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Are Males the main evolutionary tool for production of genetic variation necessary for evolution?
What I'm saying here is just a personal reflection, that might turn to be gravely erroneous, actually I'm asking that because I didn't see it presented elsewhere.
Evolution is propelled by two directions. The first one is a process that is novel in producing genetic variation, which includes: Mutation and Migration. The second is a clearing up process, something that wash out results from the first process, and those are: Natural Selection and Genetic drift.
Natural selection is more functional in the sense that it only preserves traits that are adaptive to the environment. Genetic drift is not discriminating in that sense, so it can wash out any result of process 1 whether its harmful or beneficial.
It's clear that the primary source of evolution is the first process (i.e.; mutation and genetic migration), since the second process (i.e.; natural selection and drift) only acts on what results form it.
[Note: by primary "source" of evolution, its meant here to be what's responsible for producing the basic material upon which evolution works, since evolution is change in genetic variation over generations, then "genetic variation" is the basic material for evolution, and this is produced by mutation and migration. Natural selection and drift don't produce genetic variation, they change it by an act to decrease it, and a process that acts to decrease something, can hardly be viewed as a producer of that thing. A butcher is not the primary "source" of meat, the cow is!]
Now in principle the more we have production of genetic material the more is the chance of getting a genetic change that is useful. Of course increase in mutation rates can result in injurious traits, those would be washed out by selection and drift, however its the higher probability of having a beneficial mutation that is the primary concern here.
The male spermatogenesis in mammals supplies the impression that it is the MALE sex that is the Ore of evolution. The incomparably high cell production rate of all stages of spermatogenesis as compared to Oogenesis, tends to make one think that the chance of mutation arising in spermatogenesis is ought to be much higher than that arising in Oogenesis.
The testis seems to be the Oven in which genetic variation is baked. The rapid turnover of spermatogenesis, whereby each primary spermatocyte finally results in 4 sperms (Compared to One Ovum resulting from each primary Oogonia), that's beside the very large number of sperms produced daily, that continues for years and year. While with the Oogenesis everything really finishes at the foetal life, the remaining is just maturation steps, nothing is new as far as change of genetic material inside the Oocytes is concerned, this is the state throughout most of the female's life.
When I look at the seminiferous tubules, and see all those layers of spermatocytes leading to sperms, I tend to think that there is even some small scale natural selection, that bad mutated germline cells would die off, and only the ones with good genomes would survive all the stages of spermatogensis, and possibly the ones with beneficial mutation might have an advantage in survival in that milieu and even might have better chances of fertilizing the ovum?
Not only that, the testis seems to be more exposed to stressors inside the body and even to direct external environmental stressors, while the Ovaries lying deep inside, seem to be more protected. The Oocyte actually "selects" one sperm, so it's rule is selective rather than productive of change.
All of that makes one think that it is the male germline cells that could mediate high mutation rate in response to stressors, or even without stressors by virtue of the very high production rate of germline cells for very long periods of time. It seems that this is the real source of beneficial mutations that would ultimately drive evolution.

Four connected questions:

Is the mutation rate in male germline higher than in female germline?

If Yes, then doesn't this mean that Males are more likely the source of most beneficial genetic mutations, which is the main drive for evolution?

If 1 and 2 are true, then are we justified in inferring that "being the main source of beneficial genetic mutations" is the main purpose behind evolution of a Male sex?

Was this idea proposed before?

I read until It's clear that the main source of evolution is the first process, since the second process only acts on what results form it. It depends upon what you mean by "evolution" in this sentence. And even when well defined you are likely to fall into both semantic issues in decoupling the effect of each (see for example shifting balance theory) and also into issues of estimating the relative effects of each. In any the relative importance of these two processes have been a long lasting debate in the field.

@Remi.b, possibly you mis-understood me. By the first process I meant "mutations and migration", and actually mutations mainly, it is those that are the SOURCE of genetic variation. Natural selection is not the source of variation, it acts to cut down a pre-existing variation. A butcher can hardly been seen as the source of meat. The cow is. By source I mean what manufacture the basic material of some process to be possible in the first place. Neither natural selection nor genetic drift manufacture genetic variation, evolution is change in genetic variation over generations... to be continued

..continuation, so by definition without "genetic variation", evolution is not possible, so the 'basic material' that is needed for evolution to happen is 'genetic variation', processes responsible for manufacturing this variation are mutation and migration. Natural selection and drift do not manufacture genetic variation, they actually act to de-limit it, i.e. disposing of some of it. A process hat act to decrease some material cannot be deemed as the source of this material, it is a source of change on this material yes, but not of this material itself.

I'm voting to close this question as off-topic because this is the presentation of a theory disguised as a question by the well-worn “am I right ?”

@David, but this is not a theory?! its an impression.

@David, I've edited the question.

@ZuhairAl-Johar You should focus on one question at a time. Otherwise your post would be considered too broad. While a good background is appreciated, an extensive one just becomes too much and buries the main question. Be terse and include all the relevant background but nothing more than that.

If I actually understand your premises, which is a big if, you're asking if the genetic material in the sperm has been subjected to more mutation than its counterpart in the egg... by the time of mating. In case of humans, where's there's a lot of research and the answer is almost certainly yes.

Recent [GWAS] studies have shown that 76% of new mutations originate in the paternal lineage and provide unequivocal evidence for an increase in mutation with paternal age.

The general theory how this works (which you seem to repeat) goes back to...

Haldane (1947) suggested the following general mechanism for the sex differences in mutation rate: “The primordial oocytes are mostly if not all formed at birth, whereas spermatogonia go on dividing throughout the sexual life of a male. So if mutation is due to faulty copying of genes at a nuclear division, we might expect it to be commoner in males than females.”

As for [your] choice of terminology...

Subsequent estimates of a higher mutation rate in males from molecular genetic data led Miyata et al. (1987) to suggest that evolution is “male‐driven.”

And a more contemporary term is male-biased mutation:

The concept of male-biased mutation has been thoroughly analysed in recent years using an evolutionary approach, in which sequence divergence of autosomes and/or sex chromosomes are compared to allow inference about the relative contribution of mothers and fathers in the accumulation of mutations. For instance, assuming that a neutral sequence is analysed, that rate heterogeneity owing to other factors is cancelled out by the investigation of many loci and that the effect of ancestral polymorphism is properly taken into account, the male-to-female mutation rate ratio, am, can be solved from the observed difference in rate of X and Y chromosome divergence. The male mutation bias is positively correlated with the relative excess of cell divisions in the male compared to the female germ line, as evidenced by a generation time effect: in mammals, am is estimated at approximately 4–6 in primates, approximately 3 in carnivores and approximately 2 in small rodents.

Finally one needs to be careful what one means by variation because...

The creation of genetic variation by recombination can be a much faster process than its creation by mutation.

If we could somehow turn off mutation, in a large population meiotic recombination would still result in new combinations in offspring for quite a while. Eventually, after this combinatorial space is exhausted, we'd only see organisms that repeat something that is already living or has lived in the past.

So, I've dealt with your 1 & 4. As for theories why we see this male-bias in mutation... (your 2-3) it gets more complicated:

A general theoretical perspective is that level of mutation is a balance between deleterious mutations reducing fitness, advantageous mutations increasing fitness, and cost in fitness from mutation repair mechanisms to reduce the mutation rate (Sniegowski et al. 2000). The relative importance of these factors may vary but because most mutations are generally less fit than the present wild type, selection generally should act to reduce the mutation rate by improving the repair mechanisms. However, the strength of indirect selection changing the mutation rate, either increasing it or decreasing it, is quite low and is on the order of the change in the mutation rate caused by a modifier locus (Sniegowski et al. 2000).
Using the context above, sex differences could be the evolutionary result of selection for a more efficient lowering of the detrimental mutation rate in females, a retention of a higher advantageous mutation rate in males, less cost for lowering the mutation rate in females, or a combination of these factors. One evolutionary hypothesis for sex differences in mutation rates is that there may be different selective optima in the two sexes balancing the deleterious mutation rate and the cost of efficient repair and replication (Ellegren 2007). More specifically, if we assume that the major impact of selection on mutation rate is to minimize the mutation rate per replication as much as possible to reduce rate of deleterious mutation, then any sex differences observed in mutation rate may be related to the different number of replications in the two sexes. In other words, if the major impact of selection is to reduce mutation rate as much as possible, it has been generally more successful in females, either because of more male replications or because repair mechanisms are more efficient in females than males for some reason. Consistent with this, Crow (2000) suggests that an increase in mutation rate at later reproductive ages is not surprising. His reasoning is that until recent times few men would live into their forties so there would have been little selection pressure to reduce the detrimental effects of mutations from older men. Or, the sex differences in mutation rate may not have a strong evolutionary basis and are primarily the result of sex differences in gametogenesis.

As you can see, like most theories regarding the evolutionary reason for some mechanism that itself affects evolution... it's not settled science.
So, regarding 2-3. I think I get your point that if we pick a mutation that has survived until today, there's higher chance it came from a male (2). Even if this is true, it implies little about the evolution of sex-bias in mutation.
You infer (3) that

"being the main source of beneficial genetic mutations" is the main purpose behind evolution of a Male sex

I think the discussion is getting more into philosophy than science at this point. As previous long quote says, it could simply be that natural selection was bad at reducing something that is, on-average, detrimental, but was worse at reducing it one group, i.e. in males, e.g. because it's harder to reduce there. So, assuming that's the case, the "main purpose" of evolution could have been this reduction, and the fact that beneficial mutations (like all mutations) are more often traced to males, is just a statistical artifact of the (mutation reductive) "main purpose".

Yes recombination is a source genetic variation which is why sex is there for, and Migration also acts by adding recombination, however as you said once its exhausted, it cannot push further. However as far as recombination is concerned male and female contribution seems equal. Its mutations that seem to be male driven. Not only that the conditions for a sperm to be produced, live and travel are pretty much harsh condition, as if a kind of small scale natural selection occurs, only those sperms with genetic contents that enable them adapt to the sexual tract environment would survive, cont...

continuation... this small scale natural like selection might be a kind of selection for sperms with beneficial genetic material, so it appears as if all of this is made deliberately to make the male system a machine of producing beneficial mutations to push the wheel of evolution forwards. Of course a side effect to that, is that it can be harmful as well. It appears to me form that, that the male sex from evolutionary  biology point of view is meant to be the Ore of genetic variation necessary for evolution.

I didn't say that mutations are always beneficial! On the contrary I've explicitly said that there is a side effect to that, which is production of harmful mutations. However, I see the complexity you are referring to.

@ZuhairAl-Johar: indeed, I should have said "on average".

Well your addition, seem to even further support the view point presented here, that males are primarily meant to be the source of beneficial mutations! The female sex plays the part that reduce harmful mutation rates, i.e. it plays selective role, and the cost in fitness regarding repairs is related to females.

even on average definitely mutations that are deleterious are much more than the beneficial ones, the male seems to be the source of both kinds of mutations the good ones and the bad ones, and the latter ones are of course more! The point I'm raising is not that. I think that of all beneficial mutations the proportion of those that comes from the male is much much higher than those coming form the female. Therefore as far as the source of good mutations that fuels evolution is concerned, the male seem to be the main producer! But it comes at a cost of course, hereditary disorders!

I don't know why you say "some of my premises is wrong", which ones? what you wrote in the two brackets is what I said actually?

@ZuhairAl-Johar: I've moved that discussion to the end and gave it a bit more thought.

@I see the point of view present there, as you said it becomes complicated. But I get the feeling that it is not correct. Its a little bit twisted. But of course its a possibility.

@ZuhairAl-Johar: Here's another possibility: If we assume we are at mutation-drift balance (a big if), and in males it's harder to reduce mutation, then the average mutation rate (male + female) /2 would be optimal. But it would not have this value in either group.

@Fizz How would the hypothesis that a selection on mutation rates is behind the observed differences explain why oocytes are only produced early in the female life amd stay quiescent rather than generated continuously but with a slow generation rate?

@Fizz, I'm afraid I cannot comment on your last possibility. I don't know what you mean by optimal?

@Cell: I don't think it tries to explain that.

I should have mentioned that the female has mitochondrial DNA. which is a source of genetic variation that males do not supply. However I think the higher mutation rate of males germline out-weights that. Actually even regarding richness due to recombination, its the male that is the source of sexual difference, so in some sense it contributes a little bit more to genetic variation that females even through re-combination.

The argument you've cited in the last lines, would culminate as you commented in the result that the males being the main source of beneficial mutation is just an artifact of failure of the main purpose behind sex evolution in males. I don't like that. However even if we assume this, still it doesn't change anything, still the primary source of evolution is the male sex whether that was an artifact or not, I tend to think that it is not an artifact, the artifact and the cost paid to gain these beneficial mutations is the inevitable occurrence of the harmful mutations.

Yes. The rate of de novo mutations has been found to be higher in paternally derived DNA from several papers. A recent paper from a quick search [1] found that ~80% of 15,746 de novo mutations in 225 families were paternally derived.
Based on the total mutations yes, but they are also even more likely to bring deleterious mutations. So per base probably not.
That doesn't make much sense. Consider a lowly prokaryote organism that replicates asexually. The replication process is not much different than spermatogenesis. So it doesn't explain why sex differentiation occurs. More likely sex differentiation occured to promote genetic diversity (by preventing self-replication) and rather than the male sex evolving towards increased gamete replication, the female sex evolved towards decreased  gamete replication due to selection against pregnancy at older ages (when the body is more fragile and sensitive to giving birth). This is just my speculation I have no references.
Yes. It's called Male-Driven Evolution. [2].

[1] Parental influence on human germline de novo mutations in 1,548 trios from Iceland. Jonsson, H, et al. 2017
[2] The rate of spontaneous mutation of a human gene. Haldene, J.B.S.1935


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What's a "constitutionally small penis"?
I'm reading some urology papers and came across one involving penis growth (Kim & Song, 2008); here's an intro passage that I'm confused about:

A total of 58 patients with constitutionally small penises, without chromosomal anomalies and gene-associated syndromes, intersex, and hypospadias, were included in this study. The average patient age at their first visits was 10 years and the average follow-up period was 2.2 years.

What's a "constitutionally small penis"?
Edit:
I've read the paper in detail and I don't see where the authors distinguish between a small penis and a "constitutionally small" penis.
Would a "constitutionally small penis" be the same thing as a "micro-penis"?  If not, then where do we draw the line?
References
Kim, K. S., & Song, G. G. (2008). Penile Growth After Puberty in Patients with a Constitutionally Small Penis. Journal of Pediatric Urology, 4, S63. doi: 10.1016/j.jpurol.2008.01.174

"Constitutional" refers to the physical state of the concerned individual (Merriam-Webster).
In biology, it most probably means a trait that is not pathological or environment induced.
This is in the context of size of babies:

Small for gestational age (SGA) can occur following a pathological
  process or may represent constitutionally small fetuses.
From: Ananth & Vintzileos (2009)

Between18-22% of infants SGA by population
  standards are reclassified as normally grown by customized standards
  and as the perinatal mortality of these reclassified babies is similar
  to those who are normally grown they can be considered to be
  "constitutionally  small.".
From: McCowan et al. (2018)

In most cases, it is difficult to differentiate between
  constitutionally small head size vs pathologic microcephaly, and
  available data regarding prenatal diagnosis of microcephaly are based
  on small numbers of cases of varying etiologies.
From: Ultrasound screening for fetal microcephaly following Zika virus exposure.
   American Journal of Obstetrics & Gynecology, Volume 214, Issue 6, B2 - B4

Regarding constitutionally small penis: Since the article you mentioned is the only source (scientific or otherwise) of this term, I would believe that it is based on the population average (of possibly South Korea from where the authors are). Moreover, since it is not defined rigorously, it is most likely an arbitrary classification.

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/

sort: votes


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Reptiles are a paraphyletic group because?
Here is a question I am trying to find the answer to

Reptiles are a paraphyletic group because... ?
A) They include worm lizards, which have no limbs
B) The group doesn’t include birds
C) The group doesn’t include mammals
D) Not all of them have three- chambered hearts

I’m a bit confused about the reasoning. I know a paraphyletic group does not have all of its descendants so if birds were to be included it would become monophyletic. So is B the answer? Could anyone help explain it better?

I think the question's phrasing is a little wobbly, which make it a little hard to understand. But I think you understood what your teacher was expecting. I agree with you, answer is B.

I think the question's phrasing is arguably a little wobbly, typically as to the nature of what someone would mean by the term "reptile". But I think you understood what your teacher was expecting. I agree with you, answer is B.
Reptilia is a clade (clade = monophyletic group) that encompasses all species that we traditionally classify as reptiles + all birds. Hence, our traditional definition of reptile makes up for a paraphyletic group as birds aren't included.
Related post: If dinosaurs could have feathers, would they still be reptiles?

To me it seems "Reptiles are a paraphyletic group because the group doesn’t include birds" is fine and not the least "wobbly", assuming Reptiles != Reptilia.

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


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Help with identifying creature found in brazilian beach

I don't know if this is the correct place, but I've been looking for someone
that could help me identify this creature I found while I was looking for shells. There are three mollusk-like "beings" stuck in some sort of big seed (it's definitely not a rock nor a part of their body). They
 can "spin" around with the arm that is stuck in the seed, and they continuously take some blood red hair-like tentacles in and out of a shell.
I shot a video of it,  the link is right below. Please ignore all background audio, I couldn't find somewhere without people.
This "being" was found today, at roughly 6pm, washed ashore in the beach I'm visiting - "Praia Grande" in Brazil.
Another peculiar thing is that tap water makes the "things" close for a while, and sea water doesn't do much. Also, as they dried, the single tentacle hair became multiple smaller ones. They keep coming in and out, without stop.
If anyone could give me a shine on what that animal is, it would be super helpful!
https://drive.google.com/file/d/1-rSk-WVb6pkS98Npp1VF3Aq8xxXPKiuc/view?usp=drivesdk

Welcome to Biology SE. I suspect you're not getting a response to your question because the thing that makes the question answerable - the video - is at an external site. That can cause problems down the line (for instance, if Google changes its linking structures, the question becomes uncheckable). It is possible to add video to questions, but according to this question (https://meta.stackexchange.com/questions/248249/is-it-possible-to-embed-videos-in-questions), only via youtube link. Alternatively, you could take a couple of screen-captures from the video and add them.

Those are gooseneck barnacles possibly pelagic gooseneck barnacles (Lepas_anatifera).
For comparison:

A beautiful picture and description can be seen here.


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Can a blood type O be born from AB and A parents?
I have a basic understanding of genetics, and I'm really puzzled by this. My grandma's blood type is A (I don't know if it's heterozygous or homozygous) and my grandpa is AB. Yet my mother is type O.
Grandma says that my mom is 100% my grandpa's child, so how did it happen?
I have a few hypotheses regarding this. Either my grandma is lying, which I find to be really implausible, or there's some genetical anomalies either in my mom or my grandparents.
I suspect that grandma is heterozygous, having the IAi genes for blood type, and grandpa has a weird case of IAIBi alleles, coming either from a failed disjunction which caused both alleles for A and B to be present in one sperm cell, and the i allele to be present in the egg, resulting in the IAIBi genotype. Then, when grandpa had my mom, both i alleles got combined and out came my mom with O type.
My other hypothesis is that mom is heterozygous, either IAi or IBi, but the dominant allele underwent a deletion (or something else) and was inactivated, and as such only the recessive allele remained, giving her type O blood.
Could I get some insight on how this happened? I can't seem to find anything related to it on the internet.

Never discount the prospect that someone in the lab screwed up.

Maybe have a look at the Bombay blood group. It is a pseudo 0 blood group.  https://en.wikipedia.org/wiki/Hh_blood_group

The simplest probability is that is wasn't grandpa's sperm that did the job and that grandma either "jumped the fence" or was raped, and either way was afraid or ashamed to admit the truth.

One thing for you; the "failed disjunction" hypothesis is testable; if true a genetic test would report your mother to be the child of her father's non-extant brother.

As @KaPy3141 mentioned, other genes such as the Bombay blood type may suppress the A and B alleles (epistasis). There was once an episode of a soap opera that had this exact plot.

It can't have been an error in the lab, because both my grandparents have been blood donors for years. If they messed up the blood types a lot of people would've died. Thing is my grandma and grandpa aren't on good terms anymore, nor am I with my grandpa, so I can't really have them get genetics testing. It's not that important either way, I'm not trying to test my grandma's fidelity, I was just curious if such a phenotype would be possible from this genotype.

Did any of the involved persons have a bone-marrow transplant or suffer from auto-immune diseases? Then maybe we should also consider the possibility of a change of blood-type.

The ABO blood type is controlled by a single gene (the ABO gene) with three types of alleles inferred from classical genetics: i, IA, and IB. The IA allele gives type A, IB gives type B, and i gives type O. As both IA and IB are dominant over i, only ii people have type O blood. [1]
So from this standpoint, normal Mendelian genetics cannot explain the blood-group 0 offspring, given the AB parent.
However, besides errors in testing, the (pseudo?) 0-bloodgroup could be explained by the Bombay phenotype. I don't know the incidence rate in your region, so I can't comment on the likelihood.
To give theoretical background, this would be considered a pseudo 0-phenotype, as the individual genetically does not need to be ii. Instead, the individual lacks another effective enzyme that is required for the A or B alleles to be effective; the blood-type specific sugars (N-Acetylgalactosamin|Galactose) cannot be attached to the red blood-cell membrane, as the anchor of these sugars (called H-substance) is not present.
Finally, to address your hypothesis of a gene-duplication followed by a gene knock-out: There is no need for a preceding duplication. The more probable cause is a single point mutation (or multiple) near the active center of the inherited A/B enzyme, or a nucleotide insertion/deletion in its coding region, causing a frame-shift. A completely (not partially!) inactivated A/B enzyme would effectively represent a novel 0-genotype.

Your link says its incidence is typically 4 per million, up to 1 per 10,000 in select areas/populations. IMO, unless there's a family history of it, it still seems likely that somebody's lying

Novel gene knockout is also possible; I have no data no likelihood.

incidence reports are based on tested cases - so as testing rates increase the reported rate will rise to the true rate.  Microchimerism is another possible cause.

@Joshua. I agree, I edited the text!

@Punintended that doesn't follow at all.  4 per million means that on average 4 people in a randomly selected sample of 1 million will have the genotype. Since we live in a world of several billion people, it is expected that some will have this genotype. Therefore, the fact that it is rare doesn't tell us anything about whether the grandmother is lying. Some people do have this, so why not the OP's mother?

@terdon Of course some people do have this, and if this disorder is somehow confirmed, the probability is one.  But without prior knowledge, based on the average incidence in the world (or even the subpopulation), the odds of her having it are indeed between 1/250k and 1/10k.  That's kind of the point of "average incidence"

@Punintended yes, but the odds alone are meaningless without taking into account the size of the sample pool. Essentially, here we are asking "what are the chances that a random person selected out of a pool of ~8 billion is one of the 4 per million" and that is a very different question to "how likely is it that this person is one of the 4 in a million".

@terdon If you have 100k people and an incidence of 4/million, stochasticity kicks in and the odds change. That's not the case for large sample sizes, like an n of 8 billion. 4/million * 8 billion is 32k. The odds this person is one of those 32k (given no other knowledge) is 32k/8b, or the incidence rate

@Punintended but we have other knowledge. So that’s irrelevant.

both my grandma and my grandpa have been blood donors for years, so we can safely rule out mistakes in testing. Thanks for your answers!

@PateArdealul and your mother?

@Tim she did donate blood a few times too. Most of my family got to know their blood type by donating blood.

Two highly unlikely, yet possible ways this could happen:
One extremely unlikely possibility is that grandmother was born O.  Grandmother's current A typing could be the result of interplacental stem cell transfer from bearing an A child and the mother is an XX clone of the grandmother. How similar in appearance are grandmother and mother?
A less rare yet still doubly-unlikely scenario is that the grandmother and grandfather are both chimeras and at least some of the grandmother's eggs and at least some of the grandfather's sperm are O.  We are learning that human chimeras are more common than we used to think. https://en.wikipedia.org/wiki/Chimera_%28genetics%29

Given that your grandmother is type A and your grandfather is AB, there is very small, minute chances that your mother is in fact the biological child of one or both of them.  For your grandmother to say that she is 100% your grandfather's child, maybe he had her with someone other than your grandmother, and due to unfortunate events, that woman died giving birth or shortly thereafter.  It may hurt your grandmother to admit that. Or, she could have the same views as many others, like myself, and recognizes that there is a BIG difference between being a father and raising a child, and just being a sperm donor and disappearing. There are many different situations that could be possible, that your grandparents may not be ready to admit for whatever reason, or it could very well be a simple mistake at the lab who did the testing. But does it honestly matter if she is the biological child of both grandparents, or whatever the truth may be? Will knowing the answer change anything?

Welcome to Biology.SE! On this site, answers are expected to be fact based (and are much more likely to receive a favorable response they include supporting references (primary literature is best)). Your answer is entirely opinion and thus is not appropriate here. ——— Please retake the [tour] and then consult the [help] pages for additional advice on [Answer] effectively on this site and then delete or [edit] your answer accordingly. Thanks!

Your theory of "biological grandmother is not the grandmother" doesn't really solve anything; the grandfather is AB, so the child would be A, B or AB, even if the biological grandmother was O. You'd still need to explain away the grandfather's lack of O managing to contribute an O, making the possibility of an unknown biological grandmother non-explanatory.

Did not realize that I needed to specifically state that there is a possibility of the mother being adopted and never told, thus explaining why she has neither of their blood types. My apologies, I will be sure to be more specific next time.

Please [edit] your post to make it better or, if you don't feel that is worth your time. then please delete it (click on the "delete" next to "edit" under your post. Thanks!

authors: Bob Jarvis - Слава Україні


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What is 'protein' in food?
I know that proteins perform a lot of functions and as a result there are a lot of different types of proteins in our bodies. When I eat food that has x grams of 'protein', what is this? A homogenous mix of proteins? A heterogenous one? Is it specific set of them that are general enough to be used by my body despite coming from a different organism? How can it be sure that my body can use the kind of protein in the food?

When we say "protein" with respect to food, what is generally meant is material that contains amino acids.  Every protein is, at its heart, a long string of amino acids, which then gets processed through some combination of folding, cutting, and bonding together with other molecules.
Much of our food is made out of cells, whether animal (e.g., meat), plant (e.g., vegetables, fruits, grains), fungal (e.g., mushrooms), or bacterial (e.g., yogurt).  Every cell has a widely heterogeneous mix of proteins, comprised in turn of a widely heterogeneous mix of amino acids.  Milk-based foods aren't cellular, but also have a wide range of amino acid content, because mammals produce milk as a complete food source for their babies.
Inside your body, digestion breaks the proteins, whatever they might have been originally, down into amino acids, and that's what you really need to pay attention to in terms of nutrition.
The human body can synthesize the majority of amino acids out of other molecules, but there are nine essential animo acids that we have to get from our food.  Any diet that provides a sufficiency of those amino acids, no matter what sort of proteins they may be originally bound up in, will provide what you body needs in terms of protein.

I suspect that the actual bacterial biomass in a standard yogurt is pretty darn low.

@Arthur well, if we take a standard yogurt — e.g. specified by a Russian standard, GOST 31981-2013, we get the requirement of ≥10⁷ CFU of particular bacteria (see §3.1). Dunno whether it's high or low, but the numbers are available.

@Ruslan 10^7 CFU per gram if Google reads the Russian correctly·  But even assuming we could say 1 live cell=1CFU (as I do below to get a crude guesstimate), we don't know how many dead bacterial cells are in there.  Presumably not 0.  Taking sizes for lactobacillus cells from Britannica and assuming they're mainly water from the point of view of density we get something like 1 part in 10^5 by mass live cells, or "pretty darn low".  I'm no biologist so couldn't even begin to work out the live:dead cell ratio - but can't trivially find it

It's a mix of all the proteins in whatever organism the food is coming from. Some (especially vegetable/grain) sources might have fairly specific proteins present because you are eating a specific part of that organism which is enriched in that particular protein, but ultimately the specific proteins don't matter much unless you have some sort of allergy. The reason it doesn't matter much is that your body won't use the whole proteins at all.
All proteins you eat are digested into their constituent parts: amino acids. Essential amino acids are those that a human cannot synthesize themselves, so it's important that the diet contain all of these. Vegetarians/vegans in particular should be familiar with the concept of "complete protein", or combinations of food sources that serve as "complete", to ensure they have access to all the essential amino acids.

As one might suspect, if a label says just "protein" without being more specific, it means any protein, without being more specific.
The reason we are not that interested in the details is that the body denatures most proteins in the acidic stomach and the intestines and breaks them up into their building blocks, the amino acids, without really taking a close look at them. (It's a bit like breaking up your brother's Lego stuff when you simply need grey bricks: It doesn't really matter whether it's his Millenium Falcon or his Saturn V.) The amino acids are then absorbed through the intestinal wall. They are used to synthesize the proteins our body needs (build your own star ship).
Our body can synthesize many of the 21 amino acids from scratch, some of them always in sufficient amounts; but nine of them must be ingested with food. They are called "essential" amino acids. They are like the special corner pieces you so badly need to finish your design and that are not so common.
If they are missing, which can happen with a non-varied diet, the body cannot use the other amino acids to create its needed body proteins and instead synthesizes carbs and fat from them. Therefore, a diverse diet is needed to fully utilize protein in food as building blocks for the proteins the body needs. That's the — important — exception to the rule that all food proteins are nutritionally equal.

Which is why eating collagen-rich food if you think you're body needs to build more collagen (like for joints) doesn't make any sense.  Even this site: https://www.webmd.com/diet/foods-high-in-collagens#1 gets it wrong: if your body is going to break the collagen down into amino acids, what difference does it make whether those amino acids come from collagen or from some other protein?

@MikeMaxwell if nothing else, one would think that eating collagen would ensure that you get all the amino acids required to build collagen in the human body.

The two most common amino acids in collagen are glycine and proline. ( https://en.wikipedia.org/wiki/Collagen ) The glycine-proline-hydroxyproline is the most important sequence motif for collagen structure. Neither glycine nor proline are essential amino acids (and hydroxyproline is made by post-translation modification of proline), so I think @MikeMaxwell has a point.

The other answers are correct: foods you eat include a mix of proteins, which are mostly cut into their constituent amino acids in your digestive system. However, while a burger (meat or veggie), might contain thousands or millions of distinct proteins, there are some proteins that much more common than others. For example, in blood plasma, there are more serum albumin molecules than all the other protein molecules combined.
Meat
In meat, the predominant proteins are actin, myosin, and tropomyosin. As might be expected, the function of these proteins is to allow muscles to move and apply force. Myosin heads "walk" on actin tubules. Connective tissue proteins collagen and elastin are also a major components. The function of these proteins is to provide structure and elasticity. Blood proteins such as serum albumin, myoglobin and hemoglobin are also included. The major role of serum albumin is to regulate the osmotic pressure of blood (keeping cells from accumulating too much water and bursting or losing too much water and dessicating). The function of myoglobin and hemoglobin is to carry oxygen.

Myofibrillar proteins are the main components of meat, and there are around 20 or so different types in this particular group. In perspective, out of the overall 50%–55% of myofibrillar protein, myosin and actin alone account for around 65%–70% of this figure.

From: Meat: Food and Science of the Animal Kingdom.

Actin, by Thomas Splettstoesser, CC BY-SA 3.0
Beans, peas, lentils
Pulses (peas, beans, lentils) contain mostly legumins and vicilins, which are oligomeric storage proteins. Hence, they serve no function other than to store amino acids that the new plant can use to grow from the seed. Legumins form from 6 subunits and have a total mass of 300–400 kDa. Vicilins are heteromeric or homomeric trimers with overall masses of 145–190 kDa.

Phaseolin, a vicilin storage protein in beans.
Milk
The major protein in dairy milk is casein. These proteins have an unusually high amount of proline, which inhibits secondary and tertiary structure formation. Their function is to supply amino acids to infant mammals and carry essential nutrients such as phosphorus and calcium. Together α-, β- and κ-caseins make up about 70% of cows' milk, with the rest consisting of lactoalbumin and lactoglobulin.  They comprise 20–45% of the proteins in human milk, depending on stage of lactation.


text:
Does the cytoplasm include the organelles?
I am a student in middle school. My textbook says that

Cytoplasm is the gelatinous liquid part of the cell excluding organelles.

However my teacher said this is wrong. According to her, the correct definition is "The gelatinous liquid part of a cell excluding the nucleus is known as the cytoplasm".
I am confused now as to which is the correct definition. If my teacher's definition is correct, then the organelles (other than nucleus) are part of the cytoplasm.
Is that correct? What is the correct definition?

Does this answer your question? What is the difference between cytosol and cytoplasm?

@tyersome — I don’t think it does. It is a different question — the distinction between two terms — and if taken in the context of this question it would imply that one particular definition of cytoplasm is “correct”, which, I argue, is incorrect.

Edward2007- what an incredible question by such a young mind. I'm impressed that you decided to find out more about the topic and found your way to an open forum like this. While I do not have the exact answer to your question, I do believe that Bryan Krause's response offers a very nice approach about thinking contextually. "The cytoplasm is like the ocean." It depends on how you look at things. Some times it's not very important to get the definition 100% right, but to visualize the bigger concept, for instance the makeup of a cell, in this case. Any way, I'm sure you'll do great with whatev

Francis Crick (together with AFW Hughes) famously described the cytoplasm as follows: "If we  were compelled to  suggest a  model we  would propose Mother’s Work Basket - a  jumble of beads and buttons of all shapes and sizes, with pins
and threads for good measure, all jostling about and held together by “colloidal forces”.

The cytoplasm is like the ocean.
When you talk about the ocean, do you include the fish? What about islands? Sometimes yes, sometimes no.
You could use a cytosol/cytoplasm distinction, where cytosol is "just the liquid part outside the organelles" and cytoplasm includes all the fish, but context matters and I don't think it's actually necessary to have a distinction.
If someone is talking about the "pH of the cytoplasm", you can assume they mean the liquid part, not that they're taking some weighted average of pH over all the different organelles plus the space outside of them. Same thing for ion concentrations. If someone is talking about the "cytoplasmic face" of a membrane, it's clear they mean the side that faces the liquid stuff in cells, even if you're talking about vesicles and organelles where all the membrane faces are "inside the cytoplasm" since the whole organelle is. However, if one were to "remove all the cytoplasm from a cell" you'd expect the organelles (minus the nucleus) to come along; after all, they are in the cytoplasm so they go where it goes.
If you need to memorize a definition for a class, use what the teacher gives you. Otherwise, think critically about the context in which the word is used. I like your teacher's definition better, not because the two options are "liquid only" and "liquid plus organelles", but because organelles are in the cytoplasm, so sometimes when people say cytoplasm they mean the whole ocean including the contents. Your teacher's definition allows for both uses of the term; yours explicitly does not.

"The cytoplasm is like the ocean.": great analogy!

@Bryan given the upvotes taking your post to the top answer, I think it'd be good to provide a cited example (or two) of usages

@user253751 The analogy only goes so far, but if I want to take it there then the answer would be that the nucleus in this case is the "continents". Cytoplasm was named by looking at a cell in a microscope and seeing this spherical ball in the center, calling that the nucleus, and needing a name for all the other "stuff". It was only later that it was known what other "stuff" was in the ocean.

@theforestecologist Yeah, for sure, that would be good. I've tried to find examples that make some of these distinctions I am talking about clear, but that's been a bit difficult. I will certainly try to find the time, though. For now, I'd recommend a reader try searching Google Scholar for these terms: look for papers that talk about the pH of cytoplasm, or look for "cytoplasmic face" in discussions of cellular transport or transmembrane proteins. Or, conversely, look for measurements of "cytoplasm volume" relative to the nucleus. Vacuoles add a bit of complexity if you're into plants, though

The young scientist asks:

“What is the correct definition?”.

The old scientist answers:

“As is often the case in biology, there is no correct definition — different people adopt different usages.”

This answer attempts to explain why this is the case and how to find out other than asking people who despite greater age and knowledge, may be mistaken in their dogmatism.
General Answer
Often in biology a term is coined for a new observation or concept that has arisen from scientific research. Subsequently further research reveals new aspects or details. These expand rather than negate the original discovery, but can make original definitions inadequate. Individual scientists modify the terminology, and naturally do so in relation to their own concerns, which may differ from those of other scientists. Hence different usages arise.
One might have expected that there would be committees of scientists to lay down rules, but this tends to be confined mainly to the physical and chemical sciences where precise common terminology is important. Because modern biology is fast moving, people are inclined to either wait until the dust has settled (e.g. in enzyme nomenclature) or let “terminological Darwinism” take its course.
Specific Answer
I am not really a biologist in the traditional sense, so I lacked any dogmatic attitude to the question, and, instead made Wikipedia my first port of call. This is not a definitive authority on anything, as anyone can edit it. However in this case it is, I think, useful. Under History we read:

The term was introduced by Rudolf Bon Kölliker in 1863, originally as a synonym for protoplasm, but it later has come to mean the cell substance and organelles outside the nucleus.

There has been a certain disagreement on the definition of cytoplasm as some authors prefer to exclude from it some organelles, especially the vacuoles and sometimes the plastids.

Further in the article there is a reference to the term cytosol which is used in an experimental (rather than an observational) sense to refer to the portion of the cytosol from which membranous organelles have been removed.
The date 1863 is worth noting as it is before the discovery of organelles such as the mitochondrion (1880), and knowledge of others at the time was at a primitive stage.
Addendum: Advice to the young scientist

You have eaten from the tree of knowledge and have lost your innocence. Cry a tear then wipe it dry, as you did when you realized there was no Santa Claus. If you wish to become a scientist or even just to understand science you must understand how science works.

Do not reproach your teachers. They are fallible because they are human. Be charitable towards them as you would have them be to you.

It's going to depend on what definition is useful in what context.  If was was talking about an mRNA being translated in the cytoplasm, I am saying it is absolutely not translated in the ER or the golgi apparatus.  (Most proteins translated in those places are on their way to being transported somewhere else; they will not end up free-floating in the cytosol the way proteins translated in the cytosol usually are)

If you want to know about biology, go to PubMed.  If you want to know about semantics, go to Wikipedia.
Their articles may not be tremendously detailed or accurate overall, but if there is any one thing that inspires generations of bitter snipes and threats, it is a Wikipedia discussion about how to title an article or define the title term.  In this case it is perhaps not so severe; nonetheless, their talk page suggests that they've been around this merry-go-round at least two or three times.  They seem to stick with the standard idea that cytoplasm = everything but nucleus, cytosol = everything but nucleus and organelles.


text:
How do we know the human species arose in Africa?
I have heard (from multiple sources) that the current scientific opinion is that the human species arose in Africa. What are the reasons for this opinion? If possible, simple and non-technical explanations (as far as possible) would be appreciated.

I think this is mainly based on the fossil record.

Wikipedia exists: https://en.wikipedia.org/wiki/Human_evolution

There are two big prongs of the out of Africa theory or whichever name you wish to call it.
Prong the first: fossil evidence. There are lots of different kinds of protohuman fossils. Homo erectus/ergaster are found all across Europe, Asia, and into Indonesia from about 1.5 million years or so until about 70 thousand years ago, where they stop showing up. Up until 125 thousand years ago anatomically modern humans were only found in Africa. About 70 thousand years ago they start showing up in the Middle East, and then they spread out roughly following these paths. The fossil record shows not-humans or almost-humans (Homo erectus mostly) for millions of years, then humans show up at a certain point and then there's loads of human fossils. This point gets more recent as you get further from East Africa.
Prong the second: genetic diversity. Starting with this paper (not sure if this is behind a paywall but the details are not important anyway) human mitochondrial DNA was compared using restriction enzyme mapping. This kind of mapping is super crude (roughly analogous to grinding pottery into a fine dust and grouping the dusts by color) and the original study was pretty limited by the computers available at the time. Nonetheless, they showed that the most genetically diverse geographical group was Africa, and furthermore that any two people from outside Africa are likely more closely related to each other than any two people inside Africa. Genetic diversity goes down the further away from East Africa you get, matching what you'd expect if humans hadn't been living there long. There have only been (very roughly) 60 generations since humans colonized New Zealand. All Maori people, therefore, are at most 58th cousins. All indigenous Australians are at most 1998th cousins. All Africans are at most 8000th cousins.
More recently we've done proper sequencing on the mitochondrial DNA (actually knowing whats written there) and that's allowed much more precise estimation of this sort of thing, and estimation of the timeframes involved. The genetic evidence backs up the fossil record, by and large. (There are a few interesting examples where interbreeding with Neanderthals and maybe Denisovans can be detected, and that the settlement of the middle east by modern humans about 125 thousand years ago failed. They left no descendants.)
Fun side consideration (warning, extra science, proceed with caution): all humans inherit their mitochondria from their mother, and all males inherit their Y-chromosomes from their father. This lets us trace matrilineal lines with a relatively high degree of accuracy, since mitochondria reproduce asexually. To clarify: your matrilineal line is your mother, and her mother, and so on. Your paternal grandmother is not part of your matrilineal line, nor are your aunts or sisters. These lines are statistically guaranteed to eventually converge on a single woman whose mitochondrial descendants now live in all of us. The reasons for this are complicated. There are actually lots of these women, since she inherited her mitochondria from her mother, ad infinitum (well, not infinitum. Ad failed-endocytosis-of-an-alpha-proteobacterium-leading-to-mitochondria doesn't roll off the tongue though). Science has tight estimates on the most recent mitochondrial ancestor, or "Mitochondrial Eve". To be clear: there were loads of other women alive at the time, and we inherit a lot of their non-mitochondrial DNA. Over millennia all those other women had fewer daughters, and their matrilineal lines died out. She lived about 200 thousand years ago, plus minus 20 thousand years. As a mathematical guarantee we'll never find her body or have a really tight estimate on how long ago she lived, but she's genetically guaranteed to exist. The same principle applies to patrilineal inheritance, but the estimates for the most recent ancestor of all Y-chromosomes are a little looser (200-300 thousand years ago). See here for a more detailed handling of Eve and what's going on there.
In sum: old fossils only in Africa, everyone outside Africa is only 2800th cousins with each other or less, but intra-African relatedness is less than half that (more than twice as far away genetically).

Does this mean mitochondrial eve had multiple kids with multiple men?

No, mitochondrial eve isn't real women, it is computer reconstruction according to genetic theories, mutation rate, inheritance and so on. Change one parameter (estimated effective population size, although that one have loose connection with real population size as well) and you have different estimate of Mitochondrial Eve.

Why would matriarchial lines terminate at one person in the past instead of there being multiple lines?  That doesn't make a lot of sense to me.  It would either mean that matriarchial lines never crossed, or that initially there was only a single woman.  Does the term "mitochondrial eve" actually refer to a group of women?

It's not that all ancestral lines go through Mitochondrial Eve's exclusively, it's that she's the most recent person which everyone's 'set of all ancestors going back X years' can be expected to have her in it.

@yters It's not made explicit in the answer, but mitochondrial DNA is passed almost exclusively through the female line (sperm usually only has one or two mitochondria, if any at all, while the ovum has more like fourty). There has been many lines of mitochondrial DNA, but as soon as a mother only had sons, her line was broken. Add to this how many near-extinction catastrophes humans went through (apparently, there's been times when there were only a few thousand humans on the planet!), and it isn't all that suspicious that you can trace one line that's running in all of us. Others died out.

@yters Mitochondrial eve is not a person or a group of persons (in fact I hate these creationistic connotations). It is basically a phylogenetic calculation of the Last Common Ancestor of human mitochondria (which are specifically maternally inherited). IMO addressing to this concept as her/she can be highly misleading. Resonating: you should clarify this in your answer.

@Catalept that's not quite right, you're thinking of something else I think. Most recent common female ancestor, maybe?

@Colombo Mitochondrial Eve is a single human female who is guaranteed to have existed based on what we know about how genetics works. You're confusing imprecision in the measurement technique for imprecision in the measured thing. If you had a time machine Mitochondrial Eve would be time-consuming but trivial to locate precisely.

Mitochondrial Eve was called Hera.

@LightnessRacesinOrbit We're wondering (in chat) what you meant by that. Enlighten us, please.

@Faheem: https://en.wikipedia.org/wiki/Hera_Agathon

@LightnessRacesinOrbit I see. Thanks for the clarification. I just remarked to Resonating that apparently we don't watch enough Battlestar.

@FaheemMitha: :)

@Luaan, thanks that makes more sense.  So, to restate what you are saying, there is a single female in the past that everyone shares mitochondrial DNA with.  It still doesn't make sense that there has to be a single female.  Mathematically, it seems there could be many "mitochondrial eves" from the same period.

@WYSIWYG, correct me if wrong, but you are still saying this calculation is meant to pick out a single female individual in the past with whom everyone shares their mitochondrial DNA, correct?  The calculation is not just a mathematical construct, but is meant to refer to a real individual in the past?

@yters There could have been a person but mitochondrial genome can also accumulate mutations and the rate of mitochondrial mutations is higher than that of the nuclear genome. All I said is that 'mitochondrial eve' is a hypothetical person. I said that I think the term "eve" can be misleading.

@yters Yes and no. At any given point, there's a set of women that are the 'mitochondrial eves' of that point in time.  These women between them are mitochondrial ancestors of all living humans. At this point in time, it's all mothers. If you go back further it's all maternal grandmothers. If you go back far enough the set keeps getting smaller, until it's one person. Any further back and it stays one person. Come to chat, we can back and forth faster there.

@Resonating If I had a time machine, tracing ancestral lines would indeed be an interesting use for it...

@yters Note how the single mitochondrial "ancestor" appears so long after humans did. In the beginning, there have been a lot of different mitochondrial lines - if we take the Homo genus as a whole, that's been around 10 million years, if we go from the point where modern humans diverged from Neanderthals that's around 500 thousand years. Interestingly, anatomically modern humans actually arose around the same time as MitE. But even at the time of MitE, there has been tons of different mitochondrial lines. It's just that one won out in the end - all modern Mit lines are descendants of MitE.

@yters It is indeed possible that there wouldn't be a MitE for Homo sapiens sapiens, for example. But eventually, outside of a given species, you do come to a single ancestor - maybe it was some hominid, or a fish. But with each generation, the probability of only having a single (mitochondrial) ancestor grows. If you only have sons, your MitE line just dies out, ditto if you die. As far as I know, we don't actually know if MitE was an anatomically modern human - it's not like we have her fossillised remains. Her identity is based on probabilistic analysis of human mitochondrial lines.

@yters In any case, this is really getting dragged out. Perhaps you'd like to post a question specifically about Mitochondrial Eve? I'm sure there's plenty of people who can explain this better than me - I'm no expert on human evolution or biology in general.

People previously argued for a multiregional theory in which humans arose from many different places on the globe, but have come to the conclusion that humans came originally from Africa. I believe that their reasoning is that the oldest skulls found have been found solely in Africa. This article expands on my answer if you are interested:
http://news.nationalgeographic.com/news/2007/07/070718-african-origin.html

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


text:
Do the foldings in the brain vary person to person?
Can the gyri and sulcus, which are the foldings of the cerebrum, vary from person to person? If that is true, then can we say different people have different types of thinking skills? I believed that the anatomy of the brains of homo sapiens were all the same (except mentally abnormal children with Progeria like syndrome) but then, why do we all have different thinking skills, as I have observed in my surroundings?
I know some depends on self created skills, but could different brain foldings be the reason?

The major structure is consistent but there is a lot of variation in the details, including the presence and absence of certain gyri:

Kennedy, D. N., Lange, N., Makris, N., Bates, J., Meyer, J., & Caviness Jr, V. S. (1998). Gyri of the human neocortex: an MRI-based analysis of volume and variance. Cerebral Cortex (New York, NY: 1991), 8(4), 372-384.

Kruggel, F. (2018). The macro-structural variability of the human neocortex. NeuroImage, 172, 620-630.

Bartley, A. J., Jones, D. W., & Weinberger, D. R. (1997). Genetic variability of human brain size and cortical gyral patterns. Brain: a journal of neurology, 120(2), 257-269.

However, it's not so straightforward to connect these to function and thinking skills; the layout of the gyri is more like a shape of a blank canvas that cortical function is then written on. For example, the location of prefrontal regions relative to gyri/sulci varies between individuals:

Rajkowska, G., & Goldman-Rakic, P. S. (1995). Cytoarchitectonic definition of prefrontal areas in the normal human cortex: II. Variability in locations of areas 9 and 46 and relationship to the Talairach Coordinate System. Cerebral cortex, 5(4), 323-337.

As does the primary auditory cortex:

Leonard, C. M., Puranik, C., Kuldau, J. M., & Lombardino, L. J. (1998). Normal variation in the frequency and location of human auditory cortex landmarks. Heschl's gyrus: where is it?. Cerebral cortex (New York, NY: 1991), 8(5), 397-406.

And I'd wager most other areas, too. So you can't map the size/presence of a given macrostructural feature to a specific function. You might instead look at cortical thickness in particular functional regions, or area associated with a particular function, rather than the "phrenology" of the folds.

Tl;DR: The folding pattern seems consistent among human species but they are not exact match when compared person to person.
Long Answer:
The folding is not random like a crumpled piece of paper. Rather it exhibits a pattern that is consistent from person to person. Research indicates that a network of nerve fibers physically pulls the pliable cortex into shape during development in utero and holds it in place throughout life. Disturbances to this network during development or later due to stroke or injury, can have consequences for brain shape and neural communication and may lead to mental disorders.
Over the past couple of years, several research teams have reported that the brains of schizophrenic patients exhibit reduced cortical folding overall relative to the brains of normal people so they are quite certain that brain shape differs between schizophrenics and healthy people. Similarly, people diagnosed with autism also exhibit abnormal cortical convolutions. Some of their sulci appear to be deeper and slightly out of place as compared with those of healthy subjects. Researchers pointed out that it arises from the miswiring of the brain.
Mental disorders and learning disabilities can also be associated with aberrations in the composition of the cortical layers. For instance, in the late 1970s neurologist Albert Galaburda of Harvard Medical School found that in dyslexia, the pyramidal neurons that form the chief communication system of the cerebral cortex are shifted from their normal position in the layers of the language and auditory areas of the frontal cortex.
The above information is paraphrased from this article but you can read the whole to get a better understanding of the topic.
Also, you can refer to below papers:

Toro R, Perron M, Pike B, Richer L, Veillette S, Pausova Z, Paus T. Brain size and folding of the human cerebral cortex. Cereb Cortex. 2008 Oct;18(10):2352-7. doi: 10.1093/cercor/bhm261
Garcia K. E., Kroenke C. D. and Bayly P. V. 2018, Mechanics of cortical folding: stress, growth and stability, Phil. Trans. R. Soc. B3732017032120170321, DOI: 10.1098/rstb.2017.0321
H. de Vareilles, D. Rivière, JF Mangin, J. Dubois,
Development of cortical folds in the human brain: An attempt to review biological hypotheses, early neuroimaging investigations and functional correlates, Developmental Cognitive Neuroscience, Volume 61, 2023, DOI:
10.1016/j.dcn.2023.101249


text:
Specific mechanism behind lethality of yellow coat color in mice
Our high school genetics chapter has some extra information about L.Cuenot. It only covered his research, and the fact that mice homozygous for yellow coat color would die before birth. It was an example of a lethal allele.
We have learned about sickle cell anemia, thalassemia, and hemophilia. All of them had a specific reason/mechanism which caused damage. For example, it's not the shape of the red blood cell in itself which is problematic, it is the fact that it can't carry enough oxygen. Therefore the cell will die off much quicker than normal cells.
I asked few of the biology teachers why the yellow coat color was lethal, but they couldn't provide any answer.
My question is, what causes the mice to die before birth?
Links to relevant articles or excerpts from them are highly appreciated.

Good question!  Minor quibble: the shape of red blood cells is very problematic because it can cause sickle cell crisis, the prevention of which is, unhelpfully, "live a life free of physical and mental stressors, have perfect hydration habits, and don't exercise in non-ideal conditions"

@Punintended Wow! I didn't know about this angle of the clogging of small blood vessels due to their shape. I guess there's only so much they teach you in high school.

Really interesting question: The lethal yellow mutation (also abbreviated Ay) affects the agouti signalling protein which plays a major role in pigmentation. Heterozygous expression of it leads to the dominant expression of pheomelanin (which is yellow), causing the mice to express this color (among other effects). To understand why it is homozygous embryonic lethal, we need to take a further look at the gene and its organisation.
Agouti is located on chromosome 2 of the mouse genome and downstream of a gene called "Raly" (synonymous also MERC)(Image from NCBI Genes)

The Ay mutation now deletes a large chunk of DNA, removing about 170kb between these genes. This removes parts of the coding sequence of the Raly gene and the complete promoter and (non-coding) exon1 of the Agouti gene and results in a fusion protein in which the agouti gene is put under the control of the Raly promoter. This leads to the expression of Agouti every time when Raly should be turned on.
Schematically, this looks like this (figure 4 from reference 2):

Raly is an RNA binding protein, which is highly expressed in embryonic tissues. The mutation leads to the expressing of Agouti there instead. According to reference 3 this leads to embryos which do not develop further than the blastocyst stage leading to premature death of the embryo.
So in short, the deletion removes the expression of Raly, a protein important for embryonic development. Im homozygous mice this is embryonical lethal, in heterozygous mice this can obviously be compensated. However, these mice tend to be obese and are more susceptible for certain tumors (reference 4).
References:

The embryonic lethality of homozygous lethal yellow mice (Ay/Ay) is
associated with the disruption of a novel RNA-binding protein
A molecular model for the genetic and phenotypic characteristics of
the mouse lethal yellow (Ay) mutation.
Pleiotropic effects of the mouse lethal yellow (Ay) mutation
explained by deletion of a maternally expressed gene and the
simultaneous production of agouti fusion RNAs
The molecular basis for dominant yellow agouti coat color mutations

It looks like Eif2s2 on the opposite strand would also be deleted in Ay mice. Do you know if this has any effect on the phenotype? It would be interesting to see if researchers knocked in Eif2s2 somewhere else and looked to see if there were any confounding effects.

@MattDMo I don't know, but I'll have a look into it tomorrow when I have access to journals again.

In other words, the yellow color is just one obvious manifestation of a more significant syndrome, which under 2 copies becomes massively worse and causes complete failure of the organism?


text:
Will humans and animals be harmed by frequencies outside their hearing range?
The human ear (for example) is sensitive to frequencies from 20Hz to 20kHz. Any sound beyond that limit would not be heard by us naturally.

Will it harm us (effect our ability to hear) when we hear sound more than 20kHz continuously?
Or...

Will it harm when we hear a 19,999Hz sound (which is upper limit) continuously?

this question needs to be restated to yield a sensible answer, but my explanation as to why became a little long, so I posted it as an answer below. It may actually be easier to answer if it were broken into two questions: Will sounds we can't hear hurt us (our ears specifically)? Will sounds just inside our hearing range hurt us?

The only sensible answer to these questions is "sometimes".
The reason: even a simple monotone must be described by both frequency and amplitude. Any frequency can cause harm with enough amplitude, and any frequency can be harmless when the amplitude is low enough. If you want to actually quantify the damage, you'll need something like an equal-loudness curve, but for damage rather than loudness. As a proxy, you could use the pain threshold of the equal-loudness curve.
As for the second question, there is nothing magical about 20kHz: physical damage will always fall on a spectrum, there is no single frequency and/or amplitude at which damage begins. If you set an oscillator to constant amplitude and slowly turn up the frequency, you'll notice that the sound slowly dies out around 20kHz. The damage threshold will behave the same way.

I am no an expert on this by any means. However, if I recall correctly, everything has a natural vibrational frequency. And, I imagine this would also be true for your ear-drum. So, if the eardrum is only responsive to vibrations between 20Hz-20kHz, I don't see how any frequencies outside of this limit could ever cause damage to the ear, because there would be no way for the eardrum to vibrate.

Hey @Bob. It's true that things have resonance frequencies, but you have to consider that your eardrum (and the rest of your body) can still vibrate at frequencies that you can't hear. The vibration still has to be translated to neurological impulses for you to hear them, and just because the sensory cells in your ear vibrate it doesn't mean they fire the connected neuron.

If you are talking about sound damaging the sound sensing organs in the ear, analogous to an ultrasonic heavy metal concert, I've found an interesting report just on this topic.

For ultrasonic components above 20 kHz, the limits were set to avoid hearing damage in the audible (lower) frequencies. One-third-octave band levels of 105-115 dB were observed to produce no temporary hearing loss, and were therefore judged non-hazardous in respect of permanent hearing damage.

Emphasis mine, from "Damage to human hearing by airborne sound of very high frequency or ultrasonic frequency"

If you are talking about high frequency sound from a explosion, or some sort of sonic cutter with intensities of such a level of compression or a high decibel range that conveys enough energy to physically damage something of course the answer would be 'yes this would damage your ears and the rest of the body too.
Operators of ultrasonic equipment with levels above 60 dB complained of headaches and fatigue, even nausea below 60 dB they felt no effect (reference table 7 in paper).  But they did not seem to have any hearing loss.
One soviet experiment is both informative and maybe also entertaining to read about:

An unspecified number of subjects were exposed for an hour to a tone of 20 kHz at 110 dB. Tests were made to examine shift of hearing threshold over the frequency range 250 Hz to 10 kHz. Pulse rate, body temperature and skin temperature were also monitored. These tests showed no appreciable effect, even when the Sound Pressure Level was increased to 115 dB. These same subjects were given a one hour exposure to a 5 kHz tone at 90 dB: a considerable TTS was found. The 5 kHz tone at 110 dB produced a powerful vascular response.
...
It seems safe to infer an underlying concept: A sound which does not produce temporary
dullness of hearing cannot produce a permanent noise-induced hearing loss.

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


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Can viral proteins cause infection?

Possible Duplicate:
HIV Rapid Tests

Can proteins found on the surface of RNA viruses cause infection without the presence of the actual RNA and other components used in the virus?


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Has any large-scale origin-of-life simulation/experiment been done?
I have been thinking a little about the origins of life, and was further inspired by this question: How did the first self replicating organism come into existence?
I can accept that we don't quite know exactly how, but has any large-scale/long-term simulation been carried out?
There have been experiments but they seem to have been on a small scale. As an example, according to the Abiogenesis page on Wikipedia, some experiment which spontaneously formed peptide structures was carried out by Sidney Fox during the 50s and 60s.
What would be really interesting is if there had been some experiments or simulations carried out during a very long time, plausibly allowing for extremely low-probability structures to form. I doesn't matter whether this simulation/experiment has been carried out in a lab or as a computer simulation. There is of course the interesting but old "Conway's Game of Life" simulation, but according to my search efforts nobody has really tested it on a very large scale and in 3D.
Again, I'm looking for something extensive, like a decades-long single lab experiment or a simulation that has been run for years.

much more recent experiments have been done with astounding success. https://www.nature.com/news/2009/090513/full/news.2009.471.html

What you are possibly thinking of is large versions of the Miller Urey Experiment where a mixture of reducing gasses carbon dioxide, ammonia, nitrogen and the like are subjected to electrical arcs in a closed flask reaction, resulting in some biological molecules being produced.
Opinions have changed - Miller Urey did get the atmosphere wrong and so their finding of amino acids is not as strong as supposed.  Variations of this experiment continue to be done, with different conditions in the reaction vessel which reflect typical or even unusual conditions.  I've found some nice collections and reviews. There continues to be an enthusiastic effort even today.
Looking over several of these overviews, it's clear that many different conditions are being tried - reactions on mineral surfaces, examining chemicals on meteorites, near volcanic vents, different kinds of radiation.  What I don't see is anyone going to a huge tank.
I think that this might not have been tried (perhaps someone else will find a counter example), but if it were not me, I would probably not try longer experiments either.
There's some good reasons for this, if true.
Firstly all the published descendants of the Miller experiment have produced biologically relevant compounds after a few days.  Extending the experiment a few orders of magnitude may not prove anything new.
Secondly, the longer a reaction is run the more likely the sealed containers and heaters and other apparatus has to fail, causing you to restart or include contaminants that would ruin it.
Thirdly, one is not going to run an experiment that will ever come close to reproducing the time spans or volumes over which life emerged on earth - that was perhaps a few hundred million years over the area of the planet.
That's not to say you won't find out something new - an extra week could produce a new set of compounds or even a replicating system - we don't know if we haven't done it, but the nature of science is that you have a little time and money for a project like this and you would like to prove feasibility  - 'it could have happened this way'.  By selecting the conditions and doing a series of modest experiments which allows some to fail so that you can find something new.
I would say the observation of other planets and analysis of meteorites are getting closer to your idea - they are huge systems and been going for billions of years.  Titan is especially promising.  They just aren't the same conditions as Earth.
In brief, nothing is both affordable and perfect in proto-biotic research.


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Why do some fruits have their seeds disintegrated
Sometimes I'd come across a Lychee or a Naseberry whose seeds are kinda disintegrated.. in a thick powdered form, either completely or partially. What could cause such a thing? And is the fruit with such seed harmful?
I wish I had pics to show but it happens rarely.
Here's a normal Lychee with normal seed:

And what I sometimes find in place of the solid black seed is something that has the texture like this wet dirt:

but obviously more like the seed itself that has disintegrated into a thick wet powder.

Just a guess, but I would say that the process of the seed growing into a plant started. The fruit will still be eatable in most cases. We have a similar phenomenon with peaches where the inside of the hard core changes.


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How far do 2 ant colonies of same heritage have to be in space (and generation) in order to fight?
(Kinda follow-up to this.…)
I've heard before that if you put 2 ant colonies side by side they're going to attack each other.
But then from the previous question, there could be "sister" ant colonies which (assumingly) don't harm one another.
I can probably see that generation-by-generation colonies would just naturally be either too far apart in space, (or too close in "generation"), to have any fights.
But what actually makes ants decide whether to fight or to not?
And whatever it is, is it a spectrum or a limit..? (i.e would there be a case in which some ants of a colony will fight and some wont?)

Space and generation don't directly affect whether ants fight, that's all regulated with pheromones. Some ant species are more tolerant of different smells than others (see the argentine supercolonies mentioned above) while some species of ant have 'rival' nests that they are particularly aggressive to.
So I guess the answer is 'it depends'. On pheromones produced by the queen, and species. And probably diet/weather/local food availability/ some other things I haven't thought of.
I don't think it's possible for some ants of a colony to fight and others not to, but I don't have any evidence to back that up specifically.


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Do people with colorblindness have less cones or no cones of a certain type?
https://en.wikipedia.org/wiki/Color_blindness#Red.E2.80.93green_color_blindness

Protanopia (1% of males): Lacking the long-wavelength sensitive retinal cones,

Deuteranopia (1% of males): Lacking the medium-wavelength cones,

Do they lack all those cones, or are they just (severely) short?

This is a complicated case, as it can have multiple causes.
The genes which are coding for the long (L, yellow) and medium (M, green) wavelength photopigments are located head-to-tail on the X chromosome. This is the reason why this colors are affected much more and especially in men (which only have one copy of this chromosome).
What seems to happen mostly is that the photopigment of one type of cone cells (and their neuronal connectivity) is missing, while the density of the cone cells is still the same. This means that the cells are they, but are not functioning. See these publications (when you have problems getting the articles, let me know in the comments, I can help):

The density of cones in the fovea centralis of the human dichromat
Color-deficient cone mosaics associated with Xq28 opsin mutations: a
stop codon versus gene deletions.
Functional photoreceptor loss revealed with adaptive optics: an
alternate cause of color blindness.

What can additionally happen in some cases is that these cones have a different pigment than they should have. See the third paper above for details.

You need to have faulty cones or be completely devoid of the cones that help you perceive a particular colour. If you do possess cones to visualize a colour, you aren't technically colour blind because you should still be able to detect the colour slightly (reference).


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If people with colorblindness lack one type of cone cells, shouldn't they be unable to recognize one particular color?
The 3 types of cone cells in normal humans allow them to view 3 types of colors and any color made from mixing and matching those 3.
So, 2 types of cone cells should only allow to view just 2 types of colors and any colors made from those two.
But that is clearly not the case.
https://en.wikipedia.org/wiki/Color_blindness#Red.E2.80.93green_color_blindness

Protanopes, deuteranopes, and tritanopes are dichromats; that is, they can match any color they see with some mixture of just two primary colors (whereas normally humans are trichromats and require three primary colors).

Also, from personal experience, I'm colorblind and can see and differentiate all 3 red, green, and blue. It's just the hues between red-green and green-blue I can't distinguish much...
How exactly do dichromats see all three colors when they lack one type of cone cell?

Cones do not literally interpret colors.  The three cones work together to encode a signal that is abstractly interpreted by your brain in higher processing centers.  Here is what neuroscientists currently think the decoding scheme looks like:

This leads to what's called opponent process, an antagonist mechanism whereby the perception of green/red are a matter of the contrast between the two.  In a deuteranopes, the mechanism of antagonism is missing, so the colors can not be differentiated.
What this implies is that (to some extent) a single color has no meaning.  Colors are only meaningful in the context of other colors.

Based on that decoding scheme, the problem of green/red colourblindness (assuming lack of "green" cones) should be that there is a lack of information in green and red areas. For both the only signal would be low levels of "red" stimuli (since the overlap of "green" stimuli is missing). However, this should also cause multiple correspondence pairs along the "red" stimuli curve (light green to dark orange; yellow to orange etc) at similar levels of "red" stimuli. Is this the case in green/red colourblindness? I thought that only green and red were mixed up.

The decoding scheme is direct measurement of cone activity in the presence of light.  But how the higher processing centers interpret signals from the cones is not as straightforward as you might imagine; it's actually still an open question! Opponent process is a current theory about how it works, but the experiments consist of more psychology than neuroscience so we're on the outside looking in.  But notice that the evidence suggests that R-G relies on only two cones, while Y-B relies on all three.  So there's probably some loss in YB, but not to the point where you can't differentiate them.


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Why do damaged joints or ligaments experience inflammation? Why do physiotherapists try to stop inflammation as part of the healing process?
I have had the repeated experience of going to physiotherapists with injuries to ligaments or joints and they all expressly aim to reduce inflammation.
I don’t understand this. Our mammalian (and previously reptilian ?) bodies have been using inflammation for hundreds of millions of years (mammals have been around for 167-220 million years). Surely, this is a tried and true response to injuries and healing injuries: those organisms that practice it have been selected for because it works.
Do all mammals experience inflammation in response to injuries? Do reptiles? Why is inflammation considered to be a bad response? Or in other words, why does my physiotherapist(s) actively fight hundreds of millions of years of evolution to stop this response?
I understand that stopping inflammation reduces pain, but surely, it also stops natures tried and true native healing response.

Welcome to Biology.SE. There is a (very strong) recommendation to show evidence of research (a quote with a link) included with your question. What have you read about inflammation and how it is good/healing for the body? Is there a difference between acute and chronic inflammation? Why are anti inflammatories and physiotherapy helpful? Not everything that is natural is good.

Similar underlying question: What is the benefit of fever during infections?

Agoodnurse: This is my research. That’s why I am on this forum - to ask questions and get answers that inform me of the right view on this!

This site takes your position and cites a few sources.  This may really come down to a question of social values.  Coaches say "pain is temporary and glory is forever", but that was never a quote about sports medicine.  The coach's bank account will last longer if his players keep going, regardless of the cost to them in the future.

Since my first answer was deleted a second try.
Attention: NO medical advice!!!
First of all: Always listen to your doctor. He knows best. Don´t listen to any clinical studies or internet comments. Common practices ought not to be questioned. If it is against the common narrative it warrants deletion.
Here I am trying for a balanced view of both positions. Evolution and common medical practices. I am talking about acute pain conditions not chronic ones.
Yes inflammation is conserved throughout every animal. The innate immune system developed 1 billion years ago.
https://pmc.ncbi.nlm.nih.gov/articles/PMC10168657/#:~:text=Therefore%2C%20innate%20immune%20systems%20appeared,organisms%20resembling%20primitive%20jawed%20fishes.
Inflammation is an innate immune response triggered by damage associated molecular patterns (DAMPs) that activate Leukocytes and expression of proinflammatory mediators, that cause pain, vasodilation and swelling all of which serve the purpose to facilitate recovery.
However doctors have now close to 50 years of evidence based medicine and if they say inflammation is bad then this is certainly the case.
Here are some publications that question effectiveness and safety of NSAID use in soft tissue injury:
https://aoj.amegroups.org/article/view/8367/html
https://pmc.ncbi.nlm.nih.gov/articles/PMC1320354/#:~:text=Nonsteroidal%20anti%2Dinflammatory%20drugs%20(NSAIDs,term%20healing%20may%20be%20compromised.
https://www.frontiersin.org/journals/endocrinology/articles/10.3389/fendo.2024.1428240/full
https://www.cochranelibrary.com/cdsr/doi/10.1002/14651858.CD007789.pub3/full#CD007789-sec-0106
Here is a list of studies that prove treatment of inflammation as necessary or corrobarate the view that acute pain treatment prevents chronification:

(please insert if found)

To summarise,
Yes there were and are concerns about delayed healing with antiinflammatory treatment. The effect seems to be low or even insignificant in humans when they are used short term. So if you can´t bear the pain you might wanna take it.
However your doctors view is probably based on a whole lot of studies I cannot find, that weigh more because hes a doctor. So do as he says. I found further 0 studies that would indicate a better healing with anti inflammatory treatment. Paracetamol, a non antiinflammatory drug seems to work equally for pain (see cochrane analysis), also speaking against the benefits of inhibiting inflammation.
Since there is high heterogeneity in the cause of inflammation it certainly can not be generalized and needs nuanced considerations.
As by US standards the whole response is invalid because it refers to medical stuff and this is strictly forbidden. As for eventual inhabitants from civilized countries: Here you go, I know that you have the capacity to view this from a rational perspective.
NO medical advice to be found, only opinions!!

This is a surprisingly childish response to having a post containing bits of misinformation (or worse yet, medical advice) deleted. Wouldn't learning what is and isn't allowed be better for you in the long run?  I'm not a moderator, but I think your post was deleted not so much because it was "wrong/anti-conventional treatment" as because you were giving medical advice. And here you are doing so again. Please don't.

FWIW: if people want medical advice about treatment options following injury, they really should go to a well-respected physiotherapist, who will know more about it than the vast majority of physicians. But they will not know more about fevers than physicians who must deal with them all the time. Sticking to inflammation is a good idea.

how is it medical advice when I summarise clinical studies and frame it as vaguely and carefully as possible? How is one supposed to answer a question like that? Problem is I come from a civilized country in europe so I can´t reall comprehend the US problems with medical advice. just google and everything that I said is confirmed even in popular media. What exactly is your problem? provide sources and I will change my answers in an instant. That antiinflammatory substances solely provide symptomatic treatment and are therefore optional is common knowledge where I come from.....

My problem isn't with medical advice, it's with bad medical advice. You're overly confident, and that's not a good quality in either a doctor or a researcher, let alone a layman. Inflammation is necessary for healing up to a point; there is a point at which it becomes maladaptive (e.g. in the formation of granulation tissue.) Just because something evolved doesn't mean it's hunky dory, and you're being precious about your answer(s).

thank you now please provide a source and I will incorporate it into my answer and everyone is helped.

As I stated before, it is not my responsibility to provide sources for (my) comments. It is your responsibility to answer with reliable sources that support your answers. We are all confident idiots. Read it and learn. (Also, I'm done here.)

nice, you choose to neither answer the initial question nor to correct what I am saying. Trust me, I tried finding conflicting studies. I just can´t. If it is so obviously wrong it can´t be hard to quickly provide a source. This will prevent me from spreading misinformation and help the people interested in the question. And I provided a source for every statement. How am I the confined idiot when I am just quoting from publications?!

you know that apparent confidence I get besides my biochemistry and pharmacy degree, is countless discussions with medical professions who did not give me a proof of their claims. and choose to ingore all the studies that I provide. how do you think shall I proceed in getting wiser?


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(Why) are polar bears more common in Labrador than in southern Greenland?
The Labrador Sea is between Greenland, Labrador, and Qikiqtaaluk:

Map source.
A Greenlandic source on polar bears states:

In Greenland the polar bear lives and breeds in the northernmost parts of West Greenland and in Northeast Greenland, but is also occasionally seen elsewhere in Greenland, as it moves with the drifting ice.
However, it is extremely rare for either local inhabitants or tourists to see a living polar bear. The chances of seeing a polar bear are greatest when sailing by ship along the coast.

On the other hand, Parks Canada for Torngat Mountains National Park (northern Labrador) states:

Polar bears are true carnivores and can be a significant risk to human beings. Visitors travelling and camping in the park are in polar bear country and are at high risk of encounters. Polar bears are almost always present along the north Labrador coast.

The observation that polar bears are more common in Labrador than in southern Greenland is supported by Derocher (2010), Nature:

Derocher (2010), Nature
Polar bears like the sea ice edge, but this is very far from either Labrador or Greenland when at its fall minimum.  When sea ice is at its spring maximum, both Labrador and almost all of Greenland are packed deeply in ice (see maps below).
Then why are polar bears so much more common in Labrador than they are in southern Greenland?  Arey they really?  And how do they survive all summer long, when the sea ice is very, very far away?  The occasional tourist might not be enough, I guess.

Arctic minimum sea ice from NSIDC

Arctic maximum sea ice from NSIDC

(I was hesitating between Biology and Earth Science for this question)

I'm not a polar bear biologist, but Labrador has trees and caribou and things, while Greenland has a lot less of those things. Labrador has 150 forest fires a year, but searching for 'greenland forest fires' mostly turns up ash from other places landing on Greenland. Labrador has a higher carrying capacity for large predators, I guess. On the other hand polar bears eat seals? I've heard that. So. I guess 'food' but I'm not sure.

@Resonating It is true that Greenland is almost completely treeless, whereas Labrador has forest — but the forest is mostly inland.  Inland forest is not a natural habitat for polar bears.  Also, as far as I know, Labrador polar bears are mainly in the north; see for example the Torngat Mountains links.  The Torngat Mountains don't have a lot of trees.

Then I officially have no idea. Excellent question!

I think the lack of sea ice coverage would point you somewhere- even with the maximum sea ice coverage picture, the SW corner of Greenland has next to none, which may impact the carrying capacity for both bears and prey animals on that narrow strip of land between the ice cap and the sea- less space and less things to hunt, less ways to get around, etc. And then there's not much continental shelf over there, either.
Labrador is surrounded by more continental shelf, which might contribute to higher levels of sea ice at high levels and greater seasonality. Might lead to more prey?
This article might get you somewhere:Polar Bears in a Warming Climate

Hmm.  But during maximum sea ice coverage, polar bears are hibernating, aren't they?

Polar bears don't generally hibernate- they need the sea ice to hunt seals (ambushing them at their breathing holes, for example).
See: "However, polar bears, with the exception of
pregnant females, do not hibernate like other bear species, they rather roam the ice in search of seals in winter (DeMaster and Stirling, 1981)." From Lennox and Goodship, 2007

The pregnant females tricked me!


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Salvaging a plasmid from a cell culture stored at the incorrect temperature
I have E. coli with transformed plasmid on agar in a vial.  It has been stored at -20 degree C without glycerol stock for 18 hours.
This is a continuation of: Survival of E. coli on agar plate at -20 degree C without glycerol stock
I have transfered this vial from -20 degrees to 4 degrees after 18 hours when I determined that I had made a mistake. Since this is a very important vial and I don't have another one, what should I do in this stage?
What is the procedure for saving the plasmid if I am unable to save the whole cell?

I would rinse the cells off the agar using a small volume of LB or similar rich medium. Then use a small aliquot (10 μl) to inoculate a 5 ml culture under selection to see if anything will grow. Meanwhile the remainder of the cell suspension from the vial can be used as input for your favourite miniprep procedure.
If necessary, the DNA that you recover should then be used to transform a suitable E. coli strain. Don't bother trying to analyse the rescued DNA first since polysaccharide contaminants from the agar will probably inhibit any restriction enzyme that you might use.
Good luck!