text:
What's the subpatellar tendon?
I read in Thomas Myers book Anatomy Trains:

Although the muscles themselves have attachments within the anterior
  compartment to the tibia, fibula, and interosseous membrane, the next
  station for the SFL [Superficial Front Line] is at the top of both the medial and lateral side
  of this track, the tibial tuberosity
Continuing in a straight line upward is no problem: the quadriceps
  begin their upward sweep here with the
  subpatellar tendon. The SFL  includes the patella, the large sesamoid bone designed to hold the SFL away from the knee joint
  fulcrum so that the tissues of the quadriceps have more leverage for
  extending the knee.

I can't find the term subpatellar tendon in my anatomy book. What does it refer to? Is it the patella ligament?

Can you add the text before "Continuing in a straight line upward is no problem" and the definition for SFL?

@kmm : I did so.

I suspect that you are correct, "subpatellar tendon" is referring to the patellar ligament. Although it is small, in the image below, (3) is the tibial tuberosity and (5) is the patella. (4) which is labeled "subpatellar tendon" is between the two. The only structure between them is the patellar ligament. So, I think this is what it meant (though in 20 years of teaching, I haven't heard that terminology).


text:
How exactly does long-term tension (over months) build up in the ligaments, tendons, muscles?
And is there any basis for believing that massage relieves that tension?

Can you explain a little more? What do you mean by "tension"?

Hm, here's the thing: I'm not even sure what that type of tension means. It's just what massage practitioners say when they massage one's sore muscles and tendons (and it works, at least temporarily).

So, do I understand right that you mean massage by "tension"? Not static tension or something similar?

oh, i mean, the type of tension that massage relieves.

Related: What is the difference between muscle tension and muscle tightness?

Tension is not a quantifiable thing, rather an abstract concept to describe feelings of stress in muscles.  I think I see what you are getting at but I would separate it into two questions.
"Is massage provably beneficial to muscles under physically induced stress?"
Emphatically yes, however there are so many different types of massage, some are more medically viable than others.  Most massage stimulates muscles to encourage a release of tightening, much like exercise does, though I would assume that there's also a psychosomatic that plays a significant role as well due to human contact.
The other question, more the point "Are massage therapist's claims about relief true?"
Some are and some aren't.  Unless it's by a medical professional (prescribed physical therapy for instance) they can claim whatever they like.  "Reiki contributes to your body balance and wellness by attuning your energy"  This can not be proven, but not really disproven either, so they can claim it all they want though it's purely anecdotal (if not outright fabrication on the part of less ethical individuals.)
In summary: Massage has tangible benefits, but if the claims of the therapist sound too good to be true, they probably are.

Thanks for the reply. Hmm, how exactly is "tightening" measured? And what is biologically involved in "tightening"?

@InquilineKea Have you found any information regarding your question on tightness measurement? I was wondering the same: How can I quantify muscle tightness?

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text:
Is "muscular attachment" synonymous to tendon? (when talking about the insertion of glutei medius and minimus to greater trochanter of the femur)
I have read the following two terms in an MRI report (both points refer to the insertion of gluteus  medius/minimus to greater trochanter of the femur):

mild degeneration of the muscular attachment of the left gluteus medius
mild tendinosis of the left gluteus minimus

Is muscular attachment (to a bone) synonymous to tendon? Or does the muscular attachment designate the muscle part that attaches to the tendon? Or something else?

The tendon and muscle attachment are not the same. In your example, both are affected, so they are described separately.
A muscle extends into a tendon and this into an enthesis - an actual attachment site where the muscle is attached to the bone (PubMed).

Thanks! Just to confirm, it means that muscular attachment = tendon + enthesis?

No, the tendon is not really a part of the muscular attachment.

so muscular attachment = enthesis?

Yes, that's it. It also applies for the sites where ligaments are attached to the bone.

Thanks for confirming! Good to know about ligaments.

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text:
What advantages could there be for using the unseen variant chosen by He Jiankui instead of the naturally occurring CCR5-∆ 32 mutation?
Jennifer Doudna mentioned in https://youtu.be/9Yblg9wDHZA?t=2566 on 2019-02-21 that  He Jiankui introduced an unseen variant of the CCR5 gene when gene editing the twin humans Lulu and Nana. What advantage might there be for using that unseen variant instead of the naturally occurring CCR5-∆ 32 mutation?
Figure from the above-mentioned YouTube presentation showing the CCR5 gene and some variants:

I have crossposted the question at:

https://qr.ae/TWtxdj
https://www.youtube.com/watch?v=9Yblg9wDHZA&lc=UgwInhQJsw8lhfQBVlJ4AaABAg

Interesting question, but this seems very opinion based and speculative — I suggested some edits to try to overcome this, but they may not pass muster ...

@tyersome Thanks for the edit! Understanding the impact of gene mutations on the phenotype is an important scientific question, and I assume that He Jiankui has some scientific grounding for his choice.

You're welcome!  He likely thought he had good reasons, but considering how poorly thought out his experiment seems to have been I wouldn't count on it!

@tyersome George Church, who reviewed He Jiankui's 2 papers regarding this experiment, mentioned that it seems to have been carried out quite meticulously (put aside the ethical discussion). E.g., the genome was sequenced a few times after the edit to ensure that the edit went as expected.

I don't think we can put aside the ethical issues or even completely separate them from the technical.
For example my understanding is that mutation of CCR5 may put the girls at increased risk of other diseases including: Breast cancer — https://ascopubs.org/doi/abs/10.1200/jco.2015.33.28_suppl.17; Immune system hyperactivity — https://www.ncbi.nlm.nih.gov/pubmed/23250822.

Possibly He Jiankui was using Cas9 without a template DNA.  If so, this generates double-stranded breaks that are repaired through processes such as non-homologous end joining (NHEJ) that often produce small indels (deletions and insertions) 1.
This is consistent with the apparently random small deletions and insertions around the cut site seen in both girls.
An additional, unflattering possibility is that this way he could prove that these were his edits and didn't happen spontaneously.
Useful starting points for understanding how Cas9 works can be found at the Addgene website and on Wikipedia.

Reference:
1: Brinkman, Eva K et al. “Kinetics and Fidelity of the Repair of Cas9-Induced Double-Strand DNA Breaks.” Molecular cell vol. 70,5 (2018): 801-813.e6. doi:10.1016/j.molcel.2018.04.016

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text:
What is this fruit (round, 3 cm diameter, yellow outside, 1 black seed, found on Easter Island)?
What is this fruit (round, 3 cm diameter, yellow outside, 1 black seed, found on Easter Island)?

Some fruits may have more than one seed:

I think you are looking at Syzygium jambos in the Myrtaceae.  The first link at Wikipedia has a number of pictures which are quite similar to your pictures.


text:
Does the term "upper extremity" include hands?
I see on http://en.wikipedia.org/wiki/Upper_limb that the term "upper extremity" seem to include hands. However, in many hospitals, there is a "Hand & Upper Extremity Service", which would tend to indicate that the term "upper extremity" does not include hands.
Does the term "upper extremity" include hands?

Generally, upper extremities refers to arms (and everything attached to them), while lower extremities are the legs.

I suspect that "hand" is separated out because it is often a surgical subspeciality. Hands are complicated.

Interestingly, while hands include fingers with a lot of innervation, almost all muscles for hand are located in arm. 2OP: please accept answer if it is satisfactory

As far as I know, and the same is written on Farlex Free Dictionary, the upper extremity or superior limb includes:

the shoulder girdle
the arm
the forearm
the hand

Again, on this Dartmouth Medical School page, the upper limb bones are described and the article includes the bones of the hand.
So, anatomically speaking, the upper limb includes the hand.

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text:
Where can I find the list of all tendons in the human body?
https://www.healthcentral.com/article/aging-can-take-major-toll-on-womens-tendons (mirror) claims that:

There are about 4,000 tendons throughout the body.

This claim is echoed by a fair amount of websites but I couldn't find any
decently trustworthy source.
Where can I find the list of all tendons in the human body?
I have only been able to find a list of skeletal muscles of the human body so far. I'm surprised that there are 4000 tendons even though they are only ~640 muscles: most muscles that I am aware of are attached to fewer than six tendons (FYI: Why some muscles have more tendons than others?).

Maybe that article is exaggerating?

@kmm maybe. Having a list would clarify it.

640 muscles should be enough for anybody.

@dotancohen mark my words: after a few decades, every muscular system will have at least 2~8 Gigamuscles, and many will have 16+. Technological advance will not be stopped

Your best bet is the Terminologia Anatomica, which is the international standard for anatomical terminology.
The 1998 edition is freely available. It lists only a few named tendons though, which is consistent with my experience as an anatomist: very few tendons are named separately from the muscles to which they are connected. Central tendon of the diaphragm, conjoint tendon, and calcaneal tendon are a few.
Otherwise, it's just "tendon of biceps brachii" (which actually has 2 tendons at one end and one at the other).
4,000 seems like a too high number to me. 2x the 640ish muscles plus some extra for multi-headed muscles and those with internal tendons or aponeurotic tendons seems like a more reasonable estimate.

The FMA lists 705 tendons, but note that it includes separate terms for left and right instances. As @kmm says, many of these simply shadow the list of skeletal muscles (and is likely incomplete).
You can browse the list on OLS, or if you want to extract a table you can query this SPARQL endpoint, just type in the query here:
SELECT DISTINCT ?x ?v0 WHERE {
   ?x <http://www.w3.org/2000/01/rdf-schema#subClassOf>+
       <http://purl.obolibrary.org/obo/FMA_9721> .
   OPTIONAL {?x <http://www.w3.org/2000/01/rdf-schema#label> ?v0}}


text:
What is the difference between sinew and tendon?
I wonder what the difference between sinew and tendon is. I searched for it but didn't get any clear answer:
https://www.quora.com/Whats-the-difference-between-sinew-and-tendon:

They are often used interchangably but to be technical, a tendon
  connects a muscle to a bone. The term sinew also seems to include
  ligaments which connect bones to bones. It is however, not a medical
  term.

https://answers.yahoo.com/question/index?qid=20070410182936AA2Kcnk

Sinew is another word for muscle which is the functional unit of
  movement.
Tendons connect bone to muscle to make movement possible: The muscle
  contracts and pulls the bone that it's connected to Source(s)

http://the-difference-between.com/tendon/sinew :

Sinew is a synonym of tendon. As nouns the difference between sinew
  and tendon is that sinew is (anatomy) a cord or tendon of the body
  while tendon is (anatomy) a tough band of inelastic fibrous tissue
  that connects a muscle with its bony attachment.

http://www.thefreedictionary.com/sinew

sinew = tendon

https://en.wikipedia.org/wiki/Tendon

A tendon (or sinew) is a [...]

Is sinew a synonym for tendon, and if not what is the difference?

They get used somewhat interchangeably, which blurs the lines on the definitions.
When I had my anatomy classes, sinews were regarded as an inclusive class, which included both ligaments and tendons.
For the breakdown:

Tendon: Fibrous tissue that connects muscle to bone.
Ligament: Fibrous tissue that connects bone to bone.
Sinew: Includes both of the above.

A tendon is a fibrous connective tissue which attaches muscle to bone. Tendons may also attach muscles to structures such as the eyeball. A tendon serves to move the bone or structure. A ligament is a fibrous connective tissue which attaches bone to bone, and usually serves to hold structures together and keep them stable. So sinew = tendon. Sinew is a bit more general and somewhat ambiguous. It is mostly used today synonymously with tendon, but historically it has been used to mean either tendons or ligaments, or even to mean muscle.

Please provide a citation or link to supporting evidence. Thanks!


text:
Age-associated neurodegenerative diseases
Age-associated neurodegenerative diseases encompass Alzheimer's Disease and Parkinson's Disease. What other neurodegenerative diseases could be described as age-associated? Multiple Sclerosis? Brain tumors? What might be the criteria for defining a disease as age-associated, specifically in the realm of neurobiology?

Dementia with Lewy bodies (DLB): It is characterized anatomically by the presence of Lewy bodies, clumps of alpha-synuclein and
  ubiquitin protein in neurons, detectable in post-mortem brain
  histology.[1] Lewy Body dementia affects 1.3 million individuals in
  the United States alone.

http://en.wikipedia.org/wiki/Dementia_with_Lewy_bodies

Binswanger disease is a form of small vessel vascular dementia caused by damage to the white brain matter.[1] White matter atrophy
  can be caused by many circumstances including chronic hypertension as
  well as old age.[2] This disease is characterized by loss of memory
  and intellectual function and by changes in mood. These changes
  encompass what are known as executive functions of the brain.[3] It
  usually presents between 54 and 66 years of age, and the first
  symptoms are usually mental deterioration or stroke.[4]

http://en.wikipedia.org/wiki/Binswanger%27s_disease
To name the two with the highest prevalence after Alzheimer's and Parkinson's.

And what of MS, and a definition? Should age-association be defined by epidemiological studies or some other way?


text:
What is the difference between copy number changes with and without allelic imbalance?
I require some clarification on copy number aberrations (structural gain and loss in chromosomes). From what I understand, gain/loss per se can be divided into two types.
Consider two alleles, A and B at the same locus on homologous chromosomes.

Allelic Balance: in one type of structural gain/loss, there is no resulting allelic imbalance; examples:

AB ==> AABB (duplication),
AB => -- (loss).

Allelic Imbalance: in the other type of structural gain/loss, there is resulting allelic imbalance; examples:

AB ==> AAB (duplication of A),
AB => -B (deletion LOH),
AB ==> BB (copy-neutral LOH).

First, is what I have described above correct?
Second, if it is correct, what is the biology underpinning these copy number aberration types? Are the mechanisms responsible for bringing about allelically-imbalanced CN change distinct from the mechanisms for bringing about allelically-balanced CN change? What are these mechanisms?
NB. I'm confining this to just copy number-related allelic imbalance.

Allelic imbalance is a pretty broad phenomenon difference in the expression of two alleles.  As such you have listed would probably cause allelic imbalance, but it could be the result of methylation or even differences in RNA sequences between the alleles which say interfere with post translational splicing say.
In the case of copy number variations, if a copy number region (which is often a higly repetitive sequence in the genome and not a gene duplication) might interfere or not interfere with gene regulation. In cancer cells large segments of the genome may be copied or cut out though, so in that case the mechanism you put forth may be important.

Regulatory effects on gene expression are obviously a v important consideration for AI. However, I suppose I'm confining myself to copy number. For e.g., for AI CN changes, the predominant mechanism may be NHEJ, whereas for allelically-balanced CN changes, the driving mechanism may be mitotic defects???


text:
Aren't antibiotic resistant probiotics dangerous?
Multidrug resistant probiotics are often recommended by doctors in various cases. But since bacteriae can easily exchange genes by conjugation or other means they could promote the drug resistance of other dangerous bacteriae residing in the bowels. (Which could be just "visitors" otherwise causing infections somewhere else)
Or there is something that withholds this transfer? I think not and so my former genetics professor.

I couldn't find a single paper on "multidrug resistant probiotics". What is your source?

I doubt that this is locale to our country but I can't find any international substances. Here is a google translate link for the patient information of such a probiotic. Excerpt from the end of the page: Active ingredient: 2 billion multi-antibiotic-resistant Bacillus clausii spores, 5 ml per bottle Other ingredient (s): purified water

Recommending multidrug resistant probiotics sounds fricking insane. I'm going to stop commenting now lest I start swearing...

Usually, resistance genes are located on plasmids---additional DNA rings in the bacterium that are part of the genome. These plasmids cause their own exchange with other bacteria, even from other species.
B. clausii, the probiotics organism in question here, appears to be special, though, in that it has no plasmids. His resistance genes come with the primary ring-shaped genome and should not be transferred via plasmid exchange to other bacteria. This doesn't rule out other means of gene transfer like phages or conjugation, however. In one study, it was unsuccessfully tried to transfer a macrolide resistance gene to other bacteria. They conclude

A potential hazard is transfer of resistance to microorganisms
  pathogenic for humans. The risk that this event will occur and the
  consequences in terms of morbidity and mortality have not been
  evaluated. Parameters required for risk assessment include studies on
  the nature and mobility of the resistance genes of probiotics.

The only other paper on a B.clausii resistance gene didn't look at its transferability. That clearly shows we don't know enough.
B. Bozdogan, S. Galopin, R. Leclercq: Characterization of a new erm-related macrolide resistance gene present in probiotic strains of Bacillus clausii. In: Applied and environmental microbiology. Band 70, Nummer 1, Januar 2004, S. 280–284, {{ISSN|0099-2240}}. PMID 14711653. PMC 321311.

Thanks so the conclusion is that there is no evidence neither pro nor contra. I think this makes these substances dangerous enough. If anyone can add more, he's welcome.

After all we know now about bowel microbiome destruction it's actually the antibiotics themselves that should be labelled dangerous.


text:
Skeletal muscle without antagonist
Is there any skeletal muscle that does not have an antagonist? Excluding circular muscles such as around eye and mouth.
The reason why I am wondering is because in biology normally nothing is ever just like that, there is always an exception. This would be the first biological rule without exception that I came across.
I am thinking of humans only for a start but feel free to include any other animal if any have skeletal muscles without antagonists :)

"the first rule without exception?" Didn't you just say - "excluding orbiculares"?

Good point, of course everyone can decide what exactly the rule should be and adding conditions removes exceptions. But that's not really what my question was about :-)

I would argue that the orbiculares do have antagonists. To some extent, levator palpebrae superiorus antagonizes orbicularis oculi, and zygomaticus major/minor as well as risorius antagonize orbicularis oris.
I can think of three muscle that don't have obvious antagonists:

Stapedius
Tensor tympani
Articularis genu

1 and 2 essentially perform the same action, to dampen sounds reaching the cochlea. 3 elevates the suprapatellar bursa.


text:
What is the purpose of the adrenal medulla?
The adrenal medulla is less of a 'real' endocrine organ like the others in the endocrine system and much more an extension of the sympathetic nervous system. In fact, its chromaffin cells are modified neurons by descent and secrete adrenalin and some noradrenalin upon stimulation by sympathetic preganglionic fibres, effectively turning the medulla into a sort of 'endocrine ganglion' with the whole cardiovascular system as its 'postganglionic fibres'.
Adrenalin in the circulation seems to have pretty much the same effect as all the adrenergic neurons of the sympathetic nervous system (which innervates all blood vessels, organs etc.): arteriole constriction, cardiac output increase, breath rate increase, pupil dilation, glucagon secretion and insulin inhibition, stimulation of glycolysis and glycogenolysis etc.
So what is the purpose of the adrenal medulla, if all of the effects which the endocrine adrenalin produces are essentially the same as those produced by the sympathetic mass response?

I have found the answer to the purpose of the adrenal medulla to be flexibility. Just like regulation for example of gene expression or metabolism occurs on many levels with different speeds and permanences of their effects, signalling needs to be available both quick and short-lived, and slower but with more long-lasting effects. The adrenal medulla provides exactly that.
Sympathetic adrenergic neurons are quick, but as quickly as they release their neurotransmitter, the effect is only of short duration and adrenalin is quickly cleared from the target area. Rather than giving off short bursts of adrenalin, the medulla maintains a constant systemic level of it and in response to stimulation raises or lowers that level. This response takes more time as blood circulates much slower than neurons respond, but its effects last longer.

I would also add the following distinctions: instead of releasing neurotransmitters, the cells in the adrenal medulla secrete hormones.
The adrenal medulla is where the main conversion of the amino acid Tyrosine into the catecholamines, epinephrine, and norepinephrine takes place.
The hormones are released quickly because the ANS, specifically, the sympathetic division, has direct control over the cells. Adrenaline is responsible for about 85% and noradrenaline for the remaining 15%.
Noradrenaline and adrenaline have a number of notable effects, including increased heart rate, blood pressure, blood vessel constriction in the skin and gastrointestinal tracts, smooth muscle (bronchiole, capillary), dilation, and an increased metabolism.


text:
Significance of basal lamina for outer layers of epithelium
In stratified (not pseudostratified) epithelia such as the epidermis, what purpose does the basal lamina serve for the outer layer cells which do not even stand in contact with it?
Also, how do these cells attach, all just through tight junctions to lower layers?

The basal lamina, a specialised type of extracellular matrix (ECM) that differs between cell types, acts as a base for stratified epithelia cells to layer on top of and therefore has a supportive role as well as providing a base for attachment (for the layer of cells immediately on top of it) 1. Layers of epithelial cells on top of further strata of similar cells with no differing tissue composition underneath would have no support and cell types would be able to mix freely within tissues. The different cell types within tissues are kept seperate by this ECM to maintain areas for specific functions. The importance of this can be seen through studying epithelial cancers, where the epithelial cell layer breaks through the entire basement membrance and invades the surrounding tissue. This can cause massive disruption of tissue function.
Yes, it seems that the layers of cells are attached by various junctional complexes, the desmosomes (maculae adherentes) being the most abundant for stratified epithelia.
Referenes
1 http://www.histology.leeds.ac.uk/tissue_types/connective/con_basal_lam.php


text:
Do single crossovers occur in circular polynucleotides?
Single crossovers in circular pieces of DNA do not seem to be a big topic, because if they happened, they would lead to a kind of combined chromosome with two inner strands and one large outer strand. (A bit like an 8)
 ________
|  ____  |
| |    | |
| |____| |
|  ____  |
| |    | |
| |____| |
|________|

But do these single crossovers actually not occur, for example because the crossover machinery is physically not able to do it, or do we just not observe them because they will inevitably lead to cell death and/or the chromosome somehow breaking?

this would be detected as DNA damage and normally be repaired I bet.  The RNA polymerase running around the cross over region would ruin the nifty figure 8 shape for sure.

Although crossover events can be observed in mitosis (mitotic recombination), they most frequently occur in prophase I of meiosis (crossing over in bivalents). Circular chromosomes are common in prokaryotes, but eukaryotes have linear chromosomes. Remember what meiosis accomplishes and that prokaryotes reproduce asexually. Prokaryotes don't have a need for -- or engage in -- meiotic division, so crossover events in circular chromosomes can really only be observed in instances of mitotic recombination, and I don't know the frequency of this in prokaryotes.
In prokaryote DNA replication, if any entangling of the two product circular chromosomes occurs, it is resolved by DNA topoisomerase. So perhaps a crossover would present a similar situation and the cell would resolve it by similar means.

thanks for your answer! valid thought, though crossover does occur in prokaryotes frequently - think of plasmids. the phenomenon I'm wondering about is that crossover from plasmids always seems to be doubled, exchanging a fragment between the chromosome and plasmid, and never single :)

good idea on topousomerase though! that might be

Changed the question to reflect this.

I'm accepting this answer because my understanding has improved in the meantime. As it is not possible to image recombination events as they happen (yet), it isn't possible to answer this conclusively.

Looking back at this question, I think this stems from a misconception in the first place. Crossovers are not events that affect single DNA strands but always both strands. The described double-ringed DNA molecule might exist as an intermediate in the process of a single crossover occurring.


text:
What's the therapeutic index of Pethidine (Meperidine in the US)?
What's the therapeutic index $\left(\frac{LD_{50}}{ED_{50}}\right)$ of Pethidine (Meperidine in the US) via the intravenous route for humans or whatever species you can find? The therapeutic window $\left(\frac{TD_{50}}{ED_{50}}\right)$ for humans will suffice if accompanied by the therapeutic index for pethidine via IV of another species.
Pethidine is an opioid painkiller with approximately $\frac{1}{7}-\frac{1}{8}$ the strength of morphine and a definite influence on monoaminergic neurons.
I imagine it'd be in the neighbourhood of 30-100, like most opioids that have been implemented in medicine.

I don't understand the downvotes. This seems like an answerable question.

Tell me about it... It would be nice if those that think I've done a poor job in asking this question could tell me what I did wrong.

I have not downvoted but perhaps people feel this is a medical question not a biological one. A biologist is unlikely to know the answer, a pharmacist or a surprisingly knowledgeable doctor would.

Pharmacology is a biologica/biochemical pursuit, not just the purview of medicine or pharmacy.

If so, where am I supposed to ask this question as far as stackexchange sites? This biology stackexchange is best suited for me to ask this question.

In any case I created a new tag to suite this question.

Just go ahead and ask. Remember that anyone can answer on SE, so someone with the answer may come along. Feel free to publicize your questions in other venues. Unfortunately, I'm not sure what those venues are for pharmacology questions.

Maybe someone was reading your question upside down and thought they were up-voting....

Sounds about right. I've been trying to get a pharmacy stackexchange site started but that's going to take at least a few months even if it gets a relatively large amount of support.

Closest I reached:

Source: Page 105, The Complete Recovery, By Anthea Hatfield Google Book


text:
What does "Psychomodulatory" mean in the context of potentially psychoactive drugs?
What does "Psychomodulatory" mean in the context of potentially psychoactive drugs? That is, in this journal article http://www.sciencedirect.com/science/article/pii/S0028390812001931 in the discussion (you will need special privileges to access the article via an institute or personal subscription or by paying for access) in the last sentence of the first paragraph it says

However, euphol even when given in very high doses, (up to 100 mg/kg)
  it did not show any evidence of psychomodulatory effects in the CNS

To me, "psychomodulatory" would mean "eliciting a significant change (up or down) relative to baseline or compared to a control, placebo, or carrier," here specifically in CNS function.
This statement appears to refer to the results presented in section 3.8, Effect of euphol in the cannabinoid tetrad tests. Across a range of doses (3-100 mg/kg) and across four different assessments of CNS function: locomotor activity (rotarod), catalepsy (time to move off of a suspended ring), analgesia (tail flick in response to thermal stress), and body temperature (self explanatory). The results of these four are summarized in the figure below.

Basically the effects are not significantly different from each other between dosages or times. The lines sit more or less atop one another. Compare to this figure, where the differences are significant:


text:
How is duration of efficacy estimated for vaccines?
Vaccines, especially those given in adulthood, usually have term limits attached, eg: 10 years for yellow fever or 3 years for typhoid. Since presumably the time course of an immune response is no great respecter of our calendrical conventions, and since there is also presumably a spectrum of responses across the population, how are these durations estimated? What are the criteria for deciding a cutoff time?
Also, do the estimates get revisited and updated as time goes on and new data become available? Do new data become available? Is there continuing follow-up research into this, or does the estimate just get made before the vaccine comes to market and then get taken as gospel?

Duration of efficacy is typically determined by tracking the antibody titers of a cohort of subjects who have gotten the vaccine, and estimating based on the trajectory of those titers where they will eventually cross the threshold to the point where the vaccine no longer confers immune resistance.
These estimates do get revised and estimated as time goes on - you will occasionally see new recommendations for a second or third "booster" dose of a vaccine, which is meant to extend the duration of immunity beyond the duration of the original vaccine.
Two major types of studies track this over time. Phase IV clinical trials, which are clinical trials required post-licensure, and observational epidemiology trials, which tend to be performed when disease transmission starts to occur in supposedly vaccinated populations.

Mechanical snail has raised the issue of viral evolution, so I'll touch on it briefly. The duration of efficacy discussed above is based on how long a patient's body can mount an immune response to a particular challenge. That's a concern for all vaccines.
For some vaccines, there's a secondary process that's of concern - that of the virus evolving in such a way that the antigens targeted by the vaccine are no longer those on the virus itself. This is only a concern for some viruses, notably those that are particularly fast-evolving, like influenza or HIV, and less of an issue for say, measles and HPV.
But that's typically not what people are talking about when they say "duration of efficacy" because it's inherently unpredictable, and less a function of the vaccine and more a function of the virus.

Is the cutoff determined by the first subject with titer below the threshold, the last or by some percentile of them (eg. 50)?

Usually with some form of statistical model

I read somewhere (I don't have a citation) that duration of efficacy is limited by the evolution of viral antigens; eventually the population will evolve to the point where the immune system no longer recognizes them effectively. RNA viruses have more volatile genomes and so their antigens drift faster. This explanation makes some sense but it conflicts with @Epigrad's answer.

Community wiki because I'm not sure this is correct. Feel free to edit in more information.

I've added some details to my answer. Your answer doesn't particularly conflict, its just asking about a subtly different process.

authors: w̢in̡͢g͘̕ed̨p̢͟a͞nt̡͜͝he̸r̴


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Do mitochondria simply automatically convert glucose to ATP?
I wonder whether there is any intelligent decision-making in mitochondria in the timing of their operation.
Do they simply begin ATP production as soon as the correct reactants are present?
Or, because they have their own DNA, do they have more complex strategies that vary to benefit the mutual cooperation with the host cell? This assumes that the simple circular DNA is performing higher level decisions in switching.

Mitochondria only have a handful of genes; their regulation is utterly intertwined with their host.  Additionally, only the TCA (Krebs, Citric Acid...) cycle occurs within mitochondria; glycolysis occurs in the cytosol.

@NickT, does that imply that the host 'controls' the activity of mitochondria?

Mitochondria are comprised of ~3000 proteins. However, the mitochondrial genome has only 13-14 protein-encoding genes. The remaining 99.6% of mitochondrial proteins are encoded by genes in the nuclear genome. (Wikipedia) Chloroplast genomes are only slightly larger (~100 genes).
Gene regulation and signaling between the nucleus and mitochondria (and between nucleus & chloroplast in plants/algae) occurs in both directions. Anterograde regulation is the signalling from nucleus to mitochondria and was once thought to be the only method of regulating organelle function. We now also know that Retrograde regulation occurs, in which the mitochondria sends signals to the nucleus.
To answer your question directly (but not thoroughly), both the mitochondria and the nucleus are sensing the environment and needs of the cell and signaling to each other to regulate ATP production.
If you want to learn more about retrograde signaling, googling "retrograde regulation" will bring up lots of papers on this topic in different organisms. This paper also has some diagrams of signalling pathways.

this is very interesting how there is bilateral communication between DNA and mitochondria. Does mitochondria have to work to survive? Eg. if they do not produce ATP, do they die?

Hi @Amy =)  Whilst I know that your block is quite small, we're trying to discourage extended direct quotes from wikipedia (see meta).  It might be a better idea to summarise the article yourself and link to it as a source for your answer =)

@RoryM - edited :)

@Vass That's what I think is the coolest thing about eukaryotic cells. The cell cannot build a mitochondria "from scratch" because the mitochondria have kept just enough genes on their own genome - but mitochondria cannot survive outside the cell because it has lost so many genes. If they don't produce ATP, they die, because the cell dies. Both the cell and the mitochondria have a vested interest in keeping the machinery going. :)

@Amy, why is this symbiosis so much more beneficial than the scenario of all regulation being contained in the nucleus?

@Amy thanks a lot, that really looks a lot better =D

@Vass - The current arrangement is not necessarily the perfect arrangement, it's just the best that has been achieved so far in the accidental history of evolution.  It's quite likely that it would be better if all mitochondrial genes resided in the nucleus since the sexual recombination of genes the nuclear mechanism provides allows better maintenance and improvement of genes (unlike the purely asexual DNA reproduction in the mitochondria).  This is why many genes have migrated from the mitochondrial genome to the nuclear genome, and why 99% of mitochondrial protein genes are nuclear.

@mgkrebbs, which genes migrated from mitochondria to the nuclear genome? Those that it would have needed to survive independently of the host cell?

Mitochondria have very few genes left, many fewer than a free living organism would need.  Almost all the originally present genes have been lost as unneeded, replaced by functional equivalents from the nucleus, or have effectively migrated from the mitochondrion to the nucleus.  The genes left in the mitochondria are mostly the electron transport chain proteins and the ribosome and tRNA genes needed to build those proteins.

The textbook version for the regulation of ATP involves a feedback loop with phosphofructokinase (PFK). The relative concentrations of ADP and ATP are characteristic of the energy state of the cell. If the cell is using energy, then there will be an excess of ADP. If not, then ATP.
ATP is an inhibitor of PFK, which in turn slows glycolysis (thus reducing the production of new ATP). In contrast, ADP is an allosteric activator of PFK, which in turn speeds up glycolysis (thus increasing the production of ATP).

so there is a stable equilibrium concentration between these two compounds? And is it that the use (or lack of use) of ATP ignites the production of more ATP from ADP?


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What is the average Leg-to-Foot Length/Width Ratio?
I'm making a program that estimates a probable size (widest width and longest length) for a human's foot given the length and width of the leg to which it is attached. However, try as I might, I can't seem to find the average foot-to-leg size ratio. Does anyone know this? It would be even better if you have different ratios for males and females.
As a note, I don't want to know that this varies depending on certain circumstances, just a good average number that will let me generate people who aren't grossly out-of-proportion

A brief study I conducted of my peers (10 people of varying genders, ages, and races, all about average body type) revealed a rather consistent foot-to-leg length ratio of 1:3 for males and females (variance is insignificant), and width of 2:3 for males and 1:2 for females.

Insignificant at a glance of after Chi-Squared with regards to the foot-leg ratio of males/females? How big was your sample?

@RoryM It was brief; sample of about 10 people ages 18 to 25. I didn't quite have the time to do an expansive study of peoples' legs since yesterday :P

poor effort - I'd have expected at least 100,000 samples in 24 hours!!  You might want to include that information in your answer to help future visitors from google etc =)


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What is this insect? (Location: Bangkok, Thailand; found on a rambutan; size: 8 mm long, 4 mm wide; color: black)
What is this insect? (Location: Bangkok, Thailand; found on a rambutan; size: 8 mm long, 4 mm wide; color: black)

On the rambutan:

Videos:

https://youtu.be/WwB0B_PdOT8
https://youtu.be/0DZ8nXcJIkI


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Why did the protein structure prediction accuracy in terms of GDT-TS decrease from 2008 (CASP 8) to 2014 (CASP 11)?
I read on https://doi.org/10.1038/d41586-020-03348-4:

Why did the protein structure prediction accuracy in terms of GDT-TS (Global Distance Test — Total Score) decrease from 2008 (CASP 8) to 2014 (CASP 11)?

A guess is that the tests given in the competition are of bigger proteins or the organisers have more of a pool to select challenging ones from because of the process getting cheaper in dollar terms. These proteins may be harder to model because of there being more pairwise force interactions between residues, so the average (y axis) will decrease for more difficult to model proteins unless better modelling can compensate for this.

I’m voting to close this question because it is about the historical details of computational challenge rather than a biological problem itself. As such it is, in my opinion, off-topic here, but is probably on-topic for SE Bioinformatics.


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What is this fruit from Cambodia? (orange skin, 3cm, orange juicy flesh, very stick white substance)
I saw this fruit in Thailand but was told it's from Cambodia:
Orange skin, ~3cm:

Orange juicy flesh:

The top has a very stick white substance  (the stickiness is quite similar to longkongs):

What is this fruit?

Have you tried it?

Not 100% sure, but this seems to be Willughbeia edulis, which is a climbing vine found from SE Asia through to India.
The fruit are yellow or orange, about the size of a lemon, have faint stripes on them and exude a latex from the stem end when cut. The latex forms a weak rubber after exposure to air. The latex also comes from cut stems and broken leaves.
I got this image from Plant Genetic Conservation Project Under the Royal Initiative of Her Royal Highness Princess Maha Chakri Sirindhorn, where you can see the similar shape and the stripes:


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Where does the gluteus medius attach to the greater trochanter compared to the gluteus minimus attachment?
Where does the gluteus medius attach to the greater trochanter of the femur  compared to the gluteus minimus attachment? Is it above, below, next to it, etc.? Ideally I'd like to know the distance as well and location relative to the greater trochanter.

What I have found so far: some diagrams place the gluteus medius attachment below the gluteus minimus attachment, some place it above and some place it next to it at the same height.
Example of diagram placing the gluteus medius attachment below the gluteus minimus attachment (image source (mirror)):

Example of diagram placing the gluteus medius attachment next to the gluteus minimus attachment (image source (mirror))

Example of diagram placing the gluteus medius attachment above the gluteus minimus attachment (image source (mirror)):

{1} greatly answers the question.
Regarding the insertion location (lateral view):

Note that unlike the gluteus minimus insertion, the gluteus medius insertion can also be viewed anterolaterally:

Table 2 contains more detailed insertion location data:

Regarding the insertion area:

Gluteus maximus: Average Area, mm^2 (95% CI): 473.4 (381.0, 565.8). Thick, muscular insertion along the posterior femur on the linea aspera
Gluteus medius: Composed of 2 contiguous rectangular footprints, the lateral facet oriented in the sagittal plane and the superomedial facet primarily in the transverse plane:

Lateral facet: Average Area, mm^2 (95% CI): 141.1 (117.7, 164.5).
Superomedial facet: Average Area, mm^2 (95% CI): 501.5 (442.8, 560.2).

Gluteus minimus: Average Area, mm^2 (95% CI):  280.9 (229.3, 332.5). Two morphologies noted: The majority (11/14) were long, thin, and crescent shaped and ran medial to lateral and concave facing inferiorly, while a few (3/14) were bowtie in shape.

Below are some actual pictures of the gluteus minimus insertion, the gluteus medius insertion to get another sense of their shape and location. Still  from {1}, this picture shows the gluteus medius (but not the gluteus minimus):

From {2}, this picture shows both the gluteus medius muscle and the gluteus minimus muscle:

I also find this picture good to give a better sense as to where the greater trochanter is located with respect to the human body (image source (mirror)):

References:

{1} Philippon, Marc J., Max P. Michalski, Kevin J. Campbell, Mary T. Goldsmith, Brian M. Devitt, Coen A. Wijdicks, and Robert F. LaPrade. "Surgically relevant bony and soft tissue anatomy of the proximal femur." Orthopaedic journal of sports medicine 2, no. 6 (2014): 2325967114535188. https://scholar.google.com/scholar?hl=en&as_sdt=0%2C5&q=Surgically+Relevant+Bony+and+Soft+Tissue+Anatomy+of+the+Proximal+Femur&btnG= ; https://www.ncbi.nlm.nih.gov/pubmed/26535335 ; https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4555602/ ; https://doi.org/10.1177/2325967114535188
{2} Woodley, Stephanie J., Susan R. Mercer, and Helen D. Nicholson. "Morphology of the bursae associated with the greater trochanter of the femur." JBJS 90, no. 2 (2008): 284-294. https://scholar.google.com/scholar?hl=en&as_sdt=0%2C5&q=Morphology+of+the+Bursae+Associated+with+the+Greater+Trochanter+of+the+Femur&btnG= ; https://www.ncbi.nlm.nih.gov/pubmed/18245587 ; https://doi.org/10.2106/JBJS.G.00257


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Do non-human animals suffer from insomnia?
And how do we know whether they do or not?
§
If sleep is a physiological need, it seems weird that we become unable to fulfill on demand even in the absence of any obvious physical issues. We would all probably would like to be able to fall asleep on demand on a long flight and we all know this can be hard even when we are tired.
Thus, my question is whether this is a mostly human dysfunction or a common animal property.

Cortisol is often used to measure stress levels in at least mammals and birds, and it is linked to insomnia in humans. I would therefore guess that stress-induced cortisol can cause insomnia in these groups of animals as well.

Commenting on the how, you can wire animals using EEG as you do with humans to see their brain activity. Provided you have a profile of the different patterns that correlates to different stages of sleep.

@Cornelius: You have almost the correct answer but why have you deleted it?

Insomnia most certainly occurs in other animals. One interesting example is the case of insomnia in Drosophila melanogaster. In this study 3 day old male and female flies that demonstrated reduced sleep time were crossed together over 60 generations to create flies insomnia-like (ins-l) that sleep less than 60 minutes a day compared to 800 min a day in their control flies, which are generation 0 (Fig 1B). These (ins-l) flies exhibited difficulty initiating sleep, maintaining sleep and showed cognitive impairment. They also had difficulty maintaining balance with elevated levels of triglycerides, cholesterol and fatty acids and although their core molecular clock remained intact, ins-l flies lost their ability to sleep in constant dark. Using whole-genome transcriptome profiling using Affymetrix high density nucleotide microarrays, these flies are compared against the control flies and many genes were over-represented (changed in expression compared to control flies) which are involved in metabolism, neuronal activity, behaviour and sensory perception with changes in lipid metabolism and synaptic transmission being consistent with increased adiposity and learning defects in flies. In addition, these ins-l flies were hyperactive and hyper responsive to environmental simulations and the over-representation of genes associated with sensory perception suggests that hyperarousal in insomnia may be attributed to increased activity in the sensory system and that these processes are under genetic control. Two genes in particular Filamin-A (Cheerio) and Malic enzyme (Men), which were found to be differentially regulated (changed in expression) in files are also modulated (changed) by sleep loss in humans, showing that the same processes are involved/get effected in humans and flies during insomnia.
The research above clearly demonstrated the genetic regulation and effects of insomnia in other animals and shows that its not just a human dysfunction.

Insomnia has also been observed in some fish: http://www.veterinarypracticenews.com/April-2009/Scientists-Say-Fish-Suffer-From-Insomnia/


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Overlapping genetic information in eukaryotes
In my research, I look at a lot of gene predictions / annotations. Frequently, I see loci where multiple gene models overlap. I haven't taken a systematic approach to analyzing these cases, but I do remember seeing quite a bit of variation in the direction of the overlapping genes (same vs different directions), the amount of overlap, and even the number of overlapping genes.
I know enough about gene prediction to take any computational predictions with a grain of salt--even those supported by transcript and peptide alignments. However, these cases have me thinking--does overlap of genetic information really occur in eukaryotes? I seem to remember learning (or hearing anecdotally) that it can happen in prokaryotes, and that seems to be understandable given the compactness of prokaryotic genomes. But can this happen in eukaryotes? Has this been studied, and are there cases that have been confirmed experimentally?

You might be interested in the INK4A locus (chromosome 9p), encoding both p19 and p16 genes, very close to p15. You can read a description here. All three proteins are known experimentally to exist.
Now, whether these are two different genes or the same gene with alternative splicing and start sites leading to different reading frames it's up to discussion. The point is that p19 and p16 share DNA coding sequence but not protein sequence nor function.

In general, the compactnes of genomes is a characteristic of prokaryotes, but there are several eykaryotes that have overlapping genes: many parasites and endosymbionts. The best studied of these are the fungal parasites of the phylum microsporidia and the nucleomorphs (remnant nuclei of algal endosymbionts in cryptophytes and chlorarachniophytes).
cDNA library was constructed from the microsporidian Antonospora locustae and 1,146 cDNA clones were sequenced. Here is part of the expression profile (1):

Of the 871 clones found to encode recognizable genes, 97 transcripts (11%) from 70 distinct loci encoded sequence from more than one gene (Fig. 1 A ; see also Table 1, which is published as supporting information on the PNAS web site). The polyA sites of these clones do not correspond to polyA tracts in the genome, so they are unlikely to derive from DNA contamination (see also below), but instead come from polyA RNA. In prokaryotes, polycistronic mRNAs commonly code for multiple proteins (11), but with few exceptions (12) eukaryotic mRNAs encode a single gene. A. locustae multigene transcripts encode two or three genes or gene fragments in various orientations (Fig. 1 B–I ), but they cannot all be polycistronic messages because there is no bias for genes being on the same strand.

Here is part of a review paper on the nucleomorphs genome (2):

As in other reduced genomes, the G. theta nucleomorph genome possesses a very high A+T content (75%) and gene density is extremely high: 1 gene per 977 bp and 44 genes overlap by as many as 76 nucleotides. Williams et al. (84) showed that transcription of the G. theta nucleomorph genome is affected by this compaction, with nucleomorph-derived messenger RNAs often possessing coding sequence for more than one gene, albeit with no strand bias. It appears that during the process of genome compaction, transcription regulatory elements (e.g., promoters, terminators) have moved from the intergenic spacers into the coding regions themselves (84).

I also have to point out that there are a few examples of overlapping genes in yeast: CCT6 overlaps with YDR187C and CCT8 overlaps with YJL009W (3).

A high frequency of overlapping gene expression in compacted eukaryotic genomes
Nucleomorph Genomes, Annual Review of Genetics
The Chemical Genomic Portrait of Yeast: Uncovering a Phenotype for All Genes


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Why is polyploidy lethal for some organisms while for others is not?
Polyploidy is the multiplication of number of chromosomal sets from 2n to 3n (triploidy), 4n (tetraploidy) and so on. It is quite common in plants, for example many crops like wheat or Brassica forms. It seems to be rarer in animals but still it is present among some amphibian species like Xenopus.
As I know in mammals polyploidy is lethal (I don't mean tissue - limited polyploidy). I understand that triploidy is harmful due to stronger influence of maternal or paternal epigenetic traits that cause abnormal development of placenta, but why there is no tetraploid mammals?

Excellent question! A topic of active research and without clear consensus, as far as I remember from some talk.

Great question, plenty to talk about here (give me a few days).

Looking forward to it, @RichardSmith!

We were told in a lecture that odd polyploidies were usually lethal because the third homologuous chromosome disrupted alignment during meiosis.

Diploidy is an adaptive regulatory mechanism that is not necessary to multicellular life.  Plants and cancer cells are notriously unregulated in ploidy count.

Great question, and one about which there has historically been a lot of speculation, and there is currently a lot of misinformation. I will first address the two answers given by other users, which are both incorrect but have been historically suggested by scientists. Then I will try to explain the current understanding (which is not simple or complete). My answer is derived directly from the literature, and in particular from Mable (2004), which in turn is part of the 2004 special issue of the Biological Journal of the Linnean Society tackling the subject.
The 'sex' answer...
In 1925 HJ Muller addressed this question in a famous paper, "Why polyploidy is rarer in animals than in plants" (Muller, 1925). Muller briefly described the phenomenon that polyploidy was frequently observed in plants, but rarely in animals. The explanation, he said, was simple (and is approximate to that described in Matthew Piziak's answer):

animals usually have two sexes which are differentiated by means of a process involving the diploid mechanism of segregation and combination whereas plants-at least the higher plants-are usually hermaphroditic.

Muller then elaborated with three explanations of the mechanism:

He assumed that triploidy was usually the intermediate step in chromosome duplication. This would cause problems, because if most animals' sex was determined by the ratios of chromosomes (as in Drosophila), triploidy would lead to sterility.
In the rare cases when a tetraploid was accidentally created, it would have to breed with diploids, and this would result in a (presumably sterile) triploid.
If, by chance, two tetraploids were to arise and mate, they would be at a disadvantage because, he said, they would be randomly allocated sex chromosomes and this would lead to a higher proportion of non-viable offspring, and thus the polyploid line would be outcompeted by the diploid.

Unfortunately, whilst the first two points are valid facts about polyploids, the third point is incorrect. A major flaw with Muller's explanation is that it only applies to animals with chromosomal ratio-based sex determination, which we have since discovered is actually relatively few animals. In 1925 there was comparatively little systematic study of life, so we really didn't know what proportion of plant or animal taxa showed polyploidy. Muller's answer doesn't explain why most animals, e.g. those with Y-dominant sex determination, exhibit relatively little polyploidy. Another line of evidence disproving Muller's answer is that, in fact, polyploidy is very common among dioecious plants (those with separate male and female plants; e.g. Westergaard, 1958), while Muller's theory predicts that prevalence in this group should be as low as in animals.
The 'complexity' answer...
Another answer with some historical clout is the one given by Daniel Standage in his answer, and has been given by various scientists over the years (e.g. Stebbins, 1950). This answer states that animals are more complex than plants, so complex that their molecular machinery is much more finely balanced and is disturbed by having multiple genome copies.
This answer has been soundly rejected (e.g. by Orr, 1990) on the basis of two key facts. Firstly, whilst polyploidy is unusual in animals, it does occur. Various animals with hermaphroditic or parthenogenetic modes of reproduction frequently show polyploidy. There are also examples of Mammalian polyploidy (e.g. Gallardo et al., 2004). In addition, polyploidy can be artificially induced in a wide range of animal species, with no deleterious effects (in fact it often causes something akin to hybrid vigour; Jackson, 1976).
It's also worth noting here that since the 1960s Susumo Ohno (e.g. Ohno et al. 1968; Ohno 1970; Ohno 1999) has been proposing that vertebrate evolution involved multiple whole-genome duplication events (in addition to smaller duplications). There is now significant evidence to support this idea, reviewed in Furlong & Holland (2004). If true, it further highlights that animals being more complex (itself a large, and in my view false, assumption) does not preclude polyploidy.
The modern synthesis...
And so to the present day. As reviewed in Mable (2004), it is now thought that:

Polyploidy is an important evolutionary mechanism which was and is probably responsible for a great deal of biological diversity.
Polyploidy arises easily in both animals and plants, but reproductive strategies might prevent it from propagating in certain circumstances, rather than any reduction in fitness resulting from the genome duplication.
Polyploidy may be more prevalent in animals than previously expected, and the imbalance in data arises from the fact that cytogenetics (i.e. chromosome counting) of large populations of wild specimens is a very common practise in botany, and very uncommon in zoology.

In addition, there are now several new suspected factors involved in ploidy which are currently being investigated:

Polyploidy is more common in species from high latitudes (temperate climates) and high altitudes (Soltis & Soltis, 1999). Polyploidy frequently occurs by the production of unreduced gametes (through meiotic non-disjunction), and it has been shown that unreduced gametes are produced with higher frequency in response to environmental fluctuations. This predicts that polyploidy should be more likely to occur in the first place in fluctuating environments (which are more common at higher latitudes and altitudes).
Triploid individuals, the most likely initial result of a genome duplication event, in animals and plants often die before reaching sexual maturity, or have low fertility. However, if triploid individuals do reproduce, there is a chance of even-ploid (fertile) individuals resulting. This probability is increased if the species produces large numbers of both male and female gametes, or has some mechanism of bypassing the triploid individual stage. This may largely explain why many species with 'alternative' sexual modes (apomictic, automictic, unisexual, or gynogenetic) show polyploidy, as they can keep replicating tetraploids, thus increasing the chance that eventually a sexual encounter with another tetraploid will create a new polyploid line. In this way, non-sexual species may be a crucial evolutionary intermediate in generating sexual polyploid species. Species with external fertilisation are more likely to establish polyploid lines - a greater proportion of gametes are involved in fertilisation events and therefore two tetraploid gametes are more likely to meet.
Finally, polyploidy is more likely to occur in species with assortative mixing. That is, when a tetraploid gamete is formed, if the genome duplication somehow affects the individual so as to make it more likely that it will be fertilised by another tetraploid, then it is more likely that a polyploid line will be established. Thus it may be partly down to evolutionary chance as to how easily a species' reproductive traits are affected. For example in plants, tetraploids often have larger flowers or other organs, and thus are preferentially attractive to pollinators. In frogs, genome duplication leads to changes in the vocal apparatus which can lead to immediate reproductive isolation of polyploids.

References

Furlong, R.F. & Holland, P.W.H. (2004) Polyploidy in vertebrate ancestry: Ohno and beyond. Biological Journal of the Linnean Society. 82 (4), 425–430.
Gallardo, M.H., Kausel, G., Jiménez, A., Bacquet, C., González, C., Figueroa, J., Köhler, N. & Ojeda, R. (2004) Whole-genome duplications in South American desert rodents (Octodontidae). Biological Journal of the Linnean Society. 82 (4), 443–451.
Jackson, R.C. (1976) Evolution and Systematic Significance of Polyploidy. Annual Review of Ecology and Systematics. 7209–234.
Mable, B.K. (2004) ‘Why polyploidy is rarer in animals than in plants’: myths and mechanisms. Biological Journal of the Linnean Society. 82 (4), 453–466.
Muller, H.J. (1925) Why Polyploidy is Rarer in Animals Than in Plants. The American Naturalist. 59 (663), 346–353.
Ohno, S. (1970) Evolution by gene duplication.
Ohno, S. (1999) Gene duplication and the uniqueness of vertebrate genomes circa 1970–1999. Seminars in Cell & Developmental Biology. 10 (5), 517–522.
Ohno, S., Wolf, U. & Atkin, N.B. (1968) EVOLUTION FROM FISH TO MAMMALS BY GENE DUPLICATION. Hereditas. 59 (1), 169–187.
Orr, H.A. (1990) ‘Why Polyploidy is Rarer in Animals Than in Plants’ Revisited. The American Naturalist. 136 (6), 759–770.
Soltis, D.E. & Soltis, P.S. (1999) Polyploidy: recurrent formation and genome evolution. Trends in Ecology & Evolution. 14 (9), 348–352.
Stebbins, C.L. (1950) Variation and evolution in plants.
Westergaard, M. (1958) The Mechanism of Sex Determination in Dioecious Flowering Plants. In: Advances in Genetics. Academic Press. pp. 217–281.

(I'll come back and add links to the references later)

It's a really great answer. Just a few remarks:

In next to last point you probably mean diploid gamets (gamets from tetraploid individual)
In frogs, if polyploidy changes male vocal aparatus, then it also have to change polyploid female preferences. Otherwise polyploid males would be avoided also by females of the same ploidy and it would be even more difficult to establish polyploid population.

You're absolutely right on both points Marta. Regarding the second point, the key thing is that polyploidy affecting the males' calls creates a situation where it is possible for a female to distinguish a polyploid male from a non-polyploid, which if there was a non-trivial rate of polyploidy arising would then lead to selection for polyploid females which preferred the polyploid males. Without a change in traits for polyploids there is no selection.

This answer was worth the wait. Excellent and thorough!

Beautiful answer.. I actually had the same question and referred Mable. Only if I could stumble upon this earlier! +1

Plants have a simpler anatomical structure than mammals (is anatomical the right word, or would physiological be more appropriate?). Mammals on average don't have more genes than plants, so my understanding is that this additional complexity is the result of finer and more complex regulatory mechanisms.
When you remove or duplicate an individual gene in an organism, that organism must compensate somehow. The more complex the regulatory system, more likely that even small perturbations will cause severe defects or even lethality.
Extend this to the scale of a whole genome, and it shouldn't be surprising that polyploidy is lethal for a lot of organisms. It find it extremely fascinating that it's not lethal for some organisms, but it makes sense that organisms with simpler regulatory mechanisms would be more successful handling a genome duplication event through gene subfunctionalization, neofunctionalization, etc.

This was one of the first ideas suggested when it was historically discovered that many more plants than animals exhibit polyploidy. However, it is not the explanation. I will expand on why it is incorrect when I post my own answer later. As a side point: whilst plants could be argued to be anatomically more simple than animals, they are not physiologically more simple. Animals have different constraints, environmental challenges and adaptations than plants, but ultimately are not more complex.

Thanks for answer. I also thought about it. But it is hard to measure how complex is an organism and among verebrate polyploidy also occure. Maybe amphibians are not so smart as we are, but are they really so much simpler?

@RichardSmith If there is any time to draw up your answer, it is now. I am interested in what you have to say!

@DanielStandage My finals finish on Wednesday, after which I will be back here to answer all the questions on my to-do list, starting with this one :)

In animals, polyploidy is not tolerated and very few polyploid species
  are known to exist. Those that do exist are usually asexual,
  parthenogenetic, or hermaphroditic. Most of the problems resulting
  from polyploidy occur during synapsis of homologues during prophase I.
As plants do not have a chromosomal mechanism for sex determination,
  synapsis and subsequent disjunction is not as great a problem. In
  fact, most plants are monoecious.

These paragraphs are taken from these lecture notes from an Emporia State University genetics course.
Supporting information looks to be present in Why Polyploidy is Rarer in Animals Than in Plants (H. J. Muller, The American Naturalist, 1925), but I didn't get a chance to access the article.

Thank you for your answer. The issue of reproduction of polyploid species is also very interesting, but my question was rather why some organism survive polyploidy (even if they cannot reproduce), while for other it means death at early stage of development. The last article you've quoted may be quite out of date, but I don't have an access to it either. (that's pity, becouse I'm curious what people thought about this issue at the beginning of XX century).

@MartaCz-C: Do you mean, at the beginning of the X diploid century?

My point in stating what is below is to emphasize even when polyploidy is present in closely related species there is a question of why an organism can survive one ploidy event but not another and why tolerance of polyploidy varies among similar organisms?
Several species of deciduous azaleas are tetraploid. Closely related diploid deciduous azaleas are more than happy to accept pollen and produce seedpods. We have attempted such crosses many times and they almost always success in terms of seedpod development.
Tetraploid deciduous azaleas on the other hand are very reluctant to accept pollen from diploid deciduous azaleas. We have attempted such crosses nearly 100 times without success.
However producing seedpods and producing viable seeds are of course different. Some crosses of diploid X tetraploid produce 1 or only a few viable seedlings (We have never gotten none to date.) while others produce viable seedlings measured in dozens while still others produce hundreds of viable seedlings. In some instances, the same diploid parent will produce many more viable seedlings from one tetraploid parent than from another.
To date all seedlings of diploid X tetraploid have measured as triploid using flow cytometry. Most seedlings appear to be sterile but some are fertile and occasionally some are very fertile to the point of setting open pollinated seed.
When these triploid seedling are successfully crossed with tetraploids, we get what appears based on flow cytometry to be triploids, aneuploids between triploid and tetraploid, tetraploids, and pentaploids. The few pentaploids old enough to flower appear to set seedpods when crossed with tetraploids.
In elepidote Rhododendron which has only diploid species, hybridizers over the last 150 years have had very limited success in producing polyploid elepidote Rhododendrons (less than 100 named hybrids) despite amazing success at creating and naming complex interspecies crosses (more than 20,000).
In other words, the pathway from diploid to polyploid can be a struggle for an organism even when polyploidy is present in closely related organisms.
Yet even the human lineage underwent polyploidy events. Humans were not simply created having 46 chromosomes. There is nothing to say that an organism or a set of organisms unable to tolerate almost all polyploid events are therefore unable to survive all polyploid events.
References
Rules of Engagement: Have Pollen—Will Travel by John Perkins · Sally Perkins in Azalean 2010
Ploidy level estimations in deciduous and elepidote hybrids of Rhododendron by José Cerca de Oliveira, Mariana Castro, Francisco J. do Nascimento, Sílvia Castro, John Perkins,Sally Perkins, João Loureiro in Jornadas Portuguesas de Genética, Coimbra, Portugal; 05/2011
Weighing in: Discovering the ploidy of hybrid elepidote rhododendrons by Sally Perkins, John Perkins, José Monteiro de Oliveira, Mariana Castro, Sílvia Castro, João Loureiro in Rhododendrons, Camellias and Magnolias, Royal Horticultural Society, Editors: Simon Maughan, pp.34-48 2012


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Do any animals other than humans undergo menopause?
Do any animals other than humans undergo menopause?
Also, is there any difference between animals in captivity and animals in the wild as regards menopause? For example, even if menopause has been observed in a captive member of a particular ape species, do individuals of that species typically live long enough in the wild to also undergo menopause?
I guess here's what I'm really getting at: is menopause a common thing in the animal kingdom, or is it only a common thing in humans?

So now we have one answer saying it's common and citing a Nature article, the other saying it's uncommon and citing a Science article.
Let me get my popcorn...

@arboviral Jacques linked to a summary of a paper. The original paper isn't looking at menopause per se, but rather at mammals that tend to live for a long time after menopause occurs. So it seems like the summarizer got it wrong.

Yes. Menopause is common for long-lived mammals. For instance, in the wild, killer whales go in a sort of menopause as reported in 2009 by Ward et al. Front Zool. 2009 Feb 3;6:4. So it is not due to captivity. According to a Nature review, reproductive cessation has also been documented in non-human primates, rodents, whales, dogs, rabbits, elephants and domestic livestock (Packer et al. Nature. 1998; 392(6678):807-11)

As of 2017 you can add false killer whales to the list as well (Photopoulou, T., Ferreira, I. M., Best, P. B., Kasuya, T., & Marsh, H. (2017). Evidence for a postreproductive phase in female false killer whales Pseudorca crassidens. Frontiers in zoology, 14(1), 30. at https://frontiersinzoology.biomedcentral.com/articles/10.1186/s12983-017-0208-y )

The ecological knowledge that older females have gained throughout the course of their lives can be extremely useful for the survival of their offspring. This is sometimes referred to as the "grandmother effect". For example, older females may remember key information about rare events, such as how to avoid/defend against predators, or how to find food/water in times of scarcity.
Check out this paper describing the grandmother effect in humans:
Herndon (2009). The grandmother effect: implications for studies on aging and cognition. Gerontology, 56(1), 73-9.
And in killer whales:
Brent, L. J., Franks, D. W., Foster, E. A., Balcomb, K. C., Cant, M. A., & Croft, D. P. (2015). Ecological knowledge, leadership, and the evolution of menopause in killer whales. Current Biology, 25(6), 746-750.

Only three — humans, killer whales, and pilot whales.  (Reference)

Among long-lived animals, scientists have found only three species that undergo menopause: humans, short-finned pilot whales, and resident killer whales. What makes these species so special? A new study finds that it all comes down to their unique social structures.

Your link is a summary of Johnstone et al, Proc. R. Soc. B 2010. Here's the first couple of lines from their abstract: "Human females stop reproducing long before they die. Among other mammals, only pilot and killer whales exhibit a comparable period of post-reproductive life."

Long post-menopausal life and menopause are not equal. I can assure you that mice undergo an analogue of menopause.


text:
When does one decide to refer to a virus as a new variant?
I've read that SARS-Cov-2 has several variants, e.g.:

Can the U.S. keep Covid variants in check? Here's what it takes.
Novavax’s Vaccine Works Well — Except on Variant First Found in South Africa

When does one decide to refer to a virus as a new variant?

My research:

I looked at https://biology.stackexchange.com/questions/tagged/variant?tab=Votes
The question What determines when a virus becomes a “new strain”? addresses strain. Is strain the same as variant?

For those looking at the SARS-CoV-2 phylogenetic tree it is mainly about how lineages (becomes a clade once large enough) grow, propagate from locations and locations and split in sublineages. Sometimes one lineage deserves attention not only because of its growth but also because of its mutations, this was the case for the summer variants bearing spike and RBD mutations. 501Y.v1 & 501Y.v2 emerged in this context bearing most of the interesting features spotted in the summer variants: many spike mutations and deletions, long branch/accelerated evolution, exponential growth.

We use them as synonyms. However, variant is, in my view, more colloquial than scientific. Strains are in the literature often defined by their distinct genome compared to other strains of the same species (might be one base-pair substitution or more). In microbiology, including viruses, we often think of a strain as the proliferation of a single distinct DNA/RNA molecule.
https://www.sciencelearn.org.nz/resources/184-virus-strains


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Why does the term "epicondyle" often refer to either of the two at the elbow end of the humerus?
Why does the term "epicondyle" often refer to either of the two at the elbow end of the humerus?
Example:

I understand that epicondyle means near a condyle, but there are several condyles in the human body:

On the femur, in the knee joint:

Medial condyle
Lateral condyle

On the tibia, in the knee joint:

Medial condyle
Lateral condyle

On the humerus, in the elbow joint:

Condyle of humerus (Condylus humeri)

On the mandible, in the temporomandibular joint:

Mandibular condyle

On the occipital bone, in the atlanto-occipital joint:

Occipital condyles

If something is unclear in the question, please explain, I'd be glad to improve it.

The humerus is the only of those that has a "protuberance"?

@kmm That would indeed explain. But is it true that the humerus is the only of those that has a protuberance?

There is a lateral epicondyle and a medial epicondyle of the humerus. "Epi-" is a Latin root meaning "near". Both epicondyles are near the condyle of the humerus.

Thanks. "Near the condyle of the humerus" -> Why the humerus in particular? I understand the "near the condyle" part.

@FranckDernoncourt - If you understand the " 'near the condyle' part", you have your answer. What more do you expect? Are you asking how many epicondyles there are? Are you asking what the equivalents are on the femur? Clarify, if you will. Otherwise be nice and accept (or at least upvote) this correct answer!

@anongoodnurse there are more than one condyle https://en.wikipedia.org/wiki/Condyle_(anatomy) . Why the humerus in particular? Just curious. Calm down. Why did you downvote the question?

@FranckDernoncourt - You're welcome. I also voted to close as unclear. Always happy to do my part to make a site - and its questions and answers - better. (Ha! you edited your comment. I DV'd because your question is unclear. That's one of the DV reasons (hover over the button and you'll see.)

@anongoodnurse what is unclear in the question?

@FranckDernoncourt the entire question is unclear. If you actually click on some of the links in the Google search you show, you'll see that there are several epicondyles - a lateral and a medial on both the humerus and the femur - and they are referred to as "the [lateral/medial] epicondyle of the [humerus/femur]", meaning the bone itself is referenced in the name. Google doesn't give a link as to where its definition comes from, but I suspect they said "especially of the humerus" because of lateral epicondylitis or "tennis elbow". You need to look at multiple sources to verify something.

@MattDMo unclear isn't the same as incorrect

@Franck I will admit I was unsure exactly what you were asking when I provided this answer. I will happily delete the answer but I still don't really understand what your question is - would you mind clarifying?

@HarryVervet "Both epicondyles are near the condyle of the humerus." ->  how about the Medial epicondyle of the femur? My question is: Why does the term “epicondyle” often refer to epicondyle of the humerus, whereas there are other epicondyles in the human body.


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Is the tendon width determined by genetic predisposition, and if so, is genetics the sole factor?
Tendons' widths vary widely across humans. E.g.:

{1}: "the mean patellar tendon width was 26.10mm (SD = 3.31; range 18.33mm-33.33mm)"
{2}: "Size of the patellar tendon width, measured at the same location in each patient, ranged from 24 to 35 mm"

Is the tendon width determined by genetic predisposition, and if so, is genetics the sole factor?
I read on {3}:

Tendon length is determined by genetic predisposition, and has not been shown to either increase or decrease in response to environment, unlike muscles, which can be shortened by trauma, use imbalances and a lack of recovery and stretching.{4}

But it didn't mention the tendon width.

References:

{1} Dundon, J. M., R. J. Markert, and M. W. Lawless. "Correlation between patella and patellar tendon width: an anatomic study." Clinical Anatomy 25, no. 3 (2012): 398-400. https://www.ncbi.nlm.nih.gov/pubmed/21853464; https://doi.org/10.1002/ca.21241
{2} Shelbourne, K. Donald, Richard A. Rubinstein JR, Charles D. VanMeter, John R. McCarroll, and Arthur C. Rettig. "Correlation of remaining patellar tendon width with quadriceps strength after autogenous bone-patellar tendon-bone anterior cruciate ligament reconstruction." The American journal of sports medicine 22, no. 6 (1994): 774-778. https://www.ncbi.nlm.nih.gov/pubmed/7856801; https://doi.org/10.1177/036354659402200608
{3} https://en.wikipedia.org/w/index.php?title=Tendon&oldid=885716020
{4} Young, Michael. "A Review on Postural Realignment and its Muscular and Neural Components" http://www.elitetrack.com/article_files/posture.pdf  (mirror)

My best guess is "We don't know. No study has investigated this question. However, given that tendon length has a non-zero heritability and given that a lot of bone, muscle and tendon properties are heritable , it is probably safe to assume that tendon width is somewhat heritable."

@Remi.b Makes sense,  thanks for the feedback!


text:
Why is cancer not a communicable disease?
I read another question where the author is asking about the infectivity of viruses. In the same vein, I am curious why cancer is not a communicable disease.

A cancer is not a pathogen
Cancer is a group of cells that (because of several specific mutations) start to duplicate abnormally. This group of cancerous cells are the own cells of the sick patient. It is not another species infecting the individual carrying the disease. It is the individual itself who developed the disease. Cancer is not a pathogen (but see below) that infect hosts and get transmitted from one host to another. It is more correct to picture cancer as an internal mistake of the body rather than as an external attack on our body. You might want to have a look to the wiki page for cancer for more information.
Transmissible agents that can cause cancer
Some cancers are caused by transmissible agents, such as oncoviruses. the transmissible agent may jump from one host to another and cause cancers giving the sensation that cancer is transmitted. It is just a sensation of course because in reality only the oncovirus gets transmitted and not cancer itself jumping from one host to another.
Cancers that become transmissible
Note however that it is not impossible to imagine a tumour jumping from one individual to another in cases where the immune response cannot detect cancer as 'non-self'. Some cancers are transmissible. Those cancers are called clonally transmissible cancer (As indicated by C Rags in the comments). Here is the list:

The Devil Facial Tumor Disease which occurs in Tasmanian Devils
The canine transmissible venereal tumour (article from Chris Stronks in the comments)
The Contagious reticulum cell sarcoma occurring in the hamster.

CTVT in  canines is transmissable : http://www.sciencedirect.com/science/article/pii/S0092867406009123

Please leave a comment when downvoting.

There are a total of 3 transmissible cancers in animals identified to date. One in Tasmanian Devils, another in canines, another in hamsters:http://en.wikipedia.org/wiki/Clonally_transmissible_cancer Good answer +1

I’m unhappy with this answer, and although I haven’t downvoted it, let me try explaining why it was downvoted. First of all, as you note yourself later on, your initial sentence is simply wrong: many cancers are caused by infectious agents. More importantly though, your premise is fundamentally flawed: again, as you show yourself, cancer itself is an infectious agent (ever heard of metastases?). So why, then, is it usually not transmissible between individuals? Your answer doesn’t explain that at all.

@KonradRudolph I agree with you in that the original answer sounds misleading. Isn't it a moot point though? Fundamentally the transmissible agents that cause cancer (oncoviruses) are not themselves cancer. Metastatic cancers are not transmissible cancers either...

@GoodGravy No, it’s not a moot point at all, because it doesn’t explain why cancers generally aren’t transmissible, and that was the whole question. (I also disagree with your edit, since it changed the answer substantially, and such edits are frowned upon on Stack Exchange – you should have written your own answer instead.)

@KonradRudolph I see your point. Re: edit - The fundamental answer wasn't changed too much I don't think; I removed an erroneous statement and added in the missing information in a clause along with an order reshuffle. The answer was confusing and contradictory, now its not. If this was several separate edits would it have been okay? Remi.b can roll back if they want to.

The sentence "Some cancers are caused by infectious agents" come from an edit from GoodGravy, not from me. Note, also that the edit came after the downvotes. I re-edited the answer. Please let me know if there is still something going wrong. Thanks Konrad for your feedback.

There is a very obvious answer that is missing. Cancer is a disease of the cells of multicellular organisms, and the cells of multicellular organisms evolved away from the ability to live independently. With out the proper growth medium and in the case of mammalian cells, the permissive temperature, the cells of multicellular organisms survive for only short periods of time when outside of the body. Unlike bacteria, fungi, and unicellular protists, that are equipped to survive in an external environment, the cells of multicellular organisms need the multicellular organism's systems to survive.

@AMR I couldn’t find times of survival of individual (cancer) cells outside of medium. But plenty of bacteria and viruses die almost immediately outside of their host, and are still communicable by touch (prominent example: ebolavirus). I believe bacteria are generally more resilient but many are also quite particular about their growth medium and will just up and die when left alone. In other words: I think you vastly overstate the difference in survival between cancer cells and viral and bacterial pathogens. I don’t think this specifically is what distinguishes them: Immune response is.

@KonradRudolph You cannot make an immune response argument as the reason why cancers are not communicable when in 99.9999% of every cancer in human history and all but two species of highly inbred mammals are non-transmissible. You are not going to develop cancer because you prepared the body of a family member for burial who has died of cancer; You almost certainly will develop ebola. You can have sex with someone with prostate cancer and you will not get cancer. You might get HPV which could lead to cancer, but you will not develop cancer from the cancer itself.

@AMR Immune response is the reason why they’re not communicable. That’s my point. All of the cases you’ve just listed actually contradict your survivability point, since they all rely on transmission in which cancer cells wouldn’t need to stay alive outside the body. Incidentally, I hereby acknowledge that there may be other reasons besides immune response. But I don’t know of them, and they certainly haven’t been mentioned yet here.

@KonradRudolph No. Cancer is not communicable because it has no ability to act as an infectious agent. Period.

@AMR You are still begging the question. You are saying, in essence, “cancer is not an infectious agent because it is not an infectious agent” — Not quite, but it’s simply not an answer. The question is why. You are systematically evading this.

Naïvely, there’s no reason why cancers wouldn’t be communicable. Tumours consist of abnormally multiplying cells which have switched off their response to repressive stimuli from other cells, which would otherwise cause them to stop growing (plus a few other properties which have first been collectively described in the seminal paper The hallmarks of cancer).
And tumour cells can absolutely split off and start growing elsewhere, thus effectively spreading the cancer. This happens in metastases, and it happens in the few types of communicable cancer that are known.
So why does this normally not happen between individuals?
The reason is our immune system. Our bodies are normally incredibly good at recognising and eliminating foreign bodies – so-called antigens. The problem with cancers is that they are not foreign bodies: they are our own cells, only mutated. This makes it hard for our own immune system to recognise them as foreign. (It’s worth noting that at some point tumour cells have accumulated enough mutations to be recognised as foreign, but by this point the tumour is already mounting an effective resistance to the immune system.)
It’s for this reason that most cancers are not transmissible: invading cancer cells are immediately recognised as foreign bodies, and are efficiently eliminated by the immune system before they can multiply into a tumour. Unlike other antigens they have not evolved effective ways of evading the host’s immune system.
— Let’s take a detour here and talk about organ transplantation: When a donor organ is transplanted into a new host, the host recognises this organ as foreign, and initiates an immune reaction against it (or vice versa). This transplant rejection is a huge problem, and needs to be addressed by finding a closely related donor, and administering immunosuppressant drugs.
Which brings us back to transmissible cancers: all known types of transmissible cancer occur in species which have gone through a recent population bottleneck. All now-living individuals are very closely related. As a consequence, their immune systems don’t necessarily recognise another individual’s cells as foreign, or at least produces a reduced immune response.

I'd find it useful to add that in experiments where we're xenografting cancers for experimentation, in mice for example, we're often using something immunosuppressed like  RAG−/−γc−/− so the cancerous cells aren't destroyed by the immune system.

@Kendall I have to admit that I don’t know anything about that, but please feel free to add your own answer and/or edit mine. Also, thanks for this interesting piece information, I didn’t know that.

Comparing metastatic cancer to a communicable disease is a spurious line of reasoning. I would argue that you cannot even make the case for transplant related transmission, as part of the treatment protocol is the suppression of the recipients immune system, allowing affected donor tissue to spread. Most cancer cells are not like protists or bacteria which can survive outside the body for extended periods of time without growth medium.

@AMR Please explain why you find the comparison spurious — I don't understand that at all. It's also patently contradicted by the existence of communicable cancers. And the lack of survival outside the host is in no way relevant for the comparison I'm making. At any rate, many pathogens (both bacterial and viral) have the same problem.

You have three examples in all non-human mammals and all of the human examples are iatrogenic and you want to classify cancer, a disease that affects millions of humans and countless other organisms annually with no evidence of interorganism transfer, as a communicable disease simply because it evolves genetic expression patterns that give it gain of function mutations to move to other location within the same organism, then that is a spurious argument. An infection that spreads to a different area of the body is not a communicable disease either, it is a complication of the disease process.

@AMR No, I do not “want to classify cancer as a communicable disease”. I’m explaining why it isn’t communicable by considering what distinguishes it from other diseases (which are communicable). Explaining differences this way is a common teaching technique which apparently backfired here. But I’m not really sure how to improve that—maybe put the third paragraph in bold? Incidentally, the misunderstanding seems to be related to your use of the word “compare” as if it meant “claim that they are equivalent” when, in reality, “compare” just as well may mean “contrast”. That’s what I’m doing

@AMR Put differently, since there are tumours that are communicable (no matter how few), we must ask ourselves: “what makes cancer non-communicable in general?” The other reply, which just says that “cancer is not a pathogen” isn’t answering the question, it’s begging the question. By contrast, my answer actually explores the specific difference between pathogens and tumours. This is fundamentally different from claiming that they are the same.