text:
Is the glomerular filtration rate, per kidney or for both?
We say in a healthy human being the average glomerular filtration rate is about 120 mL/min. Is that for both kidneys together (60+60), or just one kidney?
Pardon me if this makes me sound like an idiot, because I have a feeling I'm thinking about this wrong.

The definition of GFR given in Wikipedia -

Glomerular filtration rate (GFR) is the volume of fluid filtered from the renal (kidney) glomerular capillaries into the Bowman's capsule per unit time.

Since it is difficult to measure the volume entering into each Bowman's capsule, as a proxy, we measure the clearance of a solute that we know isn't going to be absorbed or secreted. For that particular solute,
GFR = (Urine concentration x Urine flow)/ Plasma concentration
The GFR you obtain here is the sum total of volume of all the fluid filtered from all the renal (kidney) glomerular capillaries into all of the Bowman's capsule per unit time.
Obviously, a single Bowman's capsule can't receive 120ml every minute, it is microscopic!!
So yes, the GFR or eGFR we use in clinical practice is the sum total of the function of both the kidneys. In fact, before transplantation, although the left kidney is preferred from the donor (since it is easier for surgery having a longer renal vein), it is more ethical to estimate individual GFR for each kidney and preserving the better functioning kidney. And yes, the total GFR drops after donating a kidney, but the body has sufficient reserve to manage.
If you still have a tough time figuring that out, think of them as many separate taps opened to fill a bucket. One tap for each glomerulus. The net rate of flow is the sum of flow rate in all the taps. The kidney has million such taps! And the taps are being clogged one at a time in chronic kidney disease - decreasing the GFR. And in a transplant, half the taps are suddenly shut down in the donor! But since this is a healthy kidney, the donor adapts and slowly reaches ~70% of original GFR.

Exactly what I was looking for. Thank you, that was very succinctly put!

It's a rate, not an absolute amount, so you wouldn't divide it up like that. It's like if a car is traveling 60 mph, each tire is going 60 mph, not 15.
You'd divide it up to describe the absolute amount, so if the kidneys filter 120 mL, then you could say each kidney filtered 60 mL (although even then each kidney isn't going to function identically).

Thank you, I understand how it's a rate and used as an indicator of the function of the excretory system.
My point is, if you removed one kidney, gradually the remaining one may grow to work more. But theoretically, the day that you remove the first kidney, the GFR is halved?


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Are humans the only species to suffer from impacted teeth?
Many humans need their third molars (wisdom teeth) removed due to tooth impaction. Are humans the only species to suffer from this?

According to Wikipedia
An impacted tooth is one that fails to erupt into the dental arch within the expected developmental window. Because impacted teeth do not erupt, they are retained throughout the individual's lifetime unless extracted or exposed surgically.
Now to your interesting question, there are case reports, that yes, animals, other than humans can also have impacted teeth.

Mandibular canine tooth impaction in young dog which was then made to erupt by surgery. Reference

Maxillary canine impaction in a persion cat. Reference

According to this article

Proper growth and development of the oral cavity depends on a series of events that must occur normally and in the proper sequence. Genetic abnormalities or trauma that affects either the developing tissues or the timing of their development can cause abnormalities. Defects that decrease comfort, health, or function require treatment; those that result in only an esthetic problem do not. Common developmental problems include persistent deciduous teeth, unerupted teeth, malformed teeth, malocclusion, and malformed jaws.

source: Stack Exchange

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

sort: votes


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how many copies of tp53 (p53) gene do we have?
I just started studying biology so I almost have no knowledge.
I learned about the tp53 gene and I just wanted to know how many copies of tp53 gene we have?

Humans have one copy of the p53 gene per set of chromosomes along with most other mammals (a notable exception being elephants with 20)[1]. Since it is located on an autosome (chromosome 17), each parent gives one copy of the gene[2]. Meaning two copies per human cell (and 40 per elephant cell).

A little extra information on p53 and the effects of only having 2 copies:
Since humans only have two copies per cell and p53 forms a homo-tetramer, it only takes one mutated copy to lose functionality.[3] This is because p53 needs to tetramerize to function, meaning only 1 out of 16 p53 proteins are effective if one copy is mutated (24 possibilities and only 1 combination has 0 mutated copies, ~6% are functional). This makes p53 a rare human tumor-suppressor gene with dominant negative mutations.
But with elephants, the more copies they have, the less and less one mutation affects the amount of functional p53. ($\bigl( \frac {39}{40}\bigr)$4 probability of having a functional tetramer = 90% functional, which is very high)

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


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What is this small brown spider?

Found in a doorway in eastern Tennessee. With its legs fully extended, it's about the size of a quarter.

I'd guess it's an orb spider by the habitus.

This spider has a roughly globular abdomen, (actually kind of egg-shaped, and pointed, which is a good clue), and is hanging upside-down in a 3-dimensional web which (if we could see it) would look pretty tangled instead of a nice, 2-dimensional orbweb.  It doesn't have any noticeable pattern other than the banded legs, and the greyish-brown abdomen looks like it has some darker blotches.  It's made its web near the top of a doorway in a house.
These clues all point to a very common Theridiid spider which goes by the name of House Spider.  It's not the House Spider that spins a flat sheet from a funnel retreat - that's the Tegenaria House Spider.  This House Spider is the Theridiid House Spider Parasteatoda tepidariorum.  It's a harmless (to us) spider that eats almost anything it can entrap in its web.  I've seen them happily eat Gypsy Moth caterpillars, centipedes and other arthropods that aren't very popular choices among household spiders.
Here's a link that you can browse to see the wide degree of variation that this spider can show - but always a kind of smudgy, blotchy greyish brown abdomen, banded legs and the tangled web in which it hangs upside-down.  You'll note that the legs of this Theridiid, like most of its relatives, aren't as burly and sturdy-looking as those of its cousin the Black Widow.  These Theridiids kind of totter along on their relatively spindly legs when out of the web, while the Widows go striding along like small Mecha-Spiders.  I always expect to hear the Imperial March from Star Wars when I see a Widow walking on the floor.
https://bugguide.net/node/view/6919

Nice answer! I've had the same kind of spider(s) at my back door every summer for years. They had/have much better webs, though, which they rebuild daily. I just assumed it was an orb spider because occasionally there was a zig-zag section in the web. She behaves just like this one. And this one. Now I'm confused. I think mine were orb spiders.

Yours probably were orbweavers - if they were hanging 'face'-down in a flat, circular spiral web, that would make it certain.  Look at these photos - see how the spider is hanging 'back'-down, with arched legs 'reaching' up?  Orbweavers hang vertically in the web (usually face-down, but some hang face-up), with their legs stretched to the sides.  You mention a zig-zag section in the web, which sounds like an Argiope, also an orbweaver.  Argiopes don't often make webs right at doors or windows, but sometimes they do.  Theridiid spiders, like this one, are different, though.

Thanks for the info! Yes, you're right on every point, including the direction she faced. But there is one every year in my back doorway, probably because the spot is good for insects (right next to a light). In fact, there is one at every floodlight as well.


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What causes the complementary copy of an RNA molecule to separate?
I have recently read an article which explains that, in the RNA World hypothesis, an RNA molecule gets 'scanned' by nucleic acid, catalysed by a different specifically-folded RNA molecule, to arrange itself complimentarily to the original molecule. However, what causes the new, complementary molecule to detach from the original molecule? I always hear people say that this complementary base pairing allows the RNA molecule to reproduce, but I never quite understood: how? If complementary bases tend to bind together, shouldn't the newly formed structure then be stable? What causes the actual reproduction?

Both complementary binding of RNA & DNA is dependent on temperature and salt concentrations (among other things), so if these factors change so does the stability of a double-strand complex

@Nicolai so both of those have to exactly spot on, or the bondings deform? Why, then, does an RNA copy itself completely most of the time? Why does it first have to scan itself completely and then detach (i.e. why can't some bases pair while the others will not due to a different temperature?)

There are many single-stranded RNA viruses in which the daughter strand must be released from the template. I imagine that this strand displacement is a feature of the action of the RNA-dependent RNA polymerase. How it works I have not been able to find from a brief search (hence comment, rather than answer), but it obviously does. So this is not a particular problem of the RNA world. I'd check the virology literature if you want more info.

@David I know it's not an issue with the hypotheses - it's my lack of understanding. So the RNA copy disentangles itself from the parent RNA because of a virus/polymerase? That seems logical, but then again, same problem: why can't it infect the RNA while it's being copied? Wouldn't it then create an incomplete copy, thus perhaps causing the whole system to malfunction? Or are these events rare because the copying stage is too quick?

The polymerase somehow starts synthesis at one end, the complementary NTP binds and the enzyme catalyses a phosphodiester bond, goes along the template strand one base so as to be able to catalyse the bond between the growing chain and the next NTP to bind, etc. etc. Your valid question is why the growing chain is released from the template rather than staying H-bonded to it. I assume that as the polymerase moves along it somehow destablizes the interaction (rather than just dissociating randomly). However I am unaware of the molecular mechanism.

Wow, what you described is very different to my current understanding of RNA synthesis. As I thought, surrounding nucleic components were somehow attracted to the RNA, and bond formation was catalyzed by other specifically-folded RNA molecules, which acted as physical shape-selective (sorry for unscientific vocabulary) enzymes and helped physically shape the bonds. I didn't know it was a polymerase that triggered the synthesis. That is very strange, because, especially if your assumption that the polymerase destabilises the bonds as it moves along is true, that would require it to have a

very particular function: it would first have to find the RNA molecule, then move along it, and while doing that it would catalyse the formation of a very specific bond, and it would also involve, as I understand, a complex negative feedback mechanism. How would such a molecule arise naturally? I know that you are right, but it just seems odd to me.

@David Sorry I forgot to tag you

First, I want to point out that the RNA world hypothesis is just that - an hypothesis. While it has been shown that it's possible for certain RNA molecules to make copies of itself, this is not a 'normal' function of any RNA.
Edit - to give a clearer answer to the question itself:
After replication of an RNA molecule it may form a stable structure together with its template or it may dissociate. Due to the various possibilities and complexity of RNA structures its almost impossible to predict this, since both the (exact) sequence itself and environmental conditions especially temperature are very important.
More background from the unedited answer:
Whether two complementary strands or RNA (or DNA) bind together is not something that can always be easily answered. For DNA of a given length (in a given environment / buffer) one can more or less predict the temperature at which complementary strands will separate (often called melting temperature), because DNA forms relatively stable helices.
RNA, however, often forms complicated 3-dimensional structures, often involving self-complementary and is not restricted to the typical helices seen in DNA. Trying to predict the resulting 3D structure of RNA molecules is still an ongoing field of research. Some of these structure are quite stable (e.g. in tRNA) but in other cases they can also be very dynamic and change quickly.
In the end it always depends on the RNA sequence, temperature and many other environmental factors.

So I assume this melting temperature is quite low, then? Seeing as (okay, I will switch to DNAs for now for simplicity) a DNA unwinds itself so often?

You mention various factors affecting base-pairing in RNA but you do not answer the poster's question, which is if the bases anneal to the template to allow polymerization in the first place, why does the product dissociate? Talking about RNA “liking to form complicated structures” won't do. It may have the potential to do so, but dsRNA viruses show that it has the potential to form duplexes.

@David I don't think it's possible to give another answer to the question than my last sentence (maybe I should make that clearer), because it will always depend on the RNA sequence and environment whether it dissociates after replication or not (even in the first place) - the fact that dsRNA viruses are possible is just another example to the ones I listed

I also remove the 'RNA likes to ...' which was indeed a bad way to describe this.


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largest and smallest gram positive, gram negative and fungal pathogens
As I stumbled through this question:

A 16-year-old female patient presented to her family physician
  with a complaint of an abnormal vaginal discharge and pruritus
  (itching). The patient denied having sexual activity and recently
  completed a course of doxycycline for the treatment of her acne.
  An examination of a Gram-stained vaginal smear revealed the
  presence of gram-positive oval cells about 4–8 μm in diameter.
  Her vaginitis is caused by which of the following agents?
  (A) Bacterium
  (B) Virus
  (C) Protozoa
  (D) Fungus
  (E) Prion

I noticed that in order to answer such question, one possible way is to know the diameter range of each pathological group because gram stain can be positive in both fungi and bacteria and so is gram negative.
I have googled and searched but found no such information; all i found was about largest bacteria in general (not pathogenic bacteria) and same for fungi.
It would be extremely useful to know the following diameter range of:

pathogenic gram-positive bacteria
pathogenic gram-negative bacteria
pathogenic fungi
pathogenic viruses

P.S. by pathogenic i mean pathogenic to Humans

I think you should search for side effects of doxycycline treatment to ànswer this question. It causes vaginal yeast infection.

Yes @Mesentery, I figured that out later. But still, knowing the diameters of pathogen groups will give extra hints and help in excluding other options even if one doesn’t know/recall side effects of drugs or whatsoever. I really hope that someone will answer this question :)

As for bacteria (most common sizes): cocci ~ 1 um in diameter; rods ~ 1 x 2 to 5 um: filamentous bacteria ~ 1 x 10 (or more) um.


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If hands are folded with both index fingers parallel, they will come closer and touch eventually?
I have a question out of curiosity. It is just something I found out/discovered:
if I fold my hands into each and let my two index fingers (see picture) be in parallel then they will eventually come closer to each other and touch.
How can this be explained?

Another thing I found out: if I fold my fingers on my left hand slightly and then with my right hand squeeze the wrist of my left hand (see picture), then the fingers of the left hand will fold more and more. Is this a coincidence of general?

The easy way to explai the first phenomenon is that at rest, your fingers - all of them - curl. Relax on your bed on your back. No matter what direction your hands face, they will curl inward as if loosely holding an egg. That's the anatominal position of the hands at rest, because the finger flexors are stronger than the extendors. So once you set the finfers up, you'll tire of keeping them extended, they'll start  to relax, and in doing so, will tough.
If I'm understanding the second example, that's because the flexor tendons for your fingers are actually in your forearm. Squeeze them and it shortens the tendons causing flexion.

the explanation for the first picture is that this is due to an invisible attraction force which is called (Ideomotor effect) which affects on the left lobe of the brain which permits to our muscles to move involuntary and unawareness.So they will come closer as if they are like a magnet and a nail.


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What allows the hypothalamus to detect a lack of thyroid hormones?
On the website www.yourhormones.com it is written:

"If there is insufficient thyroid hormone available for the brain, this will be detected by the hypothalamus and thyrotropin-releasing hormone will be released into the blood supplying the pituitary gland."

What allows the hypothalamus to detect a lack of thyroid hormones? Are there chemoreceptors in the bloodstream that send afferent signals to hypothalamus when the concentration of thyroid hormones is low (similarly to how chemoreceptors inform the cardiovascular center of the medulla oblongata in the brain stem when there is a lack of oxygen and/or excess of carbon dioxide)?

The thyroid hormone, thyroxin has a multitude of effects in various cells of the body. It is a lipophilic hormone and acts via nuclear receptors, i.e. the receptors for the hormone are not on the cell surface but inside it. This hormone-receptor complex then travels into the nucleus to attend to transcriptional changes.

The picture above is for steroid hormones but is almost similar for thyroxin too.
Inside the cell, the effect of the hormone depends on which cell it is in. For thyroxin - in heart muscles, it increases cardiac contractility, in fat cells, increases fat catabolism, and in the very same way, in the hypothalamus, its function is to reduce the production of TRH. And the control of this production is at the level of gene transcription.
Hence there is a lovely feedback loop that is formed. Increased thyroxin would lead to reduced TRH production and vice versa. So the hypothalamus responds to the thyroxin hormone by regulating the production of TRH. There is nothing special that the thyroxin is doing here. It just has different effects in different cells and in this particular cell (the neurons of the hypothalamus), the effect happens to be its own feedback loop regulation (via TRH).
The effect of thyroxin is through its receptor that is an intracellular protein and is more or less the same in all cells.
Chemoreceptors are a different ballgame. They sense changes in pH, pO2, and other biochemical parameters through their direct effect on neurons and their firing. Although their functioning is not particularly clear, they interfere with channel conductivities in particular neurons. There is no receptor and transcriptional changes as in thyroxin.

By saying that chemoreceptors "interfere with channel conductivities", do you mean that they, for instance, increase the conductivity of afferent neuron axons that signal the cardiovascular center to modulate breathing when oxonium ion or CO2 concentration is high?

Yes something of that sort. A direct biophysical change perhaps... If that's the right term.. I don't know


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How is the urea cycle regulated with respect to protein deficit?
Proteins cannot be stored in the body. Excess proteins from the diet are deaminated in the urea cycle that takes place in the liver. The liver is the first contact since these amino acids are delivered through the portal circulation.
What I do not understand is what controls the extent of amino acid breakdown in the liver. For example, suppose there is a man who hasn't had protein in a month, and has a net protein deficit, what determines that there shouldn’t be much deamination in the liver?
For carbohydrates and sugars, insulin and glucagon balance regulate the main enzymes controlling the steps in glucose phosphorylation hence maintaining homeostasis. Since this is at an organismal level and not the cellular level, like glucose, I would expect the control of urea cycle also to be hormonal. Since there is no hormone that reflects protein status (at least to my knowledge), what determines the activity of the urea cycle?

Preamble
This question is extremely broad because, rather than there being a ‘one-click’ answer, whole areas of amino acid metabolism need to be considered. This is both inappropriate and impossible to do here — even if I understood everthing about it (which I certainly don’t). However I shall provide a specific biochemical answer (or partial answer, as all is not understood) regarding the regulation of the urea cycle, after commenting on some of the assumptions implicit in the question.
Comments on the assumptions of the question
I am not sure that ‘protein deficit’ is a useful metabolic construct. From the point of view of a clinician, yes, one can say that someone is suffering from protein deficiency or malnutrition, but in metabolic terms protein is a not the highest priority and will be broken down to provide glucose for the brain during long-term starvation. And it is well established that protein synthesis is under the control of hormones and growth factors (reviewed here), and this will affect the fate of dietary amino acids or those produced by protein turnover. In addition, the emphasis on hormones in the question seems to ignore the role of the concentration of amino acids and other intermediates in regulating metabolic pathways. Finally, there is control of the expression of the genes encoding enzymes of the urea cycle, which operates over a longer time period.
The Medical Biochemistry site provides a wider perspective on amino acid metabolism and nitrogen metabolism and the urea cycle.
Regulation of the Urea Cycle
The first point that should be emphasized is that the urea cycle does not exist in isolation from other metabolic pathways, but is intimately connected to them. This is shown in the diagram below:

It should be remembered that ammonia for the urea cycle only comes from the deamination of glutamate by glutamate dehydrogenase, and the transamination of other amino acids to produce this depends on a pool of α-ketoglutarate (2-oxo glutarate). A requirement for α-ketoglutarate also exists in relation to the regeneration of aspartate for the cycle itself.
The entry point of ammonia into the urea cycle is the reaction catalysed by carbamoyl phosphate synthetase:

It turns out that this reaction requires N-acetyl glutamate (NAG) for activity, and it is thought that this plays a regulatory role in the urea cycle, as increased intake of protein has been found to increase the hepatic content of NAG. Although aspects of this remain to be clarified or resolved, it is thought that the regulation occurs at the point at which NAG is synthesized from glutamate in a reaction catalysed by the enzyme N-acetyl glutamate synthase:

This enzyme is activated by arginine, giving rise to a model for regulation described more fully in a review by Caldovic and Tuchman, from which I quote the following:

“… the hypothesis that NAG is a regulator of ureagenesis… If this hypothesis is correct, mitochondrial concentrations of glutamate and/or arginine may reflect the need for nitrogen disposal through their effect on the production of NAG by NAG synthase, glutamate as a substrate and arginine as an effector.”

But how do local intracellular concentrations of amino acids give the big picture of how much to regulate?

The idea is abundance of amino acids means the need to dispose of surplus. You are perhaps worried that this would deprive e.g. muscle tissues of amino acids following return to a protein diet after long-term starvation. I should have mentioned that there appears to be changes in amount of the urea cycle enzymes in the longer term by gene repression. There will also probably lower alpha-keto glutarate because protein and carbohydrate starvation tend to go in concert. It's multi-factorial and quite complex.


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Looking for book or article that derives formula for estimating the "average heterozygosity"
An online lecture I need to watch on population genetics describes a formula for the "average heterozygosity" as follows:

...we can theoretically predict that the average heterozygosity in the population will simply be four times N, the size of the population,
  multiplied by the mutation rate.

The formula that appears on the screen as the lecturer says this does not match what he says (but it's hard to say; the typesetting is terrible).  Furthermore, I find this description too vague (I have a million questions about each of the words in it).  Also, I would like to see how this estimate is derived.  Finally, judging by the number of egregious typos I've found in this series of lectures so far, I'd like to get a second independent rendition of these ideas.
I thought that Google would make quick work of this question, but to my surprise, when I search for "heterozygosity" or "average heterozygosity" none of the hits I get mention this formula.
I imagine that this is textbook-level stuff (i.e. not something that I'd have to go to the current research literature to find).  Can someone point to a textbook that derives this estimate?  (I am interested only in textbooks that discuss the formula alluded to in the quote above, as opposed to general textbooks on population genetics.  I've already consulted several of the latter, and not been able to locate the formula in question.)

@Remi.b: I mean a formula that matches the verbal description I quoted in my question.  I.e. an expression involving the number 4, the size of the population, and the mutation rate.

Sorry, I did not read properly! $H=4N\mu$ is the formula you're trying to derive.

$H=4N\mu$ is the formula you're trying to derive.
It is an approximation coming from an infinite site model and applies to diploid populations only. For haploids, it becomes $H=2N\mu$. The value $4N\mu$ or $2N\mu$ is often also called $\theta$ as it is a value that appears in many places in the field.
There are a number of ways to derive it. It can be derived from coalescent theory or from classical fixation index stuff from Wright.
Any good intro book to population genetics should derive this formula. (see for example in Gillespie's book). You will find more book recommendation at Books on population or evolutionary genetics?.


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How can a two genera share a latin name?
Recently, someone asked if species could share a latin name. In his answer, Remi.b said the latin name is unique to the species, and I think he is right.
However, this made me remember that I once stumbled upon a latin name that is shared between a genus of birds, and a genus of plants: oenanthe.
https://en.m.wikipedia.org/wiki/Wheatear
https://en.m.wikipedia.org/wiki/Water_dropwort
My question is: how come? Is it allowed for genera to share a name (not likely)? And why did Linnaeus, who named both, choose to do so? Error?

No, not an error. Plants, Animals and Bacteria each have their own independent nomenclatural codes. So while it is not advised, it is not forbidden by the code to have the same genera. It would be forbidden to have the same genus within one of the three codes. As a side issue, don't forget that the species ALWAYS includes the genus. Species are always binomens. The species epithet is the second word in the species binomen. Thus our species is Homo sapiens, not sapiens.

The different nomenclatural code is probably because they belong to different kingdoms in the Linnean taxonomy.


text:
Hummingbird cross Bering Strait
Hummingbirds travel to Alaska during summer. If global warming continue, allow birds stay longer in Alaska, can hummingbirds cross Bering Strait to Russia, then spread in Asia?

The ruby-throated hummingbird flies 500 miles nonstop across the Gulf of Mexico during both its spring and fall migrations
The Bering Strait is about 82 kilometres (51 mi) wide at its narrowest point, between Cape Dezhnev, Chukchi Peninsula, Russia
Based on the two facts above, it appears possible for a humming bird species to cross the Bering Straits if the weather becomes suitable to survival. Who would have thought?
That said, I am not sure how a humming bird who know which direction to fly in to make a successful crossing.

Good answer, I read Berng Strait have two Diomede Islands in center of strait, 40 km from both coasts. Probably need strong wind blow hummingbirds across, probably can't see islands from coasts.


text:
Can Anyone Identify This strange cockroach looking bug
I am looking for someone to identify this bug:
location india. It flew from my window in my room, killed it by spraying cockroach killer spray, it could fly like cockroach.

If you were a Jainist, I believe you wouldn't have killed it, right?

That is a mole cricket. Family Gryllotalpidae. They generally live underground, but as you noticed, they can fly. https://en.wikipedia.org/wiki/Mole_cricket


text:
If an antiserum was raised in a buffalo by injecting it with monkey red blood cells, what would be the full name for this antiserum?
Im confused, i've attempted this & what i got is buffalo anti-monkey red blood cell antiserum. I'm not sure if this answer is right

its actually Anti-Monkey RBC Buffalo Antiserum as the Ab formed is Anti-monkey RBC Buffalo Ab.


text:
What is the difference between Integrin to Cadherin?
My question is probably very basic but i couldnt get it in lecture and not from looking in the net.

What is the difference between Integrin to Cadherin.
By difference I am looking for say:

structural difference
functional difference

If i understand correctly both of them helps in cell adhesion.
But, probably in different way? or shortly, what is the difference?
Thank you!

Cadherins look like chains, that are stretched out only when bound to Ca++. They contribute to cell adhesion through adherens-junctions and desmosomes (cell-cell adhesion). They bind weakly by themselves, but function sort of like velcro, in that they make a strong junction when they are many.
Integrins can be of alpha and one beta type. Both types are used in a junction, and they sort of "claw" around the ECM. They also depent on Ca++ (and also Mg++) for correct binding. They join the cell to the extracellular matrix through aktin-linked cell-matrix juntions and hemidesmosomes. There's one alpha and one beta integrin per junction (i think) and they sort of "grip" the ECM by one of them going in the front and the other in the back of the ECM unit.
Both integrins and cadherins are transmembrane proteins, that also need adaptor proteins on the intracellular side.
For clarification:
Adherens junctions transfer the force of aktin filaments from one cell to another, using classical cadherins between the cells.
Desmosomes connect intermediate filaments between neighbouring cells.
Aktin-linked cell-matrix junctions link aktin filaments to the ECM.
Hemidesmosomes link intermediate filaments to the ECM.
Source: lectures at the university of Tromsø, Norway. Also my textbook.

A fair caveat, integrin CD103 binds to E-cadherin.

Thank you for the clearification! And I will also have a look in your book so thanks for that reference too!


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Why do plant leaves turn yellow?
Why do plant leaves turn yellow if they don't get enough water or get too much water? I want to know the process.
I've been searching in Google for an explanation, but none of the sites did.
Please describe the process.

Usually it is termed chlorosis, and comes about from an inability to produce chlorophyll. It can actually be determined by a whole range of things, and not just water shortage or waterlogged soil, including nutrient deficiencies, pathogen infection or unbalanced soil pH.
A lot of these factors relate to an inability of the plant root system to properly take up water. As you probably know, water enters the root system to be carried up into the shoot (through the xylem) mostly driven by transpiration, the water pressure caused by loss of water through the leaves. This water carries with it the soil-derived nutrients the plant needs to synthesise substances that can't be produced by photosynthesis. So if you change the water balance (for example by drying the soil) it becomes difficult for plants to get the nutrients they require to produce chlorophyll.
Usually this is mediated by reduced supplies of magnesium, iron or zinc, but because the precursor to chlorophyll is an amino acid, it can also be caused by shortages of nitrogen. pH comes into play because plants use a delicate balance of acidic ions to mobilise (make available to the roots) the nutrients in the soil, and if the soil pH differs too much this becomes untenable.
So in summary it relates both to shortages of key nutrients or changes in key soil characteristics, and the ability of the plant root system to uptake these key nutrients. It is mediated by these effects leading to an inability to produce enough chlorophyll, which leads to the yellowing leaves that you observe.


text:
Can anybody identify this flower for me?

One single flower on small 2 year old tree with alternate leaf arrangement

What is your location?  Do you know if this is an ornamental specimen, or something native?  The flower strongly suggests the family Malvaceae (think hibiscus).


text:
What is the tissue structure of bamboo?
If the xylem and phloem of the bamboo is not in the hollow center than where is it located/situated? cannot get clear cut answers from the above discussions

Was this not answered in : https://biology.stackexchange.com/questions/26123/what-does-the-empty-space-in-the-bamboo-stem-do

What above discussions? If this question has been asked before you cannot duplicate it.


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How are epiphytes symbiotic?
I understand epiphytes are not parasitic. But how exactly are they helping the tree on which they grow?

It's important to note that not all symbiotic relationships must be expressed in terms of a positive-negative (parasitism) or a positive-positive (mutualism) framework. I would guess that most tree epiphytes exist in a commensal framework with their host trees. That is, the epiphyte has a positive interaction (it gets somewhere to grow), and the host species has neither positive nor negative effects.

I didn't realise symbiotic relationship is superset of mutualism and parasitism!

@yathish the terminology in the ecological literature gets pretty malleable, but the Greek root basically means "living together" so can describe a range of relationships.


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Do some cells have more than 2n at some part of their cell cycle?
For example, do human cells reach 4n after s phase during interphase after replication of DNA?

For example megakaryocyte in bone marrow 8n.

Been told by a colleague that nuclei in early Drosophila embryos don't always manage to keep the rate of division in line with the rate of genomic replication, resulting in some of them temporarily housing 3n or 4n.

https://en.wikipedia.org/wiki/Polytene_chromosome


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What attacked my peach tree?

Help me please! I have to get rid of these!

I Guess Its this http://entnemdept.ufl.edu/creatures/veg/aphid/green_peach_aphid.htm. please feel free to add more information.

Please provide your location, time of year you took the photo, species/cultivar of peach tree (if known) and an approximate size for the pests. Thanks.

I am happy that i was right ať least with that fact that it is aphid.

@L.Diago yeah, nice call! Glad you added the guess as a comment. It helped me form the 2nd half of my answer :).

These are definitely some sort of aphid (small sap-sucking true bugs in the superfamily Aphidoidea).
Based on the coloration and shape of the pest and the host plant, my best guess is that you're looking at Hyalopterus pruni (or the Mealy Plum Aphid).

Note: the scientific name of this species has changed at least 21 times!

 Photo by Jack Kelly Clark

Looks like this person also found this species of aphids on a black cherry tree if you want to see more picture.

Description:

Wingless adult aphids are pale green with three dark green longitudinal stripes on their backs. Their bodies are covered with a white, mealy wax. [source].

Host Plants:
Typically trees in the Prunus genus: cherries, plums, almonds, apricots, nectarines, and -- you guessed it --  peaches. [source].
Damage:
Plant can become stunted from high numbers of aphids, but the primary concern is the development of mold that grows on the aphid's honeydew. [source].
Management:
See this University of California Agriculture and Natural Resources site for management suggestions.
Suggestions:

Biological: lady beetles, lacewings, or soldier flies
Organic: biological control + sprays of neem oil
Pesticides (typically not needed): Phosmet, Diazinon, and others in the fall; neem oil, flonicamid and others in the spring.

Final Notes:
Just because an aphid shares a name with an individual plant (e.g., the green peach aphid mentioned in the comments) doesn't mean that the species is limited to just that plant or that any aphid found on said host is that species. Many aphids feed on a wide range of host plants, so limiting your host to an individual species doesn't necessarily rule out a wide range of pests. However, it is not uncommon for an aphid species to stick to a single genus, narrow set of genera, or narrow set of families of host plants.


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How much generation of hamster's family it takes to get first bad mutations
So if I have two humsters and they start to reproduce themselfs then how much generations of hamster's family it takes to get first bad mutations?
The info here does not help to find answer https://www.reddit.com/r/askscience/comments/32x33j/how_do_animals_like_hamsters_and_snakes_avoid_the/
Thank you!

I think you're more likely to see problems related to recessive alleles than mutations. If the hamsters keep inbreeding, the odds of getting a hamster with two copies of bad recessive genes goes up, so you're more likely to see genetic diseases based on that instead of new mutations. But I don't know anything about the frequency of hamster recessive alleles, so I can't estimate the odds of seeing a genetic disorder in each generation.

@user137  Good point about recessive alleles!

Is the question aimed only at mutations (which involve changes in individual genes), or also at genetic changes  including recombination and crossover which only involve changes in gene frequency and location?  Both types of changes occur in every generation. Changes due to recombination and crossover are more likely to be harmful when both parents have a larger number of "bad" recessives.

Everybody carry deleterious mutations anyway
Your two hamsters most definitely already carry a number of deleterious alleles at segregating sites (segregating sites = polymorphic sites). Also, I will not talk about inbreeding depression in your population coming from only two individuals which will be very important but I will only answer your specific question. In short, I will assume your are not interested in segregating sites...
Probability of an offspring to carry a new deleterious mutation
The vast majority of new mutations are deleterious (Shaw et al. 2003). I don't know of estimates of mutation rate in hamsters but in mammals (and in all eukaryote species anyway generally speaking; e.g. see this post and this post or directly bionumbers#mutationrate), the genome-wide mutation rate is of the order of 1 to 100 mutations per offsprings.
If the couple of hamsters have $x$ offsprings, then the probability to have at least one new mutation in at least one offspring is given by the cumulative exponential distribution
$$P = 1-e^{-U x}$$
, where $U$ is the genome-wide mutation rate. With $U=50$ and $x=1$ (one offspring), this probability is $P = 1-e^{-50} = 1 - 1.9 \cdot 10^{-22} ≈ 1$.
In short
In short, to a fair level of approximation, every new offspring carry at least one deleterious mutation that was not present in either parent.


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Need help identifying this plant
I found this guy growing in my compost, but have no clue, what it could be.
Any expert here who want to take a guess?

What is your location?  And when was the photo taken?  You are almost certainly looking at something in the genus Persicaria and the family Polygnonaceae.  The clue is the ochrea, which is the papery sheath wrapping around the stem at the base of the leaves.

@BryanHanson This was taken in Hamburg, Germany a few hours ago

Alright someone familiar with European species in this genus will have to answer.  US species I am familiar with would not bloom until late summer.

If it is from a compost it couldn't it be from anywhere, since anything could have ended up in there?


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Molecular psychology/psychiatry literature/articles
I am new biology student which is on molecular biology subject on university. I would like to know something about genetic related to neurobiology, and certainly molecular psychiatry/psychology, perhaps evolution psychology. But i dont know where to start.
Can anybody give me type to literature/articles for beginners?

For the neurobiology I'd recommend to read: Mapping the Mind and The Quest for Conscioussness , but these are kind of long books.
For shorter articles as (merely) an introduction, I'd recommend:
Manoli, D. S., Meissner, G. W., & Baker, B. S. (2006). Blueprints for behavior: genetic specification of neural circuitry for innate behaviors. Trends in Neurosciences, 29(8), 444–451. https://doi.org/10.1016/j.tins.2006.06.006
Good philosphical and historical viewpoint can also be found here:
Marler, P. (2004). Innateness and the instinct to learn. Anais Da Academia Brasileira de Ciencias, 76(2), 189–200. https://doi.org/10.1590/S0001-37652004000200002
For something more practical: The Little Black Book of Neuropsychology.
Looking forward to suggestions by others :)


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Have Polyphyodonts ever evolved from Diphyodonts?
The Wikipedia article for polyphyodont says this:

Although most extant mammals are not polyphyodont, mammalian ancestors were. During the evolution of Therapsida, there was a period during which mammals were so small and short-lived that wear on the teeth yielded no significant selection pressure to constantly replace them.

...which was a bit surprising at first, but makes sense. So I'm wondering - have any species evolved in the opposite direction? In other words, have there been any non-polyphyodont species which have teeth, and evolved into polyphyodonts?

Not true polydonty, True polydonty is an animals that grows endless numbers of teeth like reptiles and fish do.  Elephants, kangaroos, and manatees are sometimes called polydont but they are doing something very different, they still only grow a set number of teeth, but instead of growing them in two sets they spread them out growing them a few at a time. the total number of teeth is still the same as other mammals and once that last tooth falls out they can't make anymore. It is worth noting the teeth migrate forward in the jaw as they wear out unlike true polydont in which new teeth grow from below endlessly.In essence they are rationing that limited number of teeth.
True polydonty has never evolved from a non-polydont ancestor.

I might not be understanding correctly, but it seems like this isn't really answering the question

Polydont is a difficult term there is ture polydonts and mammals that get called poly dont but aren't.


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What type of spider is this?
What kind of spjder is this? It was found in nova Scotia

The rounded carapace of the cephalothorax, and the relatively slim, banded legs indicate that this is one of the terrestrial Dolomedes fishing spiders.  The 'w' stripes on the abdominal pattern have white markings on the margins, but are not 'underlined' completely across in white, which rules out Dolomedes scriptus, in my experience.  Also (although I think this can be somewhat variable in these particular Dolomedes), this spider does not have the familiar white rim to the cephalothorax and abdomen.  Accordingly, I'll go with a rather light-colored individual of the fairly variable Dolomedes tenebrosus.
The links I enclose allow you to explore images of these spiders for your own interest:
https://bugguide.net/node/view/38828
https://bugguide.net/node/view/2011
Oh, yes - almost forgot.  Although these spiders can give a noticeable bite, the venom is less trouble than the standard Polistes paper wasp sting.  I have been bitten only once despite handling numerous females, and had almost no effects beyond a bit of pain and a small red bump.  Like most spiders, these can control the amount of venom they inject, so mine might have been a 'dry bite', but I've heard nothing about bad effects from bites by this very common spider.  I think it's safe to assume that this is a harmless spider - to us.  They love beetles and other large arthropods.


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Why are there no endoparasitic mammals or reptiles or birds?
I am curious why there aren’t any endoparasitic mammals, reptiles or birds
Endoparasite being a parasite that live In the host whereas ectoparasite lives On the host
I hope this clears up confusion

Can you please define "parasite"? Aren't humans parasites of wolves and elephants? Aren't cuckoo parasites? How about vampire bats, vampire finch, cookie cutter shark, hood mockingbird, cowbird, oxpeckers or hyena? We can largely qualify them all as parasite. Note that you might want to define reptile too (see here)

I'm voting to close this question as off-topic because it is based on a false claim that there are no mammal / bird / reptile parasites.

I mean endoparasites that are mammals birds or reptiles. I know there are endoparasites worms, protozoan sect. But I don’t think there are any mammals birds or reptiles that are endoparasites. Sorry for the confusing wording of the question

If there are any, can you give examples? I don’t know of any

Oh... you should definitely edit your post to say "endoparasite" then (and make sure to define the term). For the moment the post still says "parasite". No, I can't think of any example of endoparasitic mammal / bird / reptile except if you would consider a woodpecker a tree endoparasite, would you? Humans could be considered parasite of earth if you consider earth as a living organism (see Gaia by Lovelock) but that's a bit of a stretch. Intuitively I would think a big part of the answer is going to be "because they're big!"

I edited the question now to make it clearer. Thank you Remi.b

@Remi.b I'm not really aware of any commonly-used definitions of parasite that would classify humans as parasites of wolves or elephants (endo- or ecto-).

I would honestly suggest "parasite" is fine here, but that the question is revised to "are there any X parasites - and if not, why?"

In the most clearly defined concept of parasite, a parasite and a predator are confounded. If species A have a beneficial impact on species B and species B have a negative impact on species A, then A is a prey/host and A is a predator/parasite. In such terms, yes, humans are parasite of elephants. My point was to highlight that whether or not there are mammals parasite depends upon the definition once want to use. IMO, the question now makes much more sense with the prefix endo. It still bothers me a little that the woodpecker examples is not resolved.

@remi since woodpeckers are digging into the trees to pull out and eat insects that burrow into the tree the net impact on the tree is arguable.

If I had to guess, I would say that it's a matter of basal metabolic rate.  Birds and mammals are warm-blooded, and so have to breathe regularly (and eat a lot of food) to maintain body temperature.  It's pretty hard to do this if you're an endoparasite, and there doesn't seem to be an obvious evolutionary route to get to a lower rate.

These sorts of "why didn't this evolve" questions are not answerable without profound speculation.

Short answer size.
endo/ectoparasites need to be small to go unnoticed, and be hard to eliminate. The smallest mammals and birds are still much larger than a flea, fluke or other endoparasite. That's why larger parasites leave after feeding, if a vampire bat hung on the cow indefinitely the cow would eventually notice and do something, something as simple as rolling over could kill them quite effectively. While an animals infested with fleas can not do much to get rid of the fleas. The few large endoparasites either evolved from much smaller parasites (tapeworms) or exploit some strange insensitivity in the host(cymothoa) This means there is no path to ectoparasite which could lead to endoparasite.
Why there are endoparasites evolved by other means in vertebrates what exactly would they evolve from, there are no birds or mammals that would survive being cut off from outside oxygen or passing through a digestive system. It is like asking why no flying trees have evolved there just is no path to get there or from where they are now, or if there is a path it is so unlikely that it has not occured.


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Help on reconciling seemingly contradictory evidence about fetal experience
Fetal awareness and especially fetal pain are controversial, political issues. However, I do not wish to get into politics and want to merely stick to the scientific evidence. I have found statements about fetuses in the womb that seem to contradict each other, yet there has been no reference to the opponents in either side.
Some believe that fetuses do not have awareness in the womb and cannot feel pain. Here is an argument along those lines, claiming that fetuses cannot feel pain, even when their nervous systems and brain are developed, because the chemical environment within the womb suppresses awareness and experience that shapes the brain only happens outside the womb.
However, some other evidence seems to claim that fetuses can have experience. Twins can interact with each other in the womb as early as 14 weeks of gestation, as stated here. It is possible to learn in the womb, and newborns, even after they are born, can retain this knowledge, as stated here.
I'm not sure what to think. Are some of these statements, such as the idea fetuses are not aware, just incorrect? Or can interaction and learning occur without awareness somehow? (I know pain is distinct from awareness, interaction, and learning. What seemed particularly strange was the idea that fetuses have no conscious experience whatsoever, especially as no one making that claim, as far as I know, even mentioned the evidence about interaction and learning at all).

FYI, your third link gives a 404 response.

@vkehayas It doesn't for me, so I'm not sure what happened to you. Sorry.

I know close to nothing about the subject of self-awareness in fetuses.
But learning —and certainly interaction— can occur without anything close to human "awareness", as evident by the fact that systems without a brain (and even without neurons) can learn. Any system that can process and store information is capable of learning. Does your definition of awareness include anything more than this? Conversely, organisms with a very simple brain can display aversive behaviour.
For an example of memory without neurons, see the Wikipedia article on immunological memory.
For examples of aversive behaviour without a proper brain see Zhang, Lu, and Bargmann 2005 and Babin et al. 2014

References
Zhang, Y., Lu, H., & Bargmann, C. I. (2005). Pathogenic bacteria induce aversive olfactory learning in Caenorhabditis elegans. Nature, 438(7065), 179–184.
Babin, A., Kolly, S., Schneider, F., Dolivo, V., Zini, M., & Kawecki, T. J. (2014). Fruit flies learn to avoid odours associated with virulent infection. Biology Letters, 10(3), 20140048–20140048.

Um, don't fruit flies and C. elegans have an actual brain? Yes, I know it would be a very small brain, but it still counts as a brain, as far as I know. Anyway, stuff such as invertebrate awareness is controversial as well, to say the least, but I don't believe there has been 100% proof that they aren't conscious, and some scientists believe it exists.

Furthermore, I was actually talking about the point when the nervous system and brain do develop in fetuses. The argument I mentioned was not about whether those things had developed (they have by that time), but whether the chemical environment in the womb suppressed consciousness. The studies you mentioned don't seem to be relevant anyway, come to think of it.

@Inflationary_Bubble You asked if learning is possible without awareness. If you accept that the immune system does not have awareness, then I demonstrated one way learning is possible without human-like awareness. If you are willing to consider that the immune system and C. elegans have some rudimentary form of awareness, the only consistent thesis is panpsychism.

@Inflationary_Bubble Then it becomes a matter of identifying the degree of awareness which is an empirical question that is not really possible to answer with current methods, although it is reasonable to assume that the maturity of the fetal nervous system could be a relevant parameter. But please note that in that case the apparent contradiction also dissolves, as awareness is no longer a binary feature. The definition issue of whether you call it a brain or a collection of ganglia in the case of C. elegans is inconsequential for the answer.

@Inflationary_Bubble The fundamental problem in the apparent contradiction is then that you consider awareness as a binary feature (you either have it or you don't). However there exists no clear line dividing aware from non-aware systems. In my opinion, it is more productive to think in terms of information processing and storing.

@vkehayas - I think that your answer would benefit by including the points raised in the comments above.

@LinuxBlanket Agreed, will try to do if I find the time. Feel free to do so yourself if you'd like.


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What species of three-tailed flying insect is this?
What species of insect is this? Collected in spring in the United Kingdom near a river in an urban area during the late afternoon. They were flying up and down in the air.

Three tails mean ephemeroptera (mayfly). I don't know what species though. Mayflies can pop up very numerous all of sudden as they sometimes all hatch at the same time and fly around like crazy.

Nice pictures! What is the approximative size?

1 cm body + 2 cm tail

It only has a day to live. Let it go.

I did, don't worry. I don't keep animals unless I know how to take care of them. It was quite agitated but it flew away from my pot extremely fast into the sky.

@charlesdarwin Is the order mayfly good enough or are you hoping for a more detailed answer?

The more detailed the better but I'll accept your answer until there is a better one.

Based on this list of mayflies of the UK, your mayfly is from the genus Ephemera.  Of the three species listed at that site for the UK, the closest match is to Ephemera vulgata, and it looks quite close.  The image of E. vulgata below is from Wikipedia here.


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How do I reverse my insert within a plasmid?
I have a plasmid with:
...T7pro. -- RBS -- XBa1 cut site -- ProDpro. -- RBS -- AmilCP -- T -- Spe1 cut site -- T...
How do I design primers to reverse the portion in bold, such that the T7 and ProD promoters are on opposite sides of AmilCP? I am finding it difficult to understand how to design the appropriate primers.

Design your 5' primer upstream of ProDpro. with a Spe1 cut site added to the end (plus a few extra random bases to allow for better cutting). Add an Xba1 cut site to the end of the 3' primer, again with a few extra random bases on the end to allow for better cutting.
Amplify the insert, PCR cleanup, digest, cleanup again, and you should be able to easily clone into the Xba1/Spe1 digested vector that has been gel purified.

You are welcome, I hope it helps. As this seems a bit unclear on re-reading this, be sure your cut sites are on the 5' end (beginning) of each primer.

Also, if you feel an answer properly answers your question, be sure to mark it as the answer so others know that your question has been resolved.


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Ventricular Filling : Systole or Diastole?
As the Blood goes down from the Atrium to the Ventricles:

The Tricuspid Valve ( Right Atrioventricular Valve)
Bicuspid Valve (Mitral Valve )

The atrial pressure is INCREASES WHEN ATRIA ( THE ATRIA CONTRACTS AT THIS STAGE/ATRIA SYSTOLE) Thus:

fills the ventricles with blood ( blood goes down from the atria to the ventricles)
The Tricuspid/ Bicuspid valves OPENS since there is a higher pressure of Atria than the Ventricle

Questions:

Is the Ventricular Filling, (When Blood from Atria fills the Ventricles) itself a DIASTOLE or SYSTOLE
So during the Ventricular Diastole
Ventricular Filling is Diastole?? ,
Is it when VENTRICLES are filled with blood :

it increases THE PRESSURE IN IT SO THAT IT MAKES A
  (** VENTRICULAR DIASTOLE /VENTRICULAR CONTRACTION **)

I also saw in here that:
" The P wave represents the atrial electrical depolarization. This phase is ventricular diastole. During filling, pressure within the right atrium increases, pushing blood across the AV valves into the right ventricle."
I'd also like to clarify:

Shouldn't it be  WHEN IT FILLS THE VENTRICLE is filled,
     THE PRESSURE GOES LOW in atria gradually within the???
    I get it that the atrium has a HIGHER PRESSURE BEFORE FILLING and it makes the (TRICUSPID AND BICUSPID) valve OPEN

Kindly clarify through diagrams and steps, I'm somehow confused. Thank you!
You can kindly watch this short clip of video and this may help me clarify things:
http://highered.mheducation.com/sites/0072495855/student_view0/chapter22/animation__the_cardiac_cycle__quiz_1_.html

https://www.sciencedirect.com/topics/neuroscience/cardiac-cycle

Ventricular diastole is a period in cardiac cycle during which the ventricles are filling with blood. During this period, the atria are contracting and the ventricles are relaxed.
The diastole consist of this: atrioventricular valves open, atria contract (atrial systole), blood flows from the atria to the ventricles, the atrioventricular valves close.
When the term systole or diastole is used without saying is it atrial or ventricular, it means it is ventricular. For example, systolic blood pressure is the blood pressure during ventricular systole and diastolic during ventricular diastole.

According to what i've read and during ventricular filling the valves open because of there is  lower pressure in the ventricles, however the atria contracts  only on the later stage of ventricular filling it does not take most part of the ventricular filling

There are detailed graphs available, if you are interested in the exact timing of all events of the cardiac cycle.


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How to teach my self Biology and Chemistry?
Long story short I'm a American dreamer (a immigrant brought to the USA as a child but is illegal) and recently returned to my home country and not knowing the language here have had a hard time at school I am now 22 and think I can finally get somewhere I just need to teach my self Biology and Chemistry (Childhood dream was to be a biologist of some sorts) but I don't know where to start.
Can anyone recommend and books how how I should start my studying? I need to learn this stuff to be able to get into a university here. I wan't to start from the start and work my way up to University level.
Any sort of help would be greatly appreciated
Thank you in advance
Edit: TLDR: Basically I'm asking how I can home school my self to learn Biology and Chemistry to be able to get into a University and learn Biology and Chemistry on a University degree.

Possible duplicate of Books for beginners. There are also other posts that are more specific (such as Very introductory online source of information in evolutionary biology e.g.) that can be of interest to you.

I am sorry you've been evicted from the US to a country you know little about and don't speak the local language. As unfair as this situation sounds to me, I would like to reassure by saying that you will quickly learn this new language and will be able to attend classes like anyone else. Hopefully, this country has a decent education system and you will be able to pursue your education as you please.

For chemistry, please see on chemistry.SE

The stated clearly series is a good introduction to evolutionary concepts,  https://www.youtube.com/channel/UC_cznB5YZZmvAmeq7Y3EriQ. Personally I like Richard Dawkins books like the selfish gene and the extended phenotype, they are also fairly easy to come by.


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Why don't we find animal corpses and skeletons all throughout the woods?
Where in the forest do wild animals die?  I rarely (occasionally, but rarely) come across animal bodies.
Where are the large skeletons of bears and deer?
Detectives often investigate human bodies that were dumped months earlier.  They've partially decomposed, but are still mostly there.  Why?

Perhaps because very few animals die naturally.  They are killed and eaten.  I (or more often my dogs) often find bones of deer &c that have been killed and largely eaten by mountain lions or other predators.

Large predators can break up the bones to get at the marrow. This disperses the skeletons. But for the most part, bones are a good source of calcium, and are eaten by rodents. You can see evidence of this when you come across the gnaw marks that rodents make on the plastic boards made from recycled milk cartons. As for the reason that human skeletons are particularly resistant to this destruction, I have only a guess. Perhaps the first stage of destruction, the dispersal by large predators, is less common because these predators have been trained to avoid humans. I would also guess that many murder victims are concealed by the murderer.


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What would be the fate of protein made from D-amino acids after ingestion by humans?
There are some natural peptides made of D-amino acids, rather than the L-amino acids normally found in nature. It is now possible to chemically synthesize artificial proteins made of D-amino acids.
If such proteins were ingested by individuals, how would they be metabolized and what consequences would they have?

Please read the help on what questions are acceptable on Biology before posting: "You should only ask practical, answerable questions based on actual problems that you face. "

I believe my question meets those guidelines. To follow on from the statement you quoted, "Chatty, open-ended questions diminish the usefulness of our site and push other questions off the front page.", and that is not the sort of question that I'm asking. I'm asking what the scientific understanding of what the effects of ingesting biological material composed of opposite-chirality amino acids would be. Since the properties of those chemicals are (presumably) well understood, the effects of eating said organic matter should be answerable.

Questions about alien planets are not on topic here. Also questions to which you have applied no effort yourself, assuming that you are a 'student' of biology. If you want to ask this question you need to think about the biochemistry involved. For example you could ask "Do the digestive proteases (trypsin, chymotrypsin, pepsin hydrolyse peptides made up of D-amino acids) and on from there to the next stage in digestion, assuming they do. Until you reformulate your question in such terms I hold by my opinion.

I'm a computer programmer, I don't know anything about biology past high-school tier other than random bits of trivia. It's not my expertise; that's why I'm asking a question. If I already knew the answer I wouldn't have to ask, would I? Asking questions so that people who are experts in that field can answer them is literally the entire purpose of Stack Exchange.

I'm sorry Nick, but the first line of the Tour states "Biology Stack Exchange is a question and answer site for biology researchers, academics, and students." If I went onto Stack Overflow (as I do sometimes) and asked what a "for" loop was I wouldn't last two minutes. Indeed, if I have asked far more sophisticated questions that people regarded as too basic. And the problem of asking on a specialist SE is that you get specilized answers, that you likely wouldn't understand, or at least wouldn't be able to assess for correctness. (There's no code to run to check if it works for you.)

"If I went onto Stack Overflow (as I do sometimes) and asked what a "for" loop was I wouldn't last two minutes." I'd give you an answer for that. Probably upvote your question, too, for showing interest. I don't see why you can't do the same for me. And I tried posting this on the scifi stack exchange, and they closed it for being off-topic, so I don't have anywhere else to post it. I don't care if I can't assess the answers for correctness, since that's what the upvote/downvote process is for anyway.

OK, I'll edit your question and give you an answer.

One aspect of the basic biochemistry needed to approach this question is the fact that the enzymes that catalyse cellular reactions show various levels of specificity towards their substrates (reactants), including stereo-specificity. This is illustrated below (an ill-favoured thing, but mine own). The first example shows that the specificity of proteases may depend on the general chemical or physical nature of the substrate. The second shows the how stereospecificity works.

The enzymes that are relevant here are proteases, which are responsible for breaking down proteins to their constituent amino acids, which are then absorbed by the gut, and then the enzymes that would normally catabolize (break down) or metabolize (convert to other compounds) those amino acids. It is well known that the specificity of the enzymes is such that, even if the proteins were broken down to D-amino acids, these could not be used for protein synthesis.
I am not an expert in this area (‘for’ loops are more my sort of thing) but I found some pertinent references in a recent paper on D-amino acid analogues of peptides. To quote from the introduction to that paper:

A useful consequence of this is that (D)-proteins are highly resistant to degradation and have low immunogenicity (7). The fundamental change in backbone–side-chain connectivity and geometry means they are not recognized as proteins by many (L)-proteins—including proteases. Consequently, (D)-proteins are reported to have greatly increased gut, blood plasma, and intracellular half-lives (8). Better cell penetration has also been reported in some cases (9, 10).

The references are:

Uppalapati M, et al. (2016) A potent D-protein antagonist of VEGF-A is nonimmunogenic, metabolically stable, and longer-circulating in vivo. ACS Chem Biol 11:1058–1065.
Rabideau AE, Pentelute BL (2015) A D-amino acid at the N-terminus of a protein abrogates its degradation by the N-end rule pathway. ACS Cent Sci 1:423–430.
Nickl CK, et al. (2010) (D)-Amino acid analogues of DT-2 as highly selective and superior inhibitors of cGMP-dependent protein kinase Ialpha. Biochim Biophys Acta 1804:524–532.
Brugidou J, Legrand C, Méry J, Rabié A (1995) The retro-inverso form of a homeobox-derived short peptide is rapidly internalised by cultured neurones: A new basis for an efficient intracellular delivery system. Biochem Biophys Res Commun 214:685–693.

So it would appear that the D-amino acid proteins are less likely to be metabolized and thus would be less likely to be useful as food. I do not understand why they would have low immunogenicity, but if this is the case it seems unlikely that they would cause allergic reactions.

Could you please add an explanation about why L-amino acid could not be used to artificially synthetize proteins?

@totalMongot — Of course they can, but that is not the question.

Yes that's not the question, but I asked because the OP said that in his question: "There are some natural peptides made of D-amino acids, rather than the L-amino acids normally found in nature. It is now possible to chemically synthesize artificial proteins made of D-amino acids."

@totalMongot I think you misinterpret what the poster wrote — certainly the state of chemical synthesis of peptides from amino acids. This was first achieved at the beginning of the 20th century, led to the synthesis of peptide hormones by the 1950s, and was made much more efficient by the introduction of the solid support  methodology for which Merrifield received the Nobel prize in 1984. My mailbox is full of offers from companies that do this. Naturally L-amino acids were used, but D-amino acids will react similarly. That’s the point of needing to explain enzyme specificity towards L.


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Is this European(western), Eastern(northern) or another Hedgehog?
Yesterday this little guy ambushed my bicycle, thankfully tire-hedgehog contact was avoided at the last moment. Now I am wondering which one is it. Going by wikipedia maps and photos it should be either European/Western (Erinaceus europaeus) or Northern (E. roumanicus).
Sadly due to nocturnal nature of Hedgehog, "smart"phone camera and general willingness of Mr. Spikey to quickly leave area of incident this is best photo I have:

Incident occurred in Poland, Europe, around 21:30 local time.

There are some field marks that can be used to make the distinction but you should have taken a picture of the foot and the nose more precisely. There is still the risk of some variations in colour, then the best would be a DNA analysis in my opinion.

What part of Poland is this? Both species occur in Poland, but they are geographically seperated.

@RHA It was about here, in Opole, Upper Silesia

I think the picture you have is not enough to make a proper distinction between the two species.
By this site, they found some morphological characteristics to make the distinction but:

You have to carefully take pictures of the animal parts
The study nearer Poland has been made in Estonia and those characteristics could be slightly different in other countries.

I did not find another documents about hedgehog populations in Poland but the wikipedia page says both species are living in the country.

Downvoters: please consider to leave a comment to explain what can be improved to this answer.


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Dangers of excess blood protein?
Like glucose, amino acids are also insulinogenic as well. So, presumably, just like glucose, the body would also like to keep amino acids levels in the blood stream below (or within) some certain concentrations as well.
This question Why is too much glucose harmful? details some of the means by which high blood sugar levels can affect various cells and body function. But, would excess blood amino acid(s) levels have similarly adverse effects?

Your question is unclear and contains dubious assumptions. First the title refers to proteins, whereas the question refers to amino acids. Please correct that. Proteins are not insulinogenic. Second your assumption that because high blood glucose is harmful the primary purpose of insulin is to prevent this harm is at odds with the obvious accepted idea that it does it so the organism can obtain energy from or store this. Hence the supposition that insulin stimulates amino acid uptake to prevent harm, rather than to utilize them is completely unjustified.


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What exactly is this plant resembling Conyza?
This plant grows on my balcony in Vienna, Austria. It gained most of it’s current height (30-35cm) during the last 2 weeks. Before I didn’t notice it.

It is covered with tiny white hairs. I conducted a couple of tests. They never stung.
The leaves are toothed (I believe “serrate” is the official terminus for this type of edge).
From a central leaf vein, more veins spread out in a manner that seems somewhat irregular to my untrained eye:

Edit: Now, in July, that is about 2 months later, it bears flowers.  Furthermore it is about 3 times taller. I believe there were seed heads, which have been blown and washed away. All of this would fit Conyza mentioned in the comments, but the shape and density leaves  appear to differ from C. boranensis or C. canadensis.

Edit: now, still July some seed heads have reappeared

It is similar to Conyza canadensis, but the shape of the leaves makes me uncertain

Conyza canadensis can have these serrated leaves, although usually not this strong. The amount of flowers is also a bit much. Hmm, dunno...


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Why does doing more physical labour reduce the prevalence of disorders like OCD?
This just an observation without any study backing it. But people who do more physical labour as opposed to sitting at the couch really do have less rates of OCD.
Why this association of physical work with OCD's?
By OCD, I mean Obsessive Compulsive Disorder.
Here's a study backing up the exercise and its positive effects on reduction of OCD,
https://www.ncbi.nlm.nih.gov/m/pubmed/17568300/

What is OCD? (And don't ask me to do an internet search, I'm on this website and I shouldn't have to wrestle with niche abbreviations. And how do you think anyone is going to answer a question about pre-agricultural man other than by speculation?

I edited out that question. And added details like full form of OCD.Is it OK now?

I retracted my close vote due to your edits, thank you. To improve your question, though, it would be best to have a citation for the claim "people who do more physical labour as opposed to sitting at the couch really do have less rates of OCD" - if this is just your own observation, then we can't really answer the "why." It's hard enough to answer "why" questions when there is a known effect.

@Bryan Krause. I can see my question was a horrendous one, I'm sorry bout that. I couldn't find any valid scientific citations backing up the labour claim but here's one backing up aerobic exercise.

I would first ask which way the causation works.  Does couch-sitting increase OCD, or do people with OCD prefer to be couch-sitters as a consequence of the OCD?


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Is this Weigela?
A work colleague found this growing in a Northumberland (UK) woodland (May 2018), took a photo and sent it to me.

It was in an area with non-native species, and this was growing as a shrub. It doesn't spring out as being native to the UK to me?
The leaves are hairy, not waxy. The photo shows a collection of, what I have confirmed, are buds.
If I had to compare it to anything I would say it looks like a Weigela?

Could you please post a different picture of a leaf and a flower up close and in better lighting? It's really hard to see.  It looks very similar to a bush that grows around there. Thanks.

Unfortunately, it's all I was given by a colleague. I'll ask her if she will ever be going to the location again, or can ask another to provide another sample.

The bush that looks like this one is one of the aronia varieties. If the picture was a bit lighter, I could have compared them better. The only difference is that the regular aronia is a shrub with clusters of berries/flowers, and the bush that grows here is very short and has only a few flowers. But I am sure they are related.


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Are the sister chromatids exactly the same?
I'm having doubts about whether the sister chromatids are exactly the same or not. I know that they are the arms that carry the information genes (the alleles), but I don't know if they are exactly the same and / or in what these arms differ, since in a partial exercise they ask me the following:
Explain briefly why the sister chromatids are not exactly the same and the homologous chromosomes are different. To answer, consider the origin of both structures.
Nor do I understand quite well when the statement clarifies "take into account the origin of both structures."
Thank you very much for the help!

Well, what is the origin of the sister chromatids? In other words, by what process does a cell go from one chromosome consisting of one DNA molecule to one chromosome consisting of two DNA molecules (two chromatids)?

Then the sister chromatids would be formed from the DNA replication?

Yes exactly. Now, is DNA replication perfect or are errors introduced?

I suppose it is perfect or is it possible that there are errors?

A new chromatid is synthesized by copying the other chromatid. As such two sister chromatids are (quasi) perfectly identical.
Why did I say quasi? Because there are sometimes "errors" when replicating DNA. These "errors" are called mutations. As far as I know, most mutations occur during meiosis though and only very few occur during mitosis. So, to a pretty good approximation, yes sister chromatids are identical.

Ohh ok, with this I understood what canadianer means. Thank you very much for the explanation!


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What is the purpose of the viscous gel in the Pacinian corpuscle?
I have read that 'when the stimulus (in this case pressure) is constantly applied, the gel repositions itself to prevent the formation of an action potential'. I don't really understand what this means.

Short answer
The adaptation process in Pacianian corpuscles (PCs) is mediated via the outer capsule. This capsule is an onion-like structure that quickly molds itself to pressure stimuli, thereby rapidly desensitizing the receptor.
Background
The Pacinian corpuscles are rapidly adapting (RA) skin receptors, as opposed to the slowly adapting (SA) ones, such as the Merkel cells. RA cells become swiftly unresponsive (i.e., they adapt) when a pressure stimulus is applied, but faithfully transmit rapidly changing stimuli (such as vibrations).
Pacinian corpuscles are specialized vibration receptors. Their dendritic region is shaped as an onion-like structure with layers of stacked lamellae:

Specialized dendritic capsule of the Pacinian corpuscle. Source: Biologymad
These lamellae act as high-pass filters that result in a sharp drop in sensitivity below 150 Hz (Johnson, 2001). If this capsule is dissected from the receptor and a pressure stimulus is directly applied to the sensor element underneath the capsule, the receptor response to a sustained stimulus substantially increases (Mendelson & Loewenstein, 1964). Basically, these elastic lamellae slowly mold their shape to the stimulus and pressure stimuli are only transmitted for a few milliseconds, after which the lamellae absorb the pressure. So only a one or a few spikes are generated at the start of a pressure stimulus.
You can imagine it this way, suppose you have a gel-like substance (say Play-Do) on a weight scale. Now suppose you press the Play-Do quickly and hold your finger steady at a certain point above the scale, within the Play-Do. The weight scale will shortly display a certain weight (equal to the pressure applied in Newtons), after which the Play-Do folds itself around your fingertip, and the pressure is released from the scale.
Upon release of the pressure stimulus another spike or two are generated in the PC. Hence, a continued pressure stimulus is not faithfully reproduced. However, vibratory stimuli generate spikes on the pressure onset as well as offset as well, and this happens on every phase of the vibration. Hence, vibratory stimuli are faithfully transmitted.

Response of Pacinian corpuscle to a sustained pressure stimulus (indentation of the skin) and superimposed vibratory stimuli. Note the vigorous response to vibrations, but the rapid adaptation to the static pressure stimulus. Source: Zavantag
References
- Johnson, Curr Opin Neuobiol 2001;11:455–461
- Mendelson & Loewenstein, Science 1964;3618:554-5


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Aside from Homo Sapiens, do the males of any other species care for the offspring of those unrelated to them?
Elsewhere I heard that male Long-tailed Tits will care the offspring of their brother if they're unable to have their own. However, I'd like to know if there is a case of such behavior where the two are unrelated to one another.

Wolves? How else would the Roman Republic have come into being?

That particular wolf was of the female persuasion, I believe.

Yes most commonly in a reciprocal altruism fashion, when you aid any offspring of your species or any in your herd/pack. Crocodiles are known for this. They respond to any crocodile (of their species) distress call from any baby crocodiles. This tends to be an advantage because proximity usually means relatedness and even when it doesn't crocodiles are high enough on the food chain the risk to the males is low compared to the time and effort that would be needed to identify the offspring first.
likewise in herd animals it can be an advantage because it ends up with everyone protecting everyone else's offspring but usually has to be paired with some ability to punish freeloaders/cheaters (individuals who don't help protect the offspring).
Of course you also have males who are tricked into it, after all a male does not always know what are its offspring.
You also have males that will help with a current brood to court the mother, or even unrelated females. Basically they are showing off how good a parent they can be, some believe this is what humans are doing. This is seen in some social primates. It might happen in some birds too but I am not sure.

Would be great to have a reference for your claims.

What is cheating/freeloading in this context?

@Ludi a cheater in this context is a parent that does not help defend unrelated offspring.

I think most if not all herding species do this.
I watched one video taping a strong adult elephant (who travel alone) helped a baby elephant who was too weak to follow his/her parents and left alone.

Two examples off the top of my head:
Meerkats (Suricata suricatta).
It's well-known that each member of a meerkat group takes turns minding the pups for the whole group, and this includes both males and females.  Quote from the website http://meerkats.net/info.htm which states this specifically:

babysitter - Stays with the pups while the gang is out foraging for food.                           Different gang members take the responsibility different days, this                            is not domiated by males of females. Generally though the least                            hungry Meerkat will do the babysitting. The alpha female never                            baby-sits. This duty is for Meerkats 6 months or older.

I also found this on the same site:

After sixteen weeks [the pups] are on there own to find there food  Each pup will be taken on by a adult Meerkat which will act as a mentor, who will take the responsibility to teach the pup necessary skills for foraging for food as well as responding to danger.  Male Meerkats tend to mentor male pups and female Meerkats tend to mentor the female pups.  Many of skills Meerkats have are taught by the mentors rather then being instinctual.

(Site author says is an enthusiast compiling information from various sources: very detailed and descriptions square with information I've seen elsewhere, so I think this is a reliable source of information despite its dodgy typing.)
Canada geese (Branta canadensis).
Canada geese often have a "creche" system where one pair of geese at a time will babysit the entire group's goslings while the others forage.  Here's a discussion of this in the Guardian newspaper's Notes and Queries pages from 2011.
https://www.theguardian.com/theguardian/2011/oct/11/childminding-habits-of-canada-geese
(The first letter states that this only occurs on water.  From my own observation, I can say that that's not true.  It may be where Mr Dowsett lives, but I've sometimes seen a whole small flock's goslings asleep on a canal bank together with one pair of adults standing guard over them while the rest forage further along.)


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Why can only small molecules pass through the phospholipid bilayer of the cell membrane?
TO put simply: I am just wondering what mechanism or substance only enables small molecules to pass through the cell membrane. Is it cholesterol? My textbooks are not very clear.

The plasma membrane consists of a phospholipid bilayer which separates the internal environment of the cell from the external environment. It regulates the movement of substances in and out of the cell and helps keep a constantly regulated internal environment of the cell.
The plasma membrane consists of a phospholipid bilayer, which, as the name suggests, is made up of phospholipids(lipids that have a phosphate group attached to them.).
The phospholipid has two regions a hydrophilic (water-loving / has an affinity for polar molecules) and hydrophobic (water-hating / has an affinity for nonpolar molecules).

So what happens is these molecules come together and arrange themselves in such a way that it faces the least amount of repulsions. Hence, the fatty acid tails (Hydrophobic part) face inside and the polar part(Hydrophilic part) face the outside, to look something like this.

Now, what happens is that when a molecule has to enter the cell it first has to interact with the polar part of the lipid membrane and then with the inner non-polar part of the membrane to pass through, hence if it is a polar molecule it will face repulsions and will not be able to pass through without the assistance of transmembrane proteins (it doesn't matter whether it is small or large, it simply won't), but, in the case of non-polar molecules, there is no repulsion from the fatty acid part of the phospholipids and hence it can pass through the membrane. When the non-polar molecules are too big some other mechanisms may be utilized (like receptor-mediated endocytosis).
With regard to your doubt regarding the "mechanism" with which a molecule passes through the membrane, in the simplest case, it will simply slip in between the phospholipids and through the bilayer. But, this is, as I said the simplest case, there may be transmembrane proteins which create channels for diffusion (aquaporin is a good example), or as I mentioned earlier they may be taken into the cell by endocytosis, through pumps like the Na-K pump etc.
And also cholesterol acts like a buffer to ensure that the spacing between the individual phospholipids is maintained so that it stays fluid (i.e. to maintain optimum rigidity of the membrane).
This is what an actual membrane looks like in an actual cell:

Hope you got a general idea.
You can refer to Chapter 11 of Molecular Biology of the Cell (by Bruce Alberts et al) if you want a  more rigorous explanation.

Although aquaporins transfer most of the water, simple osmosis can occur with water due to the osmotic pressure and it is very small size.

True. I just wanted to give an example and that was the first thing that came up in my mind. Water is very small molecule and the lipid bilayer is not perfectly impermeable to water i.e. some amount of the water does get in. Once it is in the hydrophobic region, water has to go in as it will face repulsions, leading to the entry of water into the cell


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Why do bacteria use formylated methionine in the initiator tRNA, while eukaryotes do not?
Could anyone suggest an explanation for the evolution of this trait in bacteria? Does it confer any advantage?
It is also exploited by immunity receptors of some eukaryotes for the recognition of bacteria.
In the literature I was only able to find a paper suggesting a possible role in signalling for protein degradation.

Summary
The question is posed in terms which imply that the formylation of the initiating methionine (Met) of protein synthesis was a relatively late evolutionary development for some purpose not concerned with translation, such as allowing regulation of protein degradation.
My answer takes the quite different view that this was an early evolutionary development in translation, arising as part of the system for initiating at a specific codon — AUG. With time, the initiating system became more sophisticated, with the specificity of initiation residing more in a separate initiating Met-accepting tRNAf which evolved to have a distinct structure from the elongating Met-accepting tRNAm allowing it to be distinguished from the latter and other elongator tRNAs.
I postulate that in the line leading to eukaryotes and archaea a mutation subsequently occurred that resulted in a loss of ability to formylate Met-tRNAf, but that individuals with this mutation were viable as initiation had ceased to be dependent on the formylation for discrimination.
Contemporary systems for initiating translation
I constructed the diagram below for an answer to another question, but it shows some of the common features of initiation of protein synthesis in contemporary eukaryotes and prokaryotes. (The reader who wishes more detail on translation is directed to standard text books, e.g. chapter 29 of Berg et al.)

The common features of initiation in eukaryotes and prokaryotes are:
1. The use of  a Met-accepting tRNA with an anticodon that recognises AUG to insert the first amino acid in a protein.
2. That this tRNA, here designated tRNAf (but also designated tRNAi) is distinct from the Met-accepting tRNA used for inserting Met at other points in the protein during elongation.
3. That the (f)Met- tRNAf is recognized by an initiation tRNA-binding factor (I-TBF in the diagram — a non-standard abbreviation) and not by the elongation tRNA-binding factor (E-TBF in the diagram).
4. That the (f)Met- tRNAf is delivered to the P site of the ribosome (otherwise occupied by the growing peptidyl-tRNA), rather than the A site, to which elongator-tRNAs are bound.
5. In many cases the N-terminal Met is removed by proteolysis after translation.
The features of initiation that differ between eukaryotes and prokaryotes are:
1. That the initiating amino acid in eubacteria and mitochondria and chloroplasts  is N-formyl-methionine (fMet), rather than methionine, as is the case in eukaryotes and archaea.
2. The selection of the particular AUG codon for initiation is different in the two cases. In eubacteria and archaea the 16S rRNA binds to a polypurine, Shine and Dalgarno, sequence; in eukaryotes the normal method involves a complex of the small ribosomal subunit and the Met-tRNA ‘scanning’ from the 5ʹ-end of the mRNA (the secondary structure of which is first unwound.
Argument
As the question about the function of the formylation is posed in evolutionary terms, and fMet-tRNA is involved in the initiation of protein synthesis, it seems valid to consider the evolution of this latter process, however speculative that may inevitably be. The following formulation is my own, although I suspect it represents the orthodoxy in this field. This, of course, does not mean that it is necessarily correct.

It seems likely that initially translation lacked signals for start and stop (and probably also protein initiation factors). I will not deal with termination, other than to say it is probably an easier problem, but initiation would seem to require the introduction of two new features:
(i) The designation of a specific initiation codon AUG†, which, for whatever reason, corresponded to one of the existing amino acids, methionine.
(ii) Given that this initiation codon also served for incorporation of Met internally, the development of a system to select one particular AUG for initiation.
It seems simpler to suppose that (i) preceded (ii), and that is what I shall assume, although the following arguments do not depend on this.
In contemporary initiation the problem of competition between initiation and elongation factors for (f)Met-tRNAs has been solved by the evolution of two separate tRNAs that accept Met — one for initiation and one for elongation. These share certain structural features — their amino acylation is catalysed by the same amino acyl-tRNA synthetase — but they differ in recognition by the protein synthesis factors that bring them to the appropriate P or A site on the ribosome. Despite the lack of formylation of Met-tRNAf in eukaryotes, the structural similarity to the eubacterial tRNAf is such that it can be methylated by E. coli transformylase (reviewed here). However, I imagine that this structurally different tRNA took time to evolve, as, indeed did the protein synthesis factors.

My argument is that the formylation of Met-tRNA was the basis of the initial discrimination between initiator and elongator Met-tRNAs, and this could have arisen even before the gene duplication that led to separate tRNAs.

Why would fMet-tRNA bind preferentially to the P site and Met-tRNA to the A site? The amino acyl tRNAs that bind at the A site all have a free α-amino group that attacks the linkage of the peptide to the tRNA in the peptidyl-tRNA in the A-site at the peptidyl transferase centre. The peptidyl-tRNA, of course, lacks such a free α-amino group. In this respect fMet-tRNA, with a blocked α-amino group, resembles peptidyl-tRNA (see diagram below). One can imagine how structural differences in the P site could hinder binding of Met-tRNA, but allow binding of fMet-tRNA. And, of course, fMet-tRNA would not be able to react if bound at the A site, which might also have structural features to hinder its binding.

If subsequently the discrimination became magnified by gene duplication and evolution of a structurally distinct tRNAf, the need for formylation would be diminished, and one could envisage that its subsequent loss in eukaryotes may have had no adverse effects, or was easy to accommodate.
The question does arise why formylation has persisted in eubacteria, even though it is possible to obtain viable mutants lacking the transformylase. This is what the work alluded to in the question addresses. There is a 2015 paper by Piatkov et al. which suggests that N-terminal fMet can be a degradation system in E. coli. Presumably this arose after the divergence of the line leading to eukaryotes and archaea, which developed other systems for regulating protein turnover.
However I would suggest that, assuming that the foregoing is correct, it is an explanation for the persistence of the formylation of Met in eubacteria, and not the reason for its initial appearance.

Concluding Remarks
At present I know of no convincing evidence that proves my arguments and rejects the proteolysis idea regarding the reason for the evolution of fMet-tRNA. This is the problem with ideas about early evolution. It is compounded here by the facts that suggestion of a role in proteolysis only came up recently and that this is no longer the ‘hot’ field it was 50 years ago.
Nevertheless, I find it hard to imagine a system as crucial and sensitive as protein synthesis incorporating a feature like formylation of methionine if it only had a secondary function. In this case it would seem easier to formylate the N-termini of proteins post-translationally, as for other N-terminal modifications like acetylation. Furthermore, the finding that the eubacteria-derived mitochondria still use fMet can hardly be to control protein turnover, as the vast majority of mitochondrial proteins are translated in the cytoplasm and lack fMet.
†Footnote
I am aware that, in bacteria especially, there are other possible initiation codons, notably GUG, although the initiating amino acid is always (f)Met. (This attests to the importance of the tRNA structure in contemporary initiation.) It is simpler just to refer to AUG in the argument.

This answer is in the form of an argument in response to an unanswerable "why?" question. If anyone demands references to support this I can provide them. If you have access to a library with old text books, you can find them all in Adams et al. Biochemistry of the Nucleic Acids.

I demand references. Or, rather, references would be appreciated, especially so that further reading could be done. Interesting answer nevertheless.

@canadianer — Well that was fun. Let me know if there are any particular points which I haven't referenced that you think I should. I can dig them out. Also, if you — or anyone else — have any queries or notice any typos, do let me know.


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Which mosquito species is this?
Today, when I just woke up and saw this. I need to identify the species of this mosquito. I don't think its dangerous like Female Anopheles. I'm afraid if it is a carrier of any dangerous diseases such as Filaria, Dengue, etc.

Location: Bokaro, Jharkhand, India
Temprature: $ 29°C $

It is a female. From Wikipedia: "Anopheles mosquitoes can be distinguished from other mosquitoes by the palps, which are as long as the proboscis,and by the presence of discrete blocks of black and white scales on the wings." I can't see the palps for sure, but they look short (if what I am seeing are the palps).

@Karl Is it Anopheles?

I don't know because I cannot clearly see the palps. Mosquitos are not my specialty though, and I am sure that an expert will be better able to tell.