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What in the brain has gone awry during sleep paralysis?
I experience episodes of what I assume is sleep paralysis (lasting ~ 10-30 seconds) a few times a year, where I'm conscious of being somewhat awake but unable to move.  I can hear, but not see, and am quite focused on my breathing which feels labored and uncomfortable (can be accompanied by a feeling my face is covered by a sheet).  Sometimes, I've even been able to "jolt" myself awake if somehow muscle control is regained. Otherwise, I assume I drift off back to sleep.
Do we know yet what has gone wrong (if it can be assumed to be aberrant) and which neural circuits are involved? What i'm looking for is a specific explanation at the neural circuit level of how it can occur.
Is anyone aware of anyone conducting research into this or how it could be studied as it doesn't occur frequently and likely difficult to induce on demand?

Body paralysis occurs during REM sleep to keep your body from acting out your dreams.  You experience sleep paralysis when the mind awakens from REM sleep before the body paralysis has subsided.  I've had this happen before also, along with the "jolting" out of it you describe.  It usually happens when I'm very tired and trying to stay awake.  I try to stay calm but it's not easy as you know.  There is a good description at WebMD.

Thanks for sharing, @Kurt.  Yes, i'm aware of the general mechanism of muscle atonia during REM and that sleep paralysis is most likely to happen as you exit the ultradian sleep cycle.  What i'm curious about and after is a more specific explanation at the neural circuit level of how it can occur, and whether that is known/being researched (I can't find fMRI of an SP episode for example)? Is it a brain "snafu" or is a vestigial evolutionary-inherited trait that other animals have use for perhaps?

@Louis Leung.  Thanks for the clarification.  I have had trouble finding much more indepth research also.  I'll be interested to see what others come up with.

Sleep paralysis is  common, and associated with poor sleep
Isolated sleep paralysis is a relatively common parasomnia. Lifetime prevalence rates vary quite a bit from study to study, and between populations, but aggregating them gives a rate of about 7%. There are a number of associated conditions, many which are also associated with disturbed or irregular sleep in general (e.g., being an undergraduate student, shift worker, or having a psychiatric disorder).
Sleep paralysis also occurs in narcolepsy, but here it may be different
Sleep paralysis is a component of the overall clinical presentation of narcolepsy. It may have a similar but related mechanism, since these patients also experience cataplexy (muscle atonia in response to an emotional stimulus). Isolated sleep paralysis means sleep paralysis that isn't associated with narcolepsy. Some of our understanding of isolated sleep paralysis comes form studies of narcoleptic patients and animal models of narcolepsy. Because of the substantial differences in sleep patterns in narcolepsy, it's unclear if findings from these studies provide useful information for isolated sleep paralysis.
You can induce sleep paralysis by forcing sleep onset REM
You can induce isolated sleep paralysis in healthy volunteers by inducing sleep onset REM, a sleep period where REM sleep quickly follows sleep onset, instead of following a march through the phases of non-REM sleep. This was done in the linked study by, essentially, by waking the volunteers before the onset of the second REM period. Since sleep onset REM is more common in sleep deprived individuals or individuals with disturbed or irregular sleep patterns, this may be one of the reasons we see more sleep paralysis in these individuals.
Neural pathways involved in sleep are complicated, but REM doesn't directly inhibit arousal
The circuitry can be understood from studies of circuits involved in sleep in general and REM sleep in particular. You can read about this in Principles of Neural Science, Ch 47. It's quite complicated. One interesting note, though, is that the general cortical pattern for REM sleep, as measured, for example, by EEG, is more similar to waking that it is to non-REM sleep. Both states (waking and REM sleep) involve inhibition of a set of thalamic neurons that orchestrate the synchronous cortical firing seen in non-REM sleep.
Importantly, while the transition from waking to non-REM sleep involves a clear interaction between the neurons of the reticular formation that mediate arousal and non-REM sleep, there doesn't seem to be a direct pathway from REM-on neurons to inhibition of the reticular formation. It is not surprising that, during sleep onset REM periods, you could have dissociation of arousal (mediated by the reticular formation) and REM-on mediated hyperpolarization of motor neurons in the spinal cord. This review briefly discusses a possible mechanism of hyperactivity or hypersensitivity of REM-on neurons or weakness of the (still unknown) inhibition of REM.
Suppress REM and you reduce the frequency of sleep paralysis
Treatment focuses on reassurance and treatment of any underlying sleep irregularity and disturbances as well as any underlying psychiatric conditions, but when used, medications that suppress or inhibit REM in general reduce the frequency of sleep paralysis episodes.
It's probably not a big funding draw
There is, clearly, some research on isolated sleep paralysis outside of narcolepsy. It's an interesting phenomenon, but since it isn't dangerous or important clinically, I don't expect it gets much funding.

Thanks a lot for the info and particularly the link to ISP study in 1992, it was an interesting read.  I agree there seems intuitively a strong association with the epiphenomenon linked to REM states, so it would make sense to start any study with the major REM modulators.  Anectdotally, I've also noticed that my SP generally occurs in the early morning, which correlates to the time of more common bouts of REM sleep during the cycle.  As you rightly say, as it's not a major life-ruiner, there won't be much ISP study but we can leave this open until the answer is eventually found!


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Does the leaves of papaya plant help in increasing platelets in a case of dengue?
In Kolkata and nearby regions, due to sudden and huge amounts of rainfall, there has been an outbreak of dengue, a disease spread by female Aedes mosquitoes. The outbreak has been so dangerous that dozens have already died in the villages.
A problem of this disease is that, the platelets in blood are decreasing abnormally. For example, a patient had 120 thousand platelets when checked at night, but when checked on the morning, it drastically reduced to about 20 thousand. This particular patient could not be saved.
Many people say that the juice of papaya leaves (leaves of Carica papaya) helps in increasing the platelets in blood. Some doctors say it's wrong, while others say that it does effectively help. Even tablets and powders have been made, but the confusion persists as to whether they are effective or not.
I could not find any good information on the net. Can anyone, with scientific arguments, answer this question?

Dengue isnt usually fatal with good medical care. I suggest sending them to the nearest hospital immediately

@user35897 a good advice from your side, but hard to follow from our side. Hospitals are full, so much so that patients are lying on the floor, with saline bottles attached to the door handles! Such is the condition. Otherwise way will so many die every day?

I'm really sorry to hear that :( hope this pandemic end soon:(

So With some digging, I found some articles/presentations that provide evidence that fresh papaya leaf extract does increase platelet counts. The first link tested this in a rodent model and found that in the test group treated with the leaf extract, there were significant increase in platelet count and red blood cells (RBCs) from the control group. Here is the summary of their results trend from the paper:

Additionally, I found a Multi-centric, Double-blind, Placebo-controlled, Randomized, Prospective Study and a meta-analyses that supports the observation that papaya leaf extract does in fact show statistically significant increase in platelet count than that of the control groups. (Dengue fever causes platelet counts to plummet). [#2-3]
Below is the image of platelet counts from the Multi-centric, Double-blind, Placebo-controlled, Randomized, Prospective Study (2):
Fig. 1: Comparison of platelet count between two groups during different
timepoint

A good criticism of the meta-analyses on Papaya leaf extract is that something being statistically significant does not equate to clinically significant. But, the placebo-controlled, double-blind prospective clinical trial provides some evidence that in this case, it is actually clinically significant.
However, the mechanism by which this occurs is not well understood. According to the 4th article, "The secondary metabolite of plants origin makes up a vast repository of compounds with a wide range of biological activities". The presentation (5) states some possible mechanisms by which the extract can inhibit the Dengue virus/vector.

Does Carica papaya leaf-extract increase the platelet count? An experimental study in a murine model
Efficacy and safety of Carica papaya leaf extract in the dengue: A systematic review and meta-analysis
A Multi-centric, Double-blind, Placebo-controlled, Randomized, Prospective Study to Evaluate the Efficacy and Safety of Carica papaya Leaf Extract, as Empirical Therapy for Thrombocytopenia associated with Dengue Fever.
Dengue fever treatment with Carica papaya leaves extracts
Role of Papaya in Dengue fever, an evidence based Answer

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

sort: votes


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Help identifying fruit
This fruit was spotted in Kochi, India on several occassions. Nothing else is known except the fact that it seems to be irregularly distributed through Kerala.

It appears to be a noni fruit (Morinda Citrifolia).

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


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Will neurons die if they are inactive for a long time?
We know that when muscles are not used they atrophy. Does something similar also happen in neurons if they do not receive any stimulus?

Short answer
Yes.
Background
Postsynaptic neuronal degeneration after deafferentation are notorious in the peripheral sensory systems. There, marked degenerative processes are present when input to the secondary neurons is lost due to degeneration of the primary sensory neurons. In other words

When the hair cells are lost in the cochlea, the auditory nerve degenerates (e.g., Kuyama, 2010);
When the retinal photoreceptors are lost, for example due to degenerative diseases like retinitis pigmentosa, bipolar and horizontal cells in the retina degenerate due to a loss of efferent input (Mazzoni et al., 2008). For more information see the works of Marc & Jones, e.g.., Jones & Marc (2005).

Note that in the central nervous system these effects play less of a role, as neurons have ample opportunity to reconnect to other neurons, for the better or worse; e.g., in the hearing impaired and visually impaired, spontaneous sensations of sound and visuals may develop and lead to tinnitus and photopsias, respectively. These symptoms are caused by cortical sensory neurons desperately and randomly looking for sensory input after being deafferented due to peripheral loss of hearing or vision. When they cannot obtain useful input any longer, they gather irrelevant, non-useful input and start generating spontaneous 'illusionary' perceptions instead.
References
- Jones & Marc, Exp Eye Res (2005); 81(2): 123-37
- Kuyama, J Neurosci (2009); 29(45): 14077–085)
- Mazzoni et al., J Neurosci (2008); 28(52): 14282–92

These examples are related to structural loss of contacts, with the retina case occurring in a background of general degeneration. Is the loss of B and H cells due to lack of input or simply the surrounding inflammatory environment? IMO, the OP is asking about loss of inputs or absent activity in otherwise healthy neurons with contacts intact, which is a subtly different question, no? In a non-diseased context, do neurons actually die if they don't fire for a while? Consider long term memories stored in synapses which may not be activated for many years. just my 2 cents..

@LouisLeung there are no inflammatory responses afaik in the cochlea in the case of age related hearing loss and other forms of sensorineural HL so your comment doesn't apply there. In the retina I would have to double check.


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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?

"From the point of view of a neuron, its axon is efferent. From the point of view of the target neuron, the axon is afferent." Well, this is wrong. Afferent and efferent refer to the whole neuron, and indicates the orientation of the impulse (from the CNS or to the CNS, respectively).

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

It does answer. Your question is very clear: "What is an afferent axon?". If you made a different question in the body of your text I suggest you to pick just one.

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

First, it's not all neurons. Second, it's talking about the connections. Afferent and efferent are Latin terms which are not exclusive to nerve cells. They come from the verbs affero and effero. You have, for instance, "afferent arteriole".

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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Why there is no typical cells
My physiology book says that cell specialization is so great that no cell in the body could be called a typical cell.
I don't understand the above sentence, why couldn't there be typical cells? After mitosis don't we get two typical cells? Or what is meant by the sentence??
Thanks in advance!

Its because there are different kinds of cells in our body for example a neuron can't represent different types of cells found in our body like goblet cells etc., just like F1 car can't be representative of all cars. I presume that the word typical is in the context of human body.

I'm voting to close this question as off-topic because it is about language, not Biology.

It is about biological terminology which is relevant. Asmaa in this case a "typical cell" would be a cell that represents all cells in the body equally well, like an average of all cells in the body..

Typical here means representative of the whole.
from the google dictionary

typ·i·cal ˈtipik(ə)l/Submit adjective having the distinctive qualities
  of a particular type of person or thing. "a typical day"
  synonyms: representative, classic, quintessential, archetypal, model,
  prototypical, stereotypical, paradigmatic;

There is such a variety of cells in the body no one is really typical.  Like a typical human.  Who would that be?  Me?  Chinese lady?  Indian kid?  There are many of us and a lot of variety.  Maybe you could say "typical older Scotsman" or "typical arrogant Stack Question answerer".  You could definitely say "typical liver cell"; narrowing down the zone limits the variety possible and lets you more accurately characterize a call as prototypical or representative.


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Why are primary sensory cells considered neurons but muscle cells are not?
The rough picture of cells involved in neural processing looks like this:

I wonder, why primary sensory (receptor) cells (like rods, cones, hair cells, Merkel cells) are consensually considered neurons (accidently having no synaptic input, but synaptic output), while muscle cells are not (even though they have synaptic input, but accidently no synaptic output).
The last cells that are unequivocally neurons are the motor neurons. Curiously, the first cells that are unequivocally neurons are mostly called "ganglion cells", not "ganglion neurons".
Is it all just a manner of speaking/matter of parlance and words? I believe not.

I received an interesting answer from Quora:

"Muscle cells are derived from mesoderm, sensory cells (like all
  neurons) are derived from ectoderm."

But is this all that is to say? What’s the “deeper” source of this asymmetry? In the beginning there was only one type of cell, which was both sensory and muscle?

The quote from Quora has the correct answer; the distinction between neuronal and non-neuronal is an embryological rather than functional definition. Along those same lines, some of the other receptors you listed are considered sensory epithelia rather than neuronal. The retina is of neuronal origin, but hair cells in the cochlea are often not considered to be neuronal, despite the diagram you provided, nor are Merkel cells. The distinctions between epithelial and nervous tissue are often more difficult to identify because both derive from the same preceding embryonic tissues, whereas muscle is entirely separate.
In the end, these distinctions don't matter much unless you are interested in development or trivia (though I don't mean to discount the importance of development there, I just recommend that you don't worry too much about the distinctions if you are thinking only about final functions).

But muscle cells cannot be entirely separate, because they react on synaptic input: at least in this respect they behave like neurons.

What do you mean by "trivia"?

They are from a completely separate embryonic tissue: mesoderm, not ectoderm. That means that if you draw a diagram of cell fates, muscles and neurons are not on the same "family tree." You'd have to go back to embryonic stem cells to find cells that could eventually become either mesoderm or ectoderm. "Reacts on synaptic input" is not a defining characteristic of neurons, they can be excited by other sources as well, and lots of other non-neuronal cells also show some excitable properties; immune cells, for example, and many others.

"Trivia" refers to typically obscure facts that are most useful as facts rather than for some other purpose.

There seems to be a parallel to species which can have accidental phenotypical resemblances which are not backed genetically, right? (Does this observation count as "trivia"?)

I'm not after "trivia" but want to understand terminology. I always believed the term "neuron" is somehow defined functionally (phenomenologically), but now I've learned it's  defined genetically (developmentally).

Interesting thought, though the very important difference between convergent evolution, which is what you seem to be describing, is that cells with different fates do have access to the same genome and so can evolve together. I.e., a mesoderm-derived tissue and ectoderm-derived tissue can express some of the very same proteins; this of course isn't possible in convergent evolution.

Let us continue this discussion in chat.


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T1D autoimmunity causes' possibilities
As far as I've learned about T1D, the prevalence of the disease and autoimmune disorders in general over the past 5 decades intrigued me to the point it made me wonder if it's really a genetic predisposition. I've read that it could be related to a virus but as far as I've read and came to conclude, could it be the EBV virus in the first place as a primary suspect infecting the beta cells in those with no genetic hisory of diabetes in their families?

I learned that EBV infects the human body then morphs itself into a human cell look-alike, could it be why the immune system attacks beta-cells if EBV infected them?
I also learned that there is a significant population with islets' antibodies present in serum yet over the years they never develop T1D and they stay within perfect glycemic control.

My question is, were there any studies done to examine that EBV possibility being the cause of T1D and if there were any studies done to explain why some of those with islets antibodies never go through the T1D autoimmune storm?


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Exclusion Limit and permeability of outer membrane
According to this textbook:

P aeruginosa, for example, which is extremely resistant to antibacterial agents, the outer membrane is 100 times less permeable than that of E coli.[pg.no 27]

and then on the same page:

The porins of diferent species have diferent exclusion limits, ranging from molecular weights of about 600 in E coli and S typhimurium to more than 3000 in P aeruginosa.

How can P. aeruginosa have lesser permeability than E. coli, if its exclusion limit is greater than that of E.coli?

My Attempt:
This source claims that

OprF provides P. aeruginosa outer membrane with an exclusion limit of 500 Da.

This( 500 Da.) is near than that of E. coli's 600 Da., so how is it exteremely resistant?


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Is it possible for a human to live forever if he/she didn't catch any diseases?
Aging is not a disease, but it's the gradual weakening of the body, as the body gets weaker it gets more prone to diseases. So one doesn't die from aging but from diseases. So if one didn't catch any diseases, would it possible for him/her to live forever? Or just longer than the maximum life span?

A lot of deaths are mechanical, and ageing would eventually tire the muscles so much that the heart stops when the person can't even lift their arm up any more at 150 or something, heart attacks are probably eventually due to heart muscle being unfit. The nerve cells also age and dont grow new cells, the rest of the cells grow back old... avoiding blood clots in the brain requires that the person's blood flow remains pure and clean for 140 years, while in actual fact it develops kindof mechanical problems. The skin would end up so fragile at 250 years that it would be like wet paper.

just as the skin loses elasticitty, the veins do too, the person would slowly turn to mush.

Have you tried to answer why there is "... gradual weakening of the body ...".The answer is:aging manifests itself in the form of weakening type diseases termed as age related diseases and a aged human may not necessarily die of infectious diseases (if that is what you mean in the question).The weakening type diseases are inevitable because they involve mass changes at metabolic,cellular and physiological levels.

No that is not possible ever. There is something called telomere which is present in the chromosomes of cell .These Telomere triggers the action of ageging and leads body towards death. When we are in growing age the amount of telemere is very less but as we get older and older the amount of telemere get increases .
The rate of increase of telemere increases with each succesive cell disivision. Hence death is sure no matter what ever you do.

The diseases are only a part of it. Aging is also accidents and such. Cancer would still be prevalent as would accidental deaths. Even a perfect body would eventually fail because individual cell death would lead to organ failure and then death. This cellular death would come from cells failing to commit to apoptosis or from mutations. It won't be possible to live forever, but by using science and medicine, we can greatly lengthen our lives.


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Effect of hemoglobin on colloidal osmotic pressure
If Hemoglobin gets out of RBCs, my book says that colloidal osmotic pressure of plasma increases.
Hence, filtration of fluid across capillaries is prevented.
So the heart increases its work to be able to filter fluid to tissues.
Could someone explain this mechanism for me? simply please!

First:  what is oncotic pressure?

Oncotic pressure, or colloid osmotic pressure, is a form of osmotic
  pressure exerted by proteins, notably albumin, in a blood vessel's
  plasma (blood/liquid) that usually tends to pull water into the
  circulatory system. It is the opposing force to hydrostatic pressure.

"Colloid" can be any macromolecule.  It can be albumin (the normal one).  Immunoglobulins can increase blood oncotic pressure.  Intact red blood cells do too and they can be important in that role.  Blood substitutes using free and modified hemoglobin (loose in the blood not in RBC) also increase blood pressure by reducing fluid filtration across capillaries and keeping fluid in the blood vessels.
Thompson A et al.  Stroma-free hemoglobin increases blood pressure and GFR in the hypotensive rat: role of nitric oxide.  J Appl Physiol (1985). 1994 Nov;77(5):2348-54.
I think of it like rice in a salt shaker.  The rice soaks up humidity because the humidity is attracted to and stays with the macromolecules in the rice.  So too blood full of protein.  The water likes to stay with the big molecules and so stays with the blood.
If you get too much macromolecule in the blood it can increase colloid pressure of blood and raise blood pressure and that can cause trouble.  Maybe a professional bike rider has too high a hematocrit because he is abusing erythropoietin (that would be colloid pressure of whole blood, not just plasma).  Maybe someone has a cancer like Waldenstroms that churns out loads of immunoglobulin (that would be colloid pressure of cell free blood, or plasma).  High blood pressure is what you see in these cases.  I suppose if you infused a rat with too much free hemoglobin blood substitute the same thing would happen.
People with high blood pressure still perfuse their organs.  Filtration of fluid across capillary walls is decreased but the organs do ok.  The converse situation is where people have problems: low colloid pressure allows fluid to freely leak across the capillary walls and people get edematous and puffy.
The situation you propose is a weird one.  A person who has hemoglobin getting out of RBC has hemolysis: the red cells are leaking or blowing up.  Common situations for hemolysis are malaria and sickle cell disease.  Any increase in colloid blood pressure from the free hemoglobin is balanced by a decrease in colloid blood pressure because the red cells are gone.  Congestive heart failure is not a problem with persons who have sickle cell crises or malaria unless they become super anemic which is rare and involves a different mechanism.
Not simple; sorry.  But it would be easier to be simple if this actually happened (the free hemoglobin making heart work harder) and it does not.
No offense but maybe you have it wrong?  Maybe take a photo of the text you reference and edit your question to add it (that little box with the mountains and moon will let you add a picture).  Or type it in as you see it?


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What vitimins are there?
What vitimins are there and why and what are they?
they do appear in apples and other fruit but just how many are there

Vitamins are compounds that the body needs to function. They are similar to minerals but differ in the fact that Vitamins are organic and minerals aren't. There are 6 vitamins (A,B,C,D,E,K) but many are suffixed with a number, like B12 or D3. They can be found in fruits and vegetables, as well from meat or other sources.
In total, there are 13 different amount of vitamins that humans need in some amount to function:
A, B1, B2, B3, B5, B6, B7, B9, B12, C, D, E, K

thanks jacob. i need this for a project or writing informal language one

You do not appear to have read the guided tour and I imagine also not how to write a good answer. Your answer provides no evidence in its support. This is essential for anyone to judge whether or not it is correct. In fact, the statement "There are 6 vitamins...but many are suffixed with a number" is nonsense. For example Vit B1 (thiamine) and Vit B12 (cobalamin)  are completely different chemically and functionally.


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Common stains for fungal microscopy
I recently got a light microscope to start exploring microscopic features of fungi (and to explore microscopy in general).
What are some of the most common and easily available stains used when preparing microscope slides for fungi? Which situations are they each best for?


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Why can't primary RNA be used as a direct template for a protein?
Why can't primary RNA be used as a direct template for a protein

Please explain what you mean by primary RNA. This is not a standard term in molecular biology.  Preferably add a reference or quotation so it is quite clear. Also, what do you mean by "Why"? Mechanistically or philosophically/logically?

"Primary RNA transcript" is a well known term in molecular biology. OP may have forgotten the "transcript" at the end, but it is quite obvious to me what they are asking.

@GerardoFurtado then you might want to edit the question for the rest of us.

@GerardoFurtado I think half the problem with bad answers on this site is unclear questions. This is bad in many ways. Not only those I have indicated, but also that the poster has shown no evidence of having tried to solve this himself as described in the help. Furthermore, if he is asking about eukaryotes and his question is "why exons?" (philosophical) then he should have searched the site. The question would be a duplicate.

@a.baldwin Is this question about alternative splicing? Similar to the other commentators requests, please edit so no-one on SE has to guess what you are asking and you shall get answers :)


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Condition for a genetically modified group of cell to remain and to spread?
I was wondering: when a treatment modifies a group of gene (like in gene therapy), what makes a group of cell remains?
I mean, when a cell divide itself to create new ones, if a cell was initially genetically modified, it will lead to two modified one, right? But, I assume that we have a finite number of cells in our body, so if the process was going on like that, we would just have to modify one cell of our body. But, besides this, the other cells divide themselves too, so there might be something that makes a group of cell dominant (like the proportion, the number of neighbors of one cell...).

So, my question (cut in three) is:

What are the conditions for a group of modified cells to remain?
In what extend the modification can spread?
If it can't spread, why?

(I'm not a biologist student (I studied it in high school, so I may be able to understand the basics), but I'm interested in making a mathematical model of such a process. So if there is an answer, could you make it understandable for someone who has only the basis?)


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What is this insect that showed up after I left food out? How can I get rid of it?
These bugs showed up after I left some food out. I noticed a significant reduction after I cleaned up my place, but now they're back again. They're pretty small, but can you guys help me identify these bugs. I need to look up how to get rid of them.
I live in the Midwest.
I realize the quality is not the best.

What kind of food was it?

It looks like it could be some type of fruit fly.  Without clearer pictures it would be difficult to say what kind.

I don't recall, it was a long time ago. It seems to like my trash can very much.

@Kurt Uploaded a clearer pic

It is likely a fruit fly, a Drosophila melanogaster.

I've tried different methods to trap then but the most effective way I found is this. You need a container (pan, jar, bowl, whatever), vinegar (I use any type), a drop of dish soap, and plastic wrap over the top with holes poked in. Then the flies cannot stand on top of the liquid but also have issues escaping through the holes in the plastic wrap.

If it looks like the picture below it is some sort of fruit fly.  I've also attached a link telling how to get rid of them.


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Where does my extra blood volume go after giving birth?
I'm pregnant. I've learnt that during my pregnancy my blood volume will increase by 50%. https://www.ncbi.nlm.nih.gov/m/pubmed/4075604/
So I'm wondering, what does my body do to decrease my blood volume after I give birth? Where does all that extra blood go? I would imagine I lose some during labour, but I seriously doubt it's all of it.

The extra volume of fluid is due to the fluid retaining effects of high oestrogen secretion in a pregnant human female. After this high level of oestrogen subsides the extra fluid is mainly eliminated as:

urination
some is lost during parturition (labour)
lactation to some extent as well

Reference:A Textbook of Medical Physiology (South Asian Edition) Guyton and Hall

Note that this process can take some time, and in the meantime you may see some of that extra fluid show up as edema. My ankles stayed trim throughout my entire twin pregnancy, but swelled up to twice their normal width within a day of delivery. Also, you'll continue to bleed (like a heavyish period) for a couple of weeks after delivery.

The actual blood cells just get circulated out over time (e.g. broken down in the spleen). Eliminating the fluid is the easy part - consider how easy it is to drink a liter of water, absorb it and add to your plasma volume, and then filter it straight back out through the kidneys in a matter of an hour or so.

The other answer elaborates on how the fluid leaves the body, but completely glosses over what happens to the blood cells. I suggest elaborating on how the fluid leaves the body.

You phrased that very nicely.


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Why are there no large animals with chloroplasts?
Mitochondria and chloroplasts display similarities with bacteria that led to the endosymbiont theory. This theory states that an early ancestor of eukaryotic cells engulfed an oxygen using non-photosynthetic prokaryotic cell. Eventually, the engulfed cell formed a relationship with the host cell 1n which it was enclosed, becoming an endosymbiont (a cell living within another cell). Indeed, over the course of evolution, the host cell and its endosymbiont merged into a single organism, a eukaryotic cell with a mitochondrion. At least one of these cells may have then taken up a photosynthetic prokaryote, becoming the ancestor of eukaryotic cells that contain chloroplasts.
So my question is,  why is it that all the cells that took in the chloroplasts became plants or other simple animals but not large mammalian or reptilian animals?  Is there a limiting factor that restricted chloroplasts from being beneficial to large animals? Why is it that large plants can have both chloroplasts and mitochondria but not relatively larger animals?

"cells that took in the chloroplasts became plants or other simple animals" -- what does this refer to?  I am not aware of any animal (metazoa) species whose cells contain chloroplasts? There are symbionts like Elysia chlorotica that ingest algae and have adapted to make use of their chloroplasts for photosynthesis, but that seems quite different. Perhaps by "simple animals" you mean protozoa?

I'm no expert in evolutionary biology...but I suppose that it could be because of the higher energy needs in plants than animals.The plants have several more biochemical pathways than many larger animals so to maintain so many enzymes there must be more energy needs.And altogether its disadvatageous,perhaps it saved them from the intense competition during biogeny.

There are no animals with chloroplasts.

I believe the gist of it is that chloroplasts simply cannot create enough sugar from photosynthesis to significantly power the energy-intense needs of any but the simplest of animals. Consider that plants maximize their surface area to the extent possible for a living organism, and still only have enough energy to grow and reproduce - movement is essentially impossible.
Here's a pretty good article I stumbled across a while back:
http://blogs.discovermagazine.com/notrocketscience/2012/09/18/will-we-ever-photosynthesise-like-plants/

Venus fly traps manage to move pretty well, though I imagine you mean move from place to place. However, you haven't given any evidence that plants' lack of movement is because of a lack of energy. One might instead posit that plants don't move because they "chose" to get their water supply by fixing themselves into the ground. And perhaps plants could make a trade-off and grow a little less to free up energy for moving. For example, small trees seem to do just fine until they get surrounded by taller trees that block out their light.

Venus fly traps can only move a few times before they wear out, it is useless for movement.


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What is continuous selection?
I've been reading paper on ancient horse genome (Recalibrating Equus evolution using the genome sequence of an early Middle Pleistocene horse) and in abstract authors mention term continuous selection:

We also find evidence for continuous selection on the immune system and olfaction throughout horse evolution

Can someone please explain what it means? What is continuous selection? Is it selection without interruptions, but what are those interruptions?

Continuous selection is not a term; it would not be bolded in a textbook.
When studying the history of a genome/lineage, you could have two very broad hypotheses about a given trait:
1) The trait was not present in a lineage, then appeared fairly suddenly (at least on a long time scale, it could still be hundreds, thousands, or millions of generations), and since then did not change much.
2) The trait was not present in a lineage, then the trait appeared in part of that lineage, and since then, the trait has continued to change substantially among different descendants of that lineage.
You could find evidence towards (1) if, for example, you observe a trait that is fairly constant among a diverse modern taxon but you don't see a similar trait in the cousins of that taxon.
You could find evidence towards (2) if you see a lot of diversity even among recently speciated members of a taxon.
The statement in the article is just saying in plain English, rather than using a scientific terminology, that they see evidence towards (2).

I don't think it means anything more than repeated occurrence of the selection of the prefered traits.
A trait vital for survival will always be exposed to stronger evolutionary pressure. Even if the trait is good there will always be room for improvement.
It can be seen in contrast with the introduction of a radical improvement with the introduction of a new genetic mutation. This will probably happen only once until the entire gene pool is updated.

As far as I know this is not a precisely defined technical term, and there's not a huge amount of additional detail in the paper. Here's the sentence from the paper that seems to correspond to the highlighted phrase in the abstract:

Finally, we identified loci potentially selected in modern horses (Supplementary Figs 11.1–11.2), focusing on regions showing unusual densities of derived mutations (Supplementary Information, section 11.1) ... Functional clustering analyses revealed significant enrichment for immunity-related and olfactory receptor genes (Supplementary Table 11.4), two categories also enriched for non-synonymous single nucleotide polymorphisms (SNPs) (Supplementary Information, section 5.2d).

And from the supplementary information:

We used quartet alignments including the donkey as out-group, one ancient horse
  and two modern horses in order to scan for genomic regions where the two modern
  horses shared unusual accumulation of derived alleles. Those could represent
  regions where alleles reached fixation faster than the rest of the genome, as a result of recurrent positive selection along the modern horse lineage or more recent selective sweeps, possibly in relation to their domestication. ... Comparing genomic scans performed with our ancient genomes enabled us to
  dissect selection regimes at two time periods predating the tMRCA of modern
  horses.

As far as I can tell without spending much time reading the paper and supplementary methods much more carefully, the authors are comparing sets of genes that differ between between two ancient horses and the modern horse in order to determine what changes occurred during different time periods e.g. between ancient horse 1 and ancient horse 2 or between ancient horse 2 and modern horses), and are concluding that in fact changes occurred approximately equally in all periods ("continuously") rather than early vs. late.

In this picture DK is the donkey  (out-group), TC21 and CGG10022 are two different ancient horses, and M1 and M2 are modern horses.


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Why is the rough ER necessary to make extracellular proteins?
It is my current understanding that free ribosomes synthesise proteins to be used inside the cell, and the rough endoplasmic reticulum is necessary to make proteins that are to be secreted by the cell. Is this correct - and more importantly, if so, why?

Please do some research before posting questions and demonstrate that you have done so in your question. This is basic material that can be found online and in standard biochemistry textbooks.

While the default textbook will likely cover co-translational transfer of nascent proteins into the ER (which topologically corresponds to the outside of cells), there are also other mechanisms that apply to some proteins and don't necessitate rough ER ( https://en.wikipedia.org/wiki/Exosome_(vesicle) )

Ahhh I did search for a while and found nothing (in terminology could comprehend anyway) and don't own a biochemistry textbook as I am not doing a biochemistry course

Cell Biology books also cover this. You need to buy books if you are studying. Sacrifice other things, but buy books. However you could have answered this question on the web using NCBI Bookshelf, which has older editions of some excellent texts, including Berg et al. Biochemistry, Alberts et al. Molecular Biology of the Cell, and Lodish et al. Molecular Cell Biology.  Searching for Endoplasmic Reticulum brings up a list, which includes these three books, which you can then consult. Learn to save your own life.

I did research the question online beforehand - however perhaps the wording of my question brought up other results? I could find nothing that would help me when I searched. In the future, I will use that website as I've used it a couple of times (when it came up after a search) and it was very helpful

Extracellular proteins are proteins that function outside the cell, meaning they are made in cells (transcribed from ribosomes) and then are transported to the plasma membrane to be delivered to the extracellular space. The proteins that need to be secreted aren't secreted as free proteins, rather they are packaged into vesicles. Vesicles are membrane-enclosed structures. When ribosomes are translating mRNA and come across a specific sequence called a signal peptide (wiki), the ribosome goes to the ER and delivers the peptide into the ER. From here, the peptide gets packaged into a vesicle-- first a membrane budding off from the ER.
 source(NCBI)
This is also how secretory proteins get into the Golgi, by vesicle trafficking. From the golgi, proteins are packaged into vesicles. It is a hotly debated topic whether proteins are sorted into specific vesicles or proteins within vesicles (that do not belong in that vesicle) are sorted away (and degraded by the lysosome).


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Can proteins structure change depending of alimentation of an organism?
In my understanding protein are built using information caring by RNA. So a given protein should always have the same structure in a given organism has the DNA of this organism does not change.
I'm asking this question because peoples told me that "cow milk protein become longer because how we feed them today". But I don't understand how a protein can become longer or shorter.
Info: I have no background in biology. I do not try to solve a problem, but simply have a better understanding.

Hi gagarine, to me, for this question to be reopened it would at least require a more solid basis than "people told me". So, if you can cite some paper or news report or something like that at a minimum, it could direct someone to what exactly your question is about versus what is getting transformed between what you heard and what you translated that to write in your question (like a game of telephone).

@BryanKrause thanks for the pointer. Jill Hoyt mentioned it was a hot topic in the 90s, and certainly taken in the mainstream, there is a bit of history there and "legend". Removing altogether the "people told me" part would be ok also?

While it is theoretically possible for a protein to change size (based on length) because of nutrition, I don't think that's happening here.
You are right-- DNA encodes information that is transcribed to RNA which is translated into proteins. Proteins are made of a finite number of amino acids, which are the building blocks of proteins. Proteins can be modified (and can be cleaved to make the protein shorter), but I think this claim of "cow milk protein becomes longer" is a misunderstanding because there is not a single "cow milk protein", but rather many.
There are many different proteins in cow milk, and most of them are casein proteins. source
The milk protein likely at the root of this claim is beta-casein. It was a hot topic in the 1990s, because there are a dozen different variants of this beta-casein protein. Two of these variants are the most common in milk have been studied a lot: variant A1 and A2. The only way these are different is a single amino acid change at amino acid position 67 (remember that proteins are made of amino acids). Variant A1 has a histidine amino acid but variant A2 has a proline. What does that mean? That means that A1 can be cut (in your body) to produce a smaller protein bit (called a peptide). Because of the proline in the A2 variant, it cannot be cut like the A1 variant. The peptide resulting from the A1 getting cut is called BCM7.
In short:
beta-casein variant A1: can be cut to produce BCM7
beta-caesin variant A2: gets cut way less than A1 so way less BCM7 is produced.
So, what is BCM7? It had been reported to been linked to some different diseases but the European Food Safety Authority (EFSA) published this report which concludes that there is no link between BCM7 and non-communicable diseases. Despite this, there is still a lot of talk about A1 vs A2 in the dairy community. While websites such as this appear compelling, remember the EFSA report!
this paper is open source and has the information about these variants that is summarized above.
So what does all this have to do with "cow milk protein" changing size? Maybe more cows used as dairy cows have the A2 variant, which would not produce as much BCM7 (the small peptide). Since A2 is not cleaved to produce BCM7, it could be thought of as "longer"... at least relative to only a few thousand years ago.
The beta-casein A2 variant is thought to be the original version of beta-casein from undomesticated cows.
So, if this claim was originally about beta-casein, you can respond that "yes, the beta-casein protein can be thought of longer because it is not cut to produce the BCM7 peptide as much as the A1 variant is, but it is also the original beta-casein size." Whether it was 10,000 years ago or just now, the A2 beta-casein variant is the same size.
tl;dr / Good reading from the California Dairy Research Foundation.

Variation of components in milk related to different factors. Again, it's not about changing the protein structure depending of alimentation. https://extension.psu.edu/milk-components-understanding-milk-fat-and-protein-variation-in-your-dairy-herd

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Can humans distinguish light having the same color but different spectrum?
Can humans distinguish light sources that have the same color in RGB space but having different spectral composition?
I know one method, that is when the light is producesed by monochromatic laser, it looks "grained" due to interference, but this is a shape-based indicator. What about indicators not based on the visible shape, just on color perception?

flagged as "unclear what you are asking". Can you define difference between color and spectrum of light?

If by "same color in RGB space" you mean "activates human cones the same way" then the answer is no: color perception is based on the ratio that different cones are activated at. There is no difference between a spectrum that has a smooth distribution across wavelengths or one that is properly calibrated into three or more specific peaks.
This concept is why RGB monitors and TV screens work to produce just about every color (though there are of course limits to the spectrum that a RGB monitor can produce, but that is a technological limitation).

Yet, no electric lighting can emulate sun's light convincingly...

That's a completely different issue.

The "spectrum" of light refers to the relative power at each wavelength in the range of wavelengths of concern, in this case the visible wavelengths.
"Color" refers to the way we perceive various mixtures of wavelengths of light (that is, how we perceive the spectrum of light).  Most human beings have three types of light receptors (rods) in their retinas that respond rather broadly to three different overlapping ranges of wavelength (Short, Medium and Long) centered around 440 nm, 540 nm, and 575 nm.  Our brains receive neural impulses from the rods and interpret them to provide a perception of color.
The important point is that with only three types of receptors, our eyes are not able to distinguish the whole spectrum.  Our brains really just report the ratio of stimulation of the three different types.
OK, that's all background info.  I think the core of your question boils down to "Is there a way we can use our eyes to really perceive the spectrum of light?"  If there are no constraints, the answer is "yes".  For example, you can look at a light source through a prism or a diffraction grating, and it will let you see the whole spectrum. Each point of light will be spread out into a rainbow line, where each position along the line corresponds to a different wavelength of light.  There are other, more complicated ways, too.  If you would like to experiment with a diffraction grating, you can get one from, e.g., Edmund Optics.


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R nought calculation ( SIR model)
1 person gets bitten by 9vectors /night, the vector transmits the pathogen to 0.035 new hosts. Duration of infection: 9.5 months.What is R0?
I am struggling with this question for ages as I would  just multiply 9*0.035*9.5 to get R nought. However I was given a formula to use R0= βS0/v+µ+γ  but I don't know how to use because I don't get what I should.
Thanks for the help!

With $R_0$, you get $R_0$ and it looks better than "R nought"

"I don't get what I should" - what do you get? This sounds like a 'homework' question - which is fine, but you have to explain what you've attempted better so we can work out where you're going wrong.

$\newcommand{\rzero}{\cal R_0}$
If this is a vector-borne disease we don't really have enough information to compute the full $\rzero$ value (i.e. expected number of infected vectors caused by a single infected vector in an otherwise disease-free population), but we can compute a "vector-to-host" $\rzero$ (expected number of hosts infected by a single infected vector). The biting rate seems to be superfluous information unless your "vector transmits the pathogen to 0.035 new hosts" is supposed to be "infected vector has a probability of 0.035 of transmitting disease to a host it has bitten".
What are you "supposed to get"?
The formula you've given, $\rzero = \beta S(0)/(v + \mu + \gamma)$, is more generally applied to directly transmitted diseases, where

$\beta$ is the transmission rate (number of effective contacts per susceptible host per infected host per unit time) $\times$ probability of transmission
$S(0)$ is the population density
$v$ is the recovery rate
$\mu$ is the natural mortality rate
$\gamma$ is the disease-induced mortality rate

The 9.5 months is likely to be a host infection time (most biting vectors don't live that long).
Notation does vary somewhat, though.
For a vector-borne disease I would write $\rzero$ as
$$
\frac{m a^2 bc}{r \mu}
$$
where $m$=number of mosquitos/host; $a$=bites/time on host; $b$=mosquito to human transmission probability; $c$=human to mosquito transmission probability; $r$=human recovery rate (disease duration=$1/r$); $\mu$=mosquito mortality rate (mosquito lifespan=$1/\mu$).
Google Books link


text:
How come our thyroid glands don't suffer awful mutations (or do they)?
I was listening to a lecture by my Biology professor and he said that the thyroid gland contains radioactive Iodine which can break down and create reactive Oxygen species (because ionizing radiation from the Iodine interacts with water in the human body).
So, shouldn't the thyroid gland suffer awful double-stranded chromosomal breaks constantly? Shouldn't we be suffering mutations in the thyroid gland all the time?
Thanks!!!

Radioactive does not mean much in and of itself, your bones are radioactive (potassium), just being radioactive is not enough to do any damage.  It needs to be the right type of radiation and have high enough intensity before it can start damaging DNA and thus cause cancer. Second the amount of iodine in the body is miniscule, the aforementioned radioactive potassium in your body is orders of magnitude larger (if there is any radioactive iodine present at all which is unlikely).
On top of this remember we are surrounded by low dose radiation all the time so our bodies have evolved ways to handle minor damage.http://imgs.xkcd.com/blag/radiation.png

The thyroid gland contains iodine, but is usually not radioactive. In the contaminated area, it can adsorb radioactive iodine, which would lead to a health danger. In such circumstances, pills with non-radioactive iodine are prescribed as a preventive measure.


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What is the purpose of DMT in plants?
N,N-Dimethyltryptamine (DMT) is found, besides humans and other animals, in many plants(50+).
In humans (in the pineal gland) it is suggested that it is used for our immune system.

Immunomodulatory activity may contribute to significant anti-inflammatory effects and tissue regeneration. [Wikipedia]

The question is, could it have a same function in plants or it has a more defending function, like other drugs that are derived from plants?

As you guessed, tryptamine alkaloid biosynthesis is generally associated with herbivore deterrence in plants (see e.g. paper 1, paper 2, paper 3), as these compounds can be toxic to animals. I wasn't able to find a reference specifically related to DMT, as it is only one of a family of tryptamine derivatives. For example, the papers just linked to shows that expression of an enzyme catalyzing the creation of the tryptamine precursor of DMT is associated with lower herbivory by insects and nematodes. The second paper also shows that this seems to have little to do with plant morphogenesis via the auxin pathway, which was an alternate hypothesis for herbivory deterrence.
The papers also include a little speculation about the mechanism by which DMT inhibits herbivory on the animal side; it seems to come down again to animal toxicity and behavioral alteration.
So, as with other cases, likely the reason that plants express many secondary metabolic compounds is the same reason that humans use them, namely that they can have strong physiological effects on animals. But I wasn't able to find literature specifically about DMT in plants.
Hope that is helpful.
Update: found an entomology paper that goes into more detail about the effects of a variety of tryptamine derivatives on leaf-cutter ants. The compounds are toxic, but also there are some interesting insights about effects on insect behavior.
Update 2: Looking at question again, realized that I didn't address immune system response.
What's important to note is that plants don't have something homologous to animal immune systems, e.g. antibodies and so forth. They instead substitute various chemical responses, many of which are mediated by signaling factors such as jasmonate and salicylate, that have strong effects and sometimes e.g. kill off pieces of infected tissue (sort of a scorched-earth strategy). This part of plant biology is quite complex and bears further reading.
So in this sense, yeah, sure, tryptamines could be thought of as an immune system, in that their production facilitates resistance to their biotic environment. But that mechanism is completely different from any immunomodulatory effect of DMT or similar compounds in humans.

Just pointing out that there is no evidence that endogenous DMT in humans is produced by the pineal gland.    There has been much speculation, but the few studies that have measured DMT in human tissues showed the same very small amounts whether or not the pineal gland was included in the sample.    The wikipedia entry for DMT expounds on this..
In any case the amount found in these human assays was far below the amount needed for psychoactive effects.   Anyway, I hope this was helpful, six years later :)

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Entropy increase or decrease in an reaction
My question is how would you tell if the product of an reaction has more or less entropy than the reactants?
For example, in glycolysis, when glyceraldehyde-3-phosphate becomes 1-3 bisphosphoglycerate, BPG has less free energy and more entropy than G3P. Anyone able to give me a rundown as to how you would know? Thanks in advance.

The way you have formulated your question contains a major error. You can talk about the change in free energy or entropy in an overall chemical reaction, and entropy is not an intrinsic feature of a molecule but of the system as a whole. That said, an answer to your question on meauring entropy can be found on SE Chemistry, here..

@David I understand that, however the question was phrased like that on a test, as in which molecule (product) has a higher entropy than their reactants, in a chemical reaction. I know the entropy in terms of a system, but was just wondering if anything applies to a specific molecule. Thanks though.

I must say that in biochemistry the emphasis is on the free energy change of reactions. I am not sure, but imagine that there is generally considered to be no change in entropy of the molecules, unless one is considering the environment (hydrophobic or hydrophilic) or whether a polymeric chain is ordered or not (as here).


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Can bacteria only thrive in agar solution?
In petri dish, agar is most commonly used for culturing bacteria. So is there any other easily obtainable food sources for culturing bacteria.

This is the third question you have asked in a short space of time without showing any evidence of having made an effort to find an answer yourself. I have voted to close on this basis.

You seem to have some misconceptions about growing bacteria. These are cultivated using specific media, for E.coli this is usually LB Medium which contains the following ingredients per liter:

10g Bacto-tryptone
5g yeast extract
10g NaCl

This is dissolved in water and subsequently sterilized by autoclaving. Note that there are much more medium recipes for different strains and different culturing conditions.
Bacteria can then be grown either in suspension (shaking in an Erlenmeyer bottle in the liquid media) or on the surface of plates. To produce these plates, you need an agent, which solidifies the medium without having any effect on the growth of the bacteria or the medium. And this is where the Agarose is used. It can be heated up with the medium during sterilization, does not interact with the medium and bacteria do not metabolize it. If you cultivate bacteria, which produce agarase (which is an enzyme to break down agarose), you need to use a different agent to solidify your medium. And you will use a different medium anyways.
They simply grow on the surface of the solified medium and can easily be picked for further analysis or the inoculation of (bigger) liquid cultures.

Gelling agents from natural sources: agar, carrageenan potassium salt, Eladium, gelatin, gellan gum, guar gum.
Agar is not always just a gelling agent. About 100 marine bacterial species are known to utilize agarose; these bacteria produce agarase, an extracellular enzyme that degrades (liquefies) agarose; for example, Aliagarivorans marinus, Aliagarivorans taiwanensis, Algibacter agarilyticus, Algibacter agarivorans, Alterococcus agarolyticus, Aquimarina agarilytica, Aquimarina agarivorans.

Given the origin of agarose from algae, this is not a surprise to find this enzyme in marine bacteria.


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Speed of Brain Waves
Given that brain waves are characterised as such by virtue of the wave-like properties of 'electrical activity' in the brain, what is the speed of such waves; and how does it differ from neural conduction rates in peripheral nerves ordinarily in the range ~50 cm/sec.  (Oddly I have had difficulty locating an answer to this question elsewhere).

Unfortunately the term "wave" is ambiguous in neuroscience. What you are referring to, alpha waves, only means that neuronal activity tends to oscillate at about 10Hz. Neural oscillations are a widespread phenomena occurring in all brain areas. But it doesn't necessarily mean these waves travels. There are examples of traveling waves, whose speed can vary a lot (from $10^{-1}$ to $10^{-5}\ m.s^{-1}$ depending on the studies). Oscillations across brain areas tends to be synchronized during a task (so one could argue, infinite speed), and within area activity tends to hold a specific phase relationship which varies spatially (as if a wave was "frozen", in which case its speed would be 0). Traveling waves and neural synchrony/coherence might be different phenomena implementing different functions. It is still unclear what brain oscillations are for, or even if they have any purpose at all. Below are some reviews on these topics.

Ermentrout, G.B. and Kleinfeld, D. (2001) Traveling electrical waves in cortex: insights from phase dynamics and speculation on a computational role. Neuron 29, 33–44
Sato, T. K., Nauhaus, I., & Carandini, M. (2012). Traveling waves in visual cortex. Neuron, 75(2), 218-229.
Engel, A. K., Fries, P., & Singer, W. (2001). Dynamic predictions: oscillations and synchrony in top–down processing. Nature Reviews Neuroscience, 2(10), 704-716.
Fries, P. (2005). A mechanism for cognitive dynamics: neuronal communication through neuronal coherence. Trends in cognitive sciences, 9(10), 474-480.

It of course quite depends on which waves you are studying. One cool recent example from the Sejnowski group at the Salk Institute show these circular brain waves occurring during sleep, which complete within ~70msec travelling a loop of ~30cm... http://www.salk.edu/news-release/princess-leia-brainwaves-help-sleeping-brain-store-memories/ (Original paper: https://elifesciences.org/articles/17267)

Consider the simple case of 'alpha waves', with a frequency ~8-12 Hz.  What is the speed of propagation within the brain and presumably in its 'white matter'?.

@jeremiah See the answer by baca - when people refer to "brain waves" they are talking about oscillations in a recording, they are wave-like in time, not necessarily space. If they travel in space, too, that's a separate property.

@jeremiah That's right, as baca and Bryan have explained, these 'alpha waves' to which you refer are activities within a frequency band recorded from collective ensembles of neurons (e.g via EEG) where these oscillations might indicate a degree of coherence in a population.  The circular brain wave I mentioned above I thought was one of the better examples of a wave I could find (in a more normal sense of the word) where excitation spreads through space and a speed could theoretically be calculated.

Excellent and very helpful answers.  My interest is more in the spatial aspect, or I suppose, the co-ordinated relation in sequential activity between or within areas of the cerebrum--but is at this stage still ill-informed.  The implication of pyramidal cells seems interesting.

@jeremiah Yes, the coordination of waves throughout the brain is fascinating. You asked a good question and I wish I could have provided you with more well-studied examples.


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"50% of the variance in antisocial phenotypes is the result of genetic factors" means what?
How can i understand the following sentence:

Overall, the conclusions reached by these studies have been highly consistent in showing that approximately 50% of the variance in antisocial phenotypes is the result of genetic factors.

Is it saying genetic factors have a weight of 50% in the total influences on antisocial behaviour?
Source: "Natural born killers: The genetic origins of extreme violence" by Christopher J. Ferguson , Kevin M. Beaver

In a population the phenotypic variance can be caused by several underlying variance including the variance in the environment and the genetic variance (among others). The fraction of the phenotypic variance that is caused by the genetic variance is what we called the heritability in the broad sense. The fraction of the phenotypic variance that is caused by the additive genetic variance is what we called the heritability in the narrow sense.
So the sentence

50% of the variance in antisocial phenotypes is the result of genetic factors.

can be rephrased as

Antisocial phenotypes have a heritability of 0.5.

The concept of heritability is useful as it gives us an idea of how well selection can act on the changing the frequency of phenotypic traits in the population (see How to interpret the breeders equation?). Please have a look at Why is a heritability coefficient not an index of how “genetic” something is? for more information.

Let's look at the context surrounding the sentence you referenced.

A rich line of behavioral genetic research has analyzed samples of kinship pairs (e.g., twins) to estimate the proportion of variance in antisocial phenotypes that is due to genetic influences. Results of these studies, which have been based on thousands of sibling pairs, have pointed to the inescapable conclusion that genetic factors are implicated–at least to some degree–in the etiology of violence. Precisely how influential genetic factors are, however, is difficult to garner when examining single studies because heritability estimates wax and wane from study to study based on sample characteristics and methodological differences. A number of meta-analyses (Ferguson, in press; Mason & Frick, 1994; Miles & Carey, 1997; Rhee & Waldman, 2002) and literature reviews (Moffitt, 2005) have thus been conducted as a way of summarizing the findings from these extant behavioral genetic studies. Overall, the conclusions reached by these studies have been highly consistent in showing that approximately 50% of the variance in antisocial phenotypes is the result of genetic factors.

So as you said, he's basically saying that genetic factors influence antisocial behavior.  He's saying that 50% of the deviation from what would be expected based on environmental and social factors can be accounted for by genetic hereditary traits.

Sources:

Aggression and Violent Behavior, Volume 14, Issue 5, September–October 2009, Pages 286-294


text:
What is reaction time of a single c. elegans neuron?
What is the reaction time of a single c. elegans neuron?
Is sensory neuron reaction to stimulus is similar to intermediate neuron passing a signal to motor neuron? What about chemical and electrical synapses?
I want to make a simple real-time artificial network model using existing c. elegans connectome projects, but I can't find anything defining time scale.


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Why does cell differentiation start with the morula?
I suppose that cell differentation has to start by some external symmetry breaking. The first time there are two different types of cells is the morula with roughly 16 cells: there are some 12-15 cells forming the surface of the morula and some 1-4 cells in the interior of the morula. These are exposed to physically/chemically different local environments which might be the initial triggers of cell differentiation.

(source)
Questions:

Is this kind of argument/picture correct?
What are the significant differences in the environments of the outer and the inner blastomeres of the morula that trigger cell differentiation - and how do they do?

(Partial response) You're actually correct that inner vs. outer position is a differentiator, but there's still controversy whether position is a cause or whether differentiation actually happens sooner.

For a long time it has been believed that cells are identical within this ball at least until they take up distinct inside and outside positions, but is this true? A number of studies [2, 3, 6, 7, 8, 9] over the last 10 years involving a variety of markers such as oil-drops, dyes, fluorescent beads and proteins, together has challenged this view. These studies indicated that cells start to develop their identity earlier than expected, before taking inside or outside positions and, importantly, that these differences between cells are significant, as they bias cell fate [2, 3, 6, 7, 8, 9]. This view has not been universally held, however, because differences between the cells were not detected by other groups and so the view that cell fate choice is random was maintained [10, 11, 12]. It was also proposed that the bias in cell fate might simply result from the shape of the zona pellucida surrounding the embryo until implantation [13], an interpretation that has itself been questioned [14]. The random (stochastic) view of development became popular as it seemed to fit more comfortably with the experiments showing that early embryo cells are plastic and can adopt different fates upon transplantation.
The new contribution from Kevin Eggan’s group [1] now further challenges the view that early mouse development is stochastic.

And from a slightly more recent paper:

Drosophila has been found to have a pre-pattern in oocytes and zygotes. Several molecules that act as maternal determinants of the future body axis (for example, bicoid mRNA) are thus localized asymmetrically in both oocytes and fertilized embryos of Drosophila [6]. No such molecule has been identified in the mouse oocyte or embryo, although certain molecular and structural asymmetries have been described in unfertilized mouse oocytes. For example, Par4 protein is asymmetrically localized in mouse oocytes [7], but whether this protein is unevenly distributed among blastomeres after fertilization remains unknown. In addition, transcriptome asymmetry in terms of mRNA regionalization within mouse oocytes and zygotes has been identified, but no such asymmetry was detected between blastomeres within 2- or 3-cell-stage embryos [8]. However, several recent studies suggest molecular differences exist between blastomeres of the mouse embryo as early as the 4-cell stage. These molecular heterogeneities include the level of H3R17me2 and H3R26me2 (dimethylation of histone H3 at arginines 17 and 26, respectively) [9] and the level of Cdx2 expression [10].

Wikipedia also mentions this fact about Drosophila, so for insects at least it seems uncontroversial.

But isn't it received opinion that the first approx. 16 blastomeres are identical? What would "sooner" mean?

@HansStricker: I've added a quote from the paper.

Does this make my question pointless? I guess not, at least not necessarily. It might be the case that "differentiation by inner/outer position" still takes place (maybe modulated by some "pre-differentiation" before)?

One interesting question might be: If the 16 cells of the morula are already of slightly different types: Is there a correlation between inner/outer position and type, i.e. do the cells of the one type tend to be "inner", and the cells of the other type tend to be "outer" blastomeres. Has this been investigated, or doesn't it matter?

Finally: Isn't it a matter of fact, that the outer cells of the morula specialize into trophoblasts while the inner cells specialize into the embryoblasts? And that they do it for "positional reasons"? Internally, the embryoblasts may already be pre-specialized, triggered by random asymmetries of inner structure/distribution of proteins.


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Has the most recent common ancestor of all living birds lived after dinosaur mass extinction?
I wonder if one or more phylogenetic threads of dinosaurs survived the mass extinction.
In other words, are all living birds equally related to any given ancient dinosaur, or do some birds relate more to some ancient dinosaurs while other birds are more related to other ancient dinosaurs?

Birds are theropod dinosaurs

@Chinmay Kanchi: No, they're not.  They're DESCENDED from theropod dinosaurs.  Saying they are is like saying mammals are synapsid reptiles, or that all of them are really just fish :-)  And we can see this by noting that there were many different orders of birds in existence long before the K-T extinction event.

Fish is paraphyletic, but the rest is true. Mammals ARE synapsids when strict taxonomy is respected. Scientifically speaking, Donald Trump is a reptiliomorph, and Vladimir Putin is an eupelicosaur. If you deny that you'll also have to deny that you're a mammal.

I suppose that by the mass extinction, you are referring to the Cretaceous–Paleogene extinction event that happened 66 mya. The Most Recent Common Ancestor (MRCA) of all birds lived about 113.3 mya (early Cretaceous, according to this in oneZoom.org).
So yes, the MRCA of all birds is definitely older than the Cretaceous–Paleogene extinction event. As you said, this also mean that some ancient dinosaurs are/were more related to some extant birds than some extant birds are related.

You (the OP) might not need it but some other readers might need clarification about phylogeny with the post If dinosaurs could have feathers, would they still be reptiles?

That's awesome! According to OneZoom, the following groups independently survived the Cretaceous-Paleogene mass extinction INDEPENDENTLY: ostriches; [cassowary, tinamou, moa, etc]; [waterfowls, magpie geese]; screamers; gamebirds; [sunbittern, kagu]; oilbirds; potoos; nightjars; frogmouths; [hummingbirds, swifts]; tropicbirds; [flamingos, grebes]; [sandgrouses, hoatzins]; [pigeons, doves]; [cranes, rails]; [bustards, floricans]; [some cuckoos, roadrunners]; [other cuckoos], turacos, [herons, shearwaters, pelicans, penguins, albatrosses, etc].

That's absolutely amazing! Earlier I thought that a single Jurassic Park-like feathered dinosaur survived the extinction and evolved into birds, but it turns out that before the dinosaur extinction birds were already very diverse!

Of course, I enumerated the groups using names of modern representatives of the groups, and 66M years ago their ancestors might have looked differently and maybe more primitively, but they were already birds (almost?) as we know them today! All those monophiletic groups of dinosaurs-birds were already established, whereas ALL human ancestors were tiny lemur-like creatures. O_O

What was the largest bird that survived the KPG boundary and did any flightless birds do do? cool topic Remi and Andrey. From the other topic Remi, i didn't find evidence that less compact genomes can evolve more efficiently. It was an logic from lessons prior to sequencing.

I've read that all modern flightless birds are relatively young groups. All of them used flight to spread across the globe before they decided to walk. It could have happened before K-Pg, though.

I'm not sure I follow the conclusion: "this also mean that some ancient dinosaurs are/were more related to some modern birds then some modern birds". What do you call "ancient dinosaurs"? If you mean that every lineage of birds that got extinct during the C/T crisis should be called "ancient dinosaur", why not, but I find this a bit unusual.

By "ancient dinosaur" I meant any member of the clade dinosauria who went extinct before/during K-Pg.

@lolmaus-AndreyMikhaylov By your definition, there indeed are lineages of birds more related to some "ancient dinosaurs" than others, but we would probably call these particular ancient dinosaurs "birds" without much hesitation. I find it not particularly notable that some lineages of birds got extinct before the crisis. This does not make things that we intuitively call "birds" non-monophyletic, for instance.

@bli of course, as you say is right. Bird is still a monophyletic clade. The only point is that some of the birds lineage already existed before the K-P extinction. You can call them ancient dinosaurs if you want. As all birds are Dinosauria, all modern birds as well as those ancient birds are all Dinosauria. That's all. See eventually If dinosaurs could have feathers, would they still be reptiles?


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Where does the initial action potential come from?
When talking about action potentials we say that previous neurons caused an action potential in this neuron and that this neuron's action potential caused the same in further neurons.
But what is the origin of the first-ever action potential?
Maybe in a living organism, there are no action potentials initially because the brain is always "on" and some part of the brain can always initiate processes in an other. If that is the case then how is the brain turned "on" initially? If not, then how does the first action potential get triggered from the "resting state"?

The very first evoked spike is most likely triggered by spontaneous activity, as even neurons with no synaptic connections are able to fire action potentials (Luhmann et al. 2016). Later in life neurons can be excited by the external environment through sensory stimulation. At some point the central pattern
   generators also mature and, either by network synchronization or tuning of intrinsic neuronal properties, are able to maintain a self-sustained activity pattern.
The question is then what triggers spontaneous activity during development? It has to do with calcium signaling, both exogenous and from internal stores. The exogenous trigger is paracrine release of GABA and glutamate before the formation of synapses (Rosenberg and Spitzer 2011).

The first spikes are typically from sensory organs and arise from depolarization of the sensory cell by an external stimulus. This can happen in many different ways, but common for all sensory cells is that there are specialized ion channels that will open in response to the right stimulus (termed the adequate stimulus). Chemoreceptors, involved in taste and smell, have membrane channels that work in the same way as postsynaptic transmitter channels, except that they are triggered by whatever molecule or modecule-group they are sensitive to, rather than sensitive to transmitter molecules. Binding of the right molecule to the receptor channel (either directly, or indirectly through second-messenger systems) will lead to an influx of typically Ca, causing a depolarizing receptor potential, which triggers the action potential. Mechanoreceptors have membrane channels that respond by opening for Ca-influx simply by the physical deformation of the membrane (through an extremely diverse range of modifications and elaborate support structures). Sound-sensitive receptors, such as hair cells in vertebrate ears, are also mechanoreceptors, stimulated by the motion caused by sound waves. Photo-receptors typically work by second-messenger systems internally in the receptor cell, where absorption of a photon by a suitable photopigment results in a cascade that leads to release of second messengers, such as GTP, which then bind and trigger the opening of Ca channels.
An interesting special case is electroreceptors, found in sharks, many fish and al few mammals. Here the depolarization of the receptor cell is directly caused by the adequate stimulus: the change in the electric field.


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How would our circadian rhythm change over time if we had no sunlight whatsoever?
Of course, over the span of a couple days, our circadian rhythms would lengthen a few hours. But what would happen to the circadian rhythms of humans overall if we had no daylight ever? Say we can live for 10,000 years, how would our circadian rhythm be different 10,000 years from now after zero exposure to sunlight? Would it still be slightly more than 24 hours?

Your question made me curious so I found this study of fossorial species like naked mole rats. With little to no light input from the environment their societies seem to maintain a circadian rhythm: https://www.ncbi.nlm.nih.gov/m/pubmed/11134679/

Say we can live for 10,000 years, how would our circadian rhythm be different 10,000 years from now after zero exposure to sunlight?

Probably almost the same.
A circadian rhythm has - by definition - a free running period of more or less 24h. Of course this might change over time, but 10,000 years are not very much on an evolutionary time scale.
As an example there are some studies about the circadian clocks of fish that have lived in underground caves for over 1 million years: They still have a circadian rhythm (even though its doesn't react to light anymore), but even after 1million years the free running rhythm only changed from 24h to 47h. Interestingly it can also still be 'entrained' (synchronised) to other regular cues like feeding time (this is also the case for normal circadian rhythms).

Blindness has the same effect as a total and permanent absence of light: it causes an abnormal melatonin onset, and, consequently, circadian desynchrony and increased wake times. To preserve the circadian rhythm, administer melatonin (dosing and timing matters).
In sighted individuals, artificial light at night disrupts daily rhythms and suppresses nocturnal melatonin production by the pineal gland. This observation could be exploited in your hypothetical scenario: to preserve the circadian rhythm, substitute the missing sunlight by artificial light (dosing and timing matters).


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Function of Smooth Muscles in the skin
I understand that the overall function is voluntary movement, but is it the same in the skin? Is the main function in the skin movement or is there a greater function? Could anyone could provide this information or at least recommend a site that could help me with this research, as I have been searching and I haven't been able to find the answer?

Smooth muscle in the skin actually produces very little motion.  They are found in special places, such as the areolas of the nipple, the tunica dartos of the scrotum, and also around hair follicles.
Smooth muscles that surround hair follicles give you what is known as goosebumps - they contract all together, creating a bump in your skin around the hair follicle.  This can happen when you're cold, scared, or experiencing strong emotion.

Sources:

Skin Tissue Engineering and Regenerative Medicine, Justine Fenner, Richard A.F. Clark, 2016; Chapter 1


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The membrane folds of dendritic cells
Dendritic cells have a larger surface area due to extended dendrites (membrane folding into itself). Do other mammalian cells (with functions other than immunological) present these membrane folds?

Yes, these include:

neurons
melanocytes
Merkel cells

In all cases, as you suggested, their function is to extend the surface area of the parent cell. In the case of neurons, the role of dendrites, which receive the vast majority of synapses, is to maximise the number of synapses the cell receives from different pre-synaptic partners (Chklovskii et al. 2002, Chklovksii 2004). In melanocytes, they are used to transfer melanin to keratinocytes. In Merkel cells, they are again used in order to form synapse-like connections with neurons (Mihara et al. 1979).
The word originates from the Greek δένδρον, which means 'tree'. Dendritic structures are found throughout in nature, including in...trees, where presumably they are used to maximise exposure to sunlight. Theoretical studies on the formation of dendritic arborisations in neurons indicate that they are governed by at least these factors: i) repulsion between dendrites (Wen et al. 2009), ii) minimisation of dendritic volume used (Tamori 1993), possibly through resource competition (Graham and van Ooyen 2004). It is an intuitively attractive idea to think that similar processes govern dendrite-like formation in the other biological systems described above as well.

References
- Chklovskii, D. B., Schikorski, T., & Stevens, C. F. (2002). Wiring Optimization in Cortical Circuits. Neuron, 34(3), 341–347. https://doi.org/10.1016/S0896-6273(02)00679-7
- Chklovskii, D. B. (2004). Synaptic Connectivity and Neuronal Morphology: Two Sides of the Same Coin, Neuron, 43(5), 609-617. https://doi.org/10.1016/j.neuron.2004.08.012
- Graham, B. P., & van Ooyen, A. (2004). Transport limited effects in a model of dendritic branching. Journal of Theoretical Biology, 230(3), 421–432. https://doi.org/10.1016/j.jtbi.2004.06.007
- Mihara M., Hashimoto K., Ueda K., Kumakiri M. (1979). The Specialized Junctions between Merkel Cell and Neurite: An Electron Microscopic Study, Journal of Investigative Dermatology, 73(5), 325-334. https://doi.org/10.1111/1523-1747.ep12550322.
- Tamori, Y. (1993). Theory of dendritic morphology. Physical Review E, 48(4), 3124–3129. https://doi.org/10.1103/PhysRevE.48.3124
- Wen, Q., Stepanyants, A., Elston, G. N., Grosberg, A. Y., & Chklovskii, D. B. (2009). Maximization of the connectivity repertoire as a statistical principle governing the shapes of dendritic arbors. Proceedings of the National Academy of Sciences, 106(30), 12536–12541. https://doi.org/10.1073/pnas.0901530106


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Which scientific names designate eyespots?
I've found that names containing ocellata and ocellatus designate species that feature eyespots. Are there other words in the scientific names that designate eyespots?
The problem I need to solve is: I want to fill the category Eye shapes in nature, therefore any method for finding such species is welcomed.

Eyespot is a scientific name. Other names: false eyes, fake eyes.

Octopus bimaculoides ; Raja binoculata; You might want to do a regular expression search on .*oc[ue]l.*, e.g. Oligosoma lineoocellatum


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What is this strange mantis-like coral reef dwelling creature?
On the first episode of BBC's Blue Planet II they visited a coral reef and showed some odd reef-dwelling creatures as part of their establishing shots, but did not name the creatures.
In particular creature that resembles a mantis:

I tried a Google reverse image search and it very 'helpfully' identified it as "Documentary film". So close, yet so far.

The first one seems to be a mantis shrimp. No clue about the other one.

@JAB I've decided that I might have better luck if I split this into two questions. If you make that comment into an answer first I'll make sure to accept it when I do the split.

The specimen is indeed a mantis shrimp (to be specific, a peacock mantis shrimp).

These predators have highly sophisticated vision and, depending on the species, either spearlike limbs or clubs that move so fast the water can't keep up, causing dangerous cavitational effects that can even break glass.


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Any latest edition or successor of "Invertebrate zoology" by Ruppert & Barnes 2003?
I have the 6th edition of the textbook "Invertebrate Zoology" by Ruppert and Barnes from 1993. I know there is a 7th edition from 2003, but is there and will there ever be a 8th edition? Assuming they should come every 10 years, shouldn't there have been one in 2013? So if Ruppert & Barnes retired, is there any more recent successor or alternative?

There is no 8th edition. Barnes died a long time ago, in 1993. The latest edition was written by Edward Ruppert and Richard Fox, and it is the 2003 one. If you want to know if there are plans for a new edition you can email one of the authors or the publisher.

BTW Barnes is listed as 1 of the authors for the 2003 edition as well.

He will be listed on any future edition. It's just like Lehninger's "Principles of biochemistry", or Guyton's "Medical physiology": they are all dead, but they are kept as the main author.

Thanks! I would still like to know whether there is a more recent alternative.

Found it! I created my own answer.

A worthy successor to this book series is "Invertebrates" by Richard C. Brusca et al. The latest edition being from 2016, so exactly what I was looking for.
https://www.amazon.com/gp/product/1605353752/ref=pe_353720_261047730_em_sp_C_1p_1_ti

I studied invertebrate zoology using Barne's book, and I was reluctant to buy a book different from the classic one. I checked comments on the Brusca's book, and I was surprised that all of them are good ones (5 stars). It seems it's a better alternative to Barnes' book (7th edition 2003), as the last edition (3rd) was published in 2016 and includes the recent taxonomical reviews (e.g. new phyla, merged ones, etc.). I'm considering buying this; the price is quite reasonable compared to the other one.


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Dyes that won’t bind to dna
I am looking for a dye that won’t bind to DNA. I want to add dye to proteinase K to make is visible when adding to clear buffer liquid samples. I need it to not bind to the DNA so it will be removed during the purification process. Or a dye that will not show up later under fluorescence during processing.
Thank you!

You may try Crystal violet. This dye is also intercalating with DNA, though it is not fluorescent as far as I know. Disadvantage is that the dye has a low sensitivity.


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Is natural selection a force?
I often hear that natural selection, or simply, selection is a "force".
e.g.:

the forces of directional selection on correlated life history
  characters, and an adaptive topography

Source: Lande, R. (1982). A quantitative genetic theory of life history evolution. Ecology, 63(3), 607–615.

because, as is becoming increasingly appreciated, long-term studies (>
  one year) are necessary to understand the selective forces affecting
  territoriality (e.g. see MacLean and Seastedt 1979).

Source: Millington, S. J., & Grant, P. R. (1983). Feeding ecology and territoriality of the Cactus Finch Geospiza scandens on Isla Daphne Major, Galápagos. Oecologia, 58(1), 76–83. http://doi.org/10.1007/BF00384545

See also this one:

Selection is a vector having intensity and direction.

Source: Simpson, G. G. 1944. Tempo and mode in evolution. Columbia University Press, New York.

But I've also heard that selection is not a force and that should be thought as a "process" taking the analogy of a chemical reaction.

Natural selection is, in a sense, a "force" that can "act" on gene
  frequencies or trait value distributions, and this is the most common
  sense in which "act" and "force" are used. But this is only a vague
  and most improper analogy with physics. [...] The use of "force" in describing natural selection is an instance of confusion between the change in an object and the changes in relationships among objects, and can also be an artifact of typological (class) thinking.

Source: Endler, J. A. (1986). Natural Selection in the Wild. Princeton University Press.

It also seems that the way we can calculate selection (using the famous Lande and Arnold 1983 paper), using a vector field, which can be thought as a field of forces. Is there a conclusion to this debate?
Is selection a process or a force?

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

If the debate was only about semantics and not biology, then we would reconsider the term "natural selection" which is not the purpose of this question. If you want to talk about the semantics, see Darwin's letter when he says that "I suppose natural selection was bad term; but to change it now, I think, would make confusion worse confounded. Nor can I think of better; Natural preservation would not imply a preservation of particular varieties & would seem a truism; & would not bring man's & nature's selection under one point of view." My point is a clarification on a biological concept.

You may think your point is about biology but the people who answered all discuss semantics. Like many questions about evolution it is unsuitable for SE Biology in that it doesn't have a real scientific answer, and the intension in posing the question is more to initiate a discussion than to answer a problem. Tests of concept. How will you decide which answer is correct? How will accepting an answer as correct alter your future research or thinking?

Artificial preferential selection of your clothes in the morning is not a force. the force is the weather. You need to read background texts. A force is not a selection. A force is a pressure and it has encourages selection.

The main difficulty in this question is to define the terms process and force. As such it is as much a question of linguistic than a biology question.
Process
merriam-webster list a number of definitions. Below each definition I am answering wether NS would fit this definition.

progress, advance

No, NS is not a progress

something going on

Well... I guess, yes!

a natural phenomenon marked by gradual changes that lead toward a particular result.

Yes!

a continuing natural or biological activity or function

Yes!

a series of actions or operations conducing to an end

Not sure, how action is defined here...

the whole course of proceedings in a legal action

Nope!

the summons, mandate, or writ used by a court to compel the appearance of the defendant in a legal action or compliance with its orders

Nope!

a prominent or projecting part of an organism or organic structure a bone process a nerve cell process

Nope!

conk

What?
Force
From dictionnary.com, a force can be defined as

physical power or strength possessed by a living being

Nope!

strength or power exerted upon an object; physical coercion

Nope!

strength; energy; power; intensity

Hum.... no!
In physics a force is typically defined as (from wiki)

[..] a force is any interaction that, when unopposed, will change the motion of an object.

Then, no!
Conclusion
Really it is all a matter of what you want to call a process or a force. We know how NS is defined. The rest of the work is pure terminology about what you like to call a process and a force. There is no debate here. There is only people using different definition and allowing themselves to use some terms with a loose definition.
Process
I am personally quite happy calling NS a process following certain of the above definitions.
Force
I am personally not 100% happy about calling NS a force because the term 'force' already has a definition in science under which NS is not a force. Many people call NS a force because it leads to a directional effect on allele frequency. If you vision, the allele frequency as a position and moving through allele frequencies a movement, then NS is a force acting on the object that is the allele frequency. However, this is just an analogy.
Note by the way that diffusion equations can be used to describe change in allele frequency due to genetic drift (diffusion term) and NS (drift term) just like they are used to describe movement of particles. Btw, the fact that genetic drift matches the diffusion term and NS matches the drift term in diffusion equation makes me think that "genetic drift" would better be named "genetic diffusion".

Interesting. I would also call natural selection a process that, in order to work, has to fill 4 main criteria. I find it funny that 99.9% of the articles in biology talking about selection, call it a "force". I'm not sure why people prefer this way to define natural selection.

I'm curious about the way you would write a sentence such as "selection is pushing the distribution" or "selection acts against" or anything similar to this. Basically, based on a definition of selection, what would be the preferred way of talking about it? Is selection described as a force since Lande and Arnorld's paper on selection gradients?

Natural selection is a selection. Selection is an act of selecting and also the result of the act: a particular choice; choice of a particular individual or individuals; a number of selected individuals. What is selected? That which survives. What survives? That which reproduces itself. Process is the fact of going on or being carried on, as an action, or a series of actions or events. Selection is a process. Natural selection is a natural process.
Natural selection is natural. Natural pertains to nature. Nature is phenomenal. All phenomena are motions. Power is the ability to put things in motion. Phenomena are powerful motions. Force is an attribute of (powerful) motion. Force has a magnitude and direction, but no goal to reach. There are many forces acting on the individual's ability to survive. To survive is the individual's goal; if not, its chances to survive decrease. What survives? That which is strong enough to reproduce. Natural selection is a powerful selection.
Natural selection is a powerful process.