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Do xylem vessels in roots have lignin?
I learned that water enters xylem vessels in the roots after absorption by osmosis, but also that xylem cells are impregnated with lignin that doesn't allow water to pass through them to prevent water loss. Does that mean xylem cells in roots of plants aren't impregnated with it?

We have to consider the main function of lignin in xylem vessels, which is providing mechanical support for the plant. For the parts of plant above the ground, the stem where the xylem is located has to counteract the gravitational force pulling the plant down. Here's where lignin comes in to strengthen the xylem to support the plant. Remember that this is for many land plants.
Compare this to creepers, vines and aquatic plants. Lignin is absent or only present in small amounts as for creepers and vines, they have another external support, while for aquatic plants, it's weight is distributed on the surrounding water apart from the stem.
Now we can liken the case for aquatic plants to the xylem vessels in the roots of land plants. The roots of land plants are firmly anchored in the soil, and the plant's weight is distributed along the roots and soil, not just on the central root (for tapped roots). Hence there is not a need for lignin in roots of land plants.
And yes there are perforations in lignin as mentioned by @Always Confused, hence water can still enter the xylem vessel even when lignin is waterproof.


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Why are excess amino acids toxic?
While learning about deamination, I learnt that excess amino acids must be converted to urea and excreted, since the nitrogenous group can alter the pH and affect proteins. But shouldn't the pH stay the same since they have NH2 that becomes ammonia as well as a carboxyl group (weak base and acid). So why are amino acids deaminated?

"they have NH2 that becomes ammonia as well as a carboxyl group" you mean, like -$\ce{NH_2}$ converts to -$\ce{COOH}$ or that the latter cancels the pH change caused by the former?

Firstly excess amino acids are deaminated to form keto acids and not urea.
Urea is formed utilising the ammonium released as a consequence of deamination via Ornithine-Arginine cycle
Secondly the released ammonium is toxic because of two reasons:
1)pH changes in the tissues (as mentioned in the question)
2)disturbs the balance of K+-Na+ gradient between the intra and extracellular fluids.

ammonium ions compete with potassium ions for inward transport, over the cytoplasmic membrane, via potassium transport proteins like the Na+/K(+)-ATPase and the Na+K+2Cl(-)-cotransporter.

This causes increased demand for maintenance energy, caused by the need to maintain ion gradients over the cytoplasmic membrane.That is why converting the ammonium to urea is neccessary.
why amino acids are deaminated:
to form glucose via gluconeogenesis or to form anaplerotic compounds
why acidic group of keto acids fail to neutralise the basicity of ammonia:
because they keep getting utilised for the energy expenditure that increases in the tissues as mentioned above.

In addition to what @CATHARANTHUS has said I would like to mention that ammonia has its direct effects on brain metabolism.
Ammonia is an important substrate as well as a product for at least 16 different enzymatic reactions in the brain (Cooper and Plum 1987).
For instance its effect on Tricarboxylic acid cycle(TCA) is as follows:

So accumulation of ammonia will shift the equilibrium towards right hand side resulting in depletion of alpha ketoglutarate ,a key intermediate in TCA cycle which ultimately, results in decreased production of ATP, so one can say that ammonia exerts its toxic effects on brain by impairing ATP formation.

Sources:
1-Biochemistry by Satyanrayna
2-Source of last image

source: Stack Exchange

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sort: votes


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Where can I find an image of the gut/anatomy of the mealworm?
Specifically, I'm a student working on an experiment involving the dissection of the mealworm (Tenebrio molitor) but for the life of me, I can't seem to find an image anywhere on the internet. Speaking to Carolina.com also got me no results. We're looking to dissect the mealworm and extract its gut/GI tract. However, at the moment it seems like we're going in blind. Is there anyone out there who can provide some insight?

The best I could find which showed the inside of a mealworm not just the outside was this:

Taken from here. Hope this helps with your dissection.

There is a paper called: biodegradation and Mineralization of Polystyrene by Plastic-Eating Mealworms: Part 2. Role of Gut Microorganisms. I. Here you can find a picture of the midgut lumen.

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Does genetic morbid obesity exist?
With the acceptance of being a little overweight
I hear of people saying they were born morbidly obese and it was genetically passed on. I'm aware being so obese leads to countless health issues, yet we have people defending fat shaming and the likes. Is the excuse of having 'obese' genetics scientifically justified? Do people have genetics that make them ridiculously fat? Alongside, would this simply be down to the diet of the person from a young age?
Thanks.

To understand ny answer, you will probably have to make sure you understand the concept of heritability first by reading Why is a heritability coefficient not an index of how “genetic” something is? for example

It's a myth that obesity is mostly caused by genes. Yes, there are many genes that predetermine your apetite but when a baby is born obese, it's not a matter of genes but a matter of the mother's health and diet. And because till the birth, the fetus shares a single bloodflow with the mother, it gets everything the mother has in her blood. Thus, some babies are born obese, some are born addict.
Indeed, there are papers showing that there's a higher chance for the newborn to die during birth, even though you can't always say what was the main cause of death (also it depends on what you connect with obesity).

It'd be great if you could link to a peer-reviewed paper instead of livescience.com small article

Down voted this answer due to poor sources. Also the point regarding newborn obesity is certainly true, but the strong dismissal of the influence of genetics on obesity is not scientifically correct! I have provided a more balanced and better documented answer, that also focuses on the effect of lifestyle on obesity.

It is certainly a very difficult question to answer.
There are some genetic disorders that can predispose individuals for becoming obese: https://www.ncbi.nlm.nih.gov/pubmed/18230893
There are also evidence of epigenetic influences on obesity: http://www.nature.com/nrendo/journal/v12/n3/full/nrendo.2016.18.html
Typically each case of obesity is caused a combination of both genetics, epigenetics and lifestyle: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3873060/
However also keep in mind that obesity is a fairly recent problem and as such the genetic changes are likely minimal between the 1980 and 2008 populations sampled by WHO: http://www.who.int/gho/ncd/risk_factors/obesity_text/en/
A doubling in the prevalence of obesity in the two populations are most likely caused by changes in lifestyle and the availability of food, rather than genetic changes as the time frame is so short.
So to sum up: Morbid obesity caused by currently unfavorable genetics exists but is very rare. People can be genetically and epigenetically predisposed for developing obesity, which when combined with certain lifestyles can further increase the risk of becoming obese.

Genetics is not a yes or no question, every gene is affected by its environment and often the environment is influenced by other genes as well.
Are their genes that can make you more likely to be obese, Yes. There are also genes in our gut flora that influence it as well. How these genes are expressed may or may not be influenced by environmental factors. It likely varies by the gene. And of course no gene will make you obese in a absence of calories, but they can greatly change the number of calories you need to become obese.
Morbidly obese is a tricky phrase, since the BMI is not actually based on scientific measure of health. Many athletes score very high on the BMI. So you may want a more concrete definition to work from.

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Why can't I smell things that aren't there?
I can close my eyes and imagine a red cube with a yellow star on it. Although I don't literally see it -- if there was a red cube with a yellow star on the inside of my eyelids, I'd know the difference -- I can experience it in much the same way as if I was seeing it.
I can do much the same thing with sound, imagining (say) the sound of a bird, or of a bell ringing.
But I can't imagine any tastes, or smells. I know what cinnamon smells like: if several spices were placed in front of me, I could readily identify the cinnamon. But I can't call a familiar smell or a taste to mind in the same way I can call a familiar sight or sound to mind.
I don't think it's merely a memory thing. Even if I've never seen the box, I can still imagine it. I can imagine the sound of a bird tweeting in a large echoing hall, even though I've never heard it. But I can't synthesize unknown smells or tastes in my imagination in the same way I could unknown sights or sounds. I don't think I'm unusual in this respect (correct me if I'm wrong).
Are there any theories as to why this is?

I think you may be unusual.  Or perhaps I am: I can recall smells & tastes with no difficulty.  Imagining new ones is more difficult, but I think any creative cook can do it to some extent, when figuring out what foods & spices to use in a dish.

Interestingly, when I read the word "cinnamon" in your question, I automatically imagined smelling cinnamon. I would not consider myself a great smeller or taster - I can rarely guess the flavor of something without knowing ahead of time, but I still had this experience. It may be that smells are more difficult to imagine for humans, and that you are an extreme example, but it seems like it isn't truly an inability.

@Always Confused: It doesn't seem much different to me, but of course that's just an unscientific anecdotal opinion :-)  Could be it's just a function of practice, and many people get more practice with vision & hearing than with taste & smell.

the continuous nature of sound and visual stimuli--compared to the discrete nature of chemical detection--is likely at the root of your observation, which I agree with.  the specific way each of us represents odor, for instance, in the brain, is unique (see recent work by Axel lab on piriform cortex).  the direct representation of a box or sphere or whatever object is not unique.  and you can easily play with a shape in your mind, while smell is not easy to play with mentally because we have so much unexplored chemical space, in part because of the limited number of environmental chemicals.

Couple of contributing theories:

The olfactory system does not project to the thalamus, which serves as a relay to other higher processing areas.
Lack of a specialized working memory subsystem; we have fairly robust subsystems for movement,visual and auditory buffers of information, what is normally called working memory, things we can hold on for a little while, but it seems they are not as developed or engage the same areas for smell. see for instance:Working Memory in Another Dimension
It is not as useful,used or adaptive ( beyond recognizing odors) as the other senses, there is a relationship in between how much we use something ( could also be the above working memory systems )and the cortical real state devoted to it's processing, this is a competitive part of the brain and in comparison to other senses like vision the portion of the cortex devoted to olfaction is small.
Another way of looking at it, is that we do have the capability to imagine smells and gustation, but they are not as developed as the others since we don't use them as much.
Anectodally, I would argue that people whose jobs revolve around combining nice smells or tasty things do develop certain abilities like those in vision as well as for those who have been exposed to the same odor repeteadly and can imagine it at will.

Some interesting theories, but I am wondering if you can cite any academic work to back any of these suggestions up with supportive evidence? Specifically, for whether the phenomenon the OP reports is actually a real thing beyond OP's own experience, or the lack of working memory for smells?

From the citation you just added: "the results showed that prefrontal regions identified during a visual working memory task were also engaged during olfactory working memory" - This does not support your statement at all that working memory is "not as developed for smell" (edit: I see you have edited again. I still don't think what you are saying is at all supported, I see no evidence that working memory is any less specialized for any of the modalities you mention...I think it is simply true that olfactory working memory is not well studied in humans)

Also, thalamus is a relay to all areas of cortex, not just higher processing areas, and there are olfactory connections with the thalamus(for example), it is just that the olfactory bulb itself does not project through thalamus to cortex like other sensory modalities, and I am not certain the role of the thalamus in working memory is well understood


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What enzyme could you use to delipidate lipidated serine?
I have a protein with a serine modified with an O-octanoyl group (ester linkage). What enzyme could I use to remove this group? Could I use a lipase, such as pancreatic lipase?

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Does "RT-PCR" denote "real-time PCR" or "reverse transcription PCR"?
I often find the term "RT-PCR" used in articles without any further qualification. Searching for the meaning of the acronym sometimes leads to "real-time polymerase chain reaction" and sometimes "reverse transcription polymerase chain reaction." I understand that reverse transcription PCR uses a reverse transcriptase to convert RNA to DNA, which is then amplified by the usual PCR method. I'm not sure I understand what real-time PCR is, but it sounds to be distinct from reverse transcription PCR. Are these distinct methods that happen to have the same abbreviation? Or do they somehow mean the same thing? What is usually meant by the acronym "RT-PCR"? Is there some context I can use to distinguish them?

Related: https://biology.stackexchange.com/questions/95268/rt-pcr-not-seeing-how-it-can-measure-mrna-expression-levels

Does this answer your question? RT-PCR: Not seeing how it can measure mRNA expression levels

I find those answers somewhat confusing. This statement for instance seems contradictory to me: "RT-qPCR refers to real-time quantitative PCR, but some organizations refrain from any reference to quantitation (because it's really only semi-quantitative), instead using the nomenclature rRT-PCR (reverse transcription real-time PCR, I guess)."

Unfortunately, there is no real and hard definition and it can mean both, depending on the context.

Real-time PCR is used to quantify a target in real time, thus is sometimes called quantitative PCR (qPCR). Basically, any mention of Ct or Cq values indicates a real-time PCR methodology. If they are quantifying a DNA target, it's likely referring to real-time PCR (aka qPCR). If they are using it to detect (not quantify) a target from RNA, it's probably reverse-transcription PCR. If they are quantifying an RNA target (like gene expression from mRNA), it's likely RT-qPCR (real time reverse transcription PCR).

PCR means (piece of DNA) amplification with 2 primers, a polymerase, free nucleotides and temperature cycling (to favor (un)hybridization and polymerization). For RNA viruses, prior to PCR there is RNA extraction and reverse transcription to DNA. In qPCR a fluorescent probe is added in the PCR reaction, when hybridizing (with the target piece of DNA) and cut by the polymerase ExoN and excited by some light the fluorescent tag emits some detectable light. An alternative is to use electrophoresis to obtain the amplification product, followed by sequencing.

@MikeyC That was the answer I was looking for: it that states the definitions in a systematic and unambiguous way. If it were an answer and not a comment, I would accept it.

FWIW, it seems like the field is coalescing around RT-PCR meaning reverse transcriptase and qPCR meaning real-time. RT-qPCR is the combination of the two. However, there are always going to be exceptions, so context is very important.

Real-time PCR is used to quantify a PCR target by measuring some indicator of target amplification in real time after each amplification cycle, thus it is sometimes(often) called quantitative PCR (qPCR). The key to distinguishing between reverse transcription PCR and real-time PCR in the context of a paper or protocol is to look at the starting material being used and the data output.
If the source material is RNA, it needs to be reverse-transcribed into cDNA before PCR amplification. And if they're showing quantification of a specific target, it's likely a real-time PCR of some sort. Quantification of a gene target from normal DNA is likely a standard real-time PCR (aka qPCR). Quantification of an RNA target (like gene expression from mRNA), is likely quantitative reverse transcription PCR (RT-qPCR). The same goes for if the starting material is cDNA (end product of an RNA reverse transcription reaction). Lastly, any mention of Ct or Cq values (or delta-Ct, or delta-delta-Ct) generally indicates a real-time quantitative methodology.
If they are citing the use of RT-PCR to simply confirm the presence or absence of a target (sometimes called endpoint PCR) or to amplify it for downstream applications like sequencing, with no mention of specific target quantification, it's likely a standard reverse-transcription PCR.
There are exceptions to some of these rules, but it should help get you through most literature with some idea of what methods are being used.
Edit: In the past few days, I've seen multiple papers using "RT-PCR" as shorthand (I guess) when they were talking about RT-qPCR or rRT-PCR. Like I said, always exceptions to the rule. But as long as you read the methods it should be simple enough to figure out.

Why was this downvoted? Is it incorrect?

An addition: real time PCR or qPCR requires a a dye which binds to dsDNA. This will give you readings of RFU (relative fluorescence units) per Cycle. In RT-qPCR the dye binds to the dsDNA from the conversion of ssRNA by RT.


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Autoimmunity - negative selection of T-cells - APC
Through negative selection of T-cell in the thymus T-cells lose the possibility to react to antigens which are "body own" -> self antigens.
Though there are more than just this negative selection for preventing T-cells recognizing own antigens some T-cell become self reacting.
This T-cell in our case cd4 T-cells can recognize antigens presented on MHC II complexes by APC cells.
And the question is:
Who presents the self-antigens to the wrong selected CD4 T-cell, which leads to autoimmunity? How does the APC cell get this self-antigen in the first place?

Welcome Croin!  Please add a little bit of detail to this question.  Tell us a few sentences explaining the facts you are presenting, then ask the question about those facts.  For example: In autoimmunity, a theory is that the wrong CD4 T cells...." etc and provide a reference so the person answering the question can look into your source of info for more insight.  That makes the question richer and you will get better answers!

I get your point, but I'm advising you on SE guidelines for higher quality questions.  This isn't like every other Q&A site. Asking a question isn't just for you, it's contributing to building a body of knowledge.  Also without a little more info, your question sounds like a quiz or homework question otherwise.

Actually I am going to vote moving this to BiologySE.  There is a fine line between Health and Bio on physiology/pathophysiology topics, and I think there are more molecular/cellular science specialists on the Bio side, and more clinical-/pathology oriented specialists on this side.  I would love if we had more people straddling both sites, as I think more discussion of difficult concepts in physiology would really enrich this site!

I do think the underlying question about the mechanism is good.  I don't remember enough from immuno in school to answer off the top of my head.  I gave you that advice because looking at it, I know that there are thought to be multiple mechanisms of autoimmunity, and you state that like it's the only one.  Hence the recommendation to provide a better description in the question body. I upvoted your question because it is a quality topic that I'd like to see be discussed, but gave you advice how to improve the quality of the question itself.

Since you already know that the repertoire of T cell receptors is developed in the thymus, the missing half of the story in the context of antigen-presenting cells is that MHC complexes do not discriminate between self, foreign and mutated self peptides. The take home point is that selection in the thymus is meant to produce a repertoire of T cells which can overcome this fact.
In all healthy tissues, nucleated cells express class I MHC molecules loaded with self-peptides. A T cell probably isn't going to respond to it, however, because trafficking of T cells into tissues requires signals such as cytokines and chemokines. The T cells circulate to and from the lymph node T cell zones.
In the context of inflammation and cellular injury, self proteins may be released into the extracellular space where they're regularly cleared by macrophages via endocytosis. The extrinsic antigen presentation pathway loads peptides onto class II MHC molecules. In this very context, T cells are trafficked into distressed tissues by activated endothelium, where they interact with tissue APCs. Autoreactive clones that escaped thymic selection have the opportunity, then, to react to self antigens, ignoring regulatory or suppressor cells (ref).
Not just self-peptides, however, but also potential self-antigen mimics that take well meaning T cells directed against bacterial peptides, which happen to closely resemble a self antigen, and pit them against your own tissues (example). Unlike autoimmune T cells that have escaped selection and attack your cells, this invites T cells that have gone through the proper channels to do so as well.
See Cellular and Molecular Immunology, 8th ed. for an even better overview of T cell-based autoimmunity.

So basically it goes like:
Injury -> self antigen in extracellular space -> Uptaken by Macrophages -> presented on MHC II -> so the presentation ONLY goes through Macrophages which endocytosed the antigen and presented it later on a MHC II receptor to cd4 T cells?


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Why do germs live longer on surfaces than on skin?
After looking up how long germs live for on surface, I came across lots of resources that explain how long germs live on different surfaces.
A common pattern is that germs survive longer on cold/hard surfaces than on skin.
Why is that?
Wouldn't skin be a much more hospitable environment than something like a desk?

I'm pretty sure that will vary a lot from a surface to another. Can you please develop stating what surface you are talking about and also linked to your sources.

Not only will it vary from surface to surface, but will vary with microorganisms as well. I think this is too broad. If you can narrow it down to one microorganism, or provide your source, this might be better.

Some of the permanent microbial flora inhabiting the skin protects the host from other pathogens. The complex host– microbe and microbe–microbe interactions that exist on the surface of human skin illustrate that the microbiota have a beneficial role, much like that of the gut microflora. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2746716/
It is apparent that just as host immunological factors and behaviors shape the composition of these communities, microbes present on the skin greatly impact the functions of human immunity. Thus, today the skin immune system should be considered a collective mixture of elements from the host and microbes acting in a mutualistic relationship. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4219649/
Eccrine sweat glands secrete water to the surface of the skin. The water also contains salt and electrolytes which work to acidify the skin. This makes the skin a cool, dry, and slightly acidic barrier.
Furthermore, eccrine sweat glands constitutively express several antimicrobial peptides (AMPs), including cathelicidin and β-defensins. - https://www.ncbi.nlm.nih.gov/pubmed/16374474
Together, these factors are the reason why a desk would be more hospitable for some microbes

because some skin cells which are alive , secret fat and other materials , these materials make the skin acidic , and acidic environment is not good for many germs , on the other hand , there is an enzyme in  sweat (lysozyme)which destroy the wall of bacteria

Source, please?

My explanation is partly mentioned in ,junqueira basic histology , chapter skin , part protection and sweat glands , but the whole explanation exists in a book which was taugt in my college and that is not a reference book, unfortunately.

You might be an ESL (so am I) but please note that in english (and in most other language using the lating alphabeth), sentences start with a capitalize letter and end with a dot. Comas are not preceded by a space and closing parenthesis are followed by a space. Don't forget to conjugate your verbs (destroy). I think you meant secrete and not secret.  we dont write like dis on StackExchange. The term germ is never use in Biology. I suppose you meant pathogens.

Ok, thanks for your attention. I will be more careful next time.

@Remi.b I'm only linking this because of your use of the word "never", and the fact that it has 1500 citations. I do agree though, that I don't like the word "germ".

@Bob You're right. I should have said rarely. Germ is quite informal.

@minasi Btw, if english is not your mother tongue, I'd be curious what language actually puts spaces before commas.

@Remi.b, as far as I remember there was a rule for this site which told us we can not use abbreviations in our texts just like btw.

@Remi.b, no language puts space bofore commas. I told you it was all my mistake and this is because I focused on concept of my sentence.


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Why are canines not nauseated by similar foodstuffs/state of decay as human beings?
I am continually surprised at the items my pet dog is willing to ingest.
I understand part of the consumption is driven by nutritional instincts (licking salty liquids such as sweat) or nurturing instincts (eating baby faeces to prevent predators) but why does an animal with a sense of smell many thousands of times greater than our own not become nauseated by the same substances, smells or conditions that humans do?

Sweat
Faeces
Decayed foodstuffs
Assorted garbage
Untreated and/or dirty water

I have known my dog to bury a piece of rotting pork only to dig it up several months later for consumption.
In addition I watched dogs refuse to eat certain items (spicy meat etc) until their owner makes a move to take it back at which point the animal will swallow the item causing a gag, hacking couch or nasal clearance.
Is there a biological mechanism that suppresses the gag reflex in canines, is the need to consume overpowering their distaste or do they simply not find such substances unpalatable?

Your dog finds these things palatable, I assure you, and no gag-reflex suppression is needed.
I had a dog that would steal duck eggs from my flock, bury them all over the place, and dig them up when properly rotted to enjoy as a treat, and no, I'm not making this up. I saw her do it, ran across many buried duck eggs while gardening, and could immediately smell when she was enjoying one.
All that to say what smells good to a dog has nothing to do with what is acceptable to you. Many of your "dislikes" are conditioned: living in a society where cleanliness is valued and clean water is available, humans in such societies can afford to snub their noses at less sanitized things.
Manure may well elicit a completely different reaction to a farmer, who saves it carefully before spreading it on his fields to enrich the soil. To him, it might be the smell of a good crop next summer.
Many species exhibit corprophagia. It's not known why dogs (some, far from all) do this. Rabbits, for instance, eat their own feces after their first movement of the day. This is normal and nutritional for them.
Eating the feces of other species, particularly herbivores, is common among dogs and isn’t considered abnormal, just undesirable. My (same) dog followed my goats around like they were Pez dispensers. Since dogs can't digest cellulose, they get some of the advantage of eating plants this way.
Capybara, rabbits, hamsters and other related species do not have a complex ruminant digestive system. Instead they extract more nutrition from grass by giving their food a second pass through the gut. Soft fecal pellets of partially digested food are excreted and generally consumed immediately. Consuming these cecotropes is important for adequate nutritional intake of Vitamin B12. They also produce normal droppings, which are not eaten.
Young elephants, pandas, koalas, and hippos eat the feces of their mother to obtain the bacteria required to properly digest vegetation found on the savanna and in the jungle. When they are born, their intestines do not contain these bacteria (they are completely sterile). Without them, they would be unable to obtain any nutritional value from plants.
Eating garbage and human feces is thought to be one function of dogs during their early domestication, some 12,000 to 15,000 years ago. They served as our first waste management workers, helping to keep the areas around human settlements clean. A study of village dogs in Zimbabwe revealed that feces made up about 25% of the dogs’ overall diet, with human feces making up a large part of that percentage.
Coprophagia
Daily rhythms of food intake and feces reingestion in the degu, an herbivorous Chilean rodent: optimizing digestion through coprophagy
Coprophagia as seen in Thoroughbred Foals


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What actually happens to the human body during fasting/starvation?
I recently came across a UN study which advocated that controlled fasting can be beneficial for the the human body and I am fascinated by stories of wilderness survival against the odds.
It piqued my interest to ask; what exactly happens to a human body during fasting and ultimately starvation?
I understand that there is a period of glycogen use/exhaustion and functioning becomes impaired but what medically happens to the human body (organs, muscles, protein, body fat, cognitive processes etc) and over what timeline (24 hours to death).  I read that halitosis is an interesting side-effect etc.
Assume the human body has ample access to water and can avoid dehydration.

Have you read this?

I have now - it raises a few more questions though;  how long after running out of glycogen does the body wait before using adipose tissue?  Does it burn adipose as long as it exists or does it dual-use muscular fuel as well?

Please [edit] your post and update it with your current question.

This is a very broad question, there are tons of literature on how the human body adapts to fasting in various ways. Please be more specific.

Actually, the body goes into the fasting state about eight hours or so after the last meal, usually when the guy finishes absorbing nutrients from the food.
Normally, body glucose, which is stored in your liver and muscles, is your main source of energy. When in a fasting state, your body uses up the glucose that you have stored to provide energy. If you are still fasting after this store is used up, your body will start to burn fat to create energy, therefore leading to weight loss.
After fasting for a few days, there will be a higher level of endorphin in your blood which will cause you to be more alert and, weirdly, giving you a feeling of mental well being.
Eventually, if you are starved for too long, your body will start to break down muscle protein in order to create energy (that is why, during WWII, most POW's held by the Japanese were very thin - they were starved and in order to survive, their bodies had to 'eat' their own muscle)
Technically, starvation is when your body starts to eat your protein, i.e. Muscle.During starvation, your body will thin out, because your fat has been burned and your muscle is being 'eaten'. This obviously leads to weakness.
When your fat is being burned, you go through a detoxification process which is caused because any toxins stored in your body's fat are dissolved and removed from the body.
Your kidneys are very efficient in being able to maintain the body's water and salts, like potassium and sodium. But these can be lost through perspiration.
This eventually leads to dehydration which does many things to your body, like: not allowing for your body to regulate body temperature; your heart works harder (most of your water is in your blood (about %$60$) and when you lose the water, your heart has to 'catch' up and pump more to keep the blood flowing and cooling you down - now, your heart is working harder which could give you a greater risk of heat exhaustion); you can feel cranky, drowsy, confused, forgetful.
These are a lot of things that happen when your body is deprived of what it needs in terms of food and liquid.
This is what happens, and this is very general, when your body is in its starvation mode. I am sure that there are many more things, but I could only give a brief answer.

Please edit your answer, you have been misled about the detoxification. There is no scientific evidence that what you describe happens during a fast. See https://en.wikipedia.org/wiki/Detoxification_%28alternative_medicine%29 or http://skepdic.com/detox.html . Thank you.

Some people believe that muscle loss happen early when fasting. But like you rightly pointed out, it doesn't happen until the body fat is gone. This web page supports this: https://www.dietdoctor.com/does-fasting-burn-muscle. A comparison between day 42 and day 70, in Table 2, shows this clearly..

The only reason for muscle-loss during a long fast, or during many consecutive fasts, would be that weakness due to lack of energy, or at least willpower, prevents too much muscle exertion, leading to  loss of muscle strength and mass.


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Why do neutrophils have segmented nuclei?
To clarify, I'm not asking what causes high segmentation in neutrophils. I'm asking how segmented nuclei function in a regular neutrophil cell.


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What is the purpose of ultrahydrophobicity in lotus flower leaves?
I read about the lotus effect on wikipedia, but I haven't found an explanation as to why droplets collecting dirt on the surface of a leaf is helpful to the flower's survival.

Lotus benefits from hydrophobicity for that it decreases the likeliness of being infected by pathogens (found in "dirt") and increase the ability to perform photosynthesis.
According to a study by Darmanin and Guittard, the plants (not only lotus) with ultraphobicity benefits from these structure for :

self cleaning

and

these structures are able to stabilize the presence of air underwater and be submerged for several weeks

Let's talk a little about the second part : having a good access to gas is vital for plants to do photosynthesis. In an environment which is very wet (like the one the lotus lives in), it is better to be dry to maximise air/plant surface area.
Now, about the self cleaning.
First, lotus lives in backwater or muddy environment
In this study by W. Barthlott and C. Neinhuis, it is said that big particles can occlude stomas, the small "holes" that allows the plant to breath.
Wet environment is ideal for bacterial/fungal growth and different kind of disease. Unclean water could also block light and make photosynthesis less efficient.

Again, wettability
  is important for the adhesion of microorganisms to
  leaf surfaces. In addition, on waterrepellent
  surfaces, spores and conidia are deprived of the water necessary for germination. Therefore, the epicuticular
  wax crystalloids and their physical properties
  may be regarded as the first line of defense against
  pathogens.


text:
The Assumption of Weak Selection?
I was reading this question and I failed to fully understand the introductory part of it.
The OP (@Artem Kaznatcheev) says:

Most analytic models like to assume weak selection because it allows the authors to Taylor expand the selection function and linearize it by dropping terms that are higher order in the stength of selection.

I don't fully understand it. Can you help me making sense of why assuming weak selection allows one to Taylor expand the selection function. I am hoping someone would answer by presenting a mathematical model that at first does not assume weak selection and show why assuming weak selection allows the use of a Taylor series to linearize the function. I'd like to understand which terms fall down and which terms left with this assumption.

This is my take in this, without experience of using the Taylor series to analyse evolutionary game theory problems.
As you know the Taylor series expansion of $f(x)$ at point $a$ can be written as:
$f(x)= f'(a)(x-a) + \frac{f''(a)}{2!}(x-a)^2 + \frac{f^{(3)}(a)}{3!}(x-a)^3 + ... + \frac{f^{(n)}(a)}{n!}(x-a)^n + ...$
Often factors above second order are dropped as a simplification. However, to use the Taylor expansion, the function must be differentiable at point $a$, and to be differentiable it must be continuous.
As @Artem Kaznatcheev writes in his question, "...with weak selection meaning the game modifies overall fitness only slightly..." and "... it is typical to model organisms as having a base fitness that is modified slightly by the game interaction...". These statements imply that the overall fitness function/surface can be assumed to be relatively smooth and continuous (i.e. the payoff is negligible), which means that the Taylor series expansion can be used. If the game payoffs for a single game would determine a large proportion of the overall fitness, the fitness surface would be discontinuous.
An example where a Taylor series expansion is used to simplify the fitness function under weak selection is given in Andre & Godelle (2006) (see equation 20 ff).
You might also find this supplement to Nowak et al (2010) interesting (a rather controversial paper), especially page 8.

thank you! I know what is a Taylor expansion and understand how it can be used to drop polynomials of higher degree in order linearize a function. But I still don't understand what function we linearize and why it is useful to do so. I haven't read your links yet though! For example, I would love having a mathematical model that gets much more easier to interpret or to solve using the assumption of weak selection. So that I can see what function is linearized and for what purpose. I'll have a look to the links, thank you.

@Remi.b It's the fitness function that is Taylor expanded, and how the fitness function is defined naturally depends on the game being modelled. There are a lot of papers out there, but I've included one example now (haven't checked it closely though). Overall, this is a quite technical body of litterature.

I think at @fileunderwater provides a good explanation of the basics math behind it, and some good references. I would like to go more into detail about the modeling decisions and benefits of assuming weak selection and why it is done in the literature.
When you are making evolutionary models, especially one in evolutionary game theory, the first place is to start with a differential equations model of inviscid populations (this usually means that you assume very large population size). These models often result in dynamics of the form $\dot{x}_i = x_if_i(\vec{x})$ where $f_i$ is a non-linear function corresponding to the relative fitness but where the non-linearity depends on the strength of selection. Making a weak-selection argument, often allows you to come close to linearizing $f_i$ using Taylor expansion. This reducese your equations to a form like $\frac{dx_i}{dt} = x_i(\vec{c}_i^T\vec{x} - \phi)$ where $\phi$ is an average fitness. Although the transients of this dynamic are still complicated, the equilibrium is usually relatively easy to analyze and reduces to looking at the matrix $C = [\vec{c}_i^T]_{1 \leq i \leq n}$ with its columns given by your linearization of the $f_i$s.
Of course, this is only a first step, and the current trend in the literature is to move to a setting where you have spatial structure. Here, weak selection gives you a further bonus because you can use it to separate the timescales of local (dominated by the constant term) and global (dominated by first-order in $w$ -- the selection strength) network dynamics. This allows you to use the powerful pair-approximation technique. A great example of its use is Ohtsuki & Nowak's (2006) solution to the evolutionary dynamics of games on $k$-regular random graphs (you can find a brief overview here).
The final settings where this is useful is for studying the interaction of mutation and selection in finite populations. In this case, weak selection allows you to look at the selective force as a small perturbation of the mutator-balanced steady state. In the setting of EGT this rquires you to define some new solution concepts for what it means for one strategy to be "better" than another but then some interesting connections (see Antal, Nowak, & Traulsen (2009) for more) and very general analysis of the mutation-selection equilibrium can be done (Antal et al., 2009).


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Effect on fitness of mutations
What is the distribution/probability density function (PDF) of impacts on fitness of new mutations?

I very welcome any partial answer that does not give the whole PDF but just some information about the expected value or the variance of this distribution. Information of the kind: "If we consider only beneficial mutations, then the PDF is $P(X=x) = f(x)$" are also welcome.
When I say mutations, one might have want to reduce the concept of mutations only to indels and point mutations.
Of course the answer will depend on the species under consideration and from population to population but I welcome any answer that could give some insights. Eventually, some information according to what is generally assumed to be the PDF of effects on fitness of new mutations might be useful.
Here is a related question
Here is an article that assumes an exponential distribution of effects on fitness of beneficial mutations.

the PDF should be a conditional one.

also your question is quite broad and needs rational modeling for a reasonably accurate answer.

@WYSIWYG The PDF should be conditional on what? On the species. Yes obviously. But any information would be welcome. I re-edited my question to make clear what I understand by mutation. I don't feel my question is too broad. Please let me know if you can think of a way of how I could narrow down my question.

you can narrow down by perhaps assuming a hypothetical statistical model

To a good first approximation $\overline{\Delta f} = 0$. Where $\overline{\Delta f}$ is the mean change in fitness down to any point or indel mutation. The reasons for this are as follows:

In the genome of higher organisms, most of the genome is non-functional ("junk") so most mutations will not have any effect regardless of the change made.
A substantial proportion of in-frame point mutations will be synonymous mutations that result in the same amino acid being coded for (actually this can have an effect on protein expression but I don't believe anyone has - yet - shown a fitness difference?)
Even where a mutation does alter an amino acid many amino acid changes have no measurable effect on the protein produced. Especially where the new amino acid has similar properties to the one it has replaced.
Even when a mutation does alter the protein function, or render the product non-functional, in many cases this will not impact fitness since fitness is conditional on the environment in which it is measured and not all genes impact all environments.

So the distribution, whatever it is, will have a large spike at 0. Probably this spike is several orders of magnitude higher than the next highest value. Further, we can be reasonably certain that $\overline{\Delta f} < 0$ since there are more possible ways to break a Gene through a point or indel mutation than there are to improve it. If this is the case, so that there is a large excess of mutations with a negative effect on fitness, we can conclude that the distribution of mutational changes in fitness will be non-normal (negative skew and spike at zero), and that the normal distribution will be a poor approximation.

I like your reasoning, but dont understand what you mean with the last sentence.

Reminds me of Pareto optimization. But effect of each mutation on a gene still has to be sampled.

@fileunderwater: If it's left skewed and has a central spike at an exact value it therefore will be poorly approximated by any take on the normal distribution.

@JackAidley Gotcha. Suggested clarification.

Take a look at this paper. This talks of a concept similar to Jack Aidley's approach.

[This is purely speculative]
Assumptions:

impact on fitness is measured by survival chance
impact is because of protein coding genes

Probability of a mutation at position $i$
$P(m=i\ |\ g)$
where $g$ is the genome with its annotations.
Probability that activity of some protein changes by X-fold given mutation at $i^{th}$  position(s) in the genome:
$\sum\limits_{i}\sum\limits_{gene} P(a_{gene}= X\ |\ m=i)$
sum over all genes that occupy that locus.
Probability that on a given selection pressure $S$ and protein activity change $X$, the individual survives the selection.
$\sum\limits_{i}\sum\limits_{gene}P(1\ |\ a_{gene}=X,S)$
I am not an expert at Bayesian modeling. But I guess this is one way to go about obtaining the PDF. Each step has to be expanded and combined to get an equation for PDF.
I am not sure if this is of any help at all.

Thanks a lot for your answer. While it is probably interesting I have to confess that I don't understand everything. I don't really understand why defining a locus as a long enough sequence so that it occupies several genes. I don't think it really addresses the question. If $S$ is the random variable of effect that a mutation has, I am asking about the distribution of $S$: $P(S=s)$. Or as you stated, that might under some assumptions, correspond to $P(a_{gene} = x | m=i)$ but there is no need to sum over all mutations in the genome. I am not asking about the effect of the sum of all mutations

I don't think a purely theoretical model might give much insights (or only a model considering the complex network of protein interactions) but I could be wrong.

By several genes I meant splice variants that occupy the same genomic locus. Only by considering all the positions in the genome will we be able to obtain a PDF. And in this case the effect of a mutation is denoted by the random variable $X$, whereas $S$ is the exerted selection pressure.
I totally agree that a purely theoretical model wont give much insights. In this case the prior probabilities have to be calculated from experimental observations. But with a model we can make better predictions.


text:
Backcrossing in Hybrid
Can anyone help me in understanding how backcrossing helps hybrid to achieve pureline?
I have been looking into the references i possess but couldn't seem to find anything

Back crossing is the process by which a hybrid organism is crossed back (backcrossed) into a pure organism. Let's see an example

Organism 1 is heterozygous for a single gene (e.g. a hybrid), which has alleles that we can call $A$ and $a$. We can write that organism's genotype.
Organism 1 Genotype: $Aa$  (100% chance)
Right now, there is a 0% chance that organism 1's genotype is $AA$.
Goal: increase probability that organism 1's genotype is $AA$

One way to achieve this goal is to cross Organism 1 with another organism, let's call it Organsm 2, that is has a homozygous (e.g pure) genotype of $AA$.
So if Organism 1 is crossed with Organism 2 and produces a new Organism 3 what is its genotype? Well, we're not sure.
Organism 3 Genotype: $AA$  (50% chance)
Organism 3 Genotype: $Aa$  (50% chance)
Now we do the same thing again, to get Organism 4
Organism 4 Genotype: $AA$ (75% chance)
Organism 4 Genotype: $Aa$ (25% chance).
This effect keeps compounding, until there is a very high chance that the final organism has a pure (e.g. $AA$) genotype.


text:
Why is the rough ER necessary to make extracellular proteins?
It is my current understanding that free ribosomes synthesise proteins to be used inside the cell, and the rough endoplasmic reticulum is necessary to make proteins that are to be secreted by the cell. Is this correct - and more importantly, if so, why?

Please do some research before posting questions and demonstrate that you have done so in your question. This is basic material that can be found online and in standard biochemistry textbooks.

While the default textbook will likely cover co-translational transfer of nascent proteins into the ER (which topologically corresponds to the outside of cells), there are also other mechanisms that apply to some proteins and don't necessitate rough ER ( https://en.wikipedia.org/wiki/Exosome_(vesicle) )

Ahhh I did search for a while and found nothing (in terminology could comprehend anyway) and don't own a biochemistry textbook as I am not doing a biochemistry course

Cell Biology books also cover this. You need to buy books if you are studying. Sacrifice other things, but buy books. However you could have answered this question on the web using NCBI Bookshelf, which has older editions of some excellent texts, including Berg et al. Biochemistry, Alberts et al. Molecular Biology of the Cell, and Lodish et al. Molecular Cell Biology.  Searching for Endoplasmic Reticulum brings up a list, which includes these three books, which you can then consult. Learn to save your own life.

I did research the question online beforehand - however perhaps the wording of my question brought up other results? I could find nothing that would help me when I searched. In the future, I will use that website as I've used it a couple of times (when it came up after a search) and it was very helpful

Extracellular proteins are proteins that function outside the cell, meaning they are made in cells (transcribed from ribosomes) and then are transported to the plasma membrane to be delivered to the extracellular space. The proteins that need to be secreted aren't secreted as free proteins, rather they are packaged into vesicles. Vesicles are membrane-enclosed structures. When ribosomes are translating mRNA and come across a specific sequence called a signal peptide (wiki), the ribosome goes to the ER and delivers the peptide into the ER. From here, the peptide gets packaged into a vesicle-- first a membrane budding off from the ER.
 source(NCBI)
This is also how secretory proteins get into the Golgi, by vesicle trafficking. From the golgi, proteins are packaged into vesicles. It is a hotly debated topic whether proteins are sorted into specific vesicles or proteins within vesicles (that do not belong in that vesicle) are sorted away (and degraded by the lysosome).


text:
Specific primer design
I'm designing primers for species-specific amplification (inside ITS1-ITS2 region). The problem is that when I blast (GenBank) my primer pair, the Forward primer anneals with some isolates (of the same fungus species that i'm targeting) that have one base polymorfism:
Ex:
Predicted Tm= 58-61ºC
product length = 189
Forward primer  1    TTCATCTCCGACTCGCATGT  20
Template        130  ........G...........  149
Reverse primer  1    GAATACCAAGGAGCACAAGGT  21
Template        318  .....................  298
My goal is to amplify only the 100% specific sequences. Would a higher annealing TºC be able to prevent this unspecific binding?
Question 2: The fungus species i'm targeting have isolates with a diversity of polymorfisms (deletions, insertions, one nucleotide substitution,..) and sometimes the predicted amplicon lenght may vary: 189bp, 190bp, 191bp. Will it be problematic for a RT-PCR quantification assay?
Thanks in advance

If your primers are not specific enough, you should design other primers. Try shifting a few bases upstream or downstream. Also, you can add a few extra bases to your primer, you can safely reach 68C as annealing temperature.
If you want your PCR to be able to distinguish a single base mismatch, then the mismatch should occur at the 3' of your primers, ideally one of the three last bases.
If your goal is just to quantify the initial DNA, then RT-PCR will be ok. But if you want to detect the composition of the different polymorphisms, then you should go for sequencing.

Q1: You need to provide more information. How much sequence identity is shared between your target and off-target? What is the purpose of your primers?
Generally, yes a higher annealing temperature would minimise mismatches - you could try a drop-down in T_a for increased specificity during the first few rounds of amplification.
Q2: I doubt it. The difference of 1-2bp is so small that it is highly unlikely to introduce bias.


text:
Why are humans so variable in appearance
Most animals look almost identical to their peers. To distinguish lions we record the spots on their face; with whales we look at the blemishes on their tail or flukes. In other words, we have to try hard to distinguish one lion from another.
In the case of dogs, we have created many different looking breeds - but within each breed they look the same: one poodle looks very much like the next one.
On the other hand, with humans we have not only the different races (cf. dog breeds), but even within one race no two people are alike. And, not only are the faces different, the body shapes vary equally much. We use face and body shape (and voice) to recognise each other. Most other animals use smell or sound.
I thought the reason for our uniqueness might be that, with civilisation, we are not constrained us to look the same. However, even in hunter-gatherer tribes each person looks different from every other one.
So what is it in human evolution that made us unique in this regard? And, are we unique? I cannot think of any other species with as much variation as ours, but are there others?

This really isn't the case.  Humans do look pretty much alike.  Take for instance blonde Hollywood actresses: most are perfectly interchangable, and their male counterparts only marginally less so.  You only think humans look different because you have long practice (mostly unconscious) in recognizing the small differences between them.  Apply the same effort to studying e.g. dogs, and you will likewise begin to recognize the differences.

Because we as humans are really really good at picking up small differences in humans and really really bad at detecting them in anything else.
Animals are often quite good at telling each other apart, far better than humans are, birds in particular are known for this. Just because you as a human are bad at it does not mean they are.
There is a pretty strong evolutionary pressure for humans to be able to tell other humans apart and not much of an advantage for being able to tell two lions apart. We need to be able to tell mates, rivals, relatives, and strangers apart easily. We don't need to differentiating one black bird from another.
We also spend a lot of time around other humans, so we are more familiar with their differences, but the same thing happens to animal researchers whale researchers who spend a lot of time around whales can easily tell two whales apart at a glance. this is also part of the reason some people have trouble telling individuals from a different "race" apart, they are to unfamiliar and uninterested to spot differences. Or the way a car guy can spot the difference between two models at a diffrence but someone else might not.
You see the same effect chimps can tell each other apart but can't tell humans apart, unless they spend a lot of time around humans then they can. They can also match voice to face meaning the can recognize both.
Then of course you have the fact you are focusing on vision, try to tell two people apart by smell and you will likely fail but a dog will have no problem with it. likewise many monogamous song birds can identify their mates from song along, just as we recognize others by voice, penguins are another example. Humans are very visual creatures so much of our identification ability relies on vision we see the same thing in other visual species, animals tend to use whichever sense are their dominant ones. Saying organisms are more visually similar because organisms with far worse vision than humans can't tell them apart by vision alone is simply an unreasonable conclusion.

I wouldn't say that humans are inherently bad at recognizing those small differences in other species, it's just that most don't invest the amount of effort needed to learn to recognize them - a learning we do unconsciously by growing up among humans.  But if you grow up on a dairy farm, for instance, you learn to recognize cows as individuals.

We are generally worse at recognizing difference in other species mostly by comparison because of how good we are at each other, there is an entire aspect of our neural processing keyed to notice things about faces.

I didn't say animals can't recognise each other; I said they use smell and sound, whereas we use vision. Is that the main reason for our variability?
I take your point about chimps. But, do they use vision or smell? Ignoring faces, what about body shape - is there an animal species with long/short, thin/fat, muscular/flabby individuals? But I suppose evolution will rule that out in other animals

@hdhondt if you had read the linked paper you wild see they are suing vision,, in fact the same portion of the visual cortex we use, size and robustness variation is quite common in animals it is by no means unique to humans. You are assuming a lack of variation that just isn't there.

@John: Maybe your neural pattern recognition circuitry only recognizes faces; mine seems to work differently.  But how is it determined that this is innate, and not simply a matter of practice training a general-purpose pattern recognition circuitry?  Because those who have sufficient practice can make the same sort of distinctions among animals, or inanimate objects.

@John that article only says they have a built-in "face filter" like us. The chimps were asked to "select the faces of unknown apes from other objects". That is not the same as proving they use vision to recognise each other. They may do so, but the article does not state that.

except there is no reason to evolve face recognition unless you are using it for identification, and I was refering to the pubmed paper not the nature one , this one.. https://www.ncbi.nlm.nih.gov/pubmed/18085867

@jamesqf If you want to ask this as a separate question I would be more than happy to go into it, there are well documented brain injuries that impair the ability to recognize faces without impairing the ability to recognize objects and vice versa, the fact one can be damaged without affecting the other means they are separate. The condition is called Prosopagnosia.

For those familiar with prosopagnosia, which results from damage to the fusiform face area (at the fusiform gyrus), one ought to also be familiar with the area not being exclusive for facial recognition (perhaps only initially in development) but that it is also recruited for visually discerning things that we spend time on: xray images in radiologists, chess positions in grandmasters, dog faces in dog breeders, recognizing shapes related to playing music on instruments in musicians, cars and birds in enthusiasts, etc!


text:
Pasteurisation of orange juice and Vitamin C
In the UK at present, one of the examination boards has set a "controlled assessment" (an experiment that pupils do at school under exam conditions) that involves testing a hypothesis that vitamin C is removed from fruit juice by heating it (i.e. in the pasteurisation process).
I am massively skeptical about this. The teacher guidance suggests "Treating fresh orange juice in boiling water for between 10 and 30 mins gives an easily measurable decrease in vitamin C levels". Leaving aside that this hardly represents a simulation of the pasteurisation process(!), does anybody know of any solid, academic studies of the effect of pasteurisation on the vitamin C content of fruit juice? I have tried (as a scientist, but non-biologist) my usual routes to reliable information and they fail miserably - the www is full of crackpots on this one.
As a follow-up to that, is it not the case anyway that the oxidation of the orange juice when it is boiled in this experiment, plus simple exposure to light could also be responsible for any decrease in vitamin C observed?

Orange juice is pasteurized!? That's unheard of (for me, at least).

Hodgins AM, Mittal GS, Griffiths MW. 2002. Pasteurization of Fresh Orange Juice Using Low-Energy Pulsed Electrical Field. J Food Sci 67(6):2294-2299
This is a study of non-thermal food preservation, but it cites two studies that measured ascorbate loss from pasteurisation. I can't cite the studies directly because I can't find them online. According to these authors, they reported losses of 7.0-15.0% and 18.0% after 95°C for 15s. This is high compared to the pulsed electrical field method.

Yeom HW, Streaker CB, Zhang QW, Min DB. 2000. Effects of Pulsed Electric Fields on the Quality of Orange Juice and Comparison with Heat Pasteurization. J Agric Food Chem 48(10):4597-4605
This study compared ascorbate loss during storage after PEF or thermal treatment. While no difference was observed when stored at 22°C, PEF treated orange juice maintained significantly higher ascorbate concentration than thermally treated orange juice when stored at 4°C. The authors attribute this to the "higher processing temperature".

They also say (and reference other studies):

Ascorbic acid is a typically heat sensitive nutrient. High temperatures during processing and storage cause loss of ascorbic acid.

Thanks for this. The comment at the end is a bit puzzling. Table 3 appears to show that even pasteurisation at temperatures higher than normal (95 vs 72) does not decrease the vitamin C content by more than 20%. I am going to follow this up on Chemistry SE and see if I can find out what is going on.

@RobJeffries Does 20% hold some special significance?

No, I was just rounding up 18% from Table 3. I suppose if I was writing the paper I would argue this demonstrates that it is not especially heat sensitive. I also see from the graph that there is very little difference (none at 22C) between the Heat and PEF curves until you get beyond 40 days storage. So whilst the storage temperature seems important, the processing bit seems much less so.


text:
Book on current state of knowledge on the genetics of intelligence
I'm looking for a book that gives a good summation of the current state of knowledge on the genetics underlying intelligence.
I have read textbooks on human population genetics but I'm looking for something more specific.
I'd be happy for pointers to any books on neuroscience, developmental psychology, genetics that give some coverage to this topic.
I am not really looking for a popular science book.

Are you more interested in population and evolutionary genetics of intelligence or more on the molecular genetics of intelligence?

I believe that all of these aspects are pertinent, but I am probably more interested in research that point to molecular genetics and neurophysiology.

If it doesn't have to be a book, but could also be an extended review article, one possibilities would be: Toga et Thompson, 2005 ( http://www.annualreviews.org/doi/abs/10.1146/annurev.neuro.28.061604.135655 ) or Deary 2012 ( http://www.annualreviews.org/doi/abs/10.1146/annurev-psych-120710-100353?journalCode=psych)

Yeah, sure. Add those as an answer.

For current overview-like texts of diverse research topics the "Annual Review" series provides a good oversight:
Toga et Thompson, Annual Review of Neuroscience, 2005: GENETICS OF BRAIN STRUCTURE AND INTELLIGENCE
Deary, Annual Review of Psychology, 2012: Intelligence
For a very recent (and good) primary research study, - that will thus within its introductory paragraphs contain one very concise summary of the most current state of the field - one recommendation would be:
Sniekers, Nature Genetics, 2017: Genome-wide association meta-analysis of 78,308 individuals identifies new loci and genes influencing human intelligence

Thanks for that info that's exactly the kind of thing that I was looking for.

A very recent review has been written on this. See
Plomin, von Stumm (2018): The new genetics of intelligence.
For some of the latest genome-wide association studies, see:
Hill, et al (2017): A combined analysis of genetically correlated traits identifies 187 loci and a role for neurogenesis and myelination in intelligence.
Savage, et al (2017): GWAS meta-analysis (N=279,930) identifies new genes and functional links to intelligence.
However, as Robert Plomin and Sophie von Stumm report, newer genome-wide association studies are on the way which account for a larger portion of the variance. So there is constant progress at the moment.
If you're interested in the neuroscience aspect of intelligence, I recommend Richard Haier's book The Neuroscience of Intelligence.


text:
Identify this thin and strangely-shaped dragonfly, and understand why the shape looks so weird
I took these photos around noon in mid August in Hsinchu county Taiwan. I've seen many dragonfly varieties but I've never seen anything like this before.
Its body is about 5 cm long and very thin compared to the ones shown in the related questions below. The midsection looks strangely shaped to me, as if it is bent upwards in the back and suddenly ends, and a very thin "tail section" was then added below it.

This dragonfly damselfly is from the species Pseudocopera ciliata. Dragon fly anatomy changes between species and there is not definitive answer for why it looks like that, the best guess i can give is that it may assist the female as she tries to find the hookup point for mating.
General Information
More Information(Pay-wall)
This is in Chinese but confirms presence in Taiwan: http://gaga.biodiv.tw/new23/s3-37.htm

Thank you for that. :)

I added an image that addresses the peculiar shape, feel free to change it. Thank you for the very speedy species identification!

Fantastic, thank you for that. I have been to Taiwan and I think it is a very beautiful place. No worries.

If you can say something about the "...and understand why the shape looks so weird?" part of the question that would be great.

Sure, I did some research and tried my best (check the answer). Remember to click the tick, approving them definitivel answers :)

yep, I've accepted several thousand answers across multipe SE sites, I usually give it at least a few days for comments and additional answers to accumulate.

No worries, I'm new.

I've added a supplemental answer

Thanks to @Andrew's answer for identifying the genus and species, but there's an important point to be made.
I showed this page to a friend and they immediately said "Oh, that's not a dragonfly!!"
It is not a dragonfly, it's a damselfly!

...why the shape looks so weird?

While this doesn't explain exactly why it looks so "weird", it does explain why it would look weird if it were thought to be a dragonfly!
There are four ways to identify the difference between the two. The categories are

Eyes: relative sizes and distance between them
Body shape
Wing shape
Position of the Wings at Rest

For more see:

Reconnect with Nature: What's the difference; Dragonfly vs. Damselfly
Treehugger: How to Tell the Difference Between a Dragonfly and a Damselfly
Damselfly Insects – Are Damselflies And Dragonflies The Same Thing?
US Fish and Wildlife Service Facebook: Dragonfly vs. Damselfly Guide

And these two excellent videos:

All About Dragonflies and Damselflies
The difference between a dragonfly and a damselfly

Example of a Damselfly, cropped from Ischnura heterosticta: Female common bluetail damselfly. Taken in Swifts Creek, Victoria:


text:
Term for a prey animal's recognition that something potentially threatening is looking at it?
On my daily walks I frequently see individual or small groups of cattle egrets. At first I would try to photograph them but they would fly away. This vexed me because they ignored everyone else walking by as well as bicycles or loud vehicles in areas where there were roads.
I took it personally until I realized it wasn't me or my clothes, but the act of looking at them and taking an interest in them that spooked them.
This even happened at distances approaching 100 meters in open spaces, so I am not sure they could resolve my eyes and determine if my gaze was fixed on them. However, a few non-scientific tests suggested that they seemed to get nervous when I turned my head and looked at them, even though I kept moving. But even if I didn't look at them but instead continued to look forward, simply stopping and standing in place to take out my phone to snap a photo was enough to trigger them to fly away.
Question: Is there a term for this phenomenon in birds or other animals, not the flying away or fleeing part, but the recognition that something or someone potentially threatening is looking at them and/or may have taken an interest in them? Are there separate terms for responses to motion and responses to a gaze based on eyes or perceived face orientation?
Note: I have noticed a similar phenomenon with Malayan Night Herons as shown in What kind of big bird is this seen walking around Taipei? The individuals I see are more acclimated to people, but I still have to act at least disinterested when photographing them.

I have heard this from a professional bird photographer. As I remember she only looked at birds through the camera viewfinder  when ever feasible.

I have noted this phenomenon as well, exactly as you describe, with the Great Blue Herons in my area (and, notably, only with them.) It seems to derive from a combination of variation in gate and gaze, as the herons are perfectly content to ignore me standing or walking or running, but go into an alert posture whenever I alter speed or turn to look at them. However, a steady gaze does not perturb them, even at close range. As you say, acting indifferent is key, but this can be done, with practice, with one's face in any orientation.

@kheironiscus Thanks for your feedback! Based on this I'll do some more "experimentation".

"Gaze" is the typical term for the direction something is looking, including head/neck and eye position. Gaze detection, gaze following, and gaze perception are used in the literature; there might be other combinations with the term "gaze", as well, I see lots of results with a more general gaze+predator search.
These are all more general terms than the specific use by prey animals, particularly in social gaze: being able to figure out what others around you are looking at, but they are to some extent the same sort of ability.

This is exactly the kind of help I'm looking for, and now I can do further reading. Thanks!


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Identify this giant green moth(?) with great taste?
One evening in late February I sat down to eat dinner after a day of hiking in hills around New Taipei City and discovered that someone else shared my taste in clothes. A very large green moth-like insect had landed on my pants with a green floral pattern. The inset in the first photo shows that the body was about 5.5 centimeters long. Included are additional cropped top, side and front photos, the top one without flash for a better appreciation of the colors.
It frightened me at first because it was just sitting there and I have no idea how long I'd been walking around with it. After it's photo shoot I brought it outside and located some bushes and was able to convince it to move. It seemed quite sluggish though it wasn't very cool yet (I estimate perhaps 22 C)
Can anyone identify this obviously style-conscious insect, and speculate why it was lethargic and not interested in flying away?

related?

I came here for "with great taste" and left relieved, but a little disappointed. Perhaps a slight nudge to the title? Though I suspect the title may be why this is so high up on HNQ. Or maybe that's the point? ;)

Dissapointed this was not about eating moths.

@wwarriner https://youtu.be/1UM3JpcBHzY and https://youtu.be/eX97kQ8nWzo

@DKNguyen ditto, and see https://en.wikipedia.org/wiki/Charlie_the_Tuna

@wwarriner as for titles, I don't target HNQ but I think it's okay to add a little bit of intrigue to a title now and again, as long as the question itself is still there; Bird brain-eating Mantis - how does it crack the skull?

Am I the only one who finds the camouflage stunningly effective? Did it evolve on pants with floral patterns??

That appears to be an Oleander Hawk-moth a member of the Sphinx moth family.
I think the only other possibility for Taiwan is the quite similar Jade Hawk-moth, but that supposedly has a dark purplish colored head.
Image for comparison:

Source: Shantanu Kuveskar / CC BY-SA.

Interesting! Thank you for the speedy identification; it certainly looks the same. I wonder why this specimen has no antennae, while mine has a pretty big pair. Also, any thoughts on the lethargy?

If you visit the linked site you'll find pictures of male from both sides that shows the same beautiful antennae as your picture shows .. only the "lead" picture doesn't show antennae for unknown reasons

@uhoh: You're welcome. The antennae are sexually dimorphic in this species with the females having "slightly clubbed" antennae, but I don't know why they aren't visible in this picture. Not sure why he was so sluggish, but supposedly these moths are most active around dawn and dusk, so maybe you were disturbing his beauty sleep?

@uhoh: I’ve often seem moths in warm climates behaving like you describe; I’ve always interpreted it not so much as lethargy as just plain cussedness.


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Why do OX5034 GM mosquitos require the presence of tetracycline to survive? What does the drug do in this case?
I'm confused. Debug Fresno; why are the released mosquitos said to be sterile? from 2017 addresses male mosquitos released with a bacteria that will affect fertility of females after mating. They are not genetically modified.
CNN's 2021 article First-ever US release of genetically modified mosquitoes begins in Florida Keys describes release of Oxitec's OX5034 GM mosquito Aedes aegypti. Curiously, these can be kept viable for reproduction when maintained in an environment that includes tetracyline, an antibiotic.
Question: Without the bacterial infection, is it just a coincidence that the GM strain needs an antibiotic to survive? What does the tetracycline do in this case? Why was this drug chosen?
Potentially helpful resources:

https://www.oxitec.com/en/our-technology
https://endmalaria.org/sites/default/files/Enca%20Martin-Rendon.pdf

I think that those mosquitos predated this particular lethality mutation.  So it's what they had on hand to work with. That just so happens to be a means to control the population of all of their mosquitoes.

A good explanation can be found at http://hackaday.com/2021/05/03/genetically-modified-mosquitos-biohacking-for-disease-prevention/

The other answers are correct and on the right track, but I will expand on them with the specific mechanism for these mosquitos. The following paper discusses the engineering behind strain OX513A upon which the OX5034 strain is based:
Phuc HK et al. 2007. Late-acting dominant lethal genetic systems and mosquito control. BMC Biol 5:11
Oxitec mosquitos carry a transgenic construct containing two genes. One encodes for a fluorescent marker, DsRed2, for identifying genetically modified mosquitos and the other encodes a protein called tTAV:

The tTAV gene is under the control of a minimal hsp70 promoter flanked immediately upstream by a tetO site. The tTAV protein is a transcriptional activator that binds tetO and enhances expression. What that means in this construct is that expression of the tTAV gene creates more tTAV protein which binds to tetO which leads to more tTAV expression, etc. This is the positive feedback mechanism mentioned in the above image. Importantly, however, the tTAV protein can bind tetracycline and, when complexed, can no longer bind tetO and therefore cannot drive its own expression. In other words, in the presence of tetracycline, there will be minimal tTAV expression.
tTAV overexpression is lethal during development. Although the exact mechanism of lethality isn’t entirely clear, there are some leading hypotheses:
Knudsen KE et al. 2020. Genetic Variation and Potential for Resistance Development to the tTA Overexpression Lethal System in Insects. G3 10(4): 1271–1281

tTA overexpression is thought to cause lethality due to “transcriptional squelching,” that is a general interference in gene expression (Gong et al. 2005). Consistent with this hypothesis, some genes identified by the GWAS were involved in gene silencing (Su(var)2-HP2) (Shaffer et al. 2002; Shaffer et al. 2006), chromatin binding (mamo) (Hira et al. 2013), chromatin remodeling (Hira) (Loppin et al. 2000) and alternative splicing (bru1)(Spletter et al. 2015), which could all influence the level of tTA expression. Other candidate genes were involved in defense response (PGRP-LC, Lmpt)(Jin et al. 2008), the septate junction (cora) (Tepass et al. 2001) and apoptosis (out) (Coffman 2003); all of which are systems that could potentially impact survival. Four genes; eff, tey, CG32085 and CG13085, encode proteins that are predicted to participate in protein ubiquitination and degradation (Thurmond et al. 2018; Gramates et al. 2017). For example, the Eff protein is a E2 ubiquitin-conjugating enzyme (Chen et al. 2009). It has been suggested that overexpression of the tTA protein could cause lethality due to interference with ubiquitin-dependent proteolysis (Gong et al. 2005) as ubiquitination of VP16 is required for activity and also signals destruction (Salghetti et al. 2001).

To summarize, tTAV is a transcriptional activator and, in Oxitec mosquitos, it regulates its own expression in a positive feedback loop: tTAV protein binding to its response element tetO leads to more tTAV gene expression which leads to more tTAV protein. This overexpression of tTAV is lethal during development. However, tTAV can also bind tetracycline and, when it does, it can no longer bind tetO. In the presence of tetracycline, there is no positive feedback loop and and only basal, non-lethal amounts of tTAV are expressed.

Image from the Oxitec website.

yikes! Thank you for this profoundly specific and thorough answer! :-)

@uhoh You’re welcome!

Very nice answer!

@tyersome Thanks!

They don't go into any detail on the sites you link to and I don't have time to look into patents, but from the context it sounds like they may be using a tetracycline repressible promoter. This is often referred to as a Tet-Off promoter.
The core elements of these promoters were discovered in the bacterium Escherichia coli1 and several variations have been developed. These types of promoters work in organisms from bacteria to yeast to mammals1-3.
References
1: Gossen, M., & Bujard, H. (1992). Tight control of gene expression in mammalian cells by tetracycline-responsive promoters. Proceedings of the National Academy of Sciences, 89(12), 5547-5551.
2: Baron, U., & Bujard, H. (2000). Tet repressor-based system for regulated gene expression in eukaryotic cells: principles and advances. Methods in enzymology, 327, 401-421.
3: Orth, P., Schnappinger, D., Hillen, W., Saenger, W., & Hinrichs, W. (2000). Structural basis of gene regulation by the tetracycline inducible Tet repressor–operator system. Nature structural biology, 7(3), 215-219.

Yes this certainly sounds likely, thanks!


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How would a "synthetic defective interfering SARS-CoV-2" work in practice? Wouldn't it require a large fraction of all cells to be infected?
The abstract of A synthetic defective interfering SARS-CoV-2 is as follows.

Abstract
Viruses thrive by exploiting the cells they infect, but in order to replicate and infect other cells they must produce viral proteins. As a result, viruses are also susceptible to exploitation by defective versions of themselves that do not produce such proteins. A defective viral genome with deletions in protein-coding genes could still replicate in cells coinfected with full-length viruses. Such a defective genome could even replicate faster due to its shorter size, interfering with the replication of the virus. We have created a synthetic defective interfering version of SARS-CoV-2, the virus causing the Covid-19 pandemic, assembling parts of the viral genome that do not code for any functional protein but enable the genome to be replicated and packaged. This synthetic defective genome replicates three times faster than SARS-CoV-2 in coinfected cells, and interferes with it, reducing the viral load of infected cells by half in 24 hours. The synthetic genome is transmitted as efficiently as the full-length genome, suggesting the location of the putative packaging signal of SARS-CoV-2. A version of such a synthetic construct could be used as a self-promoting antiviral therapy: by enabling replication of the synthetic genome, the virus would promote its own demise.

I've highlighted "in coinfected cells"" because it seems to be key to how this would work as a "self-promoting antiviral therapy". To my understanding, the competition happens only within cells that have been infected with both viruses.
Just for example to describe my question, let's say that in an infected individual undergoing antiviral treatment with a synthetic defective interfering virus only $1 \times 10^{-3}$ pulmonary epithelial cells are infected by either virus. A naive application of statistics suggests only $1 \times 10^{-3}$ of cells infected with the disease-causing virus would also be infected by the synthetic defective interfering virus, while 99.9% of them would not be.
At that point I don't see how this is helping; it would require a large fraction or perhaps most, rather than only a small fraction of all of the patients pulmonary epithelial cells to have been infected before enough competitive events would take place for the synthetic defective interfering virus to actually cause the disease-causing virus to be threatened with "extinction" due to competition.
Is that how this would actually have to work in practice?
Question: How would a "synthetic defective interfering SARS-CoV-2" work in practice? Wouldn't it require a large fraction of all cells to be infected?

Could not find tags similar to competition and antiviral-therapy, help with tagging is appreciated.

I'd like to add on Armand's answer about the delivery method of DI RNA. The author has stated that in additional work that’s nonetheless unpublished, the workforce has now used nanoparticles as a [supply vector][1] and noticed that the virus declines by greater than 95% in 12 hours. If the delivery efficiency of DI RNA is guaranteed, the fraction of coinfected cells should be a concern anymore.
Resources
[1]: https://www.sciencedaily.com/releases/2021/07/210706153039.htm

Interesting! What does "delivery efficiency of DI RNA is guaranteed" mean? Essentially 100^% of cells that the SARS-CoV-2 can potentially infect are already pre-infected by the defective interfering virus first? They would just go into each sell and not cause harm to it, but instead just "sit tight" and quietly wait for the disease causing virus to co-infect the cell? Or does it simply need to be a substantial fraction, and the "self-promoting antiviral therapy" makes so many DI viruses as soon as the disease-causing virus starts to co-infect that they can keep up locally with the infection?

Well, that’s the problem here: you can’t pre-infect the cells with DI virus first. In the absence of WT genome, the DI RNA, even though delivered into the cells, will quickly degrade inside the cells because they are unable to replicate and package their genome. Presumably, even a small amount of RNA can interfere with the WT virus and result in the demise of each the virus and the DI genome. But the current coinfection only results in a 50% reduction in virus load over 24 hours, and this shouldn't be sufficient for therapeutic function.

Okay thanks for the insight; I'm getting the idea now.

The authors note in their article that this is only a proof of principle. In particular, they write "An efficient delivery method should be devised to increase the initial amount of DI RNA and to deliver it in vivo. "
Your question is well-founded, as nobody seems to know how such a therapy would actually work in practice.

Personally I don't think this strategy is useful, but I could be wrong.

Thanks for your answer; I was afraid that I was missing something. I'm sure the competition is scientifically interesting by itself, and even if not a realistically viable therapy as-is it may offer insight into new antiviral schemes.


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Why do only humans commit suicide?
Why is it that only humans commit suicide?
Many animals do 'brave' things to protect their children or family, and some male spiders sacrifice themselves so that they can impregnate the females. However, humans commit suicide without necessarily any intention to help their offspring. Why?

Welcome to Biology.SE. I think the answer is along the lines of Because advanced cognitive abilities

I'm pretty sure some dolphins are smarter than some people who have committed suicide :)

Probably not, although it depends on what one mean by "intelligence". Be careful, I guess some people may feel insulted by what you just said as it almost suggest that one need to be stupid to commit suicide.

I do hope nobody inferred that, I meant nothing of the sort. I do, however, think that 'advanced cognitive abilities' isn't a good explanation in itself. If those abilities make the idea of suicide conceivable, then why is that?

@NeMo Spiders and other primitive animals probably work a lot like robots, taking in input and doing output, and never actually think about what they're doing. The human brain is powerful enough to realize how crappy life can feel and rationalize that suicide is an acceptable solution. We also have the planning ability, knowledge, and technology to follow through with it.

@NeMo Spiders do not know existential crisis :P

First, I think we have to question the idea that only humans commit suicide.  How do you define 'suicide'?  Is the squirrel running out in front of your car committing suicide?

Bees commit suicide

I don't know. Did the squirrel look sad?

Untreated depression is the most common cause of suicide attempts. Many animals are capable of experiencing depression so this is a very complicated question to answer, however there is no documented case of suicide in non-humans. Perhaps cross post to Cognitive.SE and see if they can help out.

@jamesqf I should have tagged you in the above post. This, oddly enough, has been defined in the academic community. The citation explains that although sparse examples exist of deliberate self endangerment, the researchers failed to find an example of non-human species deliberately killing themselves.

This is more of a cognition question than biology IMO.

"7 Cases of Animals that Committed Suicide" and other stories in "Why do only humans commit suicide?", think upon those which are not mere sacrifices. :)

Animals can hurt themselves to save their life for example foxes and tigers falling in traps are known to chew their paws to escape from the trap. Thus one can argue that all living creatures want to live and to escape death as well as losing freedom.
looking at how animals live, an animal can always use its capabilities to escape danger or problems as well as to look for food for survival. In humans who commit suicide sometimes it is because  there is no "exit". for example some people commit suicide due to being unable to pay their loans it is the feeling of distress losing all hope and the fact that it is hard to escape from problems in a human society that lead to this thinking.
so a person doing so is trying to escape the problems instead of facing them. further, the fact that humans have the concept of "responsibility" and being held accountable by members of the society all these lead to this thinking as the only escape

You really ought to back up your answer with sources

I haven't heard of limb gnawing before. It appears it is at least controversial as to whether this has happened, although I haven't looked at either side in any detail.


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Linkage Disequilibrium in GWAS
I see a lot of studies on GWAS not filter out for linkage disequilibrium or even make the slightest mention of it. Why is this the case? I would imagine that you want to keep SNPs that are only in linkage equilibrium to promote independence (and besides, without it an additive model makes no sense)

One possible reason to not filter for linkage disequilibrium is to produce peaks/hits with multiple SNPs, thereby clearly indicating a region of a causal genotype. For example, in the manhattan plot below, each point represents a SNP, the higher it is in the plot the more it relates to the phenotype.  We see that in each of the peaks multiple points are significant due to linkage disequilibrium.  If instead we had pre-filtered all of these points out then a peak has a greater choice of representing some type of error in data collection, since there is some probability that there is some error in each SNP, but not much chance of the error occurring in all the SNPs of one peak.

I am unclear why not pruning for linkage equilibrium would prevent an additive, or any model from working.  After all a GWAS is just a series of regressions between the genotypes of one SNP and one phenotype.  In this single SNP frame of reference the LD does not affect the calculation of the betas.  Zooming out, all of the significant SNPs should group together because of the LD, thereby indicating only a few regions and not causing an increase in the false error rate.


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Cold water sour taste
Recently I underwent a wisdom tooth extraction, and while there is still numbness I have observed something peculiar. If I drink cold water, it tastes sour, however the same effect is not observed with room temperature water or hotter. What is causing this effect?

Interesting question , this reminds me of miraculin which makes us perceive sour as sweet. Maybe something like that is happening in your case.

My guess (hence not an answer) is that the regional block also affected your tongue and taste buds; signals might just have gotten crossed.

An interesting effect to note is that distilled water tastes very sweet.


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Why does our eyes got wet when we feel emotional or whenever we are hurt?
I was thinking like whenever when we feel emotional or whenever we got hurt we got tears from our eyes but why is that happen ? Why our eyes got wet ?

the other answer does not discuss specific nuclei or larger structures within the brain

The other question is only about emotions.

The lacrimal gland, the major source for tear production, is situated just above the eye. It sends it's secretions to the eye via the lacrimal duct. Tears secreted collect in the conjunctiva of the upper lid. There is also a nasolacrimal duct which drains the tears from the eye into the nasal cavity. Hence the sniffles when we cry.
How is it controlled? The lacrimal nucleus in the brain is the major source for innervating the lacrimal gland, is a subnucleus of the superior salivary nucleus in the tegmentum of the pons (part of the brain stem). The lacrimal nucleus is connected to the lacrimal gland by the facial nerve (more specifically the greater petrosal nerve). This is parasympathetic (meaning it is part of the autonomic nervous sytem) and the neurotransmitter transmitting the signal from nerve to gland is acetylcholine (the receptor is muscarinic subtype of the cholinergic... though strangely wikipedia says nicotinic subtype is involved as well, but maybe this is simply poorly worded and is just refering to the ganglia stopover between pre/post ganglionic parasympathetic neurons), this information helps explain how some drugs affect lacrimation (tearing up).
Taken from source (1) [I do not know how reliable this website is]: How is the lacrimal nucleus told to start lacrimation? The lacrimal nucleus receives projections from the autonomic nervous system as well as from various brain structures, including the frontal lobe, globus pallidus, thalamus, and hypothalamus. The projections from the frontal lobe are thought to be important in human psychic lacrimation (crying because of emotions).
What I know: Another brain area called the limbic system is involved in production of basic emotional drives, such as anger, fear, etc. The limbic system [in the case of sympathetic nervous system it would be the hypothalamus specifically, but this is irrelevant here since parasympathetic nerves cause lacrimation] also has a degree of control over the autonomic system. As I under stand it, the frontal lobe usually inhibits the limbic system.
Again from source (1): While humans across the world produce psychic tears in response to both positive and negative emotions, and while similar emotions have been identified in other animal species, no reports exist of other animals showing psychic lacrimation.
according to wiki (3): Compared to tearing for physical reasons,  tears for emotional reasons have s different chemical composition. They are composed of more protein-based hormones, such as prolactin, adrenocorticotropic, and leucine enkephalin (a natural pain killer), which is suggested to be the mechanism behind the experience of crying from emotion making an individual feel better.
sources:
(1) http://carta.anthropogeny.org/moca/topics/lacrimation-tearing
(2) http://en.wikipedia.org/wiki/Lacrimal_gland#Innervation
(3) http://en.wikipedia.org/wiki/Tears

you are explaining in great detail the process of How, but not the Why.

good catch... not only do I have no idea on "the why", but some of the info in my answer way be inacurrate for "the how"... I'm hoping someone posts a better answer and then the credit is given to them...

don't Dogs and Cows shed tears? I thought they do

maybe, but i only know about humans

Without having anything but intuition, I would tend to think that it is a communicative signal, i.e. laughter the other way round. It helps individuals in social groups to infer the state of mind of other group members.


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Term for trait that is advantageous to a population only as long as it is rare
I remember reading about a concept—in evolutionary biology or natural selection, I think—whereby a particular trait is advantageous to the population or species but only so long as that trait is only exhibited by a minority of the population. That is, the population is more likely to survive if the trait's existence and expression is maintained, but only if that expression is limited to a small percentage of the population. If the trait becomes too common, the selection advantage of having it will decrease, and the fact that most of the population has it may even negatively impact the survivability of that population.
I can't recall where I encountered it. It may have been in the context of reading about ADD, Aspberger's/Autism, neurotypicality, introversion, or mania/OCD. I want to revisit the topic and learn some more about it, but Google is failing me.
Can anyone tell me the name of or term for the concept I'm thinking of?

If I recall correctly, in humans, there is a recessive genetic trait which gives resistance to malaria in the heterozygous state (Tt) but causes  malformed red blood cells in the homozygous recessive state (tt).  Surely, this qualifies as an example, because if the gene is uncommon, the homozygous recessive becomes rare?

@nickalh I don't think that counts as an example. I think the term "heterozygote advantage" more accurately describes the behavior of the sickle-cell condition.

Frequency-dependent selection is the term you are looking for, I believe. Positive frequency-dependent selection encompasses traits that become more advantageous as they become more common. Negative frequency-dependent selection encompasses traits that become more advantageous as they become rarer.

That was it. Looks like I stumbled across the term it via http://en.wikipedia.org/wiki/Highly_sensitive_person. Thanks!


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Why do some protocols require prewarming a liquid medium before inoculating?
For example, in this protocol for E. coli competent cell preparation, it says:

Plate 10 uL E. coli BL21(DE3) cells on a LB-agar plate; incubate overnight (12 hours).
Prepare 500 mL SOB medium so it can be pre-warmed in the 37 degrees Celsius incubator the day before.
Pick a single selected colony and inoculate in 5 mL of SOB medium and grow for 16 hours at 37 degrees Celsius and 250 rpm in a shaker.
Inoculate 500 mL of prewarmed SOB medium with 5 mL of the fresh overnight culture.

and then in the protocol for overexpressing proteins after transformation of these cells, I basically follow similar steps as above but this time, without prewarming the large-scale inoculation lqiuid medium. Why is that?

Dramatically changing the temperature quickly can shock cells, both prokaryotic and eukaryotic. This could, for example, cause quickly-growing log phase cells to arrest for a period of time, depending on the temperature of the large volume of media (i.e., RT or 4C).

Growth speed also changes by incubation temp. If you put large, medium, and small sizes of culture media kept at room temp into 37 degrees incubator, times when you get the desired density of E coli may vary among the sizes

It's because E.coli BL21(DE3) are competent cells. The competent is the key here as the cells were chemically treated so the transfection can be performed by heat-shock with high efficiency.
This means these bacteria are quite fragile, due to the chemical treatment, and therefore are very sensitive to both mechanical and thermal shocks.
Pre-heating the media simply avoids damaging the cells and maximizes the growth rate.