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Why do redheads tend to sunburn more easily?
Reading Marion Roach's book on redheads she mentions visiting Rees lab where he shines UV light on her skin. Apparently this is an ongoing experiment of his regarding the propensity of redheads to sunburn more easily, but the book doesn't adequately explain why.
Why do redheads sunburn more easily?

Can you please stick to this edit, despite what the author wrote?

@R.M. Oh my,  all those references to fights and wars. Wow. This is not a fight, let alone a war. I'm just trying to keep posts as civil as possible. Some terminologies may be deemed offensive by folks. That's all.

@R.M - I was talking about keeping posts civilized. I've never accused anyone here.  You are the one that seems to take things personally and sticking labels such as 'accuse' ,  'fight', and 'war' on simple semantic changes. Dude. Relax.

@AliceD Whatever. I still maintain that if you and/or Chris believe that using the term "redhead" is "insulting" or not "civil" (your words, not mine), it's incumbent on you to back that assertion up.

You should have a look at wikipedia > melanin.

Melanin is a broad term for a group of natural pigments found in most organisms. [..] Melanin is an effective absorber of light; the pigment is able to dissipate over 99.9% of absorbed UV radiation.1 Because of this property, melanin is thought to protect skin cells from UVB radiation damage, reducing the risk of cancer. Furthermore, though exposure to UV radiation is associated with increased risk of malignant melanoma, a cancer of the melanocytes, studies have shown a lower incidence for skin cancer in individuals with more concentrated melanin, i.e. darker skin tone. Nonetheless, the relationship between skin pigmentation and photoprotection is still being clarified.

Most of the variation in skin color among humans is caused by differential levels of melanism. People with red hair have a low level of melanism (almost by definition) and therefore suffers more from sunburn than people with more pigmented skin.

The more important thing is that Melanin is formed through evolution due to Darwinism. If you lived in places which didn't get much sun you went whiter and sunnier places darker. Over generations of darkening the skin took on a darker pigment to protect itself by production of structures within the cell that was compatible with those energies to prevent deterioration and provide a medium to equalize the energy flow from the sun (Basically one of the many ways evolution was proved by sequencing ecoli strains and exposing them to synthetic sweeteners so that we could sequence the DNA structure during the evolution process). Basically the stronger you are and more adapted you are to the environment the more likely you will reproduce and propogate your characteristics. If you are whiter you required more Electromagnetic energy absorbtion for other processes so you gained characteristics that would enable that flow of energy.

This does not answer the question. And: Melanin doesn't reflect the energy, it absorbs it.


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What can cause incompatible sticky ends to be ligated?
Actual question
I have reason to believe (details see below) that in a ligation I carried out, an EcoRI sticky end (EcoRI: G'AATT_C) and an XmaI sticky end (XmaI: C'CCGG_G) were somehow ligated together, a process during which at least the EcoRI site was lost: the plasmid had a BamHI site very near the XmaI site, and a BamHI/EcoRI digest produced only one band compared to three bands in the undigested control (three conformations of circular plasmid).
How could ends as incompatible as EcoRI and XmaI be ligated?
Detailed Background or: Why I believe incompatible sites were ligated
This is chronologically further to: What are common causes of unexpected ligation products?. Briefly: I digested two plasmids, one with EcoRI and XmaI (p1), the other with EcoRI and AgeI (p2) [XmaI and AgeI produce compatible sticky ends], then carried out a ligation between a 1.4kb insert isolated from p2 (structure EcoRI-1.4kb-AgeI) into the 3.4kb backbone isolated from p1 (structure XmaI-20bp-BamHI-3.4kb-EcoRI). After transformation, I tested the ligation product by digest with EcoRI and BamHI, which should produce again 3.4kb + 1.4kb. The gel was poor quality but allowed the conclusion that there were different ligation products.
Repeating the EcoRI/BamHI digest and gel more carefully showed there were only two variants: Variant A (8 colonies) produced the two expected bands 3.4kb and 1.4kb. Variant B (4 colonies) only produced a clear 3.4kb band, nothing else visible in the lane: in other words, it only carried either an EcoRI or a BamHI site and was in total smaller than variant A (confirmed by undigested controls). Thus, I conclude that B was simply the same 3.4kb backbone, re-ligated without the 1.4kb insert. Since the BamHI site was untouched in the backbone during the preparatory EcoRI/XmaI digestion, I assume that the EcoRI site was not recovered during the ligation of variant B.
(The ligation was carried out overnight at 16 deg C, using Promega T4 DNA ligase and buffer and a molar ratio of 3:1 insert:vector at a total volume of 20uL. The E.coli for transformation were Invitrogen OneShot Stbl3 and have been routinely and successfully used in the lab for a long time. The analytical digestion used Promega EcoRI and BamHI in Buffer Multi-Core, which Promega claims offers 75-100% efficiency for both enzymes. Incubation was 1.5h at 37°C.)

incomplete digestion is one factor.

Incomplete digestion at what point do you mean? If the backbone (p1) was incompletely digested before the ligation, it should have produced a larger band than the one which I excised from the gel. If the analytical digest after ligation was incomplete, I would expect to see at least faint bands in addition to the one clear band corresponding to the backbone size.

well.. if you can provide the following details then it will be easier to troubleshoot:
1. The distance between EcoRI and XmaI site, 2. How was the double digest performed

Thanks for the hint. I added those and rewrote the description a bit, hopefully that's clearer now.

So in p1 the dropout after restriction will be 3.4 kB; A 3.4 kB difference will clearly help to differentiate between the single digest and double digests. So it seems it is not a problem of incomplete digestion. However, EcoRI and XmaI are not really compatible in a double digest experiment and sequential digest is advised. But if you anyways got the fragment of right size then it means double digest happened. How self ligation happened despite incompatible ends; perhaps due to a rare event of end joining post transformation. Just a blind guess.Anyways what was the self ligation frequency?

We actually digested EcoRI and XmaI twice using different buffers (B and MC) to see which worked better, but the results were pretty identical (and two bands easily distinguishable) so it seems that was fine. I analysed 12 of the 22 cultures on my plate, and of those 12, 4 (33%) carried the short re-ligated variant B. That seems a lot to me for a rare event.

The answer from @Armatus got me looking at star activities again. EcoRI is prone to exhibit star activity in non-optimal buffers. In the case of this enzyme this tends to be a relaxation of site specificity, so HAATTC and GAATTD would be possible cut sites. The cleavage at such sites produces the standard sticky end.
So, what if there is a star site near to the XmaI site such that a digest at the true EcoRI site and also at the star site removes the XmaI site and so allows recircularisation. If the configuration was, for example:
....GAATTC.................[XmnI].GAATTD...GGATCC....
the ligated product would have neither EcoRI nor XmnI sites.

Sounds like a valid explanation and is probably not even too unlikely. Unfortunately I haven't got access to the plasmid sequences anymore so I can't verify it :(

I want to add an extra explanation.
By personal experience I can tell that incompatible sticky-ends can ligate in some conditions. The efficiency will be lower than using compatible ends but still, some molecule will ligate if the single-stranded ends can anneal just enough for the ligase to join the DNA backbone. This can especially happen at lower temperatures where the miss-annealing of the sticky ends is more stable than at higher temperatures.
The OP states:

The ligation was carried out overnight at 16 deg C.

This condition is enough to allow incompatible sticky ends to anneal often enough to get ligated.
I propose the OP to run a comparative experiment to check the efficiency of incompatible-ends ligation by running one ligation at 37C for 15min and one at 16C overnight. I expect almost no background ligation to occur in the first case.

Sounds like a viable explanation, unfortunately OP no longer has access to any of the reagents involved 8 years later ;) (not to mention I managed to not notice this reply for more than two years)

My best guess to explain this phenomenon has been spontaneous degradation of the sticky ends, followed by blunt-ended ligation.
Alternatively, single-stranded exonuclease activity either from a contaminating enzyme or from EcoRI/XmaI/AgeI could be imaginable. For example, using buffer Multi-Core is discouraged for EcoRI due to potential STAR activity - maybe it developed exonuclease activity and some plasmids ended up blunt-ended before the ligation.

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Is Human a race?
Is it correct to say that 'humans' are a race? Will it also include apes and chimpanzees?
Can I use the terms 'species' and 'race' interchangeably?

You should clarify what are your definitions of 'species' and 'race'. It's not clear whether you are asking about biological taxonomy where such category as 'race' doesn't exist, or about human categorization where it's pretty much social construct.

"Race" is a very informal and sloppy term that you would use below the rank of "sub-species", another vague and unrestricted term that I asked about a while ago. Species is much stricter and has some biological/taxonomical meaning.

The term "race" in biology
The term "race" is sometimes used in biology as a level of categorization below the species level. It is hence not a synonym of "species" but closer to a synonym of "subspecies". The term is however quite rarely used to my experience.
The term "race" in the popular literature
In the popular literature, the definition of the term "race" has varied quite a bit through time (see wikipedia > Historical race concepts). It also vary a lot through languages and cultures. For example, in french, the term "race" is generally understood as synonym of "species", while in english it is generally understood as synonym of "ethnic group". Below, I will focus on the english definition.
From wikipedia > race

A race is a grouping of humans based on shared physical or social qualities into categories generally viewed as distinct by society.

Hence, the term "race" (in the 21st century and in english) is often used as synonym of "ethnic group" (see here). Note that ethnic groups are defined very arbitrarily and have been defined much before we started to study the genetic structure of human populations. As a result the standard categorization of humans into ethnic groups only poorly represent the existing genetic diversity. For example, consider the categorization "Sub-saharan Africans, caucasians, Asians, Amerindians, and native Australians" referred to by
@Eff in the comments. In here, the category Sub-saharan Africans, in itself represent the majority of the genetic diversity among humans (I eyeballed this claim from figure 1 from Tishkoff et al. 2009)

It is hard to read the post here. It is a phylogenetic tree of human populations. The below two third of the graph contain only African populations. Hence the non-African populations are nested within the African tree (or in other words, "African" is not monophyletic). See also the post Human genetic diversity in Africa in comparison with the rest of the world. To be clear, I do NOT mean that the classical grouping of populations into ethnic groups does not represent any genetic structure, I only mean that those categorization were made somewhat arbitrarily and hence only poorly reflect the genetic structure of populations.
Keita et al. (2004) is a very good read on the subject.
Questions of interest

Is the concept of species somewhat arbitrary?

Yes, it is somewhat arbitrary. For more information, please have a look at How could humans have interbred with Neanderthals if we're a different species? .

Are there several species of humans or is there only one species of humans?

Have a look at Does it make sense to classify all humans in a single species?

Are there different "subspecies" of humans?

Typically, we do not consider subspecies of humans. However, this decision is somewhat arbitrary. The standard classification of humans into ethnic groups is only a poor representation of the genetic structure in humans. You will note that most of the genetic diversity in humans today is found in Africa only (see the post Human genetic diversity in Africa in comparison with the rest of the world).

Is it correct to say that 'humans' are a race? Will it also include apes and chimpanzees?

Humans are usually considered a species. Other great Apes such as Chimpanzees for example are considered a separate species from humans. Some people consider neanderthals as the same species as humans but different subspecies hence calling neanderthals Homo sapiens neanderthalis instead of only Homo neanderthalis. When considering neaderthals a subspecies of Homo sapiens, we necessarily need to consider humans as a subspecies, then called Homo sapiens sapiens.

Is Human a race?

Humans are generally consider a species (or sometimes a subspecies). The term race, when used in humans is generally used to mean ethnic groups.

Can I use the terms 'species' and 'race' interchangeably?

No, you probably should not. While the term "species" is a somewhat arbitrary concept, it is a concept for which scientist work an agreement based on empirical data. The concept of race on the other hand is often used with very different definition by different people, when used in humans and in english, it poorly represent the genetic structure of populations. Also, the term "race" never really mean "species" to anyone. It either mean something like "subspecies" or something like "some arbitrary grouping" (aka. ethnic group).
On a personal note, I tend to avoid the term "race" as I prefer use the concepts of "ethnic groups" (when dealing with the arbitrary categorization of humans into groups), "subspecies" (when dealing with commonly agreed upon subspecies based on empirical data; there are no commonly agreed upon subspecies in humans), or "species" (when dealing with notion of reproductive isolation) instead so that my interlocutor has a better understanding of what I mean.

Good answer generally, however there are a few things that I think are misleading. "In other words, the standard categorization of humans into races (or ethnic groups) has very little biological basis to it and poorly reflects the reality of population structure." This is false or at least misleading. Self-identified race maps almost perfectly on to genetic clusters as they come out of cluster analysis. If you're talking about the "classic" major races such as Sub-saharan Africans, caucasians, Asians, Amerindians, and native Australians, then genetic clusters fit very well.

While I strongly agree that subspecies has a somewhat arbitrary feel to it, this is just as true for other animals than it is for humans. The reason that humans aren't generally categorized into subspecies while other animals are, is not because of a biological reason. There are many species that have recognized subspecies which have less genetic diversity, less phenotypic diversity, much overlap/continuous variation, etc, and yet have recognized subspecies. It's mostly just not done for humans because it's a socially controversial thing to do to split humans into groups.

@Eff  Thanks for your comments! I tried to clarify what I meant. Please let me know if it sounds correct to you. I have no opinion about your claim There are many species that have recognized subspecies which have less genetic diversity, less phenotypic diversity, much overlap/continuous variation, etc I imagine it is likely true but I do not know a good way to make this comparison (or do not know the literature well enough) to include that in my answer. I'll just leave it with Typically, we do not consider subspecies of humans. However, this decision is somewhat arbitrary.

I think your answer is good, and I agree with most of what you say. I think that species and subspecies are concepts that can be useful, so I don't advocate for never using them, but there is no doubt that they are quite fuzzy concepts (especially subspecies).
When I say that classical racial groupings map well onto genetic clusters, I'm saying that there are many studies that have investigated to which extend there is concordance with self-identified race and best-fit genetic cluster. What you tend to find is that there is near 100% agreement, at least 95%.

@Eff this is not an attack, I am just genuinely interested: is there a citation on hand for these?

@NatWH Sure. There are many studies testing how well best-fit genetic clusters match self-identified racial group. So many, that I won't be able to fit the citations of the individual studies in a comment. Instead, see Neven Sesardic's article Race: a social destruction of a biological concept, where he cites some of the studies testing the accuracy of cluster analysis. If you want just a single example of a study, see e.g. (Bamshad et al, 2003).

@NatWH In the study that I referenced (i.e Bamshad et al, 2003), they test how well the three classic "racial" groups, namely Sub-saharan Africans, Asians, and Europeans, fit genetic clusters (The clusters are made independently without any prior knowledge of where the individuals come from). A quote from the study that I referenced : "When data from all 160 loci were used, the mean correct assignment to the continent of origin increased to 99%–100%."

I'm curious, though: Couldn't you potentially call each node in the above tree - perhaps up to some reasonable limiting depth - a "race", and thus bigger (or "macro") races split into smaller (or "micro") ones, and moreover argue that perhaps this is the most biologically reasonable definition of race ... while of course acknowledging that it creates a crapload more checkboxes than any census form could reasonably accommodate and looks next to nothing like the traditional races of racists, but that's what happens when you use reality and not racist ideology as your basis?

Also regarding the other comments here ... there might not be an inconsistency between the two data sets/models. There is, if you look at the above tree-graph, a "Europe" cluster, i.e. a node branching to European populations, also a "Middle East" and "East Asia" cluster, and a huge "West Africa" cluster. Keep also in mind most "Black Americans" are from West African origin. So there are actually four clusters that decently approximate the four "United States Racial Hierarchy Races", and thus having "Self-Identified Race/Ethnicity" match clusters is not wrong.

The trouble is that they are at different nodal depths, and there are larger groups that also include some of, but not all of, groups corresponding to what may have been lumped under a different heading in trying to fit everyone to the US Racial Hierarchy Model. Such as all Africans as Blacks, which actually by this nodal classification would necessitate taking almost everyone as Black since Europeans are filed under East Africans as a sub-group! (The only ones that would not be would be those two green lines on the bottom ... and I can't read the labels.)

In other words, this picture both supports and rejects the "traditional racial model" used in the United States. As with sooooo many things, the truth behind these matters is not entirely what either set of duelling, polarized, and ideological partisans want to make it out to be.

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Do other animals have similar blood types to humans?
I am interested to know if there are any animals having blood groups similar to human blood groups? Is it possible to transfuse blood between humans and those animals?

You might want to have a look at wikipedia > Blood Type (non-human).

One of my cats needed several blood transfusions due to low hematocrit levels, and, yes, blood typing was involved.

I have now added an answer to the 'original post' which includes some information about cats. You will see from that that if your cat is cat-type B any human blood will contain antibodies to the N-glycolylneuraminic acid on its erythrocytes and so will be rejected. I'm not sure what the situation is if your cat is cat-type A. Also I'm not sure if cat erythrocytes have one of human-H, -A or -B antigens (they are not polymorphic but they have the ABO gene), which would also have ramifications with different human blood types. Somebody must know, but I can't find it on the web.

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Is it possible to affect a brain with electromagnetic waves?
A human brain can generate electrical signal. So it generates magnetic field as well. Is it possible to affect a brain with electromagnetic waves?

Sorry... your post is incomprehensible in its current state.  What exactly are you trying to theorize can be done, and what do you mean by "mind connect with EM wave controlling device"?  Please clarify.

Yes.  As a trivial example, put the brain in a microwave oven and cook it :-)

One can use transcranial magnetic stimulation to modulate neural activity. This is effectively inducing a current in the tissue under a magnetic coil.


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Selective breeding and Mutagenesis
I am writing an argumentative essay in which I claim that GMOs are safe. I know, it is not proved, but for the sake of my course I want to prove it. The counterargument that my professor said to me is that genetic modification is not like selective breeding. GM brings changes faster and most of the cases it is inevitable. We don’t know the consequences and they can be bad. On the other side selective breeding is changing the organism slowly and something bad can be prevented in the start of its development. What are disadvantages of selective breeding to compare with genetic modification? Can I use the mutagenesis as the example of selective breeding and use its cons?

Yes, GMO are safe to consume! See Is Genetically Modified food safe to consume?. Now, there are other (potential or real) issues related to the use of GMOs such as for example a loss of genetic diversity if every farmer plant the exact same strain. Talking about such issues will require talking about ethics, economy and sociology and it can therefore not be answered in a science website only.
Your teacher's argument does not make much sense (although a direct quote would have been helpful). GM plants also have to develop. They are organisms too!

[W]hat are disadvantages of selective breeding to compare with genetic modification?

Keep in mind that it is practically impossible to define GMO. Many of the things that we would call GMO actually don't result from much more than just selective breeding. Following this logic corn, wheat, sunflower oil, lettuce, broccoli, cauliflower, peanuts and pretty much everything else you eat is a GMO.
Attempting to let aside the semantic issue a comme argument is a lack of lack of familiarity and this is why extra precautions and testing must be done. See What risks exist with GMO, but not with selective breeding?

can I use the mutagenesis as the example of selective breeding [..]?

Mutagenesis and selective breeding are two different processes (although often used together). One is not an example of the other.


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Bacteria resistant to antibiotics?
If I use antibiotic on a specific type of bacteria, some will survive because it is resistant. Was this bacteria resistant to this antibiotic before it was even used, or did the bacteria develop resistance after the antibiotic is used?
How or why some bacteria can simply mutate to form beneficial alleles which will help in survival and others can't?

Antibiotic resistance comes from selection pressure: any bacteria that are resistant will survive and replicate, so in the next generation of bacteria you will find more resistance.
Bacteria do not simply mutate to form beneficial alleles, the alleles or genes that confer drug resistance must already be in the population; by using antibiotics, however, you're killing off their competition by killing the bacteria that don't have the resistant allele(s)/gene(s).
It's very unlikely that one individual using one antibiotic for one illness will lead to detectable antibiotic resistance. However, antibiotics aren't used in just one individual: they are used repeatedly, in many individuals, often in multiple species, etc. It is this broad use of antibiotics over time that eventually "finds" strains that are antibiotic resistant. Once these strains with resistant alleles become more prevalent, it becomes more likely that they will be present in some quantity to be selected for in the future.

Not that you said otherwise, but I'd like to emphasize that there need not be a dichotomy between complete resistance and no resistance. Some population with partial resistance could have a selective advantage, especially if the antibiotic dose is low (or short), and then continue to mutate towards higher resistance.

@canadianer Of course, I think this is a fortunate case where we've actually picked a linguistically informative word as a scientific community: resistance refers to being less susceptible to the antibiotic, that is, resistant to it, rather than invulnerable to an antibiotic, and so resistance to a given drug can be on a spectrum. It could be thought of as just a shift in the LD50 for a given drug.

I think there is too much emphasis on alleles in this answer. Resistance to antibiotics is not a purely genetic phenomenon. Some cells may resist the antibiotic pressure through epigenetic mechanisms, e.g. upregulation of efflux pumps etc. There need not necessarily even be a specific mutation required.

@JoeHealey I'm not sure I follow. An ability to upregulate of an efflux pump is going to be due to some allele, an epigenetic mechanism is just that: a mechanism. If one organism has a different propensity towards epigenetic modification of an efflux pump, that's still an allele.

@BryanKrause an allele is specifically a variant form of a gene, but the efflux pumps (or whatever other mechanism we are discussing) may only be deployed differentially - any mutations arising (which isn't always necessary) need not even be in the gene, so calling this an allele isn't wholly accurate. So, one bacteria that is killed, may simply not have responded sufficiently to the selection pressure and therefore dies, whilst another cell survives. The response could be affected by any number of other things going on in the cell such as quorum signals, nutrient levels etc.

For me 'must already be' sounds confusing. When did 'already happen? Are you talking about already drug-resistant strain (if so - where did it come from?), or any mutation that happened to happen at moment when antibiotic was poured over, or, let's say, plasmid?

@JoeHealey We're talking about evolution of gene resistance, not the variables that affect survival of individual cells and cause not all cells to die exposed to the same drug. If it isn't heritable it isn't meaningful to drug resistance. The allele need not be in an efflux pump, it could be a regulator. I suppose using a very strict definition of allele you could say that "allele" cannot refer to insertions of additional genes, etc, but I feel like that sort of terminology is unnecessarily pedantic and leads people astray to the idea of "gene for A, gene for B."

@MaximKuleshov All of the above.

@BryanKrause I'd disagree with "if it isn't heritable, it isn't meaningful". With the question as posed, it is meaningful if it allows at least some cells to persist through that specific round of selection, leaving at least some of the population viable on the 'other side'. What happens beyond then is anyone's guess, but the population has survived, and will almost certainly have used many different 'dirty tricks' over as many rounds of selection as it takes in order to survive. You don't necessarily suddenly get resistance and have it hang around forever, its much more fluid than that.

@JoeHealey If it isn't heritable, no additional resistance is carried to the next generation, and no selection has taken place. What happens beyond then isn't just anyone's guess, it would be the only thing that matters (beyond the effects of the infection on the individual we're talking about). If the "dirty tricks" are heritable then there is some gene/allele there mediating that dirty trick. Even if it's epigenetic, as long as it's heritable it counts.

@BryanKrause from the perspective of any single cell, I agree. But from the perspective of a population persisting through selection, the resistance does not need to be inherited. It can re-emerge on each exposure (though I concede this is less efficient and therefore less likely). Selection has taken place because the population will have been bottlenecked by the fact that many cells will not have survived.

@JoeHealey Starfishes (at least some of them, not sure of the exact extent) can regrow limbs that are removed. We do not say that starfishes that do not have their limbs removed lack the arm regrowing trait just because they haven't had any limbs removed. A population that has an ability to upregulate a pump for resistance has a resistance trait that has to be encoded by some heritable factor. The difference between that population and a population that does not have that ability is a gene or allele.

I think that's a bit of a false equivalency, but perhaps we will just have to agree to differ on this one. I still believe that playing fast and loose with the term 'allele' is not a triviality - terminology exists for a reason.

Let us continue this discussion in chat.


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Which synamorphy evolved last
I know that if species are on the same height level, they existed at the same time and indicates extinction. Does that apply to synamorphy? Did hair and eggs with shells evolve at the same time or did one evolve last?

A cladogram does not indicate time. That would be a calibrated phylogram. We can tell from the above cladogram that the two synapomorphies "Hair" and "Eggs" with shells are the two most recent, and happened after all the other ones because cladograms do indicate the relative timing of events. However, knowing a bit about mammals, "Hair" is the more recent than eggs with shells. Actually, eggs with shells should be on the same internode as "Amniotic eggs" in this cladogram, because Montreme mammals had eggs with shells, which were lost in the most recent common ancestor of Marsupials and Eutherians (Primates and Rodents/Rabbits are both Eutherians). So "eggs with shells" came first.

Thank you very much Karl Kier. Lets say we didn't know which came frst (ignoring your explanation that hair is more recent than egg with shells). Would you be able to tell which came first, hair or eggs with shells, SOLEY, by looking at th cladogram (by comparing their respective heights on the cladogram)?

No. Cladograms are about relative relationships. So deeper in the tree is older, but by definition, sister groups (in this case Eutherians and Archosaurs) are of equal age. There is no estimate of branch lengths in cladograms. Its just not what they do. There are ways to estimate time with clock methods and models. But cladograms don't do that.

@KarlKjer I believe they are refeed to calcified eggs which synapids do not have.

@John Pelicosuars, and many if not all the extinct synapsid mammal-like reptiles (mammal ancestors) likely had calcified eggs, all of which are placed on this internode.

Do you have a source for that because I have never heard of calcified eggs for Pelycosaurs or synapsids. And that would be a pretty important discovery.

@John Interesting. I may have fallen prey to something I have always warned others against; assuming that pelycosaurs are like dinosaurs, when clearly they are not. However, it is safe to assume that they laid eggs on land. And turtles, crocs, and dinosaurs laid calcified eggs despite their phylogenetic distance. And Monotremes lay eggs. The cladogram said "eggs with a shell", which monotremes have. Why is calcification a critical part of that definition? I confess to not knowing if monotreme eggs are calcified.

calcification varies in reptiles, some including monotremes show none, others including turtles crocs and gekko show some calcification with varying degrees of thickness and structure, hard thick calcified eggs are likely unique to dinosaurs and their descendants birds. http://www.tandfonline.com/doi/abs/10.1080/08912963.2013.829824?src=recsys&journalCode=ghbi20


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Is egg white lysozyme different from bacterial lysozyme?
Someone told me that microbial lysozyme has effect on gram negative bacteria but egg white lysozyme only affect gram positive bacteria. Is it true?

I searched about documents to prove that but i can’t find any one


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What do the letters 'p' and 'c' mean in mutation descriptions?
Example:

NM_000525.3(KCNJ11):c. 67A>G ( p. Lys23Glu) AND Permanent neonatal diabetes mellitus

Does "p" stand for "polymorphism"?
What does the letter "c" stand for?

I think c refers to cDNA and p refers to protein. Similarly there is g which most likely refers to genomic DNA.

You could check the whole HGVS guideline http://varnomen.hgvs.org/ for explanations (also @WYSIWYG is right).

According to the HGVS guidelines, a letter prefix should be used to indicate the reference sequence used. Accepted prefixes are:

“g.” for a genomic reference sequence
“m.” for a mitochondrial reference sequence
“c.” for a coding DNA reference sequence
“n.” for a non-coding DNA reference sequence
“r.” for an RNA reference sequence (transcript)
“p.” for a protein reference sequence


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Question about different gametes that can be produced
I have a question from a past exam that asks the following:
"For the organism of genotype AABbCcDDEe (homozygous for 2 genes, heterozygous for 3 genes), how many different types of gametes will be made if the C gene and the E gene are linked on the same chromosome while the remaining genes are all on different chromosomes?"
However, I have no answer key, and these answers are the choices:
A. 2
B. 3
C. 4
D. 8
E. 9
Here's my approach to the question:
We have 5 traits, and each trait consists of 2 alleles. To make functional gametes, each gamete must receive one of each allele so that it can survive. Clearly, for AA and DD, there's only one choice: A, and D.
However, for Bb, Cc, and Ee, things are a little different.
C and E are linked on the same chromosome. c and e are on different chromosomes. Therefore, a gamete can have either CE, or c and e. Similarly, a gamete can have either B or b.
Therefore, shouldn't we be able to create 4 different types of gametes?:
ABCDE, ABcDe, AbCDE, AbcDe
So wouldn't the answer be C. 4?
Please show me any mistakes I might be making, or any gaps in my understanding. This would be very much appreciated.
Thank you!

You are correct
Assuming that by linked, the question assumes perfect linkage (no cross-over ever happen), then your answer is correct! Good job!
Comments
Here are a few comments though...

We have 5 traits, and each trait consists of 2 alleles.

There are 5 loci. A locus does not necessarily match to a single trait and a single trait does not necessarily match to a single locus. Actually, it is very very rarely (if ever) the case.

To make functional gametes, each gamete must receive one of each allele so that it can survive.

This is not necessarily true. A "normal meiosis" (not leading to variation in copy number) may create a non-viable genotype and a "abnormal meiosis" (leading to variation in copy number) may create a viable genotype. But, it is true that we will only assume "normal meiosis" for this answer.

Hi there, thank you very much for answering my question and giving additional advice. Sorry that I couldn't get around to accepting your answer and giving feedback straight away. Your answer helped put these concepts I learned into greater context since it seemed like I had a kind of naive understanding of meiosis.


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Validity of Acoustic Weapon Effects on Biological Organisms?
There is alot of rather contradictory information present on the biological effects of acoustic weapons with a bevy of scientific articles claiming that they cause harm to biological organisms with effects such as nausia, gagging, and disorientation. These articles are mostly from older scientific articles and modern government scientific reports on the issue, and statements by military leaders overseeing the development of the weapons (including defence contractors). Contradictory claims are also being made by a multitude of scientific sources from a variety of different countries and backgrounds.
I am not sure which one is correct after reading about a dozen articles from both sides. Does anyone have any insight on this issue?
Of note, there are a multitude of crackpots and conspiracy theorists that believe that the acoustic weapons are real and can do outworldly things- the media seems to have bought into these speculations thouroughly and should probably not be trusted.
Here are two articles (one claiming they work and the other denying it especially pertaining to infrasound):
Bioeffects of Selected Nonlethal Weapons
Acoustic Weapons - A Prospective Assessment

technically a concussion grenade or even the bang part of a "flashbang" is an acoustic weapon.

There are a few things which can lead to miscommunication regarding the potency of acoustic weapons, but there are two main things to consider: source levels and duration.
Most organisms can tolerate loud sounds, within reason, for a short period of time. However, no matter how short, at certain levels acoustic weapons can cause temporary or permanent hearing loss, nausia, gagging, and disorientation.  Weapons with a lower source level played over a longer duration will be easier for organisms to initially ignore, but exposure to weaponized source levels over time will lead to internal issues with health, including a decrease in fecundity and nutrient digestion.
Often military and sometimes scientific reports will focus on one particular type of weapon used for a specific purpose, and deem its use acceptable or not. Many scientific studies take more factors or variations into consideration.
Ultimately, its risky because we don't have enough data about the long-term effects acoustic weapons can have on a population, and they also don't appear to be particularly effective when it comes to humans. The Acoustic Weapons (chapter 7) in 'Non-Lethal' Weapons1 by Neil Davison sums it up nicely.
Reference:
1: Davison, N. (2009). 'Non-Lethal' Weapons. Springer.

Welcome to Biology.SE! This looks like a good answer and it's great that you've provided a supporting reference. However, please include the complete reference information since links can (and do) break — for example journals may periodically reorganize their websites. One easy way to get that information is to search for the paper on Google Scholar and click on the ‟ symbol to get reference information. This is a good example of how to format references. Thanks!

Got it! Please see edit.  I hope that clear things up.

Yes that was better. (+1) I took the liberty of including the complete reference information since having the publisher can be helpful, but mostly to satisfy my OCD tendencies.

Thanks!  I see the difference now.


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What determines sex in birds?
Is there production of TDF in birds? If so which gene produces it?

Sex Determination System
Birds have a ZW sex determination system meaning that males are the homogametic sex. Or yet, in other words, males have two Z chromosomes while females have one Z and one W chromosome. You might want to have a look at Do males of all sexual species have Y chromosomes? for a short review of the diversity of sex determination system.
Dosage compensation
In birds dosage compensation exist but appear quite different than in mammals (Mank and Ellegren, 2009; Mank et al., 2011; Uebening et al., 2015; Naurin et al. 2009)
Sex determining locus
The DMRT1 gene on the Z chromosome appears to be important for male sex determination by affecting the testicular marker, SOX9 however it might not be the whole story (Smith et al. 2009). It is possible that several loci are involved in determining sex in birds.


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What's the relationship between oxygen consumption and ambient oxygen concentration for a lobster?
I was looking at a research paper by Thomas (1954) and came across a graph with ambient oxygen concentration plotted against oxygen consumption rate of a European lobster kept in water.

As we can see, this is a linear relationship, but I'm unable to figure out the reason behind this direct linear relationship.
I would be glad if anyone out there can suggest a possible reason, because just rote learning the graph is not something which should be done.

Did you read the summary? Given explanation seems legit to me: "6. Increase in oxygen uptake with temperature in sea water is mainly brought about by an increase in the gill ventilation rate. In addition, the degree of utilization increases. The relationship is a direct reflexion of the increased metabolic activity".

I read the summary and I understand why increase in temperature leads to higher oxygen consumption rate, but I can't figure out how oxygen consumption rate is dependent upon the ambient oxygen concentration.

That's how blood flow works. Gills are not 100% effective and can absorb only certain percentage of oxygen. So the lower oxygen concentration is the lower amount of oxygen is absorbed.

Now I understand. Thank you very much Maxim Kuleshov.

Increasing the ambient oxygen concentration increases diffusion of oxygen across the gills, thereby increasing the oxygen uptake by the lobster.
This can be proven by the fick's law of diffusion-
r=[-DA(P2-P1)/L]
L=thickness of diffusion membrane
D=diffusion coefficient
A=cross sectional area of diffusion membrane
P2-P1=pressure difference


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Can CRISPR-Cas9 make changes on a living organism?
Can CRISPR-Cas9 make changes on a living organism? What's the limit here? E.g. reversing/restoring hearing loss in a living adult mice.

Hearing loss is a particularly tricky phenotype to mention, because a) hearing loss has many many, sometimes unrelated, causes, and b) because hearing loss is often associated with death of cells that do not reproduce in adults.

Answer is yes, but it depends on which kind of phenotype you're going to restore/change. As you can imagine, using crispr cas9 on an high amount of cells require one condition: edited cells need to have a clear advantage in surviving besides the previous.
Here's an example of a crispr-cas9 protocol followed to restore a wildtype phenotype in adult mice.


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What spider is this? Is it dangerous to humans?
What is the species? Is it dangerous to humans?
I chanced upon this beautiful one near our water well. It stood at a height where an adult could accidentally walk through the web and the spider would land on one's face.
As a test, I dropped a piece of leaf onto its web, and the spider jumped to action, checking what it was and it took out the leaf from its web.
Size: Web, almost circular 50 cm diameter. Spider, about 8cm.
Location: Malabar region, Kerala state, south of India

Most spiders are harmless (unless you're a bug). Here are the medically significant ones.

Im in Kochi (same state in India) and I was told it would sting, so stay away. I also remember them as they appear to have only four legs (with claws) and jokes that they defy their very name, which means 8-legs in Malayalam.

This is most likely a spider from the genus Argiope, which has a few members native to India. See here for a list, I think this is most likely
Argiope pulchella, see the image from the Wikipedia:

Wikipedia also says that these spiders hunt insects, but are not dangerous for humans.

What are your thoughts about @Thomo's answer?

Its definitely an Argiope pulchella - Native to India, rather than an Argiope keyrselingii (Australian species). Either way, its completely harmless to humans, as are most spiders...


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BMI limits in interpretation in people with high/low heights
In a study, I measure BMI of a large sample of adult people.
Among them, there is some who have very low and very high height.
As I can read on the internet (like here or even in the wiki, for instance), BMI is not relevant for very short or very tall people.
Some math professor even wrote an article with a "better" calculation of BMI, but with a very low impact in science world (didn't find it on pubmed) so it's not really peer-reviewed.
Let's take some examples, assuming "normal BMI" is 21:

for a 110cm tall adult, ideal weight is 25kg
for a 130cm tall adult, ideal weight is 36kg

These weights appear really low to me. Note that dwarfism cutoff is 145cm in France.
My question is then the following: How could I choose a cutoff on height to exclude BMI values ?
NB: I didn't find anything on pubmed nor on google scholar, but maybe I missed an important article

I don't really know much about this subject, but I doubt there is a precise cutoff. Isn't it simply a continuous thing? Gradually, the more you move away from mean height (in either direction), the less value the BMI measurement has. One thing you could do is a weighted analysis, with more average height people having heigher weight.

I don't think this has been studied this precisely but I agree, it should be continuous. Still, I guess it is not linear (x3 maybe?), so there should be a value or a range of value where it become reasonable to think BMI is not relevant anymore.

The best procedure is going to depend on what exactly you're going to do with your data. Regardless, you should NOT exclude the BMI values. Just include the height, weight, and BMI. If you're simply reporting BMI as a characteristic of your study population, you can annotate that figure and let your reviewers and readers decide what to make of it. This follows the principles in Chapter 4 of Hulley's Designing Clinical Research. You want to get and maintain all the data.
If you're going run some further analysis on BMI, or if BMI is an outcome in your study, then you can evaluate the impact of a cutoff on your results, but you have to decide ahead of time how you'll do your primary analysis. I recommend using the entire data set (no height cutoff) for your primary analysis (because *there is no established practice for a BMI height cutoff in the general medical literature), and then running a secondary analysis that excludes those research subjects above some threshold (you can pick it, but depending on the size of your sample, 2 standard deviations could be reasonable). That secondary analysis would be a hypothesis generating analysis. If excluding very short and very tall people changed the results of your analysis, that's something to mention in your discussion and something to consider for the next study.
*If you're in a specialized field, then follow the practice of that field for your primary analysis.

Very interesting answer. Keeping height along with BMI is a very good idea. Still, I don't understand why excluding people is such a bad idea. My outcome is overweight and I don't have any other measurement than BMI to assess it, but I know BMI is a bad overweight assesser for very short people. Thus, by keeping short people in my analysis, I think I'd induce bias (I would not really measure my outcome for this very population), wouldn't I ?

If you're not going to apply your results to people below a certain height, then you have an excellent argument for excluding those people from your study. I was under the impression you already had the data and it included people who were very short (who, presumably, had other measurements taken that were used in other parts of the analysis).


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Irradiation positive effect on humans?
In research paper Euphytica 135: 187–204, 2004 it is written that:

434 mutant varieties of rice have been released with improved characters such as semi-dwarf height,
  early  maturity,  improved  grain  yield,  disease-  and
  cold-tolerance, and improved grain quality. Of these,
  225 (56%) were induced with gamma rays, 16 with X-
  rays, 7 with fast neutrons and 12 with other radiation
  sources

So I can see that irradiation may have positive effects on plants' genome.
Is there any information that mutations induced in this way in humans were beneficial for them? Can irradiation have positive effects on your body?

Regarding your first question, I don't know of any instance in which irradiation was used to select for a beneficial trait in humans. I italicized 'used' because I think that you could argue that naturally occurring sources of irradiation have led to the selection of traits that protect us from radiation damage.
That might sound like a bit of a circular argument, but keep in mind that in the case of the rice you mention, the discovery of beneficial traits came at the expense of a lot of dead rice that suffered deleterious effects of radiation. Unfortunately, the deleterious effects are a lot more likely to occur than than any really useful ones.
That leads to your second question. Conceivably, radiation could lead to a beneficial mutation. However, there are some pretty big caveats with that. First, in order for it to be beneficial, this hypothetical mutation would have to occur very early on in development, otherwise it would be limited to, at best, a handful of cells, probably in your skin, which would just get sloughed off anyway. So the second caveat is that in order for such a beneficial radiation-induced mutation to occur in the right place at the right developmental time, it would have to penetrate all the layers of your mother's genetic material that separate your fetal cells from the outside world without losing the energy needed to damage your DNA.
I couldn't tell you what sort of radiation might be capable of pulling that off with what probability of success, but my guess is that it's really unlikely.


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Does Alzheimer affect more than day-to-day memory?
I know that Alzheimer's damages a part of the brain called the hippocampus, which has a central role in day-to-day memory.
But, could it affect also on things in other memory centers, things such as taste and moves?

Oh, yes, though short-term memory loss is often an early sign.
"For many, decline in non-memory aspects of cognition, such as word-finding, vision/spatial issues, and impaired reasoning or judgment, may signal the very early stages of Alzheimer’s disease."  from https://www.nia.nih.gov/alzheimers/publication/alzheimers-disease-fact-sheet.  Warning: grim.
Whatever your brain does, Altzheimer's eventually undoes.  For more details:  http://www.alzheimers.net/stages-of-alzheimers-disease/

"For more details:www.alzheimers...". Just in case the link goes dead, could you summarize those details.


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Plastid and mitochondria
I am not a biologist, so please bear with me for this basic question. Although I tried googling, I am confused.

What is the difference between plastids, chloroplasts and mitochondria?
Are there any plant sequence databases for each of them (plastid, chloroplast and mitochondria)?
Can we separate chloroplast, mitochondria, plastid sequences from whole genome assemblies?

What is difference between plastid, chloroplast and mitochondira?

Plastid is a general term for an organelle which consists of Chloroplasts, Chromoplasts, Leukoplasts/Amyloplasts and Apicoplasts.
Chloroplasts (Chloro = green) are involved in photosynthesis; they express Chlorophylls and have the thylakoid structures which are involved in the electron transport chain that results in ATP formation during the light reactions of photosynthesis. As it is obvious chloroplasts are found in the green parts of the plants such as leaves. Chloroplasts also have the enzymes of biosynthetic pathways involved in carbon fixation.
Chromoplasts (Chromo = colored) express more of other pigments and less of chlorophyll. Neither do they have thylakoid structures. Therefore they are not involved in photosynthesis. When fruits ripen, the chloroplasts differentiate to chromoplasts. Flowers also contain a lot of chromoplasts.
Leukoplasts (Leuko = white) do not have any pigments and usually carry out biosynthetic processes. When they store starch they are called amyloplasts.
Apicoplasts are found in parasites like plasmodia (causes malaria) and are vital for their survival. The Apicoplast is involved in biosynthetic pathways but the precise importance of it remains unknown.
The mitochondrion is a very different organelle and has a different evolutionary origin. Mitochondria, like Chloroplasts, produce ATP from an electron transport chain but use chemical substrates (NADH, flavin etc) rather than light as a source of initial energy. Mitochondria are thought to be an outcome of an endosymbiosis between an ancestral eukaryotic cell and an $\alpha$-proteobacterium. Chloroplasts, on the other hand have descended from a Cyanobacterial endosymbiont. Therefore the structure of mitochondria is very different from that of chloroplasts.
Chromoplasts, leukoplasts, amyloplasts and apicoplasts have lost the photosynthetic ability. Similarly, there are variants of mitochondria which use different electron acceptors (other than oxygen) and some are just incapable of ATP synthesis.

Are there any plant sequence database for each of them (plastid,
  chloroplast and mitochondira)?

Chloroplast genome database: {link}
I don't know of a separate plant mitochondrial database but you can see this resource called MitBASE.
NCBI also has the organellar DNA sequences.

Can we separate as chloroplast, mitochondria, platid sequence from
  whole genome assembly?

Usually the organellar genomes will assemble as separate contigs when you sequence from the whole cell DNA prep. By homology it is possible to say if the contig is a mitochondrial or chloroplast DNA. But the best way would be to experimentally isolate the organelles and sequence their DNA.


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Healing of Skin Superficial Wound
How does the body heal a skin wound without bleeding?
I had a wound in which thick layer of skin was gone and which was too painful to touch. I could see the wound secreting clear liquid rather than forming a scab like in a blood wound. What is this yellowish thick liquid being secreted and does it form new skin?

The clear/transparent fluid you are talking about, is most likely serum, an amber-coloured, protein-rich liquid which separates out when blood coagulates

Jordi Zambrino-Are there 13 proteins? can you name them.

@TheVoid What are you on about?

@Jordi Zambrino- Ill ask a question on it in a bit, It has to do with the 13 protein factors.

@uncia- Was the wound around the knee area?

How is this primarily opinion based? Just curious.

@TheVoid just above the just above achillies tendon, so whenever i walk wound would contract and expand and more clear liquid ooze out

@uncia- Yes the areas of the body where the fatty layer is thin or on a bone or tendon or cartilage this type of reaction will occur. I would suggest liquid skin ointment to seal it up because the healing process is prolonged and will open right back up if disturbed.

Skin is composed of layers, the uppermost being the epidermis. Upper layers of the epidermis (dry, flat cells tightly packed together, and of varying thickness on different parts of the body) can be abraded off, leaving deeper layers of the epidermis (nearer to underlying blood vessels) exposed. Since peripheral nerve endings do exist in this area, the wound is painful. A wound that does not extend into the dermis does not bleed (for example, a second degree burn can lift the upper layers of the epidermis from the deeper layers; no blood will collect in the blister, but the wound is painful. Peel off the top of the blister, and you have an analogous situation.

Because the surface of the skin is no longer present, fluid (as with a blister, not containing red blood cells) leaks from the blood vessels. Initially a transudate, it can also be an exudate. And, no, it does not contain the cells needed to regenerate the upper layers of the skin. It contains many of the proteins found in serum and may contain white blood cells which help to fight off infection.
New cells are generated from the deeper cell layers (the basal cells) which are still intact. They grow from the bottom of the wound up, so to speak. The scab formed by the dried fluid keeps the layer under it moist, providing a good environment for cell growth.
Epidermis and Its Renewal by Stem Cells


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Is the human ovum visible to the naked eye?
I'm a student in a field unrelated to biology or medicine, however I very much enjoy reading about it. I just read in Merck Manual that
Human cells vary in size, but all are quite small. Even the largest, a fertilized egg, is too small to be seen with the naked eye.
A very quick google search (caused by basic elementary school biology knowledge) results in Wikipedia article that says The egg cell is typically not capable of active movement, and it is much larger (visible to the naked eye)
Did I misinterpret something here, or I'm reading an unreliable source?
Merck Manual was reccommended for learning about these things since it's maintained by MDs so I was just wondering. Thanks!

The line that you quote from the Wikipedia page is talking about ova in general, whereas your question relates specifically to human ova. The "Human and mammal ova" section of the same article states that

The ovum is one of the largest cells in the human body, typically
  visible to the naked eye without the aid of a microscope or other
  magnification device.

With the stated average size of 0.12 mm in diameter (same Wikipedia article), an ovum is very, very small, but presumably a person can still see it unaided.


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Does atrophy of the thymus not effect T-cell selection and tolerance?
The thymus atrophies as age progresses. Does the T cell selection (which happens in the thymus) continue to take place? This doubt came into my mind because in the cadaver we dissected, the thymus was hardly more than scanty fibrous tissue. This definitely should have some effect on immune tolerance right? Is this the reason why the elderly are more prone to autoimmune diseases?
Or is it that selection happens only in children? This line of thought would pose a problem since T-cells are short lived and they continuously need to be produced. Or is it that the site of selection is shifted to some other place?
P.S. I am asking these questions assuming that selection is necessary every time new T cells are made. Correct me if this primary assumption is wrong.

T cells have a long half life (both naive and memory cells have halflives measured in years), especially when taking into account the fact that memory cells in particular can slowly proliferate and renew themselves.  An adult human therefore has 20-50 years' worth of accumulated T cells by the time they grow old, and those include both memory cells and naive cells that are potentially able to recognize new antigens. The thymus does continue to produce some new cells at a slow rate, but the backlog of previously produced cells are also able to monitor for pathogens.

Thanks! Just thought memory cells have long half live, dint know about the naive cells also being similar. So hematopoiesis in later stages of life wouldn't include T cell synthesis? or rather a decilne. Does creation of new leukocutes majorly mean, new non-lymphocytes?

@Polisetty if you have a new question, please ask.

@mattDMo the question is related to the answer he's given. Was just clarifying. I'll post if the answer doesn't turn up here :)


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Down syndrome in subsaharan populations
What is the rate of occurrences of Down syndrome in subsaharan African populations? Is it the same as in white European populations?
An interesting hypothesis came to my mind:
Could it be that Down syndrome is the result of interaction of different dominant or recessive Neanderthal or Denisovan genes that European and Asian populations cary in small percentages?

See UN > stats Down Syndrome per country.
What the data says
I have not made a proper statistical test (as I am too lazy to reformat the data in anything convenient to perform a statistical test) but the prevalence seems to be consistently around 0.12499% all around the world with very very little variance. I doubt there is any significant difference in the frequency of birth that have down syndrome.
As @Markonionini rightly noticed, these estimates of prevalance are slightly far fetch extrapolation and the UN specifically advice to consider them with caution. It is probably the best data we have though.
The hypothesis seems improbable to me
Do you have any good rational behind your hypothesis? Down Syndrom is typically caused by de novo mutations and not due to standing genetic variation (Veltman and Brunner 2012) so your hypothesis seems rather implausible to me.

Well, seeing only white people having Down syndrome, made me think in this direction. Other than that, I have no other arguments for this hypothesis.

Good answer. +1 Would also be weird to have this kind of ploidy polymorphism floating around in the population ... but this gives me an idea.

@AlexDeLarge Thanks.... but now we all want to know your idea!

@Remi.b totaly!

I invite whoever down voted to comment on the reasons. A down vote without comment does not help to improve a post.

@Markonionini and Remi.b, I posted this following that idea. I hope it is not too unclear.


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In theory how fast could nerve signals travel if the nerve fibre was perfectly insulated?
My question is purely theoretical and my main aim is to find out the maximum speed that a nerve signal can travel within a nervous system and and whether this speed represents the physical limit of how fast a nerve signal can travel. This could also extend to designs not seen in nature and possible artificially designed nerves i.e. synthetic biology. Apologies for an awkward question!! Any input is welcome!!

There are multiple factors besides insulation that go into electrochemical impulse speed. For example, the thickness of the axon also contributes very much. These links may interest you: https://en.wikipedia.org/wiki/Nerve_conduction_velocity http://biology.stackexchange.com/questions/21790/how-long-does-a-signal-from-the-brain-take-to-reach-the-limbs

For some background on saltatory conduction: https://en.wikipedia.org/wiki/Saltatory_conduction
I feel that a "perfectly insulated" neuron couldn't actually allow the signal to travel. Insulation (which, in neurons, is basically layers of fat wrapped around axons so ions cannot pass) allows the electrical signal to move further along axons (less ionic leakage) and faster (due to decreased membrane capacitance-it takes less charge movement to generate the same potential difference across the membrane; see this question: How is membrane capacitance related to the increased speed of saltatory conduction?)
Also, you should check out wikipedia's page on cable theory of neurons:
https://en.wikipedia.org/wiki/Cable_theory
This is why myelination increases conduction speed, as you may or may not already know. The increased length of the ionic signal (due to the inhibited leakage) allows voltage-gated ion channels which are further away to be activated as a result of any given local membrane depolarization. This all happens faster due to the lower capacitance.
However, the only way the action potential can actually "travel" at all is due to the sequential activation of voltage-gated ion channels along the axon. This is the case in both myelinated and unmyelinated axons, it's just that the spacing is greater when myelinated. In the insulated, fat-wrapped regions of axonal membrane, there are no ion channels, voltage-gated or otherwise. If there were, the layers of fat would not allow ions to pass through anyway at this point. Thus, the "perfectly insulated" axon could never actually propagate a signal, because the signal still requires the chain reaction of voltage-gated ion channel activation and sodium influx at some point. Myelinated conduction is faster because the spacing is increased, but increasing the spacing to infinity would not allow the action potential to be passed on.
I suspect that there is a certain threshold in the extent of myelination where the spacing between nodes of Ranvier becomes to great to have effective propagation of action potentials. I wouldn't be surprised if evolution has resulted i a relatively optimal spacing of nodes. I suppose a better question might be: what is the speed of conduction between nodes?
I suppose it would be possible to send current through a perfectly insulated axon and potentially activate a voltage gated calcium channel at the terminal. However, This would be different than an action potential and would be effectively reducing the neuron to an electrical wire. Sometimes it's better to keep things simple.

I think that by "perfectly insulated," the OP probably meant "optimally insulated," as in "what is the physical limit of how fast an electrical signal can travel through an axon with the best possible insulation?" (@MICHAEL TAYLOR, correct me if I misinterpreted your question.)

OK should I delete this?

No. You have a lot of good information here, I just don't think it's what the OP is looking for. You could just edit it. But wait for the OP to clarify his question before you change anything, it could be exactly what he wanted.

Thanks for your answer Jory and your comments @CDB. Your answer is what I was looking for! Its really thorough and informative and actually clarifies my chain of thought in regards to nerve conduction and its properties and limitations.


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What is rotational diffusion and lateral diffusion in plasma membrane?
There are no good reads on internet. The idea that I have formed so far of these topics, is that lateral diffusion is translational movement of protein in a leaflet.

From this paper, rotational diffusion describes the movement of a membrane lipid around its axis that is perpendicular to the plane of the bilayer, analogous to a person spinning around while standing up.
Lateral diffusion describes the movement of membrane lipids exchanging places with each other across a face of the bilayer, rather like two dancers spinning about their mutual center of gravity.


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Which is the proportion of metagenomics reads that cannot be mapped in any genome?
I was wondering if anybody knows how many reads from metagenomic or metatranscriptomic data do not map to known sequences and are therefore unidentifiable?
I found a figure for viromics, which seems to indicate that only about 6% of the sequences correspond to known virus (http://www.pnas.org/content/111/29/10714.full). But I couldn't find a more general percentage.

I think this will vary greatly depending on the source environment. Your example (marine viruses) is probably due to the large diversity of ocean viruses of which most have no reference genome.
Referencing the Human Microbiome Project:
A total of 57.6% of the high-quality microbial reads could be associated with a
known genome (ranging from 33–77% for anterior nares and posterior fornix, respectively).

Other papers describing more recent k-mer based approaches for classification report between 40-90% classified to a known reference. See:
http://www.nature.com/articles/srep19233
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4401624/


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How to predict the effect of a non coding SNP variant on the expressed protein?
I am writing a paper for non coding SNPs on patients with metastatic breast cancer. Having used a specific gene panel (NGS) of approximately 60 genes, I'm currently running out of ideas on what to write in the discussion section.
I am looking for suggestions based on somewhat efficient methods like a bioinformatics approach or specific textbooks revolving around RNA biology/biochemistry, in order to predict the outcome of non-coding SNP variants.
Some details:

The majority of the variants are intronic (~2300/3300), so I will mostly focus on splicing.
There are two commonly repeated SNPs in 3'-UTRs in over half of the patients, involving KRAS and CDKN2A.

A) Generate exon & transcript counts for your samples, library size + quantile normalize the data.
B) Group samples into variant/wild-type categories
C) Use wilcoxon's rank sum test to see if there are differences in exon inclusion or overall expression. Remember that 3'UTR variants can also imply differential degradation by miRNA. Tools like TargetScan can help you with miR-analysis.

You might be better off using something like DEXSeq to detect differential transcript usage

You could try DeepSEA. It uses deep learning approach to predict function of noncoding SNVs. They use ENCODE and Roadmap Epigenomics for chromatin structure learning, 1KG for nonfunctional SNVs, HGMD for noncoding regulatory mutations, GRASP (Genome-Wide Repository of Associations between SNPs and Phenotypes) for noncoding eQTL and US National Human Genome Research Institute's GWAS Catalog for noncoding trait-associated SNVs. 'Predicting effects of noncoding variants with deep learning–based sequence model' paper describes the whole pipeline.

I've checked this out before, but I'm mostly looking for a way to predict the length and probabilities (sequence too, probably) of individual transcripts stemming from the emergence of the alternative splicing sites (still based in machine-learning). Do you have any ideas ?


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Why all trees have cylindrical stems?
Why a huge number of  trees/plants have cylindrical stems? I have been told that this question's answer lies in Physics but I don't know where to find. Can any one help?

Short answer: not all do.  Many tree trunks are fluted, especially at the base.  Then there's the Blue Ash (raxinus quadrangulata) which gets its botanical name from its square stems.

@ jamesqf Thanks for reply. I have edited my question taking your answer in account. But your answer raises an interesting question , why * Blue Ash (raxinus quadrangulata)* is an exception?

1)
You know most bridges have vertical cylindrical pillars.
This is probably because cylinder is among the strongest 3D structures to support anything.
So, cylindrical trunk provide best support for tree crown.
2) Most accurate
It is natural for any cell to grow equally in all directions. This, leads cells to expand in all directions equally in a circular girth.
3)
Resistance
Cylindrical girth provides least resistance to air. So, tree naturally takes this shape to prevent damage by air strikes.
4) Read
 https://m.reddit.com/r/askscience/comments/1973mh/
for more info.
5) http://www.stevespanglerscience.com/lab/experiments/balancing-act-cylinder-strength/
for strength of Cylinders.

No. Most bridges do not have cylindrical beams. Angles, channels, built up girders seem most common for bridge beams.

http://www.stevespanglerscience.com/lab/experiments/balancing-act-cylinder-strength/

@curious_cat I meant pillar. Thiss was pillar I first saw on search. http://t1.gstatic.com/images?q=tbn:ANd9GcTQKaTDU7vmR-Q64HxUcE6MYmcPMj0abgeXiIzCvYpAQZGoOM97uYofoM8

I think you have the air resistance thing backwards.  Look at pictures of trees growing where there are strong prevailing winds (coasts, mountain tops, &c), and you'll see that they are markedly non-cylindrical.  The growth part seems intuitive: trees grow (in diameter) by adding to a thin layer (the cambium, IIRC) under their bark.  In the absence of any outside force, every part of that layer is likely to grow at the same rate, so you get a cylinder.

@jamesqf Trees in costal and mountains are rather more cylindrical and straight (less branched) than at plains. I am writing from my experience from Himachal, Jammu, Goa, and Mumbai

@Anubhav Goel: Do these places have strong winds coming from a consistent direction?  I see this along the California/Oregon coast, and in the Sierra Nevada and inland mountains.

@Jamesqf For Sierra Nevada , on googling, Trees were all cylindrical. For coast of California/Oregon , I found , yes they were much branched, bent and stooping, but all had cylindrical trunk.
Well, for me Goa/Mumbai have some gusty winds.

@Anubhav Goel: Well, all I can say is go and look.  Here's an example: https://en.wikipedia.org/wiki/Pinus_longaeva Or this: http://www.gettyimages.com/detail/photo/gnarly-foxtail-pine-in-the-high-sierra-royalty-free-image/575358267

@Jamesqf Look at these trunks you link more carefully. They are more or less cylindrical in geometry. Or what you suggest, is it cuboidal or triangular prism like or pyramidal?


text:
Cross section through the right arm question
Is the largest drawn vein on first attached pictue v. brachialis or did they make a mistake and it's actually v. basilica?
Picture 1: Cross section through the right arm (source: Thieme, General Anatomy and Musculoskeletal System, p. 296)

Location of sectional plane (picture 1):

Picture 2: A similar drawing from Sobotta (source: Sobotta, General Anatomy and Musculoskeletal System, p. 240) :

do you have better quality images? its very unclear

@rg255: I've added a better quality of picture 1, but I don't have a higher quality of picture 2.

@inferoanteriorly for that top figure, how far proximal on the arm are they? In my opinion – that should say basilic vein. However, the question isn't very clear as there's no cephalic vein on that image (like the lower image) – is that picture just more proximal than the lower? Where does the book indicate that that slice is through on the arm?

@VanceLAlbaugh: I've added a picture, which shows location of cross section from picture 1.

Based on the location of that cross section in the upper arm the vein in question appears to be the basilic vein. The basilic and cephalic veins are the largest veins (most of the time) in the upper arm. Here is a nice diagram from wikipedia that shows both. The cephalic vein is much more superficial than the basilic vein, as you can somewhat appreciate in the diagram below.

I think the label "brachial vein" is probably an honest case of mislabeling.
This is another figure that supports that vein in the image in the question as the basilic vein as well:

From this image (Gray's Anatomy), you can appreciate that the basilic vein is the large and deeper vein that runs near the brachial artery. In the case of many arteries and veins there are similar names, but that does not appear to be the case in this instance.

Clinical Correlate: In vascular and/or transplant surgery, when making an arteriovenous fistula for dialysis access (for kidney failure), there are a number of common routes of access. Two of the most common are the (1) brachiocephalic fistula, which is formed by surgically connecting the brachial artery to the cephalic vein, and (2) brachiobasilic fistula, which is created by connecting the brachial artery to the basilic vein. Some additional information and a picture can be found in this open access article from Maya et al entitled Outcomes of Brachiocephalic Fistulas, Transposed Brachiobasilic Fistulas, and Upper Arm Grafts .


text:
What does "generalisation" mean?
I am trying to understand a paper about ethanol: "Generalisation of ethanol with drug mixtures containing a positive modulator of the GABAA receptor and an NMDA antagonist" (Stolerman & Olufsen, 2000)
In the abstract it says,

"After drug-appropriate responding with the training mixtures reached 85%, generalisation to ethanol was examined in extinction tests."

I can't find a definition for "generalisation" in Google searches. What does it mean? I don't have a background in biology, so simple answers are preferable. Thank you.

Generalisation

Generalisation is the phenomenon of an organism responding to all situations similar to one in which it has been conditioned.

or

Not biologically differentiated or adapted to a specific function or environment

This means that  the the rats responded to ethanol the same way that they responded to the training mixtures.
Sources:

Mangan, G. L. The Biology of Human Conduct: East-West Models of Temperament and Personality. Oxford: Pergamon, 1982. Print.
"Generalized." - Memidex Dictionary/thesaurus. Web. 04 Mar. 2016.
"Generalisation." - Biology-Online Dictionary. Web. 04 Mar. 2016.

Thanks, but I'm still not sure I understand. If a rat is given substance X, which makes it drunk, and the rat becomes conditioned to seek out that substance, but then it also seeks out ethanol, is that generalization to ethanol? Generalization to substance X? Both?

@user22316 I'd assume that it responds to all situations as in responding to all situations similar to the one in which it has been conditioned.

Thanks, I might understand it now. A rat responds to ethanol in a particular way; it responds in a similar way to substance X; therefore, it is generalized to ethanol, i.e. it doesn't need ethanol per se, just whatever the effects of ethanol (and substance X) are. Correct?

@user22316 It means the rats responded to ethanol the same way that they responded to the training mixtures

Got it. Put that in an official answer and I'll give you the check mark.

@user22316 done

Ha, I didn't notice that you were the one who posted the answer. Thanks for your help.

@user22316 You're welcome!


text:
Brain capacity of Cro-magnon man vs Modern man
Cranial capacity of Cromagnon man was about 1650cc whereas average cranial capacity in modern human is 1450cc.
My question is, why during the course of evolution, a reduction in cranial capacity is seen ?

What you call brain capacity is actually called cranial capacity (see wiki). At the end of your question you seem to try to discretely assume that lower cranial capacity induces lower intelligence but it is not necessarily true. You might want to remove this assumption otherwise, the question might get closed as being primarily opinion based.

Stanyon et al. 1993 is probably a good reading on the subject.

Some of the possible explanations are summarized in Selection for smaller brains in Holocene human evolution. It's a blog post (but from a well-regarded anthropologist and heavily referenced), but I'll excerpt a few quotes here:

Less well known is that the terminal Pleistocene and Holocene (ca. 30,000 years ago to present) witnessed a substantial decline in endocranial volume ... This decrease of approximately 240 ml in 10,000 years is nearly 36 times the rate of increase during the previous 800,000 years.  ...

He considered one possible explanation, that the smaller brain size is due to smaller stature, and determined that it's not likely:

Here, I apply a quantitative genetic model to test the hypothesis that Holocene evolution of brain size may be explained by reductions in body size. ... The net change in endocranial volume, roughly 130 ml from the terminal Pleistocene to late Holocene skeletal sample would predict a reduction in stature of 13 cm, if the brain size had changed only because of correlated changes in stature. That degree of stature reduction is not biologically impossible although it would be extreme. ... The evidence suggests substantial reductions in brain size in some recent human populations, more than can be explained by correlated changes in body size.

He then lists six possible alternate explanations, which are not mutually exclusive:

Chance.
Plasticity.
Climate.
Nutrition.
Function.
Development.

He spends some time discussing each but concludes that at the present time the cause can't be definitely determined.
Here's his conclusion:

The available skeletal samples show a reduction in endocranial volume or vault dimensions ... This reduction cannot be explained as an allometric consequence of reductions of body mass or stature in these populations. The large population numbers in these Holocene populations, particularly in post-agricultural Europe and China, rule out genetic drift as an explanation for smaller endocranial volume. ... Therefore, smaller endocranial volume was correlated with higher fitness during the recent evolution of these populations. Several hypotheses may explain the reduction of brain size in Holocene populations, and further work will be necessary to uncover the developmental and functional consequences of smaller brains.


text:
Evolution of parasite into ideal parasite
An ideal parasite is a parasite which thrives within a host without harming it (according to my NCERT textbook).
Then, quite obviously, why hasn't that happened yet? I mean, natural selection can lead to such a species, which is beneficial to us and also, not at all detrimental to the parasite.

It has happened, many times; commensal and mutualistic species are common.  Mitochondria and chloroplasts, lichens, etc are examples.   But there is no specific reason, other than common misunderstandings of natural selection, to expect this to be inevitable.  You may want to explain your reasoning for that point (or put it as a separate question).

@iayork You are right. However, how are mitochondria and chloroplasts examples of ideal parasite? Also, which point are you asking me to explain?

Do you understand the current understanding of how mitochondria and chloroplasts arose? If so, please clarify why they don't fit your question.  If not, check wikipedia, linked above. The other point I suggest you explain separately  is your claim about evolution, which I believe indicates a misunderstanding of natural selection.

@iayork Yes, I didn't know about the current understanding on how chloroplast and mitochondria arose, so that's clear now. Also, edited the question!

Why are you asking why something didn't happen, then, when as you can see it has happened many times?  Is there more to your question?

@iayork I knew such species existed, but didn't think of them as an ideal parasite. Because, when you think of a parasite, lichen, mitochondria and chloroplasts are not the first things to come to your mind. You opened up my mind :D

@iayork I think you can make an answer by developing further your comment.

Related: Why do parasites sometimes kill their hosts?

There was a recent opinion article in science which hypothesizes that mitochondria and chloroplasts could have been parasites. In my opinion, the paper has a lot of incorrect presuppositions and also makes far-fetched assumptions. IMO, mitochondria and chloroplasts would have been preys and not parasites. Anyway, an ideal parasite is the one that survives anything. What your textbook says is one possible way by which it can do that. You should see the post that @Remi.b mentioned.

Post is related to Why do parasites sometimes kill their hosts? and I think duplicate of Why have parasites not evolved to be harmless?.


text:
The alignment of fingers in our hand
I noticed that in my hand the index and middle finger are aligned in one direction and the next two fingers somewhat in the opposite direction. My question is, why are our fingers aligned in that way?
Moreover, is it of any evolutionary significance?
For clarity, I am posting a picture of my hand.

I think (and only think) its more about physics than biology. Fingers are thick at bottom and thin at top, so all fingers make an angle with others when joined together. Also, if you have a look at anatomy of hand, you might get your answer (like http://i1.wp.com/scghed.com/wp-content/uploads/2013/12/Hand-anatomy.gif or http://www.visualdictionaryonline.com/images/human-being/anatomy/skeleton/hand.jpg)

@another'Homosapien' Even if you separate all the fingers, they still seem to bend in one direction(try it). So, I don't think it has anything to do with the angle between the fingers. Also, the images too don't explain much about the orientation even as they show that the fingers ARE oriented.

Please elaborate what you mean by 'bend in one direction'. I don't think that I really did get you on this.

@another'Homosapien' What I mean is, when the fingers are separated i.e. kept at some distance from each other the apex of the index and middle finger seems to be slightly bent in the left direction as seen in the image.

Okay, this doesn't seem to have evolutionary advantage. I mean, just think of a work which a person with "index and middle finger slightly bent in the left direction" can do better than person without it, and which would provide substantial benefit to person with "index and middle finger slightly bent in the left direction" ;)

@another'Homosapien' Agreed, they don't have any evolutionary advantage, but then why are they bent at all?

Well, we would need a second/third opinion from another expert to confirm that they aren't evolutionarily beneficial. For why they are bent at all, it could be a matter of chance (http://i1.wp.com/scghed.com/wp-content/uploads/2013/12/Hand-anatomy.gif and http://www.visualdictionaryonline.com/images/human-being/anatomy/skeleton/hand.jpg again).

Notice that it takes a bit of muscular effort to hold your hand flat like that?  Let everything relax, so your fingers are slightly cupped, and if your hand's like mine, the fingers will now be aligned.

This is normal, and the effect is accentuated dramatically if you pretend to be holding an imaginary round object (somewhat smaller than a baseball, for instance.) The fingertips will all approximately point towards the very end of the thumb.

(See upper right image.) If the stone were smaller, the effect would be more visible.)
This orientation of the fingers makes the hand and fingers extremely versatile, being able to grasp and manipulate objects of a wide variety of shapes.
It also allows fine manipulation of thumb and fingers. Touching each fingertip to the tip of the thumb quickly shows the same effect - the fingertips approximately align with the thumb. If they didn't align this way, we would lose some of our very fine (as in requiring great precision, not as in quality) motor skills.
I'm not going to hypothesize on why the hand evolved the way it did; it's very efficient and that seems reason enough.

Is it always the case? Do all people have this kind of hand structure? Are there any studies that say so?

@WYSIWYG - This is, as I said, "normal". I'm sure it's in an anatomy textbook someplace. Does it sound wrong to you?

No. The theory sounds quite plausible but I haven't come across any text that actually pinpoints the morphology in this fine detail. I could find these two articles: 1 and 2, when I searched but I cannot find either of them specifying this. Can you please cite a reference as this does to seem quite obvious to me (and probably other readers)?

@WYSIWYG - I haven't had a good anatomy textbook since mine was stolen on one of my surgery rotations. I was taught this by surgeons (including orthopedists) who work with their hands for a living. They were probably wrong, because they didn't cite a source for me, either. So feel free to remove for lack of a source.

Observation: The bend in the fingers gives the straight hand a more compact appearance so that we can actually tightly close the gaps between the fingers.
Hypothesis: Without the bend small gaps would remain between the tip and the first joint of the fingers unless we press the fingers together with force. Not having this gap could protect the fingers from injury while walking or running through tight underbrush because the likelyhood of entangling the fingers in some vine or branch is lower. Also, being able to compact the hand may help us to easier scoop up water with our hands.
(yes my hand show the same slight bend in the fingers)

Could you elaborate on the part 'not having this gap.....likelihood of entangling the fingers in some vine or branch is lower' ?

well, its like the difference between running a comb and a ruler through your hair, which is more likely to get entangled?