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Does food continue to stay sequential once it is inside my body?
I may be very off on many scientific details here, but I'm always all ears.
As far as I understand, any food that is eaten goes to the stomach, gets broken down even further into smaller food molecules, and after a period goes through the intestines where nutrients are absorbed out of this chyme.
Let's say I eat food A sometime, and it's gone down and is now sitting in my stomach, waiting for the stomach to start breaking it down. After a while, I eat food B.
When digestion occurs, is it possible that the stomach only starts breaking down food A's material first before it gets to food B?
Is it possible that food B's output goes into the duodenum before food A's output?
Please help break any of this down if it's obvious I've been living in a cave. Thanks!

I'm curious, do you have a reason to believe the stomach would act in such a selective manner, when it is using muscles to churn the material around?  (also, did you get your question backwards?  Did you intend to ask " Is it possible that food B's output goes into the duodenum before food A's output?")

@CortAmmon I have had no strong reason to chase down this answer, but I was really curious because this could, if answered positively, in a way, help me figure out potentially which meal was causing any current discomfort inside.

Ahh, so you are specifically referring to the case where the meals are several hours apart?  Since the stomach usually digests food in anywhere from 40 minutes to a few hours, the amount of time between A and B would matter.

You would have to eat each meal independently and wait a ridiculous number of hours to figure out where your discomfort is coming from. Mean time from mouth to excretion is along the order of 40 hours, and so the time trial would determine something like is the discomfort originating in the stomach, the colon? An important fact to note is that food in the stomach is pulverized to chyme so if you eat meals close to one another, it can confound things.

@Kendall Thanks for the response, it is informative. I'm mostly interested in the pre-duodenum phase of digestion. What happens if you ingest food right during the process of the stomach converting the food in the stomach to chyme? Does it allow the new food into this process, to create... "uniform" chyme? Or is the new food kept separate in some manner?

@CortAmmon I'm not referring to any food-interval particularly, but am more interested in learning if food is kept sequential internally in any case/interval-between-foods. (I think) the scope of my curiosity is between the throat and the pyloric valve.

It all depends on the delay between the consumption of food-A and food-B. It is all a continuous process (without any thresholding) and there is certainly a likelihood that there would be some minimum delay below which you get a well mixed chyme of both foods. Also, depending on the nature and composition of food these kinetics may vary.

@WYSIWYG Thanks for your response, that is informative.

Eat Oreos and you may find your answer.

In general, food is not kept in any particular sequential order.  The stomach has a lot of smooth muscle which churns the food, very rapidly erasing any "order" to the food.  Beyond that, the stomach digests "the food in the stomach," in parallel.  Whatever is in it, it digests.
Now, in general, food eaten earlier will digest into chyme (the digested slurry which enters the intestines) sooner, but that's a very general pattern and doesn't account for any differences in how long it takes to digest various types of foods.
I don't have any sources to back this next claim up, but I do believe that if you were to chew some steak poorly, and then follow it up by more steak chewed properly, the later steak would actually digest first because it would take less mechanical processing in the stomach to get the digestive enzymes to where they need to be to work.

Thanks for the response.
When the chyme rests in your stomach, before it moves towards the intestines, how does the stomach treat new food that has just reached it?

think of it as a large ziplock bag.  Food goes in, joins whatever mix of chyme and bollus (chewed food) happened to be in the bag at the time.  Give the bag a few squeezes to mix things up.  It's really more of a continuous process than a batch process.  Most of the exciting stuff is happening at the molecular level, so it doesn't really care about what the mix looks like at the macroscopic level.  It doesn't care if its breaking down the last few protiens of the last meal, or fresh protiens from a newly chewed steak.

Any description of digestion I've read mentions it, so if you feel bad sans source, that's place to start looking. That said, you really, truly ought not need to cite every blasted well-known and fundamental fact. If someone really needs to get more input on the point, they can always post that specific question on Stack Exchange, too.


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Why do we blink instead of winking each eye independently?
Question
Why do we blink both eyes at the same time rather than winking each eye as needed?
Why would winking independently be better?
The benefit would be a minor improvement whereby a person would receive continuous sight of the area of vision shared by both eyes.  I'd also assume that it would be more likely for the wink-as-needed mechanism to evolve than the blink-as-needed mechanism were there no benefit to blinking over winking.
Why then has evolution favoured blinking?
My guess at why is that the overhead on our brain of switching between binocular vision to monocular vision is more significant than the overhead of momentarily pausing our visual processing.
I also believe that some animals don't blink, but wink; e.g. chameleons.  This supports my theory as their eyes operate independently, so their brains would have to cope with the variance in each eye's information anyway.  That said, their wink is different; i.e. they roll their eye inside their head, rather than having an eyelid.
Research so far
I found a couple of Reddit posts:

https://www.reddit.com/r/explainlikeimfive/comments/2kzx4s/eli5_why_does_blinking_take_me_almost_no_effort/ - explains why blinking is easier than winking; but only based on how we are rather than how we got there (i.e. why evolution would have resulted in different muscles for winking vs blinking).
https://www.reddit.com/r/explainlikeimfive/comments/3mijgw/eli5_why_do_we_blink_with_both_eyes_at_same_time/ - doesn't have any hard fact answers; just discussion of opinion.

Looking at it completely in terms of evolutionary pressure:
1.1 The whole idea of binocular vision for humans, (and some other species) is depth perception. If you suggest continuous, alternate winking, the cognition of the individual would be seriously affected.
The 'wink as needed' mechanism (assuming all other visual processes are as they have evolved today) would be like continuously alternating between a pair of binoculars and a telescope while still trying to move forward.
1.2 If you are suggesting that there would still be an evolutionary pressure for winking, then its very likely that the evolutionary pressure for coordinated motion/ efficient cognition acting together with the evolutionary pressure for depth perception would be much higher as compared to it. (This would especially be true if eye-brain coordination evolved before the blinking mechanism, as is seen to be the case, which explains your point on 'how we are rather than how we got here'. Obviously fish have evolved some eye-brain coordination, but don't blink)
This link explains evolutionary pressure for depth perception/stereopsis to an extent
https://en.wikipedia.org/wiki/Depth_perception#Survival
2.1 As for the chameleon, the winking/ eye rolling mechanism might be very closely linked to the evolution of chameleon vision. It is seen as the link for studying evolution of binocular vision and stereopsis(depth perception) from monocular vision.
https://en.wikipedia.org/wiki/Chameleon_vision

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What is the biological significance of k-mer counting?
There are many tools developed to compute the counts of k-mers present in a gene sequence. Jellyfish, Bloom Filter Counter, DSK Kmer Counter, KAnalyze, KMC 2 etc are some efficient software developed in last decade to count k-mers.
But in what purpose, these tools are used?
How they are serving biological community?

What we have used this approach for is to search for k-mers that are enriched, or over-represented, in one genomic interval (or intervals), while present at the expected, or anticipated, frequency in the rest of the genome. The hypothesis being that such k-mers may have a biological role, either in gene regulation, or chromosome structure and function. With a collection of these k-mers in hand, one can attempt to test the hypothesis. For example, if you had a list of human neuronal enhancers, you could ask if there are any enriched k-mers, etc.

@mdperry Can I also use what you said to detect repeat elements like copy-number variation?

I have not seen an application like that; but one could try. It seems to me that if you had two genomes, Normal, and Mutant, you could run the k-mer counts and compare them, to pick up repeated k-mers. However most of the CNV approaches I have seen in the literature have used micro arrays OR deep sequencing read depths.

The applications for counting the k-mer occurences in a sequence are: building de Bruijn graphs [1] for de novo assembly from very large number of short reads, produced by next generation sequencing, fast multiple sequence alignment [2], and [3] repeat detection.

Compeau PE, Pevzner PA, Tesler G: How to apply de Bruijn graphs to genome assembly. Nature Biotechnol. 2011, 29 (11): 987-991.
  10.1038/nbt.2023
Edgar RC: MUSCLE: multiple sequence alignment with high accuracy and high throughput. Nucleic Acids Res. 2004, 32 (5): 1792-1797.
  10.1093/nar/gkh340
Kurtz S, Narechania A, Stein J, Ware D: A new method to compute K-mer frequencies and its application to annotate large repetitive
  plant genomes. BMC Genomics. 2008, 9 (1): 517-10.1186/1471-2164-9-517

To be clear, here is the biological significance of each of these applications:

Sequencing any genomes (bacterial, plant, mammalian) has become very cheap and easy recently with the next generation sequencing technologies. As opposed to the Sanger sequencing (the first generation), these produce as a readout very short sequencing reads, which have to be assembled into longer ones, and subsequently, into whole genomes. Counting the k-mers is part of the assembly process and this is its biological importance.
In order to compare whether proteins might have similar function, and thus belong to the same protein family, a multiple sequence alignment is performed. This is crucial step when annotating new protein sequences and studying their biological functions.
There are many repeats in our genome, as well as in plants. Repeated sequences are also involved in neurodegenerative diseases such as Hungtingtons, so being able to identify them is of medicinal importance.

At first thank you for trying to answer me, but all these three things are known to me, because those are described in almost all papers of the tools I have mentioned like kmc2, jellyfish etc. It still not biological to me. I am seeking the last effect on biology. Say, on your answer, the question comes in mind is What is the biological significance of de Bruijn graphs, ast multiple sequence alignment and repeat detection? Thanks again.

These 3 applications are fundamental in biology. I gave short descriptions of each one. You can look them up if you want to know more.

@manetsus That should be asked in a different question. Plus, a question like "what is the importance of de Bruijn graphs in biology" is quite broad. You can have a look at Pavel Pevzner's review on how Eulerian path is used for genome assembly and ask a specific question.

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seafood muscles - how do they work?
Today, first  time in my life I ate seafood. It was a squid and a calamar. Note that I am biology layman, so please be merciful :(
While dissecting my food I noticed that the tissues of those creatures were homogenous white mass. Completely different than with pork or chicken, where you can easily see the directions of muscle fibers and different groups of muscles. Just looking at a chicken wing tells you which muscle does what.
But why are squids and calamars so homogenous? How is it possible they work? Why is it like that?

As far as I know, the squid's mantle has two layers of muscle, circular and radial muscles, and two layers of epithelium or "tunic." This is unlike animal muscles, where the parts we eat are striated skeletal muscle. The mantle would be more akin to intestinal tissue with circular smooth muscle I'd imagine. That's about all I know, though.


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How do frogs fight?
I've seen a video in this link, where two frogs fight. One of commenters asks

How...exactly...does one establish dominance in their world? I mean, they’re fat, slippery, no claws, their teeth are practically vestigial, they are hard to drown—although it is possible—so...how does one frog or toad kick another’s ass?

And this is exactly my question

Some frogs do have claws. Also, frogs have a hard lip with sharp-ish tooth-like ridges on them. I've been bitten by frogs before, it can hurt...

What attempts to answer this question have you already taken? We ask that all question posters here attempt to search for an answer to their own question and explicitly indicate what research they've already done, what they learned, and what is still confusing or unknown to them. Our goal is not to simply be an answer site, but rather a site that promotes self-learning with some expert help along the way :). Please take a moment to edit your post with this additional detail, and it will likely be received more positively by our community. Thanks!

Also, as is made clear from MattDMo's comment and answer, this question is probably too broad and we'd almost certainly expect different species to behave differently.

I found this article ([free PDF on ResearchGate) from 1989 in Behavioral Ecology and Sociobiology entitled "Fighting, assessment, and frequency alteration in Blanchard's cricket frog". The author analyzed the sound wave frequency of the frogs' dominant call to see if it negatively correlated with fighting. In other words, were the frogs with deeper calls better fighters, and did other frogs use that to decide whether or not to fight?

 Larger frogs have deeper calls, and smaller frogs tended to retreat from broadcasts of a synthetic low frequency call, which indicated a large male. In contrast, frogs attacked a high-pitched call, which indicated their "opponent" was smaller. He also found that small frogs modulated their call to appear bigger to their opponent – they bluff.

Fighting (which was apparently only between males) was initiated when one frog was calling and another nearby kept calling after a series of calls from the first that were increasingly aggressive. The first frog would search for his opponent, and

When contact was made, a male moved onto the dorsum of his opponent and attempted to grasp the lower male with his forelimbs. Contact rarely lasted for more than a few seconds and was terminated by the lower male jumping away. Such wrestling bouts were followed by another period of aggressive calling, continued wrestling, [and terminated] by either retreat or satellite behavior by one of the males. Wrestling contests were generally short, lasting from 1–18 s (N=15, $\bar x$=7.2, SE=1.42), and they were composed of from 1 to 6 bouts (N=9, $\bar x$=2.7, SE=0.58).

So, it looks like these particular frogs fight by wrestling until one of them either leaves or adopts submissive "satellite behavior". I don't know if this is representative of all frog species, but it sounds reasonable.

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How can children scream so loud and so long?
Recently I saw a small baby shrieking extremely loudly (my ears hurt) for at least 4 minutes .
How is it possible? If I yelled so loudly, I would be defeated by throat ache after less than a minute. I know that heavy metal vocalists are capable of such feats, but it takes them a lot of practice.
So how can children yell so loudly for so long? Do they ignore pain? Does the pain cause the feedback loop of discomfort->yelling->more discomfort->more yelling? Or do they have vocal chords of titanium?
I tried google search, but answers are generally "why do children scream", not "how can they scream".

4 minutes are not long,fb suporters can keep it going for 45 min.

@trond screaming and crying is a bit more physically strenuous than singing football songs, no?

I seem to remember that this question — which seems to me rhetorical — has been asked on this list before (and in life by countless parents including myself). I suspect that your real question is how to stop it, in which case I believe there is a Parenting SE. Or Doctor Spock. From memory, you let them scream themselves out.

Children are more energetic than you. Is it so surprising that this also applies to screaming? Square cube law is also probably involved.

@David this isn't a rhetorical question. I don't care how to stop crying baby. I don't have one. I'm just surprised it can go for so long and so loud.

If not rhetorical, your question seems to me to address something that has not struck others as enough of a problem to investigate.

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Should I scare the swan to help him survive?
There's a young swan in my local park. He is young and I don't see his parents around. The young swan isn't affraid of humans and one can easily feed him from one's hand, and even pet on his head.
But I think that the swan has too much faith in humanity, and someone evil (or an excited toddler) can easily hurt the swan.
Should I try to spook the swan without hitting him? This way he will learn to avoid humans.
Am I wrong, and this would be bad for the swan? Or maybe this is a non-issue, and I'm just overthinking?
I googled relevant questions, but I only get answers "how to train bird to trust you" etc.

The way I see it, if you were to try to "spook" the swan (which, for the record, I don't recommend), you would be one person trying to teach it one lesson ("Don't mess with humans, we're dangerous!") while the vast majority of the humans it interacts with would be implicitly teaching it the exact opposite. Which do you think would be the lesson that sticks? Scaring it also has the potential of stimulating it to act defensively or aggressively towards the next human it encounters, which could end badly. I suggest engaging your local wildlife protection authority and getting them involved.

+1 for your care and concern.
No
It is likely to hurt both the swan and the humans interacting with the swan. From The role of animals in education:

Animals are increasingly being incorporated into the American school
setting to help teach students important behavioral and academic
lessons (Chung 1994; Dalton 1999; Mallon 1992; Pavia 1997). In a 1998
study, Beck and Rud surveyed 1,999 elementary school teachers
throughout the State of Indiana about the presence of animals in their
classrooms. The results indicated that 20 to 25 percent of the
teachers surveyed incorporate some type of animal in their classrooms.
Researchers have found that interacting with animals can help people
in numerous ways. Levinson (1962) was the first to formally theorize
that a dog could serve as a transitional object or "bridge" with which
an individual could form a nonthreatening relationship, which could
later expand to include other humans. Beck and Katcher (1983) found
that interacting with animals almost always has positive influences on
children. Mallon (1992) suggested that animals play a role in
socializing and humanizing children. Many researchers and writers have
noted the value of utilizing animals as mediators to help people who
are not being reached by other methods (Corson, Corson, and Gwynne
1975; Johnson 1983; McCullough 1982).
Some reasons that interventions involving animals produce results when
other methods fail include issues of trust, nurturance, social
perception bias, physiological response, resistance to treatment,
nonverbal communication, identity, control, and touch.
Trust. Many researchers, including Levinson (1965) and Ruth (1992),
have observed that children who are not comfortable interacting with
other humans often do not feel the same inhibition with animals. As
Levinson (1969) stated, when interacting with an animal, a child can
assume the role of teacher, parent, or anything else without fear of
rejection. Gonski (1985) postulated that animals provide a safe means
for children to begin to trust nonjudgmental beings, before trusting
humans. Whatever the reason, some children find interactions with
animals less stressful than those with humans (Brickel 1982: Levinson
1965; Robin et al. 1984; Ruth 1992). Many claim the reason is that
animals provide unconditional acceptance and love, without the
criticism that so often accompanies human interactions (Beck and
Katcher 1983; Levinson 1969; Siegel 1962).

Further reading:

Treating Human Trauma with the Help of Animals: Trauma Informed Intervention for Child Maltreatment and Adult Post-Traumatic Stress
Research in the use of animals as a treatment for humans

There is also the ethical question of betraying an animal that trusts you.

This answer is about the utility to humans of interacting with animals, which isn't the question being asked. OP is asking about somehow trying to teach the swan to "act wild" again, to not be trusting of humans and keep its distance.

Fascinating, well researched and sadly, not what the question asked. Unless you're suggesting that the local school should be contacted as potential candidates to adopt the bird.... Maybe, but swans are not small nor quiet (and they seldom do their homework).


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How does RCSB determine the origin of the Cartesian coordinate system utilized in all PDB files
When perusing through the text version of a PDB file, I noticed in records that begin with "ATOM," there are x, y, and z coordinates for these atoms.
How is the origin of each molecule's Cartesian coordinate system determined by RCSB?

They are just arbitrary numbers, the only thing which matters are the relative coordinates. The relative coordinates themselves are determined mostly by X-ray crystallography or NMR.


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How does TYRP1 affect the synthesis of black and brown eumelanin (on a biochemical level)?
TYRP1 (aka B-locus) is a gene in dogs that determines whether black or brown eumelanin is produced (assuming eumelanin is produced at all which is determined by the MC1R gene). I've looked at many papers and flow charts and now i have a contradiction: DHI seems to be the molecule that gives eumelanin a black color and DHICA a brown color. According to many flow charts, TYRP1 seems to be involved in the polymerisation of DHICA (not DHI). Mutations that cause a loss-of-function of TYRP1 will cause dogs that carry these mutations (homozygous) to have brown fur. But if TYRP1 is important for polymerisation of DHICA to brown, why does a loss-of-function of this very protein cause dogs to have brown coat color?
Where did I get it wrong?

The actual coat color is determined by the ratio of the products of two genes: Tyr and TyrP1. The first oxidizes DHI to Indole-5,6-quinone and forms brown pigment, TyrP1 on the other hand oxidizes DHICA to Indole-5,6-quinone carbolic acid, which forms black pigment. See this pathway diagram (from here):

So loss of TyrP1 activity is not harmful to general pigmentation but prevents the formation of black color, while the inhibition (or loss of function) for Tyr will lead to albinism, since no pigment precursors (from Tyrosine to DOPA can be formed.
You may also be interested in this paper: "TYRP1 and MC1R genotypes and their effects on coat color in dogs."

Thank you! Then, my error was that DHICA forms black eumlanin and not brown.


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Density of Receptors of a mammal
I know it's a very open question. It's for a paper.
So as a reference I'm looking maybe for the average density of insulin receptors per cell of a human tissue. I want to compare it to the density of MC1R (around 1000 per cell) and it says that's a low amount.

Depends on the type of tissue.

i'd appreciate any receptor of any tissue

It would depend on the type of tissue. But if you are interested in any tissue, then have a look at this BioNumbers entry. It says that there are 100000 insulin receptors per cell in rat adipose tissue. Divide it by the surface area of the cell and you'll get the density. Cell dimensions can also be found in BioNumbers


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Why do plants need oxygen through their roots?
I was asking myself why plants die from over-watering and the simple answer was that they can't get enough oxygen through their roots. But this made me ask myself why they need oxygen in their roots since oxygen is a product of photosynthesis and plants even release oxygen through their leaves.
With this seeming surplus of oxygen, how can plants "suffocate" when their roots dont get enough oxygen from the soil?

They are mostly susceptible to stagnant water. Stagnant water gives rise to anaerobic bacteria, which use sulphur reduction and other kinds of energy chemistry. That's why anaerobic pond silt has an eggy sulphur smell. That anaerobic biochemistry can start to thrive after 2-3 days. The roots can handle low oxygen for a while, but beyone a few hours of zero oxygen pushes them into some kind of toxic cell state, which breaches the root's defenses and causes the roots to be rapidly attacked by bacteria. They benefit hugely from nitrogenated, oxygenated water.

Plants need oxygen but don't have a heart
Complex animals all have a circulatory system of some sort to get oxygen throughout the body for respiration. Plants also do respiration even though they are net producers of oxygen through photosynthesis.
Plants also have a bit of a circulatory system, but for the most part it isn't nearly efficient enough to deliver oxygen everywhere in the plant: plants don't have anything like circulating hemoglobin-filled cells we are familiar with in vertebrates, and although fluids flow in plant circulatory systems, they aren't circulating quickly like you are familiar with in your own body. This means that plants need to get oxygen near to where it is needed.
Roots, in particular, consume oxygen
The problem of a plant not getting enough oxygen through its roots isn't because the whole plant gets oxygen through the roots, it's because the roots themselves need oxygen to function. Roots do a lot of 'heavy lifting' in a plant, literally: they are pumping ions across membranes to pull in water, to concentrate other nutrients that the plant needs for survival and growth, and to pressurize the plant enough for those nutrients to make it up into the leaves. Those processes take energy, and in turn they need oxygen.
Additionally, photosynthesis isn't taking place in the vicinity of the roots: plants are both taking in CO2 and releasing oxygen from their stomata in the leaves and stems.
If roots cannot get enough oxygen, for example due to overwatering, the roots themselves are damaged, and this harms the plant as a whole.
Adaptations
Because there are always exceptions in biology, it should be noted that some plants are indeed adapted to wet environments and have better systems for promoting the diffusion of oxygen including increasing the amount of air space in the roots, where oxygen diffuses more quickly than through aqueous media. Other plants use fermentation in their roots to survive temporary hypoxia.

References
Colmer, T. D. (2003). Long‐distance transport of gases in plants: a perspective on internal aeration and radial oxygen loss from roots. Plant, Cell & Environment, 26(1), 17-36.
Drew, M. C. (1992). Soil aeration and plant root metabolism. Soil Science, 154(4), 259-268.
Justin, S. H. F. W., & Armstrong, W. (1987). The anatomical characteristics of roots and plant response to soil flooding. New Phytologist, 106(3), 465-495.
Laan, P., Tosserams, M., Blom, C. W. P. M., & Veen, B. W. (1990). Internal oxygen transport inRumex species and its significance for respiration under hypoxic conditions. Plant and Soil, 122(1), 39-46.

Great answer. This answer to a different question details differences in respiration vs. photosynthesis. Also note that anaerobic conditions around the roots can cause root rot, another pathway to death of the plant, which is related to the last adaptation you mentioned.

Plants are living things. And living things need oxygen to survive. While plants may produce oxygen as a byproduct during photosynthesis, they still require to undergo respiration, which requires oxygen.

But that doesn't explain why they cant use the oxygen they produce and have to absorb additional oxygen.

This is because photosynthesis and respiration are decoupled, they don't have an additional module to harness the oxygen produced to respire


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Exact definition of single nucleotide polymorphism (SNP)
So, I know on a higher level what an SNP is but I'm a bit confused about the details.
Firstly, our professor said that an SNP has to have at least a prevalence of 1% in the general population to be considered an SNP and not just a mutation. Wikipedia says the prevalence needs to be 0.5%. Is this actually a strictly followed cutoff? And which of the two values is correct?
Secondly, he said that SNPs never cause a disease but can only predispose you to one. However, the wikipedia article mentions thier role in diseases that are clearly caused by single mutations (cystic fibrosis, sickel cell anemia, and beta thalassemia). So, can SNPs cause a disease or not?

1% v. 0.5% is unimportant and arbitrary. The databases of SNPs need an actual cutoff. If you think of the millions of SNPs added to database by automated genome sequencing projects, the idea of weeding out any related to a mono-genic disease seems improbable,

In genetics, a SNP (Single Nucleotide Polymporphism) is the substitution of a nucleotide with a different one.
A SNP can have phenotypic effects or not.
A mutation, in genetics, is any kind of inherited change in DNA. Mutation types are: SNPs, indels, structural variants, translocations and so on.
Sometimes researchers (especially in the field of medical genetics) call "mutation" (meaning "pathogenic mutation") a SNP which is responsible of a disease (especially in case of a Mendelian disease). Since mutations causing severe Mendelian diseases are usually rare, several people use the arbitrary threshold of 1% to discriminate between a "SNP" and a "mutation".
So, probably your professor is stating that SNPs cannot cause a Mendelian disease because he uses the last definition I gave. However, while this definition may be useful for medical genetics purposes (i.e. I also agree that a very common variant is unlikely to be causing a rare Mendelian disease), it is arbitrary, if not wrong.

Single nucleotide polymorphism is the most common type of alteration in DNA, this occurs when a single nucleotide is replaced with another. SNPs are normally present in our genome, with prevalence of one in every 1,000 nucleotides, making approximately 5 million SNPs in a our genome.
These variations are commonly found in the DNA present in between the genes and act as markers for locating different genes. But when SNPs are present in gene sequence or in the regulatory region, this directly effects functioning of genes and can result in disease.
It is reported that SNPs effect person's susceptibility for developing various diseases like heart disease, diabetes, and cancer.
SNPs can also be used to track the inheritance of disease genes within families. These alterations also controls individual's response to environmental factors and response to various drugs.
Reference
https://www.snpedia.com/index.php/SNPedia
https://www.sciencedirect.com/topics/medicine-and-dentistry/single-nucleotide-polymorphism)


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Why is black eumelanin black even though it consists of black AND brown molecules?
In dogs,eumelanin consists of molecules of DHI and DHICA. DHI and DHICA are made from dopachrome. DHI through DHI oxidase and DHICA through DHICA oxidase also known as TYRP1. When TYRP1 has a mutation through which it loses its function, mostly DHI is produced which gives brown eumelanin.
Now, if TYRP1 is functional, are both DHI and DHICA produced? If no, why not? If yes, why does the eumelanin appear black and not a dark brown?


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What determines the color of the air sac of a Portuguese man o' war?
I know that the Portuguese man o' war is a colonial organism composed of many "zooids", one of which is the pneumatophore, which essentially serves as a flotation device for the whole colony. This sac may be of varying shades of pink, violet, or blue.
I'm having trouble finding a reference on how a particular man o' war gets its sac coloration. The most obvious possibilities are trace chemicals in the air and/or water or heritable genetic factors, but I'm not finding any sources.
What determines the color of the pneumatophore sac of a Portuguese man o' war? Is it genetic, analogous to eye color or hair color in mammals? Is it essentially dyed by exposure to various chemicals in the environment? Is it gender-based? Is there some other explanation as to why one man o' war might be blue while another is pink?


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How is the first Triceratops born?
To clarify at first, I have very little knowledge in biology and paleontology so there might be very obvious things I overlook.
According to the evolution theory, there must be a graduate evolution process over millions of years such that the skull and the horns of the Triceratops gradually appear over time. However why there is no fossil record of such "intermediate" form between Triceratops and earlier dinosaurs? I mean there must be some intermediate dinosaurs that has a short skull that almost looks like a small mountain on the neck and very short horns. However based on my internet search I can't find any information that confirms existence of such intermediate dinosaurs.
I just want to know is there any such evidence of graduate evolution among paleontologists or the evolution of dinosaurs is still much based on speculation (without firm evidence)?

Note btw that it is a standard layman misrepresentation of evolutionary processes to think that evolution must necessarily be very slow. This is not necessarily true.

@Remi.b Are you referring to some kind of 'evolution in bursts'? I feel I heard about it, not sure where!

@HarryWeasley I started to answer your comment and realized it would deserve its own post. So, I opened a post asking your question (and directly answered it) here.

Very related: Where are the evolutionary “inbetweeners”?.

Yes, there are many early examples of ceratopsians before Triceratops. The oldest clear member of the lineage is Liaoceratops: "the oldest ceratopsian ever found ... was about the size of a large dog. It had a blunt beak and a dainty neck frill. ... Liaoceratops was a puny forebear of the feisty Triceratops. Size, horns and spectacular frills came later in ceratopsian evolution."  Here's a reconstruction:

Protoceratops is very well known, and is a pretty obvious intermediate between famous ceratopsians like Triceratops and early ones like Liaceratops:

This cladogram shows a number of steps in ceratopsian evolution (right side of the diagram):

Note the steps it describes: Starting with early forms that have a vaguely frill-like structure, we see added: Rostral bone with "horns" that are barely visible; Frill, with jugal "horns"; Enlarged frill and skull; Postorbital horns; Nasal horn.

Thank you so much. This is exactly what I am looking for.

A quick look a the sheer variety of ceratopsians is helpful. Even right at the top of the tree there is a lot of variation. https://66.media.tumblr.com/35e87e230a6c1589aef6c474d90ed9c3/tumblr_na7av0v1Gv1srcpvio1_1280.jpg

As in any 'species' of animals, Triceratops in the ceratopsian family came about through natural selection as changes that benefited some members were passed on to the next generation. Today, we can see how a species can change by just looking at all of the dog breeds that have developed in just a few hundred years through selective breeding. All domestic dogs are descended from primitive dogs over 10,000 years ago. Today, there are over 350 recognized dog breeds and probably well over 100 'new' breeds that have not gained recognized status. You can see how over hundreds of thousands of years that 'natural selection' would create variations within a species. This does not create a 'new' animal, just a variation within the species. A dog is a dog, a ceratopsian was a ceratopsian and a human is a human regardless of the differences between individuals. https://pediaa.com/difference-between-natural-selection-and-evolution/

Welcome to Biology.SE. This looks like it could become a good answer, but answers are much more likely to receive a favorable response if they include supporting references (primary literature is best). Without that support, your answer is indistinguishable from opinion and thus not appropriate here. An example of how to format references. In addition, it is best to focus on unanswered or poorly answered questions. ——— Please take the [tour] and consult the [help] pages for additional advice on [answer] and [ask] effectively on this site.

If you are looking to a more recent evolution of Triceratops you can follow the cladogram to the subfamily Chasmosaurinae and then to the tribe Triceratopsini. You'll find there Eotriceratops, which looks very much like a bigger Triceratops and might has been his direct ancestor, as it lived 68 MYA.
The rest of your question is more philosophical than informative and echos "the chicken and the egg" paradox, or "when exactly an animal evolves into a distinct species?"


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Why are H+ ions pumped out instead of in during cellular respiration
During cellular respiration in both mitochondria and aerobic prokaryotes, the Electron Transport Chain pumps H+ ions out of the matrix or cytoplasm to create a H+ concentration gradient. This forces the H+ ions back into the matrix or cytoplasm forcing ATP synthase into action.
I was wondering, however, why the H+ ions are pumped out of the matrix or cytoplasm, instead of into it. For aerobic prokaryotes, and the early mitochondria (which were prokaryotes living on their own) pumping the H+ ions out of the matrix or cytoplasm means pumping them into the outside world, a very uncontrolled environment. There is nothing to prevent the H+ ions from diffusing out, making the pumping completely inefficient, if not pointless. Wouldn't it make more sense to pump the H+ ions into the matrix or cytoplasm, where the H+ ions cannot diffuse, resulting in much higher efficiency?

But they aren't pumped out in the surroundings they are pumped between inner and outer membrane? Add some references about your statements

@KingBoomie the OP is talking about when mitochondria were still free living bacteria

Probably someone can dig up an answer that answers this question, but I'll just repeat it here shortly:
You'll get the same gradient if you pump protons out or in. You're not specifically decreasing the outside pH when you pump protons, you're mainly increasing the inside pH. As long as there is a gradient that can be used to achieve other things for the cell, it doesn't fundamentally matter if protons want to flow in or out the cell, as long as they want to flow across the membrane.

If the protons would flow into the cell the pH would rise here, this could be a problem for the protiens present here

@RickBeeloo the reverse is also true, so your statement is not a valid argument.

but the reverse is happening in the mitochondria.... and we all still live so what do you mean? @LiuTianyi?

Because the proteins in the mitochondria have adapted for that reason? Evolution could very well occur such that proteins in the cell would be suited to work in low ph (ph decreases when protons flow into the cell, not rise) levels, which is the case for, eg lysosomes. You reject your hypothetical statement on the basis that it does not occur in the real world, exactly because it is hypothetical. That line of argument does not make sense. @RickBeeloo

Coult you cite you reference on "Because the proteins in the mitochondria have adapted for that reason"?

Here is my reference, good sir. but the reverse is happening in the mitochondria.... and we all still live

I mean a article on where to find that? You have a good point so I'm interested in why the evolution should prefer the adaption of the proteins in the matrix instead of inside the cell? @LiuTianyi . This Could be helpfull for the asker of this question.

That is exactly the point to discuss.  Why should "evolution prefer proteins adapt to basic environments over acidic environments". That answers the question. I did not add additional content on this topic. I merely said that this could be a problem for the protiens present here is not a valid reason, as the presense of proteins that adapt to high pH is inherently linked to the premise of "there is high pH in intracellular environments". I'm pointing out a logical fallacy, not a content fault. @RickBeeloo

I'll just post one more example in hopes of you understanding. Let's say chairs have 4 legs. "Why do chairs not have 3 legs?" "Because if they do, they wouldn't have 4 legs". The answer is part of the premise, it does not answer anything. If you need more explanation, feel free to discuss over chat. I'm not interested in discussing this question per se, but I feel obliged to explain why your point does not help OP.

I don't know if this is a proper answer... and this answer is really late... but if I remember correctly, the mitochondria pump H+ out to better compartmentalize the activities of the TCA and other oxygen-dependent metabolic processes within the mitochondria. This compartmentalization helps further minimize the possibility of a process or reaction to take place before the cell is ready. It also helps keep proteins that have closely related functions (as in they function in the same or complementary pathway) spatially close to each other.
Interestingly, prokaryotes have been observed to localize cellular activities as well. It is hypothesized that this occurs for the same or a similar reason as described above for eukaryotic cells, albeit it is likely less effective. This is accomplished through intracellular scaffolding of some kind of cytoskeleton. My guess is that prokaryotic cells can utilize this cytoskeleton to localize their proteins, but can't use it to localize H+ due to a lack of "binding" region (speculative).
Also, majority of prokaryotic organisms will pump the H+ into their periplasm (inter membranous space, not the "chaotic" external environment) as Rick Beeloo mentioned. This periplasm is a smaller environment than the cytoplasm and is more densely filled with proteins (and possibly others molecules) as well. I think the periplasm is more viscous as well - whether a result of solvent composition, high protein or other molecule concentration, or something else entirely, I'm not sure (relatively unfounded statement). Regardless, all these factors actually make it more difficult H+ molecules to diffuse away in the periplasm than in the cytoplasm.
Another argument against why the H+ must be pumped to the side opposite of the proteins is that ATP inhibits the TCA and other oxygen dependent metabolic processes. The ATP synthase creates ATP on the side that the H+ ion passively flows to. This causes feedback inhibition is much more temporally sensitive as ATP synthase synthesizes ATP on the same side as the proteins involved in ATP synthesis. I think that ATP synthase cannot produce ATP on the same side as the H+ ions because their is no energy to make the ATP with until the H+ ion has flowed down the concentration gradient across the membrane; by this I mean the energy used to create ATP can only be harnessed on the low-energy side of membrane (I'm guessing on this last sentence...).
As a result of these reasons and maybe more, I'm led to believe these are some reasons that it is advantageous to pump H+ ions out of the cell/mitochondria interior than in. Although 2 years late and by no means a definitive answer, I hope this adds some new perspectives or ideas to the discussion on why this process occurs as it does.

Can you add sources to your answer to allow other users to background read on your material. +1 for the elaborate answer.

Okay, I will work on that over time. It's been a while since I've gone through cell bio/biochemical engineering. It might take me a lot of time to pull stuff together, but I hope I can still find everything!

You don't have to add a zillion citations, but an image helps a lot and a few web-links here and there that back up your major claims and explain key terms would make a more satisfactory post and will give you your deserved #upvotes too. See the most upvoted answer above for example (not the best ever answer, but, well... better organized than yours for now :-).

I cannot completely vouch for how accurately my answer does answer your question. I will however try to explain the best that I can.
Here is a picture:

(source: els-cdn.com)
Firstly, in the electron transport chain the reactions that happen to metabolize the substrate are Redox reactions. As the complexes are oxidized by the release of electrons, protons are also released for counterbalancing. Statistically, the most effective route of ejection of the protons is through the H+ uniporters. There is a need for the protons to catalyze the reactions for synthesis of Hydrogen Sulfide which is required for stimulating the ATP synthase (you can check out the figure).
I am attaching some links which you can go through.
http://www.sciencedirect.com/science/article/pii/S1043661816304820 (This paper gives a detail overview of the H2S mechanism.
You can also go through this wiki article.
https://en.wikipedia.org/wiki/Electron_transport_chain
Hope I could clarify your question!
Thanks!


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What is the function of the kidney in terms of osmoregulation and excretion
Also include the role that ADH plays
I am fully aware that ADH has a role in osmoregulation  but does it also play a role in exretion?

This seems like a homework question. Per the community guidelines, homework questions are off topic unless you've shown an attempt at answering the question or doing research. I suggest looking around online for information regarding ADH. Wikipedia is a pretty good start for information regarding the hormone's role in osmoregulation/excretion.


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Resistance to Antiseptics
I know that bacteria can become resistant to antibiotics.
Why do antiseptics like alcohols, PVP-I, still work on the strains of bacteria we have today? Shouldn't some bacteria have evolved to be resistant to them? I only hear about antibiotic resistance, so my assumption was that antiseptic resistance isn't a thing that happens.
What fundamentally differentiates antibiotics and antiseptics so that antiseptics are not resistance-prone?

For some classes of antiseptics the effect is more simple chemistry or even physics than biochemical toxicity. Ethanol will just denature proteins and dissolve the membrane, and the used concentration of ethanol is so high that no amount of efflux pumps is going to save the bacterium. Some other compounds work in a similar brute force way: QACs will break the membranes, hydrogen peroxide will just oxidize everything. For iodine (like in PVP-1) the mechanism is not really known, but probably it also just reacts with all kinds of things in/on the bacterial cell and kill them.
Antiseptic resistance could happen for some other antiseptics (or low concentrations of the compounds mentioned above). For some antibiotics, resistance is caused by the expression of efflux pumps that just pump out enough antibiotics so the cell survives. Bacteria could do the same for these antiseptics. The reason why it's not that much of an issue is that the application is rather different. Antibiotics are for inside use, antiseptics for topical use, you cannot just flood your whole body with 70% ethanol to kill all bacteria, but for a wound / something dirty this is just fine. This makes it much easier to avoid creating resistance.

Please define and link to QACs. I know what they are, but many others will not, as it is not a common abbreviation, except possibly to chemists and certain microbiologists, as well as those who work in manufacturing. Overall, your post would benefit by several additional citations supporting your claims.

However, even for brute force mechanisms, there is a huge spectrum of concentrations and conditions in which we apply alcohol, bleach... That is what confuses me. What is the threshold number of ethanol molecules a bacterium's membrane could stand? Aren't a temperature that kills a whole population and other that only kills one individual appart just by a continuous gradient?

Of course bacteria can evolve resistance against antiseptics. Usually antiseptics inflict direct damage to the cell rather than interfering in some biochemical pathway. Also, antiseptics are used in very high concentrations which usually leads to complete elimination of the microbes. Moreover, different antiseptic/disinfectant agents have different toxicity to different organisms; for example anaerobic bacteria are more sensitive to oxidizing agents like hydrogen peroxide and potassium permanganate.
There are bacteria (Deinococcus radiodurans) and fungi that are even tolerant to ionizing radiation like gamma rays.
There are other extremophiles too which thrive in extreme physical/chemical environments (extreme heat/pH/salinity/pressure etc).
For more information on antibiotics vs antiseptics see this post: Why is triclosan not considered an antibiotic?


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What nutrients are best suited for growing E.Coli
I am looking to grow E.Coli (In a nutrient agar dish) to be used in an E.Coli lawn and was wondering what specific nutrients should be used to ensure the E.Coli grows optimally? Any answers or links to relative resources are greatly appreciated!

Do you have any reasons to not use standard LB agar plates?

Welcome to Biology.SE! Please consider taking the tour. You might also want to add some more information to your question showing what research you've already done yourself.
Specifically regarding your question, it's not my area but I suspect this will help: http://www.exptec.com/Bacterial%20E.coli%20Growth%20Media.htm

If you don't have any specific reason to use something else, LB is your best bet. It's cheap and it works well.

Optimal is a funny thing; it depends upon what you want. The purpose of the bacteria, is probably the most important aspect when considering the nutrients. There are many recipes capable of growing E. coli. What does optimal or best mean to you and why? Is selectivity or differentiation a factor? How important is cost? Are you aiming for industrial level production or just testing. Do you have a bioreactor? Or are you looking for something low tech... maybe from food-mart?
For what it's worth, you might find minimal salts media and solid state fermentation interesting.
Different strains like different nutrients, of course. So, phenotypical tests are sometimes helpful when figuring what an undescribed strain likes (and doesn't like).
That being said... I can offer a little insight here.
"+" for growth/utilization;  "-" for weak or no growth/utilization:
                 E. coli    E. coli inactive**  E. coli 0157:H7

Pectin                 -            -                   -
Dextrin                ++           ++                  -
Sucrose                -            -                   +++
Glycerol               +++          +++                 +++
Stachyose              -            -                   -
D-Fructose             ++           ++                  ++
D-Maltose              +            ++                  ++
D-Raffinose            +            -                   +++
α-D-Glucose            +            +                   +
α-D-Lactose            +            -                   ++
D-Trehalose            ++           +++                 +++
D-Galactose            ++           +++                 +++
L-Fucose               +++          +++                 +++
L-Rhamnose             +++          -                   ++
D-Sorbitol             +++          +                   -
D-Mannitol             +            ++                  ++
Methyl Pyruvate        +++          +++                 +++
Tween 40               -            -                   -

Gelatin                -            -                   -
L-Alanine              +++          +++                 +++
L-Arginine             +            -                   -
L-Histidine            -            -                   -
D-Serine               +++          +++                 -
L-Serine               +++          +++                 +++
D-Aspartic Acid        -            -                   -
L-Aspartic Acid        +++          +++                 +++

D-Glucoronic Acid      +++          +++                 +++

Citric Acid            -            -                   -
L-Malic Acid           +++          +++                 +++
Acetic Acid            +++          +++                 +++
Acetoacetic Acid       +            +                   -
L-Lactic Acid          +            -                   -
Mucic Acid             ++           -                   +++
D-Malic Acid           +            +++                 +++
Propionic Acid         ++           ++                  +++
Formic Acid            +            -                   +

D-Salicin              -            -                   -
Lithium Cloride        +++          ++                  ++
Na Butyrate            +++          +++                 +++
pH 5                   +++          +++                 +++
8% NaCl                ++           +                   -
D-Serine (high)        ++           +                   -
Potassium Tellurate    +            +                   +++
Na Bromate            +/-           -                   ++

E. coli inactive** is lactose-negative, non-motile- often misidentified as Shigella

As suggested by Chris, classical LB medium should be fine. There is a reason why it has been used for the last 65 years. Some people supplement it with extra sucrose or sodium chloride, but I think these are mere customs rather than experimentally-proven improvement.
If you want to re-create LB from pure components, read about minimal media. They are a mixture of glucose, ammonium salts, microelements and vitamins. A rather long list that I won't post here can be found at http://structuralbiology.uchc.edu/protocols/pdfs/nmr_sample_preparation.pdf


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Why is the "worm" body shape so prevalent in Eumetazoa?
What is the selection advantage, of this incredibly common body form? (long, cylindrical tube-like body with no limbs)
Is it just the body plan of the ancestral bilaterian and therefore remained prevalent due to absence of selective pressure against it? I.e. is it a neutral adaptation? Or is it actually a positive one?
Examples of "worms":
- Platyhelminthes
- Nematoda
- Annelida
- many kinds of insect larvae
- sea cucumbers
- lancelets, lampreys, eels, snakes, caecilians, ...
- Chaetognatha
- Hemichordata
- Acanthocephala
- Gastrotricha
- Gnathostomulida
- Nematomorpha
- Nemertea
- Priapulida
- Sipuncula

Is it just the body plan of the ancestral bilaterian and therefore remained prevalent due to absence of selective pressure against it?

Pretty much.
You can see some animals which precede the emergence of this plan, like sponges. They apparently do alright, so there's nothing precluding different body plans. However sponges also have a fairly limited niche, and perhaps there's a good reason. Similar things can be said for other non-bilaterians like jellyfish.
One could speculate that the "tall-donut" shape is the key innovation. When food moves in only one direction, it is much easier for the digestive tract to specialize and digest food much more efficiently in stages. Animals, after all, are things that survive by eating things and digesting them - the faster they can digest, the faster they can eat, the better they can survive.
Animals which have no separate anus seem to have more trouble eating things and digesting them: It's slower, and they can't eat as varied a diet.
A worm, being essentially a long tube, is a simple way of accomplishing accomplishing the one-way GI tract. If you think in an evo-devo sense, it also doesn't take a lot to progress from a "basket" to a tube (the two layers after gastrulation just have to meet, fuse, and form a second hole). If you consider the so-called higher animals, like humans, cats and dogs "worms", then we can stop there. Otherwise, we can remark that the "worm" shape also allows easy movement in water and on soil by wriggling.
Past the "pure worm" you can see a large variety of body plans, such as among arthropods, but they're really just worms with a few specialized segments, including, say, humans. This does have a fundamental reason: During early development, patterning of the body (deciding which organ or limb will grow where) relies on Hox genes, which are typically top-level transcription factors that determine a segment's identity. So the "worm" also happens to be a nice developmental "base" from which more complicated embryos can develop.

is it a neutral adaptation? Or is it actually a positive one?

This is very hard to answer:

There are necessarily many confounds, and we cannot easily find two animals which are otherwise the same, but one is a worm and the other is not. We cannot artificially generate such animals yet either.
The obvious way to infer fitness is to look at whether the trait came to dominate the population. But with since body plan establishment is something that did not evolve independently many times, it is hard to say whether it dominated due to a genuine fitness advantage or purely out of being fixed. Perhaps there are other, yet more efficient body plans, but they have not yet arisen due to random chance.

This is a really good answer -- sorry for the slow upvote, I had already maxed out on them yesterday when I got your answer, so I had to wait until my limit refreshed.


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Did vertebrates diverge from other deuterostomes via neoteny?
Question: Is there any research corroborating my suspicion that vertebrates diverged from other deuterostomes via neoteny (the attainment of sexual maturity while still in larval stage)?
Context: Most echinoderms have pelagic, bilaterally symmetric larvae, while the adults are not bilaterally symmetric (except for sea cucumbers) and live on the sea floor. The same is true for tunicates, which are supposed to be the sister group to vertebrates.
Adult echinoderms also have very reduced nervous systems, although I am not sure whether the larvae have more advanced nervous systems than the adults. For tunicates, which are more closely related to vertebrates, the nervous system definitely does degenerate when transitioning from pelagic larvae to sessile adults.
Echinoderms are also one of the few clades of bilateria, except for vertebrates, which have endoskeletons. And of course, echinoderms, tunicates, and vertebrates are all deuterostomes.
In contrast to tunicates and echinoderms, the MRCA of vertebrates is thought to have resembled a lancelet, which is pelagic and which has a more advanced nervous system than adult tunicates or echinoderms. In other words, it seems like ancestral vertebrates retained larval features into adulthood, and then just grew bigger in size.

Based on morphology some hold a conceptually related - but opposing -suspicion that ( within protostomia ) caterpillars evolved from onychophorans by hybridogenesis ( rather than being larvae ) http://www.pnas.org/content/106/47/19901.full

@tsttst This is a very interesting article and concept, which I had never heard of before -- thank you for the reference! I am looking forward to reading all of it

echinoderms are sort of bilaterally symmetrical, imagine if you took a velvet worm and then twisted it around in a big loop with the legs sticking out until the head was stuck to the tail end but still pointed away from each other. That is basically how echinoderms went from bilateral to radial. of course in practice this is done by rearranging hox genes but it is a good way to visualize it.  https://evodevojournal.biomedcentral.com/articles/10.1186/2041-9139-5-22
as for chordates look at hemichordates (which also have endoskeletons) and you can see why the general belief is that tunicates evolved that life stage after branching off(kinda like barnacles) instead of vertebrates losing that life stage.

Thank you for the interesting reference - I look forward to reading it later! The point about hemichordates is a good one which I failed to consider previously.


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Why are animals afraid of the vet?
I can understand why people are afraid of the doctor, because they have mental concepts of health and medicine.
But why should an animal be any more afraid of the vet than the post office or any other public space?
It doesn't seem like they would understand why they are there or what possible consequences it could have, the same way a human would being in a hospital.

They just don't like being manipulated the way they are. The same reason why you don't like to go to the dentist.

Because most dogs are not "dumb animals". Cats are more mysterious, and I've never taken one to a vet, so I won't speak to their behavior there.

Most animals are not afraid of the vet. When I was in practice, many dogs and cats waltzed in perfectly happily.
Of those that were afraid, I presume that many picked up expectations from their owner.  The owners who tell themselves "My dog is going to be afraid of the vet!" will be tense and nervous themselves, and of course their pet will detect this and react the same way. Many owners were far more distressed than their pets were, expecting some huge negative reaction to the vaccination or something (the pet often didn't even notice the injection, until the owner squealed or shrieked with anxiety).
Finally, animals that experienced something negative on a previous visit -- perhaps a bad interaction with another animal in the waiting room, or their owner being afraid of needles, or actually having some unpleasant procedure -- will of course remember this.

My dogs are not afraid of the vet either. They are a little bit cowed by all the smells and sounds in the waiting room, but once in a room with the vet, they are more relaxed and quite cooperative. An occasional yawn and the relative lack of tail wagging suggests they aren't stupid about it, though.


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Do marsupials ever die in childbirth?
Question: Do marsupials ever die in childbirth?
Obviously the notion of there being a linear ordering of "least advanced" to "most advanced" life forms isn't correct. Still, often marsupials are depicted as relic or archaic creatures with an inferior reproductive strategy, since besides possums they are restricted to Australia and New Guinea.
However, compared to some placental mammals, like the spotted hyena and humans, the marsupial method of always giving birth to very small young, who can finish developing outside of the mother's body, seems to be more sensible.
If there haven't been enough field observations of marsupials, then of course this is an unanswerable question, but I was wondering if anyone knew anything about papers or other materials which discuss the advantages of the marsupial reproductive strategy.


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Did insects and arachnids diverge before or after moving to land?

Question: Are arachnids and insects so distantly related that they were already diverging before their (independent) emergence(s) on land?

I am curious to know what the fossil record and molecular evidence has had to say so far about such questions.
To the extent that arachnids and insects might not be any more closely related to one another than they are to crustaceans, and crustaceans are mostly aquatic, it does not seem impossible/implausible to me that the terrestrial transitions of insects and arachnids could have been independent of one another. In fact, considering that wood lice are crustaceans, one can conclude that there have already been at least two independent terrestrial transitions for arthropods, so postulating a third seems less of a stretch to me.
I suppose the thought process behind this is related to this question. Specifically, to the best of my knowledge, flight emerged several times among distinct insect lineages after appearing on land, in cases of convergent evolution. The fact that no lineage of arachnids ever evolved winged flight while many lineages of insect evolved flight independently of one another suggests that the "fundamental recipe" for insects and arachnids is substantially different, i.e. that they are not as closely related as one might have otherwise thought.

Arachnids and Insects are exceedingly distantly related. Although both are arthropods, there are other Chelicerates, Myriapods, and all of Crustacea separating them on the tree. Both diversified on land, independently

Those are two very separate questions. Arachnids include terrestrial groups such as spiders, scorpions, and other arthropods. Arachnids are members of Chelicerata, which includes horseshoe crabs, Sea scorpions (extinct), and probably Trilobites (extinct). Chelicerates evolved in the marine environment, and invaded land afterwards. Arachnids and Insects evolved on land. Hexapods are nested within Crustacea, in a group called Pancrustacea. The likely sister taxon of Hexapoda (Insects, including Protura, Collembola and Diplura) are Remipedia, which are aquatic. See Misof et al. 2014 for the most complete molecular phylogeny, with dates. http://science.sciencemag.org/content/346/6210/763

Wikipedia appears to contain at least some part of the answers to this question, specifically here and here. Specifically, it mentions that arachnids are chelicerates, which diverged from other arthropods during the Cambrian (according to molecular evidence?) or at latest during the late Ordovician (according to the fossil record). Spiders and other tetrapulmonates (not including scorpions) apparently evolved from trigonotarbids, whose (terrestrial?) fossil record dates back to the late Silurian. So apparently not only arthropods, but even arachnids in particular, have had multiple terrestrial transitions. Chelicerates are also part of the larger clade Arachnomorpha, which is perhaps more speculative because it includes several extinct classes of arthropods for which there is only a fossil record and no molecular evidence.
Regardless of the validity of the Arachnomorpha grouping, however, their appears to be a consensu that the chelicerates are a "sister group" (i.e. separate branch) from the Mandibulata, containing crustaceans and insects. (I.e. regardless of which group trilobites and other types of extinct arthropod are more closely related to.) In fact, since insects apparently evolved from crustaceans, crustaceans are most likely paraphyletic (like monkeys or reptiles), such that Mandibulata is essentially the "monophyletic version" of crustaceans. Also apparently my belief that flight evolved multiple times independently among insects appears to be false, inasmuch as the group of all winged (or formerly winged) insects is believed to be monophyletic. The fossil record for insects apparently also consists of terrestrial specimens (well, this is also true for arachnids, since they evolved from the terrestrial trigonotarbids), and dates back to the Ordovician.
But anyway, to the extent that arachnids are chelicerates and insects are crustaceans, and that the chelicerates and crustaceans diverged from each other either during or before the Cambrian period, indeed arachnids and insects are de facto very distantly related and must have emerged on land independently of one another (in fact, both the chelicerates and crustaceans must have both had multiple terrestrial transitions, it seems, which seems quite an accomplishment). In particular, this appears to be another case where major evolutionary divergences were occurring long before the non-expert layperson would be able to identify them based on the fossil record.

Don't forget Myriapoda, which are also part of Mandibulata. But yes, Chelicerates are the likely sister group of Mandibulata. Insects evolved flight only once.


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Telomere elongation methods?
What sort of telomere elongation methods are there currently?
Would this stop aging? (edit: No, probably)
I couldn't turn up anything good on google. I was thinking that maybe you could sequence the telomeres, trim them all at a certain point, and then engineer a polymerase molecule to extend from that same point. Is this how it's done?

It would be simpler to simply activate telomerase genes or insert them using some vector virus. However, telomerase is a key component in the process of tumoral transformation. Basically, if you don't let cells die they will stack mutations until they become tumoral.

I'm confused. I thought the issue with telomere length wasn't that it effects the longevity of the cell, but its ability to reproduce and have its offspring reproduce etc. So then wouldn't longer telomeres just let you have healthy cell reproduction in old age?

It isn't as simple. Many of the things that seems to cause aging are also defenses against cancer, like telomer lenght limitation (wich prevents cells to suffer too much mutations), DNA repair systems, and autoimmunity. For instance, you could overexpress any of those mechanisms in order to prevent cancer, but they lead to accelerated aging, and the opposite is also true. While it is still a polemic topic, it seems that animals have to choose between lifespan and cancer.

I wonder if you activated telomerase in naked mole rats how long they would live. (they have cell density detection that kills all cancer, I've read)

Telomerase will not cause the tumor cells grow faster or live longer because these cells already have their own version of telomerase and adding it to them causes nothing. But healthy cells of the body will take the advantage of having telomerase around them and with a repaired and longer telomerase cancer killer and cancer detector cells will do their job much better thus tumors will be removed with younger cells trying to fight them.


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Is life in a supercritical fluid possible?
Someone claimed that the dinosaurs could only live because back then athmospheric density was around 650 kg/m³, providing some buyoncy, this claim is checked on Skeptics SE. The claim itself is beside the point now. A simple calculation shows us that an atmsphere with this density would be supercritical in underwise normal conditions, the pressure would be increased by a factor of roughly 520. See my answer to the skeptics question for a bit more explanation. I would say that a supercritical air atmosphere rules out life for several reasons:

The high effusity of the fluid may mean that cell membranes don't work
Proteins fold differently under high pressure, requiring specific adaptions
If the partial pressure of oxygen is increased proportionally, the atmosphere is highly toxic
If the partial pressure of oxygen remains at current levels, it is a trace gas and reactions relying on oxygen may run into kinetic problems (There may be a sweet spot between the last two issues)

Anyway, those are just my hunches, I never heard of experiments about life in supercritical fluids and I'm no biologist so my hunches may be totally wrong. My question is: Can we rule out life in supercritical fluids; if not can we rule out air breathing, multi cellular animal life?
Or has any life been shown to thrive in a supercritical fluid?
To stress again, the part with buoyant dinosaurs was given for background (and amusement), I'm only asking here to check my hunch that suprecriticality rules out life.


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In what forms do plants and animals excrete sulfur?
Sulfur is part of the amino acids cystein and methionin, plants take up sulfur in the form of $H_2S$. These organisms will also need a way to get rid of excess sulfur, how? In what compounds?
Judging by the smell of some farts, I guess $H_2SO_4$ plays a role, but I can't imagine that one get'S rid of all the sulfur this way.

Plants do not take up H$_2$S, this is limited to a few microorganisms. Plants take up soluble forms of sulphur as sulphates, and the surely do not build up sulfuric acid (which would destroy the cells). Have you looked at this topic: http://biology.stackexchange.com/questions/15642/can-animals-absorb-atmospheric-sulfur/

Maybe you want to comment on this answer: http://biology.stackexchange.com/a/15609/3037 'He states it's H2S

Apparently, a number of plants can take up H$_2$S. http://www.plosone.org/article/fetchObject.action?uri=info%3Adoi%2F10.1371%2Fjournal.pone.0062048&representation=PDF. (x-posted from other answer.)

Sulfur is $3^{rd}$ most abundant mineral element in the body. Carnivores obtain it from Cysteine and Methionine in the animal protein which converted in to Glutathione.
Excess of sulfur is stored into Glutathione or oxidised to sulfate by sulfite oxidase which is eventually eliminated by urine.

[1]: Nimni ME, Han B, Cordoba F (2007). "Are we getting enough sulfur in our diet?". Nutr Metab (Lond) 4 (1): 24. doi:10.1186/1743-7075-4-24
[2]: Wikipedia on Sulfur metabolism


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polarity of DNA
If currency exists in a solenoid, we can know the polarity.

However, there is no currency in DNA.how to define its polarity then?

@tomd Sorry for my poor comprehension. A DNA molecule has two chains. If at the same end of the chains both have 3'-hydroxyl and at the other end both have 5'-phosphate, then the DNA have the same polarity. If at the same end of the chains, one has 3 and the other has 5, then  the DNA has the opposite polarity, right?

DNA is never structured so that both 5' ends are at the same side, the strands are always antipolar to each other. The structure doesn't work in the opposite direction. Think about a 2-way road: you can define a direction ("polarity) for each side of the road. Proteins that interact with DNA in a directional way are just like the cars on the road: they could feasibly go in either direction with respect to the whole molecule.

@BryanKrause I hate the word always ;)

@canadianer Ugh, you're right, I hate it too and chastise others - you caught me. I even used italics to emphasize my mistake. Ok so...in most forms of DNA, like the common helix people are most familiar with, the ways you are usually going to learn about it in a basic molecular biology class, the strands are antipolar :)

@BryanKrause Haha, yes the italics were particularly damning. Didn't want to be overly pedantic, but the counter examples are interesting. Of course, you're right in almost every instance.

@canadianer No worries for the pedantry, totally warranted in this case and I thank you for it.

@tomd Please note that the polarity of DNA does NOT refer to chemical polarity (or electrical polarity), but rather structural polarity. Polarity in chemistry refers to a net dipole moment of charge density due to uneven sharing of electrons. While DNA happens be a polar molecule in this sense (it is water-soluble), that has nothing to do with the polarity of DNA's structure (that is, the ability to distinguish be the 5' end and 3' end).

Biologists occasionally play a bit fast and loose with chemistry terminology. I think this is one of those examples. Here is the definition of Chemical Polarity via wikipedia: "a separation of electric charge leading to a molecule or its chemical groups having an electric dipole or multipole moment." If you object to the source, please note that the American Chemical Society tasks professional chemists with verifying wikipedia articles on chemistry topics. (https://en.m.wikipedia.org/wiki/Chemical_polarity?wprov=sfla1)

When people discuss the 'charge' of DNA being negative they are referring to the charge within the molecule.

The Phosphates (big red red and blue in the space filling diagram) have a negative charge and make the DNA both water soluble and negatively charged.
One can also talk about the 'directionality' of DNA which simply means that all DNA is 'read' and synthesized in the 5' to 3' direction (referring to the sugar backbone carbon). That's simply how all enzymes make DNA and RNA molecules and how we define the direction of the DNA code.
As far as I know there is no current running through the DNA itself and no pole in that sense.

"When people discuss the 'charge' of DNA being negative they are referring to the dipole moment within the molecule." The way this is worded seems misleading. Does DNA even have a net dipole moment? Or if you meant the individual dipole moments of each nucleotide, perhaps "moment" should be pluralized. It is also misleading because a net charge (such as DNA's negative) is not required for a dipole moment to exist. Furthermore, a molecule may possibly have multiple charges within it, and not have a net dipole moment (if the charges are arranged symmetrically). I think it would be far better

to discuss the negative charge here without trying to associate it with dipole moments, because the two are not correlated here.

@electronpusher A DNA molecule is single-stranded, and has a negative net-charge because of the phosphates and I'm not aware of a symmetric positive charge. I agree a net-charge isn't necessary for a dipole moment, but wouldn't a net charge existing mean that a dipole moment must exist?

The symmetry would be from a like charge, for instance molecule with a negative on the right side and a negative on the right side could have no net dipole moment (assuming the atomic arrangement is symmetrical as well). Whether a single strand of DNA has a net dipole moment would depend on its configuration. If it adopted a spiral configuration, like it does as half of the helix, then the negative charges on the phosphates would all average out spatially. That is, if you looked straight down the helical acid, you wouldn't see any point on the circular cross section that has more

charge than the rest of the points (assuming a sufficiently large number of nucleotides). By the way, here is an example of a net-charged molecule with no net dipole moment: (https://en.m.wikipedia.org/wiki/Cyclopentadienyl_anion?wprov=sfla1).


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Where can we see professional discussions about vaccine development of the covid-19?
Is there any place where people keep talking about the vaccine development professionally? I need the
latest news.

Private companies, not quite open science.

oh...how about relatively professional？Guys with strong biology background, but not work in vaccine companies.

Please see Biology Meta for a question and answer giving various sources of information about coronavirus. However the links provided are to information not chat.

The New York Times maintains a decent vaccine progress tracker: https://www.nytimes.com/interactive/2020/science/coronavirus-vaccine-tracker.html
I also follow Derek Lowe's In The Pipeline blog: https://blogs.sciencemag.org/pipeline/
(It is not purely coronavirus-focused, but it has a lot of good information, and cites sources that you can go to for even more detail)


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Pseudosexual reproduction
Research projects with artificial life generally use creatures that are haploid. The offspring randomly inherit some genes from one parent, and some genes from the other parent.
Q1: Are there any biological species which reproduce similarly? I.e., they're haploid, but the offspring aren't clones. Perhaps hermaphroditic species like slugs or some plants?
Q2: Is there a name for this type of reproduction? If not, I guess I'll call it "pseudosexual" since it's a simplified form of true sexual reproduction.

RE Q1 - perhaps N. crassa is something along those lines. (http://en.wikipedia.org/wiki/Neurospora_crassa)

Yes, that looks like a good example.

Generally, all diploid species pass through a haploid phase in their life. This is called the alternation of generations and the cycle may be presented like this:

Commonly we see organisms that spend most of their life in the diploid phase, with greatly reduced haploid phase (e.g. humans "live" in haploid state only as gametes). However, this is not the only way possible. There are organisms, which spend similar amount of time in each phase, which change ploidy depending on the conditions of the environment and, of course, organisms which spend most of their lives as haploids, with only a short diploid stage.
As a rule, lower plants, fungi and protozoa may exibit this behaviour. Some examples:

Saccharomyces cerevisiae (yes, baker's yeast) will undergo meiosis and form haploid spores in unfavourable conditions, which then can grow as haploid colonies until they encounter a colony of opposite "sex"
Mosses commonly grow larger gametophytes (haploid) than sporophytes (diploid)
Some brown algae grow sporophytes and gametophytes that are indistinguishable form each other
Ferns often grow large sporophytes and small, but self-sufficient gametophytes.

Next question should be "why only lower plants and fungi?" And the shortest answer is that a diploid organism is usually more robust, it can survive more potentially lethal mutations than a haploid.

I don't know any example of haploid, but (pseudo)sexually reproducing artificial life (and hardly any at all existed 4 years ago when the question was posted!). So I assume you meant in-silico life. Then, yes, usually as you described.
There is no regular mechanism of inheriting some genes from one parent, some from the other, when parents are haploid. Such mechanism in diploid parent is meiosis, which is not, of course, possible in haploids.
Rather irregular processes that involves 2 haploid nuclei (identical or not) similar to what you describe are known in some basal eukaryotes (excavates) and in fungi lacking regular sexual cycle. In different contexts these cycles are called pseudo-, as you suggested, or para-sexual cycles.


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How can octopus walk if muscles can only contract?
From this video it is evident, that octopus can make tentacles push:
https://youtu.be/zaE-LwDowcU
How is it possible, if it is said, that muscles can only contract?
What types of muscles can distract?

Octopuses have "functionally antagonistic longitudinal and transverse muscle fibers" that "not  only  create  the  movements  but  also
supply the skeletal support".  It's basically the same as your tongue.

Can these fibres push?

One can probably extend @Armory's comment to make an answer explaining how those muscles can explain tongue and octopus movement.

Kier and Smith wrote a paper on how tongues tentacles and trunks worked. It explains in detail exactly how their legs (and our tongues) elongate, shorten and move about without any bones for support. It's called muscular-hydrostat.
Movement of the limb actually depends on which muscle is being contracted. If it's contracting the muscles longitudinally it will make the limb short and wide, while if it contracts laterally it will cause the limb to extend and be short and thin.
If you watch the video carefully you can actually see the changes in thickness of the limbs as the lateral muscles release and the longitudinal muscles contract so the octopus can move its leg forward.
If you want to see it work in person, go into the bathroom and move your tongue around and watch in the mirror. It uses the same mechanics to move your food around your mouth, lick your teeth, help you get that bit of food that is stuck up against your gum, and who can forget rolling the tongue into a cylinder or making tongue clovers.

@SolarLunix I believe Chris suggested you edit your existing answer to include the source, rather than add it as a comment. Might also be helpful if you could add more details to your answer. If I'm reading this right, figure 5 suggests that the muscles around the tentacle contract, squeezing the tentacle into a smaller diameter. Since volume must be constant, the tentacle gets longer. Once the tentacle grabs something, the longitudinal muscles contract and pull the octopus forward, allowing it to walk.

Sorry I'm quite new to this site @user137, and as for what you read, that was my understanding as well.

@SolarLunix That's fine, just make the edits and you'll be ok.

Shame for me: forgot about myself tongue :)))

@Dims lol we all forget sometimes :D


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Is it true that cats can drink sea (salted) water?
Found somewhere in the Net, that cats can drink sea (salted) water.
This fact seems to me as being urban legend, not true (because the purpose of water in body apparently implies it should be clear).
What is true and how to explain?

Can you add the link please?

This question would be better suited for Skeptick.SE if you can demonstrate that it is a notable claim.

I can drink sea water! Nothing extraordinary. You probably mean something like "be hydrated when drinking nothing but sea water"

Since cats are well adapted to dry environments, the question has some plausibility to it.
The book "Mineral Tolerance of Animals" suggests that cats may be able to tolerate slightly more salt in their diet than dogs (1.37 g salt/kg body weight for cats, vs. 0.64 for dogs).  However, these represent concentrations that were shown to be safe, not the maximum they could potentially tolerate. The reference in the book is Yu et al., 1997, and though the actual reference is not available in the Google Books version I believe it must be The minimum sodium requirement of growing kittens defined on the basis of plasma aldosterone concentration, so the goal was to identify minimum rather than maximum levels.
The ocean is about 3.5% salt.  The 1.37 value for cats came from kittens eating a diet that was about 2.5% salt, but another note in the book says that cats can safely eat a diet that is 3.8% salt, though they don't like it. I can't find the original reference ("Berger, 1979") for this claim, but I am pretty sure that this was with ad libitum water so they could flush out extra salt.  If so, cats would not be able to tolerate sea water unless they had another source of water as well.
It's often said that wild cats can get most of their water needs from their prey's blood.  It's also sometimes said (incorrectly) that the salt concentration of blood is like that of seawater; this is not true (blood is more like 1% or less NaCl) but it may be the source of the statement.

The Wikipedia article on cats makes this claim with references to https://www.ncbi.nlm.nih.gov/pubmed/13627238 and http://www.nap.edu/catalog.php?record_id=910


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Recombination fraction( frequency) in Homozygotes
I have a question about the recombination frequency I hope you have time to answer.
Background: If we look at homozygous individual A/A B/B which has been formed from the gametes AB and AB, this individual will in turn have the gametes AB, AB, AB, AB. These are the same as the gametes that were used to form the individual.
My question: Is the recombination frequency 0? Or should we consider the A's and B's as different, i.e like A$_1$, A$_2$, B$_1$, B$_2$. Then we get the possible gametes A$_1$B$_1$ (parental), A$_1$B$_2$ (recombinant),A$_2$B$_2$ (par), A$_2$B$_1$ (recomb). We then get that the recombination frequency is 50 percent (which it should be according to the source given at the bottom). Which interpretation is correct?
Definitions used in my question:
"Meiotic recombination is any meiotic process that generates a haploid product with new combinations of the alleles carried by the haploid genotypes that united to form the meiocyte." (Griffiths et. al, Introduction to Genetic Analysis, tenth edition, International Edition, p. 95)
Recombinants: "Recombinants are meiotic output different from meiotic input." (same book).
Recombination fraction: "Recombination fraction (also called recombination frequency) between two loci
is defined as the ratio of the number of recombined gametes to the total number
of gametes produced." (Shizhong Xu, Principles of Statistical Genomics, Springer, Chapter 2, page 11, 2013).
Furthermore: "When genes are unlinked, they have a recombination frequency of 0.5, which means 50 percent of offspring are recombinants and the other 50 percent are parental types." (Source: Boundless. “Genetic Linkage and Distances.” Boundless Biology. Boundless, 21 Jul. 2015. Retrieved 11 Sep. 2015 from https://www.boundless.com/biology/textbooks/boundless-biology-textbook/modern-understandings-of-inheritance-13/chromosomal-theory-and-genetic-linkage-97/genetic-linkage-and-distances-427-11654/)

Welcome to Biology.SE
Your question stems from the confusion between measuring a recombination rate and the actual recombination rate.
In the A/A, B/B individuals you describe, recombinations still occur. Those recombination just don't affect linkage disequilibrium between the Aa and the Bb loci as there is no variance at those loci in the individuals you considered. There is therefore, no way to tell whether or a recombination event occurred in a specific case. You need genetic variance at both loci in order to have a linkage disequilibrium which can be affected by recombination. But it is not because you can't measure the recombination rate that recombinations does not occur.


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Interpretation of F in inbreeding on the population level
The inbreeding coefficient for an individual gives the probability that the individual has two alleles at a locus that are IBD. What interpretation does the inbreeding coefficient have on the population level? Is it the average inbreeding value in the population?
It is possible to derive the genotype frequencies in the population when the population inbreeding coeeficient is given by F. These are given by:
$A_1A_1$: $p_{A_1}F+p_{A_1}^2(1-F)$
$A_1A_2$: $2p_{A_1}p(1-F)$
$A_2A_2$:  $p_{A_2}F+p_{A_2}^2(1-F)$
Is seems like F gives the probability that the two alleles in an individual in the population are IBD. Does this mean that F is the average inbreeding coefficient in the population?


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Meaning of "U" in "Viral Protein U"
What does U mean in Viral protein U?

Viral protein U (Vpu) is a unique gene product of human immunodeficiency virus (HIV) type 1 (HIV-1) with two well-described functions...

So does U in this case mean unique?

Source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC114397/


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Small vs Large neurons
What is the criteria for classifying neurons as small and large?
Is this classification based on gross size or the length of axon?
Do they have any physiological difference?
For instance it is said that Substantia gelatinosa of Rolando contains small neurons .
What is so special about calling those neurons as such?
Aren't they doing the same function of conduction of impulses?

I have googled it but couldn't find any explanation for such naming.

Spinal cord isn't my forte, but when there are references to "small cells" these are always in my experience related to histological appearance, and though there is no specific criterion for what makes a cell small, it usually means "relative to other tissues" - I would expect these cells to be small relative to others in the spinal cord. I looked for a couple examples, and in the situations I found so far "small cell" always seemed like a description, rather than a designation.

My guess, though based on knowledge of other areas, is that the Substantia gelatinosa of Rolando is (or was originally) defined by the presence of smaller cell bodies that distinguished it from the surrounding areas before any function was elucidated.

(note that this terminology goes back to the early 1800s)

Depending on the neuron, small/large could mean one of two things:
1: Axon diameter, larger axons have lower resistance, so transmit action potentials faster see tables here. Important for neurons that cover long distances to convey information quickly.
2: What I think you mean though is the size of the cell body, where some neurons, e.g. Purkinje cells are much larger than nearby golgi cells. In which case the size is related to the function, large cells tend to have large dendritic fields and integrate many inputs into a single output, often relayed to a different area of the brain. Small cells are typically interneurons that only have an effect over a very small area.

So, what kind of small neutrons are present in substantial gelatinosa of Rolando? Do they have large cell bodies or axons?

I pretty much have no idea, I've never heard of it, but a quick look at wikipedia suggests that small slow-conducting sensory neurons synapse with neurons here, so I guess it forms a relay, where information from the sensory neurons is sorted out before being sent up to the brain. For some reason this kind of sensory information is transmitted slowly, so small diameter fibres. I'd guess the cell bodies are pretty small as well, but I can't be sure.

In my experience, calling a neuron "small/large" is always in reference to the size of the cell body. In some areas there may be a correlation with axon or dendrite length but it is usually based on Nissl stains of tissue so people are just referring to the soma.


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What is a microsome?
This site says:

In cell biology, microsomes are vesicle-like artifacts re-formed from pieces of the endoplasmic reticulum (ER) when eukaryotic cells are broken-up in the laboratory; microsomes are not present in healthy, living cells.

Whereas this other site says:

Microsome is another name for the smooth endoplasmic reticulum (ER).

Are they both correct? Which one is correct?

Google says "microsome
ˈmʌɪkrəsəʊm/
nounBIOLOGY
a fragment of endoplasmic reticulum and attached ribosomes obtained by the centrifugation of homogenized cells."

Or see this

@Metroplex so second site must use the word fragment?

Yes it should.

The first quote is correct. 'Microsome' is more of a lab term. This is because, as said they are found (re-formed) after centrifugation and as such aren't seen in an intact cell. Differential centrifugation is a technique used to separate cellular constituents into fractions. To quote,

The microsomal fraction is the pellet produced when the postmitochondrial supernatant is centrifuged at 50,000g for 60 minutes. Microsomes are small vesicles enclosed by a biological membrane. During centrifugation, the endoplasmic reticulum is fragmented into microsomes

The microsomal fraction may also contain pieces from the plasma membranes apart from those from the ER.


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What is "multiple" myeloma?

Multiple myeloma, commonly referred to as myeloma, is a cancer of the plasma cells found in the bone marrow.(source)

Is there any significance in calling myeloma as "MULTIPLE" myeloma?

Any reason for downvote? what sort of attempt should I show in this question if I am unable to it by googling?

You often claim to have googled something but found nothing. Yet, it's that very attempt to find an answer that would make your questions more on topic. You claim, how can I include my research if I found nothing? Well, then, tell us what terms you used when you googled. Not my downvote (I never stopped to wonder so it was interesting), but yes, my closevote.

@GerardoFurtado I google etymology of multiple myeloma and myeloma vs multiple myeloma.

J. Von Rustizky, a Russian pathologist working in the laboratory of Friedrich von Recklinghausen (1833–1910) in Strassburg in 1873, introduced the term “multiple myeloma.” At autopsy, a 47-year-old patient examined had eight separate tumors of bone marrow, which Von Rustizky called “multiple myelomas,” and he noted that the nucleus of the tumor cells was located in the periphery of the cell membrane — a morphology highly suggestive of plasma cells.

source: Kyle, RA, Steensma, DP (2011) History of multiple myeloma. Recent Results Cancer Res., 183: 3-23
From the same item:

The most commonly recognized [first documented] case is that of Thomas Alexander McBean, a highly respectable tradesman from London in 1850. Mr. McBean excreted a large amount of protein that was described by Henry Bence Jones in the middle of the 19th century. Jones was a well-known physician and made many contributions to medicine.

The Bence Jones protein is in fact an immunoglobulin light chain. Purified Bence Jones protein were sequenced by FW Putnam, and
variations between patients were some of the first clues to the existence of the variable regions of immunoglobulin molecules.

Hmm, in addition to the information I get from your answer, today I learned a new googling skill, which is to get etymology we should also try History of _________. Thanks.

Another good strategy would be searching databases like PubMed for "review" articles. These will almost always have "history" sections in the beginning, and even if they're very short, they'll usually have citations to other papers that you should look up—perhaps even the original, as in this case. @JM97