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Is there a negative correlation between the mRNA produced by the cell and the time of extraction?
I am doing some data analysis about gene expression time series. When I plot mRNA produced by P. Furiosus cells irradiated by gamma radiation against the time of extraction, it seems that there is a negative correlation between them. Is it a good result from a biological point of view ?

$\gamma$-irradiation produces single- and double-strand DNA breaks, depending on the dosage, and activates DNA damage repair pathways like p53. During this time, the cell cycle arrests and most if not all mRNA production ceases. For sub-lethal doses of $\gamma$ rays, I would expect to see newly-produced mRNA levels drop off fairly quickly with time following the initial dose, then possibly begin to ramp up again later as the damage is repaired and the cell cycle arrest checkpoints released.

Thank you for your answer MattDmo, but, in this way I still wonder how can be the demage repaired if the production of mRNA in order to produce proteins for DNA repairing is stopped ?

@Manuela cells accomplish this by pre-making the DNA repair machinery so that the proteins are already present in the cell, they just need to be turned on.

Ok, so I have a last question: it also seems that the mRNA produced is higher for the samples which are irradiated with respect to the not irradiated. I am not a biologist, but I was doing this statistical data analysis hoping to find this behavior, so that I can say that P. Furiosus, when exposed to gamma irradiation, produce more mRNA with respect to the samples not irradiated in order to repair better DNA . So this reasoning is nonsense?

@Manuela I don't think you can say much of anything without more information. You may be able to show that, on a cell by cell basis, irradiated cells seem to produce more total RNA than non-irradiated cells, but you can't say anything about why they're doing it. I strongly suggest talking to a biologist familiar with the details of your project. The vast majority of my work has been with mammalian systems, and for all I know there could be different DNA repair mechanisms in Archaea that I'm not familiar with.

All right, thank you so much @MattDMo


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Polymerase Chain Reaction Specifics
While going over PCR in my biology lecture this week I have come across a few questions I have about this process.
First, since PCR focuses on trying to replicate a specific targeted DNA sequence many times in a short amount of time, are the primers used in every cycle the same sequence? I understand the forward and reverse primers would not be the same but the forward primer for one strand in one cycle, would it be the same as the forward primer for a daughter strand of let's say the 8th cycle?
Second, why are primers not reusable for different cycles? I think this would be based off of the answer to my first question. If the primers are essentially the same sequence, why do new primers have to be used for every cycle?
Thank you in advance!

are the primers used in every cycle the same sequence?

Yes.  You put the whole reaction on the thermocycler, and then walk away until all the cycles are complete.
But one could do a second round of PCR with different internal primers on that first PCR product, if you wanted.

Second, why are primers not reusable for different cycles?

Are you asking why you can't put in 10 molecules of forward primer and get a million product molecules from that?
Each molecule of primer that is used as an extension template is incorporated into a whole stand of PCR product.  It's not a primer any more.

The primer is incorporated into the start of the new strand. The number of dna strands produced is limited by the number of primers.

source: Stack Exchange

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

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Where are the ATP synthases synthesised?
The nano-machinary of energy production ATP synthase is well known to exist on mitochondrial inner membrane and chloroplasts. But how and where are they formed or synthesised ?

Welcome to SE Biology. Please read the Help on asking questions, where you will see that you are expected to show the research you have done before posting. Have you searched for ATP Synthase or Synthesis of Mitochondrial Proteins. There must be Wikipedia entries on this topic.

Sorry that I have no such things to add. I'm only a 12th grade student just interested in the topic. Thank you for the advice , I'll try to improve the way I post questions.

Yeah : ) questions don't even end there. One can go on and on endlessly to new levels of understanding. I would definitely be delighted to feed my 'what's next's but  it's inevitable after a certain level there will be none to answer. That doesn't curb the quest though ;) thank you for finding me those topics !

The interesting thing is that the mitochondrial ATP synthase consists of many subunit proteins, both encoded by nuclear DNA and mitochondrial DNA. It has long been unclear exactly how these synthases are assembled, and what differences exist between bacteria, yeast, and humans - where ATP synthase formation is normally studied. Regardless, each of these proteins is translated on ribosomes from mRNA transcripts of genes, just like regular proteins. However, these must come together correctly (in the right order) and end up in the correct location.
There are recent publications that answers your question rather directly.
Assembly of the membrane domain of ATP synthase in human mitochondria
In short:

We have shown that the assembly of human ATP synthase in the inner [mitochondrial] membrane involves the formation of a monomeric intermediate made from 25 nuclear-encoded proteins into which the two mitochondrially encoded subunits are inserted and then sealed by association of another nuclear-encoded protein, thereby dimerizing the complex. Association of a final nuclear protein oligomerizes the dimers back-to-face along the cristae [inner membrane of the mitochondrion] edges.

A commentary on the paper is also available, which provides insight into the historical and biological context and difficulties which the paper addresses and overcomes. It may be worth reading their synopsis first. You can find it here:
Assembling the mitochondrial ATP synthase

I admire the elucidation. Thank you !

And sorry that the question was closed. The mods and voters are quite overly zealous here sometimes. Neither a duplicate nor a homework question. Interesting question, certainly.

At first it somewhat disappointed me too. being a newcomer in SE I had problems understanding a dialogue box, which stated that somone suggested there's something similar to my question out there and asked me if it meets my queries. Finding that question resourceful and interesting I clicked yes and right after that my question turned duplicate . Surprised me ! Anyway, the tiny piece of machine inside our cells is marvelous enough to ignore all that, Thanks :)

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What are the differences in ultrastructure of cilia and flagella?
Cilia and flagella are aimed for similar perpose, motion. And both of them show the (9+2) microtubule arrangement. They are nearly identical in structure. But to be more specific , where exactly does the little difference lie (except the 5-6 bridge) ?

Perhaps you mean that flagella spin to provide locomotion whereas the cilia tubules themselves beat. the flagellar motor vs the fixed anchored structure of the cilia...

Thanks for the help but the question actually asked about the difference in their 'ultrastructure' or 'micro-anatomy' you may say...

Eukaryotic cilia and flagella are identical in ultrastructure.
The only reason for two different terms for the same thing is historical usage. Traditionally, 'cilia' has been used for shorter, more numerous structures and 'flagella' for longer structures which are fewer in number.

Although cilia and flagella are the same, they were given different names before their structures were studied.
Source: Lodish et al (2000)

In fact, some have suggested doing away with this dual terminology, and simply calling all these structures 'cilia'.

But isn't there at least some subtle difference like the 5-6 bridging bond in flagella that is absent in cilia ?

@Sarika I am not familiar with that... Can you please share a source for this information?

Thank you for asking me for source! That finally cleared everything :) as I thoroughly looked up once again and found out that both cilia and flagella do contain that '5-6 bond'. I'm sharing the link here: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3468612/


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Species Identification and Care
We've had this plant for a while as one of two. And both have grown incredibly over the last year. We actually know very little about these beyond watering when they look a little sad and would like to look after them better.
We can see that the plant has a 'trunk' of sorts now. Should this be under the soil? Are the plants large enough to repot? Should I change the soil?
The pot is 28cm wide at the widest and the plant is 32 cm high from the soil.

This is one of the many Yucca species, probably Yucca gigantea as this appears to be the spineless form with floppy leaves.
The trunk should protrude from the soil, indeed this species can get quite large with several trunks/branches, each with a cluster of leaves on the tip.
They are hardy indoor and outdoor plants which grow best in full sunshine and dry warm conditions. They are not particularly frost tolerant, but will survive light frosts with maybe some damage to the leaves if in a sheltered spot.
They do best in free-draining soil which retain some water and nutrients (so don't go to cactus extremes), something like 1/3 peat with 2/3 sand should do fine. They are drought tolerant and have generally low water requirements. You should be able to re-pot this plant without any problems every second year. Just water the day before, remove from the pot and replace some of the soil. Alternatively they will do well with a feeding roughly monthly of a balanced liquid feed.


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Why don't people seem to die from salmonella in bites?
As far as I know, reptiles have salmonella in their mouths as part of their digestive process. Every time I hear about someone being bitten by an python or alligator or monitor either at a zoo or in the news or from a private owner, it seems like whoever is bit recovers with ease.
How come something as virulent as salmonella that can evade an immune response doesn't cause whoever gets bitten to nearly immediately become septic? Is it because salmonella only attacks epithelial tissue and there isn't much of that deep in an arm or leg?

Important to considera as welk that a Salmonella infection isnt always that bad, even the gastrointestinal salmonella infection can be mild depending on the serotype. Salmonella is actually very common in some parts of the world and it isnt super deadly or anything.

@MikeKatz45 Others and myself been through enough food poisoning to know everything you just said is total BS.

nop, look at my answer

@MikeKatz45 I looked at the first few words and figured it was a waste of time and ignored the rest, especially considering the question is already answered. You can't speak against people's personal medical history and there is plenty of documentation that people have died from salmonella in the past. I am going to take a rare opportunity to downvote for the first time ever, congratz on being the only one to earn that.

Yes, those like you who make the mistake of assuming they are omnipotent gods. This is not a religion site, this is a biology site.

I provided all the sources to backup what I'm saying (which is relevant to responding the question because Salmonella doesn't always kill you or cause severe disease). The one who is being unreasonable is you and I haven't seen a single source to discuss this matter from your side, in that sense you are acting in a dogmatic way, not me. I commented this question because I thought it was a good question and that the answer given previously was oversimplified and I don't know why you took it like I was being an "omnipotent god" lol.

You arbitrarily mixed personal opinions with references, which doesn't change anything. If you want to go into denial over deaths across the globe, you have much bigger problems than this site.

What part exactly is a personal opinion? I never denied Salmonella can be as severe to kill you, I was only pointing out that it isn't as simple as saying Salmonella infection = dying or almost dying. The bacteria can cause a wide spectrum of things,  really don't get why you have this attitude when there is reason in all I said.

Not even ebola=dying, but that doesn't mean it isn't an enormous problem for whoever contracts it. Seeing as how that's true, your presence here has lead to no good, you clearly have no intention of contributing, you are only here for your own personal insecurities of your own intellect and nothing more. In far fewer words, Stephanie has accomplished what you failed to and without any emotional bickering, the topic is resolved and you have no purpose here.

In the case of salmonella yeah sometimes it isn't a problem at all cause you can be completely asymptomatic (as I have repeated until tireness now). I invite you to read this whole series of posts again and figure out who doesn't have the intention of contributing at all, you are the one who has been in a defensive position all the time (since you mentioned insecurities lol) . I won't make further posts here since you clearly have no interest in the question anymore whatsoever and it was all a waste of time for both you and me

Yet again you've proven my point. Whether or not it "can" be asymptomatic is regardless, the fact is that it isn't always and unless you have proof otherwise, you have no reason to be here. You are yet again reported for trolling.

Guys: First, please tone down. Then stop excessive commenting and move over to chat.

Salmonella infect via the fecal-oral route. They have proteins on their surface that match our gut cell surfaces, allowing them to attach and invade the gut. Those cell markers aren't present when you are bitten. it's the same reason that plant virus dont make us sick.
https://www.ncbi.nlm.nih.gov/pubmed/17593246
this is a bit heavy if you dont usually read primary papers, but looking for "Salmonella route of infection" or similar will yield the same kind of information

You can have Salmonella without actually knowing it, the reason behind this is that there is a group of salmonellas known clinically as non-typhoid Salmonellas (this means they are still S: enteritidis, but different serovars other than the more popular S. typhi). These most of the time cause mild infections as noted by the World Health Organization non-typhoid Salmonella. These infections can even be completely asymptomatic (carrier state) as it has been known for more than 2 decades Old paper on treatment for asymptomatic salmonellosis. We also now know thanks to modern genomic analyses that even within different strains of S. typhi some strains are more virulent than others.
There is even an atlas provided regarding the "less popular" Salmonella serovars, I suggest checking it out if you are truly interested in this topic CDC Salmonella Atlas.
Also regarding your original question there is an useful review here that mentions human-infecting serovars of Salmonella reported in relationship with snakes & lizards A Review of Salmonella and Squamates (Lizards, Snakes and Amphisbians): Implications for Public Health. As you will see the species reported belong to the group that can cause mild or asymptomatic infections so that could be contributing to the fact that people don't have that much trouble with bites from these animals in general. Of course what Stephanie said in his answer is true but also the implicated serovars are less virulent in general than the well-known S. typhi. More in favor on this last point you will see that in the review they mention that some people did develop extra-intestinal disease from reptile-derived Salmonellas like the man who got sinusitis, this means that if the strain is virulent enough in will cause disease even outside the gastrointestinal system.


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How exactly is the sunflower seed pattern calculated?
I came across this https://www.mathsisfun.com/numbers/nature-golden-ratio-fibonacci.html
and the rotation simulator just below the first section says to type in a number for each rotation. But, it doesn't explain what it is actually calculating.
If I type a number, by what angle is it rotating each cell, how is it calculating the initial number of cells, and how is it scaling each cell with each rotation to look like a sunflower? This definitely has come up in natural phenomena before like the nautilus spiral and the fern, so I want to know the generalization behind this pattern.

For a general reference, look for L-systems (the L stands for Lindenmayer) or the book "The Algorithmic Beauty of Plants". (Available online as a PDF file.)

Too broad, I am looking for something that exactly describes the simulation. The question is general only to the same extent as the simulation's parameters.


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In adverse effects of Heparin, why is bleeding from deeper organs more common?
The reason given in my book is that it i because it interferes with the secondary hemostasis..but i did not understand how that implies that bleeding from deeper organs is more common..

Skin is extraordinarily tough compared to much of our internal tissues; it has to be to protect us. To bleed, skin integrity must be breached, which usually involves sharp objects.
Think for a moment that most splenic or hepatic injuries (even complete ruptures) occur from blunt force trauma without breaking the overlying skin. For a more common example, if someone hits your thigh with a baseball bat, you will get a large bruise, maybe even a broken bone, but the skin will usually remain intact (if badly bruised) from blood vessel damage beneath and within the skin.
Many organs are delicate, and damage within them is not rare. Bleeding within/from some bodily organs is fairly common: runners bleed from their kidneys, and many, many people bleed from somewhere in their GI tract. High blood pressure may cause bleeding in the brain (a stroke) but it won't cause bleeding from the skin.
Just add to all the above the effect of anticoagulation (what heparin does.) I hope that explains things. If it doesn't, please leave a comment.

Thank you very much for the explanation. To clarify further, i wanted to know whether bleeding from deeper organs probably happens (normally) also due to pressure from surrounding tissues?

@Curious - Not necessarily pressure from surrounding tissues, no. Our bodies are well designed with things to minimize the effects of normal pressure.

Ok so..why exactly does bleeding occur more from deeper organs or delicate structures? Why is it 'delicate'?

Tissues are more delicate than skin because they serve a different function than skin, which is protective. They need protection: the brain needs the skull, the lungs, heart, liver, pancreas and spleen need the rib cage. We have minor internal injuries all the time: we damage our liver, we erode a part of the lining of our GI tract, we weaken blood vessels or break small ones, etc. Internal tissue isn't tough, it's tissue. Muscle is probably an exception, and bone is pretty tough, but even most broken bones occur without skin being damaged.

Skin is just built to be tough. I could go into histological reasons (what you'd see in a microscope) but that would be outside the range of this question.


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Why are higher doses of atropine required to produce central effects?
Reason given in my book is restricted entry into the brain..is it something to do with the chemisty?

Can you give more context as to how the book is referring to atropine being administered? If you are talking about IV administration this is wrong. Could you provide a citation and quote from the book?


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what causes epigenetic dysregulation in cancer?
Do mutations in regulatory gene sequences lead to changes in epigenetic alterations   in cancer, and if so which ones? I know abnormal hypermethylation of GCP islands occurs in promoters of tumour supressors, but what drives the abnormal methylation? Thanks

Your question is very broad. There are multiple factors that lead to epigenetic changes. I am not sure if the "first" signal that causes cancer progression has been identified but many histone modification proteins (HDAC, HMT etc) are dysregulated and are even being considered as targets of cancer therapy. So, to answer "what really causes the epigenetic dysregulation" an entire review article would be required.

But ultimately are epigenetic changes due to changes in gene sequence from mutational events? For example, would gene sequence change cause increase activity of DNA methyltransferase to cause increased methylation?


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What's the difference between the spindle assembly checkpoint (SAC) and mitotic checkpoint complex (MCC)?
Are the SAC and MCC two separate complexes? Does the SAC activate the MCC? Thanks

It can be helpful look into a few technical articles on the subject to clarify these ideas.
For example, this article has an abstract that lays it out quite nicely in the first 2 sentences of the abstract:

In mitosis, the spindle assembly checkpoint (SAC) ensures genome stability by delaying chromosome segregation until all sister chromatids have achieved bipolar attachment to the mitotic spindle. The SAC is imposed by the mitotic checkpoint complex (MCC), whose assembly is catalysed by unattached chromosomes...

So the SAC is a human conceptual model of how cells prevent the improper onset of anaphase before chromosomes are set up properly for cell division. MCC is the actual protein complex acting as an agent to make the SAC happen in cells.
The SAC could be thought of as containing the MCC and any other agents that prevent improper anaphase until spindle assembly and chromosome bi-orientation is complete, but it is not a protein complex per se in the sense of a bunch of proteins that stick together for a specific molecular function.


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Does applying a sedative via hypodermic needle anywhere in the body really work?
Bad Guy is fighting the Good Guy. Good guy miraculously produces a syringe and rams it into the Bad Guy's neck.
Cut,
  From my middle school biology I aware that capillaries are present throughout the body but I severely doubt that sedatives work by using them anywhere and everywhere. If so we're the case then why would doctors need to find my vein to give me a shot for flu?

 Yes, I'm not fun to watch movies with.

At least in my experience, having recieved a number of vaccinations over my life, they're almost always given intramuscularly, rather than intravenously.  You may be confusing vaccinations with the drawing a blood sample from a vein, where you want to draw out a relatively large quantity of blood.

On further thought, the fact that sedatives will work (almost) anywhere is demonstrated by the wide use of tranquilizer guns in wildlife management: https://en.wikipedia.org/wiki/Tranquillizer_gun

There are three basic types of injections:

intravenous (IV): An injection straight into the blood stream. Fast, but as you pointed out, one needs to find the vein first. If you are hospitalized, you will likely have a catheter in your vein already, so that you can be given drugs rapidly if needed.
intramuscular (IM): This is your second best option for fast effect. There is plenty of capilary vessels in your muscles because they need a good circulation to function (get oxygen in & carbondioxide out). This helps your body also to take up drug injected in your muscle and there is little delay until they enter the blood stream.
subcutan: this is used when you are aiming for slow uptake.

Assuming that you envision some sort of combat situation where good guy cannot just start looking for a vein on bad guy's arm, IM seems to be a reasonable choice. If they are in a fight, Bad guy will have a high pulse, so the drugs should get into the blood stream fairly quickly.
See further: https://en.wikipedia.org/wiki/Injection_(medicine)


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How are Cytotoxic T cells transfered?
We learned that Cytotoxic T cells are MHC dependent, and if CMH matchup doesn't occur between the T cell and the cancer cell for example, the former won't attack the latter.
If this is the case then how are T cells given through vaccines and transfers?

T cells are not transferred. Vaccines induce the host to expand their own T cells that are responsive to the antigens that are given.

Adoptive cell transfer incl. TIL and CAR-T are forms of T cell transfers, though.

First, they're still almost invariably autologous, and second, given that the question seems to come from a fairly naive viewpoint it doesn't seem worth confusing the issue. If the OP would like expansion on these, they should clarify the question.

I thought the same thing, fair enough.


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How does a heat-ratio sap flow sensor work and how invasive is it?
The Gizmodo article Undead Tree Stump Is Being Kept Alive by Neighboring Trees says:

Leuzinger and Bader stumbled upon the stump while out for a hike. The woody stub caught their eye because callus tissue could be seen growing over its dead and rotting parts. It was also producing resin, which indicated the presence of living tissue. This prompted a more thorough investigation in which the researchers measured water flowing through the tissues of the stump, and also its rate of respiration, which matched those seen in the surrounding trees.
“We measured water flow with ‘heat-ratio sap flow sensors’,” Leuzinger told Gizmodo. “They detect water movement in tissue by sending out very small heat pulses and measuring how quickly that heat dissipates.”
These measurements indicated that the kauri stump is inactive during the day when living trees transpire. But during the night and on rainy days, the tree stump becomes active, circulating water—and presumably carbon and nutrients—through its tissues. As the authors write in the new study, these results

"...indicate that such symbioses may be much more complex than previously assumed: by physiologically exploiting ‘‘downtimes’’ of transpiring trees during the night or rainy days with high water potentials in the root network living stumps seem to act partially autonomously, strategically tapping into resources rather than simply becoming part of the neighboring trees’ extended root networks."

I can get a general feeling for the principle. After a thermal pulse the local temperature of a probe will decay due to heat diffusion, but if there is movement of water (or sap) in and out of the area the decay will be faster...
But I have a few questions:

How exactly would you analyze a temperature decay curve $T(t)$ in order to determine if there was water, sap, or any material moving in and out of the volume or not? Is there a distinctly different shape to the curve that rules out thermal diffusion alone, demonstrating that there must be mass flow as well?
When used on trees, how is this instrument applied to the tree? Does it need to penetrate into live tissue to work, or can it work by proximity, perhaps using radio frequency or microwaves for heating and a surface contact thermometer?

@JimYoung excellent, looks like the basis of a great answer.


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What will be the deficits when left half of the brain is removed in adults?
Hemispherectomy is a surgical procedure to remove half of the brain. It is typically done on children with severe epilepsy. What will be the deficits when left half is removed in adults? Is aphasia a certain outcome in case of left hemispherectomy in adults?


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Why are Arabidopsis plant seeds being sent to the moon and not other seeds?
The latest Chang'e-4 rover brings an entire ecosystem with it, including Arabidopsis plant seeds and silkworms.
My question is: why Arabidopsis? Is this question conclusive without having to ask Chinese sources, such as just by having an educated guess as regards to the plant's own qualities?

Welcome to SE biology, please feel free to check our help center and take info tour to find out how  does it goes on this forum. I am afraid that this question is not suitable for this forum. Nevertheless, i think that the Chinese sent the plant there just because it is plant which is biggest model organism in plant physiology . We technicly know almost everything about this plant.

Without speculating further about specific decision making processes, Arabidopsis is the standard model organism in plant biology, similar to the mouse for mammals, the fruit fly for insects, C. elegans for nematodes, etc.
It's the first plant to have its genome sequenced, it's commonly used in undergraduate laboratory experiments in part because it grows very fast, etc.
If you were going to choose a plant arbitrarily for a research project, it might as well be Arabidopsis, I'd say it would be the default against which other options would be considered.


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When is it viable to remove old graves?
Societal considerations aside, when all the remaining relatives of a particular gravesite have all disappeared or forgotten about a certain grave, is it viable/hygienic to remove or repurpose old gravesites as something new?
Not all burial traditions use airtight coffins that wouldn't let the body decompose — Muslim burial tradition would wrap the body in a plain sheet of cloth and then bury.

I think it's a really interesting question, but I also struggle to see the biology in the question... religions and societies can decide on things but if you want to evoke biology you're probably going to have to come up with an operational definition for the thresholds you are asking about.

@BryanKrause I'm asking from the perspective of hygiene, mostly. I'm really nothing related to biology, but I sent this question to a bio graduate friend of mine and she mentioned soil ecology, for example.

If the question is really asking "how long under [some set of environmental conditions] does a human corpse take to decay fully?", then I think it's biology.

@kmm How does one define "fully"?

Not to speak for the OP, but I would suggests when it is "viable/hygienic to remove or repurpose old gravesites as something new".

To weigh in on this: it totally depends on soil type, moisture, and oxygen levels of medium (not tomention burial practices as you mention). See bog bodies as an extreme example -- preserved bodies after 10k years!

Also, I personally think it to be very inappropriate both socially/religiously and regarding simple decency/respect for the dead to be considering disturbing their grave sites. In many places, it is also unlawful. So I encourage you to reflect very intently on any purposes you have for gaining this information.

8-10 years
Keep in mind digging up bodies once they are nothing but bones was common practice at one time, look up the catacombs of Paris or just Ossuary.
Human remains are not actually considered infectious once they have rotted away, not that they have much risk before that, but the smell of a corpse that still has soft flesh is remarkable unpleasant, which is why waiting until they are dry bone was common.
How long it takes to reduce a body to a skeleton is controlled by the site of burial and climate. Forensics uses a baseline of 8-10 years for a six foot deep burial in most temperate soils, much longer if buried in a casket. Note changing the conditions of burial can change this time from a few weeks to never because it mummifies.
source

I think the answer to this question is open for debate, as it depends on a lot of factors.
To start with an extreme, King Tutankhamun died about 3,000 years ago. The opening of its burial grounds was attended by Lord Carnarvon, a British sponsor of archaeology in Egypt, who died shortly after attending the tomb's opening. While at first it spawned superstitious beliefs like 'Tut's curse', nowadays researchers believe it was, perhaps, caused by various bugs found in the tomb, namely Aspergillus niger and Aspergillus flavus. These molds can cause allergic reactions, including lung bleedings. The toxins can be particularly harmful for people with a weakened immune system. Other bugs, like the respiratory-assaulting bacteria, Pseudomonas and Staphylococcus have been found as well on the walls of the tomb (source: National Geographic).
However, food items were stored alongside a host of other sacramental stuff, so Tit's tomb was anything but  a 'clean' grave. A normal grave hence may, or may not lack these contents and hence its bugs. However, there are many, many more variables in play, among them the type of coffin used to bury the corpse, the type of grave, type of soil, humidity, temperature etc. etc., which all interact and can affect the duration of the various stages of decomposition (source: Wikiepdia). Up until the last phase (skeletal phase), active decomposition is taking place, and hence many bugs are around, which would raise hygienic issues.
Lastly,cleaning up graves is quite regularly performed, and a period of four decades is used on a regular basis (source: BurialPlanning.com).
In all, I guess a definitive answer to this question doesn't exist, other than longer than 3,000 years....

People do remove graves much, much sooner than that, for example: https://www.thisamericanlife.org/689/digging-up-the-bones/act-one-6 but I don't really think this is a "biology" question per se. I won't use my close vote but I do think the OP needs some clarification to make this anywhere near biology.

@BryanKrause yes wasn't done yet. The Q needs clarification, which my answer hints at. Close away. Up to you. It's a broad question, but an interesting one imo.

Oh indeed, lots of interesting concepts here but...harder to frame it in biology :) I find it really fascinating from an anthropological and archaeological perspective that different human societies have completely different ideas of what "complete" burial and decomposition means. In Greece it seems the timeline has been shrunk down to <3 years, and is driven by mostly practical concerns.

@BryanKrause wow, that's really short! Note that I'm pretty biased in my close- and answer-behavior to the type of question. Questions on sensory systems I practically never close, I'm only human. So feel free to let that mod hammer swing...

Oh definitely - I suggest listening to the linked podcast which is fun regardless :) the lack of decomposition seems pretty central to the overall experience...and yet it is all pretty separate from the ideas expressed in OP here :)


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Question in gel chromatography experiment
Here I am trying to do
gel chromatography to separate vitamin B12 and Bovine Serum Albumin (BSA)
in this experiment, I am using sephacryl s-100 HR gel column
my question is can I use Phosphate buffered saline with sephacryl s-100 HR gel column
also since the Bovine Serum Albumin (BSA) is colorless I need some kind of Protine detection reagent to see this protein (I need something other than Coomassie brilliant blue)

Is this a homework question?

No, it just that I originally not a biologist but a physicist and it is my first time performing this experiment

Within reason, you can basically use any buffer you like with Sephacryl S-100, provided that is suits your purpose in terms of protein/enzyme stability, and phosphate-buffered saline sounds ideal.
There are sometimes a small amount of positively or negatively charged groups associated with a gel-filtration resin, introduced during the manufacturing process, and it is recommended to have some salt present (100mM KCl used to be recommended) in order to counteract anion-exchange and/or cation exchange effects.  In addition, at very high salt concentrations (1M ammonium sulphate or higher), proteins may bind to the resin by a hydrophobic interaction. Furthermore, one or more of your target molecules may be unstable at extremes of pH.  NADH, for example, is unstable in acid.
In other words, you want to set up the experiment where the target molecules are stable, and where separation on the column is by 'molecular sieving' only.
A very common method of measuring protein concentration is to measure the A-280 of each fraction (the absorbance at 280nm). The has the big advantage of being reasonbly sensitive AND is non-destructive (you can fully recover the sample after the measurement).  All you need is access to a spectrophotometer and a quartz cuvette!
In addition, with (pure) BSA the method may be made quantitative as the A(1%, 280),sometimes called the E(1%,280), is known. From memory I think this is about 0.68 for BSA.  That is, a 1mg/ml solution of (pure) BSA will have an absorbance at 280nm of 0.68.  (The 'rule of thumb' for impure protein preparations is that a 1mg/ml solution has an absorbance of 1. But note that many compounds absorb at 280nm, including DNA)
You can, if you wish, calculate the A(1%, 280) from the amino acid sequence of the protein of interest. The refs (Perkins; Gill & von Hippel) are given below.
It should be possible to detect B12 by a similar method, perhaps even at 280nm, but an absorbance spectrum may yield a more sensitive/specific wavelength.
You don't give the pH of the PBS (!important), or the dimensions of the Sephacryl column.
Long, narrow columns work best, but you probably already know that.
Some Refs
Gel Filtration by Reiland (Methods in Enzymology, 1971).  A great article
Protein Purification: Principles and Practice by RK Scopes (Springer Advanced Texts in Chemistry) 3rd Edition
Sober, E. K. & Sober, H. A. (1970). Molar extinction coefficients and E (1%, 280) values for proteins at selected wavelengths of the ultraviolet and visible region. In Handbook of Biochemistry. Selected Data for Molecular Biology, 2nd edn. Sober, H. A., Ed. pp C-71 - C-98. The Chemical Rubber Company, Cleveland, Ohio.
Perkins, S. J. (1986). Protein volumes and hydration effects. The calculation of partial specific volumes, neutron scattering matchpoints and 280-nm absorption coefficients for proteins and glycoproteins from amino acid sequences.  Eur. J. Biochem. 157, 169 - 180. [Pubmed]  [pdf]
Gill, S. C. & von Hippel, P. H. (1989). Calculation of protein extinction coefficients from amino acid sequence data.  Anal. Biochem. 182, 319 - 326.  [published erratum appears in Anal. Biochem. (1990) 189, 283].


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what is this centipede like creature?
They are very big. About the size of my hand in length and I've seen two now. My cat brought one in from the Texas border region.

giant centipede. Probably a Common Desert Centipede (Scolopendra polymorpha)

Yes ,surely a centipede.Looks similar to the ones on https://extensionentomology.tamu.edu/insects/centipede/.

dark bands between segments and long tails match:

Distribution matches:

I’m fairly sure it is a centipede. However, the picture is too fuzzy to make out the exact species.
You can try comparing with the many recorded observations of centipedes around Texas: https://www.inaturalist.org/observations?place_id=18&taxon_id=49556


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Why are there otoliths in the otolithic membrane of the saccule and utricle but there aren't in the cupula in the semicircular canal?
I know both of the 2 systems work quite similar the first (saccule and utricle) detect linear acceleration and semicircular canals play the role of angular acceleration detectors. I wonder if there is a functional reason for which there are no otoliths in the cupula. Why are they important in the otolithic membrane but not necessary for the cupula ?

In the ampulla of the semicircular canals, the flow of the endolymph is blocked by the gelatinous cupula into which the hair cells protrude. Thus, during circular motions when the endolymph is accelerated in the semicircular canals, the pressure on each side of the cupula will be different and hence results in some displacement of the cupula, which the hair cells may then detect. When the rotation stops (or the rotation speed is constant), the axonal firing rate of the hair cells will return to the firing rate at rest.
In the maculae, the gelatinous layer is not blocking any canals and hence it isn't displaced effectively by fluid motions as the cupula is in the semicircular canals. The role of the otoliths (which are heavier than the surrounding fluid/tissues) is to cause a temporal displacement of the gelatinous layer during linear accelerations, which happens due to the temporal motional lag between the otoliths and the sensory epithelium with the embedded hair cells. During head tilts, there will also be a displacement of the gelatinous layer, because of the gravitational pull on the otoliths, and the hair cells will then continue to fire their axons at increased/decreased rates (depending on the tilt direction) for the duration of the head tilt.
Thus, the method for displacing the cupula/gelatinous layer is slightly different between the maculae and semicircular canals, and in the semicircular canals, there isn't a need for otoliths to make this happen.
The book Neuroscience edited by Purves et al is a good resource on this.

Great first answer Michael, especially liked the description of the physics aspect. Welcome to biology. (From review)


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Question about probability of being a heterozygous carrier
A 26-year-old woman of Norwegian descent seeks genetic counseling. Her brother died at age eight of documented cystic fibrosis. Both of their parents are deceased. The woman undergoes DNA testing for 70 CF mutations which collectively detects approximately 90% of CF carriers of northern European descent. Testing reveals that she is negative for all 70 mutations. What is the probability that she is a heterozygous carrier of CF?

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. In general, we expect you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). For "homework" questions, you are required to show your attempt to answer the question and to use the "homework" tag. (Note that "homework" can apply to questions even if they are not assigned as homework.) Thanks!

Hi, So I have tried solving this by myself. I figured that in order for her to be heterozygous carrier, she has a 2/3 chance x by the 10% of catching a rare form of CF mutation that wasn't detected. I got a 1/15 chance, however the correct answer was 1/6, so I'm not sure what I'm missing here

Please [edit] that information into your post and include your reasoning for each step (e.g. where the 2/3 came from) — comments are ephemeral and often ignored so they can not be used to convey essential information. Please also check out the links from my first comment.

I recommend to read on Bayes theorem or maybe watch one of many videos on the subject.

I figured that in order for her to be heterozygous carrier, she has a 2/3 chance x by the 10% of catching a rare form of CF mutation that wasn't detected

Based on your comment I am guessing you have correctly identified, the correct (2/3) probability of her being a carrier prior to learning the test result. Also you have correctly identified the probability of her carrying rare CF mutation prior to learning the test result.
Now you can draw a table:
She is a carrier     She is not a carrier
c                    d                      test came out positive
e                    f                      test came out negative

In this table c, d, e and f are probabilities prior to knowing the test result. So far you have calculated the e = 2/3*10% = 1/15. I will leave to you to calculate the rest of the fields in the table.
After learning the negative test result we can cross out the fields c and d. The list of all possible options has shrunk to e and f. The new probability of her being a carrier given the test came out negative is:
probability of carrying a rare mutation / (probability of carrying a rare mutation + probability of her not being a carrier) = e / (e + f)

There are 4 possibilities:
Family has rare allele,   person is a carrier
family has rare allele,   person is not a carrier
family has common allele, person is a carrier
family has common allele, person is not a carrier
Work out all these so that they add up to 100%.  The testing allows you to eliminate one of those options, so then recalculate.


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Why is the current flow shown to be flowing from the negative area towards the positive area?
When I was studying the ECG chapter in the book "Guyton and Hall Textbook of Medical Physiology", I noticed something odd in one of the pictures:

As you can see the current is shown to be flowing from the area with a more negative potential towards the area with a more positive potential.
Also here's the part of the text that alludes to the image:

This process provides electronegativity on the insides of the ventricles and electropositivity on the outer walls of the ventricles, with electrical current flowing through the fluids surrounding the ventricles along elliptical paths, as demonstrated by the curving arrows in the figure.

How is this possible? Isn't the current supposed to flow from an area with a higher potential towards an area with a lower potential?

By convention, positive current is assumed to be the direction of flow of positive charges. The trouble is that in many common situations (like this one), the current is actually carried by electrons which are negatively charged.
It can be confusing. Blame it on Benjamin Franklin. The convention for current flow was based on his work, before anyone knew about electrons, protons, and ions.

So basically what is shown in the image is the direction of the flow of the electrons and not the flow of the current, correct?

Not literally electrons, the flow is mostly Chloride ions that direction, and Sodium, Potassium and Calcium ions the other way.


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Difference in Basic Amino Structures
I'm having a hard time understanding why my slides in my biology course have two different representations of the "basic structure" of the amino acid:
1:

2:

The top one seem like what I would expect.  The bottom one, it looks like the amine group gained a Hydrogen ion and the Carboxyl group lost one.  Also, the center carbon gained an H.  I honestly don't know if this description is even correct or not.
I'm extremely new to this level of biology, so very simple explanations are much appreciated.  I just don't totally understand why there are two versions of the basic structure.
Also, I apologize if the tag is wrong, again, this isn't my major, so I'm very new to this material.

Ugly pictures in both cases :)

Your description is more or less correct, but so are both images. The bottom images shows the predominant form the amino acid would take at neutral pH (or any pH between ~2 and ~9.5). This is because the caroboxylic acid (-COOH) and amino (-NH2) groups are a weak acid and base and can lose or gain a proton (hydrogen cation), respectively. pH below the pKa of the functional group (~2 for carboxylic acid and ~9.5 for amino) favours protonation whereas pH above the pKa favours deprotonation. Also note that the "centre carbon" (the α-carbon) did not gain a proton in the second image, it's just drawn differently.
You could try this website for an overview of acid/base chemistry and perhaps these Wikipedia sections on zwitterions and isoelectric points with respect to amino acids, though there are many alternative sources of material available if you search for them. This question and answer may also be useful for you, at least eventually.

To expand slightly on this answer, this is valid for these sorts of chemical structures more generally in organic chemistry, too. When you see groups like these that act as weak acids/bases, you should think of them existing chemically in both forms, with the ratio dependent on the pH. People will switch back and forth between them freely because that's how the molecules actually exist, as well.

Thanks again for this, I now see the center H as just being drawn differently.  I must've been overwhelmed enough to miss that.

@joe_04_04 You’re welcome.


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How does hydrophilic and/or hydrophobic components of polysaccharides influence their 3 dimensional conformation?
It is my understanding that polysaccharides are insoluble in water. Does this mean they are hydrophobic? Beyond being insoluble in water how does this affect their 3D structure?
Thanks!


text:
How much of human's behaviors and preference can be explained by evolution?
I'm talking about things like the tendency to feel sleepy after eating, avoidance of excrements, general preference for sweet foods, etc. Do all those characteristics have biological or evolutionary basis?

Your question is super broad. The "evolutionary explanation" for single traits itself is quite difficult and you are asking about many complex traits.

What is heritability?
First of, please read about the concept of heritability. See for example the post Why is a heritability coefficient not an index of how “genetic” something is? You should be able to understand why all else being equal, why if environmental variance for a given phenotype increase it results in a decrease in heritability and why directional selection in a population decreases heritability.
Do you now know what heritability is and is not?... Good!
Your question is very broad...
As you now understand, heritability is a concept define for a given population in a given environment and most importantly for a given trait. There is no way to give a single answer for all traits one might want to consider.
By experience, it seems that, in humans, most behavioural traits that we decided to investigate has heritability estimates in the order of 0.05 - 0.6.
One example
I will consider just one of the trait you list, "preference for sweet foods". Sweet taste preferences appears to have a high heritability in humans with estimates of the order of 0.41-0.66 (Keskitalo et al., 2007). For heritablities about other food preferences, you might want to have a look at Reed et al. (1997; there are probably more recent papers that make better reviews though).
Preference for sweet foods

What I think is not immediately clear in this answer in response to a question like the OP is that heritability in the contexts you are presenting refers to variation in the population. If you look at the heritability of, say, height, that coefficient completely misses that evolution led to human-sized humans and not ant-sized humans, which is definitely genetically encoded.

@BryanKrause Yes, this is why I insisted that the OP looks for what heritability means and I highlighted that directional selection actually reduces heritability. But I agree with you, when rereading the question, that the question should probably be be closed as it is not asking so much about heritability but more whether "it is explained by evolution", which does not mean anything.

I actually voted to close. Then removed my close vote when starting to write a comment that was too long, so I made an answer. Maybe, I should have just kept with my close vote. Anyway, I can't vote to close anymore!

Yeah, I know that and you know that but I don't think your answer here or the linked one conveys that message in easily, quickly digestible format. I do think the right thing in the end will be to close this question.


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What is the overall end result of proteins and enzymes binding together?
My rudimentary understanding is...

a gene gets transcribed to mRNA
that mRNA is sent off to the ribosome
that ribosome pumps out whatever proteins are coded by that gene
each protein floats around in the cell until it encounters an enzyme that it fits into, and along with other molecules that may have floated into the same enzyme a chemical reaction occurs and one or more products are formed.

I'm assuming "products" are either new protein molecules or maybe the amino acids that made up the original input proteins. What I don't understand is what the overall end result of these reactions are. So there's a reaction, but what does that mean? How does that reaction, lets say, result in some physical attribute of the organism?
Any examples would be helpful.

Your question is a bit broad. Even though someone answered your question to your satisfaction, your question itself seems to ask for the entire molecular biology behind life. Can you please rephrase your question to make it precise while keeping the current answer relevant to it?

@Mowgli has been kind enough to answer this question, but it shows a basic lack of knowledge about proteins and enzymes that any answer here would not be able to remedy. You need to read about proteins in a standard text book of biochemistry or molecular biology, written and illustrated in a professional manner. There are some old editions (all you need) of very reputable books online at NCBI Bookshelf, where you can search for these terms. Alberts et al. might be suitable.

At a high level, points 1 to 3 are reasonably correct, but 4 is only a special case.
Say we're at end of point 3. You get a protein. Some proteins are enzymes (the majority of enzymes are proteins), others are not. Example of proteins that are not enzymes would be, for example, hemoglobin, which is "just" a (very high-tech) carrier.
Now, each enzyme catalyzes (at a very high level) one reaction, which may or may not involve other proteins:

Reactions without protein other than the enzyme: for example, the cleavage of sucrose into glucose and galactose (two small sugars) performed by an enzyme called sucrase. Such reactions can assemble, cut and modify small molecules or large organic molecules that are not proteins (for example, starch, which is a large polymer of sugar, or even DNA itself)
Reactions mediated by enzymes, that act on non-enzyme proteins: for example, your digestive enzymes can cut proteins from food into building blocks (amino acids) that your body can use to build its own proteins. Similarly, some proteins can ligate proteins together, or add things on them (the proteins on the surface of cells are commonly modified with small sugar chains that control their activity).
Enzymes that catalyze reactions that involve other enzymes: since enzymes are proteins, they can be the target of other enzymes. A very well described example is the cascade of enzymes called kinases. When a cell is stimulated by a hormone, a kinase gets activated by addition of a small phosphate group. Once it is activated, the kinase phosphorylates (i.e. it adds a phosphate group on) another type of kinase, which phosphorylates yet another type of kinase etc; that's a way to amplify small signals.

So the overall result of an enzymatic reaction, regardless of whether it acts on other proteins or not, is usually either

The conversion of a molecule into some other molecule (1 to 1)
The assembly of several molecules into a larger, new molecule (N to 1)
The separation of a large molecule into smaller fragments (1 to N)
The transfer of a fragment of molecule on another molecule (N to N)

Examples of these four types of processes when enzymes act on other proteins:

1 to 1: a "protein disulfide isomerase" can rearrange the topology of the so-called disulfide bridges, that connect cysteine amino acids together in the target protein. This allows a misfolded, non-functional protein to turn into a functional molecular machine.
2 to 1: a "ubiquitin ligase" can covalently attach small proteins (ubiquitin) to old, broken proteins and target them for recycling, thereby preventing the accumulation of dysfunctional proteins in the cell.
1 to 2: a "protease" can cut another protein into two smaller proteins
2 to 2: a "protein kinase" removes the phosphate from a small molecule called ATP, and sticks it on another protein

Thank you for the thorough answer. Are the physical attributes of an organism the result of enzymes manipulating molecules? So for example, is some enzyme responsible for glueing molecules together to pump out hair? nails? etc.. I'm trying to relate what's happening to some higher level biological process.

@offbynull physical attributes or phenotypes are governed by a lot of molecules and all of them have been formed because of the action some enzyme or the other (for e.g. RNA polymerase is needed for the expression of all the genes). So your statement is correct but is gross oversimplification of the biology.


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What is this furry, long-limbed, presumably tree-dwelling creature?
Can anyone identify the species below? I believe the picture was taken at the Museum Of Zoology in Cambridge so maybe someone cleverer than me could narrow it down using their collections search.

Of the species I know, it looks most like a tarsier to me. Is there any relation?

It does look somewhat like a Tarsier. I looked a second on the wikipedia and the closest thing I could find was the Tarsius fuscus. I don't believe this is what you're looking for, but if it helps you in anyway to get to the goal of identifying it, I thought I would just leave this comment.

@Eff Thanks! The limbs look a lot more similar to tarsius fuscus. Looking at their collection, they only have one species from the tarsius genus, tarsius tarsier, which does not look like it matches the photo above. If that's correct, I wonder why it looks so different? Bad taxidermy?

Yeah it was the limbs that looked alike... But I really can't tell. I'm not the one to ask for these questions. I really don't have much expertise on phylogeny. I just thought that a very slight chance of helping was better than none, so I posted the comment. I upvoted question. Hope you get help!

It looks a lot more like a loris to me. There are 10 loris species. Not sure which one this is.

I just looked at the museum list for loris and tarsier. I think the one closest fitting is probably the Red Slender Loris (Loris tardigradus).

It looks like a taxidermic specimen of a gray slender loris (Loris lydekkerianus), but it does look pale in color. The lack of color distinction in the fur may be because it is a non-living specimen. The links below may be helpful with more detail.
https://en.wikipedia.org/wiki/Gray_slender_loris
https://www.shaldonwildlifetrust.org.uk/page/grey-slender-loris.html
https://www.youtube.com/watch?v=yU3n0BlUP0A

thank you! if it's a loris then according to their collection it's either a red slender loris or a Bengal slow loris. Both specimens are hundreds of years old, might the fur discolour in that time?

@Michael If you look at their collection, there is only one mounted loris skin. All the Nycticebus cougang specimens are wet (in fixative) or bones. So, if it's a loris and it's listed in their collection, it's a red slender loris.


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What labs/companies provide comparative genomic analysis?
I’m looking for labs/companies that provide comparative genomic analysis between two different species, AND do so for the “paying” public.  I am looking to test a hypothesis regarding genetic expression and would appreciate any direction.  Thanks!

What's your starting material and your budget? e.g. animal tissue and $x.xx

Thanks for the reply.  Yes, tissue, and a budget of appx. $5000.00. But I honestly have no idea how much labs might charge.

Well first figure out what kind of work you need done. If you have tissue, you'll need extractions done. If you're doing NGS you also need the library prepared and a sequencer ran. Then multiply that cost by the number of samples. At Duke's NGS core, for example, RNA-seq with library prep on their MiSeq instrument for 10 samples will cost you around 15,000. Extractions will probably be extra. I've seen companies push QIAcube extractions for around $65 a sample.

@CKM  Understood. Thank you for your help!

Earlham Institute have the expertise for this work.  They primarily work in public-funded research but they carried out private-sector work in the past.


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Development of radial symmetry in starfishes and other animals
How does nearly perfect radial symmetry arise in an animal like the starfish? My confusion lies in the fact that cells are fluid & amorphous, & that these characteristics seem to make it difficult to form symmetric structures. Many of the sources I've read describe the formation of the blastula but not the development of the five arms following that. Also, at one point in the development it is bilaterally symmetric. Furthermore, some species of starfish can regrow from a single arm.
What process mediates the formation of radial symmetry in a developing organism? Is it that arms grow individually & there are cascades of cellular signaling that mediate the production of new arms until the desired amount is reached or is it something else? How do the arms of the starfish remain evenly spaced?

The morphogenesis of symmetry is an enigma in biochemistry, especially for echinoderms. Biologists can't agree totally and tell you a specific reason. here's all I can find(2018) "Over the last 20 years, an answer for how vertebrate embryos can tell their left from right has emerged. This model involves midline-located L-R organizers (LROs) – the node in mice. " https://dev.biologists.org/content/141/8/1603 some wiki info: https://en.wikipedia.org/wiki/NODAL wiki says that echinoderms also have the Nodal development gene.

That is the field of developmental biology which deals with organizers. Cell organizers are processes, genes and signalling proteins cells use to communicate / send and receive information from their neighbors, so that their spacial distribution in the body regulates their development.
The cells also have gradients of signaling proteins inside the cytoplasm, and cell polarity, so the cells know which way round they are:
"A spatially distributed signalling cascade can create step-like activation profiles, which decay at successive distances from the cell surface, assigning digital positional information to different regions in the cell. Feedback and feedforward network motifs control activity patterns, allowing signalling networks to serve as cellular devices for spatial computations."
All metazoans use the same types of organizers to develop different patterns of cells, so starfish use the same genes as mice to organize their axes. They are early metazoan genes/ Precambrian. Here is an in depth answer to your question: www.ncbi.nlm.nih.gov/pmc/articles/PMC5307799/
The cells know where they are, because they are receiving multiple signalling proteins from further away in the animal. Here is a picture of Bicoid morphogen in fruitflies:
The signalling proteins are received from cells far away, and that signals to other cells to make different kinds of signalling proteins to organize the local neighbors.

Given the complexity of metazoan morphogenesis, there are very many organizers and we only know a few of them. The axis formation is related to the Nodal gene which uses some kind of axial/mid-line located organizers to control symmetry, there are documentd about LRO: left right organisers, in starfish its the same chemistry in a different geometry. The Nodal biochemistry: https://youtu.be/kO8k9aiQJsQ?t=189


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The relation of a schizophrenia drug side effect and caffeine intake
I am listening to the book Surviving Schizophrenia and in the book, it is mentioned that drugs like Clozapine increases in blood level if the patient takes Caffeine, and can have side effects due to elevated levels. In case the patient takes Caffeine, can't just less amount of Clozapine work since it'll be significant enough to help the patient and cause less side effects too? I am not from a medical background, sorry if these things are pretty obvious in medical community

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] or delete your question accordingly. In particular note that personal medical questions are not appropriate for this site. No matter how good your (and our) intentions are, relying on health information from people who aren't medical professionals is unwise and could be extremely dangerous. Thanks!

In general, since everyone metabolizes caffeine and clozapine differently, it would be extremely hard to make sure that the patient got the right dose.  It's easier to say "stop using caffeine while on this".  Grapefruit juice does much the same thing; makes it harder to break down drugs, doctors do not say "drink grapefruit juice and we'll halve your dose".  They say "avoid grapefruit juice".

The place to ask about medical topics is SE Medical Sciences. Here the focus is on defined biological mechanisms, rather than complex diseases and the varying effects of drugs.

I used Google Scholar with the search terms of clozapine, caffeine.
I only found small scale studies, but they agree that it is likely that Clozapine levels are affected by caffeine intake.
To really understand the implications of this it would be necessary to research what the range of Clozapine levels actually are in patients and what the effective level is, as well as the levels that give side-effects.
Only then can the changes due to caffeine be seen to be significant or not
Example paper studying 12 volunteers below (full text available)
Hägg, S., Spigset, O., Mjörndal, T. and Dahlqvist, R. (2000), Effect of caffeine on clozapine pharmacokinetics in healthy volunteers. British Journal of Clinical Pharmacology, 49: 59-63.
https://doi.org/10.1046/j.1365-2125.2000.00111.x
Available at:
https://bpspubs.onlinelibrary.wiley.com/doi/full/10.1046/j.1365-2125.2000.00111.x

Your DOI link is incomplete.


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What's a reasonable time constant for a mathematical model of a neuron?
Background
I've been studying various mathematical models of neurons. So far I've covered the classic Hodgkin-Huxley model (to describe the potential difference of a single neuron) and the integrate and fire model for two neurons (to describe the voltages of interacting neurons). I am now studying a firing-rate model which describes the firing rate of neurons, not their voltage.
All of these models include a time constant $\tau$. For the Hodgkin-Huxley and integrate-and-fire models $\tau$ tells us how fast the channels and pumps open/close in response to an action potential.
I am currently working with a two-neuron system of one excitatory neuron and one inhibitory neuron. It is described by the equations
$\tau_E \frac{dV}{dt} = f(v_E, v_I, \theta)$
$\tau_I \frac{dV}{dt} = g(v_E, v_I, \theta)$
where

$v_E$ is the firing rate of the excitatory neuron
$v_I$ is the firing rate of the inhibitory neuron
$\theta$ is a set of constant parameters.
$f$ and $g$ are linear WRT $v_E$ and $v_I$

I have fixed all parameters $\tau_E$ and $\theta$ leaving only $\tau_I$ to be varied. Certain values of $\tau_I$ cause stability while others cause instability.
For the parameters $\theta$ that I'm using I have found that disregarding the possibilities of $\tau_I<8$ and $\tau_I>791$ greatly simplifies the analysis (because of the way the eigenvalues of the Jacobian matrix work out). I also have reason to believe that it might be alright to disregard these values.
All of the $\tau$ time constants in all the examples I've seen so far have been around $10ms$.
Question
$791$ seems very high, but is it so biologically unreasonable that it can be completely ignored? What's to stop one neuron being $1000$ times more responsive than another one given there's such diversity in neuronal structure and function over all types of neurons? Are there examples of this?
$8$ seems completely reasonable for a time constant. Surely values under $8$ can't be disregarded completely?

How these parameters relate to your firing rates? Neurons have a maximum firing rate of 500-1000 Hz.


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Looking for study/genome data for HIV in different organs
I am looking for a research study or data base that has HIV genome data available in fasta or similar format. Specifically I need genome data of HIV taken from different organs in the same subject. I am interested in studying the way HIV diversifies and changes to infect different organs and in comparing the process across different patients.
If you are familiar with such a study, or if you have general pointers as to where I may find similar data, I would appreciate it very much. I have done a few hours of searching on NCBI GeneBank, but have had no luck.
Thanks!

Could be better of migrating to Bioinformatics.SE.

This website comes to my mind
https://www.hiv.lanl.gov/content/index
It is a HIV databases containing HIV sequence data and related immunologic information


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metaphors for explaining the role of DNA in the cell
Various metaphors are used to explain the central role of DNA in a cell to laypersons. These include blueprint, recipe, catalogue, instruction manual etc. I even heard someone describing DNA as a 'boss' that yells orders.
Here are some interesting ones:

An ancestral archive
An archeological site
A prison (retroviruses and transposons)
A computer
A deck of cards
A clock

What are some useful metaphors that help to explain DNA function?

You just answered your question 11 times, if I count correctly. What is it you wish to know? Other metaphors? If yes, I think such a discussion-type question should be posted in chat, not on the main site.

It is clearly off-topic, but this doesn't appear to be homework @John. & homework questions aren't off-topic. Only if they do not conform to the other rules.

I answered. What about you? Good metaphors are essential to conveying complex or domain information and a pillar of education. Have a try!

It is a program executed by transcriptase (processor) inside a cell core (computer).

Since this is an off-topic question (it is opinion rather than fact based), it is better left unanswered. For future posts please note that answers are much more likely to receive a favorable response if you include supporting references (primary literature is best). Without that support, your answer is indistinguishable from opinion. This is a good example of how to format references. ——— Please take the [tour] and then consult the [help] pages for additional advice on [Answer] effectively on this site. Thank you!

Thats my intuition also -  that 'computation' is occurring in the transcriptome rather than the genome


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What do they mean by “most single-gene traits are recessive.” How can a gene be recessive; isn’t it an allele which can be recessive or dominant?
Here’s the paragraph pg. 45 of “Principle of Neural Science”: “Although most single-gene traits are recessive, rearrangements that lead to duplication or deletion of multiple genes often have dominant effects. For example, individuals with three copies of chromosome 21 have Down syndrome due to the increased expression of multiple genes; no single gene when present in three copies is known to cause the cognitive and physical manifestations of Down syndrome.“
In addition to the question above, when they refer to the dominant effect of multiple genes, what do they exactly mean?

Yah, that is kind of sloppy.  I guess what they mean is that single gene traits usually follow the classic Mendelian pattern.  (Though I wouldn't be surprised if that wasn't true, if incomplete or co-dominance were more common)
I'd say that having extra copies doesn't really follow the Mendelian pattern at all, so it's weird to say its "dominant".
I'm guessing that this book only barely touches on genetics.  Honestly, it strikes me as kind of juvenile to take Medelian genetics as the touchstone of genetics, and try to squash everything into that paradigm.  Perhaps that made sense historically, when Mendelian genetics was the first attempt to really understand inheritance, but with what we know now, it makes more sense to think the the Mendelian paradigm as something that applies only sometimes; easier to realize that it just isn't particular relevant when taking about, say, gene dosage.


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What is the minimum-volume : neutral-volume : maximum-volume of the molecules that make up the SARS-Cov-2 virus-fusion machine?
The "neutral-volume" is the over-lapping volume between minimum-volume & maximum-volume of the molecules that make up the SARS-Cov-2-fusion machine. Those identifying potential differences that support particle-flow inside the SARS-Cov-2-fusion machine-molecule have certain degree's of freedom. The best description of the structural dynamics of the Sars-COV-2-fusion machine that I have found was in "Scientific American", July-2020-issue/page 34,.
A base understanding of the "open-loop & closed-looped" particle-flow-symmetry is needed to explain the action of why the fusion machine of the SARS-Cov-2 virus binds to a lung-cell. The way I understand it, there is an exchange of particle-mass, starting with disorganizing lung-cell-mass by this virus at point of attachment, then re-organization occurs between the lung-cell and the SARS-Cov-2-fusion machines particle-flow grid. The SARS-Cov-2-fusion-machine may in fact accelerate into the lung cell, (to-push & bend/in the act of causing mass to dis-organize) and then deaccelerates, causing the act of organizing particle-flow between the two cells (to pull-straight/in the act of synchronizing & organizing), producing a certain closed-looped function between the virus-cell & the lung-cell. What are those unseen differentials between what is seen and what is not seen? Covalent bonding is straight-forward and well understood, except for the fact that there are other molecular actions involved. Would this be a function of two under-square vortexes, Van Der Wall-forces, Brownian motion, the action of dipoles, or something else? ALL of which may in fact contribute to an exchange of mass of which brings on those pulling forces that bind. There is a certain working-mass having a certain energy efficiency per location per time that changes the squareness of the SARS-Cov-2-fusion machine. Volume displacement of heavenly bodies plays a critical roll as to the way particles move around and through them, i.e. outer-space becoming inner-space & inner-space becoming outer-space per location per time.

I appreciate that scientists from different disciplines view problems from different perspectives, but perhaps you should consider that too if you post on lists frequented by biologists who clearly have a different perspective from you. Your concerns are not their concerns, and I cannot imagine that you will receive an intelligent answer here.  The fact that you include totally irrelevant tags such as “mutation” and “cell cycle” signals that you have come to the wrong address.

Thank you David your input is greatly appreciated and I thank biology-stack exchange for giving me the opportunity to post. I made a mistake in that I should have used the "dissociation constant" in my descriptive terminology, for I am bound to the capitalism beast and I an limited as to what I can post.


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Alcohol effect on heart and vascular system
How does alcohol weaken heart muscles and why does it increase blood pressure both temporarily and long term? Is the long term effect due to increase of plaque or is it due to other effects?

The actual mechanism through which alcohol increases blood pressure is poorly understood (1,2). However, there is a mountain of evidence that shows that there is a strong correlation between alcohol intake and hypertension (small, infrequent amounts may have positive effects whereas excessive consumption has very negative effects (3)).
Back to the underlying mechanisms however, there is a good paper by Kazim Husain, Rais A Ansari, and Leon Ferder, which presents all the possible mechanisms that may contribute to alcohol-induced hypertension. The core ideas are as follows:

Mechanisms of alcohol-induced hypertension. CNS: Central nervous system; SNS: Sympathetic nervous system; RASAS: Renin-angiotensin system and aldosterone system.
Image taken from: Husain et al - 2014 - Alcohol-induced hypertension: Mechanism and prevention
Central nervous system in alcohol-induced hypertension

[..] greater effect [of] alcohol on systolic blood pressure compared with
  diastolic blood pressure may indicate an imbalance between central
  nervous system factors influencing cardiac output and the peripheral
  vascular effects of alcohol

Baroreceptors in alcohol-induced hypertension

Alcohol diminishes the baro (presso) reflex by interacting with receptors in the brain stem, i.e. nucleus tractus solitarii and rostral ventrolateral medulla.

Sympathetic nervous system in alcohol-induced hypertension

Several studies reported increased sympathetic nervous system activation and discharge of sympathetic amines after alcohol consumption.

Renin-angiotensin-aldosterone system in alcohol-induced hypertension

The serum levels of vasoactive substances such as renin-aldosterone have been reported to be affected by alcohol ingestion in vivo or ethanol in vitro.

Cortisol in alcohol-induced hypertension

Certain studies have implicated the role of cortisol in alcohol-induced rise in blood pressure. Potter et al have reported a significant rise in plasma cortisol levels following alcohol consumption and a drop in plasma cortisol levels when alcohol intake was discontinued.

Increased intracellular calcium and vascular reactivity in alcohol-induced hypertension

Rats treated with ethanol showed constriction of blood vessels due to greater shifts in the binding of the calcium ion (Ca2+) in arterial and arteriolar smooth muscle cells causes increased sensitivity to endogenous vasoconstrictors.

Endothelium and oxidative stress in alcohol-induced hypertension

Imbalance of specific endogenous vasoconstrictor such as angiotensin II, endothelin-1 and nor-epinephrine and vasodilator nitric oxide (NO) may also play an important role in alcohol-induced hypertension. Alcohol stimulates the release of endothelin 1 and 2 from vascular endothelium in a dose dependent manner. Alcohol also increases the angiotensin II levels in the blood and vessels. Endothelin 1 and 2 as well as angiotensin II are known to be potent vasoconstrictors of the blood vessels.

References:

Husain et al - 2014 - Alcohol-induced hypertension: Mechanism and prevention
Saunders et al 1981 - Alcohol-induced hypertension
Grønbæk et al - 2009 - The positive and negative health effects of alcohol‐ and the public health implications


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Killer whale color
What purpose does the B/W killer whale color scheme serve? And what evolutionary pressure could possibly force all of them to go B/W in such a peculiar way ie with weird patches in the black. Also why not deep blue rather than black? And their diets are mostly near sea surface so I don't see how it helps them hunt, as stated in wiki

Interesting question. Can you please link to the wikipedia article and clarify where in the wikipedia article they claim that it their color pattern help them hunt (I think this the claim you are making when referring to wikipedia but I am not sure, so clarification would be welcome if I got this wrong).

https://en.wikipedia.org/wiki/Killer_whale#Feeding

You can edit your question to add this link in your question and clearly quote the passage that makes the claim that their color pattern help them hunt.

Although I'm not much into animal science, but let me try my hands on it.
The entire dorsal (top) surface and pectoral flippers are black except for the gray saddle.

The ventral (bottom) surface, lower jaw, and undersides of the tail flukes are mostly white. The undersides of the tail flukes are fringed with black.

Now let's come up to the main point, why does this happen?
The source I have referred to says there are two reasons :-

The distinctive coloration of killer whales is a type of disruptive coloration, a pattern that obscures the outline of an animal by contradicting the animal's body shape. In the flickering, filtered sunlight of the sea, other animals may not recognize a killer whale as a potential predator.
When you see the ocean from above, you see complete darkness. This helps the countershaded whale to actually blend with the darkness.

And when you see from underneath, you see light/brightness. The white ventral side again helps them to blend with it.
Source :- https://seaworld.org/animals/all-about/killer-whale/characteristics/
For the part of evolutionary pressure, it has already been answered on SE, visit
Selection Pressure on Orca Whale Coloration

Just one more question tho. Why didn't any other dolphins or well generally marine predators become as black as orcas did?

@nevertookcoursesbutwhy Because every animal has their own way of defense and their own unique way of dealing with predators or preying someone. Not all the animals (preys/predators) believe in camouflaging. For eg most of the dolphins protect themselves by having a social organisation and strong bonds b/w them.

Other dolphins do have the same counter shading! The orca is just the most extreme example. Additionally, the white patches behind their eyes is designed to a) make them look like a larger predator than they are, b) confuse prey as they are attacking from below.


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Is it possible to determine if it is the 5’-a 3’ strand or the 3’-5’ strand?
DNA is constructed in an antiparallel manner.  This means if you number each of the 5 carbons in the sugar deoxyribose the 3rd carbon will be connected to one phosphate group and the 5th carbon will be attached to another phosphate group of another nucleotide.  One strand will go from the 5th carbon atom to the 3rd carbon atom in one direction(5’ -3’).  and the complementary strand will go in the direction of the 3rd carbon to the 5th carbon in the same direction(3’-5’). Essentially they are made in opposite directions.  If I tell you the nucleotide base sequence of one strand is ACGGACTA.

I'm not clear what you are asking. If you are asking about convention, convention is to write sequences 5' to 3' (https://biology.stackexchange.com/questions/71530/what-direction-is-a-sequence-in-databases-written). If you are asking "which strand is the 5'-3' strand" the answer is both and neither: it would be like asking which side of a street is the forward side, they are both forward sides and reverse sides, it depends which direction you are traveling. Can you clarify your question?

Are you asking whether there is a convention for writing polynucleotide sequences? If so, the answer is yes, 5’ to 3’. But you might have researched that yourself.

Good analogy, @Bryan.


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How do I stimulate a neuron extracellularly, specifically the sphenopalatine ganglion
Apologies if this is too basic of a question, but I am an electrical engineer, just getting into neuromodulation/neurostimulation.
For my senior project, I am trying to make a device that stimulates the sphenopalatine ganglion. I have read as much as I can online, but some basic questions seem to not be answered. Answers to any of these would be really really helpful, as well as any resources to continue my research:

When I'm trying to 'stimulate' a neuron, I am really trying to trigger an action potential, correct?
Can I just send current across the exterior of the membrane to trigger an action potential?
Is is possible to stimulate a neuron without piercing the membrane? I know an action potential is the voltage across the membrane, so how can I change that voltage without piercing the membrane?
I believe I need to record the action potentials of the neuron, to make sure that my device is targeting the correct location and working properly, is this possible without piercing the neuron?
From the literature, I found that a 10 Hz electrical pulse works best for the sphenopalatine ganglion stimulation, but I am not sure how frequency plays a role in this.

Sorry again if that is a lot, but I am new to the field and have a lot of questions. Thanks in advance for any help!

I'd highly recommend collaborating with an electrophysiologist. You wouldn't want a neuroscientist without other training to wire up the electrical in your house (frankly, probably not even an electrical engineer, either, this is an electrician's job). Doubly, triply, 100X, 1000X more important to collaborate with someone with human electrophysiology expertise if you plan to get anywhere near a human with this. Not something that can be covered in a SE Q&A.

Hey thanks for the quick response. So I am kind of working with some neuroscientists/electrophysiologists in the field, but they are very busy and my manager says we should get some prototype finished before we meet with them.
So I need to do my background research (which now includes a SE Q&A) before I can get the help for my specific project and bring it to an actual human. It's an inefficient system, but it is what it is.

The simple answers to your 5 questions are: not necessarily, yes, yes (you're an electrical engineer; membranes are capacitors), yes but this is complicated, it's complicated - I doubt any of those really get you closer in your project, though.

As @BryanKrause mentioned, these are expert level questions. You cannot build a prototype without some knowledge of electrophysiology. There are entire books and experimental manuals written on this topic. Perhaps you can build a computer based model just to present the idea but it would not be wise to build a prototype without getting the neuroscientists on board.

Thanks to both of you for your answers. I'm wondering what books you are referring to about these specific topics. Even if I cant get a working prototype, I need to at least have a basic understanding of electrophysiology before I meet with them, just so I could have a better conversation. Any help would be great!

@Brian The two undergraduate neuroscience books I usually recommend are Purves or Kandel. The electrophysiology sections should have a lot of concepts familiar to you from the electrical part of your physics courses, but they probably focus on patch clamp electrophysiology from a technique standpoint. You have a very specialized target so from there you're probably headed to the literature. Google scholar tends to give me the most thorough results; medical indices like PubMed might miss some articles in journals with more of an engineering focus.


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How does a frog separate blood in its ventricle?
Since a frog has two atria and one ventricle, how does it separate oxygenated blood from deoxygenated blood when both are mixed in the ventricle? Or does a frog simply pump a mixture of both to the heart and the lungs? I checked a few videos and sites for this, but was unable to find an answer.
https://www.youtube.com/watch?v=MhOCzvA4KhM&ab_channel=iWorxSystems%2CInc.
My best guess, based on the above linked simulation, is that it has to do with a difference in densities of oxygenated and deoxygenated blood, but I am not sure.


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How does a diploid sporophyte form in non-recurrent apomixis?
I came across this definition of non-recurrent apomixis which occurs in angiosperms-

In non-recurrent apomixis, both the egg-cell and embryo are haploid and embryo is developed directly from an egg-cell without fertilization.

If this is the case, how does a diploid sporophyte develop from the haploid embryo? Are there any examples of the same?
I think most likely it would be by free nuclear divisions, that seems like the best bet, but I'm not sure if that's how it occurs.


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Regarding secondary growth in dicotyledonous angiosperms

I had read that (and as this image shows) the secondary and primary phloem eventually get crushed due to the repeated division of cells forming the secondary xylem, during secondary growth in dicotyledonous stems. While the primary xylem remains intact, the secondary and primary phloem are crushed.
My question: Is the phloem crushed to such an extent that it is not usable by the plant to conduct organic solutes? Then how does it compensate for this? Does the xylem take over the functions of the phloem?


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Why does a respiring mitochondrion have less cristae?
I read the following-

Number of cristae is more in resting-state of mitochondrion, but
decreases with activity, hence less in the respiring state.

cited: GK Pal, Textbook of Medical Physiology

After looking up a few sites, I was still unable to find out why resting mitochondrion have more cristae. Why is it so?
Based on this paper, the cristae undergo morphological changes in response to metabolic state and/or matrix volume (cristae remodelling), but I don't think that explains why it does so.


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Why are bees "committing suicide" in my house?
There is a beehive about 500-1000 meters away from my house.
During the last years, almost every day, one or more bees enter from the window, "dance" for an hour or two, and then drop dead on the floor. Some more details:

The bees may come in every hour of the day, but most of them come just before sunrise. This morning about 20 of them came in; now they are all dead on the floor near the window:

Often, the bees prefer to make their "dance" near the lamp. But this is not always the case.
They usually do not sting me; I was stung only twice, the bee died immediately afterwards, I took the sting out with tweezers, and it did not hurt too much.
I did not use pesticides or any other stuff that could kill the bees.

Why are they doing this? How can I stop them from coming?
I read that bees are disappearing; maybe it's because they all come to my house to die? :-)

How can we possibly know?

Welcome to Biology.SE! This is probably not an answerable question on this site since there could be many different reasons. To get an answer try contacting a local agricultural extension agent or entomology department and see whether you can get someone local interested to check for toxins and pathogens. ——— Please take the time to take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!

Abnormal behavior could be explained by use of pesticides, such as neonicotinoids. You may not be using pesticides, but agricultural companies around your place of residence may be using them. Hard to say for sure in the regulatory vacuum we live in, where our environment is concerned. https://en.m.wikipedia.org/wiki/Colony_collapse_disorder

@tyersome thanks for the welcome. I thought that maybe this phoenomenon has been observed in other places too, so maybe there is some research about it.

As @AlexReynolds indicated bee loss has been linked to neonicotinoids (a class of pesticides often used as a seed treatment), but many pesticides and pathogens can have neurological effects.  Consequently, I wouldn't believe any diagnosis made that didn't involve inspection for parasites and a toxicological workup ... Also getting someone local involved could result in the problem being solved!

@tyersome thanks! Following your advice I contacted the bee department in the ministry of agriculture in my country. I hope they will have a solution.

It's possible that there's something confusing them about the light. Does the window face the rising sun?  I've read that at twilight, bees get confused by nearby lights; maybe this happens at dawn as well. In one particular case, a beekeeper's porch light. The beekeeper moved the hive and it helped. Not a terribly helpful comment, but if the window does, in fact, face the rising sun, that might have something to do with it. Try having the hive moved.

Kind of a possibility: https://www.beebestinc.com/are-bees-attracted-to-light/

@David - Just because you don't know doesn't mean no one can know. forestecologist might know; a bee keeper might know; who knows who might kniow, but someone might. You should be less dismissive.

@anongoodnurse — No. The question relates to a particular circumstance, rather than a generality —  my house. How can anyone know the particulars of this, or even if the poster’s observations are reliable?

@anongoodnurse your guess was correct - my window does indeed face the rising sun. And the link you gave indeed describes a situation very similar to mine. Thanks!

After years of struggling with the bees, I finally found a solution. I put in my window a lot of pots with various flowers, including some vegetable plants with flowers. Now, instead of entering my house, the bees go to the flowers.
As a bonus, I get wonderful scents and some fresh cucumbers - pollinated by the bees. I have learned that bees are not a nuisance - they are an asset!

Don't forget to mark your answer as best answer.

Fragrances inside your house were probably attracting them then. I just use nets to keep out lots of curious insects. Bees and wasps, for no discernible reasons, sometimes investigate the nets pretty thoroughly... almost certainly looking for a way in, either to nest or who knows what.

Also, based on your location: in arid/desert areas bee colonies send out more scouts.

By the way, bees can see UV and of all the frequencies this is the most attractive to them https://www.nature.com/articles/s41598-020-64782-y. So it's possible the bulbs you were using, e.g. if CFL, were attracting them.

I found another solution, for a season when the flowers on the window are insufficient. I have noticed that bees are attracted to my light bulbs, especially in the early morning when it is dark outside. I have also read that bees cannot see red light - it is beyond their visibility spectrum.
So, I bought some RGB bulbs - bulbs with a remote control for changing colors. These are surprisingly cheap. Now, whenever the bees approach, I switch the light to red, and they go away.


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The Viceroy Evolution Paradox
The viceroy butterfly generates a toxin compound which make it distasteful to predators.  Biologists agree that the viceroy must have developed this trait as a passive defence mechanism to prevent being eaten.
Let’s look at it from an information point of view.
For this to work, information about the bad taste of the viceroy must be known to the predators.  This can happen by a predator eating one viceroy, discovering the bad taste, learning and never doing it again.  Unfortunately, the unpalatable butterfly had to die in the process.
The second, and most important, information path is the genetic one.  One way, evolution work is by the survival of the fittests. In this case the important trait of “tasting bad” dies with the butterfly and is less likely to have been transmitted to a new generation, unless (and this might be part of the answer) we consider the local population of butterfly as the evolving organism.
The question:
If a successful gene is only proven successful when removed from the gene pool, how does the species evolve a trait involving this gene?

Possible duplicate: https://biology.stackexchange.com/questions/24312/how-can-natural-selection-occur-at-species-level-whilst-not-occuring-at-the-indi see also: https://biology.stackexchange.com/questions/66081/how-does-natural-selection-explain-how-organisms-that-are-poisonous-evolved

@BryanKrause Thanks for finding the duplicate. I think your second link is probably more clear, but since that points to 24312, I used it as the dupe.

OP the reason this isn't a paradox is the title of the duplicate (natural selection occurs at a species level, not an individual level). The mechanism by which a toxin would be selected for is discussed specifically in this answer. If it helps, you should remember that natural selection acts on existing variation. So the toxin is already present in the population at some frequency.

I think the problems your two points. bring up can be summarized as evolution does not act on the level of a single organism.

The post marked as duplicate talks about species/lineage selection. This is unlikely to be a good explanation for the process asked by the OP. Instead, the other post @BryanKrause suggested as duplicate (How does natural selection explain how organisms that are poisonous evolved?) is a much better duplicate IMO (and talks about kin selection among other things).

@Remi.b the problem is the second post is closed as a duplicate of the first. I think we're not supposed to close a question as a duplicate of a closed question, but rather close both for the same reason.

@DeNovo Oh yes indeed. Good point. I just nominated the post for reopening as I personally don't think it should be closed as a duplicate of the other one. Thanks


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What's the percentage of zoom needed to see protozoa in an optical microscope?
I was searching for a microscope and I saw some with prices of over 10.000$. However I need to buy one that can actually show me the cells of a culture I am growing at home, and I really need to know how much "zoom" I need to see them.

Hi Caju. Welcome to Bio.SE! What attempts to answer this question have you already taken? We ask that all question posters here attempt to search for an answer to their own question and explicitly indicate what research they've already done, what they learned, and what is still confusing or unknown to them. Our goal is not to simply be an answer site, but rather a site that promotes self-learning with some expert help along the way :). Please take a moment to edit your post with this additional detail, and it will likely be received more positively by our community. Thanks!

specifically, a quick Google search can show you approximate organism sizes, approximate protozoan sizes, and how magnification and size relate. Please perform your own google searches and report back what you find and what you are still confused about. Demonstrating additional effort will certainly result in your question receiving a more positive response from most of our community. Thanks, Caju!

Not an answer since I'm a long, long way from being an expert, but 10,000 dollars is far too much to pay for a hobbyist-level microscope.  300 dollars is a reasonable ballpark, and IMHO magnifications above 400X or so aren't much use.  I found this site to be helpful: https://www.microscope.com/how-to-buy/

You can see a few like paramecium with good bare eyes. A 10 magnification loup will reveal more. For general amateur use a stand held binocular ( not distance type binoculars) is very versatile, and common, traditionally 7 X to 40 x magnification. Any more magnification will require special lights ,sample preparation , etc.

When I was much younger ( and eyes were sharper) .I watched paramecium and rotifers in my aquarium. I used various microscopes all my adult life but never published , as most metallurgists could say the same.

You don't really need special lights (other that the normal below-stage light), or sample prep beyond putting a drop of liquid on a slide and a cover glass over it, to see a good many microorganisms.

Thanks for all the help, seemingly, the microscope I'm willing to buy is more than enough for what I wanna do!