to Wikipedia, IL-6 stimulates the inflammatory and auto-immune processes in many diseases such as diabetes, atherosclerosis, depression, Alzheimer's Disease (interestingly though, Alzheimer disease is reliant on dopamine depletion, and people with Alzheimer had significantly higher levels of IL-6, which is surprising. One possibility is due to the fact that dopamine increases interleukin 6 release, and without dopamine, IL-6 cant be released, meaning more IL-6 will be metabolized but not used).
IL-6 is also the main, and perhaps only, cause of meth-induced neurotoxicity. It is responsible for neurotoxicity by means including, but not limited to, cell death, ROS generation, and neuronal damage. Lowering enviromental temprature significantly prevents neurotoxicity. To verify this claim, I Googled "methamphetamine neurotoxicity interleukin-6", and came to this article, furthering the evidence that meth vastly potentiates IL-6 and IL-6 induced hyperthermia is the result of meth-induced neurotoxocity, as mice with a mutation for IL-6 blocked meth-induced neurotoxicity, which also means that these mice won't be able to reheal faster.
To bring an update to this post, I have found this paper that shows that happiness potentiates the immune system. But this is a very minor influence as meth produces >1000 "units" of dopamine, relative to 300 units which cocaine produces. Meth would be much more efficient.
To bring further updates, it seems that my assumptions were correct. By googling "site:nih.gov methamphetamine neuroprotective", I was led to the following: https://www.ncbi.nlm.nih.gov/pubmed/24333768 and https://www.ncbi.nlm.nih.gov/pubmed/25724762
Surprisingly it is neuroprotective following stroke.
So, putting all this into account, is it possible that meth actually heals wounds and diseases (while at the same time inducing neurotoxicity)?
This assumption came to me because I have an aggressive cat and whenever I'm high on meth I noticed how wounds from a cat scratch would heal within a day or two instead of a week.

I suggest performing an empirical experiment: make some kind of repeatable, standardized wound, and measure how long it takes to "heal" (you will have to define an endpoint) on 3-5 occasions, then do the same while the analyte chemical is present in the biological system of interest (it makes it hard for even the most open-minded scientists to take an investigation seriously when it includes the words "high on meth"). Compare the ~5 control trials and ~5 experimental trials and perform statistics to determine if there is a "statistically significant" difference.

Impact of methamphetamine on infection and immunity Methamphetamine alters blood brain barrier protein expression in mice, facilitating central nervous system infection by neurotropic Cryptococcus neoformans. There may be short term benefits but long term use would lead to more overwhelming negative effects.


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How long is the typical peptide sequence recognized by a T-cell?
A naive T-cell recognizes either a certain sequence of amino-acids (even if that sequence occurs as a part of a longer sequence of amino-acids(*)), or a small set(**) thereof.  Only T-cells that do not recognize any sequences native to their own organism are allowed to mature.  Then they are released from the thymus and start searching for the amino-acid sequences they recognize, assuming that their occurrence within the body would indicate proteins synthesized, and possibly forming, another organism (a parasite).  I wonder what are the shortest, longest, and typical lengths of the sequences recognized by a matured T-cell, as counted in amino-acids.
(I suppose that if a naive T-cell recognized any very short peptide, it would be unlikely to survive in the thymus, and if it only recognized very long peptides, it would be overspecialized and evolutionarily unstable.  So there must be some limits.)
If the answer varies across vertebrate species significantly, that would be interesting, too.
Footnotes:
*: In this sense I used the term "peptide" loosely in the title formulation of my question.  Please correct me if such usage was simply wrong.
**:I don't have a good understanding of how the "sets" are represented in the T-cell, and consequently, how they can be structured - whether they tend to form a single "pattern with wildcards" or multiple independent patterns, or anything in between.


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Why do you get dizzy when exhaling with resistance?
Why do you get dizzy when breathing out while something resists the air outflow and requires more pressure? Like when blowing up balloons or breathing out through a straw.
This even happens when breathing rhythm is relatively slow. That makes me wonder if the same physiological mechanisms are at play like with hyperventilating. The effect feels very similar at least. My impression is that something changes about lung functionality when it is subjected to higher pressure (in this case only during exhalation).

A major part of it is simply blood oxygenation (O2) and levels of carbon dioxide in circulation (CO2). Breathing rate and form determine these, and effects such as light-headedness and fatigue and blood pressure depend on them.
First... you get dizzy because you aren't getting enough oxygen. You need oxygen to function. This includes your vestibular system, which, when unoxygenated, makes you feel a sense of imbalance, or dizziness.
Second... CO2 reacts with the water in your blood to form the pH-lowering carbonic acid (H2CO3). In parallel, dissolved oxygen contributes somewhat to alkalinization (pH increase from baseline). When you hyperventilate as it works very much like "exhaling with resistance". In exhalations, lungs expel CO2 out from circulation. When you hyperventilate, or breathe more than necessary, you eliminate more CO2 than usual, which makes your blood more alkaline (incidentally this is why hyperventilating into a paper bag helps: the bag retains expelled CO2 you can breathe back in). More acidic blood can also lead to dizziness, which would be the case if you were not completing exhalations - or "exhaling with resistance"). Now, this explanation is a simplification, because blood has a buffer system that keeps pH steady. It's called the bicarbonate buffer system. In lieu of this, you'll find that you are more dizzy when bicarbonate levels are increased too, so it's not directly related with blood pH in the short term.
There are probably other contributing effects too. These are probably related to blood pressure (divergence from regular blood pressure, either hypo- or hypertension cause dizziness) as it relates to breathing pattern. This is because blood circulation and respiration are coupled in many ways.
Addendum: when you exhale but don't let the air out, it's called a Vasalva maneuver. It has physiological effects too, often short-term - grunting when lifting things is an example. You can read up on it too, it could be related to your query.


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How to calculate df in the chi-square test of Hardy-Weinberg equilibrium?
We often use df=1 in Hardy-Weinberg equilibrium when there are only two alleles. Some people say that it's because we've used the frequency of two alleles when calculating the expectated values, while others may give different explanations.
The website for the second explanation:https://www.mun.ca/biology/scarr/4250_Chi-Square_HWP.html
The principle is that, if you know you looked at n experimental results that could have fallen into any of three categories a b c, the value of the first category a can be anything (up to n), and the value of the second category b can be anything up to (n-a). Having determined a and b, the third value is now pre-determined: c = (n - a - b). So, only two of the three values are free to vary. For diploid genotypic data with two alleles A & G and three genotypes AA, AG, & GG, this would suggest df = 2 in the observed data. However, given f(A), the expected frequencies for all three genotypes are automatically determined, thus there is only one degree of freedom.
This affects how to calculate df when there are more than 2 alleles. The first answer is df=3, which is from the Hartl's textbook, but unfortunately it's in the afterclass questions, and it doesn't have an answer, so I don't know why. The second one gives df=2. I found another article (in a chinese website) which says that df=m*(m-1)/2 (m is the number of alleles). Which one is right, or which one is commonly used?
Now I believe that my question is solved, so I won't open this question.

It would be helpful to have links to the sources that you have found so far, particularly so for the long quote.

You'll need to at least explain what the first method is and how it results in df=3.

After the latest edits I'm still not clear what the first explanation leading to df=3 is. If the explanation is that for 2 alleles there is 1 "free" parameter to vary because if you know p or q you can derive the other as 1-p or 1-q, therefore 1 DF, then for 3 alleles you would still get 2 DF: if p+q+m = 1, you have 2 DF because you only need two of the three to calculate the third. That's the same as the second explanation, and really it's the same explanation, too. Where did you get 3 DF from for 3 alleles? You must explain this even if the original is in Chinese.

(closing for now, because even as a good question, without this piece of clarity it would be inappropriate for someone to answer your question)

@BryanKrause I agree with you on df=2. 3 DF is from the afterclass question in Hartl's textbook. It just asks "In the situation with 3 alleles, the df should be 3. Explain why." And it's with an odd number, while the textbook only gives answers for questions with even number, so I really don't know the reason. Maybe it's just wrong.

@Planarian Ah, now I understand. Yeah, if there is no explanation and just a textbook question I'd just as soon assume a typo. You could see if your library has an instructors edition that includes odd solutions.

Better yet, what does the textbook actually say about degrees of freedom for this test? It's unusual for a textbook to come with a question on material that isn't covered...