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Is there a term for non-DNA gene?
Initially, the term "gene" referred to abstract concept of inherited trait.
Currently this term was hijacked with molecular genetics and means a continuous sequence of nucleotides. However, it omits the fact that for a phenotypic trait to be inherited, sometimes there can be more than one sequence of nucleotides, and sometimes one sequence of nucleotides participate in the formation of more than one phenotypic trait.
Is there a single-word term describing non-DNA "Mendelian gene"?

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@tyersome I replaced "sequence" to "continuous sequence". However, there are also phenotypic traits that even do not completely depend on DNA sequences, even if they conventionally claimed by the molecular geneticists to be derived from some continuous nucleotide sequence (which is nowadays called "gene"). For example, if the child will not learn language to a certain age, he will lack the phenotypic trait of speech. If he missing any of (non-continuous) nucleotide sequences responcible for development of vocal cords, he will also not be able to produce speech.

But what about Why genes in pieces?

@user268587 You seem to be referring to a polygenic trait, not a "non-DNA" trait (multiple genes affecting a single trait). The opposite, a pleiotropic gene, is where one gene affects multiple traits.

Epigenetic inheritance is one example, but it is not covering all the possibilities. https://en.wikipedia.org/wiki/Transgenerational_epigenetic_inheritance
I suggest reformulating the question in less controversial terms: less attacks on the established terminology, and more about non-genic inheritance.

Please remove the phrase “non-DNA” from your question. The only non-DNA genes are RNA genes in certain viruses, which is not what you mean. The nucleotide sequences you describe are DNA — by definition. Specific descriptive terminology is used for genes which encode subunits of a protein, both of which are required for a functional whole (1) or generate more than one product by differential splicing (2), but it only makes sense to answer your question in these terms if you transform it into something that makes sense. “Answer only well-asked questions” is a principle of this site.

@David I can use "DNA" here, because despite the fact that "RNA" also encodes genes in molecular biologist definition, all non-microscopic organisms with observable phenotypes are DNA-based, my question is fully understandable and the phrase "non-DNA" adds additional context to it in the sense that it asks about "non-nucleotide" gene.

You seem to be asking about DNA based phenomena (you wrote "sequence of nucleotides" twice), but then you say "non-DNA". This is at best confusing. Please edit your post to make your question clear. In addition, you give the impression that you may be unfamiliar with molecular genetics, so I encourage you to avail yourself of some of the introductory material available online. That may answer your question and will definitely help you ask a clearer question. ——— In addition, you may not like how the usage of "gene" has evolved, but that isn't a fight you can win ...

I have found that when learning about a new area starting with a relatively accessible and reliable source like Khan Academy is very helpful. Wikipedia is also generally a good starting point and you can then check their references. Online platforms called MOOCs offer free (or very low cost) courses on a wide variety of subjects — two I am familiar with are Coursera and edX. Finally, textbooks with a good level of detail are also freely available online e.g. from NCBI.

@tyersome I disagree. You give me impression that you may be unfamiliar with structuring of sentences so I encourage you to embrace yourself with grammatic and logic books. First, I do not wrote "sequence of nucleotides" twice. In the first example I wrote "more than one sequence", while in the second just "one sequence". Second, there is no fight. I doubt that you have seen me fighting against this trend of merging these ideas of a gene definition on a public debate. Rather there is a question if this term exist in the scientific community nowadays.

"Non-DNA gene" makes it sound like these https://en.wikipedia.org/wiki/Xeno_nucleic_acid  .

I think that what you are interested in is the original Johannsen definition of the gene as of 1909 (I translated this article, caveat emptor). Notably, Johannsen cautioned explicitly against reading too much into the abstraction of the gene, and instead insisted on reference to heritable phenomena that we would call traits or phenotypic characters, with the understanding that underneath that there is an unseen and unknowable "genotype", which can be inferred through the use of logic and statistics.
However, as you rightly point out, molecular genetics came along and changed things. At that point, many of the phenomena that Johannsen was interested in could be directly be related to genes in the sense of DNA sequences. The Central Dogma of molecular biology reorganized thinking along molecular gene-centric lines, which do have issues as you note.
However, the original Johannsen definition of the gene was never more than a a vague factor for helping genetic reasoning, no one has ever observed such a thing in the wild! There is a reason why no one speaks of genes in this way anymore, and it's because we now know a lot more about how complex molecular mechanisms that generate phenotype are. This is one of the good things that molecular biology gave us, even if you take issue with its reductive character.
If what you want is just a term that refers to a character which can be built of many genes (e.g. polygenic), or including e.g. epigenetic inputs, then "phenotype" or "trait" is perfectly good. But again, such things are subjective, and are limited by what humans can measure and observe.

The Cambridge Dictionary, CDC, and the NIH's institudes researching the human genome and cancer all agree that genes have 2 properties:

they are associated with heredity
they are a section of DNA translated into proteins

However, the Oxford Dictionary has an informal definition and formal definition. The informal definition refers to only to the first property and the technical definition refers to only the second. It also agrees with you on the etymology of the word.
It is clear to me that in the modern usage, gene refers to one factor in the inheritance of traits. The definition does not assume that no other factors of trait inheritance (e.g. DNA methylation, memes) exist. This differs from the early 20th century use of the word, which assumed that no other factors besides genes are responsible for inheritance, i.e. 'gene' was an inclusive term for all factors of inheritance.
To my knowledge, there is no single word in modern usage that has the same definition as 'gene' did in the early 20th century. The phrase 'factors of inheritance' is as close as I think you can get.
P.S. Technically detail, but not all continuous sequences of nucleotides in a strand of DNA are genes. Many sections of DNA serve structural purposes (e.g. centromeres, telomeres) or help regulate gene expression.

There are some exceptions to your (2): for example, some viruses encode their genes in RNA rather than DNA. More importantly, many genes are not translated into proteins -- their RNA transcript is the functional unit: for example ribosomal RNA genes or transfer RNA genes. Other parts of genes (such as promoters and introns) are either not transcribed or not translated, but help determine the transcribed or translated product.

Thus, a more complete version of your technical definition (2) above would be: "a distinct sequence of nucleotides forming part of a nucleic acid segment, the order of which determines the order of monomers in a polypeptide or nucleic acid molecule which a cell (or virus) may synthesize." (minor modification of Oxford Languages definition returned by Google)

Your right. What is interesting though is that of the 5 sources I had for definitions, only the Oxford Dictionary includes viral RNA as containing genes. The rest make explicit reference to DNA.

General dictionaries are a useful reference to the English language, and I would quote them on SE English language and usage, but they are hardly where one goes to discover the terminology used in specialist aspects of a subject. This is trivially obvious from definition 2, which ignores both RNA viruses and non-coding parts genes and mRNAs.


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Whether de novo mutation can be inherited or not?
Think about the following scenario: A child is diagnosed as having long QT syndrome, an autosomal dominant disease. However, neither of his parents is affected. This may be due to a new mutation in the embryo, which would explain the son having the disease with normal parents. Next, this de novo mutation could be inherited to off-spring of the child? or not?
And there are additional questions. Why do so many genetic tests performed by blood samples represent all germline mutations? Except for cell free DNA, blood cells are not germline cells. Therefore, the mutation found in the blood sample test may be a huge somatic mutation (except blood cancer). For example, for mutations that occurred early in embryo development, many cells may have been affected, and I think this might be in the form of somatic mosaicism. Doesn't it mean that it's a germline mutation if it's found at 50% or 100%?
I asked you a little more, is there only a family test (segregation test) that checks to see if it's a germline mutation?
Thank you so much in advance.
Please answer these long question, because no one answer me about this question.
If you answer me, I 'll always love you somewhere in the earth.

Thank you very much!! And I love you forever :)
And you say, in other words, de novo mutations can occur in postzygotic embryos or by germline mutations in parents.
Then I want to go further and conclude. In this case, an autosomal dominant disorder was detected as a heterozygote on a blood test. If it occurs in the embryo after conjugation, two possibilities are conceivable.
It could happens a heterozygous allele in the whole cell of a postzygotic embryo, Or can occur in one of the cells as a homozygous mutation when there are only two cells in the early embryo. In the latter case, autosomal dominant mutation would be lethal, so the child is likely not lived.
So in conclusion, if I thought that the whole cell of the child had the heterozygous mutation of the long QT syndrome, it was probably the result of the parent's germline mutation.
Am I thinkin right?

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De novo mutations can be inherited if they occur in the germline cells, those responsible for making the sperm or the egg. If you have a de novo mutation in a blood cell or a skin cell, this doesn't pass on to the next generation. But when you test the blood for mutations, it can also mean that the same mutation is present in the germline! However, if the parents are not sufferers of the dominant disease, it means this mutation is not present in their somatic (non-germline) cells. It's likely that the mutation occurred de novo in either the parent's germline during their lifetime (during the production of their sex cells in adulthood).
If your parent has a mutation in their germline, and it is passed on to you, the zygote is formed from both your parents (half of your alleles are from the mutated parent) and this zygote creates ALL of you, including your blood cells and your skin cells. This is why we can test your blood to guess what must have been the case in your germline. Of course, you may have accumulated mutations independently in the germline in the meantime, or accumulated mutations independently in the blood cells! So it's not completely the case that testing blood will tell you about the state of the germline. But you must understand that ALL of you is created from a single cell, the zygote, so at this point there is a 'bottleneck' that forces all somatic and germline cells to share the same genetic makeup.
Also, please consider that humans are diploid, i.e. have one copy from the mother and one copy from the father. And that these recombine and only one copy goes into the sex cell. This may help you think about your problem.
I trust this will help you better understand your questions.

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How octopus develops its imitation skill?
I've watched one documentary about a Mimic octopus which they can imitate another animals in several form e.g. a Lion fish, a Sea snake, a Flatfish, etc. My question is how these octopuses can have these such skills? Imagine that they can not see themselves via a mirror but their imitation is so perfect.
What is a theory behind this?

well other animals do imitation and sometimes cant see themselves, the wikipedia describes two types of mimicry that it exhibits: https://en.wikipedia.org/wiki/Batesian_mimicry  and  https://en.wikipedia.org/wiki/Aggressive_mimicry

There are even theories that some squid and octopuses have monochromatic vision, yet have the ability to change colour. Go figure!

I am confused about the use of the tag evolution in your question. Are you interested in the physiology of mimicry in octopuses or about the evolution of the mimicry?

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Fish ID? Small, yellow-finned, tropical fish in Thailand
I have not had any luck finding the yellow fish shown in the photo in any of my fish books. I saw them in many places, so they are fairly common. This observation was at around 15 meter depth.
I hope someone here knows it.

With a little Google search I found similar fishes. Says it is golden or yellow damselfish or possibly lemon damsel but I'm not sure because there are some different names for this picture or different pictures for searching same name can be found on Google.
Also, I found a fish identification page on which this fish can be found.
Is this your fish?

Yes, I think you found it. A Damselfish was also my first guess, but I thought I had ruled them out because none of the books or sites that I looked through had damselfish with fins like this.
Here is a link to the specific Fishbase entry: http://www.fishbase.se/summary/Amblyglyphidodon-aureus.html

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Cellulose Branching
I understand that humans cannot digest cellulose because there are no branches to break down the polysaccharide chain.
But why can cellulose not form branches?

Cellulose is, by definition, unbranched. If it is branched, it becomes another compound. This is like asking why blue-eyed people can't have brown eyes. If they did, they'd no longer be blue-eyed.

You misunderstand. It has nothing to do with branching. (And, as @MattDMo writes, you are attacking the problem from the wrong end.) Humans cannot digest cellulose because they do not have the enzymes needed to do so. These are called cellulases, which you can read about here. The problem seems to be one, not only of breaking the β(1→4) glucose linkage, but disrupting the higher-order structure formed by the interaction of individual cellulose chains.
Ruminants, that need to digest the cellulose in grass, also cannot produce cellulases, but they host bacteria to do the job for them in their rumen. Presumably if we humans needed to live on grass our stomach evolution would have followed a similar path.


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Somatic cell cloning always produces female offspring?
I was looking at the somatic cell cloning of goats.
One of the advantages of the process said was

All offspring produced are female.

Now I'm confused.
How is this the case?
I know that the embryo after electrofusion is injected into a surrogate mother, but I don't understand how the advantage is that they are "all ... female."

What is the sex of the somatic cell donor?

@AlanBoyd I don't know! That's what I was confused by.

Probably you should provide a link to your source.

For most species of livestock only the females are of economic value. And if you clone a female, you will only get female offspring.
I can also imagine that you would want to use an oocyte and somatic nucleus from the same animal. This way, you also preserve the mitochondrial DNA from your golden goat. And males just don't make eggcells.
It could also potentially avoid any incompatibilities between host and donor, somewhat comparable to donor organs. But I don't know if this is actually an issue.


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Xylem in the centre of the root
I want to ask a question about xylem in the centre of the root.
I am reading a book about transport in plants, and it reads this regarding the root structure:

Roots are subjected to vertical stresses - they have to be able to resist being pulled out of the soil.  A central core of strong xylem tissue gives ideal resistance to being uprooted and at the same time gives economy of space.

I'm confused about this passage.
How does the centre of the root being xylem tissue exactly prevent the resistance to pulling forces upwards out of the soil?

(+1) because this doesn't make any sense to me - I can't see why having xylem further to the centre of the root would withstand vertical stretching forces

The is something called the Pressure Stiffening Effect (turn on a coiled garden hose and watch it try and uncoil for instance), pressure in the fluid filled xylem stiffens the root, making it harder to pull out, Roots are rarely completely vertical or straight to pulling them from the soil generally involves them flexing, which the stiffening pressure resists. its the same reason an Inverted Y of steel can anchor in soil but an inverted Y of rope will not, the steel resists bending thus you have to displace all the soil above it to remove it.


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Is the CDC's reported drop today in COVID-19 cases by date of diagnosis meaningful?

I was waiting with bated breath for the CDC update on cases of COVID-19 in the U.S. by date of onset.  To my eyes this looks like absolutely wonderful news - that it means that the exponential growth of the virus has been "flattened" - but I'm still afraid I may be misinterpreting what I see.  It bothers me that the headline for the graph hasn't changed.  But it APPEARS that the number of new cases stopped increasing after 3/3.  Am I missing something?
Top: before noon on 3/16, bottom: after noon on 3/16.  Data from https://www.cdc.gov/coronavirus/2019-ncov/cases-in-us.html
Note: In today's update (the first in three days) the CDC page shows the number of cases with onset on 3/4 to be 159, and 3/9 is 307.  This doubled in five days rather than every two or three as other numbers would suggest, but given the dramatic changes in this curve, and their overall direction, I think the top answer below has been vindicated.

Did you read the text in the gray shaded area?

Yes I did.  And yes, I'm aware that on previous days some cases were added OUTSIDE the gray shaded area.  Nonetheless ... in many countries the number of confirmed cases has been growing about 33% a day.  So I was expecting to see the number of cases just to the left of the gray shaded area be something around 140 to 200 - instead, it is less than 70!  Is that a breakdown in the system ... or the system finally working?

The US has been adding more than 500 new cases a day over the last couple days; these data seem very incomplete. I would wait to have more information before interpreting them much. (There are over 4000 US cases but these data are based only on fewer than 800)

Well, there are more columns on the graph, and no cases were taken out ... yet it is still labelled as 800 cases.  So I don't think that headline is right.  Nonetheless, when I sum up their data table beneath in LibreOffice I get 970 cases, so it is still plausible this is unrepresentative (but if so, why?)

On the page those data are reported, the ** indicates: "Does not include cases among persons repatriated to the United States from Wuhan, China and Japan; does not include U.S.-identified cases where the date of illness onset has not yet been reported." I'm guessing that locations with high concentrations of cases are more concerned with reporting the cases as they come in than determining date of illness onset for everyone. They're probably quite busy.

This is against the experience of all other countries dealing with this disease. So this is most like due to under-testing.

Perhaps worth noting that the CDC is not keeping its public data current.

Any data you get from the CDC will not be current and so not accurately reflect trends. Further, lack of testing in the US means that any data that you do see will not accurately reflect true infection numbers or rates.

The information you show is meaningless unless it is also accompanied by the number of tests performed. If the CDC tested 2 people and got two positive results, that doesn't tell us anything at all about the actual rate of infection. And, indeed, the CDC has been testing a shockingly low number of cases:

‡ Data during this period are incomplete because of the lag in time between when specimens are accessioned, testing is performed, and results are reported.

(image source)
The last day they give data for, 2020-03-15, includes 0 samples from the CDC and 4 samples from other public health labs. Since only 4 samples are represented in the chart, of course we see a drop in cases, but that's because they are based on only 4 tests. As more tests for those dates and subsequent dates are reported, the numbers will change.
Date Collected  CDC Labs    US Public Health Labs
3/12            75‡         2302‡
3/13            0‡          1511‡
3/14            0‡          165‡
3/15            0‡          4‡

As you can see in the table above (from the same source as the graph), the past few days have seen almost no tests are being included in this analysis either from the CDC or elsewhere, so any drop in cases is completely meaningless.

The dates you highlight - from 3/12 on - are within the gray box, which we already know is incomplete data.  The days outside the gray box are the ones more at issue.  I see today's update increased the total cases in the chart from 930 to 1295.  The number of cases on 3/9 was 113, but all the others were less than the peak of now 90 (not 70 any more) for 3/4.  There is something complicated going on here and I think your connection to this other page IS on the right track but it is wrong to say no testing is happening or to link it with the gray box.

@mike what day are you referring to? The truth is, sadly, that the answer won't change. There is no way of looking at these data that could make them be representative of the real infection levels in the general populace, but if you clarify exactly what dip you are referring to, maybe we get get some more detail. – terdon 43 mins ago

Sorry to be confusing - I've gone back and edited the original question to add the third (current) version I was referring to.  Note that there have been cases added, but they have been added throughout the curve - so the 3/4 peak increased, yet 3/5 to 3/8 are still less than that.  So while the reported cases have been increasing exponentially, those at least might be OLD reported cases.  That means the total infected is much higher than we think ... but also leaves open the question of whether recent changes have actually reduced the spread of the disease.

@MikeSerfas any effect of the recent changes will only begin to be visible in a few weeks, not now. The main point, however, is that those data are not really helpful if you are trying to monitor the actual rate of infection because the tests being reported are way, way too few to accurately represent the rate of infection in the population. And, again, the dip isn't informative since there was a corresponding decrease in the number of tests whose results are being reported.

I added another graph from today that continues the trend.  The number of cases is not actually growing as fast as the cases reported for the country at large (the 792 is from before the weekend) but the later days seem like an exponential increase, yet the individual day of diagnosis still seems to have flattened out at 3/4.

@MikeSerfas you're still missing my point. You keep looking at the graph and ignoring the big grey warning on the last days explaining that "Data during this period are incomplete because of the lag in time between when specimens are accessioned, testing is performed, and results are reported." And you also don't seem to be taking into account the number of tests performed. Wait a few days and you will see the numbers for this period will change significantly. I understand the wish to see this flattening but there simply is no data to support that.

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text:
Does COVID interfere with internal respiration?
Siddiqi et al. wrote in January 2021,

Pulmonary ECs [= endothelial cells, in this paper] have an important role in immune surveillance, maintaining alveolar integrity and ensuring appropriate oxygen exchange. In COVID-19, direct viral infection and the systemic inflammatory response likely lead to severe dysfunction of these important ECs, compounding the resulting picture of severe hypoxia and acute respiratory distress syndrome frequently reported in hospitalized patients.

Question: does COVID infection of other endothelial cells interfere with internal respiration (oxygen and/or possibly CO2 exchange at the destination tissues)?

I find some of the responses confusing.  The quoted text says that pulmonary endothelial cells have a role in ensuring appropriate oxygen exchange - this is no surprise since the oxygen passes through the cells.  "Oxygen permeability" refers to how well the oxygen passes through the cells.  "Internal respiration" is the anatomical term for the exchange of gases at the systemic capillaries.  The mechanism of action, as stated in the quote, is a combination of direct viral infection and systemic inflammatory response - I expect more the latter.  Whether COVID infects the endothelial cell directly, affects a neighboring cell, or causes differences in serum cytokines that affect the endothelial cells, all I was wondering is whether as a whole, the wall of an infected person's systemic capillary would diffuse oxygen more slowly.

I just took a peek your reference. The likelihood of the answer being there in the paper is quite high. Look at Fig. 1.

I looked again ... in that figure they discuss thrombosis and vasoplegia, but not whether the permeability of the cells to oxygen changes.

I'm sorry to ask, but what does "permeability" mean to you? Or, for that matter, "respiration"? Because I'm not sure I understand your question without understanding your definitions, which seem vaguely to shift. To me, it's obvious that thrombosis (as a result of vascular epithelial cell damage) will injure cells distally, which of course is from oxygen deprivation. Whether a cell is permeable to O2 is irrelevant if there's no O2 around.

https://en.wikipedia.org/wiki/Respiration_(physiology)

Wikipedia doesn't cover internal respiration there - see https://open.oregonstate.education/aandp/chapter/22-4-gas-exchange/ .  We tend to take gas exchange across an endothelium for granted, because that's what it's for, but membrane cholesterol, glycocalyx, permeability and thickness affect how well it works.  I don't know if COVID affects it (putting any perfusion issues aside).

May I suggest you read more about the mechanism of action of the virus and how it causes cell (and organ) damage? Your questions show some inconsistencies in definitions and certainly the action of the virus.


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Is the central sulcus the boundary between basal and alar derivatives?
The dorsal part of the nervous system typically gives rise to sensory structures, and the ventral part gives rise to motor structures.  Because the central sulcus marks such a functional boundary, I had assumed it was an example of this zonation ... however, recently I didn't find any source to defend this position.  (I would have been sure that hunting for "fate map" and "central sulcus" would pull up something informative...)  Some of the embryology, in which I think a trace of a central sulcus might be apparent quite early, can be seen at UNSW, but none of the embryology images I considered really seem usable to answer the question.
*Note: "Central sulcus" is referenced as a visible marker for the boundary between motor and sensory functions.  Answers that trace the origin of this boundary in species where it is not marked by a sulcus are also welcome.

The basal and alar plates have an important sensorimotor separation of duties in the spinal cord. I don't see any reason to apply this to the cerebral cortex that develops from the forebrain - you're probably not finding anything about this because people don't concern themselves with alar/basal plates in the front of the brain.
Importantly, the neocortex is pretty evolutionarily new. You're placing strong developmental purpose on a sulcus that doesn't even exist in the evolutionary ancestors of humans. There is no such separation between sensory and motor cortex in a mouse, for example.
See this sagittal view of a forebrain:

(image from Medina L. (2009) Evolution and Embryological Development of Forebrain. In: Binder M.D., Hirokawa N., Windhorst U. (eds) Encyclopedia of Neuroscience. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-540-29678-2_3112)
The neocortex is just a small slice situated at the dorsal surface of the forebrain (yes, it does wrap around the entire dorsal surface and extends along the lateral sides, but that doesn't make it anything but dorsal). There is no trace of any dorsal or ventral embryonic origin within the neocortex. The dashed line that roughly separates the dorsal and ventral parts of the CNS ends in the diencephalon; in this view, all of the neocortex, including motor cortex, is part of the dorsal "sensory" part of the brain.

From the papers and images I'm seeing online, such as this one, I have the impression that the mouse forebrain has a relatively similar overall organization with motor areas in a frontal lobe.  (The motor barrel is specific to whiskers, and RFA's exact nature seems to be subject to interpretation, but the overall emphasis seems the same)  Also, I don't see how you can say the region is entirely dorsal but also that there is no trace of dorsal embryonic origin.

@MikeSerfas Yes they have a motor cortex. They do not have a central sulcus, or really any sulci or gyri besides one, the rhinal fissure. The general positions are like humans but there are no "lobes", we only call them that to reference primate brains. I'm saying there's no dorsal/ventral origin separation for cortex. It's not relevant. If you find somewhere that says it's relevant, great, but you shouldn't just look at pictures and guess.

Well, that's why I asked here. :)


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Does N-methylcocaine exist in nature?
N-methylcocaine cation (pictured) is a cocaine analog that blocks HERG intracellularly, if somehow it were able to get into a cell.  A review of tropane alkaloids in Erythroxylum does not include it, or any N,N-dimethyl derivative, but this might be attributed to the issue that a quaternary ammonium salt, though it might be technically considered an alkaloid, would not be isolated (or removed from a soft drink flavoring?) by acid-base extraction.  But before we let paranoia overtake us ... is there any indication the compound exists as a natural product?  (You don't need to look beyond Erythroxylum.  An answer just for E. coca or E. novogranatense would be welcome.)

HERG? It may make you paranoid, but please keep the rest of the list out of it.

I'm not sure which list you mean, but here's one.  The way this article tells it, anything in your kitchen probably messes with the channel. True, this makes me less sure that this was a meaningful observation about the compound in this question, but I'm still curious.

the question of whether it can exist or not is not answerable. rather i would ask can it not exist and why?. Nature encompasses the entire universe. just because humans haven't seen it or synthesized doesn't mean there isn't a planet out there full of it.  or a bacterium it there that makes it.

I admit, I wasn't literally thinking Mars. An answer from Erythroxylum or even just E. coca would be quite welcome.

My comment was an oblique way of suggesting you define HERG, and, if you must personalize please do not use the first person plural, as it suggests the reader shares your emotions. However, on a less oblique note,  may I suggest that you move your post to Chemistry SE. Not only is it a little more likely that someone there will know the answer, but, more to the point, someone there is more likely to know how to find the answer. I imagine there are books and electronic sources for information about natural products, because of their vast numbers and pharmaceutical importance.


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Were nicotinic acid/amide or flavin nucleotides ever part of primary RNA sequence?
NADH and FADH2 redox reactions are built deep into our biochemistry.  For example, pyridine nucleotides are involved in >500 enzymatic reactions.  When we look at the structure of deamido-NAD+, it is strikingly symmetrical:

The same is true for FAD, a two-headed monster of a nucleotide

in which we can recognize the two heads, belonging to xanthosine (a purine nucleotide) and alpha-ribazole 5'-phosphate, the latter of which is produced from flavin in the course of B12 synthesis:

The phosphoribose can be swapped between alpha-ribazole 5'-phosphate and nicotinic acid.
Given such enticing hints, it is tempting to speculate that one or more of these nucleotides might be so fundamental because it was actually part of some ancient RNA primary sequence, giving RNA containing this code the power to do serious catalytic chemistry with acid and amide groups, powerful options for redox and methyltransferase activity and more.
I know this is a hard question to answer, but is there any evidence that weighs in, or could weigh in, on whether this happened?  For example, if these functional groups are too unstable in regard to intramolecular reactions on a strand of RNA, or if there is no way to envision a potential base pair that would be reliably distinguished from the known base pairings.  Or if RNA editing sometimes creates them in some organism.  Or if aptamers made from these subunits show improved catalytic possibilities.  (That doesn't seem so easy to look up, since many papers look for aptamers binding these as prosthetic groups, rather than incorporating them)  It would be useful simply to have a notion of what evidence for such an idea would look like.

Have you searched the literature relating to thoughts on the adenine nucleotide components of NAD and FAD? I am not familiar with this myself, but it clearly must be extensive. My own thoughts on the subject (probably off-topic here) do not include your suggestion of these having been "bases". Nicotinamide and flavin do not look remotely like the bases, have no obvious "pair", and are essentially later oxidising agents to the likely more ancient Fe–S electron redox centres. If they arose to supply the redox function which ribozymes lack, how might they bind to the latter?

Your thoughts shouldn't be off topic - if you can make a good case for late evolution of NADH and FADH2, then it would rule out the idea.  But to my eye, nicotinamide and 5,6-dimethylbenzimidazole don't seem any more different from purines and pyrimidines than those two are from each other.  (I'm not claiming to know what they would base pair with)

There are NAD capped RNAs [1,2] but that's not what you are asking, right?

There are two reasons that I think this question off-topic. The first is that although you have asked for chemical arguments, answers are likely to be matters of opinion. The second is that it does not really conform to the question and answer format of this site, but is more to the discouraged type "I have this idea, am I right?". The way I see of resolving this (because I find the topic interesting) is given in the following comment.

@WYSIWYG: They are useful for your answer, since they show that the NAD isn't excessively reactive in the context of a longer RNA sequence.

A way of resolving the problem would be to rephrase the question to allow a variety of answers, not just the one you have in mind. This would be in of the type "NAD and FADH have adenine nucleotide components which are not involved in the redox reactions — show structures — Why?" You could then answer your own question with your idea, which could be subject to the usual criticism in the form of votes and comments. I could add mine. This would be a bit hard on @WYSIWYG who has just answered your question, but he might consider going along with it.

@David: I think a question of that type would be called "unfocused", and in any case, is a different question.  How do I ask about whether the RNA world had this range of catalytic activity - without asking it?  I think this is already open to a variety of answers and can be answered in the negative as well as the positive.

As you will. I will refrain from commenting on your idea for fear of causing offence, but I do suggest that rather than focussing on chemistry in isolation you consider the evolutionary sequence of events that your idea would entail and attempt to find out what others have written on this topic.

@David: It sounds like you have some useful thoughts to contribute regarding the evolution.  I have trouble deciding what to make of such data.  Does the metabolic relationship with tryptophan mean that nicotinic acid evolved from it, or the reverse?  If methyltransferases act on nicotinamide and RNA, but they're not closely related, what does that mean?  I'm not sure how to get to a conclusion from this sort of information.

Mike. I'd like to discuss this sort of question, but  I have been rather busy over the last few months and am only just re-engaging with the list again in a small way. I am still quite busy and have some other questions here that I need to tidy up loose ends on. I would prefer to wait until I have time to do some reading in this area and then post a question that I feel can generate some good answers. (The great thing about being a scientist is that you never retire. It's just that there comes a time when people aren't paying you any more.)

There are naturally occurring RNAs that contain a NAD "cap" at 5' end (Bird et al., 2018; Wang et al., 2019).
I could not find any papers on natural RNAs with nicotinamide or flavin as a regular base. However, a study with synthetic oligonucleotides reports that NAD containing oligonucleotides can form stable triplex structures (Göckel & Richert,2015).
There are two studies from 1970s that explore base pairing potential of flavin. Raszka and Kaplan (1974) report that FMN can hydrogen-bond with AMP but not other nucleotides. They further explore this finding to show that FAD can form intramolecular hydrogen bonds. Scarbrough et al (1976) show that flavin containing nucleotides can form stacking interaction in addition to base pairing kind of hydrogen bonds. (Compare D-X bonds)

More recently, Julius et al. (2020) have shown that NAD and FAD can act as co-factors of primase to initiate DNA replication.
Overall, it seems plausible for FAD and NAD to be a part of nucleotide chains (more plausibly for RNA as they are already known to contain a variety of unusual bases). However, I cannot comment if they really did play such a role during cellular evolution.


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Stimulating an axon causes impulses to travel both ways?

A diagram is presented as such above.
The question given states What would be the effect of stimulation to cause a nerve impulse with a microelectrode at the middle of the axon?
I thought the nerve impulse only travels in one direction to the muscle fibres, but the book says "A nerve impulse would pass in both directions."
Why is that the case?

I think Gerardo has given a very nice answer, there is just one think I would like to add:
The only reason it usually DOESN'T travel antidromically is because it is initiated at the axon initial segment at the soma. Once the action potential starts travelling (orthodromically) down the axon, it is directly followed by a section of the AP that is in the absolute refractory state. Thus, the action potential cannot turn around mid-way or start spreading into both directions.
However, when you stimulate the middle of an axon, there is (initially) no part of the axon in a refractory state which would keep the action potential from travelling in one direction or another. Both sides of the axon are ready to propagate the action potential, which is why it travels in both directions.
From the Wikipedia page on Action Potentials (under Propagation > Refractory period)

The absolute refractory period is largely responsible for the unidirectional propagation of action potentials along axons. At any given moment, the patch of axon behind the actively spiking part is refractory, but the patch in front, not having been activated recently, is capable of being stimulated by the depolarization from the action potential.


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Neurones and putting on clothes (Pacinian Corpuscle)
If I put on clothes, a gentle pressure is applied to the Pacinian corpuscles in the skin, causing Na+ ion channels to open and an action potential to be initiated - hence I feel the clothes on my skin.
However, I was reading that after prolonged time, the action potentials are no longer generated unless there is another change in pressure as the clothes again move over the surface over the skin.
I'm confused why. The reason I am given is that the Na+ ion channels remain open so a resting potential cannot be established, but I can't see how this contributes to the effect.
Can someone explain why?


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Sampling of Species counting same member of species twice
As part of the biology class, we performed a sample on the number of red squirrels in a forest a few miles away from the classroom to estimate its population.
When we returned to analyse our data, we were discussing about the validity of our sample, and I was wondering whether the idea that the same member of the species being sampled twice may have an effect.
The book I was reading stated:

a sampling procedure does not have to uniquely identify each member of a population to gain an idea of relative numbers.

I'm slightly confused as to why sampling the same member of the species twice is not something that affects the validity of our final estimate for population size.
Can someone explain why the passage in the book is correct?

Can you please explain exactly how you estimate the population size. Do you do some capture-marking-recapture or some other method? Do you take any genetic data?

Note that the quote says, "relative numbers." This means that you would need to use the same sampling procedure for each sample (true but not necessarily obvious). Then when comparing samples one would expect that different samples would have similar numbers  of species being sampled twice.
In other words, as long as each sample is obtained in the same manner, one would generally expect that the same sampling errors would be replicated in each sample, and therefore would still allow one to gain "an idea of relative numbers."


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Oncotic (Osmotic Pressure) in the blood pressure
I just wanted to ask, why is the oncotic pressure more negative in the blood plasma even though the hydrostatic pressure is higher since the blood comes from the pumping of the heart?


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Xylem Properties
 In a biology lecture, I was told that the xylem vessels were 'narrow so that the water column does not break easily and capillary action can be effective'.
My question is why is this? Is the reasoning similar to an artery in the human body, whereby the narrow property can increase the pressure of the blood and force it out faster? Or is the reasoning different?
Thanks.

While this is a slightly different question http://biology.stackexchange.com/questions/42223/why-is-the-swelling-of-bread-when-placed-in-water-not-considered-to-be-caused-by/42233#42233 , the answer will help to explain how adhesion and cohesion work to maintain the water column in the xylem. This is different from the human circulatory system,

I'd suggest reading about capillary action. The article is a bit technical in places, but what part of it boils down to is the narrower the capillary (up to a certain point), the stronger the effect and so the water column can go higher.

Related answer to How do trees lift water higher than 10 meters?

What are you referring to with "...can increase the pressure of the blood and force it out faster" (specifically the "force it out faster" part)

Xylem's main job is to transport water, and therefore the inorganic nutrients in the water. Now, to answer your question, we need to know how water is transported.
Water is transported due to both cohesion, adhesion, and surface tension. Water is known for forming hydrogen bonds, and this is known as cohesion. When it forms hydrogen bonds with other molecules, this is called adhesion. In the xylem, some of the water molecules are evaporating, but pulls the water molecules below back up. The adhesive forces also do a similar job of pushing the water up.
Now, if the xylem was smaller in diameter, then the surface the water is exposed to increases. This means the adhesive forces are stronger. Therefore, the water is transported a higher distance. This is important for really tall plants.
Now to answer your second part, the arteries analogy is so wrong. This has nothing to do with how fast the waters goes up, but the height at which is reaches. Also, the human blood vessels depend on pressure and pumping (the heart's job).

Surface tension is the result of the differential between cohesion and adhesion, it isn't a property per se. "At liquid-air interfaces, surface tension results from the greater attraction of liquid molecules to each other (due to cohesion) than to the molecules in the air (due to adhesion)."

Also, read the OPs question again, they are asking about a comparison between xylem and the circulatory system of the human body. Your answer really doesn't address that.

@AMR ok. I will edit ASAP


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Number of Chromatids in G1
I know that in G1, the number of chromosomes is 23 pairs, so 46.
I assumed there were 46 chromatids too.
Why is the number of chromatids in G1 actually 0, not 46?
Thanks.


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Role of Intermediate Filaments in cell - cell signalling
A passage in my textbook mentions briefly that the role of intermediate filaments in the cytoskeleton is to enable cell to cell signalling by extending between special junctions and alowing cells to adhere to basement membrane
What does this mean?

There are desmosomes and gap junctions (cell-cell-contact), and hemidesmosomes (cell-basal membrane-contact) which enable a stable united cell structure. I'm not so aware with this topic, but I found some papers which may help you :)
Intermediate filament in cell architecture
Desmosomes and hemidesmosomes
Review on gap junctions
Blood-testis barrier and different cell-cell-contact structures


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How much oil you can get from a dead animal
This is purely speculative, but is there a formula to calculate how much oil you can get from 1 Kg of biomass?
I've seen bioreactors in farms where they put dung, vegetable scraps, and all bio scraps, where bacteria transformed the biomass in methane gas which then was used in powering electric generators or cooking stoves.

Well as I checked the internet and noone has done this experiment. So, it is a bit hard to answer it.

Oil is not biogas. what do you mean?

I was interested to know (at some point) how many dinosaurs had to die to create 1 kg of oil. I am aware that the oil deposits were formed by other type of organism not dinosaurs, but I was curious to know what mass of biological organisms needs to create 1 Kg of oil.
I wanted to be able to tell "You know, you just burned 1 TRex driving here."


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Fruit colour related to the dissolving of pectin
What does the dissolving of pectin have to do with the colour of a fruit?

During ripening, pectinases are produced which break down pectin and render it soluble. Color change is also associated with fruit ripening.
Hence the correlation.

So there is a correlation but no causation?

yes as it seems. Both are an effect of ripening. Chloroplasts differentiate and lose chlorophyll and other metabolic changes cause pectin hydrolysis along with other things such as increase in sugar content etc.


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Can human spinal reflexes make use of a proprioceptive input?
I was out in the car when I wondered why manufacturers place pedal controls crucial for reaction time so very far from the motor cortex.  Is there anything a spinal reflex could work with, which would not be available to the brain in the same time frame?  So I looked this up and found two recent papers:

Picton, 2021, describing sensation of lateral motion by Piezo2-expressing mechanosensative neurons.
Stanchak, 2022, describing mechanosensation in the lumbosacrol organ of birds by neurons expressing myo7a and espin.

The second paper goes so far as to suggest "spinal cords across vertebrates are capable of mechanosensation and that spinal mechanosensory networks have evolved to allow unique functions"
Speaking of function:  is there any functional evidence that proprioception could directly inform a (learned) spinal reflex in humans?  Such as a human changing the pressure on a gas or brake pedal in response to acceleration or deceleration, without needing to consult the cerebrum first.  (Any other mammal would also be relevant, but it ought to be easiest to do this sort of experiment with humans)

There's been quite a bit of sidetracking about whether reflexes could be involved in driving, so I feel like I should illustrate with a common scenario.  You're coming toward stopped cars at a traffic light, braking fairly heavily, while you've turned your head to one side to look at traffic.  At one point a piece of gravel shifts under the car wheel and you momentarily stop decelerating, so you respond by braking more heavily.  This might be the result of processing a lateral motion at the inner ear, using the cerebellum to compensate for head position and directing a new program of action at the motor cortex; but perhaps it might also involve a direct spinal response to proprioceptive input originating near the sacrum to maintain the intended degree of sensation of deceleration.

What is "functional evidence"? Also, out of curiosity, did you do a Google Scholar search on, say, "Can spinal reflexes be learned?" It seems to me that the paper you quoted does suggest(?)/state(?) that.

@anongoodnurse I'm not quite sure what you're getting at.  As you suggest, such a search does readily find articles about learning in spinal reflexes. In this case an unlearned reflex would also be satisfactory, but I doubt we can name one involving proprioception since its role is (at best) not well established.

@anongoodnurse  For "functional evidence" I was imagining some clever experiment might prove quite a bit simply with reaction time.  Maybe if you jerk a person's seat backward in the lab unexpectedly, and they respond by increasing pressure to a simulated gas pedal?  But I can't say how you would prove this isn't the result of a stretch reflex, crossed extensor reflex etc.  The same problems apply even more so in the case of tripping, which all the reflexes are designed to prevent.  Still, just because I don't have an idea right off doesn't mean no one has ever come up with one!

Did you know that pedals on cars used to be purely mechanical? If you're rolling down a hill in a wagon, would you rather brake yourself with your foot or your pinky finger?

And I am confused here too; the reason driving involves cerebral actions is much because reflexes can be as dangerous as long reaction times (due to alcohol for instance). If I'm on the highway with a lot of cars around me and suddenly I see an animal on my lane, my reflex would be to smash the breakes and save the critters a$$, at a second thought, I think of the fact I'm cruising at 100 km/h with a fender bender on my tail -- now would a reflex have helped you, or resulted in a pile-up instead?...

...I understand the question, but I think you should frame it in a different way, because in its current state the driving scenario distracts folks from your real question.

@AliceD For analogy, consider the role of the quadriceps stretch reflex.  Striking your patella with a rubber mallet seems like a poor contribution to driving, yet you use the same reflex moment-to-moment to help make sure your leg is in the position you think it is on the pedal.  Higher level processing modifies the reflexes, so you can bend your leg to different positions without being defeated by a reflex action and without losing its benefit in the new position.

@MikeSerfas - I'm more confused now. You can't "override" a spinal reflex, but it is possible over time to modify it some. (Also, nit-picking, but you don't elicit a reflex by hitting the patella, except for maybe the "WTF?" reflex with a grimace of pain. You strike (gently) the patellar tendon.) An example of setting off a spinal reflex is touching a hot iron. You can with repeated effort put your hand on the iron and leave it there, but it isn't activated by other activities. Not every stretched muscle twitches, or we wouldn't be able to walk. It's not a matter of cortical overriding. ...

... IOW, your cortex isn't modifying how your leg responds to proprioception; you're simply using your leg muscles differently, and appropriately so, to achieve the same effect. You can learn (cortical) to fall flat on your face without protecting it, overriding a reflex, but that takes time and effort. Also, it's not very helpful to health or longevity. I'm not a neurologist or neuroscientist, so I don't understand the question as @AliceD seems to. The paper in the link you provided (as well as others) answers in the affirmative. What else are you asking?

@BryanKrause - I agree you would use one of your strongest muscles to stop a car. With hydraulic brakes on 4 wheels, a pinky would work as well if not as instinctively initially. (Instinctively as in, resisting a forward force, you'd use your legs instinctively.)

@anongoodnurse My point is that OP's question is based on a false premise; they're thinking that someone designed a car thinking a leg muscle would be a fast way to respond to things. In reality, cars are designed that way because once upon a time someone needed to actually transmit force through the pedals.

@BryanKrause - Understood. The whole question/premise is questionable imo. The reaction time difference between arms and legs based on their distance from the cerebral cortex is questionable when discussing a spinal reflex. What fraction of a second difference does arm length vs leg length make? I never noticed any lag in reaction time between the biceps and knee reflexes.

The intercept of 182 ms is an estimate of the time needed for internal processing and response generation; the slope of 45 ms/m for distance; (22 m/s)... So it's 45ms difference between hand/foot. Unlikely is that the number of muscles involved in coordinating the leg and foot to apply brakes, is too complex for mechanosensory response vs a learned reflex which is integrated with learnig logic and the motor cortex. A non-cortex reflex has to also know which of 250 muscles to apply when sensing 100ds of stimuli, i.e. a stone hitting the foot zone under the car.


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Blood Pressure: Significance of difference between systolic and diastolic
I wanted to understand what is the difference between systolic and diastolic readings of blood pressure. I understand 120-80 to about 100-60 is considered normal but does the difference in the two values in the reading hold any significance?
I have read some text here and here.

The difference between systolic (the upper number) and diastolic (the lower number) pressures is known as the pulse pressure:

Systemic pulse pressure = Psystolic - Pdiastolic

For a typical blood pressure reading of 120/80 mmHg the pulse pressure is therefore 40 mmHg.
It is proportional to stroke volume, the amount of blood pumped from the heart in one beat, and inversely proportional to the compliance or flexibility of the blood vessels, mainly the aorta.
A low (also called narrow) pulse pressure means that not much blood is being expelled from the heart, and can be caused by a number of factors, including severe blood loss due to trauma, congestive heart failure, shock, a narrowing of the valve leading from the heart to the aorta (stenosis), and fluid accumulating around the heart (tamponade).
High (or wide) pulse pressures occur during exercise, as stroke volume increases and the overall resistance to blood flow decreases. It can also occur for many reasons, such as hardening of the arteries (which can have numerous causes), various deficiencies in the aorta (mainly) or other arteries, including leaks, fistulas, and a usually-congenital condition known as AVM, pain/anxiety, fever, anemia, pregnancy, and more. Certain medications for high blood pressure can widen pulse pressure, while others narrow it. A chronic increase in pulse pressure is a risk factor for heart disease, and can lead to the type of arrhythmia called atrial fibrillation or A-Fib.


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How is the Concept of Simple Diffusion Possible
How can a substance pass through a lipid membrane in a cell through simple diffusion? In order for something to be able to go through the membrane, in simple diffusion, it must be hydrophobic, or non polar. The reason for this is that in order for it to easily interact and pass the fatty acid part of the lipid membrane, which is hydrophobic or non polar, it must also be hydrophobic and non polar. But in order for this substance to pass the phosphate part of the membrane, which is hydrophilic, or polar, doesn't it also need to be polar and hydrophilic?

Simple diffusion is the movement of solutes from an area of high solute concentation to an area of low solute concentration.
Here are a few ways molecules will make it through membrane into cell:
(A) Fuse with the membrane and enter due to like polarities i.e non-polar subtance fuses with non-polar membrane and passes through membrane
(B) Small polar molecules CAN move into cell but at a much slower rate
(C) Through transmembrane integral protein channels such as aquaporins, K+ leak channels, and other channels that DO NOT require energy, and are ALWAYS open
If you want to understand how it was determined which molecules were able to pass through the membrane look for some resources about Overton's Plasmolytic Method.
Alongside that the definition of the partition coefficient will give you some insight on how fast molecules will pass through membrane, if at all.
Good luck on the searching!
@ Ro Siv - Simple diffusion is not facilitated diffusion


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No bands show up in gel electrophoresis, not even marker
I haven't seen any gel lanes in neither my PCR samples nor the marker itself when photographing them.  This is not my first time performing 1.2% agarose gel electrophoresis.
I see gel lanes when I take the gel out the apparatus, but when I go to photograph them:  nothing shows up.  I only let the samples "run" for 30-40 minutes (when I ran for an hour, the bands almost ran off the gel).
Tried using different markers:  no luck.
Re-added some more EtBr to better stain the gel:  no luck.
I am also keeping the lights off in the dark room, so I do not think I am exposing the film to light early on (errors still a possibility though).
What could I be doing wrong?  Am I taking the film out too early?

I don't understand the part of your question where you refer to film in a darkroom. If you are staining with EtBr then you must be using a UV lamp to visualise the bands. There is usually no question of "taking film out" since the gel is usually photographed with a digital system of some kind. Please explain exactly what you do with the stained gel.

Do you see the color from the loading dye migrating through the gel?

since you mentioned 30-40 minutes... I run my sample on agarose gel only for about 20 minutes at 100V, and can see good bands. try reducing the time.

What I can quickly think of is that you were running the gel incorrectly: instead of from - to + direction,  You ran it the other way around and your DNA went out of the gel. Another thing might be that the UV light was not turned on or is broken.

May your gene of interest will not be cloned perfectly that is the reason, make sure that first you have to run pcr well accourding to your sequece then run the gel

This is not an answer to the question, please edit it to avoid downvotes/deletion.


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Is mate choice in non-human primates MHC-dependent?
Whether the major histocompatibility complex (MHC) affects or not mate choice in humans seems mired in controversy at the moment. Without implying that looking at non-human primates would solve this controversy, I'm still curious if some sort of scientific consensus could be reached in non-human primates regarding MHC and mate selection.

tl;dr It's messy for non-human primates too. Winternitz et al. (2017) ("Patterns of MHC‐dependent mate selection in humans and nonhuman primates: a meta‐analysis", Molecular Ecology 26(2)) review studies of MHC-based mate choice in human and non-human primates. Some of the take-home messages, mostly from the abstract:

[abstract] the overall effect sizes of primate MHC-based mating preferences
  are relatively weak ... calling for careful sampling design in future studies.

There is a

"systematic trend" for primates preferring MHC diversity (p. 679)

(I think this means "not significant" ...)

(p. 680) Nonhuman primates tend to consistently prefer MHC-dissimilar mates (Fig. 4a), but our power to detect a significant average effect is limited by our small sample size (N=6) and by the addition of random effects to control for pseudoreplication.

For MHC-diversity preferences:

Examined separately ...  nonhuman primates had a non-significant trend for mate choice for diversity (primates = 0.110 (-0.207 to 0.456), N=7, Fig. 1b)

Here are some of the key figures (these figures also include data for humans, omitted here). However, note that the overall estimates in this figure do not account for the effects of study ID and phylogenetic relatedness (see Figure 1 in the paper), which tend to make the confidence intervals wider/weaken the statistical significance.

Figure 4a, preference for MHC-dissimilar mates [disassortativity] (overall CI is [-0.01, 0.18], consistent with the "almost significant" comment referenced above)

Figure 4b, preference for MHC-similar mates [assortativity]:

For reference, the species included here are: Rhinopithecus roxellana (golden/Sichuan snub-nosed monkey); Cheirogaleus medius (fat-tailed dwarf lemur); Papio ursinus (Chacma/Cape baboon); Microcebus murinus (gray mouse lemur); Mandrillus sphinx (mandrill); Macaca mulatta (Rhesus macaque).


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Evolutionary explanation for hypoxia causing euphoria?
Why would something potentially very dangerous, such as hypoxia induce something pleasurable like euphoria? Are there any evolutionary hypotheses for this link? I'm thinking that something like the "choking game" would actually select against it, but that's probably too new.

The short answer is because evolution is more than natural selection. Many questions based on the contrary false belief are being closed a duplicate to Why do some bad traits evolve, and good ones don't? Let us know if you think the other post does not address your question and why

Your question is in essence very similar to Why can fish survive out of water?. There is an easy physiological  explanation. It evolves this way, not because it was selected for but simply as a side-effect of some other set of traits.

@Remi.b: yes, but do fish feel good out of water?

No, they don't. Feeling good is the trait of interest to you. Surviving for a few minutes was the trait of interest to this other post. Something might give us a pleasant feeling without the need for us to be selected for this feeling to be pleasant. I would recommend you to 1) follow an intro course to evolutionary biology to understand that evolution is way more than just natural selection 2) understand the physiological reason for this euphoria in hypoxia (which you can ask on a separate post) and you would then maybe more easily accept that it is just a side-effect of how the brains works.


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Do's and Don't's of Undergraduate Research?
I was fortunate enough to get a position as a researcher for the Mayo Clinic's SURF Program this year.  My PI's lab focus is on the the immune system's role in CNS axonal and neuronal injury, specifically through the lens of how innate and adaptive immune effectors interact w/ infected neurons.
Although I do research under a professor at my college and I volunteered for a state university lab during the previous summer, this is my first REU/SURF opportunity, and I REALLY want to make a good impression.  Here are my questions:
What are the do's and don't's in terms of being a skilled and efficient researcher?
Since I am still an undergrad, I know that I will be a less useful asset to the lab than a grad student or post-doc, but what can I do as an undergrad to not burden my colleagues and PI?
Thank you all for your help!  Wishing you all the very best!

This question appears to be off-topic because it is more suitable for academia.

This is indeed off topic. However, what can you do? Learn. That's all that will be expected of you.

Ask plenty of questions and write everything down. If you do not write notes when someone is explaining something to you, it will be embarrassing to go back and ask them a second time to explain it again. Before you get to the lab I would locate/Ask for review articles related to the project. Realize that you will likely shadowing a senior person while you are there, adapt to their schedule. Don't spend your incubation times face booking. Use this time to build relationships with others in the lab and on your floor and try to absorb as much information about the way the world of science works. Speaking from personal experience the small things you learn there may be insignificant but may come to be important to you in the future. If you have your own project, realize that it will probably be a small one attached to a bigger project another lab member is working on. Thats a good thing, because your time there is not long enough to get into something complicated. A simple, clear, and focused question will be key to your success.
What you should take away from the experience is not necessarily something that will amount to publication, but the actually experience in the actual process of designing experiments, performing them, and analyzing data. Assuming you are doing this to help prepare you to go on to work on a graduate degree in your favorite area of biology then remember that this is here to help you get to the next level. Programs like this allow you to demonstrate that you understand what it takes to perform graduate-level work, and potentially become a successful scientist one day.

Another thing: Take advise from people which have more experience than you, but also question things (not everything though). The last thing is especially important to understand what you are doing.


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Cloning a gene of an organism with an nonsequenced genome
What would be the best protocol to clone a gene about 5kb in size? The genome is not sequenced, but the gene itself very similar to orthologous genes of organisms with known sequences.

Do you want to clone the gene ( genomic DNA) or a copy of the mRNA (cDNA)?  (I imagine it's the latter.)

It's a hypothetical problem. If the gene is eukaryotic then the only possible course of action is to use mature mRNA (without introns) and reverse transcriptase to get cDNA, which can then be inserted into a vector. If the gene is of a prokaryotic organism, the only problem would be finding an adequate restriction enzyme?

How do you know that the gene itself is orthologous? This means that the cDNA sequence is available. So there should be no issue with designing primer for amplifying the cDNA (just that you may not be able to find out other possible targets)

I assume that we are talking about eukaryotic genomes which are split into introns and exons. Depending on what you want to do with your cloned gene, you need different strategies. The method is based on the assumption that the gene sequence has only very little differences to the known sequences of other organisms.
If you want to express your gene from a vector, you need to find the right processed mRNA which is then processed into cDNA and then cloned. Here two strategies are possible: If you have a gene, which is strongly expressed, you can design a primer primer (based on the orthologous sequences) which is anchored in the poly-A tail and has a gene specific seuqence next to it. With this it should be possible to amplify your gene specifically and isolate it. If the gene is not strongly expressed (the resulting amount of cDNA would be very small, since there is no amplification involved), I would opt for making cDNA from total mRNA (use anchored polyA primers) and then amplify the sequence from the cDNA pool with two primers (again based on the orthologous sequences) to amplify the gene sequence. I would go for TA-cloning here, since you do not know, which restriction enzyme recognition sites are present on your gene.
When you need the complete sequence containing introns and exons, there are two possible strategies. First you can use primers to amplify the gene and subsequently clone it. Then it is possible (and this is probably what I would do) to use a set of primers which bind to the end of the gene (and also the reverse strand) to amplify the sequences at the end and then sequence these PCR products. This gives you the exact sequences at the 5' and 3' end of the gene and allows you to include possible regulatory sites, since you then can design exactly matching primers for this region. Again, I would go for TA cloning.
And finally you could start by sequencing the whole region based on homologous sequence primers first and then with primers designed on the newly analyzed sequences. This is the most exact way, but is also costly and takes some time (since you need to make new primers after each round of sequencing until you are done).


text:
Was the Harcourt COVID-19 isolate paper ever published?
One very interesting paper concerning COVID-19 was the paper describing the first isolation of the virus by Harcourt et al. However, this paper as far as I can tell was only published as a preprint in May of 2020 describing research done in January and February of 2020. I used Google Scholar and other web searches and I cannot find any indication that the paper was ever peer reviewed and published in a journal. Since it is such an important paper, it seems kind of surprising to me that after a year and half the paper seems to still be unpublished. Am I missing something here?

https://pubmed.ncbi.nlm.nih.gov/32160149/ You could have found this by hovering your mouse over the author's name in the preprint link, which offered you the choice of seeing other papers by Jennifer Harcourt.

This is of course not the first isolation of the virus so what do you mean with "important paper"? Many other papers described the same thing, though with less details and cell lines.

@reuns Well, by "first" I mean the first verifiable isolation. The only ones I know of prior to it were unverifiable claims by researchers who never submitted their isolate to a repository. If you read the Harcourt paper, you can see that was a major goal of their research ("We also deposited the virus into two virus repositories, making it broadly available to the public health and research communities.").

What? The virus was first isolated in China around Jan 5. Did you read the WIV (RaTG13) and China CDC papers? https://www.nature.com/articles/s41586-020-2012-7 https://www.nejm.org/doi/full/10.1056/NEJMoa2001017

And their WA1 isolate has been used in USA only. Most countries did a isolate from one of their first patients and made a stock from it. I am not aware of much international strain sharing.

@reuns As I said in my comment, the Chinese claim to have produced isolates was that: just a claim. They did not submit their isolates to a virus repository as is standard practice when discovering a new virus. Are you even reading my comment? My question refers to the first verifiable isolate. It is important that viral isolates be verified because many types of errors can occur in a de novo genomic analysis, so it is critical that other researchers verify the results. This can only be done if the virus is submitted to a repository--hence the remark in the Harcourt paper.

Useless to discuss with someone who thinks that those papers are just "claims". A virus sequenced several times independently doesn't need to be "verified".

@reuns As I said before, an isolate is supposed to be submitted to a repository so that the genomic analysis can be verified. Also, there are experiments and checks of various kinds that can only be carried out on a live virus. A published genome is not a substitute for an isolate. The Harcourt isolate was to my knowledge the first isolate which was made available to researchers.

No, virology doesn't work like this.

It was published in June of 2020 by Emerging Infectious Disease under a slightly modified title. (It's not uncommon for journal editors and/or peer reviewers to require changes to the title of a manuscript prior to publication).
Found as the top result under "Similar Articles" on PubMed page of the bioRxiv pre-print. PMC link and full citation below.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7258473/

Harcourt J, Tamin A, Lu X, Kamili S, Sakthivel SK, Murray J, Queen K, Tao Y, Paden CR, Zhang J, Li Y, Uehara A, Wang H, Goldsmith C, Bullock HA, Wang L, Whitaker B, Lynch B, Gautam R, Schindewolf C, Lokugamage KG, Scharton D, Plante JA, Mirchandani D, Widen SG, Narayanan K, Makino S, Ksiazek TG, Plante KS, Weaver SC, Lindstrom S, Tong S, Menachery VD, Thornburg NJ. Severe Acute Respiratory Syndrome Coronavirus 2 from Patient with Coronavirus Disease, United States. Emerg Infect Dis. 2020 Jun;26(6):1266-1273. doi: 10.3201/eid2606.200516. Epub 2020 Jun 17. PMID: 32160149; PMCID: PMC7258473.


text:
How do furniture beetle larvae drink?
I have read that the furniture beetle (Anobium punctatum) has larva that will burrow for three to four years in wood before emerging and pupating. How do they obtain water during that time if they are just eating wood?

It is likely that the oxidation of the organic compounds in the wood provides the water, much like many desert animals get their water.


text:
How large is the immune repetoire and at what age does it finalize?
There seems to be a large disconnect between the Wikipedia's article on the immune effector repetoire and Janeway's Immunobiology 9th Edition, a standard textbook widely used to teach immunology to pre-meds. In the Wikipedia it puts the size of the repetoire at 100,000 unique receptors, but in Janeways it says the repetoire has typically 10^8 or between 100 million and 1 billion receptors. Also, in Janeways it implies that the repetoire is largely finalized at some point, although it gives no specific age, but in the Wikpedia article it claims that new T cells are constantly developed by the body throughout a person's lifetime.
How many unique T-cell receptors typically circulate in the body at one time and at what age is the immune repetoire largely decided (if any)?


text:
Evidence for annual rabies vaccine?
US companies that sell rabies vaccines routinely recommend that they be given annually. Obviously, these companies have a financial incentive to recommend that their vaccines be given as frequently as possible.
No human vaccine that I know of requires annual booster shots. The standard recommendation to veterinarians that they receive a single primary course of vaccinations and no boosters at all. It seems inconsistent that the CDC recommends that vets that work with sick animals on a daily basis get a one-time vaccination, but the USDA "recommends" house pets get vaccinations every year. My understanding is that this USDA "recommendation" is based on no scientific evidence whatsoever.
Is there any scientific evidence indicating the effectiveness of vaccines as a function of the frequency of their application?

Not going to research an answer, but canine rabies - and dogs as vectors in human rabies cases - has been eliminated in the US in my lifetime. Coincidence? Conspiracy? I can guess...

UK veterinarians get a boaster every 3-5 years.

Where I live, it's every 3 years for dogs.

@jamesqf That is only because your vet is not using Pfizer vaccines.

@Imprisoned Rhesus: But the fact that there are 3 year rabies vaccines, and that 3 years is the interval recommended by vet schools (e.g. http://www.vetmed.ucdavis.edu/vmth/small_animal/internal_medicine/newsletters/vaccination_protocols.cfm )  disproves the (implied by wording) claim that ALL US companies try to push 1 year rabies vaccines.


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Differences in the action of Scopolamine and Atropine
Both Scopolamine and Atropine are muscarinic antagonists, having essentially the same action: blocking parasympathetic nerve receptors.
The action on the brain by muscarinic antagonists is presumed to be caused by dilation of blood vessels, thus we might expect the effect on the brain by the two compounds to be similar.
However, in actuality the action of the two compounds on the brain is somewhat different. Scopolamine begins causing strong psychotropic effects even in very small doses before it has any effects on the skeletal nervous system. Conversely, atropine begins having effects on the muscular system long before it begins having psychotropic effects and in fact, potentially toxic doses of atropine have to be administered before significant psychotropic effects begin manifesting.
If the apparent biochemical action of the two compounds is similar, why do we see this difference in the effects between the two with regards to the brain?

It seems that the reason for the different effect of Atropine and Scopolamine on the brain is related to the structural difference between them.
From the chemical structures below it is evident that the two molecules are almost identical, save for an epoxide group that is found in Scopolamine but not in Atropine.

According to Brody's Human Pharmacology: Molecular to Clinical, 5th edition, 2010, pp. 113-115, this epoxide reduces Scopolamine's base strength and enables it to penetrate into the brain more readily than Atropine.
Faster penetration into the brain = earlier appearance of psychotropic effects.


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The Relationship between Copper and Alzheimer's Disease
I've been reading up about the research concerning the etiological factors behind Alzheimer's and I came across two papers - "Studies on Copper induced stability changes in DNA fragment (GCA ATC TAA TCC CTA): Relevance to Alzheimer’s disease" and "Copper interactions with DNA of chromatin and its role in neurodegenerative disorders." The issue I'm having is that the papers suggest that copper causes the DNA's double helix to unwind in some parts, and it causes it to coil more tightly in others (the fluorescence and circular dichroism research supports the latter).
My question is this: do high concentrations of copper cause DNA to unwind or coil more tightly?
If you could provide any help, I'd be very grateful, as I feel like I'm be missing something obvious.

I was able to find your second reference quickly and linked it above, but the first gives more trouble.  Can you post a bit more information - bibliographical info or a link?

Never mind - found the other link (Young Scientists Journal) online

I found your second reference online, which says

Hydrogen bonds are disrupted by the process of partial unwinding which induces structural changes such as loosening of base–base interaction, base tilting and destabilization of the DNA double helix leading to DNA denaturation [17]. The destabilization was due to most probable binding sites in DNA such as Cu2+ to N7 of guanine and N3 of cytosine in line with our present results and with the predictions of Eichhorn and Clark [18], [19].

With this in hand, we can Read The Friendly References.  #18 is on PMC and gets the first look - they say "perhaps the structure is"

The other references are less helpful for me right now - #17 is a paper from 1971 that's not online and never will be, and #19 talks about histone H1 blocking the copper interaction.
Now what I see here is only unwinding, and is dependent (as proposed) on the presence of G-C base pairs in the sequence.  So far from what I've seen, this is based at interactions at around 0.1 mM in in vitro studies, so I feel like it is possible a physiological situation could involve a completely different mechanism.
After writing the above, I found the other paper in Young Scientists Journal - it is quite a remarkable thing to consider.  The author is a 12th-grade student from Panama who was doing (among other things) a circular dichroism study and molecular docking with Discovery Studio 3.5.  Statistics is lacking and the experiments aren't very well integrated, and the model from the software, which doesn't agree with the image above (it doesn't bind a ring nitrogen in the cytosine), doesn't seem to be tested by the lab data.  Despite the sophistication of the software I'm afraid I'm about as skeptical as I was the first time.  Still, there is some Ph.D.-level thought there, using some methods that American undergraduates rarely access, conducted by a university in Panama with support from an Indian research institute.  Educationally, fascinating.
But I don't see much support for the interpretation in that paper that the DNA coils more tightly.  The fluorescence experiment suggests a competition between copper and ethidium bromide, but knowing what actually happens is another story.  The CD study ... well, some shifts are identified, one one way and one the other, but I don't see how they prove the DNA is coiling more.  But maybe I'm missing something!

Thank you, you have cleared this up for me!


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In human anatomy / biomechanics, what is the motion called when the arm swings sideways so the elbow moves in an arc of 90 degrees?
In human anatomy / biomechanics, what is the motion called when the arm swings sideways so the elbow moves in an arc of 90 degrees?
So e.g. if a person was to elbow somebody behind them , or if somebody had their arm out and then swung it keeping it parallel with the floor.
Like in this video
https://www.youtube.com/watch?v=IOh2-4WWzEE

It’s humeral retroversion at a 90 degrees abduction angle with extended elbow and slightly internally rotated shoulder.

Shoulder Horizontal Abduction/Adduction.
https://www.youtube.com/watch?v=R3xJDsJ_Nw4&ab_channel=InteractiveBiology
"the motion of bringing the arm across the chest is called shoulder or glenohumeral horizontal adduction. Glenohumeral horizontal adduction is demonstrated starting from 90? of shoulder flexion
with the arm slightly away from midline in abduction as seen from a front or anterior view."
Abduction would be away from the midline/body. i.e. the outward direction.
Adduction would be towards the midline  i.e. coming across/towards your body.
Starting and staying at 90 degree shoulder flexion.
Google shows this from oxfordreference.com
"Horizontal adduction
horizontal adduction (horizontal flexion)
Movement of the arm or thigh in the transverse plane from a lateral position to an anterior position. ..."
So it's also known as Horizontal flexion and horizontal extension.
as shown here https://www.youtube.com/watch?v=c0JxEZ87W40&ab_channel=BlakeMartin


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Is glycolysis the beginning part of fermentation, or does fermentation follow glycolysis?
Is glycolysis the beginning part of fermentation, or does fermentation follow glycolysis?
I see conflicting information from different sources
https://honchemistry.wikispaces.com/Lactic+Acid+and+Alcohol+Fermentation+in+Humans

"..Alcohol fermentation follows glycolysis, just like lactic acid
  fermentation..."  <-- So glycolysis is preceding fermentation, not part of fermentation

and

" The Actual Fermentation Part
Glycolysis and fermentation are two separate processes. Glycolysis was
  explained briefly to give the reader an idea of the events leading up
  to fermentation and the starting conditions in terms of molecules
  available for reaction.....Going into the fermentation, the molecules NADH and pyruvic acid are present. "  <---  so glycolysis is preceding fermentation, not part of fermentation.

Whereas these two links put glycolysis as part of fermentation, not a preceding stage before fermentation.
https://www.khanacademy.org/science/biology/cellular-respiration-and-fermentation/variations-on-cellular-respiration/a/fermentation-and-anaerobic-respiration

"Fermentation and cellular respiration begin the same way, with
  glycolysis" <-- glycolysis is part of fermentation, not preceding it.

and
http://study.com/academy/lesson/anaerobic-respiration-lactic-acid-alcoholic-fermentation.html

"fermentation, which is a process that anaerobically generates ATP by
  performing glycolysis..." <-- fermentation includes glycolysis,  so glycolysis is part of fermentation, not preceding it.

So, which is it?
Is it a)like khanacademy and study.com,  or b)like honchemistry.wikispaces.com
I have heard the idea that glycolysis is independent, in that it can produce some (not much, but some), energy on its own, and it can happen without fermentation or cellular respiration following. Though when would glycolysis occur without fermentation or respiration following? And even if glycolysis is that independent, it may still be at the beginning of respiration and fermentation and not preceding it.
Wikipedia speaks in a contrary way..
https://en.wikipedia.org/wiki/Fermentation

"Before fermentation takes place, one glucose molecule is broken down
  into two pyruvate molecules. This is known as glycolysis." <-- so glycolysis is preceding fermentation, not part of it.

so the above quote from wikipedia suggests that glycolysis is not the beginning part of fermentation, but a step preceding it
whereas still on the fermentation wikipedia page, it says

"Fermentation is a metabolic process that converts sugar to acids,
  gases, or alcohol....The first step, glycolysis" <-- so glycolysis is part of fermentation.

Links on respiration are more unambiguous that glycolysis is part of respiration.. the links on fermentation vary a bit on whether glycolysis precedes fermentation or is part of it.

This would not be a natural distinction, it is symantical. The only way to state for sure would be if some universally accepted governing board declared it so. Or, if you're a student, it's what the teacher says, at least until after the exam!

@bpedit But biologists have scientific journals.. Is there inconsistency even within a journal, with some papers defining it one way and some defining it the other way?

@barlop — There is no call to define it. Papers typically will have titles like "Delayed Lactose Fermentation by Enterobacteriaceae" (to quote a 1966 paper I found by Googling) and, for example,measure the amount of lactose converted to lactic acid or whatever in different strains (or more likely assay the activity of various enzymes). But this is not a question that concerns anyone in a field that has been moribund for the past 50 years.

The very popular college text from which I used to teach AP Biology, Biology, Campbell & Reece, uses fermentation to describe the entire process. I agree with @David below, that is probably the more standard approach.

As @bpedit indicates in his comment, this is a semantic question — i.e. one regarding the meaning and usage of words. I will explain how I and others use these words and why. If you are convinced by my logic you will wish to use them in the same way, if not you are free to use them differently. However there is no ‘universal truth’ here, and if you are student I have no idea what your instructor thinks.
The problem is that ‘fermentation’ and ‘ferment’ (both as a noun and a verb) are old words, predating any understanding of the processes involved. Thus the Oxford English Dictionary quotes a relevant early example of the use of ‘ferment’ as a verb as follows:

1663 Cowley Verses, to Royal Society iv, All their juyce did .. Ferment into a .. refreshing Wine.

From this, it is clear that the idea of the fermentation process is the conversion of some initial compound (the sugar in the ‘juyce’) to some final compound (the alcohol in the wine). This usage is still current in referring to the process of fermentation, for example a Google search brings up a BBC Science educational page which states:

Beer and wine are alcoholic drinks made by fermentation reactions that use yeast to convert sugars into ethanol.

You may or may not be aware that term ‘ferment’ was historically used to mean what we now term yeast, and ‘Zwischenferment’, the obsolete German term for certain enzymes in yeast, is derived from this. So the original concept was merely of some biological conversion effected by yeast, although this has later been extended to bacteria and the idea changed to indicate metabolic processes capable of generating ATP anaerobically.
Part of the discrepancy in definition may be the emphasis on the end-product of the fermentation — ethanol fermentation, lactic acid fermentation etc. However, it seems clear to me that the fermentation is the whole chain of metabolic events from sugar (or whatever) to alcohol (or whatever); and if glycolysis is part of that process (which it is in this example) then glycolysis is part of the fermentation. (Of course, glycolysis can occur in other circumstances where the product, pyruvate, is oxidised in the tricarboxylic acid cycle, which is not a fermentation process.)
Footnote
The extent to which one can tie oneself in knots with trying to define fermentation is illustrated in the best-selling and well-respected text book, originally written by Lubert Streyer and subsequently maintained by Berg et al. I mention this text both because an older edition is available on-line, and because a book of such value to the publishers is carefully vetted by referees. In the chapter on Glycolysis there is an attempt to define Fermentation:

Fermentation: An ATP-generating process in which organic compounds act as both donors and acceptors of electrons. Fermentation can take place in the absence of O2. Discovered by Louis Pasteur, who described fermentation as “la vie sans l’air” (“life without air”).

So the biochemical lawyers have produced a definition that very few readers will be able to take in at first sight. What is this business about electron donors and acceptors? Well what it means in relation to the fermentation process in which lactic acid is produced (note my legalistic choice of words) is that one organic compound is reduced (glyceraldehyde 3-phosphate) — by NAD+ — and one organic compound is oxidized (pyruvate) — by NADH. And as the production of ATP is included in the definition this means that Berg et al. include glycolysis in this definition of fermentation.
…except that on the same page there is the following statement:

pyruvate is converted, or fermented, into lactic acid in lactic acid fermentation or into ethanol in alcoholic fermentation

So here it seems that the word is being used for the conversion of pyruvate to lactate or ethanol, i.e. it excludes glycolysis.
Pasteur managed to talk about fermentation without being aware of glycolysis or ATP, and it is clear to me that you can write whatever carefully phrased definitions you like, but people are going to continue to use venerable terms like fermentation in whatever way seems natual to them.

I  concur, that's the way in which I generally use the term.

I see the definition apparently used by that statement from BBC science, is consistent with the old definition(that requires sugar be the start), and the new one(which mandates no electron transport chain).   I see what you mean that a current usage, from BBC science, is using the new definition but is consistent with the old one, by including sugar at the start.

However,  BBC science is a bit dodgy for example http://www.bbc.co.uk/schools/gcsebitesize/science/add_ocr_21c/life_processes/energyrev3.shtml    says "Anaerobic respiration in plant cells and some microorganisms (such as yeast) "  <-- And that's wrong.  Yeast mitochondia, are  (like most eurkaryotic organisms's mitochondria), only capable of using oxygen as the terminal electron acceptor in their electron transport chain. So, like humans, yeast,cannot do anaerobic respiration. They do aerobic respiration, and they do fermentation. So I guess their definition of respiration is wrong?

@barlop — My quote from the BBC was just to show that the 17thC usage persists to the present day. I do not intend to cite the BBC as a scientific authority. However, perhaps it was late at night when you wrote "So, like humans, yeast,cannot do anaerobic respiration". The word "respiration" is a semantic minefield as in common usage it is equivalent to 'breathing", so "anaerobic respiration" seems an oxymoron. However biochemically respiration is used to mean obtaining energy from metabolism of nutrients, and anaerobic respiration is what fermentation (in yeast and bacteria) is all about.

Glycolysis is the beginning portion of BOTH types of respiration; aerobic and anaerobic. It makes a couple of ATP. If aerobic respiration occurs, it recharges more ATP. If anaerobic respiration occurs, the organism can make other compounds (like Lactic Acid) but doesn't generate any more ATP. I actually made a diagram that you might find helpful. It's posted here on Twitter:
https://twitter.com/BOGObiology/status/829757759470067713
And have now included it in this post below

I also made a series of videos for my students that might be useful as well. They're on Youtube:  Below is a video on cellular respiration that goes into more detail.
https://www.youtube.com/watch?v=Vh7vg7zG3cQ

Can you please not advertize yourself but write an answer, which stands for itself? So adding pictures here instead of linking them, for example. References are for further reading...

Thanks.. And I think this is the case of fermentation too.   It'd be awesome if you can address this question too.  http://biology.stackexchange.com/questions/55505/are-humans-capable-of-both-anaerobic-respiration-and-lactic-acid-fermentation

@Chris i'm not sure if it's possible to add pics sometimes,  until rep is higher, but i've edited her post to add the picture from the link she gave, and i've put the references more in a context of sources and further information. It's great to have an educator contributing.

I think you're right it's part of the beginning of both. However, it's kind of wrong/questionable though to count fermentation under respiration, (which your diagram does) see my answer http://biology.stackexchange.com/questions/55505/are-humans-capable-of-both-anaerobic-respiration-and-lactic-acid-fermentation

I think you're right it's part of the beginning of both. However, it's kind of wrong/questionable though to count fermentation under respiration, (which your diagram does) see my answer  that i've just posted here

This was my first post here, so I didn't realize I could embed directly, I thought I had to think them. Sorry.

I will post an answer that uses an advanced microbiology book, as they are  careful to get their terms very accurate.
Glycolysis is part of both respiration and fermentation.
Microbiology: A Clinical Approach, Second Edition
By Anthony Strelkauskas, Angela Edwards, Beatrix Fahnert, Greg Pryor, Jennifer Strelkauskas

(Side note-  Non-introductory microbiology books don't count fermentation as part of respiration. As I discovered when looking into whether humans did anaerobic respiration, here Are humans capable of both anaerobic respiration, and lactic acid fermentation?   And as is shown in the diagram above, from that advanced microbiology text.  Biology 101 texts, and human biology texts, are more relaxed(arguably wrong), with their definition)