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What sections of the brain can be removed without causing instant death?
Years ago I've read about a young man you had lost a large section of his brain (frontal lobe) in an accident but surprisingly he survived it and continued his normal life. You may have read about that.
Now let's break down the question into 3 steps. Which parts of the brain can we remove without:

Affecting the normal life. This means, still being able to see, talk, understand, and more. Just like a normal person.
Losing conscious. This includes just being able to maintain conscious, being able to think and understand.
Dying. Which means only having the crucial organs such as heart and lungs running.

UPDATE
I'm neither looking for a list of every part of brain's million sections, nor it's possible to cover them all in a single answer. I'm merely looking for a list of widely-known largely-scaled sectioned, such as the below image.

Image credits goes to Mid Brain Power.

this reminds me of https://en.wikipedia.org/wiki/Phineas_Gage

Thank you for the link. This is a similar accident, didn't know about it :)

This question is too broad. For example, what do you consider to be a part of the brain?  Glial cells can be removed without any consequences. Neurons are constantly dying in your brain too, apparently without consequences. Perhaps you are aiming at which anatomical structures can be removed in totality? Perhaps you can define in the question at what scale you are thinking, and if you are talking bilateral transection, or unilateral only etc.

If you have examples of where my comments are not useful let me know. In general I am just trying to improve questions. The best posts are specific, clear questions and those typically receive the best answers as well.

I think you just don't recognize how broad this field is. I am in the field of studying consciousness, and it is clearly not understood within the field what structures are necessary for consciousness or even if it makes any sense to think about it in terms of particular structures at all. This thread is just going to produce speculation, and so far the only answer is horribly misleading. I agree with @AliceD that this is far too broad.

Many areas of the cerebral cortex aren't essential to life/consciousness, damaging/removing them will only destroy the function associated with that area, e.g. visual cortex in the occipital lobe, auditory cortex in the temporal lobe etc. The Corpus Callosum can sometimes be bissected without any major detrimental effects to the "patient/victim".
Edit: The point here is that what appears to be a major link between the hemispheres of the cerebral cortex can be destroyed without necessarily killing the patient. Whether it falls under the same surgical category as a frontal lobotomy or not, I don't know.
Generally the "lower" portions of the brain, midbrain and brainstem are more important as regulatory centres. However these are each made up of multiple smaller regions, each involved in multiple functions, e.g. the Pons, medulla, thalamus. Removing any of these could have wide-ranging consequences, e.g. the thalamus is important for integrating multisensory information.
So, broadly speaking, cortex damage is OK, midbrain/brainstem, probably not unless you only removed very small regions (e.g. removing the cochlear nuclei from the Pons would probably only affect hearing).
If you use the added image, you can predict what removing each brain area would affect, removing the brainstem would remove respiratory centres, certain death. Removing visual areas would lead to blindness, but probably not death.
Fully answering your question would probably require an entire book to list all of the known brain regions and the implications of removing them.

No no no - the corpus callosum cannot be bisected without major and detrimental effects. It can be bisected without causing death but that is fully different. It can be bisected and result in a higher quality of life for someone having debilitating seizures otherwise but that is fully different. The thalamus isn't important just for "integrating multisensory information" - removing the thalamus would completely destroy someone's ability to experience external stimuli.


text:
Can controlled dose of Codeine improve brain's functionality?
What I know so far about drugs (codeine, heroin, etc) is, the first time you take them you will feel better, think sharper, and act better, just like a supercharged engine. But as this goes on a regular basis, it will stop being efficient and causes addiction.
So what I can understand of this, is that our brain can function better but for some unknown reason (to me) it doesn't. However its functionality increases for a period of time after you take a dose of these drugs.
Now I have a few questions about this:

If our brain can function faster than normal, then why it demands additional drugs to do so?
Can we inject a controlled dose to brain (not by needle to the brain obviously, I mean pills, tablets, etc) of these drugs to keep the brains functionality at a higher rate?
When a drug actually charges our brain, is it taking any damage? The same way you overclock a CPU and it might cause damage to it over the time.

PS: I'm asking this on Biology instead of Health since I'm talking about brain's behavior about addiction, not just to confirm whether or not i can use drugs on a regular basis.

What on earth makes you think heroin will supercharge you? Ever looked at a person under influence of heroin? I have. And the last thing that comes to mind is charged. Burnt out gets a lot closer.

@BryanKrause, really, your comments are as good as any answer will ever get on this question :)

@AliceD I suppose I could move them to an answer, though I don't really feel like tracking down citations etc for all of this. I guess I'll do it and let people decide if they want to upvote or not.

@AliceD Take a look at someone who is on a dose of heroin for the first time. And see what happens to them in the first half an hour. Also I like how some people zoom in 6 letters of a 4 paragraphed question, to find something to criticize in the comments.

the first time you take them you will feel better, think sharper, and
  act better

You are probably thinking of amphetamines, not opiates. Militaries have used amphetamines for just that purpose for decades, particularly for situations where long periods of attention are necessary. The problems are addiction, adaptation (lessening effects over time), withdrawal, side effects, etc.
Caffeine has very different cellular effects, but is also a stimulant, albeit a much weaker one. People around the globe use caffeine to achieve much of what you are suggesting on a daily basis. I actually think caffeine is a great example of what you are proposing, because (at least for people who tolerate it well and don't have any other conditions) it is safe, effective, and has less serious withdrawal symptoms and is somewhat less addictive than many other drugs. That said, among people who use caffeine regularly, some of the benefits begin to wane, and people start needing caffeine to maintain their normal level of alertness.
People with ADHD (and some others without, particularly students) also take amphetamines to help with attention (Adderall is an amphetamine; Ritalin/methylphenidate is closely related). There is a bit of controversy over whether that's a good idea or not. All of these things have side effects, including potential for changes in personality, anxiety, and various peripheral side effects, as well as the risks of dependency and symptoms of withdrawal.
Codeine and other opiates, on the other hand, are primarily useful for blocking pain. They are often associated with euphoria, but their other psychological effects are mostly depressant: drowsiness, respiratory depression, suppression of gut motility leading to constipation, etc. I'm not aware of any cognitive enhancement from codeine, unless the cognitive task you are trying to perform is sleep.

Thank you for the answer. I get migraine attacks once in a while (a week or so) , and i use a low dose of codeine to fade it away. I feel the drastic effect of it on my mood every time. It just makes me do anything faster, better, and more accurate, however i don't stick to it since I don't want to be dependent. Does the effect wane after a while because the blood contains more of that substance by using it over and over?

In general, though there are always exceptions, tolerance occurs because of down regulation of receptors for a drug, or compensatory up-regulation of other proteins. If you suffer from migraine headaches and codeine helps your cognition, that's probably mostly from the relief from the migraine. Tolerance is usually best avoided by keeping doses low and infrequent. Sometimes infrequent dosing can encourage addiction, but if doses are low and only used therapeutically, that is less likely.

I actually tried a codeine tablet once, when I didn't have an attack. It warms the head and you know... felt way better than a smoke or 2 cups of black coffee. I don't take the pill unless the pain is unbearable, since being addicted is the last thing I would ever want ;)

That's called "euphoria" and that's basically why people get addicted to things like heroin. Especially when injected, so you get it into the bloodstream quickly, it gives a really fast immediate euphoria, much better than a codeine tablet would do. Doesn't make you better at anything, just feels really good. It basically hijacks the brain's reward system and goes right to that high. The problem is, people end up chasing after that high the rest of their lives sometimes, and they can never get it back because it won't beat the first time, unless they use more and more.

Exactly that is the point of addiction. More and more. But for example when I can't concentrate, it really helps me focus quickly and resolve a problem (math for instance) that I'm stuck in at for a while. I'll mark it as accepted a while later to encourage other answers. Gratz!

From your comment I took a brief look through recent literature on codeine and cognitive abilities in case there was something I was unfamiliar with...all studies I found showed either a mild impairment or no effect of codeine (on measures of things like attention, memory, alertness, vigilance, at therapeutic doses for pain/cough). There aren't any studies that show enhancement. Just be cautious in case the euphoric effects are tricking you into thinking you do better on the codeine.

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Does human brain store duplicate data?
There are several answers and articles about how the brain stores data, but none specifically cover whether a human's brain stores duplicate data.
I was reading in this article that a human brain can have a capacity of 1 terabyte to 2.5 petabytes. But for example, if you read a book a dozen of times, will it be stored as data several times?
Let me put it this way. When we read a book a couple of times, we remember it better. Is that because it's stored in several synapses and then retrieved better while trying to remember, or is it because reading it over and over makes the missing parts be stored?
We do recognize a familiar phrase when reading a book, which means the brain can differentiate the unknown from known. What matters is that does it decide to store it again or not? Just like a computer who refuses to save a file if the file already exists.

You might think about what gets stored when reading a book.  First there's the actual text, which (if you read it a number of times and make an effort) you might memorize and be able to recite, and which can be stored in a Mbyte or so of ASCII.  Then there's the story the book tells, which you could remember even if you can't remember the actual words.  Then there are the various experiences of reading a book that you might have read multiple times over the years.  How much space does it take to store the memory of those experiences?

@jamesqf Yes, i mentioned this in my comment to the answer indeed. Some phrase in other language that you don't even know, but you remember how to repeat it.

The way neuroscientists currently think about storage in the brain, it doesn't make any sense to think about "duplicate" data but rather about the "robustness" of a given memory to interference or confusion, which increases with consolidation and reconsolidation of memories or can degrade over time.
Repeated exposure can contribute to the robustness of a memory, but so can other factors such as the emotional content of a memory (which, depending on the emotional state, can increase or decrease memory robustness, and this can also vary with the "jist" versus "detail" of a memory).
Note that there are also very different types of memory, so that repetition is very important for motor plans and "muscle memory" whereas episodic memory can get lost in the repetition of daily recurrent events, such as parking your car or eating lunch: you might remember where you parked or ate today, but if you have a routine this can blur into all one memory, where you have a notion of eating at a particular restaurant many times, but you would struggle to remember specifically eating there on December 14th, 2011, unless there was some other special event on that day.
In your example of reading a book, there would likely be two types of memory: 1) memory for the episodic event of reading the book, which would be a separate memory because it is a separate event, though it could be confused with other similar episodic events. 2) Semantic memory for the content of the book: this would be a single memory, reinforced with subsequent readings of the book, and supplemented with all your other semantic experience with the content of a book: discussing the characters of a fiction book with your friends, learning about molecular genetics from a textbook and from a lecture course, etc.
Note also that talking about the "data capacity" of a human brain compared to a computer is a bit silly, because data isn't stored in the nervous system in bits, and a "fair" accounting of human memory needs to consider the vastly multidimensional interactions that are easily coded in a nervous system but not at all easily in a binary system. Note that other papers have come up with estimates that diverge greatly from the numbers you cite, for example Wang et al 2003 which gives a value of 108432 bits based on the number of synaptic connections. That number is truly inconceivable to our conscious experience even if it is within the capability of our brain. Clearly there are other limiting factors not involved in a simple binary system, for example confusion with similar memories, and there are types of memory that computers excel at (such as the pixel values of an image) whereas human memory deals in abstractions and hierarchical representations.
References

LaBar, K. S., & Cabeza, R. (2006). Cognitive neuroscience of emotional memory. Nature Reviews Neuroscience, 7(1), 54-64.
Walker, M. P., Brakefield, T., Hobson, J. A., & Stickgold, R. (2003). Dissociable stages of human memory consolidation and reconsolidation. Nature, 425(6958), 616-620.
Wang, Y., Liu, D., & Wang, Y. (2003). Discovering the capacity of human memory. Brain and Mind, 4(2), 189-198.

Thank you. Here i have to mention: 1- What do you mean by Robustness? For example, a signal's robustness can be divided into signal strength, signal quality, etc. 2- By reading book, i meant simply remembering words and their orders, such as you remember a phrase from a language you don't even understand.

I meant resistance to factors that interfere with signal. In memory, two of these are interference and confusion. Interference I would say is roughly equivalent to signal-to-noise, the inability to recall a particular memory. Confusion has a particular meaning in theoretical descriptions of memory as well, slightly different from the colloquial usage, but it basically means the ability to distinguish two different patterns. Also called "pattern separation" from the other direction. 2) This meaning would be the "semantic" type of memory that I mentioned.

For 1) in robustness I would also include, to some extent, the level of detail of the memory, though it could be possible for a memory to be very clear but not detailed, all of those qualities are not necessarily dependent on each other.

Nature preserves redundancy by duplicating certain parts of living things - two lungs, two kidneys, two testes, two ovaries. I believe that as an instinct of self-preservation the brain does duplicate memory in some form.  Otherwise a caveman who was clubbed on the head or fell and hit his head badly would (if he recovered) be bound to forget how to do some basic task - like remember where his cave is, or how to hunt, or how to eat.
This would explain why most Alzheimer's patients can remember the distant past, at least initially.  It also explains why they have 'good' days (where they seem like their old selves - at least until the ravages of the disease take their toll) and 'bad' days, rather than 'bad' then immediately, 'much worse'.
Another example – you hear an old song from your childhood that's not played on the radio very often. You knew you used to know the title, song, and artist very well – but now you can't remember who the artist is anymore.  You try to resist temptation to look it up immediately on the Internet because you know this can't be good for your memory recall, but curiosity eventually gets the better of you.  When you do finally look it up you say, 'No way - it can't be HIM!".  Reluctantly you accept this new memory but you realise that somewhere in the recesses of your mind this information is already stored (later you remember that you mixed this artist up with another artist at the time and performed some research and found it was this artist after all).
So what have you done?  You have a piece of information already stored in your brain and you've now stored an exact duplicate - and, because of the emotional situation attached to each piece of information, these remain as backups of one another.

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Are we deaf to water's taste/smell?
If we hold a rose in front of our nose for an hour, we can barely notice the smell after that duration, since the smell receivers ( Or the brain, I'm not an expert ) get used to it, and become sort of deaf.
Now my question is, are we deaf to the smell or taste of water simply because our body is consisted mostly of water and we are deaf to it, or is it because we do not have any receiver for this liquid?
If so, is this shared between all the living organisms?
UPDATE
By water, I mean pure water. Now what we practically have is never 100% pure, but a good place to start is distilled water.
I've come across multiple articles about this, but they lack of evidence and scientific proofs.
These are 3 of them:

Ask Anything: What Does Water Taste Like?
Does ordinary water really have no taste [...]
Water taste in man

Have you done any research into this, and if so, can you include it? And what do you define as "water"? Pure (e.g. twice distilled) water? Tap water? Spring water? Because water isn't pure. FWIW, I used to laugh at the bottled water industry; my well water tasted just fine. Until 15 years later when I had a deacidifier added, then I really disliked it (but still didn't buy it, just filtered it.) Recently I moved, and I refuse to drink what the township calls drinking water (tastes terrible!) I found a bottled water that I absolutely love. Anecdotal? Yes. Rare? Not at all.

@Jack Johansson like u said " body is consisted mostly of water " if this were true what implication would it have to bear gustato or olfactory receptors which would permanently be in its adaptive form (about which u meant by the smell of rose part) throughout one's life?secondly there are osmoreceptors in the hypothalamus and in kidneys too that handle body water content changes.

...besides there is a constant secretion of mucus in the nasal epithelium and saliva in the tongue both of which have water.so dont u think that water receptors (even if present) would always remain in adaptive state.Thus holds no meaning i think

Just anecdotat, but if you spend a lot of time in the outdoors in semi-arids areas, as I do, you learn to smell water.

@jamesqf i know what u mean...in my place (kolkata) summer temperatures can be as high as 45 celcius and u would literally love to smell the water of the first rain of kalbaiskhi...its a very nice feeling...but i think this too has something to do with the hypothalamus...its jst a guesswork though.

@CATHARANTHUS: Though I think you may mean something a bit different, "the smell you get after rain": http://discworldtour.tumblr.com/post/158020764568/then-rincewind-caught-the-smell-too-rincewind  But you can smell rain coming, too.

Related: https://biology.stackexchange.com/questions/41364/why-is-water-flavorless

It appears that little is known regarding how water is detected in mammalian mouth and throat. However, a recent study published in Nature Neuroscience(1) showed that acid-sensing taste receptor cells (TRC) participate in taste responses to water.
First, the team screened knock-out mice in order to identify which TRC were involved:

They used genetic knockout mice to look for the cells, silencing different types of TRCs, then flushing the rodents’ mouths with water to see which cells responded. “The most surprising part of the project” was that the well-known, acid-sensing, sour TRCs fired vigorously when exposed to water, Oka says. When given the option of drinking either water or a clear, tasteless, synthetic silicone oil, rodents lacking sour TRCs took longer to choose water, suggesting the cells help to distinguish water from other fluids.(2)

Then, the acid-sensing TRCs thus identified were artificially activated using optogenetics techniques:

They bred mice to express light-sensitive proteins in their acid-sensing TRCs, which make the cells fire in response to light from a laser. After training the mice to drink water from a spout, the team replaced the water with an optic fiber that shone blue light on their tongues. When the mice “drank” the blue light, they acted as though they were tasting water, Oka says.(2)

Source:
(1) Zocchi, D., Wennemuth, G., Oka, Y., The cellular mechanism for water detection in the mammalian taste system, Nature Neuroscience 20, 927–933 (2017) doi:10.1038/nn.4575
(2) Scientists discover a sixth sense on the tongue—for water, Science

Thanks for the links. However, it would be nice to include some important sections of the articles as quotes, for further visitors.

@JackJohansson I tried to do so. Hope it's better now. However, I don't quote the original study, because I don't have full access...

@JackJohansson If my answer is now satisfactory enough to you, will you please consider accepting it? Thanks! :)


text:
the meaning of "Non-primary hits" and "tags"
Can I ask you to help understand the meaning of "Non-primary hits" and "tags" in the following paragraph related to RSeQC:
The result table reports total number of reads (excluding nonprimary
hits) and tags (separate splice fragments of a read). Total assigned tags
indicate how many tags can be assigned unambiguously to the ten different
categories listed below.
Total Reads 49743155
Total Tags 63012643
Total Assigned Tags 57529077
= = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = =
Group Total_bases Tag_count Tags/Kb
CDS_Exons 36821030 34763281 944.11
5'UTR_Exons 34901580 2856644 81.85
3'UTR_Exons 54908278 9772738 177.98
Introns 1450606807 8468986 5.84
TSS_up_1kb 31234456 94103 3.01
TSS_up_5kb 139129272 161914 1.16
TSS_up_10kb 249300845 217980 0.87
TES_down_1kb 32868738 789703 24.03
TES_down_5kb 142432117 1368378 9.61
TES_down_10kb 251276738 1449448 5.77
= = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = = =

"tag" is a weird term in this context. It used to mean "read", but RSeQC likes using it in an odd way. Suppose you have a read that aligns to a single contiguous (though possibly with InDels) stretch of DNA. This would then count as one tag. Suppose instead that you have a spliced read, that is one where part aligns to one exon and part to another exon. Each aligned part of this read then counts separately as a tag. So this 1 read becomes 2 tags. By extension, if you have a read that is spliced such that is starts in exon 1, jumps to exon 2, and then finally jumps to exon 3, then it'd count as 3 tags. This is only useful if you're interested in splicing, since the higher this value is the better you're able to discern differences there.
For "non-primary hits", suppose you have a read that can align equally well to multiple places in the genome. If there are 5 equally good alignments, then 4 of these will be labeled as "secondary" and one of them will not, which is then the "primary alignment". "non-primary hits" is then an odd way of saying "secondary alignments". The number of primary alignments is equal to the number of reads that aligned.


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Why can Toll-like receptors be found either inside and outside the cell?
Innate immune cells may present Toll-like receptors either inside (TLR3 and TLR9, for instance) or outside (TLR4 and TLR5, for instance) the cell, but is there any beneficial reason for this? If so, what is it?

When you say inside of the cell, do you mean in the cytosol or inside the  ER, vesicles, endosomes? Remember inside the cell can be many places so please be a little more specific.

By inside, I mean any compartment/region which is located within the cell.

TLRs are used to identify features that are typical of pathogens. Different TLRs tend to identify different features, so that a wide range of pathogens can be identified. Some of these pathogens may be extracellular (such as some kinds of bacteria that are recognized by TLR4, which is extracellular) and some are intracellular, like viruses (some of which may be identified by TLR7, which is intracellular).
The fact that innate immune cells have these is a little bit of a red herring, because they aren't limited to innate immune cells -- they're widespread among many cell types, and are effective at protecting the specific cell, not just activating innate immune cells.


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Can I breed the most productive hen by hatching eggs from the most productive ones?
Here is some hypothetical input:

I have a set of eggs.
I hatch these eggs and get chicken from them. Say, 100 hen that can lay eggs.
I have a hypothetical technology to track some parameters of each hen during their life - one of them is the moment a hen lays an egg.
I collect the data and find out which hen laid the largest amount of eggs during her productive period. I mark this one as the most productive.
I collect the eggs from the most productive hen in the generation.
GOTO 1.

Now, if I repeat this loop of death and life, say for 20 generations, hatching only eggs from the most productive hen, will it make next generations more productive and with each iteration or is it an oversimplified picture I have?
By performing this mental experiment I want to figure out if I can use it as a clear predictable factor influencing productivity of future generations.

In theory yes, so long as you maintain genetic variation within your flock of hens (e.g. by bringing in outsider males to prevent inherited diseases spreading), artificial selection will lead to a more productive flock.
However I don't think it would be predictable and not necessarily an improvement every generation, surely productivity would be influenced by lifespan? e.g. is it better to have a hen that lays 100 eggs/month for 24 months, or a hen that lays 120 eggs/month for 12 months? Not necessarily that important, but worth considering.
You would also want to keep more than one hen per generation, maybe 2 chick hens from each of the 3 most productive hens per generation, just in case you selected one that hadn't inherited the productivity traits.
I assume you've read about milk yields. And this looks like it covers the maths of heritability of egg production.


text:
Do Pharaoh ants eat sealant?
My high-rise apartment has had pharaoh ants for the past 3 years (maybe more).  It is being handled by a pest control company.  I am not looking for countermeasures.
One of the countermeasures advised by the pest control technician is to seal the opening through which my water pipes travel.  The apartment management sprayed a sealant that looks like whipped cream, but had a distinct chemical smell (images below).
The ant sightings are usually on the kitchen counter top, mostly around the perimeter of the sink.  I try to wipe the counter often, and keep the area dry.  The sightings were getting kind of low just before the hole was sealed, sometimes going for days without a sighting.  Since that day, however, the sightings have been on the upswing.  Quite a coincidence.
I wondered whether the pharaoh ants are attracted to the chemical sealant as a source of food.  Googling doesn't turn anything up for pharaoh-ant-eat-sealant.  Does anyone know about the plausibility of this?

It's possible,. The sealant is an expanding polyurethane foam, marketed in the US as "Great Stuff", among other brands from a number of different companies. Basically, it's plastic. Ants or other pests could chew through it by removing small pieces, but I doubt they're eating it, as it has no nutritional value.

If it has no nutritional value, then it seems that the plastic foam isn't attracting the ants.  There must be another explanation for their sudden increase, coincidentally starting on the day that the foam was applied.

Just a thought, but - instead of sealing them out - might you have sealed them in?

It might be possible that at the same time the pest control company sprayed something in the basement and other parts of the building that forced out the ants.

@Jiminy Cricket: I've been told over the years that the number of an sightings in my unit is way too low for me to be hosting the colony.  So if I trapped a few scouts in my apartment (which I likely did), then why would the number of sightings steadily increase since the day the opening was sealed?

@FluidCode: It was the apartment building staff who sealed the the opening, not the pest control company.  Of course, that just leaves fewer avenues into my unit, not zero avenues.  It is possible something elsewhere caused more ants to be closer to my unit, and more ants to enter.  The timing of the increase is quite a coincidence, so I think it is not likely, but still possible.

@user2153235 Why don't you leave for few days some flypaper in some strategic points. In this way you could find out where they come from.

@FluidCode: Huh.  Never thought of that.  It's like troublehooting a technical problem.  Thanks, I'll have to mull on some locations at which to start.

It doesn't need to have nutritional value, if there's something on the other side that's attracting them. Have you looked at the foam to see if anything has been chewing on it or penetrated it? This could also be a good location to leave some of your flypaper.

It's hard to get up and close to inspect, and my vision isn't that good.  But the photo's show underside of the sink.  There's nothing there.  The outside is whatever is on the other side of the wall with the hole that was sealed.  The contents of the inside and outside did not change when opening was sealed, so that doesn't explain the presence of more ants.  I should clarify that the greater sightings are on the counter top, around the perimeter of the sink.  I try to wipe down often, and that hasn't changed.

@MattDMo: Would you care to post your comment as an answer?

@user2153235 sure. What country are you in, so I can localize my answer?

@MattDMo: Canada.

The sealant in question is a self-curing expanding urethane foam, marketed under numerous brands and formulations in the US and Canada such as DuPont Great Stuff, Loctite Tite Foam, and DAP Touch 'n Foam. It is widely available at hardware stores and home centers.
After curing it forms a hard cross-linked polyurethane mass - essentially a plastic foam. While it has no nutritional value and is solid enough to be marketed in a pest control application, it could theoretically be chewed through by a determined-enough ant colony, as the marketing material for that particular product doesn't say anything about insect repellant properties, only mice. Non-rodent-repellant formulations are known to be susceptible to eventual "chew-through" and inhabitation by both mice/rats and insects such as carpenter ants. Great Stuff markets a Pest Block formulation that supposedly is formulated to prevent chewing, but its claims regarding insects are a little vague. You'd have to ask your building management if they used a pest-blocking foam.
You say that the sightings started to swing up again a day after the sealant was applied. I would imagine that it would take some weeks for a colony to chew through the amount of foam pictured (even longer if an insect-repelling product was used), and they would need a rather compelling reason to keep at it, as the foam itself is not a food for them. It's likely that you're seeing ants that were already in your apartment when the "escape routes" were sealed, and they're simply foraging in a more visible manner now because they don't have other sources of food. On the other hand, the fact that you think you're seeing more ants now after the pipe openings were sealed could simply be a coincidence. Remember, correlation does not mean causation.

Thank you! Some time after I posted my original question, I added details, such as the fact that the sightings increased on the very day that the sealant was applied. Wiping with bleach seems to bring down sightings again. I hope that this surge is temporary due to trapped scouting ants, because I dislike the residue of bleach on the kitchen counter. The vapours aren't healthy, either. On a related note, there is no change in the food source on my side of the wall, and since the other side is just pipe space, I don't expect whatever passes as food on that side has changed either.

@user2153235 sorry, I didn't read the edited question closely enough regarding the timeline. I changed my wording a bit. Based on that, I'm pretty sure that you're seeing trapped scouts, not new ants.

Thanks!  That's a very encouraging outlook!

It has been a week since the sealant was applied, and the number of ant sightings seem to be staying at their heightened levels.  Sigh........

@user2153235 Interesting. Do you have ant traps in your apartment? Depending on their kind, they should be having some sort of effect by now, assuming my theory is correct...

The professional pest control company has laid down bait of various types and in various forms (directly dropping goop on various places versus the less messy plastic containers of bait).  The "stuff" has varied through the years.  At the beginning, I also got my own.  Each new chemical brought about a temporary lull.  The ants seem to be adapting before they are wiped out (a problem with Pharaoh ants, whose colonies can easily split). Completely wiping them out is hard in a high-rise, especially with the warming weather.

My bleach solution seems ill-advised, both because of the fumes and the adverse effects on laminate countertops.  It looks as if I will have to get comfortable again with ants on my food preparation surface.

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


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Can there be an equilibrium between humanity's increase of carbon dioxide output with plants since plants harness CO2?
Is it possible that, prior to hitting a thermal equilibrium in the atmosphere, the increase in CO2 that humanity puts out every year will come to an equilibrium due to the consumption by the world's plants, which may respond by growing, reproducing and feeding more off of the additional CO2 in the atmosphere at a faster rate?

Wow this is one single long sentence! Do you mind splitting up your question is several sentences in the hope of clarifying it? Note that a forest at its climax does not intake more carbon than it outtakes. Plants intake carbon from the atmosphere as they grow but this carbon is being released when they die. Definitely, not all forests are carbon sinks.

Also consider that even if plants could lock the CO2 produced by mankind's use (which doesn't necessarily work that way as Remi.b notes), there's more deforestation and more urban development worldwide. We have less plants and trees so where will they come from? Plant growth is set at a certain rate by its genetic code even at optimum conditions. More CO2 doesn't speed up growth.

Well, what you should also consider isn't just the static environment that exists today, but rather how plants evolve, which maybe  to intake more CO2.

Oceans, rather than forests, are actually the largest carbon sink

Yes, with 2 caveats.
More CO2 encourages plant growth up to the local plants' limit. After that limit, the plants are saturated and extra CO2 backlogs into the air. If you intend to prevent atmospheric CO2 buildup, you're better off gradually supplying CO2 rather than deploying it in large surges.
The other caveat is dead trees and other plants that should be harvested or logged to make way for new growth (while providing lumber, fuel, and employment).


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Is there any way to differentiate between a contractile and a non contractile vacuole by observation alone in any given organism
I have read about distinguishing them using osmotic experiments in books and here as well.
But is there any thing common (on a biochemistry level) from which I can tell if a vacuole is contractile or non contractile irrespective of the organism taken and only by observing?

Contractile vacoules are usually surrounded by distinguishing structures

The contractile vacuole has several structures attached to it in most cells, such as membrane folds, tubules, water tracts and small vesicles. These structures have been termed the spongiome; the contractile vacuole together with the spongiome is sometimes called the "contractile vacuole complex (CVC). The spongiome serves several functions in water transport into the contractile vacuole and in localization and docking of the contractile vacuole within the cell.

This type of arrangement is not common in non-contractile vacuoles like gas, sap or food vacuoles.


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How does transition of osmoregulation occur in fishes when they migrate from sea to rivers and vice-versa
From my high school level knowledge I can recollect that there are two types of migration in fishes-

From marine to fresh water
(like in Hilsa which grows in the marine water but migrates to the fresh water only for reproduction and then the young return back to the marine water)
From fresh water to marine
(like in eels that live in the fresh water but migrate to the marine water to reproduce)

The only mechanism I had read about osmoregulation in aquatic organisms was via the ionocyte cells in the gills of the fish.
So my question is:
How do they change their osmoregulatory mechanism during this migration?
Just a follow-up:
Are there any other mechanisms by which they osmoregulate

I found a publication related to the osmoregulation in salmon that might be interesting to you. I'm copying the abstract because it basically answer your question.

Smoltification, also called parr-smolt transformation, is a complex developmental process that consists of a number of independent, but coordinated changes, in the biochemistry, physiology, morphology and behavior of juvenile salmon in their transition from freshwater to seawater life. A key component of smoltification is represented by the physiological adaptations that enable smolts to thrive in hyperosmotic environments. Instrumental to this process is the ability of smolt gills to gradually become capable of actively secreting salt through specialized cells known as mitochondria-rich (MR) cells, ionocytes or chloride cells. NaCl secretion by teleost gills is therefore accomplished via the secondary active transport of Cl - and the passive transport of Na + . The driving force for active transport is provided by Na + /K + ATPase, which maintains low intracellular Na + and high intracellular K + concentrations. However, this NaCl secretion mechanism needs at least two different ion channels: A CFTR type chloride channel for the passive exit of Cl - and a potassium channel to recycle extracellular K + , which is a thermodynamic prerequisite to work under conditions imposed by high extracellular salinity in seawater. The characteristics of K + channels required for NaCl secretion from MR cells into seawater are still unknown for Salmo salar and only recently have begun to be studied in other teleosts.

You can find the complete paper here.

thanks for the reply.But how does the reverse happen...I mean can you throw some light  on how the adult Hilsa or Salmon transform it's osmoregulatory mechanism during its migration from the marine to fresh water?

I don't know. Maybe is easier to move from salt water to fresh water, since you'll only need to shut down the regulatory mechanisms?. @user33690

Possible, infact I thought that too at first. But in fresh water fishes the ionocyte cells (chloride cells) act to drive the reverse reaction...that is, they take up $Cl^-$ from the surrounding water. So that kept me wondering...what was actually happening- some sort of transitions or simply stopping the entire process


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Comparing Embryonic stem cell and hepatic stem cell
So, currently, I want to compare transcriptome data for liver cell development. I found 2 data sets which start from stem cell, hepatoblast, and then adult cell. The first data set use hepatic stem cell and the second data set use embryonic stem cell. I am trying to map the difference in the gene expression during cell development, so it is important to make sure the state of the cell is same. My question is, is this stem cell comparable and can be grouped as 1 category? If hepatic stem cell and embryonic stem cell is different, is there something in common that probably can be used as basis of my analysis?


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Different number of flaps in heart valves
Can anyone tell me why the different valves of heart have different number of flaps is it in any way related to evolution of homo sapiens.

This question has been asked before.. although still without an answer http://biology.stackexchange.com/questions/52276/evolutionary-explanation-of-the-bicuspid-on-the-left-and-tricuspid-on-the-right


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Does Acromegaly cause actual expansion of the zygomatic(cheek) bone
Acromegaly is a disorder in adults involving excess growth hormone production. Since epiphyseal fusion has already taken place in most bones of adults , this does not cause an increase in stature. Certain features of the face such as the jaw may be changed due the fact that the flat bones, such as the maxilla do not undergo epiphyseal fusion and may enlarge.
Several reports describe a prominent zygomatic arch due to arcomegaly, such as this. As I understand ,the zygomatic bone cannot enlarge due to its being fused in adults.
Can acromegaly cause an actual enlargement of the underlying zygomatic bone ?


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Can cancers caused due to viruses be contagious?
Generally, viruses are infectious in nature and there are several cancer-causing viruses that are known (i.e. oncovirus)
My question is:
Are these oncoviruses infectious in nature? If so, what is the way in which they can be transmitted?
(edit:just a background to connect the title and the question (as mentioned by user iayork):While reading my text(which led me to the doubt) I was considering the virus as a causal organism and the disease as cancer(malignant tumour cells).The cancer cells are non-contagious however I wanted to understand if the disease  was.Thus I was interested on the routes of the transmission of the viruses.Also note (which I had already asked user Chris in the comment) "most cancer disease are non contagious but if cancer disease was due to virus if it was contagious or not"

You may want to reword the title so that it matches the question. It should be something like "Can viruses that cause cancer be contagious?". Otherwise it sounds like you're asking if the cancer itself is contagious, which is a totally different question. I see your edit, but the ambiguity still remains.

Just to be clear, not sure whether you understand this part or not, but viruses that "cause" cancer do not guarantee cancer, they increase the risk of cancer in affected individuals.

The question title and the question itself ask two slightly (but critically) different questions.

Can cancers caused due to viruses be contagious? NO
Are these oncoviruses infectious in nature? YES

The tumors caused by the viruses are not contagious.  You can't take the tumor and transfer it to a new host and see a new cancer.  The viruses that cause the tumor are contagious, but in many cases by the time the tumor has arisen the viruses are no longer in a contagious form.  A tumor that's caused by HPV doesn't have contagious virus in it (see explanation below), and you can't transplant the tumor into a new host.  There still may be contagious virus present in the patient, but the tumor itself is not contagious.
Explanation HPV causes cancer by having a part (and only a part) of its genome integrated into the host genome, so cancers associated with it inevitably have a defective virus genome. There could theoretically be infectious virus in the neighboring tissues, but the cancer is driven by non-contagious virus. See for example The role of integration in oncogenic progression of HPV-associated cancers for a fairly basic explanation

I think your answer is pointing us to a language problem. You as a biologist may think that "a cancer" is a synonym for "a tumor" and so you wrote an answer geared towards this interpretation. For a member of the general public, "a cancer" can well be "the disease a person with tumors has" which is contagious at some stages. Maybe this should be made more explicit before people without enough background are totally confused.

@rumtscho That is not the general public definition of cancer, and it is not contagious at any stage in humans.

Generally tumors are not contagious, but we know of at least one case where that is not true. A communicable facial tumor has decimated tasmanian devil populations, though it is spread through an allograft, not a virus. https://en.wikipedia.org/wiki/Devil_facial_tumour_disease

there is also evidence of contagious cancers in clams http://www.sciencemag.org/news/2016/06/contagious-cancer-found-clams-and-mussels

Since the question is about viral tumors, it's probably actively confusing to start talking about non-viral contagious tumors like the bivalve and Devil versions.

@iayork "A tumor that's caused by HPV doesn't have contagious virus in it" a reference would be helpful.thanks.

Yes, Oncoviruses are infectious in nature. A good example is the Human Papilloma Virus, which does not immediately cause cancer, but can cause precancerous lesions in infected regions including cervix, vulva, vagina, penis, anus, mouth, or throat (see references 1 and 2). HPV is transmitted during sexual activities (hence the broad range of infected tissues due to different practices).
There is now a vaccine available since a few years which allows prevention against infections with the HPV types 16 and 18, which cause most of these infections. If it is administered before the first sexual activity, it provides a good protection against infection with these HPV types.
Other tumor viruses like Hepatitis C or Kaposi's sarcoma-associated herpesvirus, to name just two, are also infectious. If they weren't, they wouldn't be able to spread.
As @iawork says, it is important to say that the cancers which are caused by these viruses are not contagious, only the viruses are.
References:

Human papillomavirus (HPV) and cervical cancer
HPV-associated diseases.

thank u for the answer.jst to be precise,then can it be said that when we say that cancers are non-contagious it actually excludes a virus caused cancer which is actually infectious?

@CATHARANTHUS Normal cancers are not contagious. The either arise due to a genetical predisposition or acquired mutation. The virus is the agent that causes these mutations (which could also be a chemical). It happens to be that viruses are infectious.

@iayork : Huh...  Apparently reading comprehension is not my thing this morning.  Meh.  Removed.

@BryanKrause I removed this part of the comment.

Oncoviruses are most commonly transmitted sexually however in the cases of EBV (Epstein-Barr Virus) and MCV (Merkel cell polyomavirus) can be transmitted in other ways such as through an oral or respiratory route.
These viruses are contagious however as mentioned by others the cancers caused my these viruses are not contagious. In the case of HPV for instance the cancer tends to be caused through the virus integrating with the host cell and expressing two oncoproteins (E6/E7) which interact with tumor-suppressing proteins resulting in uncontrolled cell growth. The virus itself cannot bind to live tissue it instead is limited to the basal cells of stratified epithelium such tissue can be found in the cervix which is why HPV is responsible for upwards of 90% of cervical cancer cases. Because viral integration usually needs to occur for cancer to occur the virus itself needs to be contracted for integration to occur.
Also as mentioned above two genotypes of HPV (16 and 18) are responsible for most cases of cancer but there are over 200 genotypes of HPV of which there is a large number which are considered oncoviruses such as 31, 33, 39, 45, 52, 58, and 59. And another of others which are still subject to debate - many of which are not covered by the current vaccine.


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Do restriction enzymes on read 3' to 5'?
Every chart of palindromic restriction enzymes I've seen lists their restriction sites from 5' to 3', something like this:
EcoR1 cuts GAATTC between the G and A:
          5' NNNGAATTCNNN 3' --> 5' NNNG____ AATTCNNN 3'
          3' NNNCTTAAGNNN 5' --> 3' NNNCTTAA____ GNNN 5'
Will restriction enzymes match and cut a site if it's running antiparallel? For example, will EcoR1 cut this sequence?
5' NNNCTTAAGNNN 3'
3' NNNGAATTCNNN 5'

Whatever sequence (plus direction) is target, so enzyme will cut. In your example "correct" and "antiparallel" sequences are two different sites.
Actually, your example of 5'-CTTAAG-3' is cut by AflII enzyme.

Additionally, the definition of "palindrome" means that it does not matter which direction the read is in, as either direction is identical.

Another way to think about it is to look at the 3-D structure of GAATTC, I believe there is also a 3-D structure of the Eco RI enzyme. The sequence CTTAAG cannot be superimposed on top of GAATTC--well, when you superimpose them they don't align significantly. Likewise ds GAATTC fits perfectly into the enzyme active site while ds CTTAAG will fit, but poorly.

@mdperry that is what behind (in some part) specificity :)


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Why does photosynthesis occur even in blue light when the photocentres are activated in red light
From Engelmann's experiment

Engelmann used this device to illuminate a strand of Cladophora (not Spirogyra) with light from the visible spectrum, exposing different sections to different wavelengths (or colors of light). He added the oxygen seeking bacteria B. termo to this setup and noted where they accumulated (Note: Four years later, Hauser concluded that B. termo had been mislabeled and was not one, but three species of bacteria of the genus Proteus [2]). Their clumping allowed him to see which regions had the highest concentration of oxygen. He concluded that the most photosynthetically active regions will have the highest concentrations of bacteria. The bacteria accumulated in the regions of red and violet light, showing that these wavelengths of light generated the most photosynthetic activity.

It can be concluded that the photosynthetically active regions of light are present at the blue-violet region and the red region
What I am unable to understand is , if photosystems I and II are activated at light wavelengths of 680nm and 700nm (primarily at the red region of the spectrum) then what type of photosynthesis is happening at the blue region due to which there is oxygen evolution?
My attempt:
The antenna molecules (light harvesting complex) which absorb majorly at this wavelength are transferring energy to the photocentre due to which there is excitation of the photocentre and thus OEC gets activated.
Even if this were true, then should'nt blue light be as effective as red light in helping in generating the quantum yield?

See the following related questions: Why are so few foods blue?  and  Why do plants have green leaves and not red?.

While it is true that strongest activity of Photosystem I and II happens with 700nm and 680nm light, these are not the only wavelengths that can be used for photosynthesis.
The green color of plants comes from chlorophyll, which is the main light absorbing component in the photo systems. If chlorophyll had only a single absorption peak at 680-700nm, it would have a blue(-ish) color instead of a green one.
Looking at the absorption spectrum of chlorophyll (which wavelengths it can absorb how well), you can see that there is a a second peak around 400nm:

This both explains the results of Engelmann's experiment and the green color of chlorophyll (with both red and blue colors removed only green remains)
Picture taken from: http://hyperphysics.phy-astr.gsu.edu/hbase/Biology/ligabs.html

but this still doesn't explain why oxygen is evolved under blue light.The PSII is activated by red light and OEC coupled to this, splits water to reduce the photocentre... However, I am unable understand that even though blue light does not directly excite the PSII photocentre, how it is capable of causing oxygen production. As you can see there are oxygenic bacteria in the blue region indicating that there is oxygen evolution.

You didn't quite understand my answer. the 400nm absorption peak of chlorophyll means that blue light does directly excite chlorophyll and thereby PSI / PSII. Also the bacteria cause oxygen production, not evolution.

blue light does directly excite chlorophyll and thereby PSI / PSII. Do you have any references to back this up?

Thanks to @theforestecologist for giving me the lead in this answer
Just to clear up, in short:

The photocentres, as it goes by their names $P_{680}$ and $P_{700}$ cannot be said to be activated by the blue violet light directly because they can directly absorb light only at the wavelengths 680nm and 700nm for PSII and PSI respectively.
The antenna molecules are the only pigments absorbing directly at this low wavelength (also called Soret's band) which makes these molecules important in protection against photooxidation.
However the chlorophyll a as pointed out in @Nicolai's answer still show absorption at the 400nm range.
This could be explained by the transfer of energy from the antenna molecules (carotenoids) to the photocentre.
The entire  mechanism has been summarised in this paper

Thus it may account for the oxygen evolution in the presence of blue light
To the last part of my question on the effectiveness of red light over the blue light it can be said that:

Of the total blue light incident on the antenna molecules only a part of it's energy is transferred to the photocentre. Whereas in case of the total red light incident , almost all of it gets absorbed by the photocentre to be used in light reaction.

For further reference see  theforestecologist's answer on the photosynthesis

The answer you are looking for is most certainly here:
https://en.wikipedia.org/wiki/Cryptochrome

thanks for the link. But how does the cryptochrome pigments couple to the OEC? The link basically states about photosensitivity but I cannot understand why there there is oxygen evolution in the presence of blue light.


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How can I find the most studied SNP of a gene?
How can I find the most studied SNP of a gene and diseases that the most studied SNP has been related to?
I search in dbSNP database but I can't find it.
What is the process?

I have selected the BRCA1 gene.

Can you provide the gene of interest?
You can usually search Entrez for the gene symbol in the dbSNP database, which will pull up a NCBI Entrez page for SNPs located in the gene and will also give an indication of their clinical significance (benign or otherwise).
Alternatively, if you have a specific disease in mind, you can check more specific databases for a SNP, such as COSMIC for cancer-related SNPs.
Lastly, merely Googling the gene of interest (for example, "EZH2 SNP") in Google Scholar will bring up articles that present SNPs of interest.
Some combination of those methods should yield what you want, but I might be able to provide a better answer with more info.


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Optical Density conversion to cfu / ml
I am having troubles understanding the correlation between OD measurements and CFU/ml. What is the conversion factor between the two units, and does this conversion factor somehow compensate for dead cells OD might be reading? (Also lets say the OD is set at the standard 600nm).

The optical density measurement is the quantity of living and non-living cells in a sample. The colony forming unit measures only the viable cells in a sample. An OD 600nm is equivalent to approximately 8 x 10^8 CFU/ml. However, this is only an approximation and cannot fully take into account the dead cells the OD may be reading, it also depends on the microorganism that is being researched. A standard curve can be calculated from data, but it is quite difficult to attain an exact result.
A very useful article on the correlation between the two measurements can be found here (from the Brazilian Journal of Microbiology).

Welcome to biology SE - links to external material that allow further reading or offer support to content are strongly encouraged here


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How common is it for environmentally occurring bacillus strain to contain some sort of plasmid?
I am designing a method for testing whether two new bacillus isolates, that are ionic silver resistant, store the silver resistance mechanism on a plasmid or on the chromosome of the bacteria.
In my method, after I do a plasmid extraction on the bacteria, I want to use nanodrop to see if plasmids are even present in the bacteria (if no plasmids are found, then the silver resistance mechanism must be stored chromosomally). After this, I want to use heat shock or electroporation to place the plasmid in a silver sensitive bacteria, and see if the newly transformed bacteria is ionic silver resistant (this would suggest the resistance mechanism is stored on the plasmid)
I have been looking at how other people have tested for this, and I have found that the nanodrop part is not done. I thought the nanodrop would be a good control to make sure the plasmid extraction went well, and if plasmid DNA was not found, it would save me from doing the rest of the experiment.
One reason why I thought they didn't do nanodrop was that perhaps most environmentally occurring bacillus contain plasmids, and thus nanodrop would be unnecessary step.
So my question becomes how common is it for environmentally occurring bacillus strain to contain some sort of plasmid? Also, if anybody has any suggestions for improvment of my method, please let me know.


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Nervous stimuli and neurotransmitters and impacts
As far my knowledge, in body parts generally **acetacholine ** is the neurotransmitter. Which is responsible for most nervous impulses.
Consider a body part, say, foot. Only one  nerve reaches here. When ant bites there, the impulse of pain and irritation moves from there ;
Secondly, when some soothing agent comes there the impulse of comfortness moves from there
Now, neurotransmitter is the same, nerve is the same, but different impacts are observed.
My teacher said that the impulse moves to different parts of the brain.
But how are the impacts really understood, analysed and sent to different regions ( as entrance of all stimuli enter through the same brain stem,)
In short,
My question is that how does our brain analyses two different stimuli when neurotransmitter is the same, nerve is the same and enter the brain through the same brain stem. They must be going to different regions of the brain but how is that decided

Please see this related Q&A. Although that question's focus is on the motor system, the answer also provides adequate coverage for the sensory system. If you still don't understand something after reading the linked Q&A, please edit your question accordingly in order to let us know what more specific details you need help with.

Would you be kind to tell that What specifications you require?

Did you read the linked question? Does it cover your question? Or is there something more you need to know?

This related question talks about the action of peripheral nervous system. By presenting two models. I am not talking about that. My question is that how does our brain analyses two different stimuli (like i have written in the post), when neurotransmitter is the same, nerve is the same and enter the brain through the same brain stem. They must be going to different regions of the brain but how is that decided?


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why hiv genome not attacked by lysosome in macrophage
HIV cells lifecycle in macrophages suggests the early phase with naked genome entering the macrophage along with reverse trancriptase enzyme. i am thinking that macrophages are abundant with lysosomes and so called defense sodiers of the body who engulf all pathogens and kill them with lysosome action.
My questions

my question is that why this soldier is not able to distinguish a foreign and rather weird kind of genome of a retrovirus and not sending lysosome to act upon it at the very moment of entry of genome.
My second question is that why do T LYMPHOCYTES undergo lysis but macrophages are not affected?


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How do trees grow?
A nail is inserted into a tree's trunk at a young stage of its development. At which height will we find the nail after some years? Will it be found higher or at the same height(What extent of accuracy?) as when it was inserted? I have two specific questions:

Doesn't the intercalary meristem, which is responsible for the
increase in internode length, affect the relative position of the
nail?
When plants are at a young stage their branches' position would be low but after some years they would have moved higher. How does this
happen if growth only happens in the apex? As an example, in the
following image the position of the branches changes with time. Why
wouldn't the same happen with a nail?

Welcome to Biology SE! I have suggested an edit of your question in an attempt to make it more cleear. Feel free to roll-back the changes if you do not think it was useful.

One cell at a time.

You will find the nail at the same height.  Trees grow by a) adding to the tips of their branches (sometimes sprouting new branches at nodes), and 2) adding to their diameter.  (Only a thin layer inside the bark actually grows, forming the annual growth rings.)
The branches changing position in your image is an illusion.  The branches do not actually move.  What happens is that the higher branches grow larger, shading out lower ones, which die (or become leafless support branches).  You can see this most obviously in many conifers, where the dead lower branches tend to remain on the trunks.  If you cut and split a trunk, say for firewood, you will find knots in the wood where the older, now dead, branches were once attached.

Nice answer. It would be even better if you included some references.

@RHA: If you want references, feel free to add some.  I don't have any, other than high school biology and spending a lot of time observing trees.  As for instance signs & wire fences nailed to trees.  Decades later, they're at the same height, but the tree bark has grown around them.


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How to prevent a old promoter region from attaching onto a plasmid instead of a new one during ligation?
What I am trying to do is take out a existing promoter region in a plasmid, and replace it with a new one. So first I use the appropriate restriction enzymes to get rid of the existing promoter region. Next, I add in the new promotor fragment which has the appropriate sticky ends, and then through ligation, I want to place the new promotor in the plasmid.
Since the old promotor region and new promotor region will have the same 'sticky ends', how do I prevent the old promotor region from getting placed into the plasmid instead of the new one during ligation?

Performing the ligation and sequencing 5 - 10 clones is an option. You only need one clone with the 'new' promoter which will be added to the ligation in excess right?

Run it out on a gel after digestion  and extract the vector only.
Treat with a phosphatase after digestion. This will prevent religation since you need at least one of your fragments to be phosphorylated for the ligation to work.
(A must regardless) sequence several colonies at the end.

I recommend doing all three.
Edit: option 4: digest with a third enzyme that cuts in your old promoter but not the vector or the new promoter.

If your new promoter is short and you are using a pair of oligos with sticky ends that don't need to be cut, you should either phosphorylate the oligos with polynucleotide kinase, or don't dephosphorylate the vector. You need one or the other to be phosphorylated to get the ligation to work. Also, picking many colonies is mandatory. I typically do 24 minipreps at a time because that's what fits in the centrifuge. Do as many as you can. There have been many times where only 1 miniprep was successful. Speaking of which, have a good way to screen, you need nice clear results.

So to confirm, once I get rid of the old promotor region, run it on a gel to isolate the 'opened plasmid with no promotor region'. Once I have this then I preform ligation with the new promotor region....

On the plasmid I will have amp. resistant gene as a way of tracking the succesful transformed bacteria.

@RadekMartinez Yes, you are describing the standard cloning procedure, cut, paste, check for good plasmids. What is your new promoter? How large is it?

I am not sure yet. However it is not like 20 - 30bp, much larger.


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Definition of Ancestral Eudicot?
I am wondering what are examples of ancestral eudicots which can be purchased from an aquarium store, and or grocery flower store.

Have you tried googling this?

yes. that would be my first go to ...

and what did you find? Tell us a bit, so we can help elaborate!

All I found was the definition of ancestral (in terms of a cladogram). I mean, there are several plants which can be purchased from aquarium and grocery stores. However, since I am not a plant biologist it is hard for me to even guess how to go about figuring which ones are ancestral eudicots

If someone could tell me the answer, and how to go about figuring something like this in the future, I would really appreciate it.


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Does heating proteins before a SDS-PAGE gel effect gel result?
I need to isolate a protein that a bacteria has excreted into an agar plate. My plan is cut out parts of the agar, heat the agar to melt it and then concentrate the protein through some purification kit, and then run SDS-PAGE to see if I was successful in isolating the protein.
However, I am not sure whether heating the unknown protein before SDS-PAGE will effect the gel run in anyway. Does anyone know? I know if might denature the protein in some way, but I am doing that anyways with SDS.
Thanks.

I think this depends strongly on the kit you are using for the purification. Agarose doesn't need to be heated until boiling, usually they get liquid around 60°C. Or you could try to use some low melting agarose in a higher concentration. These melt around 37°C.

I guess the next question is what is the most effective way of extracting proteins from LB agarose. Are there any pre-defined methods for this?

Not that I know of. It also depends on your agarose.

I will have to be using LB Miller Agar

Could you just make a liquid subculture and isolate your protein from the medium?

As far as I know, it has an effect. If you denature your protein before running the gel, you do a normal SDS-PAGE and seperate the proteins by their size. Since you use SDS, the charge of the protein doesn't have any influence on your gel.
If you don't heat your proteins before, you do a so called native PAGE. Here the size of your protein doesn't matter so much, because you also seperate for charge, folding, pH and so on. You may have a look on this methods paper for more information.

It's native PAGE, using SDS is by definition not native. I guess a typing error?

I changed it to native PAGE :)
But SDS is the most common used, so the most will understand it.

It's not the heating per se that separates native from SDS PAGE. It's the SDS in the gel and the running buffer and the presence of denaturing agents in the preparation of the samples. Native gels you do after you know a few things about your protein and you want to get more information. But the first step in isolating and potentially identifying a protein from a culture (among SDS and native gel) is most probably the SDS PAGE as you would be able to separate all the proteins by size and as monomers.

If I use regular PAGE, how do I extract the protein from the agarose that the bacteria are growing on?

It would depend on the temperature and how long you keep it there. For SDS-PAGE we normally do it at 95 degrees Celcius for 5-10 minutes. Keeping it much longer could degrade the protein and fragment it.
You could try to do your culture on agar of lower concentration.
Alternatively, you could aim for liquid cultures, as it would facilitate handling before the SDS-PAGE.
(The whole story changes if you expect your protein to be heat-tolerant - as it could be the case that your bacterium is a thermophile)

I am not sure. I am seeing a zone of clearance around the colonies in the presence of silver, which makes we suspect that some exoenzyme is being released.

You mean you add silver in the agar? Can you add it in a liquid culture and see what extracellular enzymes you can detect in the SDS PAGE afterwards?


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MOPS Media Recipe Protocol - Well Defined
I am trying to find a clear protocol for making MOPS media. However, when looking online, I am finding that this media is loosely defined and I can not find a good protocol. (I have been looking for a couple of hours now)
In addition, there seems to be something called 'MOPS buffer'. What is the difference between the two?
Additionally, if someone could direct me to a good protocol for this media I would appreciate it.

This seems to depend strongly on what you want to do with the bacteria.  What do you want to do with you bacteria? Mops is one of the buffer substances used in bioscientific reasearch. Dissolved in water and brought to the right pH it makes MOPS Buffer.

I am doing a metagenomic anaylsis on soil, thus there are probably multiple bacterial types. It is suppose to be used for a general culturing media.


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If you have water on you, does it *actually* cool or down, or do you just *feel* cold?
I'm sure many people have noticed after getting out of a shower or out of a swimming pool that moving air makes them feel colder. It seems like one way to beat the summer heat is with water and also moving air. But, does having water on your body actually cool you off more with moving air, or is that simply what it feels like because water cools differently than air?

I'm voting to close this question as off-topic because it belongs to Physics.SE

@Remi.b It's really more about what people feel, the motivation is that people feel cold. You really think a bunch of physicists are biology experts who know the chemistry behind what would cause a different feeling? You can't determine the answer belongs in physics unless it already becomes answered and the answer is purely physics.

Could the question be rephrased Why do we not sense temperature but thermal energy transfer?? If yes, then I'd agree it belongs to Biology.SE

I don't think this is a physics question; it has everything to do with biology and how we perceive changes on our skin.

When your wet skin experiences air flow over it, water will evaporate. Evaporation causes cooling, as energy is transferred from the remaining water molecules to the ones that evaporate - energy in water molecules is being experienced as heat. Less energy -> less heat -> sensation of cooling.
This is why you feel cold, as opposed to when you stay submerged in the pool, or your skin is dry and it is just air movement - no evaporation is taking place.

For extra points do you have any references that can support that?

@DaneJoe This is rather basic chemistry, covered by any introductory chemistry text. Although we like references at biology.SE, usually we don't bother for basic textbook knowledge (it gets a bit too pedantic).

@BryanKrause Wrong. We don't know that enough water is evaporating at a high enough rate to account for this phenomena. I've studied chemistry, we definitely didn't study temperature change due to water evaporation induced by moving air.

It doesn't matter if the air is moving or not, except to speed the rate of evaporation. Surely in chemistry you learned about the heat of vaporization, which is quite high for water because of hydrogen bonds.


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Does capsaicin in food kill bacteria?
Do foods like spicy peppers have less bacteria on their interior due to their capsaicin content? Probably not, but it seems like they could. Or I guess in other words: does capcaicin provide any benefit from anti-bacterial properties?

I should also note the wording in your title doesn't make too much sense. Based on your description though, I could only assume you were asking if capsaicin can kill bacteria in food.

check this page called " https://www.quora.com/Do-capsaicin-products-have-antiseptic-or-microbicidal-properties " google is great don't you think?

@comprehensible I'm here to find references more credible than a mere quora post.

This 2015 article demonstrated that capsaicin kills streptococci (the bacteria that give you throat infection).
However, relatively high concentrations of capsaicin are necessary to kill these bacteria: The minimal inhibitory concentration was determined to be ~128 µg/ml. given that 6.6mg capsaicin correspond to 100.000 scoville, a bowl (400 ml) full of bacteria-killing chilli would need to contain 7-8 habanero chili peppers - I can't imagine that going down well - particularly not with an already inflamed throat.
Interestingly, the same paper also demonstrated, that lower - more practical - concentrations (8µg/ml or 1/2 habanero per bowl) of capsaicin dramatically reduce the ability of streptococci to enter cells. This means that while capsaicin is likely impractical as an antibiotic, it may actually help your body to fight the disease and/or reduce the risk of contracting a throat infection in the first place.

"Given that 6.6 mg capsaicin correspond..." - I just added that into the Wiki article earlier this week haha. Funny seeing it come up

@Jam good job. IMHO that is the single most important information on that page ;-)

Yes it has some bacteriostasis and antibacterial properties, The only way for you to find it is to do some Agar and similar tests on chillis to find out about their microbes. You will probably find that some chillis have zero bacteria inside them, and that the surface of all chillis have many species. Seeing as it's a weak antibacterial compound, bacteria will probably have evolved to accompany the plant.
hot chillies don't tend to go mouldy on the plant though. they just dry over time.
Fruit generally don't have many bacteria inside them, for example this study shows that a large proportion of tomatoes don't have bacteria inside them, and the bacteria that get in probably do it through the base of the stem.
http://aem.asm.org/content/11/1/7.full.pdf
Humans rarely get infections from eating ou fruit and fresh plants, they are a low microbe environment. even melons, one of the most notorious fruits which are source of deaths and food poisonings, are thought to be from bacteria that grow on the outside of melons.
activities of capsaicin and effects of its antiseptic application to ketchup
http://en.cnki.com.cn/Article_en/CJFDTotal-DLJY200903023.htm
Extract the natural antiseptic material in capsicum [J]
http://en.cnki.com.cn/Article_en/CJFDTOTAL-ZGTW200008001.htm
Study on Bacteriostatic Action of Capsaicinoid [J]
http://en.cnki.com.cn/Article_en/CJFDTotal-SDKX200702008.htm
Study on the bacteriostasis of capsaicin in Capsicum annuum
In vitro activity of capsaicin against Helicobacter pylori
https://www.researchgate.net/profile/Fadile_Zeyrek/publication/267209796_In_vitro_activity_of_capsaicin_against_Helicobacter_pylori/links/5447a8540cf2d62c30508fb9.pdf
Antibacterial activity of capsaicin-coated wool fabric

@Charles Peppers are fruits by definition. Capsaicin was even named after peppers (Capsicum sp.) What are you even talking about!?

tomatoes are related to peppers. The research papers on bacteria inside fruit and antibacterial actions of capsaicin are pretty relevant, seeing as there are no measurements of bacteria colonies inside chillie pepers on google scholar.  It's a bit of a noob website, bacteria inside of peppers is clearly a research question rather than a complex or general knowledge question that requires experience. It's fine i don't mind learnin fruit bacteriology one day if it helps out a lazy person who doesnt have the energey to do his own research.


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If people can survive being frozen some, why not indefinitely?
I've heard of cases and also personally met someone who survived with a full recovery after they were taken to the hospital after being found unconscious in the snow for (presumably) more than 45 minutes, and claimed their temperature dropped below 0 degrees (Celsius) after they recovered in the hospital, though obviously I can't go into their medical records and verify that temperature. What mechanism allows someone to survive being so cold for so long, particularly if there is a lack of oxygen to the brain, and if someone can survive it for that long, why not indefinitely like for cryogenics?
I'm no medical expert by any means, so it's possible it's a combination of things of course, but for references the first being that a doctor telling me first hand that it's possible, but rare for someone's pulse to stop in frigid temperatures and still recover after more than 10 minutes with a lack of oxygen referencing something about the decomposition of tissue slowing down, and then also news articles like these that I don't have any particular reason to doubt given the consistency of such a story across different venues, which also suggest something about frigid temperatures allowing people to survive injuries, oxygen deficiency, or tissue damage for a longer than normal time.
I'm not completely sure about the lack of oxygen part of the question because it kind of seems like they evaded that part of the question, but they definitely said frigid temperatures delay the decomposition of tissues in someone's body and suggested someone could survive longer due to that, and I don't know why tissue decomposition would be a problem unless someone had already lacked oxygen for a long time to make them susceptible to it.
https://news.google.com/newspapers?nid=1876&dat=19810109&id=CkosAAAAIBAJ&sjid=uc0EAAAAIBAJ&pg=6891,1583308&hl=en
https://en.wikipedia.org/wiki/Jean_Hilliard
http://www.nytimes.com/1981/01/03/us/dakota-teen-ager-recovers-after-being-frozen-stiff.html
http://abcnews.go.com/Health/hypothermia-save-boy-trapped-ice-30-minutes-heartbeat/story?id=9506900
http://www.dailymail.co.uk/news/article-3406926/Man-presumed-dead-frozen-solid-road-recovers-living-medical-miracle.html
https://en.wikipedia.org/wiki/Anna_B%C3%A5genholm
I remember the old saying "better cold and dead than warm and dead," I guess this makes sense for when you find someone unconscious.

Can you please provide a reference for the claim that people can survive with full recovery after their body temperature went below freezing point?  The record of the coldest body temperature recorded for a surviving human is held by Anna Bågenholm with a body temperature of 13.7ºC. I am voting to close as opinion-based (unless you can provide a trustful reference for your claim).

"heard of cases" - citation needed. I suspect, as @Remi.b suggests, that these are cases of people dropping to hypothermic temperatures, not dropping literally below freezing.

It's possible it's a combination of things of course, the first being that a doctor telling me first hand that it's possible for someone to drop unconscious due to frigid temperatures and still recover, and then also news articles like these https://en.wikipedia.org/wiki/Jean_Hilliard http://abcnews.go.com/Health/hypothermia-save-boy-trapped-ice-30-minutes-heartbeat/story?id=9506900 http://www.dailymail.co.uk/news/article-3406926/Man-presumed-dead-frozen-solid-road-recovers-living-medical-miracle.html

@DaneJoe Two of the articles you link actually report body temperatures at 13.7ºC (which seems to be the world record) and 32.22ºC. Some of the newspaper articles use the misleading expression "frozen solid" but do not actually report a body temperature (that I could find at least). I very much doubt any of them actually had a body temperature below 0ºC

@Remi.b Fair enough. Still, something about these reports suggests there's a possible correlation between frigid temperatures and surviving critical conditions that would otherwise be deemed impossible in warmer temperatures. In terms of chemistry you could say that frigid temperatures can also slow down the negative chemical processes that occur that would normally lead up to death or ensure death after unconsciousness, though could it also be random mutations?

For your curiosity... freezing tolerance ask for very specific adaptations. You can have a look at 1. How tolerant are ants to cold?, 2. How do insects survive the winter?, 3. wiki > Freezing tolerance in plants and 4. wiki > Insect winter ecology

@Remi.b Thanks but I'm not interested in etymology at the moment.

@DaneJoe I think your answer is kind of obvious then and not worth a question here: Cryogenics is about freezing people actually to (and below) 0C. All of the sources you have show people not frozen nearly to that extent. At those milder temperatures you have no ice crystal formation and no real freezing and a much less extreme recovery. It has nothing to do with cryogenics. You might as well ask "Why does food cook in my oven at 150 degrees C but it doesn't cook outside at 35C"

@BryanKrause I think scientists who get paid a salary to research it would disagree that it's a waste of time. This is about the specific mechanisms that allow people to survive frigid temperatures which could also easily be any pattern that might show itself as a precursor to such technology, especially the points about that frigid temperatures seem to allow people to survive longer with lower oxygen and reduce tissue decomposition. If the temperature is cold enough, then no bacteria is active either, which means no decomposition whatsoever.

The issue is that your question (People can survive for little time at freezing temperature. Why not indefinitely?) is based on a false prior that humans can survive at freezing temperature. The question is therefore opinion-based and must be closed as such. Asking What are the known mechanisms to tolerate below zero body temperature? would be an acceptable question (although arguably too broad but I am not sure).

You might be interested in protective hypothermia.

@DaneJoe The problem is that you made your question based on a premise that people survive frozen but can't survive cryogenics...except they do not survive frozen. They survive slightly colder than normal.

@Remi.b If it was opinion based I wouldn't be asking a question. I'm not an expert so I'm not going to rule out the possibility of someone surviving freezing given the evidence I presented, which is the opposite of opinion as it is the extrapolation of data to lower temperatures. These are temperatures much lower than "slightly" normal without doubt.


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Why the C6 intermediate molecule in the Calvin cycle is so unstable
During the Calvin cycle, it is speculated that after Ribulose bisphosphate carboxylase/oxidase carboxylate ribulose bisphosphate, a 6C molecule is created and decomposed instantaneously into two phosphoglycerates because it is extremely unstable so:
Can anyone clarify why this molecule is so unstable? and...
how we know this molecule exists?.
I did not find anything useful while researching this, perhaps I'm not looking properly or there is no debate about it.

Please cite a reference for your assertion with date. On checking my copy of Berg et al there are full details of the reaction mechanism including the components of RUBISCO involved. I imagine it's a mixture of enzyme structure, chemical logic and experimental evidence, but you will need to go to the original papers if you want the details. There may be uncertainties, but if so it won't be alone. However RUBISCO has been intensively studied.

The question of why the molecule is unstable belongs to the realm of chemistry, which is not the subject of this list. Presumably the reaction for its hydration is thermodynamically favourable and there is a reaction mechanism which allows the reaction to proceed with a low activation energy.
The question of the existence of 2-carboxy-3-keto-D-arabinitol 1,5-bisphosphate and its role as an intermediate in the RuBisCO reaction was solved in 1986 and is no longer the subject of speculation. Its synthesis was described in a paper in Phil. Trans. R. Soc. Lond. B, which is behind a pay wall, but can be found in a post on ResearchGate.
In brief, they trapped this C6 compound in a more stable form with acid, and so could characterize it chemically. Its enzymic hydrolysis could then be studied at a slower rate.
The subsequent solution of the crystal structure of RuBisCO provided further confirmation of the reaction mechanism and molecular information on the role of the enzymic groups and magnesium ion cofactor. See, for example, the review by Gutteridge and Gettenby in Cell.
So the era of speculation would appear to be long past, and the account in standard biochemical texts such as Berg et al. — shown below — would appear to be reliable.


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What is the largest culturable bacterium?
E. coli is easy to grow in the lab. It has a volume around $0.6 \mu m^3$. Source
T. namibiensis can be much larger, with a volume on the order of ${10^6}\mu m^3$. Source
However, T. namibiensis is not easily cultured. Source
So, the question: what's the largest bacterium (or failing that, a large one) that can be cultured under standard lab conditions? Let's define 'standard lab conditions' as growing with a doubling time of <48h between 25C and 50C in a liquid media with normal oxygen.

It all depends on what you mean by standard lab conditions and largest - length, width, volume, genome size?. There are lots of bacteria that grow at odd conditions (e.g. anaerobic), but are perfectly easy to grow under those conditions. Try the spirochetes as examples.

Good point. Let's say: can grow with a doubling time of <48h between 25C and 50C in a liquid media with normal oxygen. And measuring largest by volume. Is there a spirochete that fits the bill here?

It would be a good idea to add those conditions to the question. Not sure on spirochetes doubling time, and I think anaerobic from memory.

You’ve put a bounty on this so I’ll have to wait to vote to close, but it’s a “Guinness Book of Records” question quite unsuited to this site and of no interest to professional biologists. There are microorganisms which one would have much more interest in culturing where the problem is far more subtle than size.

@David I disagree, and perhaps I need to add more context to the question to justify my interest. I am a professional microbiologist. IIRC, I posted this question after a journal club about a paper comparing cell sizes in eukaryotes and bacteria, and making some arguments about diffusion and the necessity of a nucleus after certain length scales—it referenced some large bacteria that could not be cultured, so I wondered whether there was a large bacterium that could make a good model for some of the questions they raised.

OK. But there is a reason that the guidelines on asking good questions tell you to provide context. And remember questions are also supposed to relate to "problems that you face". There is nothing in your question that indicates why you want to know this, and the site tends to attract "tourists" who have nothing better to do than ask GBR-type questions. I'll delete my comment when you have read it, but would suggest that you incorporate our remarks into the question.


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Can one become suddenly ambidextrous?
Is it possible to become ambidextrous? i'm 67 and recently and suddenly became ambidextrous about a month ago. I can write w both hands at the same time.

Normally in a right handed person the left hemisphere is considered dominant.  However, a new lesion in the left hemisphere can cause loss of this dominance so it is possible that this has occurred.
Alternatively, if the subject is now able to write using both hands concurrently but different material, it suggests that the two hemispheres are disconnected, the so called split brain syndrome which occurs with lesions of the corpus callosum.  However, ambidexterity is not described in that syndrome.
Anyway, you need to consult your physician.

Nice that someone affirms that this can happen. The brain is a mysterious organ, and I agree that a brain lesion can cause this. It would be interesting to compare quality of writing in each hand.

You can't suddenly become ambidextrous.  You can train yourself to use objects with the opposite hand, and become use to using your other hand.
Your body learns on repetition- Repeating something over and over till it becomes a habit.  It takes time for your body to adjust to the change but you can become ambidextrous through training your body.
You just have to have the patience and the will to do it.

If this at all helps you.  Show some support.

Answers at Biology.SE require some references to be complete, especially for anything that goes beyond sort of "general textbook" knowledge.


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Replicator dynamics giving probabilities greater than 1?
I have a linear replicator equation and I want to simulate its dynamics to find the resting point and hopefully the Nash equilibrium.
I defined strategies' payoff as  $ \vec f = C*\vec p+ \vec b$, where $C$ is a community matrix similar to the one in Lotka volterra models, $p$ is the vector of probabilities for each strategy and b is a vector of constants. From what I understand, this is very similar to the replicator dynamics for a linear model, except that I'm adding a constant.
However, when I iterate over $\vec p_{t+1} =  \vec p_t+ \vec p_t (\vec f- \sum\vec f \vec p_t) $,   $\vec p_{t+1}$ frequently gets values greater than one or smaller than zero, which from my understanding is not suppose to happen.
An example to show the issue:
$C = \begin{pmatrix} -1 && -1.1 && 0 \\ 1 && -1.0 && -1.1 \\ 0 && 1 && 0 \end{pmatrix}; \space \vec b= \begin{pmatrix} 0.7 \\ 0 \\ 0 \end{pmatrix}; \vec p_0 = \begin{pmatrix} 0.8 \\ 0.9 \\ 0.25 \end{pmatrix} $
In this situation,  the second element of $\vec p_1 $ equals 1.448550!
What could be causing this error? Am I calculating  the replicator dynamics wrong? Does adding a constant to fitness "breaks" the replicator dynamics? Is my understanding wrong and replicator dynamics can go above 1 or below 0?

Can you please describe the meaning behind your equation because it does not really look like Lotka-Volterra equations? Lotka-Volterra equations are explained in this post.

Sorry, I mean that payoff of a strategy depends on the frequency of use of these strategies. This is represented by the matrix C. In the example, the -1 on the top left indicates that the more strategy 1 is used, the smaller is it's payoff. Likewise the more strategy 2 is used the smaller is the payoff of strategy 1 by a factor of -1.1. however irrespective of strategies distribution in the population there is a baseline payoff b for every strategy.

It is hard to tell what you are trying to compute. It is not obvious to me looking at the equation that $\arrow p$ must contain probabilities. Also, it is a bit weird that you are adding a baseline at every generation. Of course, the baseline fitness / probability (or whatever is represented of $\arrow p$) will very quickly become greater than 1.

$ \vec p$ is supposed to represent the proportion of time exercising a behavior (eg feeding). Every individual, ie every row of C and every element of in p, is supposed to have a value going from 0 to 1, representing how much of the time it spends doing said behavior. but the benefit of foraging more or less depends on how much other individuals are doing. Thus I want to know if there is any equilibrium point where all individuals stick with a certain proportion of time feeding. Hope it helps, and thanks for the time invested

This is happening because the fitness for your first strategy can be negative. In the case of the discrete replicator dynamics, the fitness cannot be negative. Otherwise, you can leave the simplex. Note that the continuous replicator dynamics doesn't have this restriction (the fitness can be negative).