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What's the Mechanism of Paradoxical Excitatory Effects with Sedating Antihistamines?
I've been reading the British National Formulary 65 (BNF-65) and it mentioned that in some, especially at higher dosages, sedating (first-generation) antihistamines, can produce paradoxical excitatory (or stimulating) effects and so I felt like asking the age-old question, "Why?" because as I hope is obvious by my questions I am fascinated by drug action and I felt there was no better place to ask this question than here on biology stackexchange.

A reference is needed for the paradoxical effects exhibited by certain H1-antagonists. I found only  one which says: We describe three CYP2D6 UMs who reported paradoxical excitation on diphenhydramine. These cases suggest that in CYP2D6 UMs, diphenhydramine may be converted to a compound that causes excitation due to the abnormally high CYP2D6 activity... Although these are only three anecdotal cases of paradoxical excitation from three CYP2D6 UMs, the reports illustrate the need for larger, more formal studies .... Not a strong evidence.


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How Do Acid and Base Loving Plants Get Enough PO4?
Acidic and Basic soils experience phosphate sequestration through binding with either calcium, aluminum, or iron. How do plant that thrive in acidic and basic soils obtain the necessary phosphate? Blueberries are an example that I particularly enjoy.

Thanks to the University of Hawaii for posting this picture.

Phycology would seem to be an ideal place to study mechanisms of phosphate absorption at varying pH.

Why is pH6- pH7 the highest range for P availability ?It seems to me like the lowest.

@biogirl it would be because the phosphorous is more likely to dissolve in water at this pH than to react with iron, aluminum or calcium. This makes it available to the plant since it cannot absorb insoluble compounds.

Fixation of phosphorous occurs when the chemical equations tip in favour of less soluble compounds. Plants are able to absorb Orthophosphate ions, such as H2PO4- and HPO42-.

Orthophosphate is most available to plants at pH values near neutrality. It is believed that in relatively acidic soils, orthophosphate ions are precipitated or sorbed by species of Al(III) and Fe(III). In alkaline soils, orthophosphate may react with calcium carbonate to form relatively insoluble hydroxyapatite:

3HPO42- + 5CaCo3(s) + 2H2O -> Ca5(PO4)3(OH)(s) +5HCO3- + OH-

Environmental Chemistry, Seventh Edition -Stanley E. Manahan
This does tend to make it more difficult for plants to obtain their phosphorous when it is stuck to something that they cannot absorb, but it is not hopeless. These equations are equilibria, so they can be made to go both directions by adding or removing reagents from each side.

The plants will pull from the left side of the equations by removing the orthophosphate ions. More will be released to maintain the equilibrium.
In acidic or basic environments, rainwater will serve as a base or acid to push the equations from the right.
Decaying organic matter releases orthophosphates that the plant can absorb.

In this way, plants living in acidic or basic environments would still obtain enough phosphorous.

source: Stack Exchange

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There are linear and rotary molecular motors in the cells. Do any of them have a fixed or stable frequency or speed?
Are there any linear, rotary or oscillatory molecular motors in the cells which can have fixed frequeny and which can be used as a reference for elapsed time timer? This question is with relevence to my earlier question 'Is there a realtime molecular clock within the genome to co-ordinate the developmental sequences in an embryo?'

There are molecular motors but the frequency is a function of energy input (ATP); similar to the angular velocity dependence on amount of current in electrical motors.
The concept of molecular motor may not be suitable for a clock like device. There are clocks based on genetic circuits, which produce stable oscillations. Examples include the circadian clock, cell division, menstrual cycle etc.
Developmental events involve checkpoints and the timing is regulated by several factors such as number of cells, concentration of some protein etc. However, I haven't come across a master clock that integrates and synchronizes all these signals for precise developmental timing. That makes it an interesting area of research.

These molecular motors' response maybe dynamic and nonlinear. But it entirely dependent on the external influence and also the characteristics of the motor itself including number of active motors involved in operation. As it is microscopic, it will not possible to analyse by assumptions and say they have some random frequency. They do have certain frequency of operation (I do not know whether they are controlled by biological clock or some master clock but they are controlled by nucleus of the cell) and "Modeling molecular motors" explains how motors act on the filament inside the cell. It mainly talks about the influence of external force on the operation of motor and also speed(v) of the motor. The following excerpt from that paper talks about the external force on motor.

The action  of  the  motor is induced by generalized forces, which for
  the motor/filament system may be identified  as the mechanical force
  fext  applied  to the  motor, and  the chemical potential difference
  Dm, which measures the free-energy change per consumed ‘‘fuel’’
  molecule. The force fext describes external forces, for example of
  optical tweezers,  microneedles, or the viscous load of an object that
  is carried. fext could also include viscous friction forces between
  the motor and the surrounding solvent if the latter  is considered as
  ‘‘external.’’ The chemical  potential  difference Dm is for the
  process of the hydrolysis of Adenosinetriphosphate (ATP) to
  Adenosinediphosphate(ADP) and phosphate (P).

The frequency of molecular motor according to "Biophysics of Molecular Motor" has been classified into two categories:

Density controlled: In the density-controlled model, it is assumed that the depolymerization rate is proportional to the motor density at the terminal site of the microtubule. Here the frequency of motor is dependent on density of the motor.
Flux controlled: Filament depolymerization is determined by the flux of motors
to the end. Here the frequency is dependent on the flux of the motor.

In both the above cases the length of the filament on which motor is acting is also important. These models have been analysed and plotted on a graph to give a clear picture of it.

The paper explains the catastrophe frequency, the frequency at which the filament shrinks. Shrinking of of a filament is due to motor. So the paper concludes saying the catastrophe frequency is 0.5 per min for a 8um length of filament.

(Catastrophe = the transition from growing to shrinking of dynamic microtubules).
To summarize, these motors do have speed and frequency of operation but they are not fixed. They vary in a non linear fashion due dynamic environment. But the motor tries to be as much stable and resistant as possible.

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Can cats use ketone bodies as only source of energy?
I recall reading that much of the energy a cat produces from its food comes from proteins which I assume would produce energy via being catabolised into amino acids which in turn, if glucogenic, would undergo gluconeogenesis and then, by means of being metabolised into glucose, enter glycolysis and the resulting pyruvate would be converted to acetyl-CoA and enter the TCA cycle to produce energy. I'm wondering whether this recollection is accurate and whether cats could, like humans, use ketone bodies for their sole fuel source if need be.

You are correct that cats consume a lot of protein, and it's safe to assume a large share of this is broken down to amino acids, which are then oxidized to produce energy. But amino acids in general are not catabolized via glucose; instead, they are converted into compounds that feed into the TCA cycle via other biochemical routes.
Almost every of the 20 proteinogenic amino acids have their own specialized catabolism pathway, so this is a large topic. The general theme is that the amine nitrogen is first removed by a transaminase to yield a keto-acid, which is when converted into a carbohydrate that can enter the TCA cycle. To give but one example, leucine is converted in the mitochondrion by a series of CoA-coupled intermediates into acetyl-CoA and acetoacetate (a ketone body; see below). The acetoacetate in turn yields two more acetyl-CoA. A description of this pathway is found at the HumanCyc database. This is a great resource for learning amino acid (and other) biochemical pathways, and provides literature references.
Some amino acids are indeed used for gluconeogenesis, mainly by the liver, but this is not a requirement for their catabolism by most tissues. (It would be energetically inefficient to first generate glucose and then break it down again!) An exception is the central nervous system, which does require glucose and cannot subsist on fat or amino acids (for reasons that, to my knowledge, are still not well understood). So in order to support the CNS on amino acids, the route your describe via gluconeogenesis does occur.
Ketone bodies (acetone, acetoacetate and beta-hydroxybutyrate) are the main alternatives to glucose accepted by the CNS. Gluconeogenesis is energetically expensive in the long run, and if deprived of dietary sugar for a long time, the body will increase its usage of ketone bodies instead of glucose. However, ketone bodies can never fully replace glucose: even during prolonged starvation in humans, blood glucose is kept > 2mM. The CNS would not function otherwise. I'm not an expert in cat physiology but I would bet the situation is similar.


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Why might you NOT observe a tradeoff between two life-history traits?
I have traditionally thought of and heard about life-history traits (e.g., size at first reproduction, number of offspring, size of offspring, survival, etc., etc.) as drawing from a finite pool of resources that an organism has, and therefore exhibiting tradeoffs. So, for instance, an organism that invests in a lot of offspring would experience a decreased probability of survival.
It has recently come to my attention that this is not always the case, and I'm not sure why. I have been directed to the work of David Houle, who wrote extensively on the topic of life-history traits, but some of his work is inaccessible to me intellectually. I was hoping that somebody had a more digestible explanation or was maybe more familiar with Houle's work.

Could you link to a few works in particular, or where you first read that?

The name of the paper I've read is, "Genetic covariance of fitness correlates: what genetic correlations are made of and why it matters". David Houle from the journal Evolution, 1991, Vol. 45. Issue 3. Pp 630-648.

It apparently has something to do with the number of loci influencing ability to obtain resources versus the number of loci influencing how those resources are allocated...

For those willing to answer: Here is David Houle's article

The simple explanation is that there are three (or more) traits drawing from the pool, and you're only looking for trade-offs between two of them. The unobserved third may show the effect of a trade-off.

Can you explain some more with references?


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A possible cause of autoimmunity
I read that

Doherty and Zinkernagel found that MHC- heterozygotes present more
  antigens to the immune system than homozygotes; yet, the infected
  heterozygous mice in their experiment all died, apparently from
  overresponsiveness.

Can MHC-heterozygotes be more susceptible to autoimmune disorders and allergies because there is a tendency of over responsiveness ?

It looks moderately muddled, but perhaps.  This paper1 is a good place to start; it's free and the intro lists a number of more recent studies.  That study found a connection to lifetime reproductive success in sticklebacks (a fish) with intermediate MHC diversity.  This 2007 study in mice2 is a particularly nice one, dealing with a inbred line outbred to wild mice, finding again, no advantage to heterozygotes.  There are others, but most deal with the concept descriptively (self-delighting in their continued refutation of a commonly-held belief) or predictively (such as this from PNAS in 19923 or a 2009 review4) but specific and proven reasons are sparse.
The general feeling is that it may remain unclear what sort of genetic interactions are involved in MHC (additive effects, overdominance, etc.) but it is probably also complicated due to the nature of immunology.  For example, a paper from 20035 points out that in an immunological response, only a few peptides dominate the response; there may be no real advantage to having extra ones if they are unused, and having those others around might dilute the useful response (That paper also takes an interesting view of serial infections, and shows that heterozygotes are indeed advantaged during coinfection).  The above PNAS publication3 gives the idea, which the stickleback paper1 recapitulated, that if more alleles are present, more T-cells will be self-reactive and will therefore be purged, resulting in an overall decreased T-cell availability.
Other hypotheses are present in the review4 I mentioned, such as perhaps positive selection efficiency is not MHC-diversity dependent whereas negative selection is, or indeed increased autoimmune reactions as you guessed.  My guess would be some combination of the above, with selection for heterozygotes being favored in the real world for multiple and repeated infections but certain specifics resulting in a homozygote preference, of which autoimmunity is likely playing a role.


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DAT1 dopamine and cocaine binding
I've searched the internet for several minutes and I've looked at DAT but I'm having trouble finding the DAT binding location. Where (and to which aa) does dopamine and cocaine bind to hDAT1?

The following paper answers your question in detail:

http://www.ncbi.nlm.nih.gov/pubmed/18568020

It seems like the following aa are responsible for the binding, but please refer to the paper for more details:

Val152,Tyr156,Asn157,Ser422,(Asp79)


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What happens if an IV drip with a saline solution slips out of the vein, but keeps dripping into the body?
A patient has a saline solution IV drip into the vein. They have somehow moved around and the needle has fallen out of the vein, but remained in the body. Nobody has noticed and for a few hours water has accumulated like a balloon in the arm.
What happens? Is it dangerous? If untreated, would the body absorb the water, or would it remain as a balloon / pocket? If a pocket of water forms, what is the treatment?

Is this a question about a real case? Or are you possibly asking about a homework question? (It sounds kind of like that to me)

Real case. I've been sent home with a puppy and an IV. It is the middle of the night. Closest vet is 6 hours away, and only available in the morning.

@Bob we need to know where the pocket is exactly.

@caseyr547 above where the needle was inserted. Between elbow and shoulder.

CALL YOUR VET ASAP. The following information is NOT from a medical or veterinary professional. It is based off of human physiology and doesn't necessarily apply to other mammals. I cannot guarantee the accuracy or effectiveness of any information that follows.

They have somehow moved around and the needle has fallen out of the vein, but remained in the body. Nobody has noticed and for a few hours water has accumulated like a balloon in the arm.

This is called "infiltration":

Is it dangerous?

It can be, depending on what was in the IV.

If untreated, would the body absorb the water, or would it remain as a balloon / pocket? If a pocket of water forms, what is the treatment?

Taken from here:
"If the infiltration is severe, you may consider the application of a compress in addition to elevating the affected limb. Check your institution’s policy regarding which type of compress (warm or cold) should be applied. Generally speaking, if the infiltration solution was isotonic, a warm compress is used to alleviate discomfort and help absorb the infiltration by increasing circulation to the affected area. However, sloughing can occur from the application of a warm compress to an area infiltrated with certain medications such as potassium chloride. In certain situations, a cold compress is recommended."

Thanks for this answer. Unfortunately the vet was not available to call, but by morning, the water pocket had been sloughed into the body. I think we dodged a bullet.

It seems like this was 'infiltration' as you say.

When we told the vet in the morning, they didn't even seem the slightest concerned this happened. I dont know - but I think that is weird. If we had of been asleep, this would have continued for another 6 hours. I am surprised they sent us home with an IV in the first place without telling us all the possible issues, such as blood clotting in the tubes (which happened earlier) due to poor circulation.

Well, I simply do not know how dangerous it is. My intuition says it's not particularly dangerous since the extra fluid is, eventually, absorbed. However, I'm not a medical professional and don't know the circumstances that dictates when it becomes dangerous. Thus, the big warning at the beginning. Better safe than sorry. :-)

The most common IV drip that would be sent home with a pet owner is Ringer's solution. This fluid is also commonly injected as a subcutaneous (between muscle and skin) bolus into both cats and dogs. Although IV administration is more efficient, this fluid is completely harmless if an IV catheter were dislodged allowing it to accumulate in the surrounding tissue.


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What is the potential function of ultra-conserved elements in the genome?
If selection pressure results in conservation of DNA sequences, what is the most plausible explanation for the existence of ultra-conserved elements (refs here and here) given that there hasn't been any significant validation of the functional significance of these elements other than a lot of bioinformatic analyses across different genome datasets? If these are of such high significance, does this mean that there is still some significant gap in our understanding of fundamental biology or is there another explanation? The second reference in particular show that there are UCEs shared between plants and animals, but are not syntenic (which is not necessarily a surprise) so it might suggest that at least a class of UCEs are associated with structural rather than functional elements.
It appears that there are at least several different 'classes' of ultra-conserved elements, based on the number of matching/identical bps, their spatial distribution across the genome and the species in which they exist. Even though there is probably no single explanation that would account for all the possible functions they can have, it is surprising that they are difficult to test functionally. This is again probably due to a lack of understanding about their properties and therefore no real method to validate their function. I think this is where we need to think outside the box to come up with the answer.
What would be the most obvious (and possibly not so obvious) function for UCEs?

What is the question? The papers you linked to already talk about the "most obvious" function for them.

I am also interested in the not so obvious functions as well.

Probably development, in particular transcriptional regulation.  To quote each link in turn,

They are found in clusters across the human genome, principally around genes that are implicated in the regulation of development, including many transcription factors. These highly conserved non-coding sequences are likely to form part of the genomic circuitry that uniquely defines vertebrate development.

and

[Highly conserved non-coding sequences] are significantly associated with transcription factors showing specific functions fundamental to animal development, such as multicellular organism development and sequence-specific DNA binding. The majority of these regions map onto ultraconserved elements and we demonstrate that they can act as functional enhancers within the organism of origin, as well as in cross-transgenesis experiments

Additionally,

Here we report that 45% of these sequences functioned reproducibly as tissue-specific enhancers of gene expression at embryonic day 11.5. While directing expression in a broad range of anatomical structures in the embryo, the majority of the 75 enhancers directed expression to various regions of the developing nervous system.

These regions tend to be highly clustered in around 200 areas, and most of them are non-coding.  ncRNA is often regulatory, and those UCE clusters are associated closely with developmental genes.  That being said, not all of them are clustered near known genic regions, which might be a good indicator that there are heretofore unknown genes in those areas; UCEs might be useful for discovery.  And here's a paper trying to give a role to one in cancer.

I definitely like to think that it is involved in development or some type of regulatory control. However, if it is unique to vertebrate, then why are they also found (exactly identical) in other branches of life? I think we also have to be conscious that sequence location proximity doesn't necessary indicate its association with particular genes. Unfortunately some of the knockout experiments haven't really provided any definitive answers, but this is a mystery that has definitely proved to be intriguing to say the least.

@MichaelLai Because that study looked at humans and pufferfish; removed enough to draw conclusions about vetebrates but not instructive beyond that.  The third link I posted deals with non-vertebrates as well.

This is a good answer about RNA world you should mention it.

It's with noting that just because something is evolutionary diverged sequentially through specialization does not mean that that function has not been to the same degree conserved. For instance non coding RNA are not characterized by sequential homology alone but through structural conservation. To a greater degree even this structure function relationship exists in other parts of the genome with retro elements and beyond the genome with proteins especially antibodies.

Does this give some hint to what their possible function(s) might be? What are your thoughts about the different types and functions that are possible?

Conservation might indicate selective pressure as a general rule, but this isn't a given; you can delete some ultraconserved elements and still get viable mice...
http://www.plosbiology.org/article/info%3Adoi%2F10.1371%2Fjournal.pbio.0050234

Does this also suggest that there are different types of ultraconserved elements? Or that they have a function that is not directly related to structural or signaling?

It suggests that high-degrees of conservation might itself not imply selective pressures - at least from a proximal perspective the deletion events should have resulted in loss of fitness if the preservation of those elements was under strong selective pressure.


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Why only heterogeneous SNVs for validation using genotyping arrays?
I am trying to validate the variants I found using whole genome sequencing . The standard practice, I have seen in the two publications below were to check for the number of heterozygous SNPs called by the SNP array.
1) Performance comparison of whole-genome sequencing platforms

To further assess the accuracy of the variant calling, ... Of the 260,112 heterozygous calls detected with the Omni array, 99.5% were present in the entire SNV data set, 99.34% were concordant calls and only 0.16% were platform-specific SNVs. This demonstrates that both platforms are sensitive to known SNVs and that few known single-nucleotide polymorphisms (SNPs) are detected by only one platform.

2) Optimised filtering reduces the error rate in detecting genomic variants by short-read sequencing

To confirm that shared SNVs are indeed true variants, we used Illumina single-nucleotide polymorphism (SNP) arrays and selected all SNPs heterozygous on the SNP array.

My question is - why are only heterozygous SNPs chosen for validation when using Illumina Omni arrays?

The purpose of validating is to find genuine SNPs and not those caused by sequencing or amplification errors. It is extremely unlikely you will have a false homozygous SNP as a result of error. Just think about it. The same error, at the same base, occuring 80%+ of the time? Its not going to happen unless you have low coverage, and these SNPs should be thrown out anyway. You may have some cases where a genuine heterozygous SNP is called as a homozygous SNP. But that isnt much of a problem. It is still a genuine SNP. It would only be a problem if you were only interested in homozygous SNPs, in which case you will just need to validate everything biochemically, which you will need to do anyways.

i think the chance of a sequencing platform calling something A/A when the microarray calls it B/B is virtually nil. Just doesn't happen.


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Do spouses begin to share genes over time?
I apologize if this hypothesis sounds strange by I was wondering if any research had been done on a phenomenon which I've seen and have corroborated with many other - the idea that over time spouses tend to start looking similar to each other.
My hypothesis is that this is really a one-way street with the wife tending to look more like the husband. The reason being that after coitus her body is flooded with his genetic material which may lead to some mixing of DNA outside of the egg. Furthermore once the woman is pregnant she enter into a symbiotic relationship with an organism whose DNA is approximately 50% foreign. Her body must then adapt to the presence of that new genetic material.
I realize this may sound strange and Lamarkian but I was curious if the phenomenon itself had been investigated.

While battling between Lamarkians and Darwinists, this sure has been investigated some time. The answer is: no. There are a lot of factors beside genes that can be a reason for this. First of all: our psychological reception of spouses. I, for example, tend to see similarities developing in people and their dogs over time. I am very sure they never ever share genetic material.

@skymninge i can show you images of couples you've never met. At their wedding they look a certain way, 20 years later they look strikingly similar to each other. From what I understand genetic change within one's own lifetime has not really been conclusively resolved.

I did not say, that I don't see those similarities. I see them quite often, EVEN between people and their dogs. But I would never account them to a genetic cause.

Microchimerism (Mc) is an interesting concept, and

refers to the harboring of a small number of cells (or DNA) that originated in a different individual. Naturally acquired Mc derives primarily from maternal cells in her progeny, or cells of fetal origin in women.

In women, it has nothing to do with transfer during/after sex but rather is due to the presence of the developing fetus.  There is definite long-term persistence of microchimerism, although not much is yet known about its effects.  Here is a nice and free review from 2010 dealing with the subject.  Most if not all of the effects have to do with immune function, in particular autoimmunity.  It is definitely not a mechanism by which couples begin to look similar.  That is social, in particular a result of living in the same environment with similar activities and tastes.  Male contribution to cellular content in the embryo is almost nil, as sperm die and the transcript count in the successful sperm is puny compared to the egg.  Most RNA content in the embryo is maternal until it switches to embryo.

Terrific, this is just what I was looking for. Very helpful and very interesting.

@user4481 There was an interesting article in Scientific American called " Your cells are my cells " by J Lee Nelson.Just google the title.

The actual article is behind a paywall, here's a pdf.  It's a great summary for sure.


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On average how many genes / alleles do people share?
I am curious about how much more a child can be alike to one parent than the other. If a child were to inherit all the alleles that are shared between both parents from one parent, but inherit all alleles from the other parent which the first parent doesn't possess, wouldn't this make the child genetically more uniquely similar to the second parent?
This question would be aided by understanding of how many alleles on average a person already shares with another person. Taking into account regional areas probably yield more similar people, I would imagine the average couple would share more than two randomly chosen people on the planet.

I will attempt to answer the question. Allele is defined, in simple terms, variation of a given gene, e.g. through deletions, SNPs etc. Humans are diploid organisms, meaning we have two sets of chromosomes, one from mother and one from father. Now since we have two sister chromosome, we can only have (share) two alleles of a given gene (one from mother and one from father) unless there are multiple copies of a gene or chromosome, which is mostly observed in disease conditions but that's not what we are talking about. Now since every humans have SNPs at roughly 1 every 1000 base pair, there are genetic variations between sequences of genes between humans, although there are some hot spots, which are more varied and some genes are very highly conserved due to their critical function such as cytochrome C. This just means that parents of the child you are describing (if not related to each other) are not likely to share the exact same, sequence wise, genetic code for a given gene selected at random.
The inheritance of a given allele of a gene on a chromosome happens through independent assortment (a process which happens maternally and paternally), meaning a child (offspring/zygote) would get one copy of a gene/allele (from the possible two that each parent themselves have) from maternal and one copy from paternal side at random. This is one source of genetic variation in a zygote. The other source of genetic variation is gene cross-over (through homologous recombination) meaning bits of the maternal or paternal chromosomes swap at gamete stage before the gametes are fused together to form a zygote, which makes the offspring unique and no offspring alike (except MZ twins but thats another discussion). This overall means that you can inherit a maximum of two alleles of a given gene (assuming again the parents of the child are not closely related) and even then the sequence of the offspring genes are not likely to be exactly the same as their parents, which makes every human unique. But saying that, you have a much higher gene sequence match to your parents than any other non-related human selected at random.
One thing worth noting here is that mitochondrial genes, are inherited exclusively from you mother (through the egg) and males inherit the Y chromosomes paternally so there are circumstances I guess you could say you inherit certain gene/alleles paternally or maternally.
What I speculate you might be thinking about is how many homologues (similar versions) of a given genes humans have and I think the average in the human genome is 3 but do check this! Flies (Drosophila) tends to have one, which is why its such a great model organism to study genetics and genetic interactions with as you do not tend to get redundancies.
I hope this answers your question

This certainly adds to my knowledge, but isn't a wholly satisfying answer. I found this helpful and interesting: "during miosis you get gene cross-over meaning bits of the maternal or paternal chromosomes swap, which makes the offspring unique and not just half versions of its parent"

There appear to be a couple spelling errors, and a few run on sentences that I find hard to follow. Maybe you or someone with knowledge can properly edit this answer?

made an edit to my original answer. Hope this is more helpful and any further edits are welcomed!


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GWAS: matched-pairs and logistic regression
Logistic regression is a common analysis tool used for GWAS when your response variable of interested is qualitative. It comes as one of the standard tools in most GWAS packages (e.g. PLINK).
Most logistic regression models for GWAS would be setup as:
$\log{\frac{P(Y=1)}{1-P(Y=1)}} = \beta_0 + \beta_1*X$
Where $X$ is number of copies of the minor allele for a particular SNP of interest and $Y$ is disease stuatus. However, suppose that my case-control data is matched (In my case matched by age, BMI, reported ethnicity, and distance to procurement site). I don't think standard logistic regression (as I have outlined above) is valid. What does everybody do? I don't see options for this in packages like PLINK.
I also posted this question on (http://www.biostars.org/p/81394/) before I realized they were no longer part of stackexchange.

My first thought was to suggest a mixed effects model, so I will describe that first. But having had a Google there are models known as "Conditional logistic regression" models in which you can include any data structure as a covariate, which may be more appropriate, but I cannot vouch for them as I haven't used them. I would suggest reading the documentation.
Mixed effects models
I only know how to do this in R (stats language - www.r-project.org), but if you're using PLINK (so presumably also UNIX) R is pretty straightforward.
There are a couple of packages available for mixed effects models, my personal preference is function lme in package nlme (CRAN link). This type of model allows you to specify 2 types of independent variable (e.g. age, BMI, ethnicity... in your case);

Fixed effects - such as age, sex (something that is a phenotype of the samples),
Random effects - such as batch or other "technical" consideration,

This means you can format a model as you would before, but include an additional "random effects" term for your "matched" variable;
model = lme( fixed= outcome ~ exposure + covariate1, random= 1|matched )

.
Conditional logistic regression models
In the survival package for R there is a function called clogit (CRAN link) which seems to do exactly what you want. Although I have never used it myself.
From what I can gather this allows you to run a logistic regression with an additional covariate strata(matched), so your model may look like
model = clogit( outcome ~ exposure + covariate1 + strata(matched) )

.
Disclaimer!
This may not be exactly what you are after, as I'm not familiar with your data, so I would suggest heading over to https://stats.stackexchange.com/ as well, and searching for questions about regression analysis and paired observations - if none answer your question then ask a fresh one.

Thank you Luke. I'm quite familiar with R, and I figured either a mixed effects model or conditional logistic regression would be needed. I was just not seeing those in the basic GWAS packages...so I was wondering if I was missing something. Thank you!

@Benjamin I find that the published packages are only so useful - they're great for performing simple analyses via an established pipeline - but there is no substitute for creating an analysis that actually fits your data. Unless there truly is an established, published method, it is better to adapt one to your specific situation - all experiments are different and have their own considerations!


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How does formaldehyde/PBS or methanol fixation of cells affect lysosomal pH?
The question is fairly simple - does formaldehyde or methanol fixation in preparation for immunocytochemistry/immunofluorescent staining affect the pH of the lysosomes?
Some background: I'm trying to look at the intracellular trafficking of a fluorescently-labeled lysosomal enzyme. Cells are grown in vitro and treated with the labeled protein, which is taken up into the cells via receptor-mediated endocytosis. The protein-receptor complex targets the late endosome-lysosome pathway, where eventually the acidic pH of the lysosome causes the two to dissociate and the receptor to recycle, while the enzyme stays and does its thing. I've labeled the enzyme with two different dyes - Alexa Fluor 488, which is supposedly pH-insensitive between 4 and 10, and pHrodo Red, which has greatly-increased fluorescence as the pH drops. Alexa488 is the brightest of the Alexa dyes, and is widely used in all sorts of applications. pHrodo is not as bright (as far as I can tell, it's been difficult to find comparisons), but its pH-dependence helps lower the effect of non-specific extracellular binding, and it seems to work in my system so far.
So what's the problem? I'm developing an assay that will measure the ability of certain substances to block the uptake of this enzyme into the cell. Since I'll be measuring a lack of signal, the higher I can get the uninhibited signal to be, the better. Like I said, pHrodo works OK, but it could be better. The problem is that my Alexa-labeled protein has an extremely low signal to noise ratio, when I would have expected the exact opposite. I'm wondering if, in my system, the Alexa dye really is somewhat pH-sensitive, and is not fluorescing as well when in the acidic lysosome. I'm encountering a few other issues as well, and while before I was performing live-cell imaging, I'm starting to toy with the idea of fixing the cells first, as that will positively impact some other things I want to try.
Hence my question: Will fixing the cells with 4% formaldehyde in PBS (standard ICC/IF protocol) affect the pH of the lysosomes? Would methanol fixation do the same thing? Any other suggestions for increasing signal?

i don't have a definitive answer.. fixation can also affect the dyes.. formaldehyde can react with the fluorophore and make it insensitive. pH should change on fixation because it dehydrates the sample.

Alas :) I see, I suggest that fixing with formaldehyde will be best, but the buffering itself will affect the pH of the system, but you're better off. Also I'm curious as to whether formaldehyde will crosslink and "plug" ion channels in the lysosomes, thus stabilizing the internal pH... As mentioned above, this will be time-dependent, so you could try fixing with formaldehyde and monitor the pH of lysosomes with pH sensitive dyes and see if changes through time... could be a quick/neat experiment..

In my opinion, cell fixation shouldn't change the pH. However unbuffered formalin will oxidize and lower the pH, but using PBS should buffer around pH 7.
Maybe Glutaraldehyde fixation would also be an option, if the others are not working...
I found this website by leica very useful, maybe it will also help you:

http://www.leicabiosystems.com/pathologyleaders/fixation-and-fixatives-2-factors-influencing-chemical-fixation-formaldehyde-and-glutaraldehyde/

Yes, they will both affect pH.
In addition to the above comment, both, but methanol especially dehydrates samples - removal of water will most definitely affect the pH in organelles. This will be time dependent. Both duration of fixation, and time after fixation before you assess the cells will affect the pH of the organelles.
Because you fix the cells in a non-aqueous environment (I presume you're using standard fixation), you don't use buffer during fixation. We might be able to answer better if you post the general protocol you follow.

thanks for answering! I actually fix with 4% formaldehyde in PBS, so it is an aqueous environment, as I mentioned in the question.


text:
How many consecutive cell divisions are required to form the adult human body from the single cell zygote?
The preferred question would have been what is the total number of cells in a full term human foetus and how many cell divisions are required to reach that number. However estimates of total cell numbers in foetus could not be found. From the abstract of the July 5, 2013 article published in Annals of Human Biology, the adult human body consists of approximately $3.72 \times 10^{13}$ cells (37.2 Trillion). The question is: what would be the approximate number of cell divisions required to reach that number (Ignoring the fact that different tissues may reach full differentiation at different times)?

Sounds like just a math problem if you allow that cells dying and different rates of division are not to be accounted for:
$2^N = 40 \times 10^{12}$
$log_2(40 \times 10^{12}) = N$
$N = 45.185$
so 45 or so divisions.
is that what you are looking for?

I think you want 40T, not 4T.

@ shigeta - Isn't 45 pretty close to the 'Hayflick limit'?

@RamManoharM Supposedly it's between 40-60, so yeah.  But if that means anything...

@ Amory - By the time you are 20 (young adult) your have near exhausted the capabilty for cell division (broadly speaking). Just wondering if the loss of Telomere has more important role during development other than merely ushering in senescence.

The Hayflick limit is entirely unrelated to this issue as the foetus develops firstly from embryonic totipotent stem cells, then pluripotent stem cells, and even in the adult body there are still multipotent stem cells, some of which are capable of indefinite replication.

that still leads me to the question of how does a whale get so big?  are the cells larger or how does a very large organism obey the hayflick limit? is it multipotent cells reasserting themselves to regenerate the tissue?

@shigeta I'm not sure what the answer is for whales specifically, but different species can have different telomere lengths. In fact, different people can be born with different telomere lengths. The Hayflick limit of 40-60 divisions is a statement about homo sapien cells.


text:
Changing the definition of life?
Viruses at this period of time do not fit the current definition of life.
Much of the reasoning behind this is that we currently believe that all life must be made up of cells.
Also, many biologist/scientists say that viruses are not living because all they are is just chemicals carrying out their predefined chemistry.
Has anyone every considered the fact that cells, the supposed building blocks of life, themselves simply only carry out predefined chemical actions? All actions cells carry out are chemically driven, not consciously or spiritually driven. Cells do not make choices, they follow chemical directions present in their DNA and RNA. Viruses act very similarly, following the action transcribed in their DNA or RNA.
How can we really even draw a defined line of what life is?

Drawing a clear line is difficult as you note.  But science typically excludes viruses because they don't have the proteins and other parts necessary to reproduce or survive on their own.  They contain the genetic code necessary to hijack the functional parts of cells in other organisms, but nothing else.  Viruses don't follow chemical directions - they rely on the host cell to do that.

Who believes life must consist of cells? I've never seen that included in the definition of life. Who believes free will is required for life? No one I have ever read.

Migrating to biology.

Relevant: http://biology.stackexchange.com/a/9455/4101

Did we have a definition of life? As far as I know, the closest thing to that is celularity. Why? Because we want to exclude viruses. That's why.

@MiguelÁngelNaranjoOrtiz: I disagree. The "classic" point against viruses being alive is that they are obligate intracellular parasites. That said, even if cellularity (whatever that means) was the "rule" for being alive that surely would not be because "we want to exclude viruses". There are definitions of life and virus may or may not fit into them, but to say (without bringing any proof whatsoever) that the definition is made specifically to exclude viruses sounds very unscientific to me...

But there are a lot of protozoa and bacteri athat are obligate intracellular parasites. In fact, many viruses have more genomic complexity than Micoplasma and many other insect associated intracellular bacteria, for example. "Life" as a term is very unclear. It is assumed that implies the ability to transform energy in order to reduce its own entropy, the ability to reproduce and the ability to evolve by natural selection. All of this is very hard to specify to many parasitic microbes, and thus the ultimate limit is celularity. Megaviruses are in a limbo, thought.

@MiguelÁngelNaranjoOrtiz it is not a matter of complexity (though I wonder about that claim, I'd like to see the genomes you mean). Also, all life has specific parameters within which it can survive. Mammals will die at -120C for example and obligate parasites need heir host, the point is that all of these, unlike viruses, can reproduce themselves without hijacking someone else's cellular machinery.

Does this answer your question? Why isn't a virus "alive"?

I'm surprised that this has survived so long. It isn't a question it's an excuse to present a point of view and start a discussion about it, clearly violating SEB principles. Given that there is already a better question on the definition of life with an answer by the top answerer here, I have no idea why it was revived, but think it should be reburied permanently as a duplicate.

How can really even draw a defined line of what life is?

It's easy, really: just make one.  In the answer I linked to I go into the reasons why viruses aren't alive and what our current definition is (spoiler alert: no ribosomes), but the bigger question is why does it matter?  We can draw the line wherever we want to, but it's still an arbitrary construct placed onto the universe by humans so we can sleep at night.  It's similar to intelligence.  We draw arbitrary lines around primates and dolphins and elephants and pigs and what have you, because they're the smartest and most thinking, but that's only for our own (legal) convenience.  Intelligence and awareness is a spectrum, there needn't be a point beyond which you "count."  There's no reason life can't be the same way.
Edit 1.5 years later to add a short, somewhat fanciful video I just watched, it goes into some of the complexity and difficulty with defining life; viruses show up about half way through.  It waxes philosophical toward the end, but that's sort of my point.  Arbitrary delineations are just that.

@PiotrChojnacki Works fine for me.  Here's the direct YT link FWIW: https://www.youtube.com/watch?v=QOCaacO8wus

...many biologist/scientists say that viruses are not living because everything they do is just chemicals carrying out their predefined chemistry.

I don't think that's correct. Many definitions of life exclude viruses because they lack the apparatus to perform the life functions themselves, especially reproduction. They don't seem to qualify as parasites because, when they've infected a cell, they no longer occupy a bounding structure (other then the cell itself.)
When viruses are acting like a living thing, they look like misbehaving cell. Here's a similar puzzle; what organism is cancer? Viruses are basically rogue genes, just like cancer cells are basically rogue cells.
"Organisms carrying out their predefined chemistry," is basically saying that living systems are deterministic. The interesting question is, are very complex systems that emerge from stochastically-driven events themselves deterministic? Are organisms like a clockwork?
Probably you should check out Schrödinger's What is Life? to get started.

"They don't seem to qualify as parasites": they do, they are obligate intracellular parasites.

I appreciate your point, @nico, but I wonder, if they were clearly qualified as parasites there would no debate over whether they are alive. Parasitism is an ecological niche, not a definition of life. So (to split the hair) they are clearly parasitic when they've infected a cell, but I question whether the annotation as parasite is accurate.

it's not really the "parasite" part which is important, but rather the fact that they are obligate, i.e. they cannot reproduce by themselves, they need a host to do that.

Every gene needs a host to replicate! Every gene is obligate; the question of parasitism is key to defining a virus as something other than a gene.

well, I do not know many people who think genes are alive...

Exactly...viruses are not alive.

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


text:
how much grass does a sheep eat in square meters per day?
I want to buy some sheeps in order to eat my garden's grass.
How much grass does a sheep eat each day ??

What species of sheep? How old? In what climate?

This: http://www.urbanshepherds.com might have the answer.

@sheep agree with terdon, some more detail would be nice.


text:
What happens in your brain when you receive information which causes you to bristle?
I'm talking about moments when you watch a film and you bristle, or when you listen to music, etc.
What kind of neurotransmitter flow changes?

Do you mean you bristle or get goosebumps?

You mean piloerection?  Adrenaline or cold tightens the muscles, which makes the hair stand on end, to trap heat and make the animal look larger.

yes exactly is it just Adrenaline or there is another flow of neurotransmitters increased or decreased ?

One thing is that we can't control the Goosebumps. It is an involuntary function caused by the Sympathetic Nervous System which is the major part of the Automatic Nervous System. The major function of the SNS is fight to flight response along with maintaining homeostasis in which case it internally will be alert maintaining body status from the background.
Before sending any response to target tissue when there is input to SNS it has to secrete neurotransmitters but before this to the sympatho-adrenal response of the body, as the preganglionic sympathetic fibers that end in the adrenal medulla (but also all other sympathetic fibers) secrete acetylcholine, which activates the great secretion of adrenaline (epinephrine) and to a lesser extent noradrenaline (norepinephrine) from it.
So whenever SNS senses (message flow is bidirectional) any stress it responds it in following action mentioned:

At the synapses within the ganglia, preganglionic neurons release acetylcholine, a neurotransmitter that activates nicotinic acetylcholine receptors on postganglionic neurons. In response to this stimulus postganglionic neurons - with two important exceptions - release norepinephrine, which activates adrenergic receptors on the peripheral target tissues. The activation of target tissue receptors causes the effects associated with the sympathetic system.

Once the receptors receive the information then the response flows to the target tissue via neurons with the help of the neurotransmitters. To explain goosebumps technically:

Properly known as piloerection, horripliation or pilomotor reflex, the bumps we get are stimulated by fear and cold and they are essentially just a temporary change in the skin. These stimulants cause a nerve discharge from the sympathetic nervous system (which is an involuntary portion of nerves we have) and the nerve discharges create muscle contractions called arrrectores pilorum that raise the hair follicles in our skin. It is the elevation of the hair that causes the Goosebumps.  The name Goosebumps actually comes from the fact that plucked goose feathers resemble the human hair follicles.

Goosebumps also occur when we listen to surprise songs, sad songs or some other kind of thrilling music. Researchers have tried to explain it and they call it "Frisson".
Check out this small video which talks about it. It is nice:
http://www.youtube.com/watch?v=-EA2eWZuYDs
Also refer to this website: Goosebumps


text:
Which human cells have the longest and shortest lifespan?
Which cells in a human have the longest lifespan? Which cell has the shortest lifespan?

Neuronal cells do not divide. Mature ones anyway

The time a cell spends before it divides should be considered its lifespan in the sense of the question? As it is often heard: cells that divide are immortal (see comment above). The question is not about the shortest span between cell devisions; there might be related questions.

If we define lifespan of a human cell to mean the period during which the cell survives with the same function in a human then..
LONGEST (LIFETIME)
Stem cells. Many types of stem cell form during embryogenesis and persist with the same functionality through to death. would be the longest lived (e.g stem cells that form blood cells such as lymphocytes, red blood cells and platelets).  Stem cells are found in many tissues including self-renewing ones such as the blood/bone marrow, gut epithelium and skin.
VERY LONG (YEARS-DECADES)
Neurons are long lived and are generally non-mitotic.  However, recent studies are raising questions about the degree of cell division in the 'mature neurons' of the brain.
Memory T-cells and memory B-cell (which can be activated and secrete antibodies as 'plasma cells') can provide long-lasting immunity from exposure to antigens in the environment and vaccines.
LONG (FEWER YEARS-DECADES)
Oocytes (eggs)..which are present at birth but which become functionally mature in waves  during puberty.
RACE FOR THE SHORTEST
Labeling studies show that mature gastric epithelial cells live for a few days.
The top layer of skin epithelium is sloughed off every few days.
Sperm cells live for days and are expended or re-cycled.
Mature neutrophils have a circulating half-life of around 8 hours but they can persist as mature forms within the bone marrow for a few days before entering the circulation and they may exit the circulation into depots such as the lung.  So the 8 hours is too short for their actual lifespan.

Some mature neurons can last a lifetime.  Gastrointestinal cells such as those in the colon might be shortest-lived, and skin may give them a run for their money.  However, depending on how you define lifespan, egg and sperm cells could beat those numbers.  Also, some immune cells only last a few days under certain scenarios, such as the aptly-named short-lived plasma cells.


text:
Renin - enzyme or hormone?
Wikipedia says :

The kidneys secrete a variety of hormones, including erythropoietin,
  and the enzyme renin.

Can a substance be both an enzyme and a hormone ? Why is renin both an enzyme and a hormone ?

Yes, something can be both a hormone and an enzyme. There are a group of hormones known as peptide hormones. These are proteins (such as enzymes) that act as hormones indirectly (and maybe directly too?). A hormone is a chemical secreted by a cell that has some effect on another cell elsewhere in the body. In this case, the chemical just happens to be an enzyme. You can read about them on Wikipedia
Renin is secreted by the kidney, but its involved in arterial vasoconstriction (outside of kidney cells), so it is a hormone. And its also a peptide/enzyme, so it is considered both a hormone and an enzyme

Hormone is just a different class of protein and is not usually an enzyme. Peptide hormones have no catalytic potential and serve only as signaling ligands.
There can be secreted enzymes which is common in the digestive tract but these are not called hormones. Hormone is purely a signaling molecule.


text:
How is it that the WI-38 cell line isolated by Hayflick in 1962 is still very much around and not affected by the 'Hayflick Limit'?
I have searched the net and I have not been able to come up with an clear answer.
Edit: Here is the para quoted from Nature http://www.nature.com/news/medical-research-cell-division-1.13273
"So began WI-38, a strain of cells that has arguably helped to save more lives than any other created by researchers. Many of the experimental cell lines available at that time, such as the famous HeLa line, had been grown from cancers or were otherwise genetically abnormal. *WI-38 cells became the first 'normal' human cells available in virtually unlimited quantities to scientists and to industry and, as a result, have become the most extensively described and studied normal human cells available to this day".*

I essentially answered this here, pointing out that telomerase negates the supposed "limit," which stem cells and cancers usually express.

@ Amory - I doubt if your comment is relevant here. WI-38 is considered to be a 'normal human cell' line. I could not find it described as a stem cell. So where does the telomerase come from? The question is a genuine one and I am looking for a serious answer or comment.

Did some digging, are you sure they actually do?  ATCC seems to disagree

From your own article: "...they so reliably stop replicating after about 50 divisions..."

Yes but the original cell line is still there and is commercially available. I just want to know how they keep it going.

The answer is that the majority of the cells were frozen from very early in their Hayflick lifetimes e.g. after 9 population doublings. They have been thawed out judiciously and only as needed thus preserving a lot of frozen stocks.  When an ampule of cells frozen at, for instance 9 population doubling, is thawed, the cells pick up where they left off and still have 41 doubling a to go.  So the magic of exponential growth combined with the fact that they keep dividing after being thawed has made for a decades- long supply . Does this answer the question to your satisfaction?

Is this Meredith Wadman of Nature?

WI-38 are the cell lines which led to the proposal of the Hayflick limit and are the classic example of cells which will only divide ~40 times.  they are not exempt - they are the example that proved the rule.
Lots of cell lines are commonly available, but have to recultivated regularly from animal/tissue source.  If they can be frozen, then the extraction of new cells doesn't happen so often without exceeding the limit of divisions.  This allows the cell lines to be used widely for experiments despite the limitations on their division in culture.
Other cell lines like HeLa and other tumor cells or Stem Cells can, under the proper conditions, divide without limit and are easier to culture in large volumes, but are often inappropriate for a given research project.


text:
What Biology topics are linked to the Nitrogen Cycle?
What other educational topics are linked to the Nitrogen Cycle? I am a Science teacher, and I need to organise my lessons. Thanks!

As phrased this is currently very broad.  You say "other" but don't say what you've already considered.  What work have you done so far?

@justin other topics may be symbiosis , root nodule formation,chemical "talks" between rhizobium and legumes. Examples of symbiosis like mycorhhizae can also be given.

The nitrogen cycle is a highly biological process. Nitrogen gas is ~75% of the earth's atmosphere and N2 is the most chemically stable form of Nitrogen for conditions in the Earth's crust.
Nitrogen is one of the four most essential and universal elements to terrestrial life (Carbon Hydrogen and Oxygen being the others).  Nitrogen fixation, the name given to the various processes which make chemically reactive forms of Nitrogen available to living things. Ammonia (NH3 / NH4+) and Nitrites / Nitrates (NO2-, NO3-) are chemically unstable compared to N2 and the conventional biosynthetic processes in the cell can use any of these forms to make proteins, nucleic acids and other biologically active molecules necessary for life.
Ammonia and similar compounds like Urea come from the biological byproducts of  living cells - waste.  These are readily recycled in the soil by plants and microorganisms and I imagine some animals and insects.  Nitrogen is a limiting resource for living things and most biomes are pretty efficient at recycling reduced nitrogen from primary (NH3) secondary (NHR2), tertiary (NR3) and quaternary amines (NR4).
But the biosphere has a great demand for bio-useful nitrogen and in most places on earth in deep water and soil microorganisms can break down N2 directly into nitrates/nitrites. This happens deep underwater or underground because the enzymes which perform this activity are delicate and ruined by O2.  This process is entirely performed by anaerobic microorganisms. In recent decades, the ecological importance of subterranean microbial communities has become better appreciated for the complex structure and ecological roles it plays.
An interesting side note to this is that up to the early 20th century, the growth of life and human civilization was really limited by the intense labor required to grow food.  While hydrogen oxygen and carbon are essentially free - obtained from water, atmospheric oxygen and CO2 by plants, Nitrogen was the limiting factor in many cases to growing more crops or animals for food.
The Haber process, which converts nitrogen and hydrogen gas under high temperature and pressure into ammonia over a catalyst was such an important discovery - it allowed the industrial preparation of effective fertilizers and was instrumental in creation of the green revolution.


text:
What is the recommended PPM when foliar feeding L-amino acids
It is said that L-amino acids such as histidine, methionine, aspartic acid, glutamic acid, asparagine and glutamine can revert plant stomata closure, increase quality of fruits and assist maturity. It is also said that the best way to apply is through foliar feeding.
I would like to start experimenting with different amino acid foliar feeds but would first like to know if there is a recommended maximum/minimum/recomended Parts per million(PPM) , for foliar feeding of these compounds.

I know that some of the amino acids you listed are commonly found in fish fertilizer. I haven't read any studies on the use of these amino acids individually and not sure where you would purchase them separately. If you're just experimenting in your own garden I would just use fish fertilizer according to the label directions. If you look for fish fertilizer studies you'll probably find more info.
Also, I've never heard of these opening up the stomata of the plants. The only references I've read indicate that foliar sprays are best applied in the early morning or late day when the stomata is already open. This is how the nutrients get absorbed from the leaves.
I don't know that I would want to intentionally manipulate stomata closure. The plant knows when it needs to breath.
Where did you read the above info? I'd be interested in seeing it.

From my understanding stomata close when light and humidity are low, and temperature and salt concentration are high. When stomata close, photosynthesis and nutrient absorption slow and the plants respiration is increased. this slows plant growth and can affect end of year yield applying L-aminos favours the opening of stomata and increases plant health and growth in adverse conditions. Body builder shops stock individual l form aminos that are easily dissolved in water thus my ppm question.

@damien I believe plant respiration decreases (not increases) when the stoma close since the stomata facilitate gas exchange. Transpiration also decreases when closed. If you're forcing the stomata open you'll need to water the plants more (or shade them?). See http://en.wikipedia.org/wiki/Guard_cell Still curious as to which sources you're referencing.


text:
What's behind the amazing colour combinations in pests & insects?
What's behind the amazing colour combinations in pests & insects ? Do this colour combination signals any character/ poison of the pest/insect ?

What pest? Which insect? Bright colors often indicate poisonous animals but you'll need to be much more specific for us to be able to answer you.

Or that's what they want you to think...

@Oreotrephes sneaky buggers :).

Why Close vote? I think, its answerable!!


text:
How do inward rectifier potassium channels work in the heart?
Apparently in cardiomyocytes, there is an inward rectifying potassium channel that operates during phase 4 of the cardiomyocyte action potential.  I have heard that despite this potassium channel being referred to as an inward rectifying channel, that in vitro the channel in fact still transports potassium from the inside to the outside of the cell.  It appears that Wikipedia seems to suggest otherwise (?).
Can someone please explain what the inward rectifier potassium channel does and its role in phase 4 of the myocyte action potential?

According to Boron's medical physiology textbook:

"Although inward rectifying potassium channels pass current better in
  the inward than the outward direction, the membrane potential (Vm) is
  typically never more negative than Ek (equilibrium potential of potassium across the membrane). Thus,net inward K+ current does
  not occur physiologically. As a result, the activation of GIRK
  channels (G protein coupled inwardly rectifying potassium channel)
  hyperpolarizes cardiac cells by increasing K+ conductance or outward
  K+ current."


text:
What is the effect of extra-cellular potassium concentration on heart rate and conduction velocity?
If the extracellular potassium concentration surrounding a myocyte increases, then the potassium gradient accross the cell membrane decreases, and therefore the resting membrane potential will become more positive.  Similarly, if extracellular potassium decreases, the resting membrane potential will be more negative.
With this in mind, how does the heart rate change when extracellular potassium concentration increases/decreases?

Pathological potassium concentration promotes arrhythmia.
Increased extracellular potassium inactivates $Na^+$ channels and opens $K^+$ channels, causing the cells to become refractory [1]:

Increased extracellular potassium levels result in depolarization of the membrane potentials of cells due to the increase in the equilibrium potential of potassium. This depolarization opens some voltage-gated sodium channels, but also increases the inactivation at the same time. Since depolarization due to concentration change is slow, it never generates an action potential by itself instead, it results in accommodation. Above a certain level of potassium the depolarization inactivates sodium channels, opens potassium channels, thus the cells become refractory. This leads to the impairment of neuromuscular, cardiac, and gastrointestinal organ systems. Of most concern is the impairment of cardiac conduction which can result in ventricular fibrillation or asystole.

Decreased extracellular potassium leads to hyperpolarization [2]:

Lower potassium levels in the extracellular space will cause hyperpolarization of the resting membrane potential. As a result, a greater than normal stimulus is required for depolarization of the membrane in order to initiate an action potential.
In the heart, hypokalemia causes hyperpolarization in the myocytes' resting membrane potential. The more negative membrane potentials in the atrium may cause arrhythmias because of more complete recovery from sodium-channel inactivation, making the triggering of an action potential less likely. In addition, the reduced extracellular potassium (paradoxically) inhibits the activity of the $I_{Kr}$ potassium current and delays ventricular repolarization. This delayed repolarization may promote reentrant arrhythmias.

References:

Wikipedia contributors, "Hyperkalemia," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Hyperkalemia&oldid=612096441 (accessed July 12, 2014).
Wikipedia contributors, "Hypokalemia," Wikipedia, The Free Encyclopedia, http://en.wikipedia.org/w/index.php?title=Hypokalemia&oldid=612818488 (accessed July 12, 2014).


text:
What happens in the synapse when cocaine administration occurs in the human brain
As far as i know when you accept cocaine in your blood some cocaine molecules reach some synapses in your brain and fill some Reuptake tunnels preventing the cell to simply "do not know that fired neurotransmitters have achieved their task" and doing so the cell fires neurotransmitters again becuase "it" simple do not know that "it" have achieved its task.
In this case cocaine molecules fill Reuptake tunnels in Dopamin Serotonin and Norepinephrine
orientated neurons.But since the firing occurs when an electrical signal occur how the neurotransmitters are fired again when such electrical signal does not exist?
If im mistaken in my physiology knowledge explained above please correct me!

You are correct that cocaine "fills the tunnel" (the pharmacology terminology is that it "blocks the transporter").  But it is not an autoreceptor, so the reuptake transporter does not send a stop signal, it just removed neurotransmitter from the cleft.  But once you've blocked it with cocaine, neurotransmitter is not being removed from the cleft so it has a much longer and stronger signaling effect on the post-synaptic neuron.
But cocaine can also block sodium channels, which assist in action potential propagation and that has more of a local anesthetic effect.
The effect you are thinking of would pertain to auto-receptors, not reuptake transporters.  Autoreceptors tend to be more like the post-synaptic targets of the neurotransmitter.

so you say a single neurotransmitter can bind to a receptor many times and can do its task many times (like neurotransmitters are not  limited) and by blocking the transporter all neurotransmitters in this case perform their task many times and new neurotransmitters are arriving just because this is the normal function of the brain ?

ligan-receptor kinetics have an "off-rate" and an "on-rate" so yes, they can bind more than once, but some receptors can become "desensitized" from being stimulated.  Regardless, having more neurotransmitter in the vicinity of receptors leads to a larger chance per unit time of ligand finding receptor and activating it.

for example if i have a long dopamine flow like being on cocaine for 1 hour will this dopamine "attack" damage your brain?
Because as far as i know cocaine consumption damage your brain or im wrong?

I'm not a medical expert, but I don't know of any damage to brain from cocaine.  Of course, using cocaine, flooding your dopamine receptors, your body will compensate in the long run by reducing the number of receptors on the post-synaptic neuron (and it will require more cocaine next time).  Once you quit doing cocaine, it will take a while to recover normal receptor levels.

Cocaine is cardiotoxic. After chronic exposure to high doses I would assume that primary damage would attack the cardiovascular system before levels of dopamine would be able to cause damage. Cocaine intoxication deaths have mostly been caused by this cardiotoxicity. Primarily, myocardial infarction, arrhythmia, heart failure, and sudden cardiac death are a result of overdose. Cocaine is a vasoconstrictor, which may be a leading cause to myocardial infarctions.
http://www.ncbi.nlm.nih.gov/pubmed/19463023

how does this answer the question?

I am saying that you would most likely overdose and suffer cardiovascular consequences that result in death before it's possible to have brain damage as a result of too much dopamine in the post-synaptic cleft.

That makes sense


text:
Difference in reptile inner ear and otosclerosis
In reptiles, the sound is conducted from the tympanic membrane to the inner ear by a single bone.
In the disease otosclerosis the stapes of humans become fused to the other middle ear bones( or to the oval window ). This disease leads to the loss of hearing.
My question is - From what seems like superficial resemblance between otosclerosis and having one bone in reptiles, what is the difference between the two that leads to loss of hearing in one case but not in another ?

Good question. To understand it perfectly, you'll need a good reference to a text on detailed explanation of sound conduction by the ear ossicles in reptiles and humans. I couldn't find anything better than these here and here.
But these are partly inadequate in addressing your questions and are a bit involved in the physics used.
But, if we leave the physical details aside below is the possible reason as to why a single bone in case of reptile conducts just fine but in humans fails to conduct.
 The reptile ear has evolved such that it uses a single bone for conduction, while the human ear is functioning with three transmitting ossicles (the only example i could think of). This is similar to the working of a watch. You can create a time-keeping device by using a combination of three gears (old play watches) or a combination of a large number of gears (my Timex Retrogade). Both have the same function, but if we fuse several gears in the second case to equal the number in the first (hypothetically only), it will obviously stop working. In our analogy, the ear has evolved such that the sound is optimally transmitted due to several effects like, resonance, impedance, transformation and simple amplification along the ossicles, and all these functions depend very specifically on the shape and orientation of the various conducting elements of the system. And therefore, even a slight disfigurement might severely impair the conduction of sound. Therefore, had the human ear system evolved to work with one ossicle, it would have evaded osteosclerosis by being able to conduct with one ossicle also.


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What is the chemical composition of an egg shell?
It ought to be some combination of C, O, and H, I presume. But really why should I care if eggshell gets in my eggs while I'm cooking?

Could you specify which animal's egg shell ?

Sure eggs from hens

Just google eggshell :) By the way, it is mostly calcium carbonate stabilized by a protein matrix. I have heard that excess calcium carbonate may cause some side effects but I don't have any good source.

@biogirl I don't want to google things; I would like to ask questions here to build a larger index of Q&A. Sure, I could always google things, but, asking questions here in the fashion that I have, is a catalyst for participation. If everyone feels that I should seek to answer my own questions through google, (which I am perfectly capable of doing), why have biology stack exchange? I would rather get the unique, human, and academic perspective from biologists and biology enthusiasts alike.

@RustynYazdanpour you should do a google search.
From the help pages http://biology.stackexchange.com/questions/how-to-ask: "Search, and research. Have you thoroughly searched for an answer before asking your question? Sharing your research helps everyone. Tell us what you found (on this site or elsewhere) and why it didn’t meet your needs. This demonstrates that you’ve taken the time to try to help yourself, it saves us from reiterating obvious answers, and above all, it helps you get a more specific and relevant answer!"

I took time to ask my question here, (help myself). My asking of a question spurred participation. SE is optimized for Q&A, so please do not tell me to google things. Perhaps they should make a biology overflow for serious research questions.

If you feel the question is obvious-- ignore it

@RustynYazdanpour I am sorry if you felt hurt by my comment. The first part of your question is easily searchable so I like the second part more because it is something I never thought before and got to learn something new ! On SE asking thought provoking questions will be appreciated. Do keep on asking good questions !!

It's the same stuff that makes up most sea shells, calcium carbonate, $CaCO_3$.
Incidentally, this explains why egg shells dissolve in vinegar (acetic acid which, since it is an acid, provides the Hydrogen ions in the reaction below):
$CaCO_3+ 2H^+ -> Ca^{2+} + H_2O +CO_2$
This simple reaction (which is what would happen in your stomach as well) produces water, calcium ions and carbon dioxide, none of which are particularly harmful.
The specific reaction with acetic acid is
$CaCO_3 + 2CH_3COOH → Ca(CH_3COO)_2 + H_2O + CO_2$
which also produces calcium acetate.
Anyway, there is nothing particularly toxic about $CaCO_3$, it's basically chalk. I wouldn't recommend eating a lot of it but you shouldn't freak out if some falls into your omelet either.
However, don't forget that an egg has exited a chicken's anus (well, cloaca) so their shells are likely to have come into contact with feces and they are porous so they are not necessarily the cleanest thing around. This is just not because of any chemical toxicity.

I thought that the calcium carbonate dissolves in olive oil, and calcium acetate forms. Should I have anything to worry about as far as calcium acetate goes?

@RustynYazdanpour calcium acetate is harmless. As you can see in that link even at very high concentrations (like those you will get if you buy it from a chemical company) it is an 'irritant'. In the concentrations you might find in your kitchen you can safely ignore it.

@Rustyn Yazdanpour: I doubt you'll get acetate from olive oil... it would rather come from the reaction terdon wrote (where he omitted acetate ions). In any case no worry about that either, although there are definitely much better uses for eggshell (composting for instance).

@terdon Ok, this is a full comprehensive answer. I really hope that the kinds of questions I'm asking are appropriate for this forum. Otherwise, if the community would prefer, I can ask some of these questions on chemistry stack exchange.

@terdon Sorry for my derisive tone that I may or may not have taken with you yesterday and thank you for your answer.

If you don't get any more chemical than this, you're fine. If you are asking about specific reactions chemistry might be better. If it is about their effect in a living system, they belong here. And no worries, you're very welcome :)

Indeed, you're more likely to find salmonella on the egg shells than in the yolk or whites themselves.


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Why does shaving dehydrate the skin? Is there an hormonal effect involved?
I want to understand why the face becomes dry after shaving and if shaving affects hormones? I've heard that after shaving, hair grows back faster, why? Shaving damages hair follicles and they become inflamed. One could get an infection JUST by shaving because tissue is ripped from the hair follicles. So maybe the increase in hair growth can be attributed to the natural blood rush that brings nutrients to the damaged follicles when they are inflamed after shaving....

You answer your own question, there is absolutely no biological reason to shave, its social. 2) One does not control the amount of sweat one produces, I wish we could. 3) You are combining multiple questions into one, please don't and post separate questions for each query instead. Voting to close.

@terdon You represent a jaded portion of this community, you don't like my question(s)? Explain to me why it they aren't valid, otherwise you have the option of nonparticipation in this thread.

I still don't see what you're asking. Of course running a sharp blade against your skin causes irritation. Are you asking why an how does skin get irritated?

@terdon is there something happening with hair follicles? And yes, I understand how the skin gets irritated-- I want to understand why the face becomes dry after shaving and if shaving effects hormones? I've heard that after shaving, hair grows back faster, why????

Ah, then please rephrase your question to make that clear. Mention the hormones and that hair grows back faster. "Our own biology rejects shaving" is really unclear.

Hmmmm... any special reason that makes you think hormones are involved?

@nico Not in particular, but through shaving we damage tissue, which might cause an uptake in hair growth hormone. If not enough hormone is available, wouldn't the body think it is deficient in the hair growth hormone and produce more?

@Rustyn Yazdanpour: I would assume it is just a local reaction, otherwise all of your skin would be affected, which is not the case... My take (but I may be wrong) is that it is just a side effect of the inflammation (e.g. some interleukins can cause dry skin).

First of all 'Testosterone' hormone controls the growth of hair on our body and also oil secretion. Depending up on the nature of a person's body, this hormone controls the growth of the hair.
Why shaving facial hair leaves the skin dry ?
First let me explain the reason behind the oiliness of the skin. Sebum is produced by the sebaceous glands and is a complex made up of cholesterol, free fatty acids, glycerides, squalene, and wax esters. Sebum and sweat, along with the epidermal lipids discussed earlier, make up the oil on the surface of the skin. Some people will have more oily skin and some have less which depends on the nature of body.
While shaving the sharp razor cuts the hair and also damages the skin and hair follicles. The level of damage to skin also depends whether you are shaving downwards or upwards. Because upward shaving usually causes more damage to skin and hair follicle. Complete detail of damage to hair follicle can be found in this article: Science of shaving.
Shaving also removes skin lipids and water content creates pores which exposes the skin. If the surrounding atmosphere is dry then skin loses water. Or if the surrounding is moist or humid then water content will be balanced. That is the reason why we use artificial face moisturizer for immediate remedy to avoid infection and balance the wetness of face. So it takes a while for the skin to get back to normal state if nothing is done after shaving which sometime leads to acne or rashes due to infection.
Another reason for dry face is use of hot water which removes skin oil instantaneously. So lukewarm water or cold water will further reduce the dryness of the skin. (Use of shaving cream with high alkaline content will obviously result in dry skin. This holds for soaps also.)
Complete details can be found in the first link provided and Drying skin after shave.


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What would classify those findings of the University of Sheffield experiment as aliens?
It's in the news that some experiment was able to capture some alien specimens during a meteor shower:
http://www.ibtimes.com/aliens-are-here-scientists-say-they-have-proof-alien-life-there-should-be-plenty-skepticism-1408322
Despite all the skepticism that has already been said about this finding, what would be a proof that such specimem came from outer space? Is there any established protocol to assure that some form of life didn't come from Earth?

Despite me having answered, I think this is off-topic for skeptics, because you're not asking us to verify/falsify a particular claim. Instead, you're asking us for "what would prove something came from outer space?", which I think people over at physics, biology, or space stackexchanges would be much better suited for. Would you mind having this migrated?

I can migrate it, but this could be a good skeptical question given the claims being made.

@LarianLeQuella As I understand it, woliveirajr is interested in the basic science question of "what would prove that something came from outer space?", rather than having the claims of these scientists examined. If he/she is also interested in having the claims examined, that question could be asked here separately, while this one is migrated elsewhere.

I wouldn't say that there is an established protocol - claims of alien life are not commonly testable or even legitimate - but if something were discovered and deemed "alive," a fairly good sign it was alien would be if its genetic makeup were based on something other than DNA or RNA.  That would be a dead giveaway the organism had side-stepped every known organism on Earth and while that doesn't prove alien-ness, it would certainly hint strongly of a non-Terran genesis.  There are arguments for and against carbon/CHNOPS-based life but that is nowhere near as definitive.
Also, there's another really good technique.  I don't like to resort to ad hominem attacks, but ideally the discovery should be by someone who has not already made verifiable false claims on the same topic.

Isotopic ratios could theoretically be useful, in particular carbon or oxygen (a la the Allende meteorite), but there are so many ways to get different numbers that an alien origin hypothesis would rank pretty low.  It could be informative but it certainly isn't a magical "push button, get number" scenario.  Wonky ratios have already been observed many times for definitely Earth-bound life.


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What would life expectancy be in the western world in the absence of Ischemic heart disease?
In 2012, the leading cause of death was Ischemic Heart Disease.  In 1st world countries, what is the life expectancy for people who do not die of Ischemic Heart Disease?  I'm interested in the USA, but I'm happy for you to provide information on other 1st world countries if USA data is unavailable.
My motivation for asking the question is a curiosity of how much our life expectancy would increase if IHD was abolished.

This will be a tough question to answer, but people tend to die from one of only a handful of age-related diseases (other deaths are either infection related, accidental, or "rare" diseases).

You may want to play a little bit with this: http://www.theguardian.com/news/datablog/interactive/2012/dec/13/how-people-die-global-mortality-visualised

This paper from 1991 is intervention-based, so it reports the effects of behavior modification on lifespan in people who turned 35 in 1990.  The authors report the gains for each individual behavior and then say:

Eliminating coronary heart disease mortality is estimated to extend the average life expectancy of a 35-year-old man by 3.1 years and a 35-year-old woman by 3.3 years

Which they feel is a modest increase but I rather disagree.  This report estimates the that reduction in death due to heart disease of over 50% between 1950 and 1995 gained around 3.5 years, although most of that is probably due to better medical treatments.  This 2004 study used 1998 data from the UK and estimated that:

The average gain in life expectancy from the elimination of cardiovascular disease risk as a cause of death was 4.0 years for all the 35 year-old men in the sample (n = 24), and 1.8 years for all the 35 year-old women in the sample (n = 32).

Although I would note the low sample size.  I didn't expect to find much, so I was surprised to find these... and with similar results!  One big issue is that a lot of the more recent research has focused on smoking, weight/BMI, and blood pressure reduction, rather than all IHD/CHD/CAD; I found tons of those.  As a side note, simply reducing TV watching to less than two hours a day can lead to a gain of almost 1.5 years.

Kind of surprising only 3.5 years, what's the point, I'd rather my KFC.  Do you think the small increase is because of other forms of atherosclerosis though, such as stroke?

Perhaps - stroke is #2 in the 75+ crowd - but don't forget about cancer.  Cancer as a whole kills more than strokes at that age, and a few forms of cancer usually come out ahead in other age groups as well.  That the number is so low is more of a testament to how successful our medical system is despite the deadliness of IHD.


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Blood pressure difference while seated and laid down
My blood pressure readings differ a lot when I read them while seated and while I lay down on a bed.
I tie the strap in both cases to my left bicep and rest for a minute before noting the readings down.
For example, one reading I took was:
Seated: 130-85
Laying on bed: 115-75
These were noted down one after the other.
I am not sure if there should be this much difference in the readings and is this something to be worried about.

Do you have any symptoms?

No. I don't have any. Any specific symptoms?

It is expected that BP would be higher when laying on the bed than when seated.  Is the cuff at the same height relative to the heart in both of your measurements?  Also have you tried measuring BP when standing?

If blood pressure increases on standing, you may have some degree of orthostatic hypertension (not to be confused with orthostatic hypotension which is more common).  This link might be of use:  http://www.medscape.com/viewarticle/543590_2

Thanks Chris. While standing and having the cuff position at the same position relative to my heart when I took the other two readings gave a fall of around 5.

I can't offer specific advice as to your personal readings, but it is normal to expect a difference in blood pressure between sitting & supine (lying down) positions.
I have taken this quote from the Department of Health Care Sciences at Wayne State University website.

Effects of body position on blood pressure
Blood pressure is commonly measured in the seated or supine position; however, the two positions give different measurement values. With that in mind, any time a value is recorded, body position should also be recorded. It is widely accepted that diastolic pressures while sitting are higher than when a patient is supine by as much as 5 mmHg. When the arm is at the level of the heart, systolic pressure can be 8 mmHg higher, such as when a patient is in the supine position rather than sitting. A patient supporting their own arm (isometric exercise) may increase the pressure readings. If the patient’s back is not supported (i.e., when a patient is seated on an exam table instead of a chair) the diastolic pressure may be increased by 6 mmHg. Crossing the legs also may raise systolic pressure by 2-8 mmHg. Arm position plays a dramatic role in value errors as well. If the arm is below the level of the heart, values will be too high; if the arm is above the level of the heart, values will be underestimated. For every inch the arm is above or below the level of the heart, a 2 mmHg difference will be found (Pickering et al. Circ 2005;111:697-716).

So if you are comparing your own blood pressure day-to-day, make sure you keep a consistent position.
Additionally, if you are reading guidelines for healthy/risk blood pressures, make sure you take this into account.

Thanks for the valuable inputs Luke. I did take a few readings this morning in different positions and they are totally different than yesterday. Now while laying down the reading is more than while seated.
Supine: 125-80
Sitting: 109-72
Standing: 102-70
So I guess my cuff position was not at the same position relative to my heart yesterday and that gave this difference in reading.
Also, as normal reading is said to be between 100-60 & 120-80, when I saw 125-80, I was a little worried.

125/80 is nothing to worry about really.  Over 140 and I'd start to worry.  So if you're taking BP medication, it's working so keep doing it, but otherwise you don't need to start taking it for 125.


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Critical pO2 threshold for cell division?
I'm a physicist asking questions on an aspect of cellular metabolism, so excuse my biological ignorance! Hypoxia is a frequent complication of certain tumour types, and has quite an implication for treatment prognosis - at certain low oxygen levels, metabolic functions become massively reduced or even halted and eventually necrosis sets in.
My question is what kind of partial pressures will cell division typically be halted at? From this review paper, it indicates that below 8-10 mmHg, adequate metabolistic functions cannot be maintained. In this case, the critical parameter being measured is ATP production. However, I've seen quotes for Chinese Hamster Ovary cells of 0.5-1mmHg. In radiotherapy, "hypoxia" as a condition is defined as < 2.5 mmHg but this doesn't tell me much w.r.t cell division or lack thereof.
Does anyone know a ball park figure for the cessation of cell division, in a typical cell line, and where I might find information on this? Thanks!

Part of your problem is that while cell lines are often cultured in "normoxic" conditions, with atmospheric levels of oxygen (~21%), no tissue in the body (except maybe the lungs) actually experiences that; it varies, but most tissues in the body see something closer to 5%, with 1% being "hypoxic."  I don't think I could grow my cell lines in 5% oxygen.


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What is this plant which closes its leaves when touched?
I came across this video on Facebook where a plant closes its leaves when touched. Unfortunately the video does not mention the name of this plant.
What's the name of this plant, and where can I see it?

Related question: http://biology.stackexchange.com/questions/249/how-does-the-sensitive-plant-detect-vibrations/

This question appears to be off-topic because it is about plant identification. These questions are usually asked on Gardening and Landscaping Stack Exchange. This topic is not found in the following appropriate topics listing in the Help center: 1) General questions about biological concepts 2) Questions about the biological mechanisms behind medical conditions 3) Questions about techniques in a biological or biochemical laboratory

Read some of the old, amazing works by J. C. Bose on this-plant here:http://www.gutenberg.org/files/48280/48280-h/48280-h.htm

It is quite common weed in India

It belong to family Fabaceae (pea-allied) and subfamily Mimosoideae (Acacia-allied). Most of the plant under this subfamily are shrubs to big trees whereas this one (M. pudica) is small, undershrub.

"LAAJWANTI" OR "CHOOIE MOOIE" IN HINDI

It is a Mimosa pudica, a wonderful plant. According to wikipedia you can find it in the following places:

Mimosa pudica is native to South America and Central America. It has been introduced to many other regions and is regarded as an invasive species in Tanzania, South Asia and South East Asia and many Pacific Islands. It is regarded as invasive in parts of Australia and is a declared weed in the Northern Territory, and Western Australia although not naturalized there. Control is recommended in Queensland. It has also been introduced to Nigeria, Seychelles, Mauritius and East Asia but is not regarded as invasive in those places. In the United States of America, it grows in Florida, Hawaii, Virginia, Maryland, Puerto Rico, Texas, and the Virgin Islands.

If you think that's impressive, look at this video of Dionaea muscipula the venus fly trap:
https://www.youtube.com/watch?v=O7eQKSf0LmY

Wow that is far more impressive and scary :D Looked like a horror movie.


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Melatonin production - requires nighttime, or just full darkness?
Is melatonin properly produced in daytime sleep in full darkness? Or does it require only nighttime sleep?
Additionally, what other biological implications are there, if any, to daytime sleeping? Melatonin production is the only biological implication I could find so far.

I think this question is answered by the answer I gave to another question. http://biology.stackexchange.com/questions/7667/what-causes-humans-to-be-sleepy.

Thank you, but the main part of my question remains unanswered - is night required for melatonin production, or does it only require full darkness (such as in a dark room, blindfold, etc)?

"It is released by the pineal gland and production starts when the light fades, as it's production is inhibited by light stimulation of the retina, the onset of the production is called dim-light melatonin onset."

The immediate thought came to my mind was relation between Melatonin and Serotonin. Because both hormones have sleep related function. I read that both are light sensitive. Melatonin is produced by pineal gland in brain whereas Serotonin is at gut and CNS.
Light dependence(Wikipedia) of Melatonin is explained here where they say blue light produces more Melatonin and wavelength of light <530nm will have effect on Melatonin production. If the light intensity is more then Melatonin will not be produced. So what they say is if there is darkness(artificial) or dim light environment then this hormone will be produced and induces sleep. Almost everywhere they explain Melatonin whose production is sensitive to light.
(But even in the afternoon when there is bright light some of us feel sleepy which is mainly due to Serotonin released after heavy meal which is produced from tryptophan. This will again effect the sleep. It is obvious that without food we can not sleep at night. So Serotonin and Melatonin are interrelated as explained here Link1 and Link2).

Thank you for the detailed answer. However one part relevant to my question is still unanswered: is Melatonin also dependent on time, hour, day\night? If I am to stay in darkness during daytime, will Melatonin be produced as well as in the same darkness at night?

@UriP: This one might be interesting for you as it explains melatonin production with respect to light: http://biology.stackexchange.com/questions/5503/what-light-intensity-starts-melatonin-release-in-humans?rq=1

It certainly does not require full darkness.  I've often slept quite restfully with the reading lamp left on all night, and children who are afraid of the dark do this habitually.  However, full darkness may PROMOTE melatonin release.

I see, thank you for your clarification. However, the main focus of my question is: Can melatonin also be released in daytime (in partial\full darkness), or only at night?