text:
What is difference between High quality and low quality proteins
I have seen in news that some bodybuilder died of taking steroids; when I went through details I learned that  "low quality proteins" contributed to their death. I have studied about linkages in proteins but I don't understand what makes them stronger or weaker. So what is the difference between high quality proteins or low quality proteins? How does low quality protein affect muscular activity or growth?

I'm voting to close this question as off-topic because it belongs to fitness.SE not biology.SE.

@Remi.b I tried to save this question for the OP - I think there is an on-topic question contained there once the personal health component is removed. There might be an additional question to send to fitness.SE about how/whether to use protein supplements that wouldn't be appropriate here.

Without a link to the news story, and subsequently the investigation into this individual's death, it's impossible to know what exactly "low-quality" means in this context. It could be what @BryanKrause talks about in his answer, or it could mean "low-quality" as in it was procured from a disreputable source that didn't take adequate care to verify the protein's purity, or adulterated the product somehow like the melamine scandal regarding milk powder in China beginning in 2008.

"Low quality" vs. "high quality" protein does not refer to anything about the linkages between amino acids in proteins. Instead, these terms are used in a nutritional context to refer to whether an individual protein source is sufficient as a sole source of protein in someones' diet.
Essential amino acids are the amino acids that humans cannot synthesize; other amino acids can be synthesized from these, but they do not need to be part of the diet. Not all sources of protein have sufficient quantities of all of the essential amino acids. Low-quality protein sources are also referred to as "incomplete" and high-quality sources as "complete."
Meat products are typically "high quality" because they contain all of the essential amino acids together. Therefore, if you subsisted on various foods but only got your protein from one animal source, you would be okay.
Some plant products do not have all the essential amino acids in large concentrations. However, if you combine protein sources from different "low quality" plant sources that together cover these deficiencies, there is no disadvantage compared to a single "high quality" source.
In the digestive process, all you take out of the proteins you eat is the individual amino acids (generally): that means that only the amino acid composition matters, not the strength or quality of the bonds between amino acids. If someone tries to tell you otherwise, they are probably just trying to sell you something.
Here is a paper that talks about some of these issues, and addresses some of the myths about balancing proteins. The quick summary is that problems develop if you get your sole protein from a source that is low in a particular essential amino acids over a long time period, but there is no need to ensure every meal contain all the amino acids.
It is possible for people on unusual protein diets, either because they are avoiding animal products or using incomplete protein supplements, to develop a particular amino acid deficiency. Otherwise, as long as all amino acids are supplied, there is no difference on health or muscles to consuming "low quality" vs "high quality" proteins.

References:
Young, V. R., & Pellett, P. L. (1994). Plant proteins in relation to human protein and amino acid nutrition. The American journal of clinical nutrition, 59(5), 1203S-1212S.

My understanding is that amino acids are not generally stored. Say you eat just corn which is first-limiting in lysine. Once you've built what proteins you can before the lysine is exhausted, the remaining amino acids are further metabolized, mostly for energy, as opposed to being incorporated into proteins. My source dates to my Biochem degree in the '70s, and textbooks from the '90s. Maybe something new has been discovered about storage of amino acids? (Still, +1 on your post.)

@bpedit Thanks, I think that's a good point, to my understanding you are correct that amino acids aren't "stored" the way fats are (at least not in humans) - and I didn't say anything about storage in my answer. However, you have a huge storage of amino acids in the form of all the proteins in your body. When proteins are degraded they aren't just junked, you can reuse a lot of the amino acids. The lysine you take in from a single meal is just a fraction of your total body lysine. So, it takes awhile for the shortage to catch up and cause problems.

@bpedit ...From the source I linked and just a general survey of "advice on the internet" it seems like a general guideline for vegetarians is to try to get a complete protein intake within the timeframe of a day, rather than worrying about being complete at each and every meal. I'm sure there is no immediate problem missing a day or two at a time, either, because fasting on those timescales isn't harmful (to my knowledge).

@bpedit You mention "many" but only gave one example. Many cultures have also suffered from things like rickets and scurvy at various points. I'm not sure what your perspective is, but I'd caution against the logical fallacies that people in the modern "paleo" movements employ, assuming that cultures they are less familiar with must have it all "figured out." Surely there are good evolutionary/anthropological reasons why there aren't extant cultures that subsist solely on corn with no other protein source, but I wouldn't read much further than that.


text:
How to calculate the percent of mitochondrial heteroplasmy
How do people calculate the percent of mtDNA heteroplasmy?
Does 7% heteroplasmy out of 10 cells, represent a mutation found in the same position on the genome among 700 mtDNA genomes out of 10,000 mtDNA genomes assuming there are 1,000 genomes per cell?
Thanks for helping me understand this concept a little better.

I emailed the authors of the paper "Age-Related Accumulation of Somatic Mitochondrial DNA Mutations in Adult-Derived Human iPSCs" and they confirmed that they calculated the % of mtDNA heteroplasmy by the following:
Aligned all mtDNA genomes against the reference sequence. Any deviance at a specific position from the reference was a "mutation". The % heteroplasmy was calculated by dividing the total number of mutations at a certain nucleotide position by the total number of genomes represented at the position multiplied 100.
So in other words, to go back to my original question- if there were 10,000 genomes aligned and there were 700 mutations at the same position, that mutation would have 7% heteroplasmy.

source: Stack Exchange

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

sort: votes


text:
Would a complete lack of heterozygotes in a population indicate the presence of a recessive allele?
This doesn't instantly make sense to me.
Lets say you have 100 people from a subpopulation who were sequenced and aligned to a reference genome. For certain variants, people were either homozygous for the loss-of-function alternate allele, or homozygous for the reference allele.
This indicates consanguineous practices within the population. However, I'm told that this also indicates that the alternate allele is recessive and that if it were dominant, there would be very few heterozygotes due to selective pressure, and individuals would not reach a breeding age. This doesn't make sense to me. If it were recessive, there would be an excess of heterozygotes, and if it were dominant, there would be very few heterozygotes, but if there are no heterozygotes, that indicates that it's recessive?
I also fail to see how either condition can be determined in this case.

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


text:
What are the blue and white things on this Sunburst lichen?
I am a amateur photographer I found some interesting things when I got home and looked at my photos. There are some blue/white cocoon. I  like structures on top of the sunburst lichen. I live in Colorado and took these photos on January 23.

I have improved your title a bit but this is not sufficient. Please describe what you tried to capture in the photograph (name of the fungus), your geographical location and climatic conditions.

Are you telling about these? Adding pointing would help the question improve a lot. If you dont like to kill the artistic value of the photoes, then you may add this one instead .

As well, the fungus is some sort of Ascocarp of apothecial type of development

Hey thank you! and please excuse me for a minute I'm trying to figure all this out so I can be more specific in questions and examples. I'm very excited to be a part of this community thank you!

I had trouble doing this on my phone but I appreciate your time. I'll keep in eye out more of these because I can't find the good image of them on Google. So I might be able to upload some better images to the Internet.

The blue part you highlight are similar to the blue parts present more generally on other portions of the lichens, aren't they ?

There you go the top photo shows them a bit more clearly the color must be pretty close my phone automatically adjust colors a little bit. I'll be revisiting the area to find more of these I'll try to get better photos.

Lichen species looks like Xanthoria parietina

The small blue creatures coould possibly be (oribatid) mites.
I have them under my the binocular when I study lichen pretty often.
Their asociation with lichen is well documented

A mite was my thought too. I had no idea of the order or anything though


text:
Thyroid transplanted to the abdomen
This question was posed in our endocrinology class, however I have no idea how to answer it:

The thyroid gland of a 5-year old boy is transplanted from its normal position in the neck to the abdomen (between the kidneys). Assume that the gland develops a good blood supply in its new position and that it remains alive.
List the abnormalities that will develop in this child:

after two months.

after 10 years.

Any help will be appreciated.

We expect people to do their own research prior to asking and to present it with the question. Otherwise the question might be downvoted and/or closed due to no effort. So, what have you found out?

do you haver any ideas what would happen? what class is this for - a college level or graduate level course?

It's for a college level course. I haven't found anything that would suggest that this is a common, or even at all possible procedure. It seems to be purely theoretical.

I know removing the thyroid would affect the child's metabolism, but whether the gland would be at all viable elsewhere in the body I guess is the question. Presumably it would still function as a endocrine gland due to the blood supply, but would it receive the relevant tropic signals from the hypothalamus and AP?

so what do you think will happen? add that to your answer and it will give us an idea that you've tried to do a little thinking in your own...

You have the answer. Just back it up.

Thyroid gland is known to absorb iodine from food.It will not be able to absorb between the kidneys.


text:
What are multiallelic genes?
Is there a clear detailed description for multiallelic genes? Are they simply genes that are more than two alleles?

are you talking about multiallelic traits?  if not, maybe add a citation for us to see the original usage of the term.

More than two alternative forms (alleles)of a gene in a population occupying the same locus on a chromosome or its homologue is known as multiple alleles.
Multiple alleles arise due to mutations of gene.A gene can mutate several times by producing a series of alternative expressions.Different alleles in a series show dominant-recessive relation or may show co-dominance or incomplete dominance among themselves.
In Drosophila,a large number of multiple alleles are known.One of them is the series of wing abnormality ranging in size from normal wings to no wings.The normal wing is wild type.The extreme expression with no wings I.e is just stumps is due to one allele 'vg',in homozygous condition .
For reference.
http://eagri.tnau.ac.in/eagri50/GBPR111/lec04.pdf


text:
Simpson's index
Simpson’s index is a diversity index which is the summation of the square of the probabilities of the species in a community.

The value varies between 0-1.
here, pi=n/N where ni=number of individual of species i in the community and N=total no. of individuals.
S=total number of species.
It is the measure that equals the probability that two individuals taken at random from a community belongs to the same species.The probability decreases if the species richness and evenness increase. It is strongly influenced by the most abundant species.
From:

Wikipedia
Fundamentals of ecology, Odum
Biodiversity of fungi

What is meant by 'It is strongly influenced by the most abundant species'?

I'm assuming that term is meant as a critique/limitation or at least a point to note when taking the index as a measure of diversity. They just mean that the value for D in that equation is affected strongly by how abundant the most abundant species is. So, if you have one species that is very abundant, you might get a high value for D (=low diversity, strangely) even if there are hundreds of other, less abundant species, because adding 1 more species with low abundance does little to the measure.

I don't know whether this math will be clarifying forr you, but it might help you understand why "It is strongly influenced by the most abundant species." It is all about finding the best p's that does the minimization for $D$. You can skip to conclusion if you feel like skipping all the math.
You want to find the critical point (where the function attains its minimum and maximum) of:
$$D = p_{1}^2+p_{2}^2+...+p_{n}^2$$
given ${p_{1}+p_{2}+...+p_{n}=1}$, for $p_{i}$ of species.
Lagrange Multiplier method is one of the techniques to find the values given to $p_{1}, p_{2}, ...p_{n}$ to make $p_{1}^2+p_{2}^2+...+p_{n}^2$  go to maximum or minimum given some constraint on this.
Assume:
$$f = p_{1}^2+p_{2}^2+...+p_{n}^2$$
$$g = p_{1}+p_{2}+...p_{n}$$
According to Lagrange multiplier:
$$\partial_{p_{1},..p_{n}} f = \lambda \partial_{p_{1},..p_{n}} g$$
We have to find the value of $\lambda$.
So after partial fractions step, we will end up with these equations:
$$np_{1} = \lambda ; np_{2} = \lambda;  ... np_{n} = \lambda$$
and we already know that $p_{1}+p_{2}+...+p_{n} = 1$
From above, we know that:
$$p_{1} = p_{2} = ... = p_{n} = \lambda/n$$ we get $\lambda = 2/n$ and from this the minimum values of the function:
$$f = D =  p_{1}^2+p_{2}^2+...+p_{n}^2$$
is when all $p_{i} = 1/n $ for i is denoting each species in ${1,...,n}$
Conclusion:
So $D$ value attains its minimum when all terms $p_{i}$ are equal. As any value goes away from $1/n$ ('n' is the total number of individuals of species you got)the value increases drastically as it is being squared in $D$.
Sample example will be like $0.5^2 + 0.5^2 = 0.25$ but a change from this say $0.6,0.4$ increases $0.5$ term by $0.11$ but decreases $0.4$ term by only $0.09$.
Hope this helps.


text:
Is there a resource for comparing categories of life along quantifiable dimensions such as species diversity, geographic range, total mass, etc?
Ideally what I would like is some sort of interactive, sliceable tabular data along the lines of my examples below. The curious individual specifies the level of taxonomic rank, e.g. Kingdom or Class etc., and then can choose to populate several rows from within that category with data on that category's "successfulness" as measured in various ways (of course all the data fields would be estimates)
CLASS        # OF SPECIES  TOT MASS   TOT RANGE    # INDIV.  # CELLS PER INDIV.
Insecta      ???           ???        ???          ???       ???
Mammalia     ???           ???        ???          ???       ???
<click to add a row>

But the user could select a different granularity, so e.g.
FAMILY       # OF SPECIES  TOT MASS   TOT RANGE    # INDIV.  # CELLS PER INDIV.
Formicidae   ???           ???        ???          ???       ???
Felidae      ???           ???        ???          ???       ???

The goal would be to be able to put "superlative" claims about various categories of life into context. I often read claims of a ____'s (species', genus', etc.) success based on one of these or other estimates, but have no intuitive way of attributing an absolute context to the number reported.
Furthermore, such a table / database would just help me form a clearer picture in my own head of "all the life out there" (that we know about). For example, if I wanted to learn all there is to know about every species of "cat" (I am on the internet, after all), how many species are we talking about? Probably on the order of dozens, versus thousands or tens of thousands for ants.
So far I've found "top 10"-style lists and the like, but no single unified searchable tabular database.

Just putting this out there: as far as I know, there isn't an available comprehensive database like this... but maybe you (or others on this site?) could kick off putting one together!

If you put "No" as an answer, I'll happily upvote it until someone else says "yes" :P

you've got a deal!


text:
Why is it unlikely that bathroom smells can pose health risks?
Based on a little bit of internet reading, it appears that odor molecules that enter your nose from human feces are of little concern to your health because the harmful stuff, like the pathogens, are not likely to be picked up and carried through the air.
This seems to make sense, however due to my limited knowledge of biology, I am having a difficult time distinguishing WHY the bad stuff is not likely to become airborne whereas other molecules can, and will cause damage by smell. Chlorine, for instance, will cause some significant damage simply by smelling the airborne fumes (which I assume are the molecules doing the damage).
I have to assume it is a natural defense mechanism that something that smells bad is not something you want to be around (CO being a major exception) but it seems that feces molecules are not a concern. Why?

Being around excreta is bad for health, because of the pathogens that breed in it. As a result, due to natural selection, we have developed an aversion to being around excreta, for safety reasons. Chlorine on the other hand, reacts with moisture in your nose/lungs and becomes HCl, which is never good to have inside your respiratory system.

So can we conclude that you can indeed get sick from simply being in bathroom that 'smells' foul, or does our aversion protect us from this?

@JAlecksen I think the point is that there are (roughly) two reasons to evolve an aversion to a smell: 1) The compound smelled is/can be harmful, or 2) The compound smelled is a marker for something that is/can be harmful. In case (2), it isn't the compounds you actually smell that are harmful, it is the presence of potentially harmful bacteria, etc. Chlorine is an example of (1); bathroom odors are an example of (2).

You can't fall ill from being in a modern sanitized toilet. You can fall ill from hanging around feces in your day to day life, and not being clean about handling it.

Mostly, what you're smelling are volatile small molecules: stuff like butyrate, indole, mercaptans, hydrogen sulfide, etc. These molecules are thousands of times smaller than even the smallest pathogens, being measured in Angstrom vs. nanometer scales. Pathogens are just too large to be actually volatile, in the sense of freely escaping into the air. And fortunately, these volatile organics are not nearly as reactive as something like chlorine gas. (If they were, imagine the damage they would do, at a much higher concentration, to the person they were just inside.)
Now, if someone had literally just projectile-vomited (or if excreta were churned around, e.g., by flushing), it's possible that a very small pathogen like norovirus could spray outwards in an aerosol. Since norovirus has a very small infectious dose (on the orders of tens of viral particles) this could be enough to make you sick, and indeed, aerosols have been implicated in norovirus transmission, though it's not that common. But the smell would remain long after any viral particles in aerosols had settled down onto surfaces.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4692156/

Great answer, of course it also makes me wonder why our bodies have not evolved to recognize the bad pathogens as smelling bad. This seems like it would be a good defense mechanism...

@JAlecksen I think one issue might be that by the time there's enough pathogen in your nasal passages to be able to detect it as a "smell", you're hopelessly contaminated. Far better to be able to detect pathogen-associated volatiles which can be detected before you get close enough  to pick up the pathogens. That way you can keep your distance. The smell molecules themselves are not harmful, they just indicate that harmful things are nearby, and you should keep your distance.


text:
Personal Genomic Data Samples
a quick question. I am looking for complete personal genomic data of human individuals. The only requirement for the genomic data is that it contains the complete set of SNPs of a human individual. So far I found only one, a hispanic female.
Are there any similar personal genomic data available on the web?
Any database I can access with a collection of SNPs per individual?

Here is the link to the 1000 Genomes project, all the data is available for download. They already have a comprehensive list of SNPs as well.
It is not the only project around but it is definitely the one with more accurate data on so many genomes right now.

Another source would be the Simons Genome Diversity Project published by Mallick et al. in 2016. This set covers way more populations than the 1000 Genomes, and therefore includes more overall human genetic diversity, but also has only few individuals per populations (and populations do not overlap with 1000 Genomes as far as I know).
Which database is better for you depends on the actual question.


text:
Is chocolate poisonous?
I have heard that chilli peppers and coffee evolved to contain toxic chemicals which help to protect them from predators.  And recently I learned that star anise, liquorice and aniseed are not actually related plants, but each independently developed the ability to produce anethole, which can also deter predators.
However humans have evolved resistance so they can ingest all these substances, and tend to enjoy their extreme flavours.  Some more examples are onions, garlic, peppercorns and tea (for its stimulative effect rather than for its flavour).
It made me wonder:
Did the active ingredient in chocolate also evolve to deter predators?
And I am also curious, are there any other foods which I haven't mentioned that humans also enjoy due to their toxic or deterrent components?  (I'm thinking more about flavour than psychoactive effects here, as I know there are many examples of the latter.)

Are you sure people enjoy those flavors because they come from toxins? Even though it sounds very interesting, I can't think of any evolutionary reason we would like to consume them because of their toxicity.

Caffeine is also present in chocolate and toxic to many carnivoras.

I will add some info in my answer

@Probably I think with coffee, nicotine, alcohol, and perhaps also chocolate, we enjoy them less for their bitter flavour but rather for the association with the changes they cause in our brain chemistry. For things like spices, the strong flavour seems to be related to the toxicity. Presumably before our resistance had developed, those strong flavours were a warning signal, but now the residual effect is an exciting taste. (Chilli has the additional effect of causing a release of dopamine.)

Alkaloid synthesis is energy consuming for plants and have complex metabolic pathway.
If their evolutionary history is not known with certainty, they have numerous uses and are often toxic to potential plant or animal aggressor.

Chocolate contain many alkaloids including caffeine and theobromine. But apparently do it with a different pathway and is the result of convergent evolution.
It is safe to assume these alkaloid protects cocoa plant in the same manner it protects coffee and that the benefits of such poisons allowed poisonous cocoa plant to become predominant.
However, alkaloids of chocolate are solely responsible for its bitter taste. (Cf. Wikipedia page "Alkaloids" for more info).
If bitterness is part of its flavour, we prefer its fats the numerous volatile compound gained during fermentations of the beans. According to this article published on academy.org :

The distinctive chocolate flavor evolves throughout its production. Odorless, tasteless “precursors” form during fermentation, and these precursors react during roasting to form taste and aroma compounds.

Also many essential oils are poisonous to insects, fungi or bacteria. These properties are sometimes used by humans : for instance cinnamon oil is toxic to mosquito larvae


text:
How Anopheles crop doesn't digest gametocytes of P. vivax?
Background
According to my A-level textbook: When Anopheles mosquitoes inject their proboscises and suck up blood from human host of malaria agent, they suck all stages of malaria parasite present in the blood like merozoites, cryptozoites, gametocytes etc.
But, Anopheles mosquito's crop digests all other stages of malaria schizogony except the gametocytes.
Question
Well, how does the digestive system of Anopheles distinguish the gametocytes from other stages of malaria parasite?
Or, is there any protective mechanism for gametocytes to stay untouched in face of digestion in Anopheles crop?

Short Answer: Nothing prevents it, most Plasmodium (gametocytes/gametes/zygotes/ookinetes) are killed.
Background: After lots of search, I finally found a definite answer about this. According to Smith et al, 2014, the survival rate of Plasmodium in the Anopheles gut is very low. At each developmental step during their life cycle, a large proportion of Plasmodium face the deleterious effects of the gut (albeit they are not certain that the effect possesses contribution from enzymes). As an example, even if an Anopheles mosquito ingests thousands of Plasmodium gametocytes, about 50-100 are able to develop into ookinetes while only about five survive to form oocyst. This is why even in high transmission areas, majority of Anopheles mosquitoes are not infected by Plasmodium parasites. See this image:

Pay attention to 'parasite #' and see how the number of parasites keeps on decreasing during different stages of development of Plasmodium.
Reference: Smith RC, Vega-Rodríguez J, Jacobs-Lorena M. The Plasmodium bottleneck: malaria parasite losses in the mosquito vector. Memórias do Instituto Oswaldo Cruz. 2014;109(5):644-661. doi:10.1590/0074-0276130597

Perhaps worth emphasising the points made in the paper (and shown in the Figure you have reproduced) that much of the reduction in parasite numbers may be attributable to factors present in the blood bolus such as complement, that come from the blood meal.

Why is there a sudden increase after a continuous decrease? O, I get it it's cleavage in epithelium.

@Another After this answer, do you still think the primary host of Plasmodium is Anopheles? I don't think without paleontological data, nothing can be said about which was the prior host of Plasmodium, mammal or Anopheles

"blood bolus such as complement, that come from the blood meal." Do you mean complements from human blood?" Do you mean complement proteins gathered from human host blood? @Alan Boyd

@Mockingbird yes, the paper that is linked to in the answer includes extensive discussion of the role of human complement in killing during the early stages - it is shown in the diagram along with blood-derived antibodies. The article also suggests a role for reactive nitrogen species generated  by incoming haemoglobin, amongst other things.

@alanboyd the paper said that the gametocytes (inside bolus) are resistant to complememnts while ookinetes (which come out when complements and bolus are digested) are sensitive to complements. Enlighten me if I got this wrong, but this is why I didn't bother to add it.

@mockingbird well I don't specialize in this field, so I can't say anything definitely

@another'Homosapien' I thought that you had broadened the scope of the discussion beyond gametocytes. If you didn't mean to do that then fine, but looking at the information in the Figure I don't think it is fair to say that 'most of them are killed' if 'them' means gametocytes only.

'nitrogen species' What kind of nitrogen species? @Alam

@Mockingbird why not read the paper?

Okay. I will do it

@alanboyd nope I didn't mean to broaden the topic, 'them' meant Plasmodium in general, not just gametocytes (does it convey that meaning?)

Disclaimer: I am trying to answer the question without finding any academic research on the topic. So, appreciate hypotheses and feel free to point out mistakes.
Short Answer : Co- Evolution

Broad Answer: 2 hypotheses

The gamete stage of Malaria parasite simply co-evolved with Anopheles sp. to develop a protective mechanism to survive digestion in crop. Whereas, the other stages of Malaria parasite didn't co-evolve,  so they get digested.
Parasites had already the protective mechanism for surviving digestive enzymes in Anopheles crop. They entered mammals later and evolved a life cycle with a new protective mechanism for new host's immune system.

Why is that?
The answer to this question is not so clear according to known biology, as I haven't found much research in this phenomenon.
But, we have to remember that biology sometimes (or always?) doesn't explain why rather explain how.
The following words are corresponding to what I think about the mechanism of this co-evolution
Hypothesis 1:
It could have simply happened that some point in ancient times, the gamete entered the Anopheles crop from a mammal, but not only that; it tried to continue its life cycle on this new host. But, the environment of crop was unsuitable for the gamete to survive due tto digestive enzymes. So, the first few million or billion tries went into vain. But, the parasite slowly started to evolve to adopt in the Anopheles crop.
After 'some' time, the parasite developed a working protective mechanism from digestive enzymes and continued it's life cycle in Anopheles.
As @Another Home sapien points out, there should be some benefits for this evolution. While it's hard to tell exactly what the benefits could have been; I think it's simply to adopt to new potential host's physiological environment.
But why didn't other stages evolve of Malaria parasite in a same way?
This is another hard question to answer. However, it's not so that only the Anopheles and the parasite co-evolve; the mammal host co-evolved too in this period. And the whole system evolved gradually to get to the present life-cycle of malaria.
Hypothesis 2:
It might have happened that the original host to malaria parasite was indeed Anopheles. So, it had developed a protective mechanism long before entering any mammal host. Then, after entering the mammal host it developed another protective mechanism to survive host's immune system and continued  it's life cycle.
I think hypothesis 2 is more probable as insects pre-existed mammals. Another hypothesis can be drawn the life cycle of parasite is shaped up simultaneously in mammal host and Anopheles host. But, it's hard to hypothesize what could have happened in this scenario.
Reference : 1. Wiki: Co-Evolution
2.Article on this co-evolution

I must say, you are assuming just too much in your answer. How do you know that Anopheles wasn't the original host of Plasmodium? And what benefit would sporozoites get even if they developed a protection against digestive enzymes? In evolution, selection pressure can be both in favor of or against a trait. Also, I won't recommend using phrases like "it chose to..." Also, usually its the parasite that co-evolves with the host, while the host just evolves to get rid of that parasite (which Anopheles too seems to be doing now)...

Thank you @Another You are free to edit my 'answer'. I too felt that my understanding is limited in this case. So, I will edit now.

@Another Do you think you would be able to add some quality reference on this phenomenon?

well, I've already been searching for the 'how' part for hours :P regarding the 'why' part, I'd love to improve the answer, but I feel I should first wait for somebody more specialized in evolutionary biology (since I ain't)...

@Mockingbird Just as an additional information: the definitive host of Plasmodium is the mosquito, not the mammal.

@Gerarddo Furtado Thank you for your comment. I hope you can add some reference and details to my answer.

@Gerardo Are you sure about it?

Yes, totally. Do you know what a definitive host is? I used to warn my students to this detail all the time: the definitive host of Trypanosoma is the fly, humans are only secondary hosts; the definitive host of Anopheles is the mosquito, humans are only secondary hosts... maybe the fact that humans consider themselves so important has something to do with this common, yet incorrect, conception that we are the primary hosts for those parasites.

Then, the 2nd hypothesis is more probable, I think.

@Mockingbird indeed a very imprtant & essential question to ask...@Gerardo Furtado said its totally correct.The Plasmodium's primary host is the Anopheles.There r reasons why but this logic is merely basic level only:The encysment of oocyst is due to partially secretion of cyst material by the stomach of the primary host and partially by the zygote itself.Without encystment sporogony doesnot initiate in them. This could be an important phenomenon which makes the mosquito not just a vector but a vector host.Otherwise they could hve cmpleted the entire cycle in humans alone.

I just realised that I wrote "the definitive host of Anopheles is the mosquito", what I meant was: "the definitive host of Plasmodium is the mosquito".

@Catharanthus What's the difference between vector and vector host?

vectors only transmit the disease and vector hosts not only transmits the disease but also plays the role of a host during one phase of a digenetic life cycle like in malaria.I only read the term in a textbook on a digenetic cycle.

Would I have to award the bounty to myself?

What if Nobody answers without me? Would I have to award the bounty to me?

Umm sadly AFAIK you cannot award a bounty to yourself. Its probably gonna go to nowhere.

@Another Ha Broke my heart

Sorry for that, but now you have another option :P

@another'Homosapien' and Mockingbird: There is a reason why you cannot award the bounty to yourself (in any SE site). Suppose this situation: 1. You post a question and start a bounty of 500 (the maximum allowed). 2. People do a good research, excited about those 500 virtual whatever. 3. You get one or more well written, extensively documented answer. 4. You post your own, crappy answer. 5. You benefit from the canonical answer but award yourself the bounty, not loosing any point.

@gerardofurtado lol :P yeah that would be injustice with the whole purpose of bounty

@Furtado I understand.


text:
Are there animals that are present in two different classes?
Are there animals that are present in two different classes, like amphibian and bird, reptile and mammal etc.?

Like mammals also being vertebrates?

@WYSIWYG FOR EXAMPLE frog is an amphibian and a mammal (this is not correct it's just an EXAMPLE)..Are there animals present in two different classes?

@WYSIWYG Wouldn't taxonomist propose a new class if some species (somehow) showed characteristics of 2 close classes?

Short answer: No. Taxonomy is about categorizing and an organism cannot be placed to different taxa.

@WYSIWYG Mammals are a class, vertebrates compose a subphylum.

An organism is not placed into two classes, an amphibia is very different from a mammal. During classification the characters of an organism are considered before it is placed in a particular taxon. You may read ncert class XI biology(the chapters are available online), the concept is explained in the most comprehensible way.

Classes are a holdover from Linnean classification that don't have any real taxonomic meaning in modern systematics.


text:
A hypothetical emergency situation
This question was posed to me by my Biology teacher:
Consider a hypothetical emergency situation of a person shot by a bullet in the heart. The bullet goes into the body and comes out from it, causing a total of two "holes" in the heart, one each in the "dorsal" as well as "ventral" side of the heart. Blood starts coming out.
Now in an ordinary situation, if the blood continues to flow out, the person will die. But there is a twist, the person has been given an infinite supply of blood from some sort of medical equipment. (Nothing like this actually exists in real life, but you might consider this a "conceptual Biology textbook problem".) The person's heart beats at a normal rate of ~72/second.
Now here is the question :

Considering, the "infinite" supply of blood available, will the person survive?

Will the heart develop some sort of clot or something similar to prevent further leakage of blood, as it forms due the cuts on arms or legs? Is some medical assistance required besides the "infinite" supply of blood?
NOTE : You might make the following assumptions ---

There is no doctor/surgeon to help. Just you and your faithful "machine".
The blood provided by the "machine" is 100% compatible with the blood group of the person.
The "machine" is connected in such a way that after the complete loss of the "original" blood of the person, now the blood provided by "machine" runs in the arteries of the person.
The veins and arteries of the person are 100% OK. The only part affected is the heart "perforated" by the bullet.

At some point there will be clotting, but if it is fast enough is probably influenced by the size of the bullet holes and the coagulation factors in the infinite blood.

There are at least three other points to consider. First, you need to make sure the blood is sufficiently loaded with dioxigen and nutrients. Second, the blood pressure must be monitored. Third, your machine has to pump the blood, and not only supply it, since a heart with two holes probably won't do it properly.

Where is this leaked blood going? Is it filling the thorax to interfer with physiological respiration? I say dead. And how does "Life Blood" compare to regular blood?

What about the pneumothorax from the GSW?

@kmm - Hemothorax would be a much greater problem.

The person cannot survive for long, in spite of the infinite supply of blood.
In real life
There is no blood delivery system that can add blood to the vascular system as fast as it would be lost by two bullet holes in the heart. But I guess that's covered by your conditions.
As mentioned in comments, where would the blood go? Despite a thoracic entry and exit wound, blood volume inside the thorax would not squirt out of those holes fast enough to prevent a life-threatening accumulation of blood which would interfere with expansion of the lungs, so unoxygenated blood = death.
Theoretical
I suspect this is what your teacher was hoping would be the answer. Blood - like most things - will follow the path of least resistance. Which has a higher resistance, the aorta and arteries  (if it hit both the right and left ventricles, the pulmonary vasculature as well) supplying life-sustaining blood to vital organs, or two holes? Theoretically, there would be little resistance against blood flow through the holes, so no flow into vasculature means death.
Regarding clotting, nope. Rate of blood flow would preclude a functional clot.
In real life, even with surgeons at the ready, this is a deadly scenario. One hole: doable (depending on the caliber of the bullet); plenty of people have survived this event. Two holes, it would take particular circumstances and would basically be a miracle.

So does it mean a person shot at point blank range has negligible chances of survival unless something miraculous happens... ???? Also please tell in as few words as possible whether a person can survive a bullet shot in "real life" and my "theoretical question", as your answer seems very ambiguous to me......

@QUANTUM - I'm sorry the answer is ambiguous to you, but I'm not sure I can be any clearer. It was your scenario, not this new comment, that I answered. Two holes in the ventrical(s) is not a survivable injury unless they are very small and a trauma team is able to operate immediately.


text:
Can a species populated solely by males be saved from extinction?
How, if possible, can a species be saved from extinction if the only surviving population are males that cannot reproduce with each other?

The article does not say it died. I vote to close this question.

It does not say anywhere in the article that the female died.

This question does not apply just to the linked species.

If the "males" can self-reproduce: yes, if not: no.

Than it's too broad and pob

Its more complex, I am going to provide a quick answer.

"How, if possible, can a species be saved from extinction if the only surviving population are males"... it sounds like you are questioning a specific paper/article/book etc that claims "the only surviving population are males" or something like that. Is it? if yes; then please give a link to that article. If no; then the question does not make sense because why only males of a population would survive.

I would request moderators to revert the edit because otherwise the question does not make useful sense. It looks the OP seeking skeptic analyses on a particular blog... not about whole living world.

@AlwaysConfused Consider the fact that a lot of species are critically endangered due to habitat destruction and climate change, populations will dwindle and there is a chance that the population, however small, will only be populated by one gender. Is that not possible?

May be the bloggers meant some other method of propagation like gene bank and ivf etc.

In 2012 we weren't able to save an species with one male and no females https://en.wikipedia.org/wiki/Lonesome_George .

@Pere Would it be possible for a sole female to save their species?

Well, in 1999 they couldn't but in 2003 they tried again.https://www.nationalgeographic.com/magazine/2013/04/species-revival-bringing-back-extinct-animals/ However, I must admit that neither the failures nor the hope for success were related with the fact that the last individual was a female. I haven't been able to find examples more similar to the question, with several individuals but all of them of the same sex.

The following answer only deals with theorical feasability

Can a species populated solely by males be saved from extinction?

Short answer : No, not with certainty
Nuanced : yes, in some species, it could be possible
It varies in function of how you determinate the sex of your species.
Sex determination is a wide topic, see the appropriate wikipedia page
Some reptilian species are not sexually determined by chromosomes but by temperature. An example is the painted turtle, of which thermal sex determination has been studied by Carrie Lynne Morjan in an article titled Temperature-dependent sex determination and the
evolutionary potential for sex ratio in the painted
turtle, Chrysemys picta
Thermal sex determination allows you to get 2 different sexes from the "same" genome, as temperature will be the driver of the hormonal differentiation.
Cross-species cloning: influence of cytoplasmic factors on development, by Sun and Zhu states that cross species cloning has been successfully made with fishes and mammals.

Nevertheless, cross-species NT has succeeded in cloning some endangered mammals, such as the gaur
In fish, a type of relatively primitive vertebrate, cross-species NT [nuclear transfer] could be achieved in quite a few genetically distant species

It means we are able to use as a mother and egg-layer a different, albeit related, species.
We can, with a massive grain of salt, hypothesize that we could, in a specie solely constituted of sperm producing male, use the oocyte of another specie to clone it, then use the thermal differentiation to make a female out of our clone.
However, I am not aware of any information about how much genome and spermatozoids genetic payload is modified by the sex differentiation. Therefore, it is possible that sex-determined genes cannot produce a sexually naive clone.
For more information, and if you want to research more about it, I recommend you to see the current state-of the art in de-differenciation technics and DNA-demethylation for cloning.
I hope I provided a sufficient answer for you.


text:
What does self-perpetuating mean?
From Wikipedia

The community begins with relatively few pioneering plants and animals and develops through increasing complexity until it becomes stable or self-perpetuating as a climax community.

From Wikipedia again,

Self-perpetuation, the capability of something to cause itself to continue to exist, is one of the main characteristics of life.

What I  don't understand is every organism has the capability to perpetuate (except the sterile ones, which are not under consideration) even a seral community does then why is climax community specifically labeled self-perpetuating?

Here self-perpetuating means that the community is able to sustain it'self and continue, more or less, as it is. A seral community is an ever changing one, so it can't be considered a self-perpetuating one.

"Climax community" suggests a long enough history to have tested, and perhaps evolved, relationships between the member species such that a high degree of stability exists. Among other needs, members have enough to eat, places to live and controls on overpopulation. It suggests a dynamic equilbrium between the member species. It should be noted that the concept of climax community, although having theoretical uses, is currently "abandoned" as an actual construct in favor of terms like "old growth".  https://en.wikipedia.org/wiki/Climax_community

The key here is to recognize the distinction between a community as a whole and the individual species within that community. Just because individuals have the capability to self-perpetuate, doesn't mean that a community as a whole does.
For example, imagine an island with a whole bunch of caterpillars. Now imagine that you introduce a non-native caterpillar-infesting wasp. On the mainland, the caterpillars have evolved resistance to this wasp and so can fight off the infestation. But on the island, they never evolved that resistance, and rapidly succumb. Upon introduction of the wasp, you have a "community" of wasps and caterpillars. The caterpillars can reproduce, as they have been, so they're self-perpetuating within their species. The wasps can also reproduce by laying their eggs in the caterpillars, so their species is self-perpetuating. But the wasp infestation is killing caterpillars faster than they can reproduce, so the community is unstable. Over time, the population of both wasps and caterpillars will crash as all the caterpillars die off. Each species can self-perpetuate, but the wasp/caterpillar community, taken as a whole, does not.
That, in a slightly more complex way, is what happens with non-climax communities. The pioneer species change the environment in a way that permits other species to grab a toe-hold. These species are more suited to the changed environment, and thus push the pioneer species out.
For example, species which can survive in nutrient-poor soil grow and die in that soil, enriching it with nutrients. Now that the soil is no longer nutrient poor, faster-growing plants can grow in the soil, and push out those species which started there. Each individual plant can reproduce, but the community as a whole is changing from one which favors the nutrient-poor adapted plants to the nutrient-rich adapted ones.
It's only in a climax community where the members of the climax community create/maintain an environment which is most conducive to the climax community species. This is why it (the climax community) is being called "self-perpetuating". The community as a whole is maintaining an environment which favors those species which make up that community.
Wipe out the climax community species (e.g. through a forest fire), and you no longer have an environment which favors the climax community species. A new set of species comes in, changing the environment, which then allows other species to come in, changing the environment further, which then ...

'The community as a whole is maintaining an environment which favors those species which make up that community' to forever last, at least theoretically ?

@SanjuktaGhosh Well, "forever" is a very long time. The concept of a "climax community" is no longer well accepted by ecology researchers, for this very reason. Many think it's inaccurate to pick out a particular community as "climax", as no community lasts forever due to fires, floods, storms, plagues, etc. But the use of the term "climax community" - in as much as it has any meaning - implies that the community is stable, ignoring "outside" influences like fire, etc. -- it's part of the definition of what a climax community is.


text:
How does vitamin C increase iron uptake?
I've read that vitamin C increases the iron uptake in the human body. How does that work, physiologically?

Vitamin C both enhances iron uptake, and affects iron metabolism:

in addition to the known ability of dietary ascorbate to enhance nonheme iron absorption in the gut, ascorbate within mammalian systems can regulate cellular iron uptake and metabolism. Ascorbate modulates iron metabolism by stimulating ferritin synthesis, inhibiting lysosomal ferritin degradation, and decreasing cellular iron efflux. ... Importantly, this iron-uptake pathway is of particular relevance to astrocyte brain iron metabolism and tissue iron loading in disorders such as hereditary hemochromatosis and β-thalassemia. Recent evidence also indicates that ascorbate is a novel modulator of the classical transferrin-iron uptake pathway, which provides almost all iron for cellular demands and erythropoiesis under physiological conditions.

--The active role of vitamin C in mammalian iron metabolism: much more than just enhanced iron absorption!

stimulating ferritin synthesis, inhibiting lysosomal ferritin degradation, and decreasing cellular iron efflux. Is it possible to translate these 3 things into simpler language?

Just v various ways of increasing iron metabolism: Making more of the handling proteins, preventing them from being broken down, and keeping iron in the cell


text:
Can a bacterium survive without GroEL protein?
In prokaryotes, GroEL protein (together with GroES) is required for protein folding.
Question: Can a bacterium survive without GroEL protein?

In E. coli, GroEL/GroES is found to interact with about 10% of all soluble proteins (Kerner et al. Cell 2005) and is the only chaperone essential to the bacterium under all tested conditions (Horwich et al. Cell 1993).

There doesn't appear to be a knockout for it in the Keio collection (they systematically knocked out genes in E coli to assess essentiality, via recombineering).
If they couldn't knock it out, that strongly suggests it's an essential gene and the organism cannot survive without it.
http://cgsc.biology.yale.edu/KeioList.php
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1681482/

There is a groEL knockout: http://cgsc2.biology.yale.edu/Strain.php?ID=109235

That's only a GroL knockout, so I'd say the point still stands.

I'm fairly sure groL and groEL are synonyms.

You may be right, I assumed they were a pair, but I think I'm confusing this with it's interaction with ES.
If so, I stand corrected.
And that nomenclature is stupid :p

Haha agreed. Also, in the page I linked to: "There is some question as to if this strain has a complete knockout of groL".

Yeah I know with the KC they've been plagued by false results.

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


text:
How does chromosome number get halved in meiosis I?
In meiosis 1, it is said that chromosome numbers become halved in the two daughter cells. For example, in a 2n human cell there are 46 chromosomes. During meiosis 1, the cell will undergo interphase and probably the S-phase, where chromosome number becomes duplicated. Now the cell is 4n (i.e. 92 chromosomes). During anaphase 1, 46 chromosome out of 92 would go towards one pole and 46 would go opposite. Thus the resulting two cells will have 46 chromosomes in each. So why should we say that, in meiosis 1, the chromosome number is reduced? I say that S phase shouldn't occur in meiosis 1 but rather it should occur in meiosis 2. Is my reasoning incorrect?

If you consider sister chromatids to each be a chromosome, meiosis I, rather than halving the chromosome count, separates the homologous chromosomes, which result from sexual reproduction, from one another. Meiosis II then separates the sister chromatids from one another resulting in the final halving of chromosomes.
On the other hand, many if not most biologists don't consider the sister chromatids to be individual chromosomes until they are segregated during meiosis II. In this sense, meiosis I does reduce the chromosome count to half.


text:
What kind of fish is this? I don't remember the full name but it started with Tiger
name starts with tiger, forgot the rest, please help

Where is it from? Do you know that?

I got it from a local pet store called Elliot's

In which country is it?

Please add some more information about it, like its size, habitat (where you live), etc.

You could just go to the pet store and ask.

It's probably a juvenile tiger loach, or tiger botia.

Adult Tiger Loach

Younger individual of another species
These fish are from the genus Syncrossus and the family Botiidae which include many common aquarium fishes. This genus comes from India, Myanmar, and Southern Asia.
These fish can grow up to 20-25cm (~10in).
Syncrossus species can be told appart using appropriate litterature. This specie sheet from seriously-fish is well documented and provide interesting links from further reading and a quick explanation of its taxonomy easily accessible for the average guy,


text:
Hardy Weinberg principle
The principle is that sum total of all allelic frequencies is 1.
Individual frequencies for example can be named p,q.In a diploid cell , p and q represent the frequency of allele A and a respectively . The frequency of AA individuals in a population is p2  as the probability of an allele A with a frequency of p appear on both the chromosomes of a diploid individual is simply the product of the probabilities. Similarly for aa it will be q2.Can anybody explain that how it will be 2pq for Aa?
I am getting it as pq.

This question is really more about probabilities than H-W. Basically, you can arrive at Aa in two ways; either getting A from the father and a from the mother (Aa), or the opposite (aA). The probability of each combination of Aa is pq and the total probablility of both (Aa and aA) is therefore 2pq.

@fileunderwater: oops, my explanation might be super misleading. Thanks for clarifying!

@AlexDeLarge The binomial expansion that you gave (if I remeber correctly) is also correct to apply.

You almost said it all! Here are two ways to think of this problem
Finding the missing probability
Let's denote the fraction yz genotype in the population with $f(yz)$. The sum of of fraction of all genotypes must be equal to 1. In equation it means
$$f(aa) + f(aA) + f(AA) = 1$$
Here, of course I don't make a difference between $f(aA)$ and $f(Aa)$ (whether A is inherited from the mother or from the father). Knowing as you said
$$f(aa) = p^2$$
and
$$f(AA) = q^2$$
and feeding this value back to the first equation result into
$$p^2 + f(aA) + q^2 = 1$$
Solving for $f(aA)$ yields to
$$f(aA) = 2pq$$
Directly calculate the probability
Another to reach this result is to ask the following questions

What is the probability that the maternal allele is A?

The answer is $q$

What is the probability that the paternal allele is a?

The answer is $p$

What is the probability that the maternal allele is a?

The answer is $p$

What is the probability that the paternal allele is A?

The answer is $p$
Therefore, $$f(aA) = pq + pq = 2pq$$


text:
Meaning of “cognate genes encode the basic biological functions of proteins”
In the introduction to a review article entitled “Interpreting the protein language using proteomics” the author uses the term ‘cognate genes’ in a manner which I do not understand:

Whereas cognate genes encode the basic biological functions of
  proteins, the real-time dynamics and regulation of protein structure
  and function are generally carried out by specific post-translational
  modifications (PTMs) of proteins such as phosphorylation,
  glycosylation and acylation.

What does it mean?

Could you provide a reference. The word "cognate" implies relatedness, so that "cognate gene" on its own is meaningless. It has to be cognate to something else. Unless the preceeding sentence inidicates this, I suspect you have a poor text using terms that you should certainly not use yourself. I personally have never heard cognate used in this way and it would seem to me to be incorrect.

Perhaps the reason you ignored my request is that you are on a different time zone. An internet search found the article you (mis)quote. I have rewritten your question citing this article, which is what you should have done in the first place if you wanted people to help you. My brief opinion is the author (not a native English speaker) is misusing the word for effect. I will compose a detailed answer when I have time.

The sentence quoted accidentally misuses the word ‘cognate’ because in attempting to appear profound it has become overweight and off-balance. Notice the sentence also contains the meaningless nonsense of “real-time dynamics”, and in the rest of the paper the word ‘cognate’ is (fortunately) nowhere to be found.
What does the author mean? His review is on proteomics, and he wishes to emphasize the importance of post-translation modification of proteins. He needs to refer to the unmodified form of proteins, and so he associates them with the information in their genes, which is limited to the unmodified amino acids. The word ‘cognate’ in plain English has the meaning of ‘related’ or ‘corresponding’, so the author would appear to be using it to imply the relationship between particular genes and the individual proteins that they encode. What he may have meant to say is:

“Whereas genes encode the basic biological functions of their
  cognate proteins…”

This would have been linguistically correct, although the word ‘cognate’, in my opinion is unnecessary as it adds nothing to the sentence.
You can find a biological definition of cognate on GenScript:

cognate
A term borrowed from linguistics, signifying a correspondence;
  e.g. a receptor and its cognate ligand, a tRNA and its cognate amino
  acid.

These two examples are of the most common uses of ‘cognate’ in molecular biology — that for tRNA can be found on the Wikipedia page for aminoacyl tRNA synthetase. A quick search brought up few examples of ‘cognate proteins’ or ‘cognate genes’, and in these cases I found the word was used to refer to similar genes or proteins in different organisms or strains.

I think it may be referring to constitutive expression of those "cognate genes". So, cognate genes are those who codify for essential proteins which are constantly produced in the cell, and their function is regulated by said PTMs (Post Translational Modifications). Sorry if I had grammar mistakes in this text.

Please add some references to your answer.

yeah this is confusing - the writer just means 'the primary structure of proteins' probably.  the primary structure directs the 'job' of the protein, but the small modifications to the protein, such as those PTMs s/he mentions, are responsible for directing the protein to/from its 'workplace' and determining its level of activity and its specific shape.


text:
Help me find out what this bird is (description, no picture)
A while ago I read about this bird(s) whose species status was not confirmed. This was because they had a very large distribution and birds in adjacent population could breed with each other but birds at each end of the distribution (western Europe and South Asia I think) couldn't. I am pretty sure that they were some kind of gull and from Europe to Asia their wings got lighter, from black to grey. I think I might have read about them in a Richard Dawkins book.
Does anyone know the species I'm talking about?

Do you have an image of that bird, and some more specifications?

You're describing a Ring Species: "a connected series of neighbouring populations, each of which can interbreed with closely sited related populations, but for which there exist at least two "end" populations in the series, which are too distantly related to interbreed, though there is a potential gene flow between each "linked" population".
The classic ring species is the Herring Gull complex, and that's probably what you read about:

The classical example of the ring species model was originally based upon the herring gull complex (Mayr 1942). This group comprises more than 20 taxa of large gulls (Haffer 1982) which together occupy a circumpolar breeding range in the northern hemisphere. ... Mayr envisioned all taxa of the circumpolar chain to be connected by gene flow, while herring and lesser black-backed gulls in Europe, the hypothetical endpoints of the ring, have reached full reproductive isolation and now coexist as distinct species.

--The Herring Gull Complex (Larus argentatus - fuscus - cachinnans) as a Model Group for Recent Holarctic Vertebrate Radiations
However, recent genetic work shows that the situation is even more complicated than this, and it's questionable whether they really are "ring species":

Contrary to the ring-species model, we find no genetic evidence for a closure of the circumpolar ring through colonization of Europe by North American herring gulls. However, closure of the ring in the opposite direction may be imminent, with lesser black-backed gulls about to colonize North America.

--The herring gull complex is not a ring species.


text:
Help with analogy: Competition among similar species
I'm not from this field, but I'm trying to make a biology/ecology analogy for companies with similar products competing for the same market segment.
I was thinking of using the competitive exclusion principle to illustrate that the products will have to each find their own niche, or disappear from the market.
In a market, when opportunity arises (lots of capital available, and interest from the consumer side for an new product) many competing products spring up, and then we slowly arrive at an equilibrium similar to the exclusion principle mentioned before.
My question is this: Is there a similar "opportunity stage" of this process in nature? Like an increase in resources available that drives many different species to "appear" and compete for the newfound wealth?
Pointers to Wiki articles etc. for further research will be appreciated.

The Cambrian explosion may be an example of what you are talking about: https://en.wikipedia.org/wiki/Cambrian_explosion

Here are some definitions of interest to you

Ecological succession is the process of change in the species structure of an ecological community over time. The time scale can be decades (for example, after a wildfire), or even millions of years after a mass extinction.
A seral community (or sere) is an intermediate stage found in ecological succession in an ecosystem advancing towards its climax community. In many cases more than one seral stage evolves until climax conditions are attained.1 A prisere is a collection of seres making up the development of an area from non-vegetated surfaces to a climax community.
In biology, a disturbance is a temporary change in environmental conditions that causes a pronounced change in an ecosystem. [..]  Because of these and the impacts on populations, disturbance determines the future shifts in dominance, various species successively becoming dominant as their life history characteristics, and associated life-forms, are exhibited over time.
Ecological facilitation or probiosis describes species interactions that benefit at least one of the participants and cause harm to neither.1 Facilitations can be categorized as mutualisms, in which both species benefit, or commensalisms, in which one species benefits and the other is unaffected. Much of classic ecological theory (e.g., natural selection, niche separation, metapopulation dynamics) has focused on negative interactions such as predation and competition, but positive interactions (facilitation) are receiving increasing focus in ecological research.


text:
Non-Lifestyle related diseases
Given the obvious importance for global health, I've found it easy to track down lists from Google of the top lifestyle related causes of death (like heart disease, lung cancer etc), but as a consequence it proven difficult to find a source of the opposite, the leading causes of death which have no (or very little) relation to lifestyle choices (like smoking, obesity etc).
What I'm interested in is those chronic and generally quite fatal disease which just happen for either genetic or spontaneous reasons, or perhaps due to environmental causes which are so ubiquitous as to be unavoidable.
I'm not looking for an exhaustive, or even very large list, the top five to ten would do, and I understand that there's no clear distinction between lifestyle and genetic factors, but obviously health organisations make some estimate of what is mainly the cause otherwise lists like these would not be possible. I just want the opposite list.
To clarify in the light of some answers, I'm looking for diseases which one might contract in adulthood (this could include pathogens) which could in a normal healthy person living within reach of modern medicine still present a more than 50% chance of being fatal. Basically I'm after a risk figure (my field of research) which would act as a baseline presuming a safe, healthy life.

Getting impaled by a giant metal rod might leave you pretty deadish

Fair point, have edited the title to specify diseases. Mind you standing precariously above sharpened metal rods might well be considered a lifestyle choice.

I think it's somewhat fallacious to equate all heart disease to lifestyle choices. The heart of someone living a very healthful life will eventually give out. Cancer is not always caused by something we've done. So there's plenty of overlap.

@anongoodnurse I quite carefully did not relate all heart disease to lifestyle choices but put it  (quite uncontroversially) in a list of diseases which are "related" to lifestyle and then go on to specify that I'm interested in differentiating disease by what is "mainly the cause". Having already specified in the question that "I understand that there's no clear distinction between lifestyle and genetic factors" I'm not sure what to make of your contribution that "there's plenty of overlap".

So the CDC has a list of total leading causes of death
https://www.cdc.gov/nchs/fastats/leading-causes-of-death.htm

Number of deaths for leading causes of death
  • Heart disease: 614,348
  • Cancer: 591,699
  • Chronic lower respiratory diseases: 147,101
  • Accidents (unintentional injuries): 136,053
  • Stroke (cerebrovascular diseases): 133,103
  • Alzheimer's disease: 93,541
  • Diabetes: 76,488
  • Influenza and pneumonia: 55,227
  • Nephritis, nephrotic syndrome, and nephrosis: 48,146
  • Intentional self-harm (suicide): 42,773

Cancers can be further subdivided into types which may or may not be related to lifestyle. There are lung cancers and skin cancers that are not linked to smoking or skin damage respectively. Cancer is very complicated.
Most of the causes on this list have lifestyle or environmental components to them. Influenza and pneumonia have less to do with lifestyle and more to do with the immune system either being too robust or not robust enough but the immune system is influenced by lifestyle as well.
To get a list of diseases that are the leading causes of death and not influenced by lifestyle or environmental, you'd probably be looking at genetic diseases like cystic fibrosis for example.
The WHO has a list of these monogenetic diseases. These are diseases that are caused by a single gene (either one or two copies of the gene depending on the disease) and are independent of lifestyle and environment.

Thalassaemia
  Sickle cell anemia
  Haemophilia
  Cystic Fibrosis
  Tay sachs disease
  Fragile X syndrome
  Huntington's disease

You can read more about these diseases here: http://www.who.int/genomics/public/geneticdiseases/en/index2.html

Thanks, that's something like what I was looking for although I failed to specify in my question (my mistake) that I'm looking for causes of death which would not be apparent within early childhood, something which could just happen and you'd have no way of reasonably avoiding it.

If the main goal is trying to avoid death, then living a healthy lifestyle, going to the doctor for checkups and getting blood work done regularly are your best bets to identify diseases early on and hopefully prolong your life.

I'd think even influenza &c could be said to be lifestyle-related.  After all, you catch them from other people, so if your lifestyle is such that you spend a lot of time in crowded places, you're probably more likely to get them than if you're a hermit living in the wilderness.

As I've specified in my edits I'm not looking for medical advice, I'm a statistician, my interest is in risk perception, I'm trying to establish systems for communicating risk that are more accurate than Lifetime Risk (which gives the misleading impression that your risk would be zero if you avoided whatever factor is being discussed) but more meaningful than Odds Ratios which most laymen cannot relate to. I have access to mortality statistics, but in order to extrapolate the data I need to know which causes of death would give the best indication of a "random, unavoidable" cause.

I'm getting the distinct feeling that the information I need is tantalisingly there but not being specified, you mention in your previous comment "living a healthy lifestyle, going to the doctor for checkups". If the only diseases not influenced by lifestyle are monogenetic ones then what are you going to the doctor's regularly to get check for? This is exactly what I'm asking, you seem confident that a person leading a healthy lifestyle should still visit the doctor regularly for check ups. If you could just list the things a healthy person might need checking for, that would be my answer.

This is a list of the top ten most common genetic diseases.
This is a link to a list of the 'worst' genetic diseases
This is a link to some fatal genetic diseases
I hope that helps, I think genetic diseases are the only ones that would not be considered a lifestyle disease. Other diseases would be caused by a pathogen; I have never heard of one arising spontaneously (although I could be wrong about that).

The OP asked for causes of death. Some on your list are not fatal. Also, diseases arise spontaneously all the time that are unrelated to lifestyle. Many cancers come to mind.

@anongoodnurse Could you perhaps list some of the many cancers that come to mind or point me to a reliable source. This would be pretty much what I'm looking for, but whilst it's easy to find a list of cancers broadly related to lifestyle (lung, skin, colon etc) I've found it harder to get a list of ones which really aren't.

@Pseudonym - That's a matter of taking all cancers and subtracting those that are influenced/caused by lifestyle. Too many to list.

@anongoodnurse I presume from your comment that you personally cannot supply me with an answer, but for the sake of any other experts potentially willing to help, l'm only asking for the top few, not the entire list, just ten of the highest risk cancers that are not strongly connected to lifestyle factors would do, even one would be a good start.

@Pseudonym - I can supply you with an answer, but believe in the value of working to get what you want (seriously. I didn't become a physician by asking other doctors for help all the time.) I gave you a formula to find the answer: google the top, say, 10 cancers and delete those with known lifestyle causes.)

@anongoodnurse I am certain that Biology.SE is not the primary source for any of the information given in its answers and so all of them could be deduced by Googling eventually. I have mortality statistics ordered by coroner's code numbering in the several hundreds of causes. I could re-sort them all in order of mortality, and Google each one to see if it's lifestyle related but it seemed eminently sensible to first see if any one had already done this. A simple "no, I don't have that information to hand" will suffice, I don't need to be chided like a child who hasn't done their homework.

http://www.slate.com/articles/health_and_science/science/2014/02/deadliest_cancer_chart_shows_mortality_and_incidence_rates.html Here is a detailed chart for the deadliest and most common cancers. However, they don't mention how many of these are related to lifestyle so additional research may be needed for that.


text:
Would we know about a virus that causes no symptoms?
I've heard that there are a number of viral illnesses that humans can get from animals, which cause no symptoms in the animals. If there was such a virus in humans, which was very widespread but caused no symptoms, would we know about it?
As far as I know most pathogens have only been discovered when people were specifically looking for the cause of some disease. With bacteria, I think we know / can discover any that can be found in a human body, though we don't necessarily know what each type does. But viruses are much smaller.

With the modern rise of meta-genomics, symptom-less viruses can be identified by the presence of their genomes. Certainly, there is more interest in pathogenic viruses than in harmless passengers, but today it's not necessary to have symptoms to identify viruses.  For example:

Investigators can now go beyond pathogenic viruses and have access to the thousands of viruses that inhabit our bodies without causing clinical symptoms. By studying their interactions with each other, with other microbes, and with host genetics and immune systems, we can learn how they affect health and disease. This article reviews current knowledge of the composition and diversity of the human virome in physiologically healthy individuals. It focuses on recent results from metagenomics studies and discusses the contribution of bacteriophages and eukaryotic viruses to human health.

--Metagenomics and the Human Virome in Asymptomatic Individuals.
Even prior to metagenomics, some "silent viruses" were identified:

Viruses are the most abundant obligate intracellular entities in our body. Until recently, they were only considered to be pathogens that caused a broad array of pathologies, ranging from mild disease to deaths in the most severe cases. However, recent advances in unbiased mass sequencing techniques as well as increasing epidemiological evidence have indicated that the human body is home to diverse viral species under non-pathological conditions.

--Describing the Silent Human Virome with an Emphasis on Giant Viruses

So it's not just true that we could discover such a virus, but we already have discovered many of them in humans. That's fascinating!

It's still a very new field, and many of the newly-discovered silent viruses are bacteriophages that infect the normal gut bacteria, but there are a handful of apparently non-pathogenic viruses that infect humans.

I would add that the silent virome might not have been silent upon the infection of the first animal acquiring it.

Sure, but in some cases that first acquisition may have been millions or hundreds of millions of years ago (consider spumaviruses of primates) -- so it becomes questionable if it's even the same virus, or host, as in the first acquisition.

@iayork - That's exactly my point.

Theoretically, I think we can. We are able to identify viruses in humans that are asymptomatic or have yet to produce symptoms (e.g. HIV, Zika Virus). However, unless this virus causes an impact on humans, like causing death in cattle, I don't see why people in our society would invest in finding out about it. Most organisations award grants for research that they could profit off in some way.


text:
Why do plants store energy as carbohydrates and not as fats?
In my introductory biology class, we are learning about biomolecules. The textbook says fats are a more efficient energy store than carbohydrates.
So my question is - why would plants store their energy as carbohydrates and not as fats, if fats are a more efficient energy store?

What research have you done before asking it here?

Asked my professor :P He suggested it might have been because plants don't have an inconsistent source of energy in the same way that plants do, but that didn't make much sense to me.

Not a homework problem! Although I guess there's not much I can do to convince people of that... Just a question I asked in class that my prof. didn't have a satisfying answer for.

I'd imagine since plants are already making carbohydrates and it would waste energy turning sugars into fats, there is just no benefit for them. Keep in mind that for plants and animals the majority of the calories we burn are carbohydrates, but plants will make more everyday while animals have to find it, and thus could go several days without. This is just supposition however.

Note that plants do commonly use fats for storage in at least one context, that of seeds (which humans exploit for edible oils). Seeds need to be compact for dispersal, so the high energy density is an advantage.  The stored fat is used by a small plant (the seedling), so transport issues are less severe than in larger plants.

Great question!  Agree with @John 's ideas.  Also, the main advantage of fat is that it is compact --- it stores more energy per volume than sugar polymers --- and a compact storage form is important to animals which need to move around, but probably not such a big factor for plants.  Just a thought.

Found this page  http://www.techno-preneur.net/technology/tech-trends/agriculture/animals.html  that contains several arguments that make sense to me at least.  It's hardly a textbook, but perhaps gives some ideas.

There are quite some reasons for why plants prefer carbohydrates for energy storage rather than fats. I will reach some of them one at a time.

Fat hates water: By just applying some common sense, one would get to know that fats are hydrophobic, meaning they literally 'hate' water i.e. don't dissolve in water. So, they cannot be transported very easily. On the other hand, most carbohydrates are water-soluble and can be easily transported via phloem fibers. So, plants prefer to use carbohydrate instead of fat. But they can store fat, by converting them into lipoproteins, by binding them with fatty-acid binding protein, by storing them as fatty-acids (i.e. with terminal -COOH which makes them a bit water-soluble) or by storing them in special compartments called elaioplasts. Yet, as one might assume, this would require more energy intake than using carbohydrates, so plants don't prefer this process too much.
source
Plants don't want to store everything: Obviously, plants photosynthesize because they need energy, and because they need energy to survive. So, storing every bit of energy would not be very clever, they need some of it handy. Fats are storehouses of energy i.e. they store energy for extreme conditions, when there is no primary energy source left. Under normal conditions, and at night, carbohydrates are the primary energy source.
Cells don't let them in: Plasma membranes are semipermeable, quite a general fact. So, they do not allow large molecules to enter inside. And fats are one of the largest biomolecules (after, obviously, nucleic acids). So they cannot be transported inside or outside cells. You would say 'but cells are the ones which make fats, so they are already inside!' No, that is why there is phloem, because there are cells which don't synthesize them (say, root cells). On the other hand, carbohydrates, being much smaller, can be transported through small channels or even through simple diffusion through the plasma membrane. Also, as already stated, fats are quite hydrophobic, unlike carbohydrates. So, they are, in a sense, repelled by hydrophilic layer of cell membrane just like water itself hates it. So, they find it even more difficult to cross plasma membranes because of combined effect of size and hydrophobicity.

There can be lots of other reasons which I can't think of right now, but I hope even this much is helpful.

A good effort, but I'm afraid I don't find the arguments very convincing. (1) "Fat hates water" -- but lipoproteins and fatty acid binding proteins solve this problem. (2) "Plants don't want to store" -- possible, but sidesteps rather than answers the question I think, and probably plants do need some energy stores. (3) No, membrane impermeability is due to hydrophobicity, not size; and see nr 1. (4) This is pure speculation, and the description of cardiovascular disease is completely off -- lipoproteins are nanometer scale particles and they do not "get stuck" in blood vessels.

(1) Still, molecular mechanisms have evolved for handling lipid solubility, and plant cells do in fact use these to store fat, see for example http://www.sciencedirect.com/science/article/pii/S0968000498013498. Therefore, solubility is likely not the answer. (3) No, I mean lipids are not that large (triglycierides ~1000Da) and size is not the important factor. (4) I think you have got the wrong impression from that web site. Atherosclerotic plaques result from inflammation, not cholesterol "sticking" to the vessel wall. I suggest you delete/revise this part of your answer.

The reasons stated are equally true for animals (specially first, third and fourth), but animals they do store fats.

My point is not to criticize the poster for accepting your answer — I should have expressed myself better. Clearly he doesn't know the answer to the question, so one cannot expect his judgement to be perfect. However, when an accepted answer is incorrect, as in this case, it is important to comment on the incorrect answer, pointing this out. Otherwise other readers may not realize why it is wrong. No hard feelings. We all have our areas of experties and we all make mistakes. In your place I'd delete your answer,  but that's entirely up to you.

Actually, hydrophobic means "lacking affinity for water", and literally means "fearing water", not hating it, from the Greek phobos meaning "fear"

It doesn't change much about the answer, except you said literally hating water, which is wrong. So at least that part of your answer is incorrect. It was a comment, not a down vote.

No, the problem is not just wording ("sticking", "clogging" or whatever). The idea that triglycerides or even lipoproteins would get stuck in vessels because of their size is simply wrong. Even the thinnest capillaries are several micrometers, and lipoproteins are tens of nanometers. And this does not occur in atherosclerosis --- the lipid buildup occurs inside the vessel wall and is associated with inflammation. (This atherosclerosis stuff is really beside the question here, but the analogy is still misleading.)

@another that's not the point. The point is you said literally, which is incorrect. Hydrophobic does not literally mean "hates water". It literally means "fears water". That is a fact. I'm not saying "hydrophobic" isn't the right word to use, or that "hates water" does not convey an appropriate meaning.  I'm saying that your claim of what it literally means is incorrect. I have now said the same thing half a dozen ways; hopefully you understand. I can't think of way other ways to say it, so let's leave it at that.

@another you still don't understand what I am saying. There isn't a significant difference in meaning, but it's nevertheless incorrect. Let me try this way: Remove the word "literally".

The question was:

Why would plants store their energy as carbohydrates and not as fats, if fats are a more efficient energy store?

But before trying to answer it you have to be quite clear what is meant by efficient. Without qualification this term is meaningless. A little reflection will tell you that whatever positive properties are implied by ‘efficiency’ may have different importance in relation to the very different modes of existence of animals and plants. One will also want to test any explanation on the exceptions — the instances where animals store carbohydrates (generally polysaccharides) and plants store fats. With this in mind I argue as follows:
1. Carbohydrate is the straightforward solution
Plants synthesize glucose from carbon dioxide, animals take in carbohydrates in their diet and break them down to monosaccherides. Hence, storing excess as polysaccheride (glycogen in animals, starch in plants) involves developing and using a relatively simple polymerization/depolymerization system. One would therefore assume it to be the default. The question is then, “in what circumstances is it advantageous to store surplus as fat?”.
2. Fat is a more concentrated energy store, so is used to minimize weight
Dull eh? But that’s the answer. The following extract from Berg et al. explains this clearly (triacylglycerol is the chemical name for triglyceride or fat):

Triacylglycerols are highly concentrated stores of metabolic energy because they are reduced and anhydrous. The yield from the complete oxidation of fatty acids is about 9 kcal g–1 (38 kJ g–1), in contrast with about 4 kcal g–1 (17 kJ g–1) for carbohydrates and proteins. The basis of this large difference in caloric yield is that fatty acids are much more reduced. Furthermore, triacylglycerols are nonpolar, and so they are stored in a nearly anhydrous form, whereas much more polar proteins and carbohydrates are more highly hydrated. In fact, 1 g of dry glycogen binds about 2 g of water. Consequently, a gram of nearly anhydrous fat stores more than six times as much energy as a gram of hydrated glycogen, which is likely the reason that triacylglycerols rather than glycogen were selected in evolution as the major energy reservoir. Consider a typical 70-kg man, who has fuel reserves of 100,000 kcal (420,000 kJ) in triacylglycerols, 25,000 kcal (100,000 kJ) in protein (mostly in muscle), 600 kcal (2500 kJ) in glycogen, and 40 kcal (170 kJ) in glucose. Triacylglycerols constitute about 11 kg of his total body weight. If this amount of energy were stored in glycogen, his total body weight would be 55 kg greater.

The animal exception — glycogen
A limited amount of fuel is stored as glycogen in animals. The increased weight load is offset by the advantage of rapid mobilization and the fact that glucose is obtained (animals cannot convert fatty acids to glucose).
The plant exception — oils in seeds
Plants do not walk around, so weight is not generally a consideration that would induce them to store their reserves as fat. They can develop large tubers under the ground, for example. However there is an advantage to minimizing weight in the energy reserves required for the development of seeds — it allows for easier spreading in the wind or through animal consumption. Thus one can rationalize why the energy reserves in seeds are oils (lower melting point triglycerides on account of their greater unsaturation).

Here is my try.

Why do plants store energy as carbohydrates and not as fats?

Is it because they can't? That isn't the answer as we have corn oil, palm oil, coconut oil, olive oil, sunflower oil etc. So plants can and do store energy as lipids.
Perhaps the question is better rephrased as "Why isn't the main store of energy in plants lipids like mammals."
My guess is because plants do not move as actively as animals. A plant is rooted to a spot by its root system. Hence there isn't an advantage of a storing energy in a high density manner, particularly when lipid synthesis takes more energy compared to sugar synthesis.
So aside for specific examples, there is no advantage to store energy in lipids for a plant. There is no need to pay for a compact source of energy when you will never move as an adult.
As a seed... that may be useful... and this is why all our plant oils comes from seeds of one sort or another.

Quick answer: Animals need mobility while plants favour stability.
Explanation: As you mentioned fat is a more effective storage form of energy. Plants though, reserve energy through starch (carbohydrate) and not through fats as it would be expected. This doesn't mean they don't use fats at all (i.e. oil seeds).
An energy storing molecule must save energy (as the name indicates), but it shouldn't be too heavy and it should be stable enough so that it's functional within the organism. Fat is the most lightweight molecule storing energy. One gram/fat stores more energy than one gram/starch or protein. Thus, the weight of a moving organism would be less if it stored fat instead of starch. But plants don't move around so weight saving is not a real necessity.
So, a heavy starch molecule is more stable than a lighter fat molecule which is comparatively more important for plants in order to provide long-term stability. Another reason why they store mainly starch instead of fats is alternate flowering for example, where the plants save up some starch every year (depending on the plant) and then use all the saved energy at once while blooming. Fats wouldn't have lasted for that long because when fats or oils are exposed to air, they react with the oxygen or water vapor and form short-chain carboxylic acids.


text:
Potential immunization against airborn viruses
I have had an idea based on the principals of a virus and their properties and how they enter the cell by tricking it into believing it is a protein etc.
If we coated a copper particle (or another type of metal which should neutralize the atomic structure) and utilize the process they use to induct themself into our cells by mimicing the methods they connect by, would ejecting it in an aerosol steralize the earth from that specific airborn virus?
My ideology seems to fit that if we don't immunize the atmosphere against viruses that they will always naturally occur due to the Entropic nature of the universe. Does this fit into current medical science?

A lot of airborne viruses enter through sialic acid receptors. If someone can make a spray that blocks those, viruses will have no receptors available to bind. It's similar to closing unused ports or banning incoming connections on a computer network interface to prevent hack attacks and block self-replicating malware. I'm surprised there aren't known examples of cells that retract or alter/randomize the shape of commonly infected receptors when they aren't in use.

Could you clarify what precisely do you want to coat the particles with. Ligand molecules to block the cell receptors or receptor molecules to "mop up" the viruses?


text:
Infant Death Adjusted Historical Human Lifespan
I had found a good paper at one point to describe this but I can't seem to locate something similar now. I am looking for a manuscript that describes average human lifespans throughout history/prehistory especially adjusted for infant and child deaths but it would be nice if there was un-adjusted data as well. Does anybody know of a reference with this information?

Related Q/A with some relevant references: Survival curve in early humans

I assume you are asking about expected (mean/median) age of death, for people that survived young childhood(?).

@fileunderwater Unless I'm missing it I do not see the answer at the linked page, but yes I am looking for mean/median age of death for those that survived childhood compared across time (ideally prehistoric times up until recent times).

The link goes directly to the answer (Q above). This doesn't directly answer your question though, but contains some information on infant/child mortality in different types of human societies.


text:
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.


text:
Why do cats' claws retract?
Humans have nails, horses have hooves - but they are always exposed. Why are cats' claws retractable rather than always exposed? Is it related to "Why are there nail growth differences  between humans and other mammals?"?

Just a speculation, but cats' claws are a lot sharper than the other examples you gave, and are more likely to get caught on things(particularly when a cat is stalking prey), dulled by the environment, or cause self-injury. The purposes and uses of hooves, in particular, are quite different. When would it ever be beneficial for a horse to retract its hooves?

Retraction of claws is a feature of the cat family, Felidae along with some civets that helps them keep those sharp by preventing unwanted wear.These claws are important for the members of cat family, including domestic cats that hunt preys by grasp attack rather than bite.
However cheetah among the big cats that usually hunt through bite-attack, has evolved to have semi-retractable claws that help it generate traction.
In pet cats it has offered another advantage:
Retraction keeps them from getting tangled in fabrics.
Sources:

Wikipedia
Russell AP, Bryant HN. 2001. Claw retraction and protraction in Carnivora: the cheetah (Acinonyx jubatus)
as an atypical felid. J Zool ,Lond 254:67-76.

A footage of cat hunting.

from my understanding the reason cats claws are retractable due to the tendons in the cats paw http://kids.britannica.com/comptons/art-53056/All-cats-except-the-cheetah-have-retractable-claws