How long do zebra fishes remain transparent?

The upper limit of transparency time of zebrafishes is anywhere from two to three weeks for normal zebrafish for optimal high-resolution imaging. However, there is a modified species of Zebrafish called 'Casper' which is now the preferred zebrafish strain for studies in cancer and other research, because the length of transparency lasts into adulthood.

Sources:

http://medicalphysicsweb.org/cws/article/research/51394
https://biology.mit.edu/people/lisa_steiner#research_summary
http://www.the-scientist.com/?articles.view/articleNo/34834/title/Models-of-Transparency/


Role of ATP and AMP in functioning of Phosphofructokinase

This is clearly explained on the Wikipedia page for glycolysis under the heading Phosphofrucokinase. AMP is an allosteric activator of the enzyme and ATP competes for binding at the same site but is not an activator.

You should think of the interaction between the two regulators in terms of reversible binding of both: since they compete for binding at the same site the proportion of the enzyme with bound AMP will go down if [ATP] goes up, for example.

Neither of your proposed schemes is   correct: the enzyme is more active with AMP bound and less active with ATP bound. The idea that AMP binds, activates, then wanders off is wrong.


How does a test like the Natera Panorama distinguish the child's genome from the mother?

As you correctly discerned, distinguishing the fetal cell free DNA from the mothers cell free DNA in the blood stream is one of the major challenges in this type of diagnostics.

Consequently, the results that can be directly linked to the paternal DNA are the most reliable.

In the case of the example you give, the high accuracy stems from the fact that in case of Monosomy X, there is no indication of neither a paternal Y nor a paternal X chromosome. While the Y chromosome is the most easily discerned, a paternal X chromosome could also be detected because in that case the cell free DNA would contain fragments of three distinct X chromosomes.

This publication summarizes the issue nicely:

  Once the cell-free DNA fragments have been purified, small differences
  between the fetal and maternal DNA sequences are exploited in order to
  make a specific fetal diagnosis. To date, the majority of studies have
  focused on the detection of paternally inherited sequences that are
  entirely absent from the maternal genotype, such as those on the Y
  chromosome of male fetuses. This target is particularly attractive as it
  comprises a large portion of DNA which is not otherwise present in
  women.

  Variable regions of repeated DNA (short tandem repeats or
  STRs) can be used to identify paternally inherited sequences, by comparing
  the number of repeats present with the paternal and maternal sequences.
  Paternal alleles on the autosomal chromosomes can also be detected, if
  they are known to be absent in the maternal genome, but this requires
  detailed sequence knowledge of the paternal genotype of interest, as
  well as detection methods that can distinguish DNA sequences that
  might only differ by a single nucleotide. Importantly, all these methods
  rely upon the fetus inheriting a uniquely paternal sequence that is conveniently
  located for a particular diagnosis.

The reliability of these tests can apparently be improved by enriching the fetal cell free DNA:

  Selective enrichment of fetal DNA, based on a difference in the
  average physical length of fetal and maternal DNA fragments, which
  can be exploited to increase the relative amount of cffDNA. Fetally
  derived DNA fragments are generally smaller than those that are
  maternally derived, being predominantly ,313 base-pairs in length
  (Chan et al., 2004). Therefore, by using standard size fractionation
  to select only DNA fragments ,300 base-pairs, circulating cffDNA
  can be enriched such that it comprises around 70% of the total cellfree
  DNA (Li et al., 2004b), prior to detection and identification by
  either PCR (Li et al., 2005) or mass spectrometry (Li et al., 2006).


IMO, the question is unclear

The question is unclear to me. I understand we expect a triploid nucleus plus a diploid zygote (double fertilization) but I don't understand what (TTT + TTt), TT means.

Which book did the question come from?
Is there any preamble to this question?

Double fertilization

I am not so used to thinking about double fertilization in plants. In short, two pollens are involved. One fertilize a haploid gamete from the mother and the other fuse with two haploid gamete (polar nuclei) from the mother (triple fusion) resulting in a triploid "individual".

In my below answer, I am assuming that any two polar nuclei can fuse with the pollen. I am not sure this is true. If it is systematically polar nuclei resulting from the same meiosis II (that is they have the same parent cell after meiosis I), then t story is a little different.

How I understand the question

In my understanding, we are talking about a single locus with two alleles T and t. Both pollens are T. The mother is Tt.

Answer

There are two possible gametes from the female side T and t. Only one possible gamete from the male side T. Therefore, the diploid zygote is either

$\frac{1}{2}$ TT
$\frac{1}{2}$ Tt

, where the numbers indicate probabilities

Now, for the triploid nucleus resulting from the fertilisation of two polar nucleus from the mother and one pollen grain can be either

$\frac{1}{4}$ TTT
$\frac{1}{2}$ TtT or tTT
$\frac{1}{4}$ ttT

Now, I have no idea how that matches to the possible answers as I don't understand the notation.


What does the total membrane current vs time plot of an action potential look like?

Check out panel b for total current, panel c for K+ and panel d Na+ currents separated...

This is from this website: imageWebsite


What does units/mg mean for Streptavidin

16 units/mg means 16 units per milligram of protein.

Many companies, including Invitrogen, define 1 unit streptavidin as the amount of streptavidin necessary to bind 1 microgram of biotin.


How should species density be calculated for a clumped distribution?

To me, there are two issues that are mixed up here (if I understand you correctly). First, do you want to estimate the mean and variance for a statistical population (i.e. to characterize a larger population by independent samples), or do you want to calculate the actual density for a particular area, where you have counted all occurences in that entire area (but maybe divided the area into subareas out of convenience when counting)? This is not clear from your question.

In the second case, your second option of pooling counts and areas is suitable. However, then you have only calculated the actual density in that particular area (ignoring issues of detectability of the organism when counting), and you cannot draw any inferences about a larger statistical population.

If your aim is to draw inferences for a larger statistical population, a start is to calculate the mean and standard deviation (sd) of your sample. In that case, I assume that your samples are chosen randomly and independently from a larger statistical population. Your first option is then the right approach. However, since your samples have different sizes, you might want to attach more weight to larger samples, since they can be assumed to better describe the population average than smaller samples. This is called a weighted mean.

Generally, the weighted arithmetic mean is defined as:

$$\bar{x}_w = \dfrac{\sum_{i=1}^nw_ix_i}{\sum_{i=1}^nw_i}$$

where $w_i$ are the weights for each sample ($x_i$) and $n$ are the number of samples. Using this formula, you will arrive at exactly the same value for the weighted mean as you calculated in your second attempt (0.458), if you use the areas as weights.

The weighted standard deviation is a bit more problematic, in the sense that there doesn't exist one single standard way of calculating this. However, a commonly used formula is:

$$ \sigma_{w_1} = \sqrt{ \frac{ \sum_{i=1}^n w_i (x_i - \bar{x}_w)^2 }{ \frac{(M-1)}{M} \sum_{i=1}^n w_i } },$$

where $M$ are the number of nonzero weights. Other definitions of the weighted standard deviation can be found at Wikipedia: weighted sample variance.

Another version is defined as (called "reliability weights" on the wiki page):

$$ \sigma_{w_2} = \sqrt{ \frac{ \sum_{i=1}^n w_i (x_i - \bar{x}_w)^2 }{  \sum_{i=1}^n w_i - \frac{\sum_{i=1}^n w_i^2}{\sum_{i=1}^n w_i}}},$$

If I haven't made a mistake, these will give the standard deviations 1.15 and 1.22, using your data.

As for the biological interpretation, all calculations of average densities indicate a clumped distribution, since the coefficient of variation (CV) is larger than 1 (CV = sd/mean), but more so if you use a weighted mean. The CV using the arithmetric mean is 1.5, while it is 2.5-2.65 for the weighted mean, which is reasonable since you are giving more weight to the large area sample with a zero count. However, I should also note that you should be cautious about using a weighted mean when you have a strongly clumped distribution, since your run the risk that e.g. a large sample plot land on an area with no occurences, which might bias your density estimate. Generally, when you have a clumped distribution, you need to sample more intensively to get a good estimate of average density, and many small samples is often better than a few large ones.


Are these Gram stain substitutions acceptable?

I'm not a biologist.

From a chemist's point of view, these molecules should have similar polarity. Their structure is very similar, actually.

Considering your replacement rule is correct, I would say there wouldn't be much effect other than observing different colors. What is also plausible is that you'd have to reverse the interpretation of your results, e.g. methylene blue stains X, but crystal violet stains Y whereas carbol fuchsin stains Y and safranine stains X.

Was that clear?


can magnesium bicarbonate be absorbed in the mouth?

Technically, the human mouth do not absorbed anything. The human mouth is just a first line of defense mechanism against external microbial (In terms of saliva). If in terms of physical aspect, it just helps you to reduce food size and shape it for consumption.

Real absorption do not happen in the stomach neither. Stomach is where acids are used to break down your food and subject to higher lethal effect to kill microbial. The absorption only begins in the small and large intestine. (This is why drug delivery is such a hot topic in research labs).

To answer your question, yes. We need magnesium to survive and so we do absorb magnesium. In fact we can't live without magnesium, we need it for certain vital functions for our body to be normal. (Only in small magnesium amount, we don't need a lot of it).

As for bicarbonate, our body do not need it. In small amount, it is not toxic to our human body but in high volume, this would be a serious issue. When we breath, on cellular level, gas exchange occurs. Oxygen is supplied into our healthy cells while carbon dioxide is removed from our cells into our blood.

This is where it gets tricky, we do not store carbon dioxide in the form of gas when removing it via breathing out. We actually store carbon dioxide in the form of Bicarbonate in the plasma of our blood (Do note that its plasma, not RBC). When it is transported to our lung, this bicarbonate will be converted to CO2 and removed as we breath out. Hence, we do not absorb bicarbonate unless it reacted with some other elements or salt to produce some byproduct that we could use.

I hope you find this useful.

Regards

Price


Why would hawk moths evolve long tongues for Darwin's Star Orchid when there are other flowers around?

I think the key terms are niche and co-evolution;

Why would hawk moths evolve long tongues for Darwin's Star Orchid when
there are other flowers around [?]

Because the moths have grown a long proboscis as an adaptation to a certain niche. As you say, not much other species can feast on the flower's nectar, so it makes perfect sense to narrow your niche by elongating your proboscis, and reap the benefits of this little visited flower.
A niche is

[T]he range of environmental conditions in which a species can exist.

As the University of South Africa explains:

One important part of the idea of the niche is that it is controlled
by how the species exploits resources in its environment.  If there
are two species living together and exploiting the same resources,
then one will usually be worse than the other at doing this –
eventually, that species will disappear because the other species will
outcompete it. However, species can live together because they
exploit different resources or because they exploit the same resources
in different ways.  These species then have different niches, even
though they occur in the same place.

Then how would the flower benefit? Now I'm going a bit more into a hypothetical explanation, but flowers need cross-pollination to reproduce and genetic mixing. If a plant species can bind a certain pollinating species to itself, it can make sure that that pollinating species only forages on that particular species of plant. Hence, that plant species can ascertain that the pollinating species carries only the right pollen and therefore make sure the transferred pollen is from the same plant species. This is beneficial, as pollen from other species won't pollinate them.
It's all a matter of co-evolution, in this case of two mutualistic species, nicely and succinctly explained by the University of California, Berkeley:

The term coevolution is used to describe cases where two (or more) species reciprocally affect each other's evolution. So for example, an evolutionary change in the morphology of a plant, might affect the morphology of an herbivore that eats the plant, which in turn might affect the evolution of the plant, which might affect the evolution of the herbivore...and so on.
Coevolution is likely to happen when different species have close
ecological interactions with one another. These ecological
relationships include:

Predator/prey and parasite/host
Competitive species
Mutualistic species

The hawk moth Xanthopan morganii praedicta pollinates the Madagascar star orchid (Angraecum sesquipedale) with its long proboscis. source: Encyclopedia Briattanica


How Do White Blood Cells Learn? Or Do They?

So while some kind of a biological database might have been an evolutionary option, the way we evolved is different from this. Rather than 'planning' what diseases could be recognized in the environment and recording this, our bone marrow constantly pumps out naive B and T cells that have a randomized receptor on them. The effect of this is that every new B and T cell that your bone marrow makes will recognize a unique, random protein sequence, and you will have billions of these cells floating around in your blood circulation at any given time. These cells however will only float around in circulation for a short period of time before dying and being replaced by other cells with new random sequence receptors.

When you get a vaccination, you are injecting in specific protein sequences from a specific pathogen. As these injected protein sequences circulate through your blood they will eventually bump into a B or T cell that has a receptor that recognizes them. When this happens, the B or T cell will now start to divide and give rise to long lasting memory cells that express the exact same receptor and will therefore recognize the exact same protein sequence again in the future. These cells will float around in your blood for most of your life and make you 'immune' to the recognized pathogen. When you get reinfected with the same pathogen or the pathogen to which you were vaccinated these memory cells will rapidly divide upon recognition of the pathogen and give rise to a large number of effector cells that eliminate the pathogen before it can 'make you sick'.

What is really cool about this is that because each T or B cell carries on it a receptor that recognizes a random protein sequence, you currently have in you B and T cells that would recognize a protein that does not even exist on Earth, but might exist on Mars or somewhere else in the Universe. This makes our immune system quite valuable because any protein that nature creates for all of time anywhere in the universe will still be recognizable by our immune systems.


Is it possible that there are two people in the world who belong to a different species?

At the beginning, the population of the parents who we are talking about should be made more specific. Let's limit it to adult, healthy individuals (let's skip pathologies, various kinds of random body injuries, personal sexual preferences and close relatives).

From the descendants group, let's also exclude children who would die from random causes, body injuries (unintentional :-( and intended :-((( ), genetic diseases, etc.In addition to the genetic variation (A global reference for human genetic variation), epigenetic variability (Worldwide patterns of human epigenetic variation) should also be taken into account.

If we give the most popular definition of a species (and there are very many of them), as individuals capable of giving fertile offspring, of course all humans belong to one species. Contrary to popular opinion, we are similar to one another like drops of water.


Does antibacterial soap work chemically?

What the comments are trying to say might go something like this.

The antibiotic triclosan that's used in almost all 'antibacterial' products works pretty quickly - by interfering with several processes in the bacterial and fungal membrane.  It doesn't need much more than contact to work.

That being said, the longer your exposure to the antibiotic, the more thoroughly it will work.  Triclosan can penetrate the blood stream through the skin.  If you have soap suds scrubbing may or may not get the triclosan into more contact with a greater surface area as it diffuses into the skin, but probably won't affect the substantial effect it has killing surface bacteria and fungi/yeasts.

Its worth noting that the FDA doesn't recommend the use of antibacterial soap or other antibacterial products.  Soap itself is a powerful agent for killing bacteria and other microorganisms and biocides like triclosan probably encourage the emergence of antibiotic resistant strains which present a medical risk to people.


How it is possible that blood group shows that a person is not the son or daughter of their parents?

Each person has two alleles for the blood type. The two A and B alleles are dominant. So, you don't need A/A to end up with blood type A, it could also be A/O. Having both A and B results in blood type AB. Having none of these, results in blood type O.

Following these rules, from parents being AB and B (genetically either B/B or B/O) you would expect these possible blood types for their children:
- A/B
- A/O
- B/B
- B/O

The Rh factor (positive or negative) is inherited similarly. The positive allele is dominant, so genetically +/+ or +/- would be positive, only -/- is negative.

There is a rare case of a "cis AB" mutation, where the A and B antigens are in just one allele (wiki, paper). Then the genetic alleles of an AB type could be AB (in one allele) and O.
The children of the couple could then be
- AB/B
- AB/O
- B/O
- O/O

So, there would be two possibilities for the case you describe.

The parents are not the biological parents of the child.
The mother is cisAB/O +/- and the father B/O -/-

edit: or a third way would be of course some de novo mutation in the child, resulting in the loss of A/B from the mother

edit2: maybe to answer your actual question "How can a child not be the child of its parents?".. adoption, in-vitro fertilization with donated eggs and/or sperm from other people, mix-up in the hospital..


What kind of spider is this from Nova Scotia, Canada?

That is an Araneus diadematus, a kind of garden orb-web spider.

Orb-weaving spiders are quite common, and can be found nearly anywhere in the world, excluding Greenland. The following is a distribution map for the species A. diadematus, of which, as you can see, is mostly contained to North America & Canada.

Dark gray: present; Light gray: no record. (source)


Effect of soap on the survival of non-enveloped viruses

Yes, hand washing with soap is effective at removing non-enveloped viruses. Here is a study showing that washing with soap is effective at disinfecting norovirus, which is a non-enveloped virus: https://aem.asm.org/content/76/2/394


Have we succeeded in building a living organism from inanimate material?

It depends on your definitions.

we have built organisms with an entirely synthetic genome. basically the genome was "printed" from a computer file and inserted in a cell which had its DNA removed, it continued to function and replicate just fine.

We have not built a modern cell from scratch, mostly because even the simplest living cells today need to compete with other more complex cells so they are still extremely complex in their own right. The simplest possible cells would never survive in the current world due to competition and "predations" so we don't know exactly how it has to be arranged to function.

You may want to look at the much more modern experiments like the Urey-miller one, Jack Szostak has been trying to work up to what you are looking for, his lab has created RNA from abiotic (non-life) sources.
This is probably the closest since we know a slightly longer sequences of RNA can be self-replicating. And Harvard scientists have put manufactured self replicating RNA in an artificial lipid capsule and gotten it to function.
 Getting the right sequence of RNA to form by itself is possible but would probably need several billion repetitions of the first experiment.


Your question already answers a fundamental point: namely that there are several distinct quantitative measures that can be associated with enzymes (the list could also be extended, and you will discover more in biochemical textbooks...).
If experimentally or theoretically accessible, one additional important quantity is the formation of product over time divided by biomass ( e.g.: Jacob et Monod 1961)


How increased potassium intake increases sodium excretion?

That's because cell membrane could have a protein, called Na/K pump who's able to regulate the level of Sodium/Calcium using the energy gained by the hydrolysis of a phosphate bond from ATP.


Why do wild lizards often tap with their front leg?

I found a paper(1) about the 'tail in the mouth' behaviour in the whiptail lizard, Cnemidophorus ocellifer:

Every time that the female moved, the male followed her. During these periods, he often maintained physical contact, covering her hind legs and base of tail region . The male also performed a series of tongue-flicks on the female's back during this activity. During the observation, the female twice executed a sequence of two or three sinuous, figure-eight movements, which were confined to a small area, and after which, the female moved away. After each movement, the male remained motionless for a few moments and then resumed following her while foraging. After 45 minutes and nearly 15 m from their initial positions, the pair entered in dense underbrush, where we could not continue to observe them. While we observed the pair, there was no agonistic encounter between the accompanying male and other males for access or copula with the female.

The paper continues to explain this behaviour as simply a mating strategy:

Two conditional mating strategies have been described for teiid males (Zaldívar-Rae & Drummond 2007).  1) In consensual copulations,
the male courts the female, slowly circling her for several minutes,
then straddling her and copulating; this strategy is often performed
by a male companion, and thus is linked to accompaniment.  2)
Opportunistic copulations are not preceded by courtship, and are
characterized by a male chasing and holding a foraging female, and not
accompanying her after copulation (Zaldívar-Rae & Drummond 2007).

The 'taping the surface they are on' seems like an attempt to induce vibrations, which is a method of communication.(2)

Some chameleon species communicate with one another by vibrating the substrate that they are standing on, such as a tree branch or leaf. Animals that use vibrational communication exhibit unique adaptations in morphology (i.e., body form) that enable them to detect vibration and use it in communication. These include unique adaptations in ear and jaw morphology that give the animal direct contact with the surface they are standing on, and enable them to detect subtle vibrations. Lizards that live on substrates that can be easily moved (such as thin tree branches or leaves) are probably more likely to use vibrational communication than lizards that live on substrates that do not transmit vibrations as easily, such as the ground or thick tree trunks.

1- https://www.scielo.br/scielo.php?script=sci_arttext&pid=S1676-06032011000400031#:~:text=The%20most%20commonly%20reported%20mating,Bull%202000%2C%20Ribeiro%20et%20al.
2- https://en.wikipedia.org/wiki/Lizard_communication


Enzymatic Protein Deglycosylation of TCL

So we went ahead and did this.  The efficiency was much lower, which you might expect, and dehydration did aid the process.  We found that taking raw lysates and running them through the linked protocol, had about ~20% the efficiency of conducting it on purified protein.  I assume the majority of the loss was due to reagents being expended on proteins that were not of interest.


What are these tiny, swarming, jumping bugs?

Very useful image updates! These are actually not arachnids but hexapods called springtails (order Collembola). Although springtails are often very tiny and hard to see without a lens, you happen to find some "larger" specimens. Specifically, these appear to be some species in the family Dicyrtomidae.

 Credit: M. Bertone (source)

Your species resembles the image of Dicyrtomina minuta seen here or Dicyrtomina saundersi seen here (though I can't be certain of these source's accuracy).

In general, springtails usually feed on decaying matter, and -- you guessed it -- they're known for their ability to jump!

  Springtails are so-called because they have a unique structure, the furcula, that allows them to jump for considerable distance relative to their tiny size. [source].

 Springing mechanism of a generalized springtail. Credit: Marianne Alleyne [Source]

According to NC State Extension:

  Rarely springtails may become exceedingly abundant and may congregate in heaps several inches high on driveways, sidewalks and poolsides.

Collembola.org has many excellent close-up images as well as detailed descriptions of nuances and sexual dimorphism seen in the Dicyrtomina group of springtails.


Why can't ciliary muscles in the human eye relax like other muscles?

First of all, I should correct some points that were misunderstood.
Don't change the question because this will lead to confusion.

"The way the lens becomes flat is by using spring-like connective tissue called choroids that pull it taught."

In classic ophthalmology you don't need to think about choroid in direct relation to accommodation: choroid is a sponge-like layer between the sclera and retina and in general it is consisted of blood vessels. The anterior part of the choroid continues anteriorly to became a ciliary body which in turn contains ciliary muscle - one circular muscle per eye. From the ciliary body/muscle spread zonules (zonule fibers) and they are fixed on the lens equator.

Physiology: contraction of ciliary muscle causes zonules to became loosen and "free" the lens to became more convex and move the focus anteriorly (not choroid contracts itself). If the ciliary muscle relaxes then zonules are tighten up and the lens consequently becomes more flat (less convex) moving the focus posteriorly. In other words you can say it in the terms of depth of focus - convex lens gives less depth, less convex gives more depth of focus.

Thus, the classical choroid layer does not perform any action (look at your choroid related link - there are almost nothing about accommodation).

"Permanent state of contraction" can be physiological (=normal) as well as abnormal one, and it is very common in some conditions (muscles spasms). One example is priapism, where corporal smooth muscle contraction causes permanent and dangerous penile erection which can be medical emergency (priapism is by far more complex, so take the explanation like a metaphor).

If we refer to "accommodation spasm" there is analogy to "muscle spasm" (and partially to priapism), but I should state we believe that spasm of ciliary muscle exists - since we don't see it directly. Probably (and take this sentence as speculation, since I cannot give you reference right now) the causes of this is not a muscle spasm itself, but the state of zonular fibers which cannot come back to their base state. I like the example with iron rod - if you will contract it fast and many times, at some point it can be "loosen" as well as fractured (and probably it does happens to zonules too). Probably (I say "probably" to underline the point we do not exactly know this), the "accommodation spasm" is partially misname and in future the investigations will clarify that.

Probably, you will learn some interesting facts from definition of "pseudoexfoliation" syndrome, but I do not explain it here because it is not related directly to the question. From wiki "has been known to cause a weakening of structures within the eye which help hold the eye's lens in place, called lens zonules"

Another example for analogy for continued "spasm" is the situation when one should care something heavy for a long distance without releasing the grasp - finally one can get not only spastic contraction but also severe ischemic damage to the fingers.

Considering your case, you should know about pathological (degenerative) myopia where the eye expands posteriorly and consequently the focus is before the retina which should be corrected by minus lenses. It is well known fact that myopic eyes have longer axial length then normal eyes. Probably, it is your case.

So, as you can see, the answer to your question is not a clear cut, but assumption. The ciliary muscle does can relax, but probably the problem is more complex then only ciliary muscle related issue.

PS The image you reposted is a little bitconfusing one and is not exact. This one is classical and gives better understanding of the anatomy -


6kDa are usually enough to seperate two proteins in my experience. Try the other way, use a 7 or even 8% gel. They run longer but have a higher separation capacity. If you look at this figure from the LabFaQ, you see that you can use a higher percentage gel:

The other thing are the antibodies: Where are your isoforms different? 6kDa are 55 to 60 amino acids more for the long form, so there should be enough possibilities to make specific antibodies.


How quickly is antibiotic resistance lost?

Antibiotic resistances in bacteria is commonly encoded by extrachromosomal DNA, the plasmids. These are circular pieces of DNA, which are much smaller than the hosts genome and which replicate independently from it. See the image from the Wikipedia:

These plasmids can be transfered between different bacterial cells, which then also get resistant. Plasmids are divided between daughter cells, when the parent cell divides. One of the few exceptions seems to be Mycobacterium tuberculosis, which does not seem to carry plasmids but also develops resistances. It has been hypothesized that they contain extrachromosomal single-stranded DNA ("Does Mycobacterium tuberculosis have plasmids?")

Regarding your question: Plasmids which carry antibiotic resistances will only disappear, when the antibiotic is not seen for a while, since the cells, which don't carry it, have a growth advantage over cells who are still carriers (since they save the energy of forming the plasmid). However, these resistance plasmids are nothing new, evolutionary speaking. They appeared as a countermeasure against fungal toxins.

In the lab, bacterial strains loose plasmids within a few days, when not kept under selection pressure according to my experience. There are a few paper who looked into it:

Natural selection, infectious transfer and the existence conditions
for bacterial plasmids.
The persistence of parasitic plasmids.
The evolution of plasmid-carried antibiotic resistance


How and why did mouth and nasal cavity evolve separate?

Neither the nostrils nor the mouth originally evolved for breathing.  Fish have (two pairs of) nostrils which they use to smell and mouths which they use to eat, but they breathe through their gills.  Some lobe-finned fishes (the ancestors to tetrapods) evolved a connection between the posterior nostrils and the oral cavity called choanae.  A fossil called Kenichthys is a transitional form in this development.  The evolutionary reasons behind this development are not particularly well understood.  (This should not be surprising when discussing something that happened in the Devonian.  It's only recently that the discovery of Kenichthys ended the controversy of whether chonae in tetrapods are homologous to posterior nostrils in fish.)

Basal reptiles have nostrils and mouths and can breathe through both of them, but do not have a separation between the oral and nasal cavities.  The next important development is a secondary palate (which separates the nasal and oral cavities).  This allows animals to continue breathing while swallowing food.  Animals without such a separation must hold their breath while swallowing.  This ability is certainly useful in many situations, and unsurprisingly several solutions to this problem have evolved in different lineages.


It is not a pseudoscorpion as those would have 8 legs and then the two front large pincers. This is most likely a kind a jumping spider where the two large front legs count as two of the 8 legs.
Depending on your geography (not given in the question), this looks to resemble a jumping spider in the genus Chalcolecta (or some regional variant of that based on where you are). Hard to see any detail (like eyes and body segments) from your photos. But have a look at some of these and see if any of them match your specimen. Here are some pics of C.prensitans and C.simon.


How do female hormones cause blood to clot?

These combination contraceptives contain two substances: Estrogen and progestin (a synthetic progesterone). Both are used together to overcome the negative effects of single substance drugs as acne or sickness.

The risk for blood clots has been known for quite a while (see reference 1 and 2) and is generally caused by raised levels of clotting factors (especially VII and X), increased plasma fibrinogen, increased platelet aggregation in the blood and reduced activity of antithrombin III (which inhibits coagulation). This can happen as well in pregnancy when the factors are naturally elevated (that's the way these contraceptives simulate pregnancy to the body). The paper shows this nicely for two of the factors of the blood coagulation cascade (factor VII and X):

This risk is relatively rare, it affects only about 1-5 in 10.000 women, but is still not negligible. The risk is much higher in persons with defects in the blood coagulation cascade. Compared to this, pregnant women have a risk for blood clots of 5-20 per 10.000 women (for details see here).

Blood coagulation is really fine tuned to ensure proper function when necessary but no blood clotting when not. Basically activating and deactivating hold a balance, as depicted in figure 1 from reference 3:

Smoking now disturbs this balance by inhibiting fibrinolysis and promoting the accumulation of fibrin and pushes it more to the site of coagulation. What causes the problem here is the elevation of clotting factors in combination with the disturbance of the balance between activation and inhibition of clotting. See reference 3 for the details.

This effect seems to be limited to high concentration single estrogen and estrogen/progestin combination preparations, while there seems to be no such effect in progestin single preparations (although data is limited here). There is also a significant difference in the type of estrogen used. See references 4 and 5 for more details.

The mechanism of how this works is relatively straightforward. The estrogen binds to the estrogen receptor on the cell surface and forms a receptor-ligand complex. This leads to signalling inside the cells which finally results in changed gene expression. Additionally the complex can be internalized by the cell. Inside the cell this complex can bind to the so-called "hormone response element" and also regulate the expression of genes. This is explained in detail for Factor XII in reference 6 (and works like this for other parts as well). See the image for illustration (from reference 7):

References:

Relation between oral contraceptive hormones and blood clotting
Use of combined oral contraceptives and risk of venous
thromboembolism: nested case-control studies using the QResearch and
CPRD databases
Hemostatic effects of smoking and oral contraceptive use
Coagulation effects of oral contraception.
Lower Risk of Cardiovascular Events in Postmenopausal Women Taking
Oral Estradiol Compared With Oral Conjugated Equine Estrogens
Molecular basis of estrogen regulation of Hageman factor XII gene
expression.
Estrogen synthesis and signaling pathways during aging: from
periphery to brain


Expected time for a neutral allele to reach a frequency of $p_1$ when starting at frequency $p_0$

Plain English Answer:

I have written a computer function which simulates neutral evolution to solve this problem. It's not an exact mathematical answer, but it is basically the same approach as Kimura and Ohta took in (the second half of) their paper, except that my computer is more powerful than their one, so I could get far more precise estimates by simulating more populations than they did.

Figure One is a lattice plot of the relationship between P0 and the expected time to reach P1, for different values of P1 (by column) and different population sizes (by row). It is clear that the same relationships between P0, P1 and expected time to get from P0 to P1 are seen in every population size, but with larger populations, you should expect a longer time to get from P0 to P1.

When P0 and P1 are close together, you generally expect a smaller time to get from P0 to P1 than when P0 and P1 are far apart. You might think of this as a rule like 'it takes a longer time to travel further'. Expected time taken to get from P0 to P1 is smaller when P0 and P1 are on the same side of 0.5 as each other and P1 is further from 0.5 than P0 is, than when P0 is further from 0.5 than P1 is. You might think of this as a rule like 'it is quicker to travel when you're closer to fixation or extinction, than when you're in the middle frequencies'.

Figure One: Expected time for a neutral allele to go from frequency P0 to frequency P1, given differences in P0, sub-plotted by P1 and population size. Modelled frequencies of P0 and P1 are 0.1, 0.3, 0.5, 0.7, and 0.9. Modelled population sizes are N = 10, N = 50, and N = 100. Each sub-plot represents one combination of P1 and population size, with P1 increasing from left to right, and population size increasing from bottom to top. All expectations are estimated from 10,000 simulated populations.

Some populations take longer than others to go from P0 to P1. Generally, most populations take a small number of generations to reach P1, and a smaller number take a long time – but a very few can take a very very long time.

I've attached my code, so if you know how to use R you can use it to estimate the expected time to get from P0 to P1 for any combination of P0, P1, and population size.

Additional details and assumptions for the technically inclined:

Relevant theory:

In a diploid, sexually-reproducing population of size $N$, there are $2N$ copies of a given locus. Each locus is occupied by some allele. All variation at our locus of interest is selectively neutral. For our purposes, we can consider that each locus is occupied either by our allele of interest ($A$), or another variant ($a$), ignoring variation in the 'other' alleles. The number of copies of $A$ in the population at the start of the process, $A | t=0$, is given by  $2N*P0$.

Let us assume that population size is constant ($Nt+1 = Nt$ for all $t$), and that mating is random. Let us further assume that generations are distinct. Let $t = 1$ be the first generation born, and so on.

The expected number of copies of $A$ at time $t+1$ then follows a binomial distribution:

$At+1$ is distributed $Binom(2N, At/(2N))$

Since we have a transition rule for $At → At+1$, it is a fairly simple matter to simulate populations undergoing this form of evolution. I have written the R function neutralFPT to carry out this simulation and estimate the proportion of all populations which reach $P1$ at some point in their history, the expected time for a neutral allele to reach $P1$ from $P0$, given that it will reach $P1$, and the distribution of lengths of time taken to reach $P1$, given that a population will reach $P1$. The script is given in the final section of this answer.

Probability densities of first-passage times:

Probability densities of first-passage times over plausible values of $P0$, $P1$, and $N$ follow a similar structure – unimodal near the left margin, with a long right-tail of longer first-passage times (Figure 2).

Figure 2: probabiltiy-densities of first-passage times from P0 to P1 under different values of P0, P1, and N. A: P0 = 0.5, P1 = 0.9, N = 50; B: P0 = 0.9, P1 = 0.5, N = 50; C: P0 = 0.5, P1 = 0.9, N = 500.

Function: neutralFPT, with examples of use.

 ## this function simulates the number of generations taken for a
 # neutral allele to go from a starting proportion, P0, to a final
 # proportion, P1, in a random population, given that it will at some
 # point reach P1. Allele frequencies are not modelled after the point
 # when P1 is reached.
## neutralFPT was generated in response to Stack Exchange user Remi.b, at
 # http://biology.stackexchange.com/questions/30812/expected-time-for-a-neutral-allele-to-reach-a-frequency-of-p-1-when-starting-a
## neutralFPT was written by Shane Baylis, 2015
 # for R version 3.2.2

neutralFPT <- function(P0, P1, N, niter) {

tOut <- c(rep(NaN, niter))
 # create a vector of blank t-values
statOut <- c(rep(NaN, niter))
 # create a vector of population status values (reached P1, or didn't)

if(P0 == P1) stop("P0 and P1 are set to the same value!")
if(P0 == 0 | P0 == 1) stop("P0 is set to zero or one, so its frequency
                           cannot change!")
if(P0 < 0 | P0 > 1) stop("P0 must be between zero and one")
if(P1 < 0 | P1 > 1) stop("P1 must be between zero and one")
## work out whether you're heading upwards or downwards
if(P1 > P0) { # i.e., our target is above us
    for (i in 1:niter) {
        NAllele <- round(2*(P0*N))
        Target <- round(2*(P1*N))
        t <- 0
        while (NAllele < Target && NAllele != 0 && NAllele != 2*N) {
            t <- t+1
            NAllele <- rbinom(1, 2*N, (NAllele/(2*N)))
        }
        if(NAllele >= Target) {
            statOut[i] <- 1 ## 1 indicates that P1 occurred
            tOut[i] <- t
        }else{
            statOut[i] <- 0
            tOut[i] <- Inf
        }
    }
}else{ ## i.e., our target is below us
    for (i in 1:niter) {
       NAllele <- round(2*(P0*N))
       Target <- round(2*(P1*N))
       t <- 0
       while (NAllele > Target && NAllele != 0 && NAllele != 2*N) {
           t <- t+1
           NAllele <- rbinom(1, 2*N, (NAllele/(2*N)))
       }
       if(NAllele <= Target) {
           statOut[i] <- 1 ## 1 indicates that P1 occurred
           tOut[i] <- t
       }else{
           statOut[i] <- 0
           tOut[i] <- Inf
       }
   }
}
successes <- sum(statOut) # the number of populations in which
                          # P1 was reached
propSuccesses <- successes / niter # the proportion of populations
                                   # in which P1 was reached
successTimes <- subset(tOut, statOut == 1)
expectedFPT <- mean(successTimes)
medianFPT <- median(successTimes)
outs <- list(successes=successes, propSuccesses=propSuccesses,
             successTimes=successTimes,expectedFPT=expectedFPT,
             medianFPT=medianFPT, trials=niter)
return(outs)
} # function close

## neutralFPT examples #################################################

sim <- neutralFPT(0.5, 0.9, 500, 10000)
sim$expectedFPT # Numeric. shows the expected (i.e., mean) first-passage
                # time from P0 to P1, in generations, given that a
                # population reached P1.
sim$medianFPT # Integer. Shows the median first-passage time from P0 to P1,
              # in generations, given that a population reached P1.
sim$propSuccesses # Integer. The proportion of simulated populations which
                  # reached P1. Other populations reached fixation
                  # or extinction of A without reaching P1.
sim$successTimes # Vector. The number of generations taken to reach P1,
                 # for all populations which reached P1.
hist(sim$successTimes, xlab="First passage time (generations)",
     main=paste(sim$successes, "successes from", sim$trials,
         "populations"))  ## histogram of first-passage times

PZero <- c(rep(c(0.1, 0.3, 0.5, 0.7, 0.9), 15))
POne <- c(rep(c(rep(0.1,5),rep(0.3,5),rep(0.5,5),rep(0.7,5),rep(0.9,5)),3))
PopSize <- c(rep(10,25),rep(50,25),rep(100,25))
FPTs <- c(rep(NaN, length(starts)))
testFrame <- data.frame(PZero, POne, PopSize, FPTs)
testFrame <- subset(testFrame, starts != ends)
for(s in 1:nrow(testFrame)) {
    sim <- with(testFrame, neutralFPT(PZero[s],POne[s],PopSize[s],10000))
    testFrame$FPTs[s] <- sim$expectedFPT
}  ## estimates expected first passage times from P0 to P1 for a variety
    # of values of P0, P1, and population size. Outputs the estimates to
    # a table called testFrame.

require(lattice)
with(testFrame, dotplot(FPTs~PZero|POne*PopSize,
   main="Expected First-Passage Time by P0, P1, and Population Size",
   xlab="starting frequency (P0)")) ## generates the lattice plot used as
                                     # Figure One.


Wikipedia actually has a note on the evolution of kissing.  They point out that there are grooming behaviors such as licking and social behaviors like dogs touching noses in many species even insects.  They note that it is not decided at all whether kissing is learned or from some sort of instinct.  They also mention that its reminiscent of feeding behavior common in birds (and other animals) where food is pushed down the throats of young.  (try thinking about that next time!)

I seem to remember though that there are some culture which do not kiss. with their lips at least. This would favor kissing as a learned behavior, but these cases are very rare and isolated peoples and it might be simply a taboo to talk about kissing with researchers or at all, which is a hazard of that sort of work.  In addition, bonobos, one our our closest primate cousins, do kiss frequently with the lips, as a social and intimate gesture and the parallels with most human cultures are difficult to ignore.


What is the reason for having an extra recognition site for a restriction enzyme?

The scenario in your question can be explained if the "extra" recognition site mapped very close to another recognition site for the same enzyme.

For example, if there were 2 EcoRI sites separated by between 0-50 bp of plasmid DNA, then depending on the type of gel being used, the resulting tiny DNA fragment generated could be difficult to detect (either because small fragments run off the bottom of the gel, or because they don't resolve well unless the gel contains a higher percentage of agarose or acrylamide).

Similarly, depending on the size of the adjacent fragments in the various digests, and this assay's limitations on estimating fragment sizes, you might not detect that an "extra" fragment was generated, and "missing".


Corpus luteum during the luteal phase and gonadotropins

Lots of questions, so I'll break them down one at a time:

  Does the corpus luteum operate independently of the hypothalamic-hypophyseal-ovarian axis?

The corpus luteum does depend on intact pituitary signalling.  Hypophysectomy at the beginning of lutenization will result in cessation of corpus luteal growth and subsequent drop in progesterone; in essence, the corpus luteum won't grow and function properly in the absence of pituitary hormones.  In some species, estradiol is needed, so intact gonadal steroidogenesis is also required.

  In an ovarian cycle where there is no pregnancy, do FSH and LH affect the corpus luteum?

Elaborating on the above, yes pulsatile secretion of LH is required to fully develop and maintain the corpus luteum (not so much for FSH).  Other pituitary hormones, such as growth hormone are also involved.  In pregnancy (or pharmacologically), a large dose of hCG can sustain the corpus luteum.  hCG and LH are homologous.  Depending on the species, prolactin and estradiol are also required.

  Is it true that the corpus luteum degenerates because of low FSH and LH levels?

The corpus luteum degenerates (luteolysis) because of prostaglandin produced by the uterus.  In the absence of a uterus (and therefore prostaglandin), luteolysis is delayed.  It is reported that estradiol from the next batch of follicles triggers oxytocin release by the posterior pituitary and subsequent release of prostaglandin and thus is the penultimate cause of luteolysis.

  Why doesn’t the corpus luteum degenerate immediately after the LH surge, then, whereafter FSH and LH levels are so low?

As described above, it is not low FSH and LH that cause luteolysis.

  If not, then why does the corpus luteum degenerate?

Described above.

Source: http://physrev.physiology.org/content/80/1/1.long


I assume you mean "why can't glutathione, NAC .. be added"

From lef.org

  There is one problem. The FDA prohibits combining existing drugs and
  dietary supplements unless a New Drug Application is filed, tens of
  millions of dollars of clinical studies are performed, and the FDA
  agrees to allow the combination to be sold. The whole process can cost
  upwards of $100 million and take a decade to complete.

It's sad that would would be very likely an effective solution for the deaths and liver damage is not available or made more widely known.

Only about 10% of acetaminophen is metabolised through the glutathione conjugation pathway via NAQBI (the other 90% is direct sulfation and glucuronidation of acetaminophen). Many people take NAC supplements regularly (I used to).  While high does can have some side effects, a typical supplement level dose of a few hundred milligrams daily are well tolerated.


What are the major differences between good study habits for biology vs mathematics?

I started in cell and molecular biology, but moved to applied math and computer science, so perhaps I can give my thoughts.

Personally, I found that biology learning was more about big ideas and visualization. The first is because biology has an extraordinary amount of details (e.g. Molecular signaling pathways, biochemical properties of different molecules, the location of different foramen in certain fossils, etc...), so it is truly impossible to remember them all. You should focus on learning what to look up, not what is actually occurring. Something you work on will be gradually memorized on its own, so don't spend effort memorizing things you can look up (you're not an undergrad :) ). So don't remember that histone acetyltransferases use acetyl-coa to act upon the NH3+ groups of lysines. Just remember that those enzymes modify chromatin in a way that alters transcription, thus changing the cell and its behavior. The second (visualization) is because it is very hard to understand biology without pictures! So use them, not text (no kobayashi and nomizu style). Mathematicians like symbols but (at least in the molecular case) there are too many of them (and they are mostly useless names... e.g. P53). Much of biology is about seeing  visual results (blots, fossils, medical images,...) and interpreting them.

Note that (I think) the first suggestion is harder in biology than in math, because math partitions naturally into theorems, corollaries, lemmas, and their applications (roughly in order of importance of what you need to know :) ). Biology as a field is more of a fast moving chaos of  observations and changing inferences. But of course there is a constantly growing core of the field that is not in flux.

One good thing about biology is that one can be an expert in one area but know little about most others. Math is a little more intertwined. So there's no need to read a "general bio" book. Just read an intro book to your target topic (e.g. Ecology, evolution, cell bio, molecular biophysics, bioinformatics ...). They will cover the relevant parts of other fields, usually. I know genetics experts who know basically nothing about cell trafficking for example. But you will definitely need some background to read the latest literature (i.e. Don't skip straight to Cell papers).

One issue that occurs throughout science, but also in math, is that learning is a process of improving models. In math, we might start with linear algebra, then basic manifolds, and eventually with, say, finsler spaces. In physics, we go from Newton to Einstein. In biology, we start with a basic model and set of rules, but gradually add exceptions and details to it. I think this is where much confusion can arise, because things that were correct in the simplified model might be wrong in the better, more complex one.

Also, models are being updated at an insane rate in biology. Often that means that previous models were wrong (though the evidence underpinning them is not); hence definitions and results might change over time! Science improves over time, and this is a good thing. Of course, in math, once something has been proved, it will never change. (Although definitions, or at least notation, in math can be very inconsistent too). Of course, if there are inconsistent definitions, you can ask here and see what people think. I will agree that biologists are less concerned about detailed rigor than being correct overall. Generally scientists will either define such things themselves or cite a reference with their chosen definition.

My suggestion for your question is to learn the basic widely accepted definitions first, then go to the literature. Often it is the case that different groups think different things. Most likely, one or both will be proven wrong eventually. Each paper is likely to be internally consistent; the only ambiguity is usually in areas where no one knows the correct answer or interpretation. Two groups in conflict usually have reasonable hypotheses consistent with the evidence, and if they can't decide how to mesh their ideas, probably we can't either. So don't worry about it too much.

So when a topic has multiple interpretations that are possibly true, use your math background and consider it from a Bayesian perspective :) most likely all the interpretations are at least partly true, and have some non zero probability of being true. And as you read more papers, update your posterior. :)

Also, don't worry about talking to biologists (as the other commenter states). In fact, among the sciences and engineering fields, my opinion is that biologists are on average the friendliest and least arrogant :)


What is the optimal sampling method for modeling of microalgae growth?

For these kind of experiments, especially when you talk about modelling, it can be worth to set up a chemostat or at least a turbidostat. An example of such a study can be found in: Simultaneous growth and neutral lipid accumulation in microalgae by Klok et al. (Pubmed).

Alternatively you can use lipid dyes such as Bodipy but these are often very tricky to get to work and they might not penetrate in your Chlorella. Nile Red in any case is almost impossible to get working quantitatively despite it being used quite extensively, see details in this publication. Be very cautious when going down this route.


Can plants survive indefinitely without external supply of gases at compensation point?

If the plant is growing the system will fall out of equilibrium due to more carbon going into biomass than oxygen.


difference between "Petri dishes" and "Petri plates"?

Typically you'll hear either "petri dishes" or "plates", not usually "petri plates". Either way though people will understand what you're talking about.


Can crossing over between X and Y chromosome of sex chromosomes take place?

Yes, it can, but it is rare, and typically only in the pseudoautosomal region, meaning those sections on the X and Y chromosome that have homologous genes.
The reason it's rare and more difficult is that the DNA does not match as well, so the chromosomes have trouble interacting along the length of the chromosome.  Furthermore, there are less recombinant zones available.

Sources:

Kauppi, Liisa, Marco Barchi, Frédéric Baudat, Peter J. Romanienko, Scott Keeney, and Maria Jasin. 2011. Distinct properties of the XY pseudoautosomal region crucial for male meiosis. Science 331 (6019): 916-20.
Hinch, AG, N. Altemose, N. Noor, P. Donnelly, and SR Myers. 2014. Recombination in the human pseudoautosomal region PAR1. Plos Genetics 10 (7): e1004503.


Why do cows (and other hooved animals) need a hierarchy?

Could not fit in a comment...

There are several issues with your question.

The correct question is not why such species need something but rather why it occurs in this species. In other words, why did a hierarchy evolved in a given species?
It is unclear to me why your are interest in cows (or other grazing animals) rather than any other species that has some kind of hierarchy and therefore your question is a bit unclear.
There are several questions in your post. A post should always be limited to one question.
I personally have never heard of the concept of "advertised fitness". How do you define it?
I am not sure how much you are interested in the evolution of social traits and especially about reputation and how much you are interested in Machiavellian intelligence. In any case, you may probably want to read about the evolution of social traits (kin selection, it may take you some time) and about the social selection pressures for the evolution of cognition, such as Machiavelian intelligence.

For all those reasons I vote to close. But I hoped that those comments can help you to clarify your post and to seek for more information.


It is a species of silverfish such as Ctenolepisma longicaudata or Lepisma saccharina for examples (thanks @RHA for correction in comments).

Silvefish are well known very resistant pest typically found in washrooms and sometimes in kitchens. They are not directly dangerous but can cause property damage. Here is a webpage giving advice on how to get rid of them


Relation of conformational entropy and protein folding

This question is an example of important general problem in chemical biology: “How does an ordered system arise without violating the second law of thermodynamics?” Berg et al. address this in the following manner:

  The Second Law of Thermodynamics states that the total entropy of a system and its surroundings always increases for a spontaneous process. At first glance, this law appears to contradict much common experience, particularly about biological systems. Many biological processes, such as the generation of a well-defined structure such as a leaf from carbon dioxide gas and other nutrients, clearly increase the level of order and hence decrease entropy. Entropy may be decreased locally in the formation of such ordered structures only if the entropy of other parts of the universe is increased by an equal or greater amount.

Your question is about the spontaneous folding of proteins. You ask:

  In this context the meaning of conformational entropy is that the higher the stability of the proteïn is the lower the conformational entropy is (I think).

  Why does the surrounding entropy increases because of the burial of
  hydrophobic residues?

Comments on your interpretation: Do not use the term ‘stability’ in this context. It is not a thermodynamic term and its meaning is imprecise. If we think of entropy as the degree of disorder or randomness, then we can see that Conformational entropy is used by the authors to mean the entropy of the protein as a random coil which can adopt many different structures. This has clearly a greater entropy than the folded protein with (to an approximation) a single structure. The adoption of the folded structure is thermodynamically favoured because it represents a state of lower energy (specifically Gibbs Free Energy) compared with the random coil structures, but entails a loss of entropy.

My answer: The surrounding entropy increases for the following reason. The surrounding entropy is that of the water molecules vibrating and interacting with other water molecules by means of the δ+ and δ– charges on H and O, respectively. In a system containing a protein with a random coil, the movement of these molecules is restricted by the hydrophobic side-chains they encounter, hence limiting the entropy, as it were. When the protein folds into a globule with polar residues on its surface, the vibrating water molecules are less restricted in their movement and hence have a higher entropy.

Further you ask:

  Why does the burial of those hydrophobic residus couterbalances the large loss of conformational entropy?

  I think maybe because the unfolded protein has more conformation then
  the protein when it's folded because of the hydorphobic core, it
  lowers the possible conformation because the hydrophobic interaction
  restrict the possiblities. Am I right?

My Answer: I have explained that in general terms above, in response to your first question. If you want a quantitative, mathematical justification you’ll be pushed to find one. Assuming that there are no other factors involved, we assume that it must be so because of the second law.

Comments on Your Answer: I don’t understand what you mean by “it lowers the possible conformation”. You can decrease the number of possible conformations — you cannot "lower possible conformation”. I assume English is your first language. You must try to use it more precisely if you are going to write about science (as well as checking your spelling, grammar and capitalization). If I were marking this paragraph as an exam answer I would put a line through it as unintelligible. The key thing is that you are comparing a single conformation of the lowest energy involving specific weak interactions and a polar surface, with a number of conformations which expose hydrophobic residues and restrict the free vibrations of the water molecules.

Further Clarification

The diagram below illustrates the problem:

The protein is changing from a disordered to an ordered state so, its entropy is decreasing:

  ΔSprotein = x ,  where x < 0

Whereas the water is changing from a more ordered to a less ordered state, so its entropy is increasing:

  ΔSwater = y ,   where y > 0

and

  ΔStotal = ΔSprotein + ΔSwater = x + y

If ΔSprotein + ΔSwater = 0 (x + y = 0), we would say that the increase in entropy of the water counterbalances the increase in entropy of the protein. For the folding to occur spontaneously, the total entropy must increase (ΔStotal > 0 , i.e. x + y > 0) and we would change the previous statement to  “more than counterbalances”.


Why is propanoic acid often added to the diet of C. elegans?

Propanoic acid is toxic against many types of mold, fungi and bacteria (wiki), but same time has almost no effect to C. elegans ("fivefold less", reference). This is why propanoic acids and (more commmon) its salts are used as conservants for C.elegans cultures (as well as for other animals, like Drosophila).


Formation of disulfide bonds in protein expressed after transduction

I am not an expert on expression of genes from viral vectors, but as I requested the poster to clarify his question I feel an obligation to provide at least a partial answer.

The first question to address is whether the mRNA for the protein of interest is expressed in the same way as normal cell proteins. In the case of the lentovirus vectors which are integrated into the genome there is no reason to think otherwise.

In this case the factors determining the formation of disulphide bonds would be the same as for any similar normal cell protein translated from mRNA.

In summary:

Only secreted proteins have disulphide bonds.
In eukaryotes these protein are synthesised on ribosomes on the endoplasmic reticulum, which obviously must be present in the cell in which one is trying to express the protein (i.e. it must be capable of secreting proteins). One assumes that if one is restoring a function found in normal cells this will be so.
Oxidation of sulphydryl groups occurs in the intercisternal space before secretion. It involves a number of proteins and there are reduction and chaperone systems to deal with inappropriate oxidation, which occurs to a greater or lesser extent. A recent freely-accessible account of this topic can be found in a Cold Spring Harbor perspective by Neil Bulleid in 2012.
The (small?) proportion of incorrectly oxidised proteins that are not recycled are presumably removed by the cellular mechanisms that degrade aberrant proteins.

It would not seem possible to answer in a literal manner the question what the numerical ‘chance’ is of correct oxidation, but this would not seem to be pertinent. The question of interest is whether the protein would be oxidised to the correct native structure with the same efficiency as in normal circumstances. There seems no reason to think it would not.


Role of epigenetics in evolution and transmission of defects caused by drugs

Generally speaking, epigenetic modifications are not inherited as they are reset during embryogenesis. However, subsequent epigenetic modifications can be acquired during the period of pregnancy, which as a mechanism depends on the epigenetic state before the reset and on the physiological conditions of the mother including nutrition, health, stress, etc.. Obviously drug-intake years before pregnancy can still affect the mothers health-state.
Answering your first question: Epigenetic modifications generally cannot be directly passed, but indirect effects could theoretically pass through multiple generations without hard limit.

A major barrier to transgenerational epigenetic inheritance is germline reprogramming, during which histone variants and their modifications, as well as small RNAs and DNA methylation, are all reset. In mammals reprogramming occurs both in the germline and in the zygote immediately after fertilization. (Source: Heard & Martienssen 2014 doi: 10.1016/j.cell.2014.02.045)

2: The great potato famine is said to still have epigenetic effects, generations later. 3.: Epigenetic changes cannot directly "become permanent" as genetic changes, although hypothetically speaking, epigenetic states can lead to viability of certain mutations that would otherwise be lethal and can therefore in theory influence evolution.


Where happens MHCII coordination to a self-peptide, and what happens if the bond would be irreversible?

It appears that in cases self-pepties are bound to the MHC-II proteins (say HLA-DP2) when they are at the surface already. Where do such self-peptides come from?

Class II MHC molecules are capable of presenting any peptide of appropriate length, regardless of where it came from. Contents in a phagolysosome will contain both self and non-self peptides.

  Do they come from inside the endosomal active cell

Some do, yes. While many proteins are degraded by the proteosome, some are actively imported into a lysosome and degraded there. This is termed chaperone-mediated autophagy. Full organelles may also be brought into the lysosome through "regular" autophagy.

  or could they also come from "outside" from where the T-cell comes?

This is the case as well. Any ingested material from the outside could contain cellular debris, protein agglutinations, or foreign organisms. Peptides from all of these sources can be presented at the cell surface.

  What would happen if (for some reason) a) the self-peptide binds "irreversibly" to the MHC-II?

According to this study, MHC II molecules are recycled, and their turnover is carefully regulated. There is no need for the bound peptide to dissociate during antigen presentation, so likely problems would occur when MHC II turnover is disrupted.

  the self peptide binds irreversibly to the MHC-II and at the same time is structurally significantly distorted (e.g. if there is something, like a heavy metal bound in-between the MHC-II and the self-peptide)?

If the MHC itself is structurally distorted, it will not be recognized by any other cells. Remember that, during T cell selection, the cells must be able to recognize the MHC itself with a low affinity. T cells which bind strongly to the MHC itself undergo death by negative selection, whereas those which do not recognize the MHC at all undergo death by neglect. As a significant structural change would result in either an excessive affinity, or no affinity, no T cells capable of recognizing the complex would be present.


These are a kind of ramshorn snail, as Jestep correctly guessed.  Now they are grown up and they are clearly identifiable as ramshorn.

I will post photos of adults when I get the opportunity.


Why do squirrels have twitchy bushy tails?

Tree jumping.
The obvious answer is that having a balancing ballast is incredibly handy for some of the death defying jumps squirrels perform. The tail is needed for that.
A big bushy tail might be a good counter to predation.
You make the assumption that an inconspicuous tail would be bad for predation. I would challenge that assumption, but I am making an educated guess so feel free to debate this.
Tail flagging in ground squirrels is used to deter predators and communicate vigilance. Perhaps something similar occurs in tree-dwelling squirrels too.
Rabbits have a short white tail which isn't particularly camouflaged. It helps to confuse the predator allowing the rabbit to make sharp turns that the predator cannot anticipate.
In the case of this big bushy "twitchy" tail (which like rabbits, some squirrel tails have white tips, like in your picture), a predator probably cannot see the body and importantly cannot see or is distracted from the footing and pacing of the squirrel. If you've ever seen a dog chase a squirrel, the squirrel is easily able to outmanoeuvre the dog long enough to make it safely to a tree, probably because the dog can't predict the squirrel's trajectory due to the distracting and writhing tail.
Let's say a predator did get its jaws or claws near the squirrel and tried to take a chunk. There is a good chance all the predator will grasp is a bunch of tail fur. The squirrel will probably be sore but will live to tell the tail. (I couldn't resist)


Is this is a parasitic wasp, which I found in Blackpool Lancashire?

Yes it is ! If you look closely at the wing patterns, they are characteristic of the Ichneumonidae family, as you can see below*. This family contains thousands of species which all are parasitoids. Species identification is very tricky for this family, but the patterns on the abdomen (2nd and 3d strips are yellow, the others are black, yellow spot at the tip) and on the tibia (yellow strips) are very characteristic of the species Ichneumon stramentor, which parasitizes caterpillars.

Based on the width of the abdomen, this is probably a female (ovipositor is not visible for this species).

It's actually quite common in the UK (they live in habitats such as hedgerows or woodlands), but not so frequently seen on windows!

*Image source : DrawWing.org

Derived from: Comstock J.H.
(1918) The wings of insects. The Comstock Publishing Company, Ithaca, N.Y.


Has anyone tried Gibson Assembly Optimizations?

I haven't tried Gibson Assembly myself, but I do know the Cambridge iGEM Team in 2010 and 2011 developed a web-based tool - Gibthon - for automatically generating primers for Gibson Assembly.

You could try running your difficult sequences through their tool to see what it suggests for primers.  It apparently gives you a "value for the Gibbs free energy of the worst case secondary structure of the primer."


When you yawn, the muscles surrounding the glands which are responsible for bringing tears, i.e. the Lacrimal glands get squeezed leading to teary eyes. This is the location of Lacrimal gland (it's present at the top left corner in this image):

https://upload.wikimedia.org/wikipedia/commons/c/cf/Gray896.png

These glands actually work all the time as they've the responsibility to coat the surface of our eyes (that's the reason our eyes appear glistening). When they get squeezed, due to the tightening of facial muscles surrounding the eye, or maybe because your closing eyelids too tightly while yawning, they release a small amount of "tears" they would have otherwise used at a later moment.

Also, as a side note, there are more than one type of tears, this specific type of tears are called reflex tears. Quoting a Wikipedia article as a reference (https://en.wikipedia.org/wiki/Tears#Types):

  $\ldots$ It can also occur with bright light and hot or peppery stimuli to the tongue and mouth. It is also linked with vomiting, coughing and yawning. These reflex tears attempt to wash out irritants that may have come into contact with the eye.


I think that enzyme-linked immunosorbent assay (or ELISA) is the best way to do so, given you have an antibody against the protein to coat the sample wells with... You could use mice to create polyclonal antibodies against your protein by injecting the protein and collecting the serum and purifying it...as long as there isn't similar proteins to the bacterial one in the sample you are testing for...but to diagnose an infection you could use something like q-PCR assuming you can get the bacterial DNA from the sample (you could use typical bacterial DNA extraction techniques).

For more on ELISA go here. Here is a good animation on ELISA:
http://highered.mheducation.com/sites/0072556781/student_view0/chapter33/animation_quiz_1.html


Yes, this is a book louse (order Psocoptera). They feed on all kinds of organic matter, and are very common. Fun fact - they are called "book lice" because they are often associated with old books, feeding on the organic glues in the bindings. (they are also called bark lice - I'm sure you'd know why).


Yes, this can happen, although the risk is low. The problem is that some tumors need to be irradiated since the cannot be operated (this is true for some brain tumors). Here the radiation therapy is the therapy of choice. The effect of the therapy is that the tumor cells get a high radiation dose which either kills them or drives them into apoptosis.

The problem the irradiation is that you will always affect healthy cells, of which most will die. This causes some of the negative effects of the radiation therapy, but it is also possible that a healthy cell receives a dose which is "only" damaging and causes a secondary tumor. Here a benefit analysis needs to be done to see if the benefit from the therapy is woth taking the risk of acquiring more damages. See the references for some more background.

References:

Long term side effects of brain tumour radiotherapy
Second Cancers Caused by Cancer Treatment
Therapy-Related Secondary Cancers


Which of the two mitochondorial membranes relate to bacteria according to the endosymbiotic theory?

The inner membrane is that of the engulfed bacteria. The bacterium would have been phagocytosed by a larger cell. Hopefully you can see in this image the smaller cell being engulfed in the membrane of the larger cell:

[ source ]


Why are there 2 copies of RNA in the HIV virion?

You are not totally correct because these two strands don't have to be the same, they can be genotypically different, which occurs when a cell is infected by two distinct HIV strains. Also HIV uses reverse transcriptase which can "jump" from one strand to the other so sometimes pieces get repeated, skipped etc. So you will get a recombinant --> more genetic diversity(see this article) I won't go into to much detail but if you want to know more I would highly recommend to read the article I linked after genetic diversity. So to summarize:

genetic diversity, because of switching between the two strands (this makes it so hard to cure AIDS e.g.)
If one RNA strand gets damaged it can use parts of the other RNA strand as template, so to synthesize DNA
apparently the dimeric form of RNA in HIV is essential for successive replication of the virus

Source: previous mentioned article(HIV-1 RNA dimerization: It takes two to tango.)


How does Isoxaben kill newly germinating seeds, with almost no effects on established ones?

As with your other question on mitotic inhibitors ("How does Trifluralin kill newly germinating seeds, with almost no effects on established ones?"), inhibiting cellulose synthesis will inhibit growth. Hence, an established plant will stand its ground, but newly germinating plants cannot grow without cellulose synthesis and hence will fail to germinate.


How can I verify my true genetic relationship with my close relatives with simple physical traits?

Here are the answers for your four questions:

Widow's peak (hair in V): dominant: Dominant and recessive characteristics, blinn.edu; Dominant Inheritance, Genetics Generation
Dimples: irregular; tendancy toward dominant *: Mendelian Genetics, uni.edu; What Is the Genotype for Dimples?, seattlepi.com; Understanding Genetics, genetics.thetech.org
Curling tongue: complex; tendancy toward dominance: Myths of Human Genetics, udel.edu; Debunking the biggest genetic myth of the human tongue, Cathrine Woods
Phenylthiocarbamide detection: dominant: Phenylthiocarbamide tasting, Encyclopedia Britannica; Genetic study of phenylthiocarbamide (PTC) taste perception, Egyptian Journal of Medical Human Genetics, Volume 13, Issue 2; PTC The Genetics of Bitter Taste, genetics.utah.edu

Hope it helps!

*See comments


Does anybody knows name of this bird I found in my backyard in India?

I am pretty sure that this is a  Indian Paradise-flycatcher (Terpsiphone paradisi). Since we cannot see the length of the tail feathers, we cannot distinguish between male and female, the later have a much shorter tail.

See the image (from here) for comparision:

More information can also be found here and here.


Does physical exercise following lack of sleep increase the risk of sudden cardiac death (SCD)?

Sleep is an important aspect of our life. Sleep disorders are acute due to their effects in physiological and mental health of a person.Sleep occupies nearly 30% of our daily life and people were gradually decreasing the sleep time in order to adjust their busy schedule. According to the United States National Sleep Foundation, adults need to sleep 7-9 hours each night. The decrease in sleep time contribute mostly towards cardiovascular disease, including hypertension, coronary artery disease(CAD),risk of arrhythmia, stroke etc.
The circadian and dirurnal rhythms influence the neural circulatory control causing the changes in heart rate, vascular tone and blood pressure. The REM(Rapid Eye Movement)sleep and nonREM sleep affects the cardiovascular system. Researchers found it important that normal sleep is a complex and dynamic process with profound effects on cardiovascular homeostasis.
Insufficient sleep is a stress stimulator that acts through the sympathetic nervous system elicit changes in blood pressure, heart rate and barroreflex setpoint.
Sleep deprivation is a state of having less or no sleep which is a major reason for cardiovascular diseases.Which may cause
Inflammation
Cardiovascular disease is mainly driven by atherothrombosis, which is an inflammatory process. Increased levels of C-reactive protein(CRP) and interleukin-6(IL6) have been implicated as the predictors of cardiovascular disease risk.Both CRP and IL6 have been found elevated in both totally and partially sleep-deprived subjects.Inflammatory cells such as monocytes and neutrophils were also found to be elevated during acute sleep deprivation, supporting that sleep deprivation is an inflammatory process.
Endothelial Dysfunction
Endothelial Dysfunction has been reported after a combination of sleep deprivation and stress, also increased heart rate, blood pressure are reported in sleep deprived subjects may result in Endothelial Dysfunction.
Hypertension and Stress
Hyper tension and stress hormones are released by the body when lack of sleep occurs, this results in elevated bloop pressure and may lead to CAD.
CardioArtery Disease
The American Cancer Society , the Almeda County study and Partinen also showed an increased risk of CAD in subjects who reported sleeping 4-6 hours a day.
Diabetes Mellitus(DM)
Diabetes Mellitus is a major risk factor for CAD and it has been underlined from several studies across past decades that sleeplessness can result in DM.

A sudden cardiac death is highly probable for a person who follows increased physical exercise and decreased sleep durations. For a sleep deprived person the risk of cardiac diseases are so high, then for some one who spend lot of time exercising can cause chronic cardiac problems. Physical exercise and over training can cause more stress hormones and increased heart rates, these factors along with prolonged sleep deprivation can cause serious cardiac diseases or even sudden cardiac death.

Levels of cortisol (the "stress" hormone) are elevated for long periods of time.
The body spends more time in a catabolic state than an anabolic state (perhaps as a result of elevated cortisol levels).
Excessive strain to the nervous system during training.
http://en.wikipedia.org/wiki/Overtraining

References

Critical Care Nursing: Synergy for Optimal Outcomes - Roberta Kaplow
Sleep Deprivation and Disease: Effects on the Body, Brain and Behavior - Matt T. Bianchi


Document the incident and notify your supervisor. For environmental testing where SOP is involved, this would count as an incident, i.e. anything that falls outside SOP. Whether the incident is a non-conformance, deviation or nothing at all is up to your quality team. You can always take another sample, supplies withstanding, too.


How does evolution explain the apparation of different group like: mammals, insects etc

Insects and mammals diverged from one-another over 500 million years ago. For most of Earths 4.5 billion year history, life was single-celled, or organized into colonies of single-celled organisms. Likely sometime shortly before the Cambrian, multicellular animals evolved. The first multi-celled animals were likely a kind of colony that was not differentiated into tissues. It didn't have a head, or tail, or look much like an animal. From these simple undifferentiated, multi-celled building blocks, came most of our animal phyla, during a burst of innovation called the "Cambrian explosion". At this time, one lineage headed down a path that would lead to insects, and another lineage, toward mammals. Although theoretically, it is possible, given enough time (as in billions of years) for a fly to evolve into a rabbit, this is highly unlikely. Evolution works with what it starts with and modifies it under natural selection to favor fitness. So having six legs and wings works pretty well for flies, and having 4 legs and fur works pretty well for rabbits. The hurdles to go from one form to another, given that these lineages are already well adapted, would be enormous. It was much easier, 500+million years ago, to go from one colonial lump of cells to a rabbit, and another lump to a fly. As an example of how evolution works with what it starts with, virtually all tetrapods (amphibians, reptiles, and mammals) have 5 digits on their limbs. This is because they share a common ancestor that did. Not because 5 is somehow special. Another example, humans choke to death because we share a common ancestor with fish, and fish share a tube that connects both the mouth with their swim bladders and their gut. Swim bladders were modified into lungs, but the common connection from our fish ancestors remains (a really bad design, but we are stuck with it).


Interesting Insect, possibly a beetle (Northern Indiana)

That is a carrion beetle. Family Silphidae, in the genus Necrophila
https://www.insectidentification.org/insect-description.asp?identification=American-Carrion-Beetle


Are there any viruses or bacteria which have evolved to withstand higher temperatures due to fever

Fever is just one of the many ways of the body's defense mechanism work. Under infection, human body can raise body temperature, release cytokins and activate white blood cells etc. Sometimes the bacteria can evade immune suppression or immune complement fixation so that they can stay inside a "fever-ish" body like they just don't care. Example: Pseudomonas aeruginosa. They can grow in 42 degree Celsius which surpass the normal fever temperature.

My answer may not be the best for your question. All I'm trying to say is that fever acts as a supportive role during an infection. Human body relies on heavy artilleries such as white blood cells and cytokin to clear the infection. That's why it will be more beneficial for the bacteria to evolve abilities to evade immune suppression and immune complement fixation. And bacteria know how to do those.


Analysing the ERP (Event-Related Potential from EEG recordings) in terms of the P-300 wave

So, are repetitions wanted in this kind of experiment?

Yes: repetitions reduce random noise and increase the chance to tell artifact from response. Adaptation is a serious issue, typically becoming apparent by decreasing amplitudes, or even skipped responses. Reading the existing literature and/or performing experiments with various stimulus intervals may help to identify adaptation effects, if any.

  ...there is allways a background activity in the brain...

Correct - if not, you are either not recording properly, or subject is brain dead.

  are there certain frequencys that are more likey to happen under these conditions

If you repeat your recordings and average them out, this is not an issue. Otherwise, yes, FFT analysis shows several frequency bands, dependent on the state of the subject. For example, awake subjects show primarily fast beta activity (13-30 Hz), drowsy or sleeping subjects much slow-wave alpha (1-4 Hz).

  should I assume anything on the P300 response?

In short: The P300 response is most commonly elicited in an "oddball" paradigm when a subject detects an occasional "target" stimulus in a regular train of standard stimuli. The P300 wave only occurs if the subject is actively engaged in the task of detecting targets (Picton, 1992).

  What is the recommended sample Rate I should use. I guess there should be an advantage for high sample rate for more resolution bu[t] I am not sure about that. Am I right, or maybe a lower samp[le] rate has advantages th[a]t I am not aware of?

The higher the sample rate, the better. Downsampling can always be done later. Typically 1000 Hz is sufficient for fast responses. For a P300 this should already be kind of an overkill.

Reference
- Picton, J Clin Neurophysiol (1992); 9(4): 456-79


difference between neurotransmitters and hormones

At heart, the distinction between neurotransmitters and hormones is how they are transmitted - not necessarily a difference in the chemicals themselves.

Neurotransmitters are sent over synapses, between neurons. They may be small molecules (e.g. dopamine) or larger molecules such as proteins (e.g. substance P). Conversely, hormones are sent through the circulatory system but could also be small molecules (e.g. adrenaline) or large molecules (e.g. growth hormone).
Looking at the structures of these chemicals, we can see that both neurotransmitters and hormones have an enormous variability in the chemicals they involve. Furthermore, dopamine looks much closer to adrenaline than it does to substance P. But dopamine is primarily a neurotransmitter and adrenaline is typically thought of as a hormone!
There may also be overlap between roles of chemicals as neurotransmitters or hormones. In fact, adrenaline may act as both a neurotransmitter and a hormone. So, to answer your question of "why do some neurotransmitters act as hormones?" - the distinction is in the context of how the chemical is sent through the body. There's variability in which chemicals are used for either purpose, and no rule saying a chemical can't be sent via multiple mechanisms.

Furthermore, neurotransmission also involves spillover of neurotransmitter, which in theory could find its way into the circulatory system. So there could be overlap between neurotransmission and hormone signaling. And lastly, as @Remi.b points out, the particular mechanisms of neurotransmission and hormone signaling have implications on the dynamics of the signaling.


If the human atlanto-axial joint is pivotal only, what accounts for the craniums additional degrees of freedom?

The additional degrees of freedom are provided by the entire cervical spine, rather than the atlantoaxial joint alone, which is the joint between C1 and C2. What you're describing as roll (when you point one ear to the ground), is provided by contraction of the sternocleidomastoid. The sternocleidomastoid muscle pulls the mastoid process (behind the ear) down and in, toward the fixed clavicle and sternum.  The joint that provides lateral flexion in response is the entire cervical spine.

Here you can see the sternocleidomastoid muscle (the SCM):

And here, a drawing with a reasonable approximation of the way the cervical spine responds to lateral flexion (due to contraction of the SCM). I can't find a good c-spine film at the moment to demonstrate it in a human person, rather than an artists imagination. But this drawing is accurate to my recollection. You can see the space between C1 and C2 on the right is quite limited (that atlas and the axis are in close apposition). C2 and C3, as well as the other cervical vertebrae, have more space between them on the right:


Besides hemoglobin, what proteins are present in red blood cells?

Reticulocyte stage is when the ribosomes are still present and after that no new protein synthesis occurs. However RBCs have a lot of proteins and major proteins other than haemoglobin are cytoskeletal proteins and ion channels/pumps (In fact, cytoskeletal proteins are more abundant than haemoglobin). It is the Na+-K+-ATPase that consumes most ATP. As you correctly identified the RBCs produce ATP via glycolysis and glycolytic enzymes are also present. Note that deficiency of pyruvate kinase leads to haemolytic anaemia.

For a detail on the proteins present in human RBSs, see this paper. They have studied the RBC proteome by ion-trap MS. The top 5 proteins (from Table-1) are:

No.    Protein description              Molecular mass (Da)    Gi Number    Sequence     No. of identified
                                                                           coverage(%)      peptides
1      Spectrin α chain, erythrocyte         279,916.5          1174412       48.0           77*
2      Spectrin β chain, erythrocyte         246,468.1          17476989      48.0           76*
3      Ankyrin 1, splice form 2              206,067.9          105337        45.0           55
4      Ankyrin 1, isoform 4, erythrocytic    203,416.6          10947036      45.0           50
5      Ankyrin 1, isoform 2, erythrocytic    189,011.2          10947042      46.0           48

Although in this table you cannot find glycolytic enzymes other than GAPDH and Aldolase, but other enzymes are also present. They are perhaps not detected in this experiment because of overwhelming levels of structural proteins. You can check this old paper that shows a study of different glycolytic enzymes from erythrocytes. It is also to be noted that the glycolytic pathway flux is not as smooth as in other cells. So some accumulated metabolites are probably exported out of the cells to keep the flux smooth[ref Full text not found].


At what age does the mouse skull stop growing?

This doesn't fully answer the question, but for those mouse skull sutures that do fuse, fusion is complete by about 45 days of age, according to Studies in cranial suture biology: IV. Temporal sequence of posterior frontal cranial suture fusion in the mouse.  That suggests that most cranial expansion is more or less complete by about 6 weeks of age.  I think there is still the potential for remodeling of the skull, especially bone thickness and so on, but since your interest is on the internal size of the cavity, this may help address it.


what does the "two photon" means?

Ordinary confocal microscopy uses single photon of laser light to excite the molecule of fluorescent dye.

In two photon microscopy you use two photons, with lower energy, which cannot excite the molecule of dye on their own, but their interference in a specific place leads to summation of their energies and to excitation.

This has benefits such as decreased phototoxicity and increased precision (resolution) especially in z-plane.

  how does the implement look like?
  Does all relevant (genetically engineered) neurons light in the same color?

There are two types of fluorescent dyes for 2-photon Ca2+ imagining. Since you want to measure local concentration of Ca2+, you can either use a chemical which chelates the calcium ions and changes its conformation and fluorescent properties based on that e.g. fura-2.

Alternatively, you can prepare fused protein from calmodulin ( CALcium MODULated proteIN) and some fluorescent protein e.g. GFP and transfect the cells with this product.

This means you can transfect different cells with different GFPs and get different colors. Depends on the actual experiment design.

Source

  Is it the color that is measured or the intensity of the color?
  Is it sensitive to absolute voltage or voltage changes?

You can analyse fluorescence intensity changes. The derived fluorescence intensities and ratios are plotted against calibrated values for known Ca2+ levels to learn actual Ca2+ concentration. Source

  Is the purpose of this technique single neurons or brain paths?

Actually, with a good interpretation of the data it can be used for analysis of both.

For more information about calcium imaging, see for example: http://www.cell.com/neuron/fulltext/S0896-6273(12)00172-9
or http://www.pnas.org/content/100/12/7319.full

or corresponding wiki articles:
https://en.wikipedia.org/wiki/Two-photon_excitation_microscopy
https://en.wikipedia.org/wiki/Calcium_imaging


What is the biological limit on hearing resolution?

Short answer
The main limitation to frequency discrimination is loudness.

Background
The cochlea is tonotopically organized - it basically acts as a Fourier transformer, where different frequencies are analyzed on a place map  (Fig. 1). Frequency tuning of cochlear hair cells is mainly limited by sound intensity. The louder a pure-tone sound stimulus gets, the larger the area on the basilar membrane that is activated and hence the wider the range of cochlear hair cells that is activated, and hence the worse the frequency resolution becomes (Fig. 2).

Fig. 1. Cochlear tonotopy. Source: Cochlear Implant Help

Auditory nerve fiber tuning. The louder the stimulus, the worse the tuning to frequency. Source: - Fettiplace & Hackney, 2006

As to the quantitative aspect of this question, namely what the frequency difference limen is, and an indication how many frequency bands can be distinguished I refer you to below linked question. Both depend highly on the method used to determine the just-noticeable-difference, and as said also on the sound intensity applied. Moreover, it is dependent on the frequency under consideration. The higher the frequency, the larger the frequency band becomes expressed in Hz. This is an example of Weber-Fechner's law (Hecht, 1924). The cochlea is organized in octaves, meaning that higher frequencies have less cochlear space devoted to them and hence less hair cells to code a particular frequency range.

Further Readings
- What's the frequency resolution of the human ear?

Reference
- Hecht, J General Physiol (1924): 235-67
- Fettiplace & Hackney, Nature Rev Neurosci (2006); 7: 19-29