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What kind of larva is this? (Southern CA, USA)
I need help identifying this larva:

(Click images for full size versions).
There's about a dozen of them in my parents' bathtub and I'm not sure what they are or where they are coming from.
They are about a centimeter long, maybe a little less. They look flat and are hardly noticeable. When they are upside down they look more like a maggot.
My parents didn't even notice until I pointed them out. They move around very little and stay at the bottom of the tub. I haven't seen them anywhere else.

3 Important questions: 1. Is your parent's home currently under renovation/construction? 2. Have you noticed any insect damage in the bathroom or nearby? 3. Have you seen any flying insects in or outside their home?

Also, a definitive length may rule out certain species...

That looks a lot like a Common Southern California Termite. I would check any wood that you have around your home just to prevent any damage. If you want more information just look it up online, but that's most likely what it is.

Note the eyes, the short, segmented antennae, the mandibles (better seen in your second photo.)

Please add a link to an image of your id/ add an image directly. Also mention why do you recognize it as one. That would make your entry complete. Thank you for writing an answer.

Hi Askansce. I edited your post to bring it to our site's requirements. Feel free to roll back if you desire. :)

@anongoodnurse, thanks for the help. I'm really new to all this and don't quite know the format for everything just yet. I definitely appreciate the assistance :)

 Short Answer
These look like termites, and based on appearance and size they are likely Drywood Termites of the family Kalotermitidae.

Specifically, these appear to be either workers or "pseudergates$^†$", and likely those of the species western drywood termite (Incisitermes minor).

 Source: UCANR

However, without mature soldier or swarmer specimens, conclusive species ID is very difficult.
 Long Answer
General Termite ID
According to Orkin, there are 3 distinct groups into which termites are divided: subterranean, drywood, and dampwood.

Since the worker termites in these groups more or less look the same, the appearance of the reproductive caste (alates) [or swarmers] and soldiers is important..

In other words, it will not be possible to properly ID your specimen without pictures/descriptions of the soldiers or swarmers.

However, It is critical to identify the species of destructive termites to formulate an appropriate control program.

According to this UC IPM page, there are at least 23 different species of termites in California.
I'll give you support for the options that I think are most likely:
 Option 1:
My initial guess is that you have some species of drywood termite (family Kalotermitidae), because these are common.

Based on the following picture (and numerous others from a google search), your specimen looks more like the size/shape of a drywood species vs. either dampwood or subterranean:

 Workers (from left to right) of subterranean, Reticulitermes hesperus; drywood, Incisitermes minor; and dampwood termites, Zootermopsis nevadensis. [Source: UC IPM].
Without swarming specimens, further confirmation will be difficult.

However, drywood termites have very distinct hexagonal 1mm-long fecal pellets called frass that you could try to locate to confirm.

 Zoomed in frass (or fecal pellets). Sources: Termiteweb and UC IPM

 Fecal pellets collecting under a door Photo by B.J. Cabrera, University of Florida
Do you have this??

However, even given that initial guess, another UC IPM page suggests that drywood termites are not often seen:

Drywood termites are cryptic insects that are difficult to detect. They live deep inside wood; and except during periods when they swarm or when repair work is being done on infested homes, they are seldom seen.

So my guess could be wrong....

Possible Candidate Species
If your specimen is a drywood species, it is most likely the western drywood termite (Incisitermes minor).

 Source: Himmi et al.(2016)
From UC Berkeley:

Pest Status: Second most destructive termite in California.

Key Characteristics:

Present throughout California, but most prevalent in southern CA.
~ 1 cm long
Live in and eat dry wood (typically found throughout wooden structures of homes)
Nests of most species remain entirely above ground and do not connect to the soil.

For more info, see here.

 Option 2:
Subterranean termites (typically of the family Rhinotermitidae ).

Shelter tubes (sometimes called mud tubes) are the most commonly seen evidence of a subterranean termite infestation.

Common species:

Western Subterranean Termite (Reticulitermes hesperus) [also see here].

The most destructive termites found in California [Source: UC IPM page].
Unlikely your species because they typically are only about 0.3 cm long. [Source: Termite.com].

Formosan subterranean termite (Coptotermes formosanus)

 Source: Nolawoman

Invasive termite from China, that has invaded US (including CA).
Nicknamed the super-termite because of its destructive habits due to the large size of its colonies and its ability to consume wood at a rapid rate
Again, these are likely too small to be your specimen as the body length is approximately 4-5 mm. [Source: CABI].

Conclusion
Based on size, it is more likely that you have a drywood species vs. a subterannean species.
However, again, without more evidence (frass vs feeding tubes and/or pictures of mature soldiers/swarmers) a definitive ID will be difficult.
I advise that you contact a local exterminator or termite expert to have them check your parent's house more closely.
Good luck!

$^†$  Note: "pseudogate" = a blind wingless nymph performing some of the functions of a worker. [See here].


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Betaine HCl stomach pH
It seems betaine HCL is often recommended for those suffering from "low stomach acid" -- which, as I understand, is having too high stomach pH for proper digestion (especially for proteolysis via pepsin). However, I have a few questions then -- though I'm not sure if my reasoning is correct here:
Understandably, one wouldn't want to drink pure or highly concentrated HCl by itself to increase stomach acid! But then, what role does the betaine play?
I'm guessing betaine HCl probably does not dissolve in water to give the same pH as just straight (or concentrated) hydrochloric acid -- since then it would seem just as dangerous as drinking plain HCl!
In that case, if it doesn't decrease the pH as much, making it safe for oral consumption, what value does it bring for "lowering stomach pH" anyway? I mean, one could just drink a little vinegar or citric acid for the same effect?
Or, perhaps, is betaine-HCl just a means of some "delayed release" of HCl to lower stomach pH without hurting the mouth and esophagus during its initial consumption? Betaine may just be a useful carrier here, given it's quaternary ammonium and carboxylic acid groups (e.g., a zwitterionic carrier)
Alternatively, could the value of betaine HCl simply be in providing a source of Cl- anions, possibly for increased pepsin activity? (I'm not sure if pepsin requires merely low pH or specifically also needs Cl- anions as well) Betaine-HCl does seem to be often formulated with additional pepsin enzyme(s) as well...

Betaine HCl (trimethylglycine) was present in over the counter "stomach acidifiers" but the US FDA says there is no evidence for its efficacy and has banned its use for this indication (source: US FDA) - it may be freely available elsewhere, I am unaware of the regulatory status in other jurisdictions.
There is no biological reason to expect the "HCl" portion for most drugs to have any substantial effect on stomach acid. Lots of drugs are packaged in an acidic form as "drug HCl" - this is usually because the acidic form of the drug is more soluble. Drug doses are commonly in the microgram to milligram range (though obviously this varies for different drugs) - at those concentrations, the stomach acid is much too concentrated to be affected by the small amount of acid added from the drug.
The catch with Betaine HCl is it looks like websites are advocating for taking several grams to provide enough HCl to affect stomach acid. I suspect that supplement makers suggesting these high doses is what led the FDA to ban the drug OTC in the first place. Although betaine is produced as part of normal metabolism, there are some side effects reported, mostly mild.
Note that anhydrous betaine is prescribed (and approved by US FDA) for homocystinuria, and used as a supplement to animal feed, but neither application is related to stomach acidification (and the anhydrous form is not acidified).
One recent study supports use of Betaine HCl with patients who are being treated with acid-suppressing drugs such as proton-pump inhibitors, to be given along with other drugs that require an acidic environment to function/be absorbed. However, it is important to note that this study was in fasted patients: they consumed nothing but a little water with the betaine HCl. In this circumstance, the little bit of HCl in a moderate to large dose of betaine was sufficient to lower stomach pH. However, the results likely would have been very different if the patients had eaten a recent meal.

+1 Great answer, looks like skepticism was the right call here indeed, according to WebMD as well : ) http://www.webmd.com/vitamins-supplements/ingredientmono-312-betaine%20hydrochloride.aspx?activeingredientid=312&activeingredientname=betaine%20hydrochloride

@ManRow Yeah I actually saw the webmd note first but then went looking for some more robust sources. :)

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What is the oxidation state of iron at the photosynthetic reaction center?
Is the iron at the reaction centre  in the $3^+$ or $2^+$ oxidation state?
For instance, 1AIG is $2^+$ or, perhaps it will depend upon charge separation state? I checked the PDB: some are $3^+$ while some are $2^+$.

At what reaction centre?

The question needs more information. The pH is critical to the answer.

Iron in these complexes is used to transfer electrons and so can exist in both oxidation states.

in chlorophyll it is Mg but in RC it is iron. I am asking the role of Fe. I don't care about Mg. I am not doing catalysis. By the way, what is the role of Mg?

How will PH influence the oxidize state? Just the normal living plants and bacteria. I saw in PDB various molecules. They marked out whether they are 3+ or 2+ ......I think they did not specify the PH?

Iron is fixed at the RC. It is not moving. It cannot transport electrons.

no....in the reaction center of (bacteria)  light harvesting antenna

Is there anything interesting about Fe in cytochromes?

@latra yes, Fe in cytochromes is also fixed, but it also functions to transport electrons. Like cytochrome c oxidase, or generally, all cytochromes in electron transport chain in respiration.

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Help me identify this... plant? fungus?
Today I found several of these in my back garden in Sydney NSW, Australia (specifically the north shore). They seem like flowers, except I don't see any attached plant and they have a weird brown goo around the mouth. I've never seen anything like this. Any ideas?

That's absolutely an Aseroe stinkhorn. The way stinkhorns disperse their spores is rather interesting - rather than producing powdery wind-dispersed spores like most fungi, stinkhorns make flies do the disposal by placing the spores in a foul-smelling gel called gleba(the brown slime visible on your specimen). Flies pick up the stench, and land in it and eat it, thereby spreading the fungus to any suitable patch of soil that the fly lands on.

After some Googling, it seems maybe this is a stinkhorn fungus, specifically Aseroe rubra.


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Why is western blotting used to confirm positive ELISA HIV tests?
I know that when an ELISA test indicates a positive result for HIV, a western blot is done to confirm. When I search online for the reason why, all that I see is that western blotting is "more specific" than ELISA. If they both use antibodies, shouldn't these procedures have similarly accurate results?
My only guess would be that the combination of Ab-Ag binding in addition to expecting your antigen to be a certain size is sort of a "double yes" and thus western blot results would possibly be taken as more accurate.

The only other thing I would add is most commonly used ELISA employ an indirect approach of detecting Antibodies in the serum against HIV antigen attached to the ELISA plate

One reason a Western blot is more specific than an ELISA - even one using the same set of antibodies - is background.
Antibody-linked colorimetric reactions aren't completely on/off. There's always some background reaction. The antibodies are a little bit cross reactive, or non-specifically sticky, or the colorimetric coupling enzymes aren't completely washed away, etc. There's a number of reasons you'll get a small amount of signal even in the abscence of the desired reagent.
So imagine how this non-specificity looks in an ELISA assay. You're only getting a single readout. Any non-specificity/background in the assay adds noise to your output level. Hopefully for any decent assay the noise is normally well below the threshold for crossing over into a "positive" readout, but if the noise is Normally distributed, there's always a small chance that the noise will exceed that threshold. (There's also those non-normal failure modes, where you mess up a wash step, or you get a bad tube of antibody, etc. Negative controls help, but only so much.)
In contrast, think about how non-specificity/background looks in a Western blot. If you get non-protein linked background, the presence of this background will be across the entirety of the blot. It's very obvious that something went wrong with the assay in those cases. Even if you get random spots and not overall background, the chance you'll get a random spot at just the correct molecular weight is very, very unlikely.
An additional benefit is that Western blots first separate the proteins prior to doing antibody-linked detection. This means if there's some protein in the sample which cross-reacts with the antibody, it's very likely it will migrate at a different molecular weight and not be counted as a false positive. (As opposed to ELISAs, where every signal counts toward the total.)
These effects mean that if you're looking for low false positives (as you would with an HIV test) a well-done Western blot is likely to give a more confident signal than a well-done ELISA would. (At the cost of time and effort.)
A final issue is that combining the two will give you more confidence in a positive result than either one alone, especially if you use different antibodies for each. The final confidence in a positive result is not just the confidence from the Western blot, but the confidence that both the Western and the ELISA report positive results, so there's a benefit of doing both, even if they were equally specific.


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How can antibodies in rapid antibody tests be kept at room temperature without denaturing?
The normal temperature for long term antibody storage is around -20 degrees Celsius. However, when developed into rapid antibody tests, they can be kept at room temperature for prolonged periods. How is that possible?

Antibodies have no problem with room temperature. Naturally, antibodies expect to survive for many days or weeks at body temperature, which is much higher than room temperature (at least, mine is).
-20°C is recommended for very long-term storage (many months or years) of antibodies, but they are typically very stable proteins and don't denature very readily at all. Storing them at room temperature can be done for a long time -- certainly weeks, in my experience, with the only real concern being the possibility of bacterial or fungal growth if the antibodies aren't sterile.


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Why are these trees leaning, but no trees around them are?

This was observed in Florida.The trees on the left have a distinct lean to them, but none of the other trees in the area are leaning, why is this?
I'm not sure what other information is pertinent or what else I should look for.

Could it be that this location is in close proximity to the sea and that the sea (or a large lake) is located to the right of the picture?

How far away from the ocean are these trees?

@kmm Not close to the ocean. There is a small lake not terribly close (800ft). I'll have to check how much it aligns with direction of leaning.

Related: http://biology.stackexchange.com/questions/35622/what-could-cause-a-forest-of-bent-trees/35627#35627

There are several reasons as to why a tree might lean. Normally, it is a combination of some/all of the points below:

Weight distribution: Depending on the diameter of the trunk and especially the height of a tree, gravity can create problems. So the main question is how the weight of the crown is distributed over the tree's trunk.
Species variability: Different species of trees have different root systems, some go deeper and others don't. The depth and width of the root system are factors to consider when assessing a leaning tree.
Environmental factors: There are a variety of environmental factors that will contribute to a tree leaning. For example, a
tree that leans because it has grown towards the sun often has a curved trunk. The trunk curves due to the tree's ability to adapt over time to the changing
availability of sunlight. Its root system will grow to accommodate the “off center” weight distribution, up to a point. Additionally, storms or constant wind can obviously cause a tree to lean.
Structural damage: Leaning trees that don’t have a “sweep” (caused by wind) but tend to have a fairly straight trunk generally have a history
of structural damage to the root system or storm damage that has
caused the root system to slip, break, sink or simply fail to support the
tree in some fashion. If the trunk appears to enter the ground without
a mound of soil on the side away from the lean, then the root system
has sunk, either from rot, mechanical fracture, physical cutting of the root plate or soil subsidence. If the mound does exist on the back side of the lean, that's a sign that the root plate is being tipped
out of the ground and the roots have failed - either through mechanical wounding or structural failure. As roots break under stress from wind or off center crown weight pushing the trunk away from the soil holding the roots, the up-wind side of the root plate will tip out of the ground.

In addition, it may be worth mentioning that time plays an important role here too. Older trees will have been exposed to the forces of nature and plant pathogens for longer than younger ones so it certainly makes sense to take the life cycle of a tree into consideration, some live longer than others and thus may have been subject to wind while the other surrounding trees weren't "tall" enough to shield off any of the wind etc.
Sources: Georgia Forestry Commission - Leaning Trees - What's up with that

Interesting stuff, I'll have to look at the ages of trees nearby. What really struck me is how spatially localized the phenomenon is though, maybe some sort of localized weather effect.


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In which direction does ATP synthase rotate?
I heard about the rotation of ATP synthase in a biochemistry course. The professor said it will rotate counterclockwise. Is that true? If so, what mechanism defines its direction?

Short answer
The direction of rotation depends on the viewing point of the observer and the reaction catalyzed by the ATP synthase. When synthesizing ATP, and viewed 'from the bottom' (observer faces the intermembrane space looking into the mitochondrial matrix) it rotates clockwise.
Background
ATP synthase is a membrane bound enzyme with two large subunits; F0 and F1. F0 is inserted in the membrane and funnels H+ ions from the intermembrane space into the mitochondrial interior (Fig. 1). The stalk region connection F0 and F1 contains the γ subunit, which basically forms a rotating shaft powered by the flow of H+. This causes the entire F1 unit to rotate during ATP synthesis.
Now importantly to know before continuing; enzymes basically work two ways, as they merely establish equilibrium. As such, any ATP synthase is also an ATP hydrolase. When it synthesizes ATP, the γ subunit runs in clockwise direction when observed from the “bottom” (the side closest to the F0 and the membrane, see Fig. 2). When it hydrolyzes ATP (e.g., under non-physiological laboratory conditions) it runs counter-clockwise as the reaction, as well as the movement of the γ subunit reverses (Nakamoto, 2008).
The direction in which the rotation takes place is dependent on the steps involved (Fig. 3). In this figure, ATP hydrolysis is shown and that can be compared to burning fuel in a combustion engine. Now the direction of H+ reverses, against its concentration gradient and needing energy (the road speeding below a car if you like). Because ATP binding, hydrolysis and release of waste (ADP + Pi) each cause a 120o turn of the rotor, the F1 subunit rotates one full turn in each cycle (Yoshida, 2001). During ATP synthesis the opposite direction is established, as waste (ADP + Pi) is taken in and phosphorylated to ATP, during which the flow of H+ reverses (akin to a car going downhill, only combustion engines cannot generate gas from carbon dioxide and water, unfortunately).

Fig. 1. ATP synthase subunits. source: Penn State University

Fig. 2. ATP synthase. source: Noji, 2004

Fig. 3. ATP synthase compared to a combustion engine. A combustion engine converts fuel energy into rotation of a rotor. It can drive the intake of the fuel gas, compression, ignition and exhaust sequentially just by a simple rotation of the central rotor (right panel). The F1 gamma-subunit has and three reaction chambers (the catalytic beta-subunits (left panels). The three reaction sites each go through three cyclic steps in a 120° phase difference to cause rotary motion, very similar to a combustion engine. source: Yoshida, 2001
References
- Nakamoto, Arch Biochem Biophys (2008); 476(1): 43–50
- Noji, Biohistory journal (Winter, 2004)
- Yoshida, Nature Rev Mol Cell Biol (2001); 2: 669-77

It should be F_o instead of F_0

Why does it rotate in that direction?

@latra figure three shows why.

I have read the caption of figure 3 and the third paragraph, but it only says ATP synthase is similar to a combustion engine.  It did not tell me why that direction.

@latra I can't explain it in more detail. Why does the crankshaft of an engine rotates left or right; because it is structurally engineered to do so.

@latra it's all about conformational changes in the protein


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Why are deciduous teeth shed?
Why do we have two sets of teeth? Why do earlier shed and new teeth replace them? In humans, kids do not have any need for replacement of the teeth. Why don't the milk teeth grow themselves? Or why don't we have a set of small permanent teeth as our first teeth?

Teeth grow beneath the gums in the mandibles. They don't grow once erupted. "Baby teeth" are small to fit small mandibles; too small to be as efficient as needed for the longer life of an adult. Teleologically it makes sense to have small  teeth for the time we're small, and exchange then for bigger teeth for the rest of out lives.

@anongoodnurse And since we do not grow as an adult, new teeth are not required as mandible size is fixed! Why don't you post it as an answer?


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Why is competence useful for a starving cell?
I know that some bacteria become competent when there is not much food available in their environment.
I don't really understand why this is useful for the cell. I've seen some other organisms form a biofilm or get together to become a slime when starved and I understand the utility of this mechanisms (reducing energy consumption and being able to move around easily to look for nutrients).
The only plausible explanation that I see is that being competent might be useful to take advantage of the DNA of dead cells. Am I right?

The wikipedia article you link gives four current hypotheses: genetic diversity, "DNA as food," repair of DNA damage and Horizontal gene transfer. Are you looking for additional hypotheses, or a clarification of what's in the article?

@AJK I would like some clarification. For instance I don't understand the "DNA as food" hypothesis. In my understanding if all the cells became competent then there would be no available DNA in the medium they're growing in and they would die, making one of the above forms (biofilm - slime) preferable.


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Does a queen wasp sting also have poison?
Last night I got sting by a wasp and because of the time of the year I suppose it is a queen. But usually it swells and hurts for a day after it, but this time nothing happened only that I woke up of the sting which hurt a little for a short time, but in the morning I couldn't find any signs of the sting.
Now is this because of the poison is worked out because it could be a pretty 'old'  new wasp queen and her enzymes like histamines and aptoxine are got too old? Or do queen wasps not use/have poison or less? Or is it my body that just reacted different?

A good read.

Ok interesting, so higher levels of spiroacetyls in the worker venom are more harmful than the acetamide in the queens.

I'm voting to close this question as off-topic because question is based on an anecdotal example.

@AliceD although I agree the bulk of the question is based around an anecdotal experience, the root of the question is both on-topic and interesting. I'm voting to keep open. Marijn, perhaps you could edit this a bit to reflect more on the biology and less on the personal experience.

@Marijn If you read that article carefully, the focus of the research isn't on the potency of the venom itself with repsect to how much harm is caused to the victim; but instead, the research was exploring a comparison between a queen wasp's venom with that of a worker (or guard) wasps, in regards to how well the release of the venom alerted other wasps to attack -- i.e., the signaling efficacy of the venom, not the potency of its damaging effects. ".. as soon as a guard wasp stings an attacker, the venom releases an alarm-signalling odour picked up by the workers .."

@Marijn "As soon as the queen's venom was released, the workers mobilised but limited their aggression to flying towards the bobbing disc. However, it was a different matter when the workers' venom was released. The workers mounted a full-scale attack, landing on the disc and even stinging it. While queen's venom was sufficient to stimulate the early stages of an attack sequence, only the volatile components of the workers' venom provoked a full-on assault." -- last paragraph of that article.

Yes, all female wasps are expected to have venom. In the case of social wasps, which I am inferring is what stung you, all female wasps are equally potent as they're morphologically the same. [This opens the question of how could you say this was a queen wasp.] The only difference between a wasp worker and a queen is that a worker is forced to fly around and forage by the queen so it doesn't have the time and energy to invest into laying eggs.
The following paper discusses this: http://dx.doi.org/10.1590/S1519-566X2008000600011
However, not all individuals are the same, both wasps and people, so you may have been stung by a rather weakened wasp/species to which you're not particularly sensitive.
I'd like to recommend the following paper which isn't about wasps, but discusses fundamental venom composition differences between fire ant workers and queens.
Fire Ant Queen Venom is Fire Ants' Secret Weapon
This is the DOI reference: http://dx.doi.org/10.1016/j.toxicon.2018.11.428
(Free Version)
This is the DOI reference: https://doi.org/10.1101/454637
Contrary to wasps, most species of ants present a marked caste specialisation, meaning queens are quite different from workers. However, they still produce (and deliver) venom.
Thanks for your account!

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How do aerobic Rhizobium bacteria survive in root nodules while fixing atmospheric nitrogen?
I read that rhizobium carry the enzyme nitrogenase, which is irreversibly damaged upon the exposure of oxygen. Inside the root nodule of legumes leg-haemoglobin keeps a microaerophilic environment where nitrogenase enzyme can function and molecular nitrogen can be fixed (source: Brock's Biology of Microorganisms).
Shouldn't therefore Rhizobium bacteria die in such microaerophilic condition inside the root nodules?

Welcome to Bio. What makes you think rhizobia are anaerobic environments?

I read that rhizobium carry the enzyme nitrogenase that is irreversibly damage upon the exposure of oxygen, that's why, inside the root nodule of legume plants leg-haemoglobin keeps a microaerophilic environment where nitrogenase enzyme can function and molecular nitrogen can be fixed.

That's interesting to note. +1. I added those details in the question. If you could add the source of that info that would be awesome. Thanks for this question.

The source is 'Brock Biology of Microorganism', it is 14e I believe

Great book! I love that one, especially the edition with the hot water springs in Yellowstone NP :)

TLDR
One hypothesis for survival is nitrate respiration.
Long Answer
Ampount of oxygen available in root nodules is controlled by the host plant by two ways:

By presence of leghemoglobin
By the diffusion resistance
Under anaerobic condition the bacteria survives by making use of denitrification process which could be used to produce ATP under anaerobic conditions.

It is known for a while that, beside nitrogenase activity, in many symbiotic associations between legumes and Rhizobium the activity of nitrate reductase also exists 12. Most of the nitrate reductase ativity has been found to be concentrated in infected bacterial body i.e., bacteriod3. The bacteriod uses the process of conversion of nitrate into nitrite for creating a proton gradient which is inturn used for generation of ATP.
Reference.

Leghemoglobin fan here.  My boy needs equal time with that loser nitrate reductase.  Got another diagram?


text:
When does the kinetochore form?
According to Wikipedia,

the outer plate... is assembled in the surface of the chromosomes when the nuclear envelope breaks down.

However is makes not mention of when the inner portion of the kinetochore forms, and I cannot seem to find this jn formation elsewhere. Is it present from DNA replication and helps to hold the sister chromatids together?

Have you checked wikipedia? https://en.wikipedia.org/wiki/Kinetochore

@FilipeRocha as you can see I referenced Wikipedia in the first line of my post. So yes, Wikipedia was my first port of call. As I stated above, it says when the outer plate of the kinetochore forms, but I do not know if the kinetochore chore exists from DNA replication in s phase. It makes no mention of this.

Oops, that's true, you did! What do you mean "exists from the DNA replication in S phase"? My idea is that the chore is also formed during mitosis, prophase , at the same time as the outer part, but I can't give you a sure answer :/

@FilipeRocha i thought that perhaps the inner core is present in s phase and prevents the sister chromatids from separating (as well as the cohesins)

That is the function of the centromere, may you be confusing the names? The inner kinetochore is the part of the kinetochore which attaches to the centromere during mitosis, but only forms then, in contrast with the centromere, which is always present, even when the chromossome is made of a single chromatid. I think historically the word "kinetochore" was used to describe the centromere, but no longer. Also the cohesins only do their function when chromatid condensation begins (prophase).

@FilipeRocha from what I am aware, the cohesins are present from the dba replication on s phase and they mostly break during chromosome condensation in mitosis.

you are right about the choesins, they are present from after the dna replication a break during anaphase


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Is the amount of cholesterol the body produces affected by how much cholesterol you take in with food?
In the past I've been told multiple times that if you don't eat foods containing cholesterol, your body will increase its production of cholesterol to balance out the lack of nutritional cholesterol. On the other hand, if you eat sufficiently much cholesterol, the body will adapt its production of cholesterol in the other direction.
What evidence is there to support this statement?

Here's a study in which they measured a decrease in endogenous cholesterol synthesis after various amounts of dietary cholesterol: Dietary Cholesterol Feeding Suppresses Human Cholesterol Synthesis Measured by Deuterium Incorporation and Urinary Mevalonic Acid Levels (Arteriosclerosis, Thrombosis, and Vascular Biology, 1996):

The objective of this study was to measure the response of cholesterol
  biosynthesis in subjects to three different amounts of dietary
  cholesterol: 50 (low), 350 (medium), and 650 (high) mg cholesterol per
  2800 kcal. Individuals with low (n=7), normal (n=12), and elevated
  (n=11) plasma cholesterol concentrations consumed in random order
  solid-food test diets (15%, 55%, and 30% of energy as protein,
  carbohydrate, and fat, respectively) at each dietary cholesterol
  level. The three diets were consumed for 4 weeks each, and each
  dietary phase was separated by a 4-week washout period. During the
  final week of each diet, 0.7 g D2O was given per kilogram of body
  water and deuterium incorporation into the erythrocyte cholesterol
  pool was measured for 24 hours. Urinary mevalonate levels were also
  determined in samples obtained during two consecutive 24-hour periods.
  Both techniques provided measurements of whole-body cholesterol
  biosynthesis. In all subjects the cholesterol synthesis rate as
  measured by deuterium incorporation was significantly lower (P<.05)
  after the transition from low- to medium- and low- to high-cholesterol
  diets. Urinary mevalonate excretion decreased after the change from
  the medium- to high- (P<.05) and low- to high- (P<.01) cholesterol
  diets. Although correspondence between the two methods was poor, they
  both indicated some suppression of cholesterol synthesis by dietary
  cholesterol. The response of cholesterogenesis to different amounts of
  dietary cholesterol was related to the rate of synthesis under
  depressed conditions of the low-cholesterol diet. These findings
  indicate modest downregulation of synthesis in response to dietary
  cholesterol in humans, independent of plasma cholesterol levels.
Metabolic responses to increased dietary cholesterol potentially
  include reduced endogenous synthesis, decreased absorption, and
  increased biliary excretion of cholesterol.

In some people, who are cholesterol hyperresponders, dietary cholesterol does not effectively suppress endogenous cholesterol synthesis, so it results in elevated blood cholesterol levels (Comprehensive Biotechnology, 2011). In one study, a decrease in dietary cholesterol intake resulted in a decrease of blood cholesterol in hyperresponders but not in hyporesponders: Endogenous cholesterol synthesis, fecal steroid excretion and serum lanosterol in subjects with high or low response of serum cholesterol to dietary cholesterol (Clinical Nutrition, 1986):

In this study we addressed the question whether hypo- and
  hyper-responders to dietary cholesterol differ with regard to the
  flexibility of endogenous cholesterol synthesis after changes in
  cholesterol intake. Whole-body cholesterol synthesis was measured as
  faecal excretion of neutral steroids and bile acids minus cholesterol
  intake. In addition, we determined serum concentrations of lanosterol,
  a precursor of cholesterol and a possible indicator of cholesterol
  biosynthetic activity. The study was carried out with 2 hyper- and 4
  hypo-responders; these subjects had shown a consistently high or low
  response of serum cholesterol to a decrease in dietary cholesterol in
  two previous experiments.
The subjects received controlled high- (on average 697 mg of
  cholesterol per day) and low-cholesterol (109 mg/day) diets for
  periods of 4 weeks in succession; cholesterol was the only dietary
  variable. The two hyper-responders again showed a significant decrease
  in serum cholesterol. There was essentially no decrease in serum
  cholesterol in three of the four hypo-responders. The decrease in
  cholesterol intake caused an increase in cholesterol synthesis in five
  out of the six subjects.

In conclusion, in most people, dietary intake of cholesterol does not increase blood cholesterol levels because of decreased absorption and endogenous synthesis and increased excretion of cholesterol.

Some info about the mechanism would be interesting and not  off topic, I guess: "because of decreased absorption and endogenous synthesis". How is cholesterol intake downregulated, by enterocytes?

This question has also been answered on MedicalSciences.SE:

"The net daily synthesis of cholesterol is equal to the amount of cholesterol lost in the feces minus the dietary cholesterol"
The body synthesizes an amount approximately equal to the amount it absorbs
Source: Balancing Cholesterol Synthesis and Absorption in the Gastrointestinal Tract David E. Cohen, M.D., Ph.D.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2390860/

copied from this answer https://medicalsciences.stackexchange.com/a/17712

Duplicating answers from elsewhere on StackExchange is okay, but make it abundantly clear that this is what you are doing. Additionally, I would much prefer some level of original content to be added especially when it isn't the same person answering both questions. This answer also doesn't really add much that isn't already in the existing answer here.

Your question asks if/how "the body will adapt its production of cholesterol".
Literally, any cell - that should include the hepatocytes of the liver - of "the body" produces cholesterol, as it is an essential part of the membrane (of animal cells, by the way, by a factor of 100 more so than of plant cell walls), and it should be empirically well ascertained that there is adaption of cholesterol production to dietary input (reflected, especially, by delivery of cholesterol by - so called "remnants" of cholesterol transporting lipoproteins and chylomicrones, which may very much seen as a regulatory system that balances production between specialized cholesterol producing cells, i.e. especially hepatocytes of the liver and adipocytes of the tissue).
However, refering to any mechanism your question may be about, there are still open questions. See quote below, last sentence.
Here's the only pertaining quote I found.
Takizawa, Cellular control of cholesterol:
"When cells are faced with low cholesterol levels, they respond by increasing the gene expression of proteins that stimulate biosynthesis of cholesterol, such as HMG-CoA reductase, and proteins that increase the uptake up cholesterol from the external environment, LDL receptor. These genes contain a common upstream regulatory element called the sterol response element that binds a transcriptional activator, called the sterol response element binding protein.
When bound to the element, the binding proteins turns on transcription of downstream gene. So, a key question is how the cell regulates the binding of the binding protein to the response element and how that regulation is sensitive to cholesterol levels."


text:
Adam's Apple and Voice box
Why is Adam's Apple more prominent in males? Is it due to bigger voice box pushing the cartilage more, or is the cartilage indeed bigger than that in females? I am assuming bigger voice box as males have a "deeper" sound. Is it correct to do so?

Yes, you nailed it!
Adam's apple (aka.  laryngeal prominence) exist in both men and women. It is a piece of bony cartilage called thyroid cartilage that wraps around the larynx (aka. voice box).
The Adam's apple is more prominent in males because males have have a bigger larynx (giving males a deeper voice). In males, the prominent Adam's apple typically appears during adolescence, when the larynx increases in size and the voice becomes deeper.

So the cartilage is prominent because the  voice box pushes it out, right?

It was maybe not clear before. The larynx is what people call voice box (I now clarified this point in my answer). Adam's apple is the cartilage that wraps around the larynx so if the larynx is big, the cartilage will be prominent.


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"Treatment" of allergy.
Is there any treatment for allergy? I am not saying about solutions like epi-pen which reduce the symptoms. Is there any way to modify our immunity so that it does not identify the allergens? Can we modify our WBCs to not identify them?

See Allergen immunotherapy and eventually Enzyme potentiated desensitization.

@Remi.b in the article on EPD, there was this in mechanism section:- "The treatment uses dilutions of allergen and enzyme to which T-regulatory lymphocytes are believed to respond by favouring desensitization, or down-regulation, rather than sensitization. Once activated these lymphocytes travel to lymph nodes and reproduce or stimulate similar T-lymphocytes." What does it mean by "are believed to"? How does GIVING allergen desensitise T-lymphocytes?


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How can we decide at which level does natural selection apply?
Here is a passage from The Selfish Gene

If selection goes on between groups within species, and between species, why should it not also go on between larger groupings? Species are grouped into genera, genera into orders and orders into classes. Lions and antelopes are both members of class Mammalia, as are we. Should we then not expect lions to refrain from killing antelopes, 'for the good of the mammals'? Surely they should hunt birds or reptiles instead, in order to prevent the extinction of the class. But then, what of the need to perpetuate the whole phylum of vertebrates?

So shouldn't it eat the other animals? Also in the next line, it says about vertebrates that since reptiles and birds are vertebrates, the lion should go for invertebrates.
It sounds illogical, but what stops lion from eating his "relatives", or from sparing a deer? And till what extent is the term "relatives" valid?
Is the question is too broad, please give a source where I can get an answer.

It would be helpful if you could cite the actual passage. It is a bit unclear when reading your post whether the subject is lineage selection or group selection (aka kin selection).

It feels to me that the title of the post ask another question from the content. "What level applies" is different from "How does selection at this level make sense". Generally speaking evolutionary biologists assume that selection at level higher than variance in individual's fitness within population is often negligible but I don't think there is much data and much of a good argumentation for the extent of the validity of such assumption.

@Remi.b so individual fitness and that of close ones determined by Hamilton's equation. And that would also explain the lion example as they are too distantly related to outweigh the advantage.

I did not say that. I said I would need a clear quotation from the book to be able comment on it.

@Remi.b Actual statement in next comment.

If selection goes on between groups within species, and between species, why should it not also go on between larger groupings? Species are grouped into genera, genera into orders and orders into classes. Lions and antelopes are both members of class Mammalia, as are we. Should we then not expect lions to refrain from killing antelopes, 'for the good of the mammals'? Surely they should hunt birds or reptiles instead, in order to prevent the extinction of the class. But then, what of the need to perpetuate the whole phylum of vertebrates?

I haven't read the book, but these questions seem rhetorical. It seems like Dawkins is setting the stage for an answer, which I suspect he gives later.

the follow up to the portion being discussed is that while those other form may exist they are swamped by gene/individual level natural selection. genes that benefit the species at the expense of individuals can't compete with genes that benefit themselves or individual lines at the expense of the species.

Natural selection favors genotypes that produce phenotypes that survive to reproduce.  To the extent that natural selection drives the instincts that drive predation, the (essentially tautological) answer is that, "It has proven selectively beneficial for that particular genotype to eat whatever it's eating."
Indeed, nature has shown us a variety of solutions to these selective pressures.  Cannibalism is not hard to find.  In the extreme case, mothers from diverse species are known to kill and eat their own offspring, which at first glance may seem like the height of failure when it comes to propagating one's genes.  And yet we can hypothesize a number of selective advantages of that behavior.  (E.g., the mother can produce large litters when food is plentiful, and then adjust for shortages to shore up a smaller litter when food is scarce.)
We also know that there are selective pressures against eating similar animals.  For example, pathogens that kill an animal are likely to afflict its genetic relatives, and so that could drive the aversion of some carnivores (including humans) to eating close relatives.
There are plenty of examples of evolved symbiotic organisms.  Alligators don't eat plovers, and sharks don't eat remoras.
But it is hard to imagine selective pressure for altruistic behaviors that don't benefit a particular genotype.  E.g., if there are mammals to be eaten, the lions that eat them will survive and the ones that don't will die.  If the entire class Mammalia is under pressure, population dynamics trump evolved behavior: If prey become scarce, predators will become scarce.  But if any predators survive, it will be the greedy ones.


text:
How do different sensory stimuli differ in nerve signal?
Every day, we experience different types of sensory stimulus, like heat, pain, cold, etc. However, in each case, the transmission of the stimulus to the brain through the neurones is carried on in the same way: through propagated depolarisation and repolarisation in axons, while through the release of acetylcholine at the synapses.
So, how does the different sensory stimulus differ if they are transmitted the same way? (I mean to say that how does the nerve signals differ for two different kinds of stimulus?)
Let's put the question simply:
How do two nerve signals originated from two different stimuli differ? If they do not differ, then how does the brain differentiate between different nerve signals if they are all alike? How does it understand what nerve signal carries what message?

I think the short answer to your question is that the contents of different types of sensory stimulation are communicated to different populations of cells in the brain (note this transmission is mostly glutamatergic, not cholinergic). From there, the remaining associations and experiences derive from connectivity with other networks of brain neurons that result in different types of experience, based on the networks that those networks form and learned associations over development and a lifetime.
Computer analogies aren't always appropriate to understanding things about the brain, but maybe it could work out a bit here. How does a computer distinguish between input on your keyboard vs your mouse? On many modern computers, it is common for both to be connected with USB. The computer has some software that distinguishes between the different inputs - the brain has hardware that does the same.
Later on in the brain, or at a different stage in a computer program, those inputs can be mapped to functions that underlie experiences or functional outputs. Movement of the mouse can be converted to the movement of a screen cursor ("motor output"). Proprioception (the sensation of the relative position of the body from receptors in the muscles, tendons, and joints) can be combined with motor plans to create an error signal to move a particular muscle to match the intended movement.
Explaining any further than this probably requires entire textbooks of material, so I will leave it there.

Agree, this is a massive question, with many subsections of the brain to consider, e.g. the lateral geniculate nucleus for visual input, cochlear nuclei for auditory, not too mention touch/pain/temp that all gets bundled up in the spine. Anyway there's some extra google food.

This is exactly the area of study known as neural coding. The representation of information is not universal and differs for different modality, different stages of information processing, and what not. It's an active area of research.
That said, for the peripheral nervous system, the simplest code is pretty much rate code with label line. In other words, knowing which nerve fiber is firing what rate carries much of the sensory information. There are adaptation and some timing information if you look closer.

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


text:
What's cosmic VCF?
The popular MuTect variant tool:

http://archive.broadinstitute.org/cancer/cga/mutect_run

has the following VCF option:

--cosmic < comic.vcf >

Q: What is this cosmic VCF file? What's the purpose of the file?

VCF is an abbreviation for Variant Call Format. It is a file format for SNPs.
COSMIC stands for Catalogue Of Somatic Mutations In Cancer. It is a database.
Have a look at the links for more information.
A COSMIC VCF is likely just a file in VCF format file containing data coming from the COSMIC data base.

Without looking at any mutect docs and how it might use this, the COSMIC VCF would refer to a VCF from the cosmic database http://cancer.sanger.ac.uk/cosmic/


text:
Protein diet composition
I have read that non veg food are better for proteins while veg food is deficient in either one or other protein. If it is so are herbivores protein deficient always in case of animals as well as humans?

http://health.stackexchange.com/questions/9124/is-all-protein-the-same/9130#9130

Link from VonBeche is good.
Proteins vary in amino acid content.  Humans can make some but we need 9 of them in our diets.
from https://www.ncbi.nlm.nih.gov/books/NBK234922/
    Nine amino acids—histidine, isoleucine, leucine, lysine, methionine, phenylalanine, threonine, tryptophan, and valine—are not synthesized by mammals and are therefore dietarily essential or indispensable nutrients.
This guy http://michaelbluejay.com/veg/protein.html
is clearly a vegetable enthusiast but he makes a good point (and provides a nice table): just about any vegetable can provide enough amino acids if you eat enough of it.  Getting your entire caloric requirement from iceberg lettuce would a project, it is true.  But until I did the back reading for this answer I thought it would be impossible to take in the calories it would require to get all necessary amino acids from some of these plant foods.  Thanks michaelbluejay.

I here assert that animal foods have more amino acids per calorie than vegetable foods.  So, if you wanted to limit calories but meet your amino acid requirement it would be easier to do with animal proteins than with vegetable proteins.
But even all calories from potatoes can get you your amino acids.  The people who get into trouble are people who are not getting all the calories they need because they are starving, and the calories they do get are from low protein source foods like yams or bananas.  That is protein-calorie malnutrition.


text:
How does one determine the sex ratio of a ZZ and ZW cross?
In Campbell's Biology Chapter 14-15, Mendelian Genetics & The Chromosomal Basis of Inheritance, question 12 reads:
12) In birds, sex is determined by a ZW chromosome scheme. Males are ZZ and females are ZW. A recessive lethal allele that causes death of the embryo is sometimes present on the Z chromosome in pigeons. What would be the sex ratio in the offspring of a cross between a male that is heterozygous for the lethal allele and a normal female?
A) 2:1 male to female
B) 1:2 male to female
C) 1:1 male to female
D) 4:3 male to female
E) 3:1 male to female
The correct answer is A. In my Punnett square, there were two male and two female so shouldn't the answer be C?

Let $Z$ be the chromosome carrying the non-lethal dominant allele, and $Z_l$ the chromosome carrying the lethal recessive allele.
The Punnett square goes:

$Z_lW$ is not viable, so there are two possible male genotypes ($ZZ$ and $ZZ_l$) and only one possible female ($ZW$). So the correct answer is A. indeed.


text:
How to remove protein contamination in plasmid isolation.
I have already tried phenol chloroform extraction, isopropanol precipitation, did not work. It is giving high 280 reading.

Can you please give some more details on your protocols and probably also show some spectrum?

I used Resuspension(mixed with RNase) buffer,then vortexed and added lysis buffer,shaking and then neutralization buffer and centrifuged. Took the supernatant,added 100%ethanol and incubated for 1hour,centrifuged,took the pellet(huge pellet came,must be because of protein), 70% ethanol wash ,dried and resuspended in TE buffer.

i also did phenol chloroform step next time after collecting the Supernatant after neutralization, protein layer did not come much.


text:
Are oysters really aphrodisiacs?
Oysters have been thought of as aphrodisiacs for millennia.
Is this a case of the bark of a willow tree as a precursor to modern paracetamol, or some sort of marketing ploy.
Is there any biological evidence that foodstuffs such as lobsters, oysters and other sea delicacies boost our sexual health and desire? If so, what biological mechanism underlies this property?

What research have you done before asking it here?

Positively, a lot of people consider seafood an aphrodisiac for various reasons. I am interested in the scientific point of view.

Welcome to Bio. It feels more like a rumor than anything else. I am unfamiliar with the specific stack, but Skeptics.SE may be more appropriate. The question as it stands may be anecdotal and it is too broad for this site. If you could add a credible source that claims your hypothesis, it would already improve your post. Why and How questions generally fair well here. 'Is X true questions' are generally much less well received.

I'm voting to close this question as off-topic because I think it may be better suited for Skeptics.SE

@LadyFickle To be answered in Skeptics.SE you will need to provide a specific source for the information which has to show that it is a notable claim (for example, something like a major newspaper publication, not a copy of a Facebook post). I am sure you can find such a source but you have to do that work rather than having us do it for you. Second, I somewhat disagree that this question doesn't belong here. I think if you provide a decent source we can answer it as a biology question.

(also note that "notable" doesn't mean you have to find a well-referenced source, just something to show that it isn't just speculation among a group of people but rather a wide-ranging idea, see this meta )

I've heard this before. Apparently, oysters have been thought of as an aphrodisiac for millennia: https://theoystersmyworld.com/tag/casanova-and-oysters/

http://www.telegraph.co.uk/news/uknews/1486054/Raw-oysters-really-are-aphrodisiacs-say-scientists-and-now-is-the-time-to-eat-them.html


text:
Is survival probability the same thing as relative fitness?
I created a model where I calculate the survival probabilities from a Mark-recapture design.
I'm wondering if I can call the survival probabilities as "relative fitness".

Phenotype or genotype: $X$
  Absolute fitness: $W(X)$
  Relative fitness: $w(X)=\frac{W(X)}{\bar W}$

Since relative fitness is a ratio, I would have the tendency to say that it's the same thing as survival probability (keeping in mind that survival is only one component of fitness, so conceptually not exactly the same thing).
If I refer to this article, since I'm computing survival probabilities per individual, I would just need to call it "individual fitness".
It seems that "relative fitness" is more appropriate with a certain categorical phenotype: the relative fitness of tall vs short plants. If you have a continuous trait, how is the relative fitness interpreted?


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Anomaly in growth of fungus in Potato dextrose broth.. turbidity is not seen in one flask
I have inoculated six flasks of 200 ml potato dextrose broth, one of which does not show any turbidity and the medium is clear with a fungal disc in it.
All were inoculated at the same time and from the same pure fungus culture.
What might be the reason for this anomaly?

Several explanations are conceivable. Knowing what type of fungus you are working with and how exactly you proceeded to inoculate the cultures could help narrowing down the possibilities.
Here are some possible explanations:

Since you inoculated six liquid cultures from the same stock culture, the process might have been too long. Let me explain. Most fungi are strictly aerobes and do not tolerate well even short lack of oxygen. So, as I can guess, while you were inoculating the dextrose broths one after the other, the stock culture just remained unaerated on your bench. Since it can take a few tens of minutes to prepare everything and to proceed to the inoculations, it is possible that while you were doing so, the physiological state of the fungi just kept deteriorating, to such a point that one of the last inoculations did not contain enough viable cells to initiate a growth in the broth.
You might have forgotten to shake the stock culture just before taking the sample used in order to inoculate the broth. So it is possible that all the biomass in the stock culture was sedimented and you just inoculated your broth with the supernatent.
Also, a classic mistake is to mix up some of your broths. You think that you have inoculated all six broths with the stock culture, but maybe you unintentionally skiped one, or maybe you inoculated the same broth twice.


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Do neurons feature a collective "resistance" to firing too often beyond the refactory period?
My understanding is that neurons are prevented from firing too often by a 2-part refactory period: an immediate inability to fire again for a period of time followed by an increased threshold for firing for an extended period of time.
My question is simply whether or not there is an additional "collective" aspect of the refactory period or other mechanism which prevents too many firing based on frequency within a period of time. In other words, the refactory period as I understand it is the same each time a neuron fires, regardless of whether or not it has repeatedly fired as often as possible for a period of time before hand. I'm asking whether there's a mechanism that takes into account how many times the neuron has fired within x timeframes collectively to prevent further firings or weakens the output, sort of like a "resistance" (in which case it would be a mechanism having more to do with the synapse than the action potential / refactory period).
Do neurons feature a collective “resistance” to firing too often beyond the refactory period?

My last question was deemed too broad and low effort, hopefully this one is soecific enough and demonstrates a reasonable understanding of the relevant concepts :)

I think this one could be answered, though again, it might be more broad than you even realize. Another benefit to doing some textbook study on your own is that you would learn some of the terminology to use which will help you search for answers on your own. A question like this should probably include terms like "plasticity" or "homeostasis" and the issues you talk about at the end are a completely different area of study than the issues you begin with. :)

@BryanKrause you're right, I struggle with lack of terminology in asking neuroscience questions, I'll have to study up. So far I've been winging it with a highschool Biology knowledge level plus some Wikipedia reading and Youtube videos lol. With that I've been able to create a neural simulation from scratch that teaches itself to play Super Mario Bros, but I'm having to go into deeper understandings to push the limits beyond that.

At some point you will have to decide if you want to get serious about learning neuroscience, or if you are only interested in machine learning. Although neuroscience is great for motivating machine learning, and there is crosstalk between the fields, they are really unique fields in their own right. There are a lot of things that biological neurons can do that no one would ever use in an artificial network unless they were specifically trying to model the biological one, and there are a lot of things that an artificial network can do that biology just doesn't.

I would also add that it is a lot simpler to teach a computer to play a game than it is to understand how exactly a person learns to play a game. :)

@BryanKrause I'm experimenting with the idea that perhaps evolution has created the best possible model in terms of dynamic capability for complex thought process - better than machine learning algorithms - and so my strategy is to model the functionality of the neuron as close as possible, requiring me to go deeper and deeper into neuroscience.

Let us continue this discussion in chat.

No there isn't. Take the case of methamphetamine for example, the more methamphetamine someone has, the higher dopamine concentration in the synapse would be. An overdose of meth is the result of TOO much epinephrine metabolized from dopamine resulting in a heart attack. So, any amount of dopamine could be released, to the point of death.


text:
plausible science for why an enzyme breaks down a substrate better at 4 degrees rather than 20 degrees
An enzyme was found to have an optimal temperature of 20 degrees. The same enzyme in sheep liver extract was found to have an optimal temperature of 4 degrees. What are some of the factors that can contribute to the differences observed?

What enzyme? What substract? Who defined its optimal temperature? Who collected the data? How was the experiment conducted? As you can see, a lot of questions must be addressed for anyone be able to write an answer.

I can think of examples in living cells where the apparent optimal temperature for the activity of certain biochemical processes change in different chemical environments. But, I've never really thought about this occurring in extracts/purified enzymes. I agree with @tomd, this should not be closed.

Seems like this question does have a pretty simple answer, i.e. that chemical kinetics can vary with the solution, whether through biologically explicit mechanisms like enzyme inhibitors/activators or through more mundane mechanisms like the solution's ionic strength.  So, the performance of an enzyme'll vary with its environment, so that an enzyme was found to behave differently in two different environments is a really unsurprising result.

Then, when the question asks, "What are some of the factors that can contribute to the differences observed?", the answer's basically that stuff: inhibitors/activators, ionic strength, relative concentrations of reactants, possible denaturation during extraction, etc..  Additionally, these factors can act on not just the enzyme itself, but also the substrate(s).

tl;dr-  This question can probably be re-opened, as it has a pretty simple answer.


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Why should we use the NA12878 dataset for benchmarking?
As far as I understand, the human genome sample called NA12878 provides high confidence variants for a human sample. It is being used as a benchmark for many genomic research projects.
Q: Why exactly the NA12878 is such a popular benchmark dataset? Just because we have a set of high confidence variants? But we can also get some high confidence variants from the 1000 Genome project. Does that have something to do with the sequencing technology? Anything to do with the sample itself? Why do we want to benchmark our experiments with NA12878?

It would be a good idea to explain abbreviations you use, so other people could understand them as well.

@Chris NA12878 is the name. It is not abbreviation of anything.

Still, your answer might be closed as unclear.

@Chris I know you are a mod, but I disagree. NA12878 is a very well known human sample, covered in many high quality papers. My question is about why it is a good benchmarking data set.

First: This has nothing to do with me being a mod. Then: It is well known to people from the field, but questions/answers here are expected to stand on their own without reading further literature.

@Chris I still disagree. This is like explaining DNA for any question related to genetics. Prior knowledge is assumed and required for most questions in this site. Anyway, I did give a brief introduction on what NA12878 is in my first sentence. The title and the question could be a potential useful resource for anyone googling NA128278.

No it isn't. I work with NA12878 daily, so I happen to recognize it, but that doesn't mean that everyone who could answer your question would know the code on sight. I have been working in genomics for almost 10 years now but didn't know what NA12878 was until last year when I started doing variant calling. More to the point, if another user, let alone a mod, suggests that your question could be clearer, why don't you just clarify instead of arguing? Obviously it seems clear to you, but equally obviously, it isn't so clear to everyone.

@terdon Chris is a mod, he could have just closed the question if he really believed it was inappropriate. Furthermore, a user who doesn't know what NA12878 will not be able to benefit from it. The question will benefit NA12878 users, and we know there're many. I did introduce NA12878 in the very first sentence. I ask because I don't understand NA12878 very well. I can't summarise something I don't really know. What else do you want?

It's not about closing, it's about making the question easier to understand. And nobody said it was inappropriate. The only thing inappropriate here is your reaction to a helpful suggestion telling you how to improve your question and increase your chances of getting an answer. You took it as criticism and started arguing when all you needed to do is provide a link as I just did. That way, people can click on it and see that you are referring to a DNA sequencing sample and can look up information about it.

@StudentT It's not about closing, this is something I would have done if I think a mod intervention is necessary. It is about improving the question and understandability, nothing else.

@StudentT jumping in here - you shouldn't start ranting, but be glad folks try to help. Also understand a little introduction is always nice. This site is not only about you you know. The best questions are relevant and interesting for the community at large. A short introductory sentence on NA12878 (what is it, why do you use it) may provide useful information for others such that they can actually learn from the question.

This might be helpful: NA12878 is part of the Illumina Platinum Genomes dataset.
https://www.illumina.com/platinumgenomes.html

@Chris, NA12878 is a 'known' reference genome in the variant/structural genomics world. The question really is what was this particular standard choosen over any other and it is valid. The name is the name though.

@Artem Great. Then why it is so complicated to add this information to the question?

So to clarify for people unfamiliar with NA12878, that's the sample identification for a particular Utah woman. Her parents are NA12891 and NA12892. In human variation data-sets that's what we are given to identify individuals, an ID, sex and population. All the other data is removed to protect patient privacy. So the question is why was NA12878 (this Utah woman) chosen as the reference patient in genomic analysis...
I don't know the real practical answer but from what I gather it's inertia.
I don't have a full history for her but I do know somethings which make her genome a good choice for a benchmark. NA12878 is a fairly old to geneticists and her DNA is included in multiple legacy projects, specifically HapMap.
She has a genetic disease (CYP2D6 mutation) which is probably what initially included her and her family genetic analysis. This is a better reason to study this genome in detail instead of it simply being someone famous (i.e. Venter).
She's Utah mormon (small founder population with extensive pedigree information), has 11 children (can do recombination/inheritance analysis). What this means is that a deep understanding of her genome will have applications to this population.
Her lymphoblastoid cell line GM12878 was included as tier-1 ENCODE cell of study. This means there's terabytes of epignomic data for her as well.
When I choose to do human genome analysis, NA12878 is the obvious choice because of how much data is already available, which also means more data is going to be available. Thus I think the answer is largely inertia.
Also consider it this way, if you're trying to say your pipeline or sequencing technology is better then other ones, and everyone uses NA12878 to benchmark their technology, then it's wise to also use NA12878 so the results can be comparable.


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Translation of RNA into proteins
What's the least number of tRNA molecules needed to form a polypeptide chain that contain 50 amino acids of 15 types?

I know that each type of amino acid has at least one unique type of tRNA that recognizes it and transport it, so according to my understanding the 15 types of amino acids need at least 15 tRNA molecules of different types unless there was a reason that prevents one tRNA molecule from transporting two identical amino acids (two alanine) to the same polypeptide chain

•In other words:
Can one tRNA molecule carry two identical amino acids (ex: two alanine) to the same polypeptide chain that's being synthesized or not?

No, there is no way the same species of tRNA can carry two different amino acids no matter how similar they are. Each tRNA carries only one particular species of amino acid and there is no way it can just "switch to" any other one.

@YordanYordanov although physiologically I agree, and it answers the question, I just am wondering: there must undoubtedly be chemically modified amino acids variants that will be inserted into the growing peptide as well right?

I have to check this out but aren't the amino acids modified after they become inserted into the growing chain, not before. I will make a quick search online now. Here is one paper I managed to find with a very "quick" online search-https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3130931/ . As far as I can see all modifications are done after translation, not before. But there might be exceptions yet. I guess I would have to go deeper for this question.

@YordanYordanov — "Use comments to ask for more information or suggest improvements Avoid answering questions in comments." You see these instructions when you click in a comment box. Please follow them or you are breaking the SE model.

Please clarify what you mean by "of the same type".

@David amino acid having the same code ex: two amino acid molecules with (GCG) code.

@David - it often happens that users do not feel confident writing up a full answer and comment. In my opinion, that is not breaking the model but making helpful comments to the user that won't do as a full blown answer. See e.g. meta

Jasmin, each codon (not code) specifies only one amino acid (in a given organism and subcellular compartment). GCG is the codon for alanine. If you think a codon can specify more than one amino acid (except in the special cases of selenocysteine) then you should study an elementary text on the genetic code.

@AliceD — I didn't make the rules, but I subscribed to them when I signed on. I also understand them. They are clearly explained on http://biology.stackexchange.com/tour. When the people who have set this site up feel so strongly about this rule that they put a reminder in the comment box, there is really no justification for flouting it. If one person does it others think it is permissible and one ends up with the sort of discussion forum and chit-chat that StackExchange expressly is not. If people are uncomfortable with the rules they should go somewhere else.

The only thing that comes to mind would be an error in tRNA charging.

@David  Can't there be two amino acids of the same codon be found in one polypeptide chain of protein, as alanine to be present more than one time in the chain?!

Jasmin — Of course. But it was not obvious to me that this is what your question was about. Assuming that this is not a homework question  (is it?) you need to explain very clearly what your question is. 1. When you say "particular tRNA molecule" do you mean the same identical one molecule in the cell or molecules of the same class, i.e. with the same anticodon. 2. When you say "two similar amino acids" you need to make it clear that you are refering to two alanines or two glycines (I would use identical, rather than similar). Your question is still unclear, which is why it has close votes.

@David I hope that my question is clearer now. (Sorry for the inconvenience, but English is not my first language)

Jasmin — OK, but a strange question. And there are 20 different amino acids encoded in the standard genetic code, so I don't know why you picked 15, although a 50 amino acid protein could conceivably be lacking five amino acids. I suppose I have to answer your question now though.

Yes we can imagine that a tRNA can be recycled to incorporate the same amino acid into the same peptide chain multiple times so 16 tRNA could form a 50 amino acid chain but that will never happen thermodynamically. You need large concentrations of tRNA of all kinds for this reaction to take place, if you mix a single ribosome, mRNA and 15 tRNA with abundant free amino acids the reaction chemistry won't function.

@David - I know the rules and you are right. The thing is that it is a gray area. Personally, I indeed never give answers-disguised-as-comments, only when I expect the question to be closed and close-voting myself. Anyway, point taken.

In the basic model of protein synthesis the events involving tRNA and amino acids are as follows (see any standard text, e.g. Lodish et al. section 4.4):

An amino acid is attached to the appropriate tRNA (the one with the anticodon that recognizes a codon for that amino acid) by one of twenty specific amino acyltRNA synthase enzymes in a reaction requiring ATP. This is called charging or aminoacylation of tRNA.
The tRNA corresponding to the mRNA codon is brought to the ribosome by an elongation factor (EF1) and the peptidyl transferase activity of the large ribosomal subunit catalyses the formation of a peptide bond between the growing polypeptide chain* and the amino acid of the tRNA, releasing deacylated tRNA.

I am unclear why you are concerned with this problem, but if there were two alanine codons in the mRNA, in theory after a particular discrete tRNA molecule had inserted the first alanine it could be recharged by the aminoacyl tRNA synthetase and then be used to insert the second alanine. However the concentration of tRNA molecules in the cell needed to support protein synthesis is such that the actual probability of this same discrete molecule being used, rather than another tRNA carrying alanine, is remote.
*A real-life complication is that a polypeptide chain has to be initiated by an initiator methionine-tRNA that is distinct from the methionine-tRNA that inserts internal methionines (see Lewin et al. section 4.5).


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Can a ribozyme be present on two different RNA molecules?
Suppose we have a ribozyme that consists of an 'enzyme' strand and a 'substrate' strand. (e.g. hammerhead ribozyme)
Is it possible to have the enzyme strand of the ribozyme on one RNA molecule and the substrate strand on another RNA molecule (such that it allows multiple-turnover reaction)?

Are you asking specifically for hammerhead-like ribozymes or would any ribozyme do? The spliceosome, for example, may match your description.


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Etymology of PAX proteins
What is the reasoning behind naming proteins first found in Drosophila as paired box? All I could find on internet is that it was first found in Drosophila as a protein with paired domain, but I couldn't find anything about the term box along with it. Could anyone please signify the terms paired and box in the name of that protein?

According to InterPro, a paired domain is a DNA-binding element consisting of paired N-terminal and C-terminal subdomains, separated by a linker. PAX proteins follow this motif, and as such typically represent a class of helix-turn-helix transcription factors.
Box is the more interesting term here. In genetics, a box can be used to describe any regulatory element of a gene, including its promoter, UTRs and any enhancer or silencer elements. More loosely they also use box to describe coding segments of a gene, but in older publications.
Going back to Drosophila, however, studies in embryogenesis initially identified a protein called paired, a.k.a. prd. Homology studies into mammalian transcription factors found the presence of a prd-like domain in human HUP transcription factors, and these were renamed to PAX (ref). Thus, the naming of PAX family proteins classicaly denotes the presence not of a PRD regulatory element, but of a coding region for a prd-like domain in the gene product.

Can I say that they form the shape of box when they attach to a transcription factor?

@JM97 I think that would be difficult to prove!

In addition to the other answer, the following is some historical context on the naming of these genes.

1980 October: Discovery of pair-rule genes in Drosophila.
Nusslein-Volhard C, Wieschaus E. 1980. Mutations affecting segment number and polarity in Drosophila. Nature 287:795-801.

We have undertaken a systematic search for mutations that affect the segmental pattern depending on the zygotic genome... In [pair-rule mutants,] homologous parts of the pattern are deleted in every other segment

1986 May: Isolation of the paired gene in Drosophila.
Kilchherr F, Baumgartner S, Bopp D, Frei E, Noll M. 1986. Isolation of the paired gene of Drosophila and its spatial expression during early embryogenesis.

Here we report the isolation of the pair-rule gene paired (prd)... Transcripts of prd exhibit a pattern of seven evenly spaced bands during late syncytial blastoderm, reflecting a double-segment periodicity...

1986 December: Characterization of the paired box domain in paired.
Bopp D, Burri M, Baumgartner S, Frigerio G, Noll M. 1986. Conservation of a Large Protein Domain in the Segmentation Gene paired and in Functionally Related Genes of Drosophila. Cell 47:1033-1040.

...we show here that the prd gene contains a third domain about twice the size of the homeo domain, the paired box...

1988 May: First use of the abbreviation Pax to describe paired box containing murine homologs to paired.
Deutsch U, Dressler GR, Griss P. 1988. Pax 1, A Member of a Paired Box Homologous Murine Gene Family, Is Expressed in Segmented Structures during Development. Cell 53:617-625.

With the objective of isolating murine paired box homologs, a mouse paired box sequence (Pax 1) was identified that shows extensive nucleotide and amino acid sequence homology to all three known Drosophila paired box genes.

In response to a comment on the other answer:
Paired box refers to a DNA sequence/motif. The actual paired domain is a DNA binding motif present in some transcription factors. The crystal structure of the paired domain from prd has been solved. PDB: 1PDN. Expectedly, it doesn't really look like as box.
Xu W, Rould MA, Jun S, Desplan C, Pabo CO. 1995. Crystal structure of a paired domain-DNA complex at 2.5 Å resolution reveals structural basis for Pax developmental mutations. Cell 80:639-650.


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When do fireflies glow in their lifetime?
Does a firefly glow only when adult or larva? Or does it glow during its whole life. By glowing, I mean that they glow only when they require, not all the time.
Is there a reason (evolutionary reasoning) why they glow? Also, if the answer is all the time, then why, or if the answer is specific period in life then why?

Is this a homework question? And why would they be required to glow? And what does the last sentence mean?

@AliceD It is not a homework question. Is there a reason (evolutionary reasoning) why they glow? Last sentence means that if the answer is all the time, then why, or if the answer is specific period in life then why?

Gotcha. The way the question is posed it just tastes like homework. In fact, two of the close votes are based on homework suspicion. I would edit the question to remove the demanding undertone and improve its clarity.

A reason is a reason. Keep it simple. Ask whether it performs a function and keep evolution out of it unless your question is specifically about evolution (which it isn't).

@David I think AliceD suggested corrections the way that the meaning of my question won't change. It is clear enough. Maybe you should make the edits. (If you feel so.) :)

Fireflies 'glow' in larval and adult stages but for very different reasons. It is thought that glowing behaviour first evolved in larvae to deter predators(Branham and Wenzel (2003)). This is an example of an aposematic warning, which uses bright colours, smells, sounds, or in this case light, to tell predators they are undesirable as prey. Sometimes a prey animal will use an aposematic warning to tell predators they are poisonous, or simply to mimic a prey that is poisonous. In the case of firefly larvae, they don't taste good to predators because of a steroid compound in their bodies (Branham (2005)).
Adults also glow, but do so in a synchronized pattern of flashes to communicate with mates (Carlson and Copeland (1985)). Mates will time their flashing with physiological fluctuations and even respond directly to another individual's flashing pattern with appropriate delays and timing of responses.
So to answer your first question, fireflies are not continuously glowing, but flash at night as larvae to deter predators, and during active mating as adults.
Your second question can get into a long-winded explanation of how certain traits evolve in response to a pressure, but to simplify, it's likely that fireflies evolved glowing because it relieved predation pressure. This ability then evolved further to communicate the quality of mates more efficiently than phermone signalling.


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Coracoid vs. Coronoid - Etymology/Naming Choice?
The word coracoid (e.g., coracoid process of scapula) literally means "resembling a crow/raven" or "of the form of a crow/raven." In this case, I assume, resembling the hooked characteristic of a corvid's beak.

Etymology: korax ("raven",Greek) + -oid (from Greek -oeidēs meaning "form").

However, the word coronoid (e.g., coronoid process of the ulna or of the mandible) also refers to a hooked projection of bone. Its etymology, however, is more straightforward:

Etymology: korōnē ("hooked", Greek) + -oid (from Greek -oeidēs meaning "form").

My question: Why the distinction?
 - Why is one termed the "coracoid" while the other structures are referred to as "coronoid"?

Since the coracoid process looks no more like an actual corvid's beak than the other structures, it seems that they should have all been referred to as "coranoid".

I get that we've just kept things the way they originally were b/c we like to do that in biology, but what was the original reason for the naming of the  coracoid to break from the trend?

It appears that both naming conventions originate with Galen, the Greek physician, almost 2000 years ago (for example, see: Singer, 1952).
Although the precise motivations behind the naming conventions aren't entirely clear, it seems that the origin of the coracoid naming convention is quite simple: Galen thought it looked specifically like a raven's beak, as you state, rather than the beak of some other bird.
Fortuine (2000) seems to suggest that the origins for both words originally applied to beaks of different birds, which implies that Galen may have thought some bone structures looked like beaks of one bird, and other bone structures looked like the beaks of another bird, so he used the corresponding terms of description. Specifically, "korōnē" may have referred to a crow or cormorant (I feel like the cormorant link makes more sense, though both are supported by Arnott (2007) - it may not be possible to know how the distinction was applied from surviving texts), as well as referring to a hooked shape. The same source mentions several other bird-derived terms, including the coccyx resembling the beak of a cuckoo and "rostrum" used more generally for beak-like structures.
Today, coronoid and coracoid may sound similar enough to be easily confused by students of medicine. However, giving these different bones distinct names does allow for some useful shorthand, such that one need not refer to the "coronoid of the scapula": I would assume, though I'm not sure if it is possible to find a good reference on this, that this is the motivation to keep things as-is, besides of course the history.
References

Arnott, W. G. (2007). Birds in the Ancient World from A to Z. Routledge, New York.
Duckworth, W. L. H., & Lyons, M. C. (2010). Galen on anatomical procedures: the later books. Cambridge University Press.
Fortuine, R. (2000). The words of medicine: sources, meanings, and delights. Charles C Thomas Publisher.
Singer, C. (1952). Galen's elementary course on bones.

I emphasize to my anatomy students the "coraCoid of the sCapula" and that the coracoid and coranoid are in "ABC order" from proximal to distal along the upper limb. (Of course, "coraNoid of the maNdible" or "of the ulNa" works, too).


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Why do human females have periods?
Why do human women have periods when most animals don't? It is known that the unfertilized egg needs to be shed from the uterus. But why shed the whole endometrium? Why didn't evolution put macrophages to work to simply digest the ovum and only the ovum, instead of the physiologically, energy-draining process of menstruation and accompanying blood loss? Also, are there any other purposes for menstruation, besides wiping out dead ova?
Sites I used for references:
 1. Jensen et al., Am J Reprod Immunol (2012); 68(5): 374–386 -                       Menstruation seems energy draining, in my perspective, given that 30-40 ml of blood is lost × 3-4 days × 12 months × 15 years on average - that is a lot of blood loss.
 2. Also see this Quora post.

Related question: Why is menstruation in wild animals not a disadvantage to organismal survival?.

My question is different from this related question because there the OP is concerned about the survival advantage of the menstruation with respect to the predators. Here I've asked why menstruation and why not phagocytosis as the former to me seems to be highly energy consuming process. Also as the fellow post writer had earlier suggested though the two questions  seem to be one and the same, they are subtly different and aimed for two different audiences as I emphasise more on the physiological aspects of menstruation and the related question's OP needs clarification about survival advantage and other ecological aspects of menstruation.

This video may be informative: Why do women have periods?

Short answer
Shedding or reabsorbing the endometrial lining is energetically advantageous to the female.The advantage of shedding over re-absorption may be that sperm-born pathogens are removed from the uterus. A more parsimonious explanation, however, is that the endometrium in primates has developed into too large of a structure to be completely reabsorbed by the uterus wall.
Background
Basically you ask why are estrous cycles in mammals accompanied by regression and build up of the endometrial lining? The main reason for either reabsorbing or shedding the endometrial lining is thought to be to save energy. It has been calculated that, when implantation fails, a cyclical regression and renewal of the endometrium is energetically less costly than maintaining it in a metabolically active state required for implantation. In the regressed state, oxygen consumption in human endometria declines nearly sevenfold. Metabolic rate is at least 7% lower, on average, during the follicular phase than during the luteal phase in women, which signifies an estimated energy savings of 53 MJ over four cycles, or nearly six days worth of food (Strassmann, 1996; Crawford, 1998).
In fact, impaired shedding of the endometrial lining may lead to pathologies. If no egg is released and the estrogen/progesterone system becomes imbalanced, the endometrium may continue to thicken, instead of breaking down and being shed normally as a menstrual period. This abnormal thickening is called endometrial hyperplasia. Periodically, the thickened lining is shed incompletely and irregularly, causing irregular and more heavy bleeding. If this cycle of abnormal thickening and irregular shedding continues, precancerous cells may develop, increasing the risk of cancer of the uterine lining (endometrial cancer), even in young women (source: MSD manual).
Now the question of why human females shed the endometrial lining instead of resorbing it? Indeed, shedding the endometrium is mainly limited to primates, as opposed to reabsorbing it (like in most other mammals). Here, I do not have a definitive answer, but I like to share two opposing hypothesis on the matter.

Hypothesis 1:  Profet (1993) hypothesized that shedding the endometrium may be an effective way to get rid of sperm-based pathogens. The accompanying bleeding, Profet hypothesizes, delivers immune cells into the uterine cavity that can combat pathogens.
Hypothesis 2: Strassmann (1996) surmises that the endometrial microvasculature is designed to provide the blood supply to the endometrium and the placenta, and that external bleeding appears to be a side effect of endometrial regression that arises when there is too much blood and other tissue for complete reabsorption. The relatively large blood loss as seen in humans and chimpanzees can be attributed to the large size of the uterus relative to adult female size and to the design of the microvasculature in the uterus wall.

References
- Crawford (ed), Handbook of Evolutionary Psychology: Ideas, Issues, and Applications, Psychology Press (1998)
- Profet,  Quarterly Rev Biol (1993); 68(3): 355-86
- Strassmann, Quarterly Rev Biol (1996);71(2): 181-220

WebMD lists the most common reasons for missed periods as weight disorders, eating disorders, increased exercise, and stress.  It seems like the body's tuned to undergo the costly process of shedding/regenerating the lining only when the metabolism is working correctly and not under significant stress.

Sidenote: I read recently that a contributing factor is that the human endometrium is bigger than in other mammals, which it needs to be because human fetuses are more aggressive when implanting and could otherwise connect directly with the mother's bloodstream as in an extrauterine pregnancy.


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Do species ever go extinct by becoming too successful?
Are there examples of species that have driven themselves into extinction by being too good at what they are doing? Like a predator that evolves to hunt so efficiently that it kills all it's prey and then goes extinct itself.

Humans seem like they're on this course. You may be interested in predator-prey dynamics.

There is evidence that lemming populations approach this in ~4-year cycles of population proliferation and crashing. They've rebounded through these cycles, so it's not quite an extinction example, but it shows that catastrophic success definitely has precedent. Here's a brief article on the relationship between predator-prey trends: http://vetmed.illinois.edu/wildlifeencounters/grade9_12/lesson2/adapt_info/predator.html.

Seems like there's a need to define "success".  If a predator wipes out its own food source, is that really "success", or just a different kind of failure?  If a human becomes wealthy and uses all of that money to eat McDonalds until they die, then would you say that they died from "success"?

@Nat It is a success in the species's ability to gather resources and proliferate. The failure is in both its predators and prey. I suppose it could be argued that it has a failure to adapt to starvation conditions, but in the case of lemmings at least, they evidently are adapted well enough to have some survivors and rebound.

@HarrisWeinstein Seems like any species that drives itself to extinction's failed in the most basic of senses.  But, this question words it is in such a seemingly positive way - "becoming too successful".  Like a heroin addict who overdoses dies from being too successful at getting heroin.  Or like gunshot victims are die from being too successful at getting free bullets.  Positivity's great, but when examining how a species drove itself to extinction, it'd seem appropriate to characterize that suicidal behavior as something other than "success".

yes, infectious bacteria are a good example, a highly destructive infection may often kill its host before it can spread the disease.  https://www.ncbi.nlm.nih.gov/books/NBK27114/


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What step of the cloning process requires an egg cell? Have alternatives been attempted?
In the famous Dolly the sheep an egg cell was required. Why was specifically an egg cell required compared to say sperm cells or any other cell types?
Given that egg cells are not trivially harvested and culturable, have clones from alternatives been attempted?

This question doesn't show a lot of effort or nuance, but I am a bit puzzled why someone voted to close it for not being clear without providing some sort of comment.

I think this question deserves a chance and could yield some interesting answers. I've edited it to clear up any uncertainty.

egg cells are not required for cloning, plants for instance can be cloned just fine without them. Oocytes are commonly used in animals becasue they already contain some of the chemical markers and enzymes to begin development in the mother's body and keep her immune system from attacking it. In more derived animals development is not solely controlled by the the embryo but also by the mother, so using an egg cell helps trigger those processes of the mother. If you used a standard stem cell likely the mother immune system would just destroy it as a foreign entity.

"some of the chemical markers and enzymes to begin development" is almost an understatement.While it is almost possible to make specific cell types out of stem cells, the processes needed for embryo development are even more complex than that and as of today noone would be able to make a stem cell into an viable egg cell or embryo

Actually they have in mice, http://www.the-scientist.com/?articles.view/articleNo/47256/title/From-Stem-Cell-to-Oocyte-In-a-Dish/

oh wow, I didn't know that (was already possible). Thanks for the link.