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Why do human have continuously-growing hair on their head?
Why do hair continuously grow on human heads, while the same doesn't happen on other parts of the human body? Where there are hair, they only usually grow to a fixed length; but they seem to have no limit (or at least a much higher limit) as long as the head is concerned (and the face, in men).
Why does this only happen on humans? When did it start happening? What kind of evolutionary advantage could there be in overly-long head hair, so that humans have them while other primates and mammals don't?

I know there are various questions around about why humans have much less body hair than other mammals; mine is related but different: why are we the only species with so much hair on our head, to the point that they might even become inconvenient if we don't cut them?

There is a limit on hair growth - http://biology.stackexchange.com/questions/1267/why-can-hair-grow-without-limit-while-eyebrow-cannot/1273#1273
As for the rest of your question, we still haven't found the "missing link" in human evolution, so we can't really say "when" because we don't know the stages in-between. As for advantages and disadvantages, well, that seems like it might be more opinion based as I don't know if we can ever know for sure "why".

Thanks for pointing that out; however, even if waist-long hair is the limit for most people (and I know for sure there are exceptions to this rule), the question still stands: why does this only happen on human heads?

@SolarLunix there is no such thing as the "missing link". It's a fallacy dating back to the ancient Greeks, and used by creationists to attempt to disprove evolution. Look it up.

@Massimo Actually, it doesn't really only happen in humans. If you look at a lot of long hair breeds of dogs, there are some that need CONSTANT attention or their coats will become too long and get in their way. As for why it started, that's more of an opinion based thing, it could've been a mutation, or it could've started and continued due to a mating preference.

@MattDMo I wasn't aware, thanks for pointing that out. Is there any research/evidence on how humans evolved? I mean I've read a bit about Neanderthals and other species in the phylum Homo (such as ones who were amazing runners), but I haven't read much more than that.

@SolarLunix check out https://en.wikipedia.org/wiki/Timeline_of_human_evolution and https://en.wikipedia.org/wiki/Human_evolution for starters. And, BTW, Homo is a genus, not a phylum.

@MattDMo sorry, I'd change it but it won't let me edit that comment. Sometimes I get my terms mixed up (thanks for the two corrections)

This post should give some insights on the mechanism of hair length control.

Suggested edit by user @JustinMasters:  "I would like to suggest taking a different approach towards asking questions that have to do with science.  Rather than ask why something happens, try to ask "how" or "what" questions that can provide you with the the information you seek.  "Why" implies reason or purpose in such a way that one can get comfortable thinking about things the wrong way, especially when you ask "why" in a physics or chemistry class. In zoology, most why question about an animal's traits can be answered with fitness to compete for resources or mates." [cnd..]

[cnd..]: "The more interesting information comes from trying to figure out the how. How do the genes / gene expression for hair and fur differ such that hair will continue growing unchecked while fur will grow to a specific length?"

The above comments were a suggested edit to the Q, but I think they fit better as comments, since the edit wasn't a rewrite of the Q but rather suggestions or an alternative perspective.


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Exhalation while holding breath
If you inhale to your maximum capacity and hold your breath for an extended period of time, it begins to feel uncomfortable; slowly releasing your breath at this point seems to provide relief from this discomfort.
Is there a biological reason why this is so, or is this something psychological?

The exact causes of the discomfort relief  after the breath-hold breakpoint  is unknown yet.
It has been stated that breath "pacemaker" continue to work independently of voluntary breath holding. Thus, while breath holding, the breath center is trying to activate the diaphragm and the afferent feedback from the diaphragm normally causes the feeling of discomfort. Thus, upon starting breathing again, i.e. actual diaphragm movements, the discomfort will diminish and the subject will feel relief.
Breath-holding and its breakpoint. Experimental Physiology Volume 91, Issue 1, January 2006.
full text of cited article

This occurs because the feelings of needing more air to breath result from changes in the concentration of carbon dioxide in the bloodstream. This happens because the carbon dioxide gets dissolved in blood, turning into carbonic acid (H2CO3). This, since it is an acid, dissociates into ions, and your body can detect that change in acidity. These changed PH levels are not desirable because they reduce the efficiency of proteins and can cause negative effects. Therefore, the body detects these changes and creates the discomfort from the desire to breath out. This also holds true for too little carbon dioxide, because it will result in the reverse effect on the acidity in the blood stream (it will raise the PH/make it more basic). Passing out occurs when the acid levels are too high and nothing is making them return to normal (breathing out) so the brain says "this idiot cannot breath correctly" and shuts off the control center to do it itself (unconsciousness).

Welcome to Biology! Although your answer is well formulated, it doesn't address the question why the release of air seems to provide relief.

You should add references for whatever you are saying.

source: Stack Exchange

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IC50 and area under the curve
I was hoping to get some clarification on how drug response data (i.e. IC50) are presented. On publicly available datasets like Genomics of Drug Sensitivity in Cancer, area under the curve (AUC) values are also presented alongside IC50 values. How are these AUC values for a particular drug/cell line calculated and are they correlated with the IC50 values?  If I want to compare the potency and efficacy of many drugs for a cell line (i.e. rank the drugs from highest potentcy/efficacy to lowest) should I use the AUC or IC50 values?
Any help would be greatly appreciated!

Have you read this: wikipedia: area under the curve (pharmacokinetics)?

Area under the curve is the integral of the curve where plasma concentration is plotted against time. A xenobiotic can be potent but still have a large area under the curve, and vice versa. Toxicokinetic factors that affect the area under the curve is absorbance, distribution, elimination etc. Even a less potent xenobiotic can become a lot more potent if its half-life is increased (has a high AUC). If the xenobiotic is really potent (exerts its toxic effects at lower concentrations) it can become less damaging if its elimination rate from the blood plasma is high. Compare IC50 values.

Are you referring to area under dose-response curves? This is very different from pharmacokinetics. A comparison of AUC and IC50 in this context is given in http://www.sciencedirect.com/science/article/pii/S0092867413009604 . Basically, AUC takes effect size (% cells killed) into account, while IC50 does not reflect this.

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What is the meaning of conservation site in miRNA-mRNA pairing context?
I am not biologist and just work in Bioinformatics field.
Does anyone know what is the meaning of conservation in the context of miRNAs and their pairings to mRNAs?
Example:
Each of these duplexes has a region called the “seed”, a site located at 5’ part of miRNA (positions 2-7) which is characterized by a strict or almost strict Watson-Crick pairing between miRNA and its target site and shows the best conservation among the miRNA sequence.
(from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3182075/)

As far as I know this is unknown. Binding sequences for miRNA where empirically found to be more conserved overall (this is actually used by and very important for algorithms to predict miRNA binding sites) than the rest of the transcriptome but the actual reasons behind it are still unclear. For the meaning, well the seed in particular is very conserved which means that this information can be used to better predict where miRNA will bind and therefore which genes they will silence, i.e. mismatches in the seed regions are more heavily penalized than mismatches in non-seed regions.

What the conservation scores denote is how well is the miRNA binding site conserved between different organisms (orthologs). PicTar uses an HMM based methodology to do that. TargetScan and miRanda also provide conservation scores. I shall give you a detailed answer in a while.

So, generally miRNA binds several different target RNA? If yes is it relevant? Thanks.


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If a trait does not appear to be advantageous to organism, why does the organism have it?
Why do organisms have some traits that do not appear to have any evolutionary advantage?

Also, let me know if this question should be merged should be merged with this thread: http://biology.stackexchange.com/questions/35532/if-a-trait-would-be-advantageous-to-an-organism-why-hasnt-it-evolved. They are fairly similar.

You could have answered there itself.

@WYSIWYG Fair enough, the reason I didn't is because I figured the question "Why didn't X trait evolve if it would be advantageous" and "Why did X trait evolve if it isn't advantageous" are different enough to warrant two separate questions.

There are many reasons why an organism might have a trait that does not appear to be beneficial.

The trait is actually advantageous even if it does not appear to be.
The trait is a byproduct of another trait, which is beneficial. Not all traits are the product of direct selection; traits that are byproducts of other traits are known as "spandrels", a trait coined by Stephen J. Gould and Richard Lewontin
The trait was fixed by some process other than natural selection, such as genetic drift. Genetic drift can fix traits that are neutral or even evolutionarily disadvantageous.

Also, the trait may have been beneficial at some point but no longer is. See: http://biology.stackexchange.com/questions/34466/is-there-a-name-for-the-evolutionary-loss-of-vestigial-structures


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Which pair of primers should be used to amplify the ORF in PCR?
So I want to choose the correct set of pair of primers to amplify the ORF of the gene that corresponds to amino acids in a protein. The start and stop codons are underlined. (I know that these need to be synthesised by the primer also for correct PCR technique)

The boxed sets of nucleotides are the primer options I have at hand. I know that the DNA synthesis can only carry out from 5' to 3' and there is a forward and reverse primer. The forward primer should be easy enough but non of the options seem acceptable? Could someone please explain to me how to go about this problem?

So you've identified the ORF by marking the start and stop codons. You'll want a primer on either side of the ORF. You said none of the options seem ok, but why do you think that?

First of all, if this is a homework question, add that tag to it. And show what work you have done so far.
Secondly, primers for amplifications should lie on opposite strands. Primers are typed in 5'-to-3' direction (aka left-to-right on leading strand).
Appropriate primers will be: primer 4=GTG... and primer 5=GAA.... Note how those primers are always in 5'-3' orientation. That is how you order those.
Again, if this is homework (looks like it) it is very bad taste to just ask question without any work shown. It displays laziness and usually not respected behavior when asking for help.


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Why does the face turn pale in dangerous situations?
I know what the effects are of a dangerous situation on the brain, i.e., an activation of the hypothalamic-pituitary-adrenal (HPA) axis which eventually results in an increased heart rate and elevated blood pressure. However, I do not understand why enhanced blood circulation would result in a paling of the skin? Do red blood cells actively change direction?

Red blood cells are not equipped with a motor system to propel them through the blood stream. Instead, they are passively transported through the vasculature by the the pumping action of the heart. The effects of dangerous situations on the skin have to do with hormonal effects on the blood vasculature, and not with direct effects on red blood cells.
Dangerous situations trigger the fight-fright-flight response, and is a direct result of adrenaline being released into the bloodstream. Adrenaline prepares the body to fight for its life.
Adrenaline has a variety of effects including enhancing perspiration (or diaphoresis, which prepares the body for the increase in temperature associated with fleeing/fighting), dilation of the pupils (which increases light sensitivity, but reduces acuity), dry mouth (gastric juices and saliva production decreases because blood flow to the digestive system is decreased), enhanced smell and hearing, and a cool, pale skin.
The cool and pale skin is caused by a reduced blood flow to the surface of the body, while blood flow to the arms, legs, shoulders, brain, eyes, ears and nose can be increased. Besides getting ready to run and fight, the body is preparing to think quickly and be aware of threats by hearing, seeing and smelling things better. Pulling blood away from the skin also helps decrease bleeding from cuts and scrapes (Source: Army, Navy & Air Force Australia).
Adrenaline stimulates alpha-adrenoreceptors in blood vessels, which causes the smooth muscles around the vessels to constrict (Bolli et al., 1984)

Adrenaline (epinephrine) released from the bloodstream dilates vessels in the skeletal muscle via beta-receptors, and constricts them in the digestive system and the skin through alpha-adrenergic receptors. Source: Marian University College, Indiana.
Reference
- Bolli et al., J Hypertens (1984); 2(3): S115-8

It has nothing to do with blood cells per se. Blood vessels constrict in areas not necessary for flight-and-fight response (sympathetic nervous system response).
By constricting blood vessels around face, blood is redirected to organs more important in resolving dangerous situations: muscles of legs, spinal cord, and brain. Same way pupils get dilated to capture more light..

Totally agree with the answers already provided: It is directly caused by constriction of blood vessels in the face.
However, from a behavioral perspective, I feel there is an additional function for 'turning pale', that is not yet mentioned:
For social animals (such as humans), the face has great expressive value.
The face turning pale might fulfill the function of warning our fellow species that there is a certain threat. This form of communication might be preferable over, for example, yelling. Yelling might attract to much unwanted attention from predators (if predator was reason why individual is afraid).
If this is true, then we should expect turning pale of the face would more often occur in groups than alone and would also happen more often to the 'weaker' individuals of the group, because stronger individuals that seek help from their weaker friends would not be so advantageous.

Welcome to Biology and thanks for your behavioral perspective. However, the question is not so much on the why, but more on the how.

Ps. Dutch by any chance? :)


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Database of medically validated SNPs
I'm looking for all possible sources of clinically tested human SNPs. There is a handful of databases that store SNPs (like dbSNP), but I only need those that have validated presence/absence of phenotypic effects with some additional metadata. Thank you in advance.

Any type of disease, or just a subset?

@mdperry any Mendelian disease will do.

@EliKorvigo Did you not find the desired information in the GWAS databases that I mentioned below?

@WYSIWYG I'm struggling to find true negatives. I've already found plenty of true positives though. Thank you for your answer. I'll wait a couple of days before accepting it in case someone else comes up with a valid way to find true negatives.

@EliKorvigo I think for that you may have to check the original study and get the statistics

@EliKorvigo - Be wary of the statistics for GWAS studies. Clinically we don't get too excited about them because the cost-effectiveness of doing a study has surpassed the ability for appropriate statistical analysis - the sample sizes are almost always much too small - too much noise to signal - there are several reviews to discuss this, e.g. [http://www.ncbi.nlm.nih.gov/pubmed/18464043] (review)

@VanceAlbaugh Thanks for pointing that out. Yes, at this moment we have a lot of data but we should be careful before making inferences. There have been a lot of discussion about doing the right statistical analyses.

@VanceAlbaugh exactly. That's the whole point of this question - I can't rely on available bioinformatic GWAS studies to come up with a set of true negative SNPs due to statistical issues. Hence I desperately try to find something that was clinically validated.

@EliKorvigo - yeah, good luck with that - I don't know of any GWAS studies that have reproduced externally in a statistically sound way and have been published. If someone did that it would be a big deal because the analysis of the data hasn't been perfected. We have similar questions in metabolomics, proteomics, and RNAseq. Too much noise, not enough signal.

I've added some references to the data I've managed to collect.

You can search by traits (mostly diseases) for genome wide association, in these databases:

Gwasdb2
Human genome variation Database: it also links to a Copy number Variation (CNV) database.

Just to make this post a tiny bit more useful, I must add that there are several additional sources I've found:

UniProt has an open dataset called humsavar
ClinVar database
HGMD database
OMIM
A paper with a manually collected database based on recent publications in Nature Genetics.

Different datasets intersect to some extent, but all in all you get over 200k somewhat validated SNPs.


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Autotrophic and heterotrophic organisms in anaerobic condition
Can both heterotrophic and autotrophic organism survive in anaerobic conditions? If an autotrophic organism does not produce carbon dioxide but requires oxygen, it should not be present in anaerobic conditions, instead the heterotrophic organism can develop. Is this correct?

I am confused by your question ;) Can you clarify what exactly you wish to know?

Whether in anaerobic conditions both auto and heterotroph organisms exist. Actually I am too confused, but I have tried to answer my question by myself, but I am not sure about it. My guess is that because the autotrophic organism requires oxygen even though does not produce CO2, should not survive in anaerobic conditions; instead, the heterotrophic organisms can adapt.

You can edit your question to clarify instead of saying it in the comments.

It is not necessary that all heterotrophs are aerobic. Many are anaerobes (yeast etc.)
Anaerobic Heterotrophs
These anaerobes live on glycolysis and fermentation (as far as I know). These two processes don't require Oxygen for release of energy.
Glycolysis
Alcohol Fermentation
Lactic Acid Fermentation
Alcohol Fermentation takes place in yeast (just an example) and Lactic Acid Fermentation in Muscle Cells.
The autotrophs will take care of themselves as photosynthesis require no Oxygen. If place in correct conditions (light and water are available), then they will thrive.
So, the answer to your question would be that both can survive. It varies from species to species. If you select the correct one then, both would survive or only one of them.

Autotrophs: Organisms that can synthesize organic carbon from inorganic carbon (carbon fixation). Nitrogen fixation is not considered an essential condition to qualify as autotrophs. True autotrophs can fix both carbon and nitrogen (Some algae. This true autotrophs is not an actual terminology).
Aerobes are organism that require oxygen for metabolism; it is not really dependent on whether the organism is autotrophic or heterotrophic. Anaerobes do not use oxygen for metabolism. Some anaerobes are aerotolerant i.e. they can tolerate oxygen (oxygen is highly reactive and can damage tissues) while others are not.
You can have a look at this post for some basics on aerobic and anaerobic respiration.
Examples of anaerobic autotroph include Ferrobacillus sulfooxidans and Methanobacterium thermoautotrophicus.
Some organisms are called microaerophilic i.e. they need oxygen but not in high concentrations.


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What is this small black bug found in Turkey?
What species is this? It was found in Turkey. It was dead, I did not kill it.

Looks like a scarab beetle (Coleoptera, Scarabaeidae). Species is difficult to tell without better pictures, but perhaps Scarabaeus typhon?
Edit: OP has IDed in comment as Scarabaeus jalof

@Oğuzİsmayiluysal If you think this answer is correct, we encourage you to accept it.

Definitely looks like a member of Scarabaeus but why S. typhon?

@augurar I forgot to edit my comment it is not typhon. It is a S. jalof. https://c4.staticflickr.com/4/3510/3847992837_b3aa34f400_b.jpg

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Are we more attracted to people of the same ethnicity?
Are humans more attracted to people from their own ethnic groups? I ask this because most of the time people have relationships with people of their own ethnicity, and I wonder if it's purely social, or if there's more behind it.

What do you mean with "own race"? Talking of "human races" is political and not biological backed.

I'm not sure, but would this me more apt on cognitive.SE? The reasons are  underpinned by complex social and historical structures and talking about them in biology rather than sociology doesn't quite make sense. Having said that it might actually be inappropriate on  cognitive.SE too...

I agree with both earlier comments. Once edited to exclude improper terminology it is fit for Cognitive-sciences. I vote to close therefore.

I'm voting to close this question as off-topic because it is a better fit for CogSci, but only after suggested edits.

How would you possibly test out whether the preference was "purely social" or not? Either way, it is an expressed preference. For a not quite scientific but entirely depressing big-data take on this issue, see the famous OKCupid blog post about race and internet dating.

Biologically we are attracted to people that smell similar to our parents but different enough that they aren't close relatives. I'm too lazy this morning to find the paper, however. I might come back to answer later. The rest is more of social convention, and I'm not qualified to answer that. Bill Nye is also quoted as saying "there is no such thing as race scientifically". That being said there still is racism and pressure from parents to marry "your own kind".

I'm voting to close this question as off-topic because race is not a biologically meaningful or accepted concept, and such questions are not on topic http://meta.biology.stackexchange.com/questions/372/why-questions-about-race-do-not-belong-to-biology¨

@AliceD Are psychology questions on-topic in cogsci?

@WYSIWYG - yes - "Cognitive Sciences is [...] cognitive science, psychology, neuroscience, and psychiatry." http://cogsci.stackexchange.com/tour

There is a good chance that there is a relation mediated by oxytocin, a hormone which influences both romantic attraction and distrust against outgroup members. But I don't know its exact mechanism of action (especially the causal direction of oxytocin release, falling in love, and stranger distrust) to post an answer, so I hope somebody with better understanding will post an answer about that.

@rumtscho Oxytocin release will be the molecular mechanism, but it would take a lot of conjecture to tackle sociology using molecular biology!

Edited the word "race" to the more scientifically relevant "ethnic group". I would argue at this point this question can be considered on topic as a behavioral/sociological aspect of biology.

@SolarLunix: If attraction is mediated by smell, how to account for movie stars, Playboy, on-line dating & internet porn, that attraction across a crowded room, et cetera ad infinitum?

@jamesqf (and SolarLinux) - there is more than one contributing factor - smell is one, visual stimuli also affect attraction

@MarchHo Although ethnicity is a less troublesome word, it even less useful here as it's is very plastic and more culturally dependent.

I also think it's necessary to clarify just what's meant by attraction.  If it's purely sexual, that's one thing; marriage is quite different, and friendships different still.  That could explain a lot about those OKCupid numbers: I might be sexually attracted to a person, but not want a relationship unless they shared my views on desireability of hiking, skiing, horses, etc, or my distaste for urban living.

The answer in extreme brief is yes.  Only about 9% of whites and 16% of blacks engage in interracial marriage in the U.S.
But really this deserves a fuller discussion.
The predominant pattern of mate selection in human beings is to marry within their ethnic group.  I say 'ethnic group' rather than 'race' because 'race' has no strong scientific definition. Racial groups as usually understood have about the same genetic variance as the overall species.  I need to point out here that races can have a strong geographical point of origin and thus races can in some cases be genetically identified, but these correlate poorly often with, say health risks or other clinical data.
Because its clear that interracial marriages are on the rise in the US, mating choices are often argued to be socially defined preferences.  Social attitudes affect men and women differently and different cultures too, as tracked by regional differences. Not the least is a limit of opportunities.  Being comfortable with people from other cultures or who simply look different.
Interestingly, Women at least in American studies are much more likely to state a same-race preference (see p17), while men are likely to demur from stating a preference, but act out a bias unconsciously, making both genders equally biased.
As mentioned in the comments by @AliceD, Mating preferences as described in traditional population biology are adapted from availability.  That's to say people don't meet because of ethnic boundaries such as geography, socioeconomic or social strata. Then there are socialized preferences.  I.e. growing up we are imprinted by the sorts of people we see, which can create preferences later in life.
Lastly there may be genetically conveyed preferences. The human race has been spreading out over the past 200,000 years or so.  That's a pretty small amount of time.
There are cases where such mating preferences have evolved.  There are 17 species of arctic penguins, species caused by migration around the globe.  Each species can actually mate with others nearby, but where the penguins met at the far end of the globe, the species do not mate because they have been separated for so long they have diverged.
But speciation events can take millions of years.  Its clear that human beings from the far corners of the globe can produce offspring - we are one species.  It seems as if we are only a fraction of the way towards two neighboring penguin species in the example above.  There doesn't seem to be any evidence that we are genetically predisposed to ethinic self mating.
Only by way of example (not to offend anyone!) you can choose an ethnic group which has divergent behavior and try to get an estimate of how big a role the social context plays.  Looking at the jewish community we see that 47% of jewish people have married out of group in recent statistics.  They are thinly distributed over a wide geographical region and availability is high for out-group marriage.  All this while orthodox jews have a practically non-existent out-group marriage rate. Not judging here, but only for illustrative purposes we can guess that social attitudes and behaviors are playing a large role here.
As and endnote, I'd also like to point out that since whites are about 50% of the US population and african americans are about 10%, the percentages not so disparate as they seem - all things being equal the average person one meets in the US is white.  For caucasians, approximately 50% of the population the average interracial marriage rate with no racial biases is is 50%.  For blacks its 90%.  Again, just using random shuffling for statistical point of view.

There exists a marked geographical segregation of whites and Afro-Americans in at least some cities, like Baltmore. This has its roots in history and the standard of living. Hence other factors may and will likely play a role in partner choice.

yes @AliceD - i thought i'd try to list other factors like geographical, socioeconomic, cultural separation, but the list is quite long.  given all that its not surprising that not a lot of racial intermarriages are happening compared to the rates one would get from at random pairings.  Its a lot like the factors cited in population biology, is it not?  humans are picky for more reasons than animals tho I think..

This answer doesn't really address the biological aspects of the question.

@shigeta - great answer +1

@augurar - the question is not biological (see the comments string under question). Therefore this answer is great.

@augurar of course biology concerns itself with inherited and environmental aspects of behavior.  Sociobiology and Ethology has informed social psychology and behavioral economics, and now literary crit and cultural crit.  They are not as prominent today as biology departments have gone more and more molecular in the past 30 years, which has obscured the previous forms of the science.

The problem here is that attraction is not the same as marriage.  Personally, I've been attracted to - oh, perhaps thousands of women, but haven't to date married any of them.  As far as I can tell, the likelihood of physical attraction is pretty much the same for all races/ethnic groups.  Perhaps if we could find data for casual sex encounters, and correct if for opportunity, we might get a more realistic picture, but I don't think that's possible.

Of course you are right.  Marriage is not a bad statistic to look at because its more easily measured with less slippery subjective critiques.  I'm borrowing from couples research in psychology which only took off when they started using divorce instead of qualitative satisfaction metrics.  Few would argue that attraction is even more broad than marriage, though some might not admit it....

@jamesqf marriage is a good measure to use - while we don't marry everyone we are attracted to, most marriages have some kind of attraction at some point (remember that attraction is more than just a visual thing - biochemical, behavioural, and other biological stimuli are important)

@rg255: As I said above, I think the OP needs to clarify just what sort of attraction is meant.  I'm working on the premise that we're discussing purely sexual attraction.  For marriage, you need not only that sexual attraction, but (in most cases, anyway) shared interests and desire for compatible lifestyles, which makes the set of acceptible marriage partners a very much smaller subset of those to whom we're sexually attracted.

"Lastly there may be genetically conveyed preferences." Do you have a citation for this?

One of the precursors to speciation is that different isolated groups stop mating with each other even if they are exposed to each other.   I'll see if I can find a good link for the penguins, which is a specific example of this phenomenon.

To keep it simple: The term here is assortative mating which describes the tendency of individuals to select reproductive partners based on some arbitrary measure of "likeness" considering the available within-species variation. The "likeness" could be anything from a general evaluation to being based on one specific trait.
This is a evolutionary significant phenomenon, and when it comes to humans there are a lot of factors that seems to be related to human assortative mating, including both race (whatever the term's biological significance) and ethnicity, among other things like height, religion, politics and even altruism. See wiki for ref.
As seen in the article Shigeta liked to, racial belongingness is generally very significant in human assortative mating.
So the concept of choosing "similar" partners as we see in humans is a common biological phenomenon with evolutionary significance, although by what exact mechanisms this selection works in humans and how culturally dependent it is (maybe some assortative selection traits are more or less biologically/culturally founded than others) is probably in need of more research.

But are we really talking about "reproductive partners" here?  Personally, I've always gone to some lengths to ensure that reproduction does not occur - and that's not even considering that it's even going to be a possibility with only a small fraction of those I'm attracted to, because the attraction is so seldom mutual :-(

@jamesqf I think it's quite reasonable to generalize 'attraction' as the selection of productive partners in the context of biology and evolution, especially considering the tags of the question.

But then you're asking a much different question, something like "Do humans generally want to have children with partners of the same ethnic background?"

@jamesqf The OP has tagged his question sexual-selection and evolution, I cannot see that I make any unfounded assumptions about the intentions behind the question even if we can split hairs about sexual attraction not being the same as actual sexual reproduction. I interpret the question as asking about sexual selection - If I'm wrong then the OP is most welcome to correct me and/or clarify his question.

I wouldn't say that differentiating between sexual attraction and reproduction is "splitting hairs".  Certainly not in the context of modern culture, and not in a lot of past ones, either.  (Or among bonobos, perhaps.)  Consider marriages made as economic/political decisions, where the married couple might not even see each other until after the wedding.

@jamesqf Since this is about biology and evolution, I choose to use an approach to this question that is applicable to this general biological domain, and to avoid going into sociology and "modern culture" while still flagging for the issue of cultural dependencies in the answer. And in this context I see limited use of trying to differentiate sexual attraction to sexual reproduction. (Maybe except the odd cases like where dolphins and penguins apparently regularly rapes other species for some kind of stimulation, but that might as well just be instincts gone haywire.)

@jamesqf Arranged marriages sure, but what is the rule and what is the exception here?

The point I'm trying to make here is that in humans (unlike many other species) reproduction is no longer the primary function of sex, otherwise females would come into heat a few times a year, and be unreceptive at other times.  Human sexuality (and bonobo, apparently) has become a form of social bonding & recreation, with only a small fraction of encounters intending to result in offspring.  Therefore reproduction is not a good way to measure human sexual attraction.

@jamesqf I'd argue that reproduction is still very much the primary function of sex even in humans, but that it also have very important secondary functions as well. Even if a human individual might have different priorities. (Although, that human females are receptive throughout their menstrual cycle is easily explained by a little bit of evolutionary game theory in regards of the battle of the sexes and our general human sexual behaviour. I don't see how that would invalidate the significance of mating in sexual activity and attraction). But I think we both have gotten our points across now.

@Alex, this is a good answer.  I do not know why it was downvoted.


text:
Evolution of diversity and extinction resistance
I saw a comment on an answer to another question that touched on an interesting topic:

keeping diversity is useful for parameter exploration or to adapt to future environmental change

My initial thought was that evolution doesn't "know" about the future, so natural selection might decrease genetic diversity even if it meant dooming the species in the long term.
On the other hand, species that have low genetic diversity may be more likely to go extinct eventually.  So perhaps over time the surviving taxa are those that have evolved mechanims to "hedge their bets" against future environmental changes.
It's clear that some of the parameters that affect genetic diversity within a species (e.g. mate selection, mutation rate) are heritable, but it's unclear to me how the short-term processes of natural selection relate to the extremely long-term processes of speciation and extinction.  This gets into some of the same issues as group selection — how can natural selection, acting on individuals, lead to traits that benefit entire populations or clades?  (Perhaps this simply cannot happen.)
Has any work been done on the topic of extinction resistance or the evolution of mechanisms to create and preserve diversity within populations or taxa?
This is a big question so I don't expect a full answer here.  I'm just looking for some references as a starting point to learn more about this topic.

This is a big question, that one of the evolutionary biologists here can probably give a fuller answer to, but you might check out this article by Jablonski

The topic you describe is very interesting and known as "species selection." Some traits exist that not only affect the reproductive success of individuals, but also affect the diversification rate of the entire species, either through affecting the extinction rate, the speciation rate, or both.
To give you an example, I'll summarize this paper by Goldberg et al 2010. Self-incompatibility (SI) in plants is the ability of a plant to reject its own pollen to prevent inbreeding. This mechanism is expected to increase the genetic diversity of the plant's offspring. Self-incompatibility has been lost many times in the history of flowering plants, yielding self-compatibility (SC), which allows a plant to breed with itself. A plant that can breed with itself has an advantage in that even if the population size is low and it can't 'find' another individual to breed with, it can still breed with itself to produce offspring. However, this trait is expected to result in decreased genetic diversity in the offspring due to inbreeding.
The transition from SI to SC is a common transition that cannot easily be reversed. One might expect, then, that SI would be very uncommon as lineages would lose it to SC. However, it turns out that SC lineages have a lower diversification rate than SI plants in the Solanaceae due to the fact that SC lineages have a higher extinction rate than speciation rate. This difference in diversification allows SI to persist. This is an example of trait-dependent net diversification rate. It is not known exactly why SI lineages have a higher net diversification rate, but it could be related to the higher effective population size which results in "increased polymorphism,
lower linkage disequilibrium, more
efficient response to purifying selection, more
extensive geographic distribution of genetic diversity,
and lower rates of extinction".
If you want to read more, I can suggest a few more papers:
The Units of Selection by R.C. Lewontin
Darwainism and the Expansion of Evolutionary Theory by S.J. Gould
Species Selection: Theory and Data by D. Jablonski


text:
Parents are Rh +ve and child Rh -ve
Suppose the two parents of a child have blood groups A+ve and O+ve, and the child has O-ve type. For blood group, there are two alleles. Since the child has O, the father must have one 'A' allele and one 'O' allele.
Does such a reasoning hold for the Rhesus factor too? Should I interpret that both the parents have one + allele and one - allele?

Since the Rhesus antigen is inherited in a dominant negative way, both of your parents need to be heterozygote for it, so you can carry -/- for your alleles.

I edited the question to remove reference to self. Good question.

Rhesus antigen (Rh-D) is inherited in an autosomal dominant pattern.  Therefore you are correct in your reasoning.
Simple problems like this are often best worked out using Punnet Squares, shown below for the scenarios you have considered.

Because the inheritance pattern is dominant, if either parent was homozygous (DD) for Rh-D then 100% of their offspring will be Rh+ve.

In order to have a rhesus negative child, neither parent must be homozygous for the D allele.  You are correct that one possible scenario is a matching pair of heterozygotes:

In this situation 3/4 of the children are rhesus positive and 1/4 rhesus negative.
There is an alternative where one parent is Rhesus negative and the other positive.  In this case there is one heterozygous parent and one homozygous negative parent:

In this scenario, half of the children are rhesus positive and half rhesus negative.

Thanks. The second case does not arise because the mother is Rh- positive, in my question.

@Bravo ah of course, I missed that element!


text:
Can a lizard shed a regrown tail again?
Some lizards are famous for their ability to voluntarily shed their tail to elude predators (Autotomy). After a while, the tail will be regenerated, though with slightly different qualities, as visible in this photograph:

(source)
My question: Can this regrown tail be discarded again voluntarily, or is it a one-time feat?

Yes, a regrown tail can be dropped again. It is the primary survival trait of some species.

Short answer: many species can drop a regrown tail again and again again, however a few can only drop it once, while some lizards cannot drop their tails at all. It all depends on the species.
Background information:
According to this site the tail will only be able to be shed above the site it originally broke off. Although according to UCSB there are a few species of lizard that only have their tail grow back once.
Every site I've visited has said that the tail is nearly a completely different structure than the one it originally had. The original tail has "score marks" (fracture planes) which were studied by Sanggaard et al. (there are a few figures that you can see in their paper).
However, according to W. N. F. Woodland, D.Sc. (Lond.), there is no apparent limit to the amount of times a Gecko can drop its tail, "save the longevity of the animal". His paper goes into great detail, and has a lot of information about autotomy (limb dropping) of the gecko. I highly recommend going through it if you're interested.
So tail re-dropping looks like it primarily depends on the lizard that you're studying.

Doesn't actually answer the question: Can this regrown tail be discarded again voluntarily

The last paragraph says there is no limit to the amount of times they can disgusts their tail...

But @FloriOn , I added a summery bit to make it more clear.

But you've written, that the tail is nearly a completely different structure. And actually the regrown tail doesn't have those fracture planes, you have mentioned, so can't be discarded voluntarily.

Again, it depends on the species of lizard. Some can drop it again and again, others can only drop it above the place that it had been dropped before and others can only drop it once. @FloriOn


text:
Animal identification (larva)
I found a tiny, white animal in my mouth on the morning of June 28, 2015, in Toronto, Ontario. Luckily I don't seem to have hurt it. I was eating some sunflower and pumpkin seeds at the time. I believe that's how it got there.
The pictures include a toothpick and a Canadian cent to give an idea of its size.
I also took a video of it crawling around. I will post it if the pictures are not sufficient for identification.

Did you see any dots on it?

@Ilan I don't see any dots on it. It looks very much like the picture you posted. I still have it. I might try to keep it until it molts.

Oh, is it still alive? So keep it, it would be nice to see the actual moth!

This animal is moth larva. The images presented are blurry, but if there are no any dots on the larva my first suggestion is:
pantry/Indian meal moth larvae -

"They are a common grain-feeding pest found around the world, feeding on cereals and similar products."
(picture source)


text:
Toronto spider identification
I found it in Toronto, Ontario, during early June, 2015.
When prodded it seemed to jump around, or at least to move very fast.
I can also post a short video of it if needed.

That jumping spider is a Jumping Spider! (That is, family Salticidae, commonly called Jumping Spiders).
There's a lot of diversity in the family, but your pictures look similar to the Zebra Jumping Spider.


text:
Accuracy of best plant growth models?
Given a plant $P$, predict its height $H$ at time $t$ since planting given some environmental variables $E_1, \dots, E_n$. How accurate are the state-of-the-art models for such thing? What data is used to make the prediction?

You should add some more details. What do you mean by state-of-art models. Note that the utility of models depends on the question that is asked.

I've worked on a couple of these for biofuel production. The answer varies widely according to plant P and how well studied plant P is. In terms of what data is used, it includes but is not limited to: temperature, insolation, length of the day, cloud cover, rain, soil composition, soil type, soil density, other local effects like wind or pests, altitude, humidity, and pH. For corn(food) and miscanthus(experimental biofuel crop) the models are quite good if the year is pretty normal and you're in a well-studied parameter space, mostly because corn and grass grows straight up. For trees, non-crops, non-corn crops, etc the models are almost completely useless. It's a question of testing nearly every possible combination of parameters for each plant P, and how much people care about how tall it gets.
Given how much data goes in, it surprises me that even under ideal conditions(well-studied) some of the parameters the model spits out are impossible/wrong. There's a measure of leaf overlap(just as an example) that's especially poorly defined but a rough proxy might be "number of leaves that shade a specific point, on average" and it's regularly measured at <10 and regularly predicted at well north of 50.


text:
Why do many DNA solutions contain additional compounds?
DNA solubility data in only water is scarce.
A previous question asked for a quantification of DNA solubility in water. It seemed like it would be easily answerable, however isn't quite that simple since no data seems to exist for DNA solubility in exclusively water.
Even the small amount of data about water was in the context of washing away organic compounds from the solution. This got me thinking. DNA is in an aqueous solution in biological situations, and is usually handled in aqueous solutions in labs. So why is solubility data so scarce for pure water? What is important about organic compounds for DNA solutions?
Why are other additives important for laboratory DNA solutions?
So my question is why is DNA dissolved in exclusively water seemingly "uncommon" in laboratories? Is there something about pure water that is bad for DNA storage? Is it that functionally DNA never needs to be in water because it is inaccessible to proteins? Or have I misinterpreted the lack of solubility data; water is common-place and no data exists because there is no need?
I imagine PCR is where most of the data on DNA solutions exists. What about the polar organic solvents/compounds makes them important for DNA solutions?

I routinely dissolve minipreps and maxipreps in water or Tris buffer. It is most certainly not irrelevant in laboratories. PCR can't use water as the buffers are necessary for the activity of the polymerase.

@MarchHo Thanks for the insight. I think the idea of buffers probably also goes beyond PCR. I didn't intend to dismiss water as irrelevant - I just wanted to highlight there is little/no research that has been done on water as a solvent by itself.

Double-stranded DNA, with its strongly polar sugar-phosphate backbone, is negligibly soluble in non-polar organic solvents. Could you please provide a link or cite a reference where they dissolved any nucleic acids in non-polar solvents?

@GoodGravy DNA is evolved to function in aqueous environment. Perhaps it may dissolve in other polar non-aqueous solvents but I don't think non-polar solvents can dissolve it. As you might already know, even polar non-aqueous molecules like ethanol precipitate DNA (It precipitates with acetone too- I tried it a few times as a fun experiment).  Which solvents are you talking about?

Thanks for pointing out the "non-polar" mistake. I meant polar: ethanol for example.

@GoodGravy But DNA is never dissolved in any non-aqueous solvent. DMSO and formamide are used in PCR but not as solvents.

@WYSIWYG Ah I see your point. Your point also re-enforces why it's so weird to me;  no pure water solubility data seems to exist despite DNA being dissolved almost exclusively in aqueous solutions. Some other compound is always present. I cannot believe that there has never been a control done on DNA solubility in pure water.

http://www3.idtdna.com/pages/support/technical-vault/faq-old/application-support/storage/faqs/2011/07/01/what-is-the-maximum-solubility-of-dna-in-water-(weight-unit-volume-unit)- How about this.

DNA dissolves perfectly in plain water - there are no other additions needed. The reason you use Tris-EDTA  buffer is that is better for storage. About what other organic compounds are you thinking?

The only organic solvents I have used with DNA/RNA are isopropanol and ethanol to precipitate the DNA, and phenol:chloroform mixtures to extract proteins away from the DNA. I always resuspend the precipitated DNA in an aqueous solvent, sometimes just nuclease free water. It's not the best storage solution, but I don't have to store it forever.

The question received a -1. Do folk see it as being too broad, or simply unclear as it stands?

I'd like your reference for claiming that many DNA solutions contain organic solvents, Aside from extraction and clean-up procedures which utilize the differential solubility of cellular components to isolate DNA, most laboratory procedures (all of them that utilize DNA + enzyme reactions) are performed in aqueous solutions. While there are a few exceptions (highly concentrated synthesized oligonucleotides, perhaps large quantities of genomic DNA in a low volume), DNA is soluble in water at relevant storage and working concentrations for the vast majority molecular biology experiments.

Isolated DNA and RNA are stored in water or Tris-EDTA for the reasons mdperry mentioned. The addition of other solutes to various reactions (ATP, Mg2+, various buffers, etc) is to provide for the enzyme acting upon DNA. Enzyme activity can be highly dependent on temperate, salt concentrations, pH, etc. The concentrations and compositions of the substrates and salts added to reactions involving DNA are optimized for enzyme activity.

@InactionPotential I see the problem. I think I put focus on the wrong thing and perhaps semantically called additives solvents (which is incorrect). I'll edit this to remove any inaccuracies. I'm simply asking why pure water seems to not be used (and according to mdperry, ssDNA is temporarily in pure water).

DNA in pure water.
The only time that nucleic acids would encounter pure water would be in a laboratory setting--for example after an oligonucleotide is synthesized in vitro, the protecting groups are removed from the reactive atoms in the finished sequence and the final product is cleaved from the supporting matrix.  At that point you can lyophilize (freeze dry) the ammonium hydroxide solution, and resuspend the single-stranded oligo in pure water.
Additional compounds enhance heavy oligomer solubility.
However, as noted in the comments, nucleic acid solubility, particularly high molecular weight DNA, like genomic DNA,  is enhanced in solutions with dilute monovalent cations. 10 mM TrisHCl, pH 8.0, 1 mM EDTA suffices for almost every application. The EDTA inhibits any errant DNAses, and also slightly inhibits microbial growth.
Compounds act as pH buffers.
Tris is not the best biological buffer but has high solubility and is relatively cheap and stable. If the solution becomes too basic the DNA strands will melt, and if the solution becomes too acidic the purines will start to deaminate.
DNA never experiences pure water in biology.
From the moment that DNA is synthesized in a cell until that cell dies and its DNA is ultimately degraded, it does not encounter a pure water environment.

Good explanation. I would reiterate in your answer (in addition to your comment above) that DNA is maintained and used in an aqueous solution. Organic solvents (phenol:chloroform) are used primarily to separate DNA from other water soluble cellular components (proteins, RNA). PCR and its variants, restrictions digests, thymidine kinase... reactions of interest performed on DNA in the laboratory are performed in aqueous solutions, they may utilize different buffers to maximize enzyme activity, but water is the solvent.

This answer does an excellent job at explaining a lot about why other compounds are important and when DNA might be in pure water. It's odd to see that even ssDNA appears in pure water. Exactly what I wanted to see, thanks!

I've added some headers. Feel free to roll back if you want.

And as user137 said, DNA does dissolve in pure water. I dissolve PCR products in nuclease free water sometimes (especially if I need huge amounts of the sample for some downstream step).

While physiological experiments could be conducted without organic solvents, chemical syntheses of DNA or analogs, chemical modification of DNA, and purification after chemical reaction could be performed in the presence of organic solvents. Such experiments are not directly relevant to physiology, but we use chemically synthesized DNA and DNA analogs. In addition, chemical properties of DNA in the presence of organic solvents may tell how DNA behave in physiological conditions.
People doing PCR and/or molecular biology may not be interested in the solubility of DNA, because under the condition they are using, the concentrations are far less than the saturated condition.


text:
What are all of the currently known variations of the G zipper motif?
The G zipper motif is found in transmembrane proteins at an above random frequency and there are models explaining how it might help with multiple transmembrane intra-membrane helix bundle assembly.
However there are a bunch of different "flavours" of these G zipper motifs. Here are the ones I have come across so far:

GXXXG
GVXXGV
GXXXGXXXG
AXXXGXXXG
SXXXGXXXG
GXXXGXXXS
GXXXGXXXT

I don't think I am completely up to date so that is a non-exhaustive list. Have I missed any? Broadly speaking what accounts for their variation?
note: X refers to a non specific amino acid in FASTA protein sequences.

It seems to be a small family as per pfam. And frankly I had never heard of glycine zippers till now (so thanks for that). Perhaps this may be useful.


text:
Phosphorylation-Dephosphorylation : ATP-driven VS spontaneous
Is protein dephosphorylation most commonly spontaneous (without need of ATP)? I came across some papers that mention it, as well as the opposite case (ATP-driven), but I can't figure out which is common or which is rare.
In the case of protein phosphorylation, I would say ATP is always needed since it provides the phosphate? Or could you have a spontaneous phosphorylation using free phosphates that float around?
I am aware that in the end, pretty much everything is possible, so I am more looking for likelihood. What is commonly accepted, wide spread, and what may happen but is rare.

Well of course why not. Look at ATP, which is not a stable molecule, because it can spontaneously dephosphorylate.  Whether a phosphate group can be spontaneously hydrolysed depends on the nature of the molecule it is a part of. Are you asking about protein phosphorylations? In almost all cases that I know of, dephosphorylation in not ATP dependent.

Yes I am asking about protein phosphorylation.

Do you know of cases where dephosphorylation is ATP dependent. I certainly don't. You can add that info in your question.

I'd rather say google returns some articles, like this one. Again, It is hard for me to figure out whether this is well established science or not.
http://www.ncbi.nlm.nih.gov/pubmed/21401736

This is fine. Can you add this example in your question?

First, I would like to clarify what is meant by "spontaneous". In chemistry, thermodynamically favorable reactions ($\Delta G < 0$) are indeed termed spontaneous because they will eventually occur, regardless of how slowly. But if transition states are unfavorable (high energy barrier), the reaction rate can be extremely slow --- millions of years in some cases. For example, combustion of wood is highly favorable and, chemically speaking, it is spontaneous. But that doesn't mean trees are unstable and likely to catch fire any minute.
Most biologists would probably call a reaction "spontaneous" only if it actually happens on a reasonable time scale, perhaps on the order of hours, depending on the context. So the terminology is a bit messy. But neither chemists nor biologists would call a molecule "unstable" if it has a reasonable half-life, I think.
Now for the actual questions. Dephosphorylations are typically not ATP-driven, because breaking the P-O bonds is usually favorable already (although I'm sure there exceptions). However, the reaction is typically too slow to be useful to cells, so it is not "spontaneous" in this sense, and therefore needs to be catalyzed by phosphatases. A typical example is alkaline phosphatase which dephosphorylates a wide range of proteins and other substrates.
Phosphorylation requires a phosphate source of course, but also an energy source, because forming P-O bonds is not a favorable reaction on its own (the reverse of the above). So adding a lone phosphate would not be favorable, but transfering one from ATP is much better, because this simultaneously involves breaking a P-O bond in ATP, "freeing up" energy to drive the reaction.
Finally, an interesting point is that ATP itself is actually a quite stable molecule, with a half-life of about two weeks. So ATP hydrolysis is not "spontaneous" in the biologist's sense, and enzyme catalysis is required (kinases). In fact, the combination of a high "energy content" and good stability is probably key to the role of ATP as an energy currency in cells: if ATP was indeed unstable, it would randomly phosphorylate everything. Stability means enzyme catalysis can be used to control phosphorylation events. Truly unstable compounds are never used by cells, because their reactivity causes damage and toxicity.


text:
Crow branch pecking behaviour
I was walking through a small park when two crows started cawing at me, and followed me, flying from tree-to-tree as I walked. I speculate that this is a territorial or protective behaviour, but what I found different was the crows were violently pecking the branches nearby them. I have no memories coming to mind of seeing this behaviour beforehand. I speculate that this behaviour could be threat displays, but a quick search on Google did not reveal to me any authoritative studies on this phenomenon. I'd appreciate more information and sources.

This question has been added as a casual observation on iNaturalist.

Anything like this? https://www.youtube.com/watch?v=rQZj59-Kufc

@theforestecologist That is strikingly similar.

This is a good question. This type of behavior -- pecking at a branch, wiping the side of the beak on a branch, pulling off twigs and dropping them, or knocking off pieces of bark -- is quite common among many corvid species, particularly when they are interrupted by something or someone that they might consider a threat. This includes not only potential predators but also potentially hostile conspecifics.
It is typically considered to be a form of displacement behavior. The concept of displacement behavior, from classical ethology, posits that when an animal experiences two conflicting drives to do two different things, it doesn't know which to do and does a third thing instead to dissipate the drive or anxiety. For branch-pecking in crows, see E.g Kilham and Waltermire 1990 Ch. 12.
Referece: Kilham, L., & Waltermire, J. (1990). The American crow and the common raven. Texas A&M University Press.

Sorry but I couldn't resist. It is certainly amusing that the answer comes from you (with the name corvus and a crow for DP)

Indeed - as the resident corvid I felt somewhat obliged to answer this question.

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


text:
How does tearing work?
I found the question about tear gas very interesting. Shigeta says there that crying helps the cells of the eye to wash themselves clear of the toxic components in the tear gas.

Does non-emotional tearing always work this way? Is tearing not caused by cells in the tear duct working as receptors? If not, why we have tear duct (the first in-eye part of it)?
What is the cause of tear-production associated with crying during strong emotions? Is it due to hormones or nerve activation?

I slightly reworded your question for clarity. Please feel free to roll back.

Tear cleaning can be experienced when dust blows in your eyes.
Your eyes water at that time.

The regulation of tear production (lacrimation) involves reflexes initiated by sensory neurons in the cornea. Corneal pain receptors (nociceptors) and mechanoreceptors detect damaging stimuli and induce tearing to cleanse the ocular surface (and, hence, Shigeta is right as tear gas stimulates pain receptors). Corneal neurons sensitive to drying of the ocular surface also appear to increase tearing. These neurons also respond to cooling and hyperosmotic stimuli (Kurose & Meng, 2013). The tear duct is necessary to drain the tears away from the eye into the nasal cavity (Fig. 1).

Fig. 1. Tear glands and tear ducts. Source: Mayo Foundation for Medical Education and Research.
Strong emotional responses like crying can result in an overflow of tears (epiphora). Epiphora is mediated by the limbic system (the emotional center of the brain), especially the hypothalamus. Such strong parasympathetic stimulation is accompanied by other symptoms, like reddening of the face and convulsive breathing (University of Minnesota, Duluth).
Reference
- Kurose & Meng, J Neurophysiol (2013); 109(10): 2517-22


text:
Has anyone modelled calcium oscillations using Matlab software?
I have been trying to model calcium oscillations using MatLab, but I cannot obtain the oscillation.
I created a function where I put all the equations and used ode15s to call the function.  I have listed the equations and the code.
Can anyone tell me why I am not obtaining the oscillations?
These are the equations along with the codes:

r(:,3) = ( (((.029*0.13*1.049 + .21.*.5.*.144).*initi(:,1)) ./  (.144.*1.049.*(.5+ .13)) ) .*( 1- initi(:,3)) ) - (( (.21 *.5 + .029 *.9434) ./ (.5 +.9434) ).*initi(:,3));

The values of the upper case Ks are obtained as follows:

and the value of p is 0.5

a(:,1) = power (( (.5 .* initi(:,1) .*(1 - initi(:,3))) ./ ((.5 + .13 ).*(initi(:,1) + .0823)) ),3); % p_o

Jserca is directly substituted in the equation shown below

r(:,1) = (( 1.11.*  a(:,1) + .02 ) .* (  initi(:,2) - initi(:,1) ) ) -( .9 .*  power(initi(:,1),2)) ./ ( power(.1,2) + power(initi(:,1),2) );

 r(:,2) = - r(:,1) .*5.5; % Ce

The constants are shown here:

And this is the desired result:

But I obtain this!

And this is my code:

function[t, initi, r,a]= deyoung()
clear all;
clc;
close all;

%--------------------------------------------------------------------------
% Initial conditions
%--------------------------------------------------------------------------
initi(:,1) = 0;  %  C
initi(:,2) = .9; %  y
initi(:,3) = .5; %  Ce

%--------------------------------------------------------------------------
% ODEs
%--------------------------------------------------------------------------
icon=initi;

tspan=[0 100];

options = odeset('RelTol', 1e-08, 'AbsTol', 1e-08);

[t,initi] = ode15s(@(t,initi) oper(t,initi),tspan,icon, options );

[r,a] = oper(t,initi);

figure();
plot(t,initi(:,1),t,initi(:,3));

end

function [r,a]=oper(t,initi)

    initiSize = size(initi);

    initiColumnCount = initiSize(2);

    if ( initiColumnCount == 1)
        initi = initi';
        a = zeros(1,1);
    else
        initiRowCount = initiSize(1);
        a = zeros(initiRowCount, 1);
        r = zeros(initiRowCount, initiColumnCount);
    end

    % y
    r(:,3) = ( (((.029*0.13*1.049 + .21.*.5.*.144).*initi(:,1)) ./  (.144.*1.049.*(.5+ .13)) ) .*( 1- initi(:,3)) ) - (( (.21 *.5 + .029 *.9434) ./ (.5 +.9434) ).*initi(:,3));

    %Po
    a(:,1) = power (( (.5 .* initi(:,1) .*(1 - initi(:,3))) ./ ((.5 + .13 ).*(initi(:,1) + .0823)) ),3); % p_o

    %C
    r(:,1) = (( 1.11.*  a(:,1) + .02 ) .* (  initi(:,2) - initi(:,1) ) ) - ( .9 .*  power(initi(:,1),2)) ./ ( power(.1,2) + power(initi(:,1),2) );

    %Ce
    r(:,2) = - r(:,1) .*5.5; % Ce

    r = r';

end

Welcome to Biology.SE. The problem is either specific to programming (there's a bug in your code) or to biology (you did not understand the process you want to simulate). I don't actually know the concept of calcium oscillation but no one can correctly answer your question for the moment. You should add your code, describe it, describe the output and explain why the output is different from what you expected. I vote to close for the moment and will retract my close vote when the question will be improved.

@Remi.b Is that okay now?

Yep, that seems to be answerable now. Good improvement +1.

A general programming tip: define your parameters beforehand instead of directly hardcoding their values in the function. I did not go through your code but it seems that you have incorrectly typed the value of a parameter. As it stands, this question is off topic.

I'm closing this question as off-topic because it is about coding and not really about the computational model of the biological system.

@WYSIWYG Can you please tell me which parameter has been coded incorrectly?

@nashynash It is difficult for me to look through. I just guessed that might be the case. You can try defining the parameters in the beginning of the code and then use them in the equations. Difficult to troubleshoot otherwise. Something like a=1; r(1)=somefunction(a);

@WYSIWYG - your not voting anymore..

@WYSIWYG I think you should have at least checked the  code and the equations before you make such a comment.

@AliceD That is the default line that comes if I select the custom close. Anyways this is clearly off-topic.

@WYSIWYG - oh really? Sorry then! It's an interesting post given my post at meta. I think this one is indeed across the line. Happy I could help on the brink of closure anyhow.

@nashynash This is not the right site for code-checking and troubleshooting. You should do that in stackoverflow. And I commented based on my empirical understanding of systems and codes like these. Oscillations can disappear if some parameters change (Read about Hopf bifurcation). As I said, try to improve your coding style and you may find where you could have gone wrong. And it is better to write 0.5 instead of .5. General stuff.

@WYSIWYG Yes I know that it is more to do with the coding. But just wanted to try if someone from biochemistry would be familiar with Matlab and help me know where I am going wrong. But I will take you tip as well.
Ps: I have tried in stackoverflow, but since most of them are unaware of the mechanism behind calcium oscillations, they cannot fully grasp the idea.

@nashynash You are using the equations from a published study, right. So they should work: therefore I assume that the problem must be with the code. In stackoverflow, you need not explain calcium oscillation because your question is not really about if the model works (it works because it is already done by the people who published it. Your program is not replicating it). But before asking in SO try editing your code and examine if you have mistyped any parameter. Do the basic bug checks. You can try this site too: http://scicomp.stackexchange.com

Okay @WYSIWYG. And thanks for pointing out that page. Didn't know such page existed.

I wish to share an open-source modelling study on Ca2+ oscillations in astrocytes which contains a detailed description of the underlying math and even better, it has supplementary Matlab code published alongside (Zeng et al., 2009). This may be of help to check your formulae and script.
Unfortunately I do not feel inclined to start troubleshooting and bug-fixing your formulae and Matlab code, because, as mentioned in the comments, the issue can be anywhere in the chain of events.
Reference
Zeng et al., Biophys J (2009); 97(9): 2429–37

@nashynash - good luck. I'm sorry to see this question closed after all the efforts you put into it. Perhaps you can try another SE and hope for better luck there.


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Can you recharge without sleeping?
Sometimes it's difficult falling asleep for almost an entire night. You might feel like getting up and being productive instead, or 'pull an all-nighter'.
Or you can try to simply lay in bed to relax and rest, even though sleep does not kick in. In this situation, you may eventually fall asleep, only to be woken by your alarm just an hour or two later. Upon waking from such short sleep you can feel completely wrecked.
It leaves me wondering if you would feel more rested if you didn't sleep for just one hour. Maybe if you could relax throughout the night without really sleeping, you'd feel more rested by the time your alarm goes.
But is it physically possible to recharge as if you were sleeping without actually sleeping?

wikipedia says:       https://en.wikipedia.org/wiki/Sleep                                                                                If sleep were not essential, one would expect to find:
Animal species that do not sleep at all
Animals that do not need recovery sleep after staying awake longer than usual
Animals that suffer no serious consequences as a result of lack of sleep

Hi Marc - this has received a number of close votes because personal medical questions, or questions relating to your own personal health, are considered off topic. To make this "on topic" just remove the references to your own situation, therefore any answers/recommendations cannot be misconstrued as personal medical advice (which the vast majority of people here are not qualified to give). Thanks!

I suggested a very radical rewriting edit in order to remove all "personal health problem" wording and thus have the question qualify for reopening. You don't have to accept it, of course. But I think that with it, your question has a chance of getting open again and gathering more answers.

Was the edit I made not sufficient?

No, you cannot. Although we don't know how sleep works, we know that lack of sleep is very devastating to the body, and nothing (including laying in bed relaxed but awake) can replace it. If a rat experiences 100% lack of sleep (somebody keeps it awake all the time), this will kill it sooner than 100% lack of food would. There are no wake-until-you-die studies in humans, but even reduced sleep has very bad effects, both cognitive (it impairs you similarly as if you were drunk) and physiological (metabolic changes: you need more energy for the same actions, and food intake increases disproportionally).
If you have insomnia (and yours sounds severe), you need to get it treated. There are different options depending on whether an underlying cause is found, and whether behavioral therapies turn out to work for you. There are no alternatives which replace sleep.
The above is just a summary. For a dry but very reliable source on sleep, see Principles of neural science (ed. Kandel et al), Chapter 51 written by David McCormick and Gary Westbrook. For a very good popular science book on the subject, see Sleep thieves by Stanley Coren, I can recommend it for anybody with insomnia.

Hi, this is a well-written answer, but can you include a few references (e.g. that lack of sleeps would kill you sooner than lack of food). Thanks!

@Luke I did. Kandell (or rather the chapter author, K. is the editor) says that part about the "kill you sooner". I don't think I can find the exact page because I have the Kindle edition.

Ok. Didn't realise that reference was for all the points due to the vague wording - my apologies, it is an interesting answer.


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Does the anatomy of our hand result in (computer) mouse-accuracy that varies by direction of movement?
First off, I apologize if this isn't the right stackexchange sub-site for asking thsi question.  I was torn as to where I should post this question: it could plausibly belong in Biology, User Experience or even Arqade.  However, given the root of my question has to do with the "wiring" of the human hand, I elected to post it here.
My hypothesis/question:
Let's assume that wrist adduction/abduction is responsible for horizontal movement of the mouse cursor and that finger extension/flexion is responsible for vertical movement of the mouse cursor.  (I am, of course, willing to revisit this assumption, if necessary.)  Would it be accurate to say that we are "hard-wired" to be capable of higher precision in vertical movement of the mouse cursor than in horizontal movement?
Description of mouse grip:
In making the above assumptions, I assume a fingertip-grip style of the mouse (as opposed to the claw and palm grips). The (corner of the) wrist rests on the table and acts as a pivot for allowing side-to-side motion (i.e., horizontal motion of the mouse cursor).  Meanwhile, flexing/extending the fingers allows for pulling/pushing the mouse away from us, (i.e., vertical motion of the cursor).  The main (admittedly unscientific) reason behind my hypothesis is that vertical movement of the mouse cursor uses similar finger motions as those used for hand-writing (which is, after all, a highly precise activity).
(I understand that my question makes the assumption that we are capable of more precise movement with certain muscles of our body than we are with others - please let me know if that's a flawed assumption.)
Why do I care about this?:
If my hypothesis is correct, there would be implications on mouse settings (namely, horizontal and vertical DPI*) that are conducive to both high accuracy and speed.  The key issue is that if we keep our wrist in place (i.e., no sliding/lifting of our pivot point) - then we're able to move the mouse a greater distance side-to-side (i.e., horizontal motion of cursor) than we're able to move it toward/away from us (i.e., vertical motion of cursor).  However, if there is evidence to support my hypothesis, than an appropriate adjustment (which wouldn't result in a loss of accuracy) would be to have a slightly higher vertical DPI than horizontal DPI.
*DPI = dots (i.e., pixels per inch).  For example, I have a resolution of 1366x768 (which is in units of dots or pixels) and a 600 dpi mouse, which means that my (physical) mouse needs to be moved ~2.3 inches (1366 divided by 600) in order for the mouse cursor to move the full horizontal distance of my monitor.  To put it simply, lower DPI results in higher accuracy but it is preferable for our wrist to remain in-place in the interest of speed.

Finger movement is more precise than wrist movement. Further, because of RSI, it is better to move the arm than the wrist :) BTW: your question seems to mix up maximum distance and accuracy. Accuracy is better in fingers because of their function, not because their maximum covered distance is smaller..

Thank you!  That is exactly what I'm looking for.  Feel free to copy paste into an answer.  I'm probably unclear in how I described the issue.  I simply meant to say that because the maximum covered distance (by finger movement) is smaller, it would be convenient to be able to use a higher sensitivity in this direction - but that making this change would only make sense if your fingers were capable of more precise movement to begin with (which, thanks to your answer, I now know to be true!)

Assuming the case where you move a mouse left and right with the wrist and up and down with the fingers, then yes, finger movements are more precise. The fingers and facial musculature are body parts with the most exquisite fine motor-control. The wrist, on the other hand, probably less so. The wrist is definitely involved in fine motor skills such as writing, but the fingers even more so.
I wasn't able to find a good reference about the level of precision for different body parts at the behavioral level. I can, however, approach the question from a neurophysiological point of view. The amount of motor control available for different body parts can be visualized by means of a motor homunculus. The motor homunculus shows how many neurons are available in the cortex for a given body part. The larger the cortical surface dedicated to a body part, the larger the corresponding body part is presented in the homunculus (Fig. 1).

Fig. 1. Homunculus drawn on the motor cortex (left) and the homunculus presented as a figurine (right). Sources: Conference on Human factors (1997) and Autism Index, respectively.
The fingers have a huge amount of motor cortex dedicated to them compared to the wrist. There are a lot of 'buts' to add, most notably the larger number of muscles in the fingers versus the wrist, which explains part of the difference. Nonetheless, the homunculus does show the relative functional importance of the fingers in motor processing power of the brain, while the wrist is virtually invisible on the homunculus (Fig. 1, left panel).
Lastly, you seem to be mixing up 'distance' and 'precision' in your question. While the wrist may cover a greater distance, it is not because of this that the precision is smaller. The fingers have more neuronal processing power behind them and can be exquisitely fine tuned. In other words, the precision is not determined by the dynamic range (distance), but by the processing power dedicated to the motor function.
As a side note, because of RSI, it is recommendable to use gross arm movements instead of fine wrist and finger movements.


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What does this equation about DNA replication mean?
Could someone help me understand this equation please? I found it in a paper which said that it was DNA replication, but why?
$\ce{dNTP + dNMP_{n} -> dNMP_{n +1} + PPi}$
I found that dNTP means deoxy nucleotide triphosphate and dNTP means deoxy nucleotide monophosphate. Deoxy nucleotide monophosphate is a monomer in DNA, but dNTP isn't.
I also would like to know if there is an equation like this in other processes in the central dogma (such as transcription and translation)?

NTP stands for nucleoside triphosphate. A subtle difference. With nucleotides, the phosphate is implied.

The notation you are referring to is a way to express the elongation of a nucleotide strand (Fig. 1).
dNTP + dNMP(n) → dNMP(n+1) + PPi
means
Existing strand  +  deoxynucleotidetriphosphate  →  elongated-strand  +  pyrophospate.

Fig. 1. Elongation of DNA. Source: Concepts in Genetics.

This reaction holds for DNA replication as well as transcription.
Translation is all about protein synthesis from amino acid precursors. Each subsequent amino acid is coupled to the growing peptide by a peptide bond between the carboxyl of the growing peptide and the amino group of the new amino acid. A water molecule is eliminated during the reaction (Fig. 2).

Fig. 2. Peptide bond formation. Source: An Introduction to Molecular Biology
Hence translation can be written analogously to replication as:

amino acid + peptide(n) → peptide(n+1)
However, also in this polymerization reaction energy is needed and amino acids are activated while they are bound to the messenger RNA (mRNA) through the action of ATP. Moreover, during translation the ribosome (i.e., the protein synthesizing machinery) uses another source of energy to move across the RNA template, namely GTP. Hence, the net reaction can be written as:

amino acid + peptide(n) + ATP + GTP → peptide(n+1) + AMP + GDP + PPi + Pi
Note that this notation in itself is not a dogma as other ways are in use to denote DNA and RNA synthesis. According to Merriam-Webster a dogma is:

A belief or set of beliefs that is accepted by the members of a group without being questioned or doubted.

It's incorrect to say that amino acids are not activated. tRNA charging is the activation step of protein synthesis and creates an ester bond with high and negative free energy of hydrolysis (whose cleavage subsequently drives peptide bond formation). tRNA charging requires ATP. A net equation for peptide synthesis could be written as amino acid + peptide_n + ATP -> peptide_(n+1) + AMP + 2Pi. This equation (like that discussed in the question) is over simplified, but gets the point across.

@canadianer - Great point, will include shortly

Additional point to what @canadianer said. Each elongation step requires a molecule of GTP per codon. So the reaction for translation elongation should be: amino-acid + Peptide(n) + ATP + GTP → Peptide(n+1) + AMP + GDP + PPi + Pi

@WYSIWYG - I edited the answer. Thanks. I must say that both mRNA activation and the ribosome movement are both indirectly related to the translation reaction. The direct substrates are mRNA and the growing peptide. ATP and GTP are indirectly involved. So I reverted to my old answer and added your comment alongside Canadianer's in a separate section for clarity's sake. Thanks for your suggestions and the edits!

DNA is a polymer of dNMPs (dAMP, dTMP, dCMP, and dGMP). That's why you could describe DNA by dNMPn (n base length). When another dNTP is added to DNA (dNMPn), one pyrophosphate (PPi) is released. It is obvious that the length of the DNA results in n+1 bases.


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What could cause a forest of bent trees?
While hiking on the northern Idaho-Montana border, I encountered a large area where virtually every tree is bent at the base in the downhill direction.  Only the very largest and very smallest trees are straight.  What could cause this?

Avalanche?  Or just a heavy accumulation of snow bending them towards the ground one year.  I could find you some hereabouts that are bent into U-shapes, or even S-curves.

Forgot to remove the fisheye lens?

This case is much different, but you might find it relevant: Crooked Forrest.

A forest near my grandparents farm has a bunch of bent trees due to a tornado 40 years ago. That being said, if they are all bent at such a similar angle geotropism seems more likely.

Prevailing winds, you see a lot on the coast.

Also see,the Dancing Forest https://en.wikipedia.org/wiki/Dancing_Forest they think it might have been caterpillars.

The phenomenon in question is probably related to geotropism.
If the hill soil is "on the move" it will cause the bend on the trees -

If the soil in a slope is moving downward, the trees on this slope
  will tip downward.  As the tree continues to try to grow upward, the
  trunk will show a curve. The degree of bending could indicate the rate
  or amount of movement of the soil.

source

This was a surprisingly interesting question and answer.

@canadianer :) thanks, nice to help to community %)


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Calculating the canopy size (crown) of a newly planted tree at a future date
Assuming that one knows the maximum area of the canopy and the age of the tree when it achieves this. And given an initial canopy size from the nursery. How would I calculate the canopy size at a future date.
Whilst certain aspects of the growth are obviously variable... how would I model the growth over the year(s)? I'm looking for a simple formula that I could give to a user in a planning department to develop adaptive lighting solutions for trees in streets.

Maybe trees branch randomly so there might be no such formula.

If you can tell the weather years in advance this might be possible. Other than that just interpolate linearly and that'll be close enough maybe?


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Where do the H+ ions come from in light reactions?
In the light-dependent reactions of photosynthesis, H+ ions pass to the thylakoid space. Where do these protons come from?

Photolysis of water. It is the first step of the light reactions. BTW, H⁺ is ubiquitous.

And the electrons go to PhotoSystem II?

Is this a homework question? It really looks much like it. Additionally: Please have a look at the reaction chart on the Wikipedia page on photosynthesis which explains both questions.

No, I have a biology course in Univeristy, and I just want to be sure I know it before the exam.

@Benjli Read our homework policy. If you have not put an effort in answering a basic question then we consider it as homework. Can you add some points on how you analysed this problem?

All right, I will keep the homework policy in mind. But again: that question was not a part of any homework. I had tried to search it in my biology book. It was written in it that electrons come from water to Photosystem II only when there are no electrons left in it, but H+ ions are being passed into the thyalkoid space even when there are enough electrons left in the photosystem! So I tried to solve the contradiction.

@WYSIWYG I think you meant H+ (not H-) is ubiquitous. H+ is everywhere in the aqueous system. H- is pretty rare and unstable in aqueous/biological systems, that's why there's NADPH.

The photolysis of water is coupled to the reduction of plastaquinone (Q) in photosystem II (PSII) as summarized in this diagram, adapted from Berg et al.:

The overall reaction (which balances) is:
2 H2O + 2 Q + 4 H+ = O2 + 2 QH2 + 4 H+
But the 4 H+ on both sides of the equation are not the same. The generation of the hydrogen ions in the thylakoid lumen is coupled to the uptake of hydrogen ions from the stroma as the plastoquinone is reduced. This is made possible because of the membrane disposition of the components of photosystem II. Hence an electochemical gradient is established that can be used for generating the ATP needed for photosynthesis.


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Identify bee in photo (found in Utah, USA)
A friend took this photo of a bee in his back yard in central Utah (© Jon Mott, CC-BY 3.0). I have no formal training in systematics or entomology, so to me everything looks like the bees' poster child Apis mellifera. Can someone with a bit more experience confirm or refute this?

Maybe You should contact a local apiary and ask them about common bees in your are.

Yes, this looks like Apis mellifera, which is also one of the most common bees you'll run into. If you have other pictures, you could check the identification tips at the bugguide page for the species.
As a side note, in general to really confirm an identification a specialist would need to see a collected specimen (that is, a live or pinned bee) as the distinctive characters (things like size, wing veins, or in this case, long hairs on the eye) may not be visible in photographs.


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What have the L-systems (Lindenmayer systems) been actually used for in biology?
From Wikipedia:

An L-system or Lindenmayer system is a parallel rewriting system and a type of formal grammar.
L-systems were introduced and developed in 1968 by Aristid Lindenmayer, a Hungarian theoretical biologist and botanist at the University of Utrecht. Lindenmayer used L-systems to describe the behaviour of plant cells and to model the growth processes of plant development.

I tried to find biological research that has actually used this system but I could not find any. Perhaps this is because I do not know biology that well.
Are these models important? Still taught?
They do produce pretty pictures (again from Wikipedia)

The Wikipedia article points (in the references at the end) at least to a potential impact in developmental biology with this book (which I haven't read): http://www.amazon.com/Lindenmayer-Systems-Theoretical-Computer-Developmental/dp/3642634745

BTW awesome images.

http://ftp.tuebingen.mpg.de/pub/kyb/bweber/papers_db/2001/Zamir/J%20Gen%20Physiol%202001%20Zamir.pdf

The main point is not that biologists do use l-systems in their research (although those interested in artificial life do), but that plant growth is (in mathematical sense) a l-system.

I've been considering using them to produce realistic branching in neural simulations, but I haven't actually implemented anything yet.

Great photos... here's a paper from Researchgate that may help you. I suggest reading the abstract + intro thoroughly and skimming over the paper. https://www.researchgate.net/publication/27481070_Derivation_of_L-system_Models_from_Measurements_Biological_Branching_Structures_Using_Genetic_Algorithms

Greatly suitable to proposed bioinformatics

Are these models important? Still taught?

Yes!! These models are extremely important, however, the application of L-systems most definitely isn't confined to just the scope of Biology. I myself first came across L-systems when taking Calculus in university, and then later in several Computer Science courses (I study Bioinformatics).
What's (probably) most significant to mention about L-systems is that they produce fractals, which is acheived by defining a substitution system and utilizing recursion.
Fractal mathematics can be used to describe extremely complex phenomena, starting with just a few simple rules and initial conditions (which is why it's so powerful/attractive to study). Also, fractals have the nickname of, "God's Thumbprint", or, "The Fingerprint of God", just from where they're found so prevalently in nature. To name a few, fractals can "easily" model:

Coastlines
Blood vessels
Brain structure (neuronal connectivity)
Plant foliage
Lightning bolts
Diamonds
Snowflakes

I tried to find biological research that has actually used this system but I could not find any.

As you can see, some of these examples are biologically related, however, the use of L-Systems have been broadened to many other fields of science, such as mathematics (coding theory) and theoretical computer science.
Unfortunately, very rarely do biologists have the mathematical or algorithmic backgrounds to work with L-systems, since L-systems are more related to mathematics, algorithms and logic, than they are with (practiced) biology.


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Why do some medicines induce sleep?
I have seen lot of people sleep or say that they are feeling sleepy after taking some medicines. Why? I mean, if a medicine acts on some cell of the body because that cell has got its receptors and other cells have receptor for another part of that molecule, then too why do a large range of medicine induce sleep?
This also points to a doubt that there are only one kind of receptors for sleep inducing medicines (the real ones not the ones which have sleep as side effect) or many? If many are there, then it can be possible that a large range of medicines induce sleep.
Is it due to induction of sleep gives relaxation and thus give time for action of other medicines? Or is it just a natural process? If latter, why only some?
I don't want metabolism, just a reason.

Potentially too broad here - many medicines induce drowsiness/sleep but they may (and probably are, particularly comparing sleep medication and those that induce drowsiness as a side effect) by different mechanisms. I think you may need to narrow this down a little.

I'm torn between flagging this as way too broad and thinking that it is a good opportunity to clear up basic misconceptions about drugs in an answer. In any case, I recently noticed that a standard book on pharmacology has three separate chapters entitled "how drugs act", this should give you a hint why the question is hard to answer in this state. Note that these were basic overview chapters, before delving into what specific classes of drugs do.

@rg255 can you suggest what specificity should be added?

You can answer three-four methods. Please give me the common ones.

@InfiniteLight I don't see how reducing it to three-four mechanisms will help. "Why are there many medicines which are H1 receptor antagonists" is not a good question, there is no good reason why there are several of them. Also, I wouldn't say that some mechanisms are more "common" than others, common by what count?

Common meaning here that many medicines exibit them

agree with @rg255 - too broad a question... but could easily just give a broad answer - drugs/medicines are not as specific are they are made out to be - any side effect, not just drowsiness, is an off-target effect

I don't understand the question? Is it why various parts of the same molecule can act on different receptors (atomic level), why a molecule can bind various receptors (molecular level), or why activation of different classes of neurons activate the same brain area (cellular and tissue level). Voted to close because it's unclear. Feel free to edit though. There's enough comments to make this question a cracker.

Hi - I agree with some previous comments that this is too broad because (and this is an assumption) the mechanisms will probably differ between medicines - if you have a few in mind then list them in the question and this will hopefully be answered (I am very interested to see an answer - particularly for antihistimines I take around this time of year... makes me very groggy some days)

Your edits do not fix the problems with this question

I just mean to ask that what can be the advantage of induction of sleep? Is it just as a side effect (like @VanceAlbaugh sujjested) or is it some part of a metabolism?

Is there any general relation which all pathways follow?

@InfiniteLight - within the body naturally occurring compounds as well as medications (i.e. legal and prescription) target a variety of receptors (even if drug companies or other people say they specifically target one single receptor in the body). Almost ALL drugs we prescribe to patients have side effects that are off-target effects. Anti-histamines are probably the most common class that cause people to be sleepy. Even though those drugs "act" through one type of histamine receptor, another type of brain histamine receptor is also targeted unintentionally - causing sleepiness.

@InfiniteLight - you are trying to ask why so many medications cause drowsiness in people. This is a common side effect of many drugs. There are a number of receptors that can cause drowsiness or sedating effects - there are too many drugs to name that act on these numerous receptors. These effects are off-target effects - which we call "side effects" in clinical medicine.

@VanceAlbaugh So, they are always side effects as drowsiness?

I mean drowsiness is always a side effect? I know others are there, I mean to ask if drowsiness is common to all or not

@InfiniteLight - drowsiness isn't always a side effect - it's just a common side effect for a lot of medications. Anticholinergic side effects (i.e. dry eyes, dry mouth) is another very common side effect we see. Those are mediated through cholinergic receptors. I will try and answer this question and give some citations for this stuff.

Give the answer in the answer column now. Don't just comment

Voting to reopen this question. I disagree that it should have been closed for being too broad, because I think this question can be answered with a relatively concise answer that clears up the misconceptions present in the original question.

Me too! @BryanKrause me too!


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Forward versus backward numerical simulations in population genetics
My question is closely related to this post.
There are a number of existing platforms to perform numerical individual-based simulation in populations genetics. An almost exhaustive list of such platforms can be found here.
Some program (like NEMO or SFS_CODE for example) perform forward simulations while some others (like SIMCOAL2 for example) perform backward (coalescence) simulations.
I am asking for a general comparison between those two methods.

Is one faster than the other? Why? (Intuitively I'd expect backward simulations to be faster).
Does backward simulation allow for simulating selection, recombination, gender-specific mutation rate, complex demography, etc..
Why/when would one use a backward/forward simulation model rather than the other type of model?

Your intuitions all seem correct. Coalescent simulation should be faster, because you don't track the entire population history over all t generations as you do in the forward simulation. Rather, as you work backwards in time you are tracking a smaller and small population. And with coalescent simulations it is probably very hard to incorporate the full range of evolutionary processes whereas doing so is more or less trivial with forward simulations.
A 2008 paper by Carvajal-Rodriguez reviews some of the issues in more detail that I have here.


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How do steroids travel in the bloodstream?
Cholesterol, which is hydrophobic, cannot simply travel in the bloodstream, and instead is enclosed in lipoprotein (LDL, HDL). Steroids, which are derived from cholesterol, are also hydrophobic (right?). So how do they travel in the bloodstream? If they are enclosed by anything, what is the molecular mechanism of their entering the target cell?

Steroid hormones are transported in an inactive form bound to proteins in the bloodstream. Androgens and estrogen are bound to Sex hormone-binding globulin (SHBG), while glucocorticoids and progestins are bound to transcortin.
References:

Transport of steroid hormones: binding of 21 endogenous steroids to
both testosterone-binding globulin and corticosteroid-binding
globulin in human plasma.
Plasma protein-mediated transport of steroid and thyroid hormones.
The Functions of Corticosteroid-Binding Globulin and Sex
Hormone-Binding Globulin: Recent Advances

They also bind to albumin.