text:
How do you increase eumelanin but not pheomelanin?
Are Scientists currently looking into this?

Where do you want to increase eumelanin, in the skin? And why would you do so?

I read that it is more efficient in protecting against skin cancer. I have also read that you usually cant increase Eumelanin without increasing Pheomelanin. Is there a way?

Please edit your question to include those details (where, why,...) for future readers , as they will then be more likely to attempt an answer.

I doubt that this will be really successful, since the synthesis is rather complex and can be influenced (positively and negatively) in many ways. First, the synthesis pathways looks roughly like this:

The first step is identical for both melanin forms, it is the conversion of the amino acid tyrosine into dopaquinone by the enzyme tyrosinase. The next steps are different for each process and only one of the possibilities can happen at any given time. The decision is done by the availibility of the necessary components. When the cysteine concentration in the cell is high, the pathway goes exclusively into the direction of pheomelanin, only when the cyteine concentration is lower than 0,76µM eumelanin is made (see here and here for details).
But this is not the only influence on the reaction. The availibility of dopaquinone is critical, and the activity of the tyrosinase can be influenced by the pH of the melanosome (the compartiment in which the pigment production takes place). The tyrosinase activity for people with dark skin is about 10 times higher than for people with pale skin (see here and here for details). The difference here is mainly the pH, which is neutral for dark skinned people and acidic for pale.
Then there is of course the availibity of tyrosine (which is less of a problem, as this amino acid is not essential) and also the availibity and activity of downstream enzymes for the eumelanin production as tyrosinase-related protein 1 and dopachrome tautomerase.

Thank you Chris, very interesting. I am guessing that there isn't a way to naturally reduce the amount of Cysteine (to increase the chance of producing Eumelanin) or influencing the pH to neutral?

I don't think so.

Is this a "no goer" on any level then? Surely if we can increase Eumelanin we can increase the efficiency against skin cancers.

Is there a way to take an Eumelanin supplement?

I wouldn't say it is completely impossible, but it will be difficult. And the question is, if it is wise to do so. You have to mess around in some pretty fine balanced pathways and nobody knows what side effects this could have. Using sun protection and/or avoid to short clothes in the sun works as well and is non-interventive. If you supplement melanin with the food it will most likely be metabolized.


text:
What does chromosome CHR_Un, CHR_MT in the ftp site of NCBI mean?
I am not a biologist. But need some genetic data. So I searched internet and reached NCBI's website. I came to know from the FAQ page that I can the complete genome data of organisms from ftp://ftp.ncbi.nih.gov/genomes/. So I went to the FTP site and opened the homosapien section ftp://ftp.ncbi.nih.gov/genomes/H_sapiens/. I found folders CHR_1 to CHR_22, CHR_MT,CHR_Un, CHR_X and CHR_Y.
My doubt is this : Normally there are only 23 pair chromosomes right? 1 to 22 pairs OK. XY make another pair. Then what are MT and Un ?
And the folder which I am looking is a genome of male right?

chr_MT: List of variations that map to the mitochondria
chr_Multi.txt.gz: List of variations that map to multiple chromosomes
chr_UN: List of mapped variations that are on unplaced chromosomes
see here for more information.
This is the reference genome for human, as far as I know there is no discrimination for it into male/female.

If it was female genome , do we have to consider X twice.

@terdon : Do you mean the AGTC sequences as 'List of variations'?

@dexterdev I did not answer this, Chris did. I just edited which is why you see my name there. I don't know what Chris meant by that since I can't find that file on the FTP site nor see it mentioned in the FTP's README (which, by the way, you should read).

OK @terdon I will read it.

@dexterdev "List of variations" simply means variations from the reference sequence.

@Chris I will have read more to understand these. For example what is the "reference sequence" here then?

The reference sequence is the sequence of a genome which is considered to be the "normal" sequence of this species. This varies from individual to individual due to a individual set of insertions, deletions, polymorphism and so on.

source: Stack Exchange

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

sort: votes


text:
Why Rh conflict happen but no ABO conflicts?
I wonder why Rhesus conflict can happen during pregnancy and mother can make antibodies against Rh protein (I think the correct name is D protein), but it doesn't happen if mother has different ABO type than the child?

It happens, but it is very rare.
Anti-A and Anti-B antibodies are IgM type. They do no cross the placenta. Sometimes IgG can be produced and lead to the hemolytic disease of the newborn.
Anti-D antibodies are IgG type and can pass through the placenta.

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


text:
Relationship between action potentials and EEG recordings
It is possible that I am overthinking this but I have difficulties relating the neural activation to the amplitude and frequency of EEG recordings.
For example; if at the EEG location P3/P4 we observe alpha waves at 10Herts, what will that tell us about the action potentials and membrane polarisation within the population of neurons generating the wave at this frequency?
Also, high amplitude within alpha frequency may indicate attention deficits, but how is the high amplitude related to or explained in terms of electrochemical activity within a neuron?
Informed replies are very much appreciated!
Many thanks

Most of the EEG waves are not directly generated by action potential, because it is too short and has a high frequency. They are generated by synaptic activity (overall propagation potential of axons).
The amplitude of this propagation potential depends on the impedance of the brain. Higher impedance means higher amplitude. Impedance is higher for low frequency signals.
The amplitude is also affected by the direction of the EEG vector so parallel axons which go in the same direction should produce a higher wave in amplitude.

Reference: Rudell AP, Fox SE. The propagation potential. An axonal response with implications for scalp-recorded EEG. Biophys. J. 1991 Sep;60(3):556-67. doi: 10.1016/S0006-3495(91)82085-9. PubMed PMID: 1932547.

Hi Cornelius, Your answer is really helpful, and thanks for the link.


text:
Have there been any theories put forward as to the reasons behind Temperature-Dependant Sex Determination in reptiles?
This applies to most if not all reptiles, but I'll write about leopard geckos since that's what I know.
Incubation temperature of the eggs makes a big difference in the development of the gecko. Obviously excessively high or low temperatures will kill the embryo, but inside the safe temperature range there are some interesting effects. The most well-known is Temperature-Dependant Sex Determination (TDSD).
Studies have been done and it is quite well-documented that:

Incubating eggs at the mid-point of the safe range results in predominantly male offspring.
Incubating eggs at the high or low end of the range both result in predominantly female offspring.

According to my gecko book, there are also some interesting effects regarding males that hatch from female-biased temperatures being more sexually active but less aggressive to females than the "macho" males produced at male-biased temperatures, females at female-biased temperatures being the most fertile and high-temperature females being more aggressive than lower-temperature females.
(Incubation temperature also affects colour - specifically melanin production levels. AFAIK it's not known whether this is a direct effect of the temperature or an indirect effect from the changes in sex hormones at the different temperatures. It's probably a different enough issue to warrant a separate question, though.)
Going back to TDSD, my question is: what theories have put forward to explain this sex determination? Evolutionarily speaking, how did this come about? Are males less likely to survive so they are only produced at safe temperatures? Does the optimal male:female ratio for propagating the species change in adverse conditions?
I'm not looking for random guesses. I'm interested in knowing if there have been any theories put forward from knowledgeable and reputable sources.

How is this possible? per Wikipedia Y chromosome defines gender in mammals but it is different in Non-mammals i.e for reptiles.

@JamesJenkins Not really sure if you're attempting to answer the question or just providing extra info. In case it's not clear in the question, I'm not asking how it's possible, I'm asking why reptiles have evolved that way; what advantage it gives. Though I did find that link interesting as I was unaware of the differences.

Not answering, I was only aware of the mammal process and thought it applied to all species.

I had the chance to read part of this book before its releasing. I'm sure you'll like it.

Welcome to Biology StackExchange!
Environmental sex determination is tremendously interesting.
It looks like the most common explanation is that temperature-dependent sex determination (TSD) is the original form of sex determination, and genetic sex determination has evolved multiple times in different animal groups since then. Reptiles are a mish-mash of different mechanisms.
If TSD came first, then the real question is not why did it evolve, but why is it still around. And the answer is likely because it works well enough. I couldn't find a lot of evidence that females make varying choices for next temperature, so in "real life" it might mostly be that plenty of males and females are always born. There is also recent evidence that genes affect when the temperature has an effect, so again, temperature alone is unlikely to drive sex ratios.
As far as possible advantages of TSD there is no definitive explanation that has held up to testing. It is possible that ideal female development has slightly different requirements than male development, so nest location choice by the parent may act to produce more females if the current environment supports them more than males. For instance, it has been shown that having more female offspring when temperatures are higher results in larger females.
Sorry to not have a simple answer for you. The whole idea is fascinating, along with other environmental triggers to development, like worker ant larvae becoming a winged queen if given the right nutrition, or butterflies that add "eyespot" pigmentation to their wings in wet years with increased predators.


text:
How does Oedipus complex fit in the evolutionary theory?
This is somthing that really makes me curious. How is posible that trough a  evolution process the best posible candidate is the one that falls in love whith his progenitor?

Can you provide (biological) scientific evidence that the Oedipus complex is real and not just a psychological theory?

It doesn't.  The Oedipus complex is one of Freud's theories to explain human behavior, not something that is endorsed by the fields of psychology or psychiatry.  Freud had a lot of interesting theories, some of which remain core concepts in psychology, and some of which have been marginalized or rejected.
There are some professionals who feel it has merits for consideration, to one degree or another, but if you look at publications by the APA (American Psychological Association) and Psych.org (American Psychiatric Association), you won't see in their practice guidelines.
APA: http://psycnet.apa.org/journals/pst/32/4/535/
Wikipedia: http://en.wikipedia.org/wiki/Oedipus_complex#Criticism

If you're asking how might it fit with evolution if it were to be true, that's more of a philosophical question - which perhaps is the better angle from which to approach the question.
In "survival of the fittest" - "fittest" is better described as "those who most successfully reproduce and produce offspring that are also highly successful in reproducing."
Reproducing with one's immediate family results frequently in severe birth defects, the opposite of "fit."  Those who want to reproduce with their mother but don't, and reject all other mates, will not reproduce.  Not "fit."  The only possibility similar to the oedipal complex is that males choose mates that are like their mothers.
What is true is that we often marry someone similar to our parent - but it is not a result of an actual oedipal complex.  Freud wrote the oedipal complex in part to try to explain this phenomenon.  But there are better explanations - we are attracted to that with which we are most familiar, to that which makes us feel comfortable, to that which makes us feel warm and fuzzy.  Our definition of beauty is largely shaped by family faces - because that is what you are surrounded with as your mind develops.  Etc etc.


text:
Do there exist publicly available Genome sequences of a family?
I would like to explore the genome sequence of a publicly available genome sequences of a family (like mother, father, son, daughter...). If such human genome sequences are not publicly available at least any animal's family data is also OK. :)  I am not a biologist, but aims to just understand things more clearly.

For animals and other organisms, NCBI has a database for publicly-available sequences:
https://www.ncbi.nlm.nih.gov/guide/howto/retrieve-seq-org/

I know that 1000 Genomes has sequenced Mother-Father-Child genomes from populations around the world (I think at least some of these samples were obtained from HapMap) and their data is publicly available by following the links in their website.


text:
Is it possible to be (briefly) aware you had been decapitated?
If a person's head was cleanly and rapidly decapitated by a sharp blade slicing through the neck, such as would happen on the guillotine, could that person remain conscious? If so for how long? Long enough to be aware of (the head) falling down and hitting the ground?
Obviously it would be brief due to lack of blood supply, but it seems plausible that it could be a few seconds.
Or is there some inherent neurological shock due to the severing the top of the spinal cord that would cause near instantaneous loss of conciousness?
Could Marie Antoinette have seen her own severed neck from the basket below the blade?

According to this, in rats it takes about 17 seconds after decapitation for the EEG to become iso-electric. But there is no known correlation between EEG and consciousness. Also at 50-80 seconds after decapitation, EEG being iso-electric, a very slow, late wave appears on the EEG record.
The same article concludes that it takes about 3-4 seconds after decapitation for the animal to lose conscience and perceive no stress and pain.
Also, dr. Harold Hilman states in An unnatural way to die article from october 1983 issue of New Scientist, page 277 that:

Consciousness is probably lost within 2-3 seconds, due to a rapid fall of intracranial perfusion of blood.

So "yes", Marie could have looked up from the basket and seen her own severed neck. Whoa...

interaction with the head covered in extreme detail by this "classic"

I remember reading that during the French Revolution Antoine Lavoisier arranged with his assistant condemned to death to blink after the cut off if he still had conscience (Lavoisier was to call his name first to limit automatisms). He reported a possibility that the assistant did hear him (the blinking was apparently not that obvious)


text:
Why humans have the temperature they have?
It is obviously very onerous to generate heat at all, although it has advantages. We don't have to lie on the sun like a crocodile to get warmer. And we avoid the freezing of our body water by out own means. But wouldn't just a little of heat be enough?
Why do humans go as far as 37 C? Couldn't we just have a temperature of 10 C to avoid freezing but stay at it?

Read this article http://www.ncbi.nlm.nih.gov/pubmed/15217694. It says that a lower temperature may have anti-aging effects, but it seems the human body is not 'designed' for other temperature http://en.wikipedia.org/wiki/Human_body_temperature#Human_temperature_variation_effects

It's simply not possible for humans to live with an absolute body temperature below 20 C for the simple biophysical reason that it would prevent flux of protein through the Golgi and therefore biosynthetic and secretory pathways, as well as endocytosis. The lipid membranes become too "stiff" to correctly function.
My own sense is that the nominal 37 C body temperature is a result of all of the ATP hydrolysis reactions that happen all the time. The chemical reaction is not efficient, and some of that energy is absorbed, heating the tissue.
There are various grades of hypothermia, from mild (33–35 °C) to severe (< 28 °C). Death from hypothermia results only from prolonged exposure, for example, being in ice-cold water results in death after 50-100 minutes. The basic mechanism is that the body dies from a combination of decreased electrical conductance of pacemaker nerves in the heart, and a slowed heart rate incompatible with sustaining life. Ultimately, hypothermic death is a dysregulation of the body's thermoregulatory mechanism, rather than an immediate biochemical problem as I've pointed out above. For a detailed review, there is an open access article detailing hypothermic etiology and pathophysiology.
M.L. Mallet. Pathophysiology of accidental hypothermia. QJM (2002) 95 (12): 775-785.

And why are temperatures of 35 C or less already life threatening? What happens (or probably doesn't happen) when the temperature drops 3-4 degrees?

it isn't out of the question for eukarotes to flourish at low temperatures - see http://en.wikipedia.org/wiki/Psychrophile , membrane fluidity could be adjusted via the content of unsaturated fatty acids in phospholipids. What would be challenging would be frequently undergoing large temperature shifts.

@Alan - that's true. I should clarify I was talking about humans only since that was the focus. I've edited  my answer.

If I had to guess, the reason human have the body temperature we do is because the ancestors of placental mammals had that body temperature. You will notice that all placental mammals have nearly the same body temperature http://www.infonet-biovision.org/AnimalHealth/Tools-livestock-care-and-treatment
That being said, birds have a higher body temperature than placental mammals http://www.sciencedirect.com/science/article/pii/030096299190122S
But why the higher body temperature....as you say why not just high enough for muscular activity?
One potential answer is at higher temperature, animals are better able to resist fungal infections for the simple reason that most species of fungus don't grow well at temperature above room temp. Declining by 6% of species for every 1C rise https://www.sciencedaily.com/releases/2010/12/101222121610.htm.  The optimum as calculated in terms of energy cost to maintain that high body temp vs number of fungal species to fight against was estimated to be 36.7 C, about body temp for mammals, and resting body temp for birds.


text:
Biology in romantic love
Hi could anyone explain the biological basis behind romantic love. What is the biological basis of falling in love?I know that serotonin and dopamine are secreted when we first fall in love. What happens after that as we move on to the more advanced stages of love. Why is it that after some time, we no longer feel the initial feelings of love. What is the biological basis behind it. And also why do we feel so heartbroken if we happen to fall out of love? What is the biological basis behind it?

courtship rituals like romantic love are a product of evolution. for humans they are often engineered to create a long term bonding.  all human cultures have romantic love.  Human love is more biological than we often expect.  I'm not an ethologist, but these behaviors are so unusual when you stand back and look at other animals and primates.

I have a theory that we may not feel the same after a few years with a person because maybe like when we need higher quantities of a drug to get the required effect in addicts over time, the same amount of dopamine/serotonin cocktail just doesn't do much to our senses after a couple of months/years..

Dopamine, norepinephrine, and serotonin are more commonly found during the attraction phase of a relationship.
All these chemicals stimulate the brain's pleasure center. But this stage only lasts 1.5 - 3 years [2]. That's why 'we no longer feel the initial feelings of love'.
Oxytocin and vasopressin seemed to be more closely linked to long term bonding and relationships characterized by strong attachments [1].
Attachment makes relationships last for years and decades. It is based on commitment and mutual friendship. Oxytocin and vasopressin are at higher levels [2].
The neurological process involved in the perception of heartache is not known, but is thought to involve the anterior cingulate cortex of the brain, which during stress may overstimulate the vagus nerve causing pain, nausea or muscle tightness in the chest [3].

Image from Wikipedia [1]
References:

Wikipedia contributors, "Biological basis of love," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Biological_basis_of_love&oldid=613867553 (accessed June 26, 2014).
Wikipedia contributors, "Love," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Love&oldid=614240299 (accessed June 26, 2014).
Wikipedia contributors, "Broken heart," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Broken_heart&oldid=613979584 (accessed June 26, 2014).

Great answer.  Has there been any solid work on pheromone-like molecules and human compatibility?

@PlaysDice there are a few articles about that. Here is one http://www.ncbi.nlm.nih.gov/pubmed/15653193


text:
What is the normal duration of human sexual intercourse?
Wikipedia is saying:

Men's typical ejaculatory latency is approximately 4–8 minutes

How the researchers measured this? How did they know if the test subjects weren't suffering from premature ejaculation?
And is this measured from the start of erection or from the start of penetration?

First, "premature ejaculation" is a matter of definition. Here is an authoritative source. From the American Urological Association's news site, a 2008 notice:
'The ISSM [Int'l Soc. for Sexual Med.] has defined premature ejaculation as “a male sexual dysfunction characterized by ejaculation which always or nearly always occurs prior to or within about one minute of vaginal penetration; and, inability to delay ejaculation on all or nearly all vaginal penetrations; and, negative personal consequences, such as distress, bother, frustration and/or the avoidance of sexual intimacy.”'
The main author of the ISSM paper was Sharlip. Sharlip ID, Hellstrom WJG, Broderick GA: The ISSM definition of premature ejaculation: a contemporary, evidence-based definition. J Urol, suppl., 2008; 179: 340, abstract 988.
If this is the threshold for PE then it is not a stretch to say that almost anything else is within normal limits. If "typical latency is 4-8 minutes" then 1.5 minutes would be near the low extreme of normal.
I think the issue of stress is at least as important as duration. If something isn't bothersome it never becomes a medical issue.
A nice study involving 491 men is reviewed here. The mean IELT (intravaginal ejaculatory latency time) is 5.4 minutes. As you can see from the graph on the site, most of the results are contained in the first few minutes with a tail of longer times to the right.
The original source for that information is MC Waldinger et al. A multinational population survey on intravaginal ejaculation latency time. Journal of Sexual Medicine 2005 2: 492-497. This also addresses your question about the timing of measurement--it's post-entry.
An expert in this area could update my information but it's a recent average so I don't think things have changed much.


text:
What types of light can't a plant photosynthesize in?
I have a plant on my desk, and it got me to wondering: Can my plant use the light from my monitors to photosynthesize? If so, what light (apart from green light, to a degree) can't plants use to perform photosynthesis?
I know that plants have the photosynthetic pigments to absorb many different wavelengths of light (primarily red and blue) but would there be certain types of light it can't use?
(The specific plant by the way is Schlumbergera truncata)

possible duplicate of What does "chlorophyll photosynthesis peak" mean in relation to photon wavelength?

The other is a duplicate of this, not the other way round?

Chlorophyll can use a quite broad range of light for photosynthesis, the only range where it is not working is approximately between 500 and 620nm. See this adsorption spectrum of chlorophyll (from the Wikipedia article on Chlorophyll):

The lack of chlorophyll to absorb light between 500 and 620nm (roughly) results in the green color of leafs, because this light is reflected.
Besides the wavelength also the energy of the light is important, so plants will grow better in sunlight than in the light of your monitor. This link about the maximum effectiveness of photosynthesis is also interesting.

I like this image because it also shows why chlorophyll is green.

Would I be right to assume, then, that the monitor's red and blue pixels would be useful for the plant, while the green would not? (granted, a monitor produces so much less light than the sun that having it nearby isn't doing much for the plant...just theoretical)

Theoretical, yes. And this is what special growth lamps for plants do. They leave out parts of the spectrum. The Wikipedia article I linked contains a photo of such an installation.

"Besides the wavelength also the energy of the light is important" - wavelength defines the energy of light and vice versa. What you wanted to say was the intensity of light field.

It might also be of use to know that plants 'use' certain wavelengths of light as a sort of sensory input, in addition to providing the photosynth energy . The same can be said for light-dark cycles. Plants know when winter is coming as the days get shorter. https://today.duke.edu/2015/07/plantlightsensors                Phytochrome https://en.wikipedia.org/wiki/Phytochrome      Phototropism  https://en.wikipedia.org/wiki/Phototropism


text:
Is there an evolutionary explanation for the black spots around a pandas eyes?
I couldn't seem to find one elsewhere, at least not with a scientific source.
It would seem as it's quite a striking feature there would be an advantage it would infer.

From Wikipedia: "Although scientists do not know why these unusual bears are black and white, speculation suggests that the bold coloring provides effective camouflage in their shade-dappled snowy and rocky habitat." With a reference to Giant Pandas by Karen Dudley (1997).

One can create a selectionist explanation for any trait, but all such explanations have very little scientific content.

It could be related to stopping light glare too, not entirely sure why a panda would need that but living in snowy areas there is a lot of sun glare... athletes use this trick, particularly in ball sports http://en.wikipedia.org/wiki/Eye_black but remember, not everything has some wonderful evolutionary explanation, some stuff just exists for no real reason.

As your commenters have suggested, no.
In order for an explanation to be a good evolutionary explanation, it needs to have a testable hypothesis and a mechanism to test it.
The most common mechanism for testing the crypsis (camouflage) hypothesis is to take a large number of closely-related species, and see if their coloration differences are correlated to a particular habitat. Since pandas have few black-and-white relatives, there is no statistical power in this analysis.
Another option is to take a large number of pandas, create a treatment and control group and bleach the treatment group (or their eyespots) white, and compare survival or visual acuity. Unsurprisingly, this has not been done.
Here's a nice article to animal coloration for those that have access:
Caro, T. I. M. (2005). The adaptive significance of coloration in mammals. Bioscience, 55(2), 125-136.

I quite like the explanation I found on the website of "Exploring the BioEdge". Robin and Honeybadger explain the black and white colouration as follows: To minimize the risk of being attacked by the tiger, the colouration of the giant panda is aposematic, warning would-be predators of its vice-like hug and bite. This warning signal, visible even in poor light, consists of a black-and-white contrast on the face (ears and eyes) as well as the body as a whole.”
http://explorebioedge.com/bio-bullets/item/43-warning-colouration-in-the-giant-panda.html


text:
Has it been enough time for evolution through simple natural selection?
Let first state that I understand natural selection. I am not asking if evolution happened. I see evolution as a fact, but I do not assume the current theory of natural selection as fact.
I wonder if there has been enough "time", or number of generations, needed to create enough mutations that lead to the known genetic complexity of all species today (or even just until dinosaurs), since the Last Universal Ancestor.
Is it possible to prove, or estimate this time?
Note: There was obviously enough time for evolution to occur. My question is if, the known mechanisms of mutation and theory of natural selection, are enough to justify the evolution in this amount of time.

The evolution to the current state of life on earth has occurred through some 3.8 billion years. During this time it has gone from the most basic forms of life, simple self-replicating units, to the complex beings we see today. Evolution, the process of change within a collection of units, is caused by 4 factors, mutation, selection, drift, and gene flow. So firstly, the current state is not thought to just be the result of natural selection but instead a result of all the mechanisms of evolution.
Selection can itself be subdivided in to two types, natural and sexual selection. Therefore "natural selection" does not even contain all types of selection. Selection is not a simple process, but occurs in a very complex manner, simultaneously affecting the many levels upon which selection can act (nucleotide, gene, organelle, cell, organs, organism, population, species, ecosystem etc.).
There are a number of things to consider when discussing whether enough time has elapsed for the mechanisms of evolution to produce the variation we see today, a primary concern is quantifying how much variation there is in the world that has evolved. Here are some other factors which would determine the likelihood at arriving at that level of genetic variation:

Mutation rates (per generation)
Generation times
Offspring per generation (affects the number of potentially new lineages per generation)
Genome size (number of potential sites)
Complexity and strength of selection
Population size (affecting drift and the efficacy of selection)
Genetic admixture/inbreeding/potential gene flow
Recombination rates
Social structure
Environmental variation

These all vary wildly in contemporary populations and would also have varied in ancestral lineages too, this makes it, in my opinion, near impossible to even get a rough estimate of how likely our current state of variation evolved via the known mechanisms of evolution. But there is a simple answer, all variation you see today arose from simple life and evolved in the last 4 billion years via the four known mechanisms of evolution - which, in part, includes natural selection. The proof is in its existence and the absence of other possible (plausible) mechanisms.
To illustrate the complexity of the problem and the high likelihood of these mechanisms leading to substantial genetic variation (this is highly unscientific):
I'd suggest a very conservative estimate of just mutation rates and time since life began (3.8 billion years, Last universal common ancestor [LUCA]), using approximate human mutation rates (175 per generation and 25 years per generation = 7 bp mutations per year), would suggest a single lineage from LUCA to now could have had some 26 billion mutations, an average of 8 mutations per site in the human genome (this would assume constant mutation and generation rates, and starting genome size of 3 billion BP in LUCA - obviously completely ridiculous, but it's just an illustration and assumes evolution purely by drift and mutation).

" the absence of other possible (plausible) mechanisms" - who is to decide what is plausible? what i cannot see cannot exist?

Whatever there isn't evidence for might as well be treated as non-existent.
If your preferred theory is that an invisible dragon is secretly directing mutations in order to reach a desired outcome then show me evidence for that. Without evidence for this dragon or even a hypothesis for how it might work in the world while simultaneously avoiding detection then this theory isn't anything more than an unsubstantiated hypothesis.

"The proof is in its existence and the absence of other possible (plausible) mechanisms." This is precisely the same argument religious people use for God.

As in, the existence of so much diversity, which we know came about by evolution, is proof that there has been enough time for evolution of so much diversity.

There was a paper that attempted to assess this published in 2010
There’s plenty of time for evolution - Herbert S. Wilf and Warren J. Ewens
There is also a layman's explanation of this here
Basically when we account for the fact that genes evolve in parallel under a number of simultaneous trials, it appears that there is indeed enough time for species to have evolved as far as they have.

What's your average contemporary DNA pol error rate? Something like 10^-9 errors per bp? Your average prokaryote generation time is maybe something like 10 days. LUCA is thought to be about 3.5 billion years old. However, it would be expected that DNA pol error rates were far higher in the past. In fact, if RNA + protein world existed (I think a strong case can be made for it), we're looking at multiple orders of magnitude faster change. Eukaryotes with their longer generation times don't pose much problems to the calculations, since the vast majority of domains in Eukaryote proteins were prokaryotic inventions and Eukaryote proteins are mostly just prokaryotic domains shuffled around. I agree with the above answer of there being way too many variables involved (that we would basically have to guess) for robust calculations..

-1. This doesn't actually answer the question.


text:
Why doesn't Diabetes cause death by starvation?
The main cause for diabetes is lack of insulin in the body. Insulin is the hormone that allows body cells to absorb glucose from the blood. With out insulin, the body cells can't get glucose from the blood. So, why doesn't diabetes cause death by starvation?

I mean, the short answer is "it does". But on a cellular level, and unevenly. So the effects are a little different. Most of this stuff happens with regular starvation also: http://www.diabetes.org/living-with-diabetes/complications/ketoacidosis-dka.html

Diabetes before the advent of insulin therapy

Not all cells depend on insulin to take in glucose from blood (e.g. vascular endothelial cells). But the majority do (muscle tissue and fat tissue).
The lack of insulin causes the cell to use auxiliary metabolic pathways to generate its energy [1]:

in muscle, the protein breakdown is stimulated
liver gluconeogenesis is stimulated by low insulin levels and high amino acid levels in blood and using substrate from muscle and fat tissue
glucocorticoids stimulate lipolysis
liver starts ketone body synthesis, which along with medium chain fatty acids prove to be quite a good alternative energy source for the brain

Energy from nutritional principles is as follows:

Lipids = 9 kcal/g
Proteins = 4 kcal/g
Carbohydrates = 4 kcal/g - the most important because they are used as is. Lipids and proteins require energy from other sources to start chemical reactions which yield energy.

References:

Mark Brandt, Ph.D. Endocrine Notes Supplement from Rose Hulman Institute of Technology, pages 78-80
Wikipedia (links)

Glucose enters your cells via a family of transporters.  A primary transporter in muscle and fat cells is known as GLUT-4.  Insulin stimulates GLUT-4 to move from the interior of a cell to the cell surface, where the glucose can then bind to the GLUT-4 transporter and enter the cell.  However, there are plenty of glucose transporters on the cell surface, even when there is no insulin.  In fact, there are enough transporters on the cell surface to allow the cell to get enough glucose to sustain its energy needs.  Thus, glucose transport into cells is never truly dependent upon insulin.  Insulin enhances the uptake of glucose into cells, but it is not required for it.  In fact, when you knock out the insulin receptor in mice so that insulin cannot stimulate glucose uptake into muscle or fat cells (yet you keep the insulin receptor intact on other cells like brain and liver), the animals do not become diabetic and they have normal blood sugars.-https://www.ncbi.nlm.nih.gov/pubmed/15254588
Metabolic tracer studies have allowed us to learn how insulin operates in humans in vivo. When you take a type I diabetic off insulin, blood glucose climbs sharply. However, it's not because glucose can't get into cells. In fact, glucose uptake into cells actually increases. This is because the concentration of glucose in the blood is so much higher than the cellular concentration that glucose must move into the cells (remember, there's already enough glucose transporters on the cell surface even if there's no insulin). So why does blood glucose climb so high? Remember that the amount of glucose in your blood is both a function of how much glucose is entering the blood (the rate of appearance), as well as how much glucose is leaving the blood (the rate of disappearance). In a fasted diabetic without insulin, all of the glucose is coming from the liver. Remember that your liver helps maintain blood sugar levels when you are fasted by releasing glucose; this glucose comes from both gluconeogenesis (the formation of glucose from non-carbohydrate sources, like protein) and glycogenolysis (the breakdown of glycogen stored in your liver). Insulin acts as a brake (a chalone as Dr. Schafer described it) on these processes. Thus, when you do not have insulin, you have runaway gluconeogenesis and glycogenolysis. The high blood sugar in an uncontrolled diabetic is thus caused by overproduction of glucose from the liver, not because glucose can't get into cells.-http://m.bja.oxfordjournals.org/content/85/1/69.short


text:
What are the blood groups for human beings?
Human blood groups are of 4 types with negative and positive of each types (Wikipedia). But according to this forum thread there are some other types too:

A+,A-,B+,B-,O+,O-,AB+,AB-,A1+,A1-,A2+,A2-,A1B+,A1B-,A2B+,A2B-

I'm going to make software for blood donation, where I need to put a dropdown list of actual blood types. I had intended to use:

[ Select Blood Group V ]
[ O Negative           ]
[ O Positive           ]
[ A Negative           ]
[ A Positive           ]
[ B Negative           ]
[ B Positive           ]
[ AB Negative          ]
[ AB Positive          ]

But now I am uncertain whether this is appropriate. What is the most suitable list of blood types for donors?

I've edited your question, mainly because you started it with "We all know...".  This is unnecessary and is often either offensive (you have no idea what I know, and you are suggesting I am ignorant if I am not aware of your assertion) or a ploy (presenting something dubious as a fact). If you really must, use "It is well known...". I've condensed the rest, which was too verbose. Also note that in English "software" is uncountable, it never has an indefinite article — either "software" (in this case) or "the software" (referring to a specific program), but never "a software".

@David thanks for the edit and the enlightenment. You are always welcome.

As far as I am aware it is the RhD and ABO blood groups that matter with blood donation - though you may wish to contact a blood donation organisation for more specific information on how they handle & categorise the blood.
But using just RhD and ABO gives 8 combinations, positive and negative of A, B, AB, and O. You can find out more about the blood groups, blood donation, and the characteristics of blood groups here.
The subgroups you allude to are due to differences in the number of the antigens on the surface of the blood cell, for example the A1 group have ~1,000,000 A antigens per cell whereas A2 variants have ~250,000. The A group has ~20 subgroups, the vast majority of people are A1 (~80%) or A2 (~20%), and the other groups make up less than 1% of the population.

These two subgroups are interchangeable as far as transfusion is concerned, but complications can sometimes arise in rare cases when typing the blood.

If the blood donor is filling out the info, I recommend you have one dropdown that offers: A, B, O, AB, don't know....  And a second dropdown that offers Rh +, Rh -, don't know. And be aware that the average person is not likely to correctly know their blood type.
Actual laboratory blood typing checks for a large number of possible differences between blood cells beyond just ABO types. The clinician or technician will not use anything as simple as either your drop-down OR the slightly more complex drop-down in the referenced forum post.
If you still want to know more about "what the actual blood types are," recognize that there are LOTS of blood types, including the MNS system, the Kell system, and the Lewis system: http://en.wikipedia.org/wiki/Blood_typing

Thanks. And, And be aware that the average person is not likely to correctly know their blood type. - kudos for the point. :)

don't forget AB blood. :)

Gah. Yes. Corrected.

I would have assumed that someone performing the blood test is typing in the information. I doubt anyone is relying on self-reported information for blood transfusion.

Well, that's the thing. If it's the clinician, they need to enter a LOT more information about blood type than just ABO and Rh. And if if the user is the general public, they aren't likely to be correct. So I'm not seeing how this will be very helpful software.
Unless it's a dating site. Or one of those sites that gives you an ideal diet based on your blood type.


text:
Curious about Brazzein
What is in compound "Brazzein" that it makes it 2000 times more sweeter than sugar?
Can anyone please explain the science behind it?

Does someone care to answer?

If you are pressing people, nobody will care to answer. A common thing here is that we expect people asking questions to try and find out the answer first and then explain in their questions what they already know or at least what they tried to find an answer. This is a stack exchange site, not google.

@skymninge I know that but at least they should initiate something!

No, actually what I meant to say is that it is you who should initiate something.

Brazzein is not even a sugar - its a protein that comes from Oubli, a West African climbing plant.
While I think nearly every living thing from bacteria up to large animals can perceive some carbohydrates as a food source, the mechanisms vary over the tree of life.
Because of this the taste of sweetness in animals varies a lot.  Aspartame, a non carbohydrate sweetener does not register as sweet in all the primates.  Brazzein and aspartame as capable of activating one or more of the human taste receptors.  Receptors are just proteins which sense a stimulus.  They can be activated by other compounds - this is how most pharmaceuticals work.  Sweeteners which are not glucose/sucrose can bind more tightly or affect the structure of the receptors, causing them to send a sweetness signal. Often these compounds also register with other sense receptors and so the sweetness is accompanied by other tastes as well.  It sounds like Brazzein is a clean taste, less likely to have such side effects.
I've not dug fully into this - its clear that some human sweetness receptors are known, but I'm not sure they are all known.


text:
Evolution and the levels of selection
Reading Okasha's "Evolution and the levels of selection" he talks about "the levels of selection problem." There is a bit of a problem with this opening chapter because, while he talks about why the levels of selection problem is a problem, he doesn't define what the levels of selection problem is.
The opening line from the book..

"The levels of selection problem is one of the most fundamental in
  evolutionary biology, for it arises directly from the underlying logic
  of Darwinism. The problem can be seen as the upshot of three
  factors..."

I think what he means by the "levels of selection problem" is that selection acts on many levels, and what is adaptive at one level may be maladaptive at another. Therefore we can not define selection as acting at one single level, and studying it as such is likely to lead to incorrect conclusions - studying selection is not a simple process. Can anyone provide a firm definition of what Okasha, and the general community on the matter, mean by the "levels of selection problem"?
(Note: The factors are the abstract nature of the principles of selection, the hierarchical nature of biological organisation, and the process of adaptation via natural selection).

Reeve and Keller in the first chapter of Levels of Selection in Evolution (Princeton Univ. Press,1999) seem to address this question in the second item in the following paragraph.

The purpose of this volume is to sample current theoretical and empirical research on (1) how natural selection among lower-level biological units (e.g., organisms) creates higher-level units (e.g., societies), and (2) given that multiple levels exist, how natural selection at one biological level affects selection at lower or higher levels [boldface added]. These two problems together constitute what Leigh (chap. 2) calls the "fundamental problem of ethology." Indeed, as Leigh further suggests, they could be viewed jointly as the "fundamental problem of biology," when genes and organisms are also included as adjacent levels in the biological hierarchy. This generalization has the desirable property of immediately removing the long-standing conceptual chasm between organismal and molecular biologists.

The authors suggest definitions of fitness that account for hierarchical relationships (the level of selection problem) by considering the effect of a trait (nepotism among social insects) on "adjacent" biological levels, such as individual and colony.
By measuring what they call 'absolute fitness force' they propose to eclipse what they see as spurious debate over the fundamental level of selection (genes vs. individuals, say).
A somewhat surprising aspect of their discussion emerges here:
"It is still embarrassingly common to read inaccurate statements...that frogs have to produce many eggs to ensure the survival of the species because tadpoles suffer extremely high rates of predation, or that wolves have evolved ritualized displays to establish dominance hierarchies because physical combats would be too disadvantageous for the species. These naive statements betray a widespread and persistent misunderstanding of the level at which natural selection most commonly operates."
Their point is that such statements focus on the wrong level of selection (group), and that stronger selection may occur at the individual level; their overall argument being that both levels should be factored in.
I cannot present this as a 'community definition' but it may be a representative example.

So I am pretty close with my understanding already then? Including selection at all levels is essential to understanding how traits and populations of the units of selection will evolve.

I think there is a debate with 'DNA fundamentalists' claiming that there really can only be one mediator of selection (there is no level of selection problem!) and the multilevel folks claiming that there are forces beyond kin selection that influence evolution.  You might be just representing one pov here. The debate has been published in Science/Nature recently so I think its fair to say that it is not resolved.

@shigeta: Yes, the answer really only deals with the definition. Your comment is a good caveat or if you think it's preferable I can add a note to the answer. Thanks.


text:
Signaling through G protein Coupled Receptors?
There are two different cell lines but we do not know that these cell lines have Gs or Gi proteins, associated with their G-protein coupled receptors. If we wants to know about this. Can we design a experiment through which we would be able to identify specific Gs or Gi proteins in cell lines?

You can design such experiments. Do you know which receptor you're interested in? What have you learned from the literature about how GPCR signalling pathways are evaluated?

I have studied about Adrenergic Receptors. Beta Adrenergic receptrs and alpha2 Adrenergic receptors.. ?

Wat else do you know about your cell line? Are you sure that the two receptors are expressed in the cells in a mutual exclusive way?

I want to know that how can i distinguish between these two cell lines that whether they are Gs or Gi cell lines associated with the G protein coupled receptors..? Beta-Adrenergic receptor (epinephrine) is for Gs and alpha-adrenergenic receptor (acetylcholine) is for Gi.I have this information about the two cell lines..

Thats why I ask if you know if these proteins are expression mutual exclusive. If they are, you can do a simple RNA extraction, cDNA preparation and then do PCR (doesn't have to be realtime PCR) with specific primers to sort this problem.

i've read extensively about these kind of experience and worked in a lab as such. my answer is better do it.

Depends on if you've got antibodies for the associated subunits and the GPCR. If you do a pulldown (Immunoprecipitation) + western blotting would be a good way of checking.

Bez experiments are too difficult and costly you don't need to do that.
Take, label samples then apply ligands and sustenance. The inhibitory will have have a slower rate of growth not death and use a control with replicates. Also if you have the money buy an epac FRET to measure cAMP. Find someone to do the FRET if you can't. It will take a longer than a day but you avoid the whole I gave it too much it was going to die anyways. If you did not initially separate your cell lines by proteins and have a mix of Gs Gi within the cell lines and you need to find which ligand causes a dominant response then you will have to do individuals of these test. There are companies that specialize in growth response.
If not FRET. Find some business with an ION torrent and sequence the genome its really really cheap. If your proteins have known homology to Gs or Gi this will give the best results quickest. If you're proteins function is novel add ligands and the Gi will have less PCR amp than the Gs. Don't do your own NA extraction just let them. I've seen so many samples go bad in delivery because people tried to save a buck.
Also since you had trouble designing this experiment find a company which will run the whole of the experiment for you. Most places with ION torrents have the whole lab setup to run such an experiment and do so on a weekly basis.

ION torrent processing is a great option too! But regarding epac FRET, as far as I know speaking to a few friends, FRET based experiments takes a while to optimise/make them work but could be wrong as I have never done them personally. Getting a company to do this for you is always the most convenient, i agree, if it isn't part of your project.

@Bez yeah pay someone who has one was the theme of my answer

@caseyr547 I don't understand how sequencing genomes would get you anywhere: assuming these cell lines are from the same organism then they will both have the same genome carrying genes encoding all G proteins.

EDITED ANSWER
Based on comments and responses my original answer to this question received I have decided to edit the answer and respond to some questions.
Since I work on proteins, I tend to favour protein based approaches specially when wondering about the presence of a protein. This is simply the case because protein is what is important functionally (purely talking about protein based problems/questions here and not talking about RNAi stuff here) so what I have experienced editors require for majority of papers, they want to see some sort of protein work. Now I'm aware that is not always possible since the antibody (Ab) might not be very specific or sensitive specially for low expressing proteins. If a protein is highly transient that makes the problem even worse, which is why many people resort to mRNA expression to make deductive reasoning for the presence of proteins although that makes a number of assumptions about how the mRNA is processed and whether the relationship between mRNA expression and protein expression level is linear but thats another discussion. So all I'm trying to say is that it's important check for the presence of a protein using Ab based techniques, which are immunohistochemistry (IHC) and western-blot (WB).
So my primary recommendation is to use Gi and Gs species specific (non-cross reactive) antibodies to check for the presence of your proteins of interest and always use Ab heavy chain control for IHC and a negative control for your WB using a sample that you know doesn't express your proteins of interest, if thats available. IHC also tells you some spatial information and whether Gs and Gi are both present in the same cell line or not and if they co-localise etc etc! Obviously check for Ab availability and if its compatible for IHC or WB procedures.
The other method that is feasible is if you know your two different cells express only one of the Gs or Gi exclusively, you can look at their specific inhibitors and add it to some of your cells and the chances are if the dose is high enough it will cause the cells to die since Gs or Gi are crucial for cell function. You can probably get away with an experiment like this using wells in a 24 well dish so you don't have to use that much media or drugs. But with stuff like this it might not work and you might get off-target effects so just do this as a complementary test. For your drug test always do a DMSO control since the chances are that's what the drugs are dissolved in and if not just use whatever solvent the drugs are dissolved in and add them to your cells in your control experiments.
Now the other possible and commonly used method to check for the gene expression of protein and subsequently infer its presence as a protein is to use a reverse transcription based PCR, such as RT-PCR although it doesn't have to be real-time as correctly mentioned in the comments. Please note that I'm not at all an expert in this and do check my answer in this section since I haven't personally done reverse transcription based PCR. As far as I'm aware, the basic procedure is to extract cellular mRNA, which can be performed using kits such as RNeasy or a similar product (I'm not promoting any products here and these are just what I have came across!). The protocols come with the kits and available online, and tells you exactly what min/max cell number/RNA levels should be present and how your cells should be (pelleted) before processing. Another method for RNA extraction is CsCl but thats pretty messy and complicated and requires high expertise to get it right but I know its inevitable for certain situations but for cell processing, a kit will do. At least RNeasy protocol states it enriches for mRNA and selectively exclude other types of RNA. Once you have your cellular mRNA you can proceed to reverse transcription using the appropriately designed primers for your gene of interest using a thermocycler. Again I'm not sure what tools to use for designing the primers for making cDNA from mRNA and what to look for (apart from the fact that make sure your primers are specific) as I only do regular PCR but would welcome any edits! Once you get from mRNA to cDNA, you can then run them on your (Ethidium Bromide or whatever DNA staining based) agarose gel and see if your amplicon is present and is the correct size (again based on the primers you have chosen you would know what the correct size is) and hence whether your gene is expressed or not. At least RNeasy kit says you do not need to use DNase digestion to get rid of any DNA before reverse transcribing your mRNA as most of it gets cleaned up when using the kit but you have that option. Now regarding the next-generation RNA sequencing I do not know anything about them so would again welcome any edits but seems unnecessary since you only want to know if the gene of interest is expressed so don't need any sequence info but thats an option too (although I imagine a little expensive?). Just to mention something very obvious, it's important that the species, which your lines have been generated from are sequenced or you have good sequence information about the Gs and Gi genes in your lines otherwise designing primers would be guess work. Its always best to see if anyone has done what you are trying to do and ask for their primers as most people are happy to share reagents.
Now you have probably noticed so far that my methods are quite biased towards molecular biology approaches and that's simply because that's what I know more about, however a great suggestion was to use cAMP levels as an indicator for Gs or Gi expression. Again I'm not an expert in this since I haven't ever analysed small molecules but I imagine that involves something like a HPLC, which you need to discuss with a chemist/biochemist how to extract and clean up your cells from everything and leave only the cAMP. There is probably a procedure/kit/biosensor for it but I will avoid getting into it as I know virtually nothing about this. However I have a note of caution for these types of indirect experiments. I have no idea what your cell lines are and how well they are characterised but since lines have all sorts of mutations and deletions and insertions in them, it's not a good idea to make inferences from cAMP levels. Since considering cAMP presence is quite important for cellular function, their absolute levels in a cell line is not necessarily a good indicator of whether one cAMP production regulator is present or not and I'm sure if you do something like this you open yourself to major criticism by any journal editor/referee. What will be a good idea though in any future experiments you do with these cells is to over express Gs or Gi and see their effects on cAMP production but I just don't recommend using cAMP levels as a sole indicator as to whether Gs or Gi is expressed or not.
If everything else fails and you got tired and wanted to wash your hands off this identification task, you can always lyse your cells and send them for mass spectrometry (MS) if there is such a facility at your institute. It's crucial that the species, which your lines originate from are characterised in terms of their global protein sequences since programs such as Mascot query the raw spectral data against databases such as UniProt to get protein coverage and subsequently protein hits. Also before you go ahead with you MS experiments, just speak to the facility manager and ask for guidance as to what lysis buffer is best to lyse your cells in and what components should not be in your lysis buffer and how sensitive their machines are and how likely you are to get detection and what your protein concentration should be. I think the best machine to use is Orbitrap and as a general rule, the higher the protein amount, the more likely you are to detect it. Since cell lysate is pretty messy and the MS machine columns can get saturated by abundant proteins such as actin, it would be best to run your lysates on an SDS-PAGE gel under reducing conditions (you can even do multiple loads by running your samples in the gel, switching off the WB machine, loading more samples and running them in the gel and continue doing this a few times. It works, I have done it myself but for pulled down samples which are a bit cleaner (less contaminants/unwanted proteins) in general). Once your gel runs through just cut the region of the gel corresponding to the molecular weights of Gs and Gi and send that for MS identification. This method (running your lysate through SDS-PAGE gel) gets rid of unwanted proteins that can interfere with the identification process. But MS is very expensive!
Again I would highly welcome any edits to my own edited reply! I'm here to help and learn.

As in G protein coupled receptors, the Gs protein is associated with adenylyl cyclase and thus increase the level of cAMP in the cell by activating adenylyl cyclase but when  Gi protein is associated with adenylyl cyclase it will inhibit the level of cAmp in the cell by inhibiting adenylyl cyclase, so is their any technique by which we are capable to detect the elevated presence or absence of cAMP in the cells.

based on your comment, you should edit your answer to describe making cDNA from mRNA and sequencing those, or using next-gen RNA sequencing protocols.  You are correct, 'genomic' sequencing won't address expression.

Ok, i have now extensively edited my original answer. hope the information are helpful.

@ Shigeta, thanks for the spelling corrections. My keyboard isn't working well for some reason. Just thought I point out it's not RNAeasy its RNeasy! But thanks to all anyways!


text:
Identification of species found in fly lab
I just found this in my Drosophila lab (within a closed vial) - unfortunately it was dead having been frozen for two weeks. Can anyone help id what it is, and whether it poses a risk to my flies (like mites do)? My inclination is that it is some kind of (moth?) larvae. Note the awesome corkscrew tail...
Found in Uppsala, Sweden, May 2014 in a vial of Drosophila with food (a yeast, sugar, and agar mix). Length is about 3-4mm excl. tail.

I'd guess it's a larva of one of the carpet beetles (Dermestidae), some of which are synanthropic. They probably would be interested not in live flies, but in their food and cadavers.
Its appearance seems to be very characteristic - someone would be able to identify it to generic or even specific level.

Attagenus gebus is known for having longer tails than other dermestid beetles. See Orkin, for example.


text:
Is this statement in agreement with Darwin's theory of evolution?
Is the following statement in agreement with Darwin's theory of evolution?

The number of offspring is not related to fitness.

If so, why? This is not a homework assignment, I just want to justify the reason for which this statment is in agreement (which I really hope it is).

could you explain what makes you think it is inline with Darwin's theory of evolution?

@GriffinEvo Not necessarily inline, but in agreement with. Darwin's idea of natural selection consisted of differential reproduction, which portrayed his concept of fitness. Fitness, is a measure of an organism's ability to survive and reproduce. Nevertheless, it solely stated reproduce and it did not pertain to the exact amount. For this reason, I think that it is inline, (or in agreement), with Darwin's theory of evolution.

what's your source, I'm not convinced the statement makes sense in isolation

@GriffinEvo It seems this quote is an answer to an evolution jeopardy. Google the phrase in "" and see for the outcome.

@chris what is an Evolution Jeopardy game? I was quizzing the OP because the statement made me think it was a creationist trying to start a debate

It's a stupid statement. I'm not sure how it's supposed to help review evolutionary concepts(It's on flashcards?), because as is the statement is just vague to the point of meaninglessness. Fit creatures have offspring. Creatures with offspring are not necessarily fit(see: mules, seedless watermelons). A convincing argument could be set up that they are related, because adding more offspring often increases fitness. But: there are counterexamples that imply a better statement might be "the fitness, and not number, of offspring is related to parent fitness". It's a trick question.

Short Answer
The statement "The number of offspring is not related to fitness." is wrong! In other words, The number of offspring is related to fitness.
Various definitions of fitness exist depending on the model you want to use but whatever is the model you want to use the number of offspring is always related to fitness. For the purpose of a beginner in evolutionary biology, it is probably enough to assume that the number of offsprings that managed to survive to some adult age and fitness are actually the exact same thing.
Long Answer
Darwin's theory of evolution?
What do you call Darwin's theory of evolution? Do you mean the theory of evolution as it was formulated by Charles Darwin at its time or do you mean the current theory of evolution? Charles Darwin never used the word fitness (if I am not mistaken), so I will talk about the modern theory of evolution only.
Generalities
For most of the purpose it is enough to consider fitness as being the expected number of offsprings that manage to survive to some adult age of an individual given its environment and its genotype. The word "expected" used above refers to the first statistical moment (mean) of the random variable which is the number of offspring of an individual given its genotype and its environment. In other words, the number of offsprings is "related" to fitness.
Absolute versus Relative fitness
In general, we talk about absolute and relative fitness, where the absolute fitness of an individual is its number of offsprings and the relative fitness of an individual is its absolute fitness divided by either the mean fitness of the population or more often divided by the absolute fitness of the fittest individual in the population.
Fitness is a function of fecundity and survival
To be a bit more accurate, fitness is a function of both age-specific survival and age-specific fecundity. A very good measure of fitness is given be the elements of leading eigenvalue of the Leslie matrix $L$ in $\overrightarrow n_{t+1} = L \overrightarrow n_t $ where $\overrightarrow n_t$ is a vector that gives the number of individuals of a given genotype of each age living at time $t$. $\overrightarrow n_t = (n_{1t}, n_{2t}, …, n_{nt})^T$, where $T$ indicates transpose and $n_{xt}$ is the number of individuals of age classe $x$ at time $t$.
Definitions of fitness slightly varies depending on the model you want to use
One may want to use an even more complex definitions of fitness, typically when using models that apply to species that have an alternation of generation. Or when considering, genotypes that have different norms of reactions and considering a changing environment through time.
Anyway, whatever is the model you want to apply, fitness is always related to the expected number of offsprings. It would be wrong though to reduce fitness to the expected number of offsprings only, because a more complex definition might be necessary in some special cases. In any case, fitness is always an index of how much will a variant spread in a population and is therefore closely linked to the number of offsprings.

It is definitely in line with Darwin's theory.  You can look at living things as having two sorts of reproduction strategies (for the sake of this question - of course there are many diverse strategies, but this is just one dimension of it).  r and K strategies.
K-selective strategies try to select the best mates and produce the strongest offspring, which they invest a lot of resources in so a to maximize their chances of reproducing.  Human beings are a classic example of K-selective evolution.  A human child will take a decade or even two before it is independent.  Birds might give their offspring a few weeks.  That is why as a person you might tend to think that all animals succeed by investing in offspring.
r- selective strategies do not value their offspring at all.  They produce hundreds or thousands of offspring and don't invest in any of them at all.  A common example of this is cockaroaches or guppies, which are as likely to eat their offspring as acknowledge it, having thousands or hundreds of eggs in one clutch respectively.
For these animals, life is cheap, the fit and the unfit all come out together, but those who survive are the strongest.


text:
Why are red blood cells considered to be cells?
Wikipedia states that a cell is

the basic structural, functional and biological unit of all known living organisms. Cells are the smallest unit of life that can replicate independently.

It then goes on to state that

All cells (except red blood cells which lack a cell nucleus and most organelles to accommodate maximum space for hemoglobin) possess DNA.

Then why are red blood cells still considered cells, while they can't replicate? Is the definition on Wikipedia just a bad definition? Or are red blood cells wrongly considered cells, but remain so for historical reasons? Or are they considered cells for some other reason, such as this answer which states that red blood cells do contain a nucleus at some point?

that's why they are referred to as corpuscles

Many fully differentiated cells can't replicate: neurons, for example.

Animals such as birds and amphibians have nucleated red blood cells...

The most prominent other non-nucleated corupscules are platelets. If you consider why they aren't called "cells", you'd arrive at the conclusion that it's something to do with one RBC originating from one precursor by eliminating its nucleus, rather than one precursor producing lots of non-nucleated membrane bubbles (i.e. megakaryocytes). Then again, jargon calls platelets thrombo-"cytes" ;)

A very good question, and it is most likely because of the last option.  It had a nucleus for part of its life. After the RBC jettisons its nucleus, it still remains very metabolically active for approximately 3 months.  It maintains its cell membrane integrity, it metabolizes glucose, it interacts constantly with its environment, numerous cellular functions and structure remain intact...  It is extremely specialized for a primary purpose, and no longer requires the nucleus to provide more proteins.  It has limited capacity to heal from injury, so it has a limited life span.
Speculation:  I wonder if it might lose the nucleus early on so that when it is destroyed in the spleen at the end of its life as RBCs are, the spleen macrophages are not overwhelmed with additional processing of nucleic acids?  Macrophage type cells are already working hard in there to clear infectious agents and some immune cells from the blood.

I'd say it's much more likely eliminated simply to free up the space. The nucleus is a massive organelle and takes away lots of space the cell could fill up with haemoglobin.

I definitely agree with @Armatus about space being the likeliest explanation for the early loss of the nucleus. Also keep in mind that the total "nuclear flux" (and the processing load of the waste from that flux) would be the same whether the nuclei were lost early or lost late


text:
Why is there no way to remove an immune response?
We've known for a long time now how to "add a new entry to the database," as it were, of immune responses.  It's called vaccination, and it's been one of the greatest success stories in the history of medicine.
And yet, allergies and autoimmune disorders, both caused by an immune system gone rogue, are still serious problems today.  If it's so easy to add a new immune response, why don't we have any way of deleting one?

I estimate about 25 years of hard work until we know enough to do that. It is not as easy as you think to create a vaccine or modulate immune responses.

It is an interesting question. The reason for why new immune responses can be launched but the memory of old ones are not deleted is based on the concept of irreversibility of certain chemical reactions.
Launching an immune response involves clonal expansion of cells expressing the epitope sensors such as the immunoglobins and T-cell receptors, accompanied by maturation of these receptors. Some of the reactions involved in this process are irreversible, which include VDJ recombinations, class switching and affinity maturation.
In an overall sense, immune response is analogous to natural selection- in the presence of the antigen the best binders are selected and expanded. Now to make a species extinct you would have to find each individual and kill it. Or you may have to develop a technology that will identify and kill a certain species in an automated manner. This is difficult to implement; how to engineer a mechanism that will precisely seek and destroy all the epitope sensors for a particular antigen. In contrast selection happens spontaneously because it does not proceed with a reason. It just selects the best from available stock.

"how to engineer a mechanism that will precisely seek and destroy all the epitope sensors for a particular antigen" it's called a virus. Sounds like the solution would be synthetic virus particles that specifically latch on to those epitope sensors and sabotage the rogue immune cells. Another alternative would be a synthetic programmable organ that produces antibodies specific to the epitope sensors.

Too long for a comment: Because we don't know how to do this.
The immune system is an extremely complex and highly regulated function of the human body and it is not easy to shut down single pieces of it without affecting the whole rest. We can completely block immune responses (more or less), which is beneficial for people who got a transplant. These people couldn't survive without this intervention, since their immune system would otherwise turn against their transplant.
The downside for them is, that they are more likely to get severe infections. A friend of mine, which got a kidney transplanted has to be very careful to not get pneumonia, since his immune system can barely fight this.
The other problem with fighting of these immune responses is that they are widely distributed. Lets take allergies as an example: Here you make antibodies which are highly specific for the antigen. This means that you make relative short living plasma cells which actively make large amounts of this antibody and long living memory cells which keep this memory alive. The later are then homing into the bone marrow and wait for another exposure to make them proliferating into more plasma cells and a few memory cells again. This process works for every antigen for which we acquire immunity, including vaccinations.
How should we selectively delete one subgroup of memory cells from the bone marrow without affecting all others? How do we find all versions (one protein, which causes an immune reaction has a lot more than one antigenic peptides) of it? And what else do we mess up, when we try to do so?


text:
Why are some scorpion species fluorescent under UV light?
It's known for some scorpion species such as Pandinus imperator, Heterometrus Petersii etc. to be shining under UV light. That makes them easier to capture and collect by humans.
Is there any evolutionary advantage for this property?
Usually, in articles you stumble upon the phrase "It is not known" for this matter (example). Maybe someone knows of recent discoveries.

As far as I can see from different articles, this seems to be a study in progress. Dr Kloock from the California state University states that scorpions might be more active when not exposed to UV light. If not fluorescing, they know that they are hidden and have a lesser chance of being preyed on. He argues that scorpions are less active on full moon nights rather than other days. (reference) Dr Kloock has also stated that the pigment could get used up on repeated exposure to UV light. He made an observation that scorpions whose pigments got used up were more active than those still fluorescing when exposed to UV light mimicking the moon and the stars. (reference) Dr Gaffin from the University of Oklahoma, in his studies have reported that scorpions might be converting UV light to turn it into the colour blue-green which is what they see best effectively turning their body into one big eye. His studies are consistent with Dr Kloock in that scorpions try to hide and avoid UV light (reference). Some scientists have also hypothesized that scorpions might glow to warn predators or that the pigments that make it glow are the accidental by products of certain chemical reactions in its body (reference). There is no definite proof on this subject though.


text:
What is the effect of Montelukast on the amount of IgE in blood?
I know that it decreases the amount of leucotrienes in blood.
I saw a patient with high IgE altough under Montelukast medication.
This suggests me that Montelukast does not affect the immunoglobulins, but somehow restrict the allergic reaction indirectly.
What is the effect of Montelukast on the amount of IgE in blood?

I was interested in this question because I have always been a little confused about allergic responses, so I did some rather superficial research (i.e. I looked at some Wikipedia pages). As far as I can see there is no reason to think that Montelukast will have any effect upon IgE levels.
Montelukast is a leukotriene receptor antagonist. It is used to treat allergies and asthma.
Leukotrienes are lipid signalling molecules that are used by cells to regulate immune responses. One role of leukotrienes is to promote contractions in the smooth muscles lining the bronchioles. If they are over-produced they can cause inflammation in the airways leading to symptoms of asthma. Since leukotrienes act through a receptor, an antagonist of that receptor such as montelukast can reduce their effect.
IgE is involved in allergic responses because it interacts with Fc receptors on the surface of certain cells such as mast cells. If the IgE molecules are associated with one another through Ig-antigen interactions this leads to clustering of the Fc receptors which triggers an intracellular signalling pathway leading to mast cell degranulation - the release of histamine by fusion of storage vesicles with the cell membrane (i.e. exocytosis). Histamine causes constriction of the bronchioles via effects on smooth muscle, just like leukotrienes.

Thank you for your work and clear answer! It is interesting to note that HIV virus leads to clustering of CD4+ cells so total CD4 cell count decreases. Here,  Fc receptors cluster (IgE interaction) so all total count of Fc cells decrease. - So histamine can interact with Fc receptors and cluster Fc cells, like leukotrienes.


text:
Is there a possibility that medicine will affect the efficiency of natural selection?
I mean, saving sick people means that they possibly can propagate something that nature does not allow. I know that there is already something that operate at genetical level producing alteration, i.e. genetical mutation. And i am well aware that natural selection and genetical mutations take place really slowly.
p.s. i really want medicine to work!!

You might be interested in this Q&A: How is evolution possible in contemporary humans?

Slowly? On mutations: https://biology.stackexchange.com/q/19908/24354

Summary:  Yes it can, but not the way you might think.
Humans aren't under a lot of selective pressure on a large scale right now.  We have a lot of control over our environment, and you're accurate that disease (or I'd add massive, fatal natural disasters) are the biggest ways we would see a large genetic shift.  (Or genocide, which is an extremely unnatural, artificial selection, but some of our species have historically been horrific enough to try to do this.)
Small local natural selection has happened in areas where Malaria is endemic: many people die from malaria. some people die early from homozygous sickle cell anemia, but those who are heterozygous have "sickle cell trait" (because of incomplete dominance) and have deformed enough RBC that malaria isn't able to infect them well.  So the survival advantage is enough that the prevalence of sickle cell alleles in these areas is higher.  There's a similar story with Glucose-6-phosphate dehydrogenase deficiency.
But on a scale you might be thinking of, the primary mechanism would be a global pandemic infection that targets people with a specific trait.  For example, if suddenly an incurable contagious, virulent, highly pathogenic, and fatal virus/bacteria that was only fatal to those with an allele for blood type A were to emerge.  Theoretically it would cause a genetic shift to eliminate type A blood from the gene pool, and reduce prevalence of type B (by eliminating AB due to the A).  Or if it attacked only one location of the world, but that's highly unlikely due to global travel.
Medicine could theoretically catch it in time - mitigate impact and prevent a large shift by creating a vaccine or cure that is effective and easily mass-produced.  The most likely to succeed would be a vaccine (yay for public health!).
Variations on this have happened to reduce or eliminate pathogens (such as polio and smallpox because of the vaccine) and their effect on mankind, but those have little to do with selection for human traits that would cause genetic shift.

"Humans aren't under a lot of selective pressure on a large scale right now." : That is completely wrong. Of course we're under selection! We live in a specific ecosystem and changes to that system affect our survival. We are under strong selective pressure to be animals that can survive a specific range of temperature, acidity and oxygen concentrations to name just a few. Anyway, the main driver of selection is always the way that mates are chosen and that is still going strong today. Not everyone in a generation reproduces => selection. Disease is a relatively minor player in this.


text:
Is a double-yolk egg capable of producing two viable chicks?
As per title: If fertilized, is a double-yolk egg capable of producing two viable chicks (that could survive to adulthood)?
Have there been any reported cases of such (presumably) fraternal twins?

According to the discussion here they normally fail to hatch because the chicks cannot get enough leverage to break the shell.
Here is a video of an assisted hatching. It is claimed that these two survived.

I wonder then, if someone assisted to break the shell, or the shell was particularly thin, then perhaps they could survive. I was wondering if there would be enough physical room in one shell, although I have noticed that double yolk eggs are typically noticeably larger than normal.


text:
Why is the mosquito a definitive host in malaria?
I thought that the definition of a definitive host was that the parasite had to sexually reproduce in that particular host.
I've been told that mosquitoes are the definitive host for the plasmodium parasite, but I thought that the fertilization (and thus the sexual reproduction) takes place in the human?

Plasmodium falciparum (the main causative agent of malaria) and other Plasmodium species have a very complex life cycle, with stages in the female host Anopheles mosquito, in the human liver, and in the human circulatory system, where it primarily resides in the erythrocytes (red blood cells, or RBCs):

During a blood meal, a malaria-infected mosquito injects sporozoites in its saliva into the human host (1). Sporozoites travel through the circulatory system and first infect hepatocytes (liver cells) (2, stage A) and mature into schizonts (3), which rupture and release merozoites (4). After this initial replication in the liver (exo-erythrocytic schizogony (A), which can last a minimum of 5.5 days), the parasites undergo asexual multiplication in the erythrocytes (erythrocytic schizogony (stage B)). Merozoites leave the liver and enter the circulatory system where they infect red blood cells (5). The ring stage trophozoites mature into schizonts, which rupture releasing more merozoites, which continue the cycle of infection of RBCs (6). Some immature trophozoites, in the so-called "ring stage," differentiate into sexual erythrocytic stages (gametocytes) (7). Blood stage parasites are responsible for the clinical manifestations of the disease.
It is important to note here (in answer to your question) that while the male and female gametocytes are formed at this stage in the human (the equivalent of meiosis), sexual reproduction does not occur until the micro and macrogametocytes are taken up by a mosquito.
The male (microgametocytes) and female (macrogametocytes) gametocytes are ingested by a female Anopheles mosquito during a blood meal (8) - only female mosquitoes (of pretty much any species) drink blood. The parasites' multiplication in the mosquito is known as the sporogonic cycle (stage C). While in the mosquito's stomach, the microgametes penetrate the macrogametes generating zygotes (9). The zygotes in turn become motile and elongated (ookinetes) (10) which invade the midgut wall of the mosquito where they develop into oocysts (11). The oocysts grow, rupture, and release sporozoites (12), which make their way to the mosquito's salivary glands. Inoculation of the sporozoites into a new human host perpetuates the malaria life cycle (1).
Sources

The Centers for Disease Control and Prevention: Malaria
Wikipedia: Plasmodium falciparum biology

The answer contains a lot of information, some incorrect, and does not answer the question.
The mosquito is the definite host of plasmodium, despite the humanocentric way this parasite is always looked at.
What happens in the human is the generation of the gammonts (named gametocytes). In the mosquito, these develop into the gametes (microgametes and macrogamete) and sexual reproduction takes place. In the then formed zygote, meiosis occurs, but is not immediately followed by cytokinesis.
As Plasmodium is haploid, the occurrence of meiosis relative to the formation of gametes is shifted in time, but this does not effect the definition of when sexual reproduction takes place (anyway both occurs within the mosquito).
Mirko Singer

Please add some references to your answer.


text:
Fastest and slowest action potential
When our instructor asked us about the speed of action potentials in cells, I told him that action potentials and two-wheelers travels at similar speeds. He thought that this is an 'interesting' way of looking at it.
Needless to say after the class I tried to figure out the minimum, average and maximum speed of action potentials in neurons. Wiki helped but its not authoritative. Some place it says that the fastest is 110 m/s and other place it is 120 m/s. While slowest one varies between 7 m/s (in Rana frog) to 0.5 m/s (Nociceptors) on Wiki. The average speed would be hard to calculate.
I am looking for any references where slowest and fasted action potentials are described. They would be interesting cases to write a note for classromm.

You can search on Bionumbers.
Here is what I got after searching action potential:

Speed of action potential along non-myelinated invertebrate axons of ~10μm diameter = less than 1 m/s
Action potential speed in myelinated axon = 50 ... 100 m/s
Velocity of action potential in pyramidal tract at 37°C (in Cat Felis) = 164 m/s

It offers you references for every number.


text:
To determine no beating cardiomyocytes from ECG or video recording
I am trying to find data and some method by which I can see and say that there are some cardiomyocytes not working.
I have reviewed many arrythmia data where I think I can see much cardiomyocetes there and there which are not beating at all.
Is there any method with available data for the recognisition of cardiomyocytes without beating?
I am particularly interested in the paediatric data.
I am using at the moment ECG data after cardiac infarction.
What is the name of this video record?
Picture from House season 3 episode 2:

A number of cardiomyocytes is lost during an infarction. Instead, fibrous tissue forms, but it only preserves structural integrity, having no contractile function [1]. Myocardial infarction is an uncommon condition in pediatrics, happening very rare, when embolization occurs due to blood coagulation affections or heart congenital defects [2].
The fibrous tissue has different properties, thus modifying:

MDE-MRI images [3]
ECG: deep Q wave [4]
echocardiography: hypoechoic and hyperdense echoes inside the fibrotic material (the latter compatible with calcium) [5]

That video record is probably about 3D Echocardiography (look here at Video 2 and figure 2).
References:

Yao Sun, Myocardial repair/remodelling following infarction: roles of local factors
Nicola Carano et al., Acute Myocardial Infarction in a Child: Possible Pathogenic Role of Patent Foramen Ovale Associated With Heritable Thrombophilia
Harikrishna Tandri et al., Noninvasive detection of myocardial fibrosis in arrhythmogenic right ventricular cardiomyopathy using delayed-enhancement magnetic resonance imaging
ECGpedia - Pathologic Q Waves
Berenzstein CS et al., Usefulness of echocardiography and doppler echocardiography in endomyocardial fibrosis

The video in House series is probably fake. I cannot understand from which angle you can get so circular picture. Those real-life pictures are much more challenging than the one in House.

@Masi I could't understand that either.


text:
Why is there no cure for Dandruff?
It looks like a simple problem, affecting almost half of the population at the post-pubertal age and of any gender and ethnicity [wikipedia]. What is so complex about finding a cure? Also, if you know some of the most effective treatments, they're welcome.

http://curebird.com/condition/search?keys=dandruff

Dandruff is dead scalp, i.e. skin. Your skin everywhere is constantly renewing itself. Everwhere else in your body, dead skin gets scraped off on e.g. clothes, things you touch etc. so you don't notice it - dandruff gets caught in your hair and thus you do notice it. Dandruff is not a condition, it's a consequence of natural healthy skin turnover. If you aimed to prevent it from forming, you would interrupt a natural process and most likely also incur some sort of damage. Thus, the best way is to get rid of it periodically once it has formed - i.e. wash your hair ;)

Ok this seems like a natural cause, but Dandruff has other causes such as Seborrheic dermatitis, psoriasis.. The results are similar (dry skin flakes) and they have nothing to do with washing. Some literature state fungi like Malassezia furfur as a cause, but it doesn't seem to be clear evidence for a permanent cure

For dandruff caused mainly from dry scalp, I imagine that there is a delicate balance between moisturizing the scalp and getting oily hair. In my uninformed opinion, this is what shampoos like Head and Shoulders attempt to do.
Taking a more general look at skin health, growing research suggests that the right compilation of microbiota dictates lots of skin health issues. Just like your bowel has an endless supply of mutualistic bacteria, so does your skin. Disruption to this ecosystem (whether genetic, by way of a pathogen, or environmental) could have various negative effects. Dandruff, I imagine, is one of them. It is unfortunately very difficult to understand what a healthy ecosystem looks like, as every person is different both in genetic and environmental factors. This is part of the reason why other dermatological conditions like acne are difficult to treat.
You may be interested in research done through the Human Microbiome Project. Additionally, this article includes some discussion of the fungi mentioned above in the comments and postulates the role of microbiota in determining their success.