Poultry raised for meat in the US (called broilers) reach butchering size in 5 to 8 weeks (compared to 10 weeks for half the size 40 years ago. It's not a GH miracle; it's a result of generations of selective breeding (as cows have undergone for unhealthy udder size).

GH use is illegal in the US and many other countries. Honestly, it's an unnecessary additive/expense.

I raised poultry for more than a decade, mostly chickens and ducks (but almost everything else as well). Once I bought 25  1-day-old broiler chicks (early broilers were a Plymouth Rock X Cornish) alongside my usual mix.  Within 2 weeks the broilers were at least 3 or 4 times the size of the other chicks, and more than a couple of them died (under ideal conditions - all free-range outside, cooped only at night). By 10 weeks, they were enormous.

They were also dumber than a bag of hammers, unfortunately. I felt so sorry for them that I let them live out their natural lives, which wasn't terribly long, partly because of their docile stupidity.

Growth hormone is unnecessary in the poultry industry.

Murray McMurray Hatchery: Jumbo Cornish X Rocks
Modern Meat Chicken Industry


How is it thought that phosphine is synthesized by living organisms on Earth?

The background to phosphine production on Earth can be found in a review entitled “Natural Products Containing ‘Rare’ Organophosphorus Functional Groups” by Petkowski et al. in Molecules  24, 866 (2019). The four authors are also co-authors of the Nature Astronomy paper. They state (my emphasis):

The detailed biosynthetic pathway for microbial phosphine production
is currently unknown. For detailed discussion of the biological
production in the environment, its biochemistry, and atmospheric
chemistry see three recent papers by Bains, Sousa-Silva and colleagues
[482,494,495].

These three papers are from the authors, one of which I followed up:

Bains,W.; Petkowski,J.J.; Sousa-Silva,C.; Seager,S. New environmental model for thermodynamic ecology of biological phosphine production. Sci. Total Environ. 2019, 658, 521–536.

The abstract to this includes (my emphasis):

In this paper we show through thermodynamic calculations that, in
specific environments, the combined action of phosphate reducing and
phosphite disproportionating bacteria can produce phosphine.
Phosphate-reducing bacteria can capture energy from the reduction of
phosphate to phosphite through coupling phosphate reduction to NADH
oxidation. Our hypothesis describes how the phosphate chemistry in an
environmental niche is coupled to phosphite generation in ground
water, which in turn is coupled to the phosphine production in water
and atmosphere, driven by a specific microbial ecology.

The paper itself is not of the ‘author-pays’ type, so you may need institutional access to read it. There is a graphical summary provided, however, which summarizes the hypothesis:

The paper consists of detailed thermodynamic arguments for the scheme suggested at the particular temperature, pH and anaerobic environment of marshes and swamps. Under these conditions, the authors postulate that the purpose of posphine production is to gain energy†. The analogy would be with the production of NADH as in anaerobic glycolysis to gain energy, but needing to be reoxidized to NAD+ to allow this to continue. The reduction of phosphate to do this would be analogous to the reduction of pyruvate to lactate or to ethanol. Like ethanol, phosphine would be a by-product of no value to the organism.
However the possible role envisaged for phosphine production in Venusian clouds is different. In the Supplementary Information for the Nature Astrobiology paper, there is the following:

Initial modelling based on terrestrial biochemistry suggests that biochemical reduction of phosphate to phosphine is thermodynamically feasible under Venus cloud conditions. Biological phosphine production on Venus is likely to be energy requiring. However, life can make substantial energy investment into compounds that provide important biological functionality. There are many potential useful biological functions including signaling, defense, or metal capture for which phosphine has useful properties, so endergonic biosynthesis cannot be ruled out.

The suggestion here is that phosphine is a useful product, synthesized at an energetic cost.
The only biochemical connection between the two would be that if, as appears likely, life on Earth can produce phosphine (by biochemical pathways that remain to be discovered), then these same biochemical processes would be candidates for phosphine production by life on Venus if the authors are correct in arguing that (at least known) non-biological candidates have been excluded. The question does not ask for opinions on the latter, nor would I presume to present those that I hold.

† The thermodynamic approach involves calculation of Gibbs Free Energy changes (ΔG) for reactions. Often on this site discussing standard biochemistry we (or at least I) talk in terms of standard free energies — ΔG˚ (or ΔG˚′ for normal cellular conditions). However the actual value of ΔG for a reaction is influenced by temperature and the concentration of reactants (which will include hydrogen ions), so that the ΔG calculated for terrestrial marshes and the like is likely to differ from that in Venusian clouds.


Why do fetuses have membranes between fingers and toes?

Short answer
The transient membranes between the fingers and toes in embryos are a myth.

Background
The presence of transient membranes in developing embryos supposedly points to our fishy evolutionary origins. However, I couldn't find any credible sources to support this myth. In fact, I couldn't find any source mentioning the presence of webbing between the fingers and toes at any stage during development.

To support this lack of evidence, I have posted several photos of embryos and fetuses in various developmental stages. None show any signs of the "swimming webs". Note that the age mentioned is the developmental age, counted from the moment of conception (add 2 weeks to have gestational age):

Fig. 1. Five-week embryo. source: Palm Reading Perspectives

Fig. 2. Seven-week embryo. source: Wikipedia

Fig. 3. Eight-week embryo. source: WemMD

Fig. 4. Fourteen-week foetus. source: WemMD

Fig. 5. Eighteen-week foetus. source: WemMD

Fig. 2 may seem to show some webbing, but if we look at some close-ups of the hand and feet at week 7 in Fig. 6 below, we can see that there is no real webbing; fingers and toes are simply budding from the primordial hand and foot structures.

Fig. 6. Developmental stages of the hand and feet around week 7. source: I am Pregnant

Note that an embryo is called a fetus only after the first trimester, i.e. after some 12 weeks. There is certainly not any sign of webbings in healthy fetuses.

Also note that webbings may be the result of birth defects, such as syndactyly and pseudosyndactyly (Fig. 7):

Fig. 7. Infants with Syndactyly (left) and Pseudosyndactyly (right). sources: Wikipedia & University of Columbia

Original photographic image source (Figs 1 & 5)*
- Nilsson, Ett Barn Blir Till

* Credits go to rg255


Is this ladybird larva secreting a protective fluid?

In larvae stage Ladybird beetles secretes yellow gooey alkaloids from its abdomen.

Ladybird beetles oozes hemolymph(in other word its blood), which is toxic and very smelly, when threatened. It's a mixture of various alkaloids and repulse the predators.

Good Job, There might be no picture more clearer than you provided

source:

[1]: Ladybird defence alkaloids: Structural, chemotaxonomic and biosynthetic aspects (Col.: Coccinellidae), Désiré Daloze, Jean-Claude Braekman, Jacques M. Pasteels

[2]: 10 Fascinating Facts About Ladybugs


It is impossible at present to reproduce all the conditions of a womb.

A womb is more than a warm fluid-filled home for nine months. A few days after fertilization, the trophoblast portion of the conceptus attaches itself to the uterine wall where it develops into a placenta and umbilical cord while the rest (the epiblast) becomes the baby.

Throughout the pregnancy, the mother delivers oxygen, nutrients and hormones through the her blood flow to the placenta, while carrying away waste. The womb also prevents infection of the placenta and amniotic fluid.

In addition, the placenta contributes to amniotic fluid production. Production and reabsorption of amniotic fluid is a very dynamic process; it isn’t just there. It is estimated that more than 95% of amniotic fluid turns over on daily basis, and the fluid composition changes throughout pregnancy.

While cell cultures of the womb's endometrium have been grown, there is nothing artificial which is close to this kind of environment yet, nor is there likely to be in the near future.


Energy transformations in chemiosmosis and ATP synthase

ATP synthase is basically a pump operating in reverse: while transporters such as the Na/K ATPase uses ATP to push ions against a chemical gradient (resulting in potential energy), ATP synthase uses the H+ gradient across the mitochondrial membrane to make new ATP.

A pump uses ATP (chemical energy) to achieve one-way transport by inducing conformation changes in the protein (mechanical energy), which either opens the channel only when ions come in contact with the low-concentration side, or closes the channel when ions come in contact with the high-concentraton side. In either case, the result is that ions can pass only in one direction, and a concentration gradient will build up (potenial energy).

In the case of ATP synthase, the process is simply reversed: an H+ ion entering the channel from the high-concentration side (the intermembrane space) causes a conformation change that opens the channel, and is coupled to the synthesis of ATP. Precisely how the ATP synthase accomplishes this on the molecular level is a complicated topic, and still an active area of research. See this article for an overview.

Note that ATP synthase is clearly reversible: if the mitochondrial H+ gradient collapses, for example if respiration is blocked, then ATP synthase can run in reverse, consuming ATP to pump H+ out of the matrix. There is even an ATPase inhibiting protein dedicated to blocking the ATP synthase in this situation, to prevent the depletion of ATP. Also, the lysosomal ATPase is structurally similar, but operates in the reverse direction to create low pH in lysosomes.


Identify brain junk - What are all the known intracellular and extracellular substances which build up with age and clog the brain?

Another example is the paired helical filament of Alzheimer's disease, so-called because neurofibrillary tangles have a ribbon-like structure when viewed under the electron microsocope.

It is now accepted that paired helical filaments consist of a single protein, microtubule-associated protein tau, in a polymerized and hyper-phosphorylated state. (see Lee and co-workers).

This old answer might also be of interest and contains a fuller reference list.

Neurofibrillary tangles are one of the two characteristic lesions of brain first described by Alzheimer, and are intracellular. The other characteristic lesion is the extracellular neuritic plaques caused by the build up of amyloid-beta (as the OP points out), which is itself part of a much larger transmembrane protein (of unknown function), the amyloid precursor protein or APP.


How can green algae be both multicellular and unicellular?

Because Algae are represented across four kingdoms, namely Bacteria (unicellular prokaryotes), Plantae (multicellular eukaryotes), Chromista (multicellular eukaryotes), and Protozoa (single-celled eukaryotes).

For example, I. Chlorophyta is unicellular:

I. Chlorophyta. Source: University of Wisconsin

While kelp can become huge and can form underwater forests:

Kelp. Source: Nature

Reference
Guiry, J Phycol 2012; 48, 1057–63


Does alcohol really do more damage to the body of a child compared to an adult?

As is stated in this article by Hiller-Sturmhöfel and Swartzwelder from the National Institute on Alcohol Abuse and Alcoholism, there are ethical issues surrounding research on human subjects that preclude direct testing, however studies in model mammals and observational studies do find that "adolescence is a unique stage of brain development which is particularly sensitive to the disrupting effects of alcohol."

A research review by Tapert, Caldwell, and Burke, also finds that studies support the conclusions that alcohol use by adolescents and young adults has a negative effect on cognitive abilities.

Hope that begins to provide you with an answer to your question.


What causes the preliminary changes in resting membrane potential in neurons?

You have already listed two possibilities:

  1) mechanical changes (stretching, pressure, etc)

and

  3) Ligands (neurotransmitters, etc)

In the central nervous system, ligands and in particular neurotransmitters are going to be the overwhelming cause of most initial depolarization. Ligand-gated ion channels are the simplest mechanism: some examples include AMPA receptors, GABA-A receptors, and nicotinic acetylcholine receptors, but it is also possible to change the membrane potential via second messenger systems that open or close other channels.

In the periphery and in sensory organs, sensory-evoked potentials can be caused by mechanical gating, as you mention, as well as by specialized channels that respond to particular stimuli, for example the TRP family which includes channels sensitive to temperature (for example TRPV1, which responds to heat and also responds to capsaicin, the chemical that makes chili peppers 'hot') and to certain chemicals in food (resulting in taste).

The other category you missed is that some cells generate a spontaneous depolarization because they contain channels that are activated around the resting potential (and/or potassium channels that close, which also depolarizes the membrane). This is crucial for the cardiac pacemaker but can also be found in the central nervous system in some cell types.


Yeast Strain with squalene synthase / farnesyltransferase (ERG9) gene deleted

Yeast strains have two mating types MATa (since it secretes a pheromone named 'a factor'), MATα (secretes pheromone 'α factor'). Both MATa and MATα strains are haploid and when they fuse together they form diploid zygote. A haploid yeast has only one set of genes and utilize chemicals like histidine and tryptophan (amino acids) and adenine (part of DNA, ATP and other molecules) for growing. Yeast strains mutant with any of genes to
make these chemicals they will not grow unless they can get these chemicals from their food (yeast media) or allowed to mate with strain having normal genes.

Interpreting the strain notation:

BY4743; MATa/MATα; ura3Δ0/ura3Δ0; leu2Δ0/leu2Δ0; his3Δ1/his3Δ1; Met15Δ0/MET15; LYS2/lys2Δ0; YKL019w/YKL019w::kanMX4

Strain name: BY4743
Genotype: MATa/MATα; ura3Δ0/ura3Δ0; leu2Δ0/leu2Δ0; his3Δ1/his3Δ1; Met15Δ0/MET15; LYS2/lys2Δ0; YKL019w/YKL019w::kanMX4

To understand clearly, you can dissect the genotype in individual strains

BY4743;MATa;ura3Δ0;leu2Δ0;his3Δ1;met15Δ0;LYS2;YKL019w/YKL019w

BY4743;MATα;ura3Δ0;leu2Δ0;his3Δ1;MET15;lys2Δ0;kanMX4

Yeast genetics nomenclature:

Normal or wildtype genes are written in capitalized form - MET15 in MATα
Mutated genes are symbolized with small letter and Δ - ura3Δ0
ura3Δ0/ura3Δ0 - allelic mutation:  mutation in same genes of both strains (MATa/MATα) - They are two mutant alleles in the same gene locus. Both alleles of same gene are knocked out, so even both strains mate, they need external source of uracil in media to grow. Defect in one strain is NOT complemented by the other.
Met15Δ0/MET15 & LYS2/lys2Δ0 - Non-allelic mutation: Defect in one strain is complemented by the other. MATa has Met15Δ0 (mutation in methionine gene) and MATα has wildtype MET15 gene, capable of met synthesis. Complementation works here.
YKL019w/YKL019w::kanMX4 - Critical aspect of yeast strain in functional complementation assays. In all commercially available yeast strains, one gene will be double knocked out (both alleles of same gene) and replaced with an auxotrophic markers like antibiotics - tetracycline, kanamycin, ampicillin - for selecting the diploid cells after mating two strains. It is similar to plating Kanamycin mixed LB media to pick E.coli colonies harboring Kanamycin resistance vector in it.

The gene that is replaced is the gene of interest, i.e. if I am looking to study role of putative PGPS in Plasmodium falciparum, I get yeast strain knocked out with yeast PGPS (pgsΔ). When I do complementation test, I provide external DNA template cloned with Plasmodium falciparum's PGPS to check whether it complements in yeast genome and yeast grows - gene essentiality study.

I am not sure of the gene YKL019w/YKL019w, but it implies that wildtype of YKL019 is replaced with Kanamycin - kanMX4.


Is viral single-stranded RNA in the absence of reverse transcriptase infectious?

In RNA viruses with a single-stranded genome, this RNA can be positive or negative sense. Positive sense RNA is directly translatable by a ribosome, while a negative strand RNA cannot be directly translated and therefore non-infectious. It either has to be converted to a positive strand RNA with the help of an RdRP (RNA-dependent RNA polymerase, carried in the virion) or reversely transcribed into a DNA which then serves as the template for generation of translatable mRNAs. In either case, this RNA is non-infectious in absence of the necessary proteins.
Note that positive strand RNA has to be propertly capped in order to be translatable. This is also not always the case - some viruses generate or steal the cap from the cellular mRNAs once uncoated in the cell.
Another aspect worth mentioning is that positive-sense retroviruses usually code for their genes in multiple reading frames and make heavy use of splicing to produce their proteins. Thus, directly translating their positive sense RNA is not sufficient for infection.
From Chapter 3 in Viral ecology:
For plus-strand RNA viruses except retroviruses, translation of the viral RNA
follows immediately after uncoating. The viral RNA extruded from the capsid is then
used by the host translation machinery for directing protein synthesis (Fig. 9).
For all other viruses, whether of DNA or RNA genome, the step immediately following
uncoating is either transcription of the genome yielding functional mRNAs or
reverse transcription of vRNA yielding proviral DNA (retroviruses).

References:

Viral Ecology
Principles of Virology


Linkage and LD: quantitative or qualitative?

Linkage disequilibrium (LD) occurs when there is a non-random association or correlation between genotypes. Note I used the word correlation; this is a quantitative trait.

Some genotypes may well correlate perfectly (R=1), i.e. they are always inherited together. Others may not be in 'perfect' linkage (e.g. R=0.9), but are still considered to be in LD because there is a strong correlation between the genotypes (I think 0.8 is generally seen in published papers as the 'cut-off').

The correlation coefficient is derived from the D' value - this (simply) denotes the observed vs. expected frequencies of the genotypes (whether they are in linkage or not). Therefore either value can be used, but I think it is more common (and more interpretable) to express the correlation coefficient (or to be more precise, the coefficient of determination, R^2).

If you'd like an example: I might be interested to know if any SNPs are in LD with rs10757278 (located on 9p21, associated with heart disease). Using SNAP (by the BROAD) I can input my search, choose my options (e.g. use 1000 genomes data, and an R^2 cut-off of 0.8) and search. ~5 SNPs are found to be in 'perfect' LD (R^2=1), but a further ~40 are still considered to be in linkage with the input-SNP because their R^2 values are above 0.8.

So in summary, both statements can be used correctly, but it is always more informative to state the degree of linkage (otherwise it might be assumed they are in perfect correlation).


XXY (Klinefelter's) & Trisomy 21 & X-inactivation

X-inactivation does occur in XXY individuals.

In phenotypically normal XX females, one X chromosome is inactivated.  Which one of the two X chromosomes is inactivated in any given cell is random. Therefore, about one half of the cells should have the maternal X active and the other half should have the paternal X active.

XXY individuals show a wide range of clinical symptoms and intellectual ability.  Iitsuka et al. (2000) suggested that this variation may be explained by a bias in X-inactivation.   They found that about 31% (5 of 16) individuals (either XXY or XXYY) shows a very strong bias of X inactivation, which they defined as at least 80% of the cells inactivating one particular X chromosome. Two individuals has biased inactivation of the paternal X and the other three had biased inactivation of one of the maternal X chromosomes. The sample size is rather small (not surprising) but X inactivation is occuring.  Samango-Sprouse (2001) argues that incomplete inactivation of one X chromosome may also explain some of the more severe clinical mental disorders.

For Trisomy 21 (Down's Syndrome), the individual as three copies of chromosome 21, so X inactivation is not an issue. However, scientists are studying whether Xist can shut down the third copy of chromosome 21.  The Xist gene is transcribed to produce a large molecule of RNA. That RNA is what usually causes X inactivation.  Jiang et al. (2013) were able to show that Xist can coat one of the chromosome 21 copies, performing essentially the same inactivation function that it does for the X chromosome. So far, though, this work has been entirely in the lab (in vitro).


Are free-nuclear division and endomitosis the same?

No. If you google the terms you'll get a lot of sites with definitions. For example:

Nuclear division
Definition
noun
The process by which a nucleus divides, resulting in the segregation of the genome to opposite poles of a dividing cell.

source: http://www.biology-online.org/dictionary/Nuclear_division
Edit:
or

free nuclear division    mitotic division of nuclei without accompanying cytokinesis, i.e. nuclei divide in a common cytoplasm, the cells walls only forming around each later

source: http://ecflora.cavehill.uwi.edu/bio_courses/bl14apl/Gloss.htm
versus

endomitosis
mitosis taking place without dissolution of the nuclear membrane, and not followed by cytoplasmic division, resulting in doubling of the number of chromosomes within the nucleus.

source: http://medical-dictionary.thefreedictionary.com/endomitosis
or a bit more revealing:

Duplicated chromosomes produced by endomitosis exist as discrete units
in a single polyploid nucleus or may be packaged into separate nuclei,
depending on the phase at which mitosis is aborted

source: http://en.wikipedia.org/wiki/Endoreduplication
So as you see by definition nuclear division is part of a bigger process (cell division), and accoriding to the first source karyokinesis is a synonim for nuclear division (karyo = nucleus kinesis = moving, both come form greek language).
Edit:
If you check the definition above, you can see that free-nuclear division is a mitosis without cytokinesis, thus chromosome separation still occurs.
In endomitosis the can end up with a polyploid nucleus, in contrast to the other two aforementioned mechanism where no polyploidy occurs.


How would a medication cause a one to maintain a different weight?

Based on my reading, weight gain, as in resetting your maintenance set-point, which is what it sounds like you are describing, is a very well-known side-effect of the serotonin selective reuptake inhibitors (SSRI).  In some cases, patients may even discontinue the medication.  As far as I know, the underlying physiology behind this specific example is not well-understood.

In recent years, the use of next-generation sequencing (NGS) of DNA has been used to characterize the so-called microbiome in the gut of individual humans (sequencing faeces).  Some studies have reported that thin, or skinny people have somewhat different microbiomes than fat, or obese people, leading to the hypothesis that some overweight people might have bacteria that are more efficient at breaking down their food such that more of the calories are available for absorption.  Some evidence supporting this interpretation comes from experiments with fecal transplants.

If a medication also affects a patient’s microbiome (in addition to the drug’s intended therapeutic effects) then that could be another, less obvious(?) mechanism for weight changes.


will a plant grow faster if it is exposed to concentrated sunlight?

In nature, there is often ample sunlight available to plants. From this NIH page:

  However, even at the maximum light intensity encountered by photosynthetic organisms (tropical noontime sun, ≈1.2 × 1020 photons/m2/s), each reaction-center chlorophyll a absorbs about one photon per second, which is not enough to support photosynthesis sufficient for the needs of the plant. To increase the efficiency of photosynthesis, especially at more typical light intensities, organisms utilize additional light-absorbing pigments.

In other words, plants are not entirely photosynthetically efficient and do not typically use all of the light available to them. From Wikipedia:

  Photosynthesis increases linearly with light intensity at low intensity, but at higher intensity this is no longer the case (see Photosynthesis-irradiance curve). Above about 10,000 lux or ~100 watts/square meter the rate no longer increases. Thus, most plants can only utilize ~10% of full mid-day sunlight intensity.


I think the quoted answer is correct.

First, the probability of getting a son( and not a daughter) is $P_s=0.5$.
Next, since both the parents are heterozygous, the probability of genotype $hh$ is $P_h=0.25$. This genotype will not produce any antigen precursor, and hence there will be no antigens on RBC. As blood group O is defined by the absence of antigens, this can be classified as blood group O.For the expression of the antigen (dominant at the $H$ locus), the probability is $P_H=0.75$.

Again owing to the heterozygosity of both the parents at $I$ locus, the probability of getting a blood group with genotype $I^oI^o$ is $P_I=0.25$. This is the probability, that if the antigen precursor is made, $75%$% of the times the expressed blood group will be O. Therefore the probability of blood group O due to homozygous $I$ locus and dominant $H$ locus is $P_I\times P_H=3/16$.

Net probability for blood group O=(probability due to homozygous h+probability due to homozygous I and dominant H)*probability of a son.

$$P_{net}=P_s(P_h+P_HP_I)\approx 0.22$$


Modelling how much cadmium a cell will be able to chelate with phytochelatins

One of the best ways that I have found for modeling reaction pathways is to set up a boolean network for that specific pathway. The boolean will give you an idea of the possible different states in that pathway (dependencies) and while not really necessary I find it helps orient you to the system.

The next step once you have yourself oriented is to set up Michaelis-Menten equations which you can then use to run you ODEs. Here is a great primer on how to set up these equations: http://depts.washington.edu/wmatkins/kinetics/michaelis-menten.html

The subsequent modules provided in that link are also helpful in explaining how to set-up quadratic velocity equations and do different sequential models.

Also, I'm sure you know this but, it bears saying: these are all steady-state kinetics. If you are looking for a more accurate model of what is occurring in that reaction you are going to have to set-up stochastic models of your system.

Hopefully, that answers you question. Good luck!

EDIT

I have found a paper that seems to relavent to the process you are trying to model. It goes into a bit more detail than I think you are looking for but the basics seems sound. Mendoza-Cozatl and Moreno-Sanchez, 2006


Anatomical differences between herbivores and omnivores

"Is there a clear distinction at all, or is the border between the two groups somewhat fuzzy? Or are omnivores merely herbivores who are less picky?"

On second thought, I'll tackle those questions.

The "border" between herbivores and omnivores is very fuzzy among mammals, birds and at least some reptiles. Amphibians are a treat - they're all carnivores. Among reptiles, snakes are exclusively carnivorous.

Most lizards are also carnivores, though there are some herbivores. I'm not even sure about omnivorous lizards, though.

Omnivores are all over the map. If some are described as herbivores that are less picky, others could be described as carnivores that are less picky.

Note that certain species can be herbivores, carnivores or omnivores in certain parts of their range or during certain seasons. For example, bears may feast on salmon or ungulate calves when they're available but spend most of their time foraging for plants and small animals.

The most familiar omnivores include humans, pigs, raccoons and (some) rats, so you might look for some similarities between these species. Humans and raccoons are plantigrade, for example (as are bears - and rats, too, I believe). Humans, pigs and rats are known for their intelligence. Pigs and rats are very popular in medical research, for some interesting reasons.

Another thing to note is species that defy their group's general dietary tendencies. For example, the giant panda and palm nut vulture are herbivores, whereas other vultures are carnivores and most bears are omnivores - except for the polar bear.

There's another general rule; omnivores may be more rare in habitats that are lacking in plants. I don't think any marine mammals are considered omnivores, for example. All cetaceans (whales and dolphins) are carnivores, as is the sea otter. However, sirenians (manatees, dugong, etc.) are all herbivores.

That might give you something to work with.

EDIT: To my surprise, there are some good resources comparing omnivores and carnivores. Check out The Comparative Anatomy of Eating. The source might look a little flaky, but it looks very accurate to me. (It uses some of the same examples I did. ;))

To my surprise, there is apparently a closer correlation between carnivores-omnivores than herbivores-omnivores. But bear in mind that this article apparently focuses on mammals. Thus, differences in jaws and teeth can hardly be applied to birds.

Regarding my comment on omnivore intelligence, see Intelligence, Evolution of the Human Brain and Diet, though I can't vouch for its accuracy. Intelligence can be related to diet; it takes more brainpower to capture active prey than sneak up on a clump of grass, for example. This would suggest a preponderance of "intelligent" organisms among carnivores.

Intelligence can also be related to anatomical differences, like bipedalism, opposable thumbs and binocular vision.

In fact, most of the animals that are renowned for their intelligence appear to be carnivores or omnivores. Exceptions include gorillas, orangs, gibbons and the giant panda.

While whales, wolves/dogs, squids and octopuses are carnivores. Crows and ravens - regarded as among the most intelligent birds - are omnivores, as are humans, chimpanzees, pigs and at least some rats. As far as I know, pigs are generally regarded as the most intelligent ungulates (hoofed mammals); they're also among the few that are omnivores. (I can't think of any other omnivorous ungulates offhand.)

Pigs are also more compact than other ungulates, with stocky bodies and short legs. In fact, there don't appear to be many long-legged omnivores (among mammals, at least). Similarly, most (if not all) long-legged birds are carnivores (or insectivores, vermivores, etc.).


How is the number of mitochondria in a cell regulated?

The concept you refer is recognized as mitochondrial biogenesis and it is regulated by AMPK which senses the cellular energy demand. If you have few mitochondria in the cell, the electron transport chain works suboptminally generating less ATP. When the AMP/ATP ratio is high (low ATP) AMPK is activated, and turns on the catabolic pathways required to produce more ATP, included mitochondrial biogenesis.


Why can all animals swim in water without learning to swim but humans cannot?

While I am not sure I buy your assertion that all mammals know how to swim, I would say that humans are at least as good as dogs when swimming. If you drop a human in water we will instinctively flap around and try too keep our head out of the water in about as elegant a way as a dog. The main problem for humans is panicking. Someone who does not know how to swim is likely to panic and not manage to keep their head out of the water. Remember that humans float in water, if you keep calm you should be able to keep your head above the water line easily enough.
Dogs can't swim as such, they simply do the same motions in the water as they do on land. There is no different action happening, they don't instinctively do a breast stroke.
In addition, human infants actually have a couple of instincts that make them "swim" (source):

The Diving Reflex
The diving reflex, or bradycardic response, means that infants whose heads are submerged in water will naturally hold their breath. Their heart rate will also slow down while they are underwater. This reflex disappears after about six months of age.
The Swimming Reflex
Newborns placed stomach-side down in water will move their arms and
legs in a repetitive "swimming" motion. This is known as the swimming
reflex. This reflex, too, begins to fade at about the six-month mark.

That is no better and no worse than any other non-aquatic mammal can do. Try dropping a cat in water* and telling me she is a graceful swimmer :).
* Don't, that's not nice.


Secondary structure and function in mRNA and single-stranded virus RNA

Summary

Both mRNA and the RNA of ssRNA viruses can have secondary structure, which is often important in regulating translation
The extent of secondary structure of RNAs depends on the base composition and sequence, so that RNAs of various degrees of folding are possible.
Weak RNA–RNA hydrogen bonding can be competed for by weak RNA–protein interactions, so that a dynamic situation is possible — secondary structure in some circumstances which is unwound in others.

Evidence for Secondary Structure in mRNA and viral RNAs

Work in the late 1960s and early 1970s on the translation of the polycistronic single-stranded virus RNAs (MS2, R17,Qβ etc.) provided evidence for their secondary structure. The extent of masking of the ribosome binding sites (Shine and Dalgarno regions) of different cistrons affected their translation, and treatments and mutations that destroyed the secondary structure stimulated translation. This 1980 paper by Iserentant and Fiers and this 1982 paper by Hall et al. provide entries to that literature.

Eukaryotic mRNAs do not normally have ribosome binding sites, although those of certain RNA viruses like polio do, and these have distinctive secondary structure (ribosome landing pad) — see e.g. this paper from Sonenberg’s group. However the majority of eukaryotic mRNAs have extensive secondary structure at their 5'-ends, which requires a specific helicase — initiation factor eIF4A — in conjunction with eIF4B and eIF4H to unwind — see e.g. Svitkin et al., RNA (2001).

Secondary Structure varies with Sequence

A little reflection is enough to convince oneself that the extent of self-folding of a single-stranded RNA depends on its nucleotide sequence. The extent of hydrogen bonding of, for example, an (AG)n polymer (A does not base-pair with G in a Watson–Crick helix) would be expected to be much less than that of an (AU)n polymer where A–U base pairing can occur. Likewise, continuous stretches of complementary bases are likely to result in extra stabilization by base stacking, and hence in a more stable secondary structure than the same number of interspersed base pairs. The fact that the secondary structure of a mRNA can be altered by changing the nucleotide sequence without changing the amino acid sequence of the protein product is illustrated by the algorithm described in this paper by Gaspar et al., Nucleic Acids Research, (2013).

Competition by Proteins

It has already been mentioned that proteins (eIF4A and other initiation factors) are involved in unwinding eukaryotic mRNA, and there are numerous examples of the interaction of proteins with specific nucleic acid structures (including the ribosomal landing pad (aka internal ribosome entry site — IRES), previously mentioned above and shown below).

[IRES for Hepatitis C virus RNA, showing areas of interaction with various proteins. From Hellen and Sarnow, Genes and Development (2001)]

The general concern that mRNA secondary structure would impede secondary structure has some basis, but the movement of the ribosome can disrupt secondary structure, as the initial RNA phage experiments indicated. One should remember that after each peptide bond is formed, the ribosome causes the translocation of the mRNA by three nucleotides with respect to the A and P sites, so that it is continuously applying a motive force to the mRNA.

Turning to viruses, tobacco mosaic virus (TMV) — a positive single-stranded RNA virus — was the first virus the structure of which was determined by X-ray crystallography. There is, therefore, a wealth of detail as to the organization of RNA and protein in its virion — this PDB ‘Molecule of the Month’ article (illustrated below with the RNA in red) is quite accessible (in both senses). (A schematic of the virion of a different virus — vesicular stomatitis virus — VSV — is also shown.)

The assembly of the TMV virion involves initial protein self-assembly followed by the looped RNA (secondary structure) being fed in and winding round the inner core. The secondary structure origin of assembly of the TMV RNA is shown below.


If dolphins can see sound, can they say images?

As I understand your question, dolphins (and other echolators) can more or less map out their "surroundings" (which might include nearby ice floes, for example). It sounds like you're asking if they can then transmit that knowledge to other members of their species.

I don't know the answer, and I suspect no one does. However, it's hard to imagine why one dolphin would need to tell another dolphin about its surroundings when the second dolphin ought to be able to map its surroundings all by itself.

Cetaceans do communicate with each other, presumably alerting each other to danger (e.g. predators) and the presence of prey.

Incidentally, I worked on an acoustic study of bowhead whales in the Arctic Ocean years ago. We recorded bowheads and Arctic seals, which make some unbelievable sounds. We operated under the presumption that they were primarily "sounding out" their environment - searching for open areas in the ice where they could breathe, for example. It's possible that one whale might say "Hey, I found a breathing hole!" without mimicking the echoes that alerted it to that hole.

Sorry, that's not really a direct answer, but it might help put things in perspective.


The second model is the one. No tags, flags, or routers, just a 1-to-1 system.

A striking example of this is are the different effects of spinal cord injury, which depend on the place where the injury occurs.

And I quote from the apperalyzed website:

  Spinal Cord Injury Overview

  When a person suffers a spinal cord injury, information traveling
  along the spinal nerves below the level of injury will be either
  completely or partially cut off from the brain, resulting in
  Quadriplegia (Tetraplegia) or Paraplegia.

  [...] The brain will still be trying to send messages downwards to the
  muscles in the body, known as motor messages. These messages however,
  will be blocked by the damage in the spinal cord at the level of
  injury. Nerves joining the spinal cord above the level of injury will
  be unaffected and continue to work as normal.

  Quadriplegia / Tetraplegia [occurs] when a person has a spinal cord injury above
  the first thoracic vertebra. Paralysis usually affects
  the cervical spinal nerves resulting in paralysis of all four limbs.
  [...]
  Paraplegia [occurs] when the level of spinal cord injury [is] below the first thoracic spinal nerve [and leads to] paralysis of the legs and abdomen up to the nipple line, [but] paraplegics have full use of their arms and hands

This example shows that there are strict one-to-one connections (2nd model) and that messages are not simply flagged and routed to their destination via the shortest or quickest route available among a bunch of redundant, ill-defined pathways (1st model). Hence, there is only one way from the brain to the periphery; once severed the message cannot be simple re-routed via parallel lines.

Another example is the make-up of the sensory-motor cortex:

The picture shows that the motor cortex (muscle control/motor output) as well the sensory cortex (sensory input) contain a complete image of the body. Each part of the motor cortex and sensory cortex is devoted to the control or sense of one specific part of the body, respectively.

Nerves are indeed typically bundles of 1-to-1 fibers. For example, the optic nerve contains fibers that carry info from one, and only one well-defined and localized pixel from the retina to the brain.

Principles of Neuroscience by Kandel and Schwartz is a great book with a wealth of info.


Are there real world examples of one way isolation between two populations?

You might want to look for asymmetric dispersal.
Asymmetric dispersal has been found in many freshwater fishes (such as bullhead; Junker 2012), freshwater mussel (Terui et al., 2014) and in marine kelp (bull kelp; Collins et al., 2010).
That being said asymmetric dispersal does not mean that dispersal goes exclusively one way. Maybe Blondel et al. (2020) reporting asymmetric isolation caused by waterfalls in guppies can be helpful to you.
I am also thinking of polyploid and invasive lines of sunflowers that often live along rivers and reproduce clonally through cutting, where cuts gets transported by the water stream. I co-authored a paper on the evolution of these invasive sunflower lines (Bock et al., 2018) so I should know the literature well but I don't and I am not able to cite a paper that really describes the dispersal and population structure of these sunflower lines. Such patterns might be found in Mimilus as well.
Planctons follow water streams and can therefore have very asymmetric dispersal too (Pringle and Franks, 2001).
I am also thinking of plants reproducing with seed flying in the air and living on a windy sea shore or in windy wide open plane (e.g. tumbleweed). But I cannot give you a reference.


How many human proteins are very well characterized?

To address your list:

a high quality 3D structure: this you can easily get from PDB, using the answers to the question you linked as starting point. However, it is become increasingly clear that intrinsically unstructured proteins also play important roles in the cell, and for these you won't get a good 3D structure.
known activity in vivo / known associates in its activities in the cell: interaction partners can be found in databases like STRING, although just knowing the partners doesn't mean we understand what's going on :)
kinetics of its activity: I know of no good resource on this one except BRENDA for enzyme kinetics. But of course there are also kinetics to protein–protein interactions that would be interesting to know. (Update: There is AffinDB.)
regulatory elements for expression: there are databases like TransFac, but ChIP-Seq experiments show that we only know a tiny part of the regulation.

But, I think the key to a good answer lies here:

  (probably most importantly) a general consensus among experts that it is well described

I would check how often the genes are described in the literature. The GeneRIFs from NCBI may be a good starting point, because these are snippets from the literature that are curated and shown on the NCBI Gene pages. E.g. p53 has >3800 of these. The length of the summary could also be a good proxy. (Or, the length of the Wikipedia page?)


Oculus rift (or, what do other eye placements see?)

It would probably be quite disorienting, maybe even make you sick.

There is a much more limited fun classroom demo that my institution uses with kids, where they wear goggles that shift their view a couple degrees to the left (this demo is quite common, you can find many examples on YouTube as well). They stand a couple meters from a wall and throw a ball at a target: inevitably, they miss wide right for the first few throws, but eventually they adapt and hit the target no problem; then when they remove the goggles, they miss again to the left.

So, your visual system can adapt to some shifts in visual field. However, if the view was very skewed, oriented for example like the eyes of cattle, on the sides of the head, it would be much more difficult to adapt to where it feels natural. I would expect the strategy people would use would be to attend to only one visual field or the other, since there is no longer any binocular area of vision, sort of like if you would look as far to the right as you possibly can you see a lot of visual space with only one eye.

An important element to immersive VR is that you feel like you are actually having the experience - in VR when you have some sort of joystick or controller to manipulate, for example, it is really helpful to orient people by allowing them to see the controller in virtual space. Providing the eyes with very unusual inputs is going to make it much harder to maintain the illusion.


What mechanisms tell temperate trees when to drop leaves?

Here is a good USDA link:

http://www.usna.usda.gov/PhotoGallery/FallFoliage/ScienceFallColor.html

It would appear that the shortening days are a main trigger, and there are other factors. I did a basic search using Google for "what triggers leaf fall in deciduous trees?", since I always thought temperature and changing seasons were major triggers and wanted to double check.


Is there a way to prevent an HIV infection after exposure to HIV infected Blood?

The standard protocol for treating a healthcare worker that accidentally comes in contact with HIV infected body fluid is to receive HAART treatment.

HAART is an acronym that stands for Highly Active AntiRetroviral Therapy, and is a multi-drug cocktail that acts on a number of pathways to block the HIV virus from replicating.

There are early inhibitors which seek to block the binding of gp120 to CD4/CCR5.
There are Nucleoside analogs that are able to block the activity of Reverse Transcriptase.
There are Reverse Transcriptase inhibitors that can bind to allosteric sites on the enzyme, thereby effecting its ability to catalyze the reaction which produces the viral cDNA.
There are protease inhibitors which inhibit the viruses ability to make the necessary post-translational modifications, thereby causing the viral proteins to be non-functional, as they are produced from a single, long mRNA transcript.

UPDATED

This is the link to the CDC guidelines from prophylactic treatment for occupational exposure to HIV. http://www.cdc.gov/mmwr/PDF/rr/rr5409.pdf with an update to the guidelines here http://stacks.cdc.gov/view/cdc/20711

After confirmed exposure to HIV infected bodily fluid, it is recommended that HAART begin as soon as possible after exposure, that toxicity be monitored, and that the treatment be continued for 4 weeks.

The recommendations weigh the toxicity of HAART with the HIV status of the person. Even in cases where the status is not known, but the risk factors of the source are low, HAART is often not recommended.

Note that post-infection prophylaxis is less effective than preventing exposure in the first place. That is why barrier protection during intercourse (in the general case), proper handling of sharps, screening of the blood supply, and barrier protection to mucous membrane for healthcare workers is vitally important in preventing an HIV infection from taking hold.

These are the CDC guidelines for Prophylactic treatment from non-occupational exposure. http://www.cdc.gov/mmwr/preview/mmwrhtml/rr5402a1.htm

UPDATE

In the original, unedited question by the OP, they asked

  Yes It is possible to save a person when snake bites him, by sucking the poison from the bite region. so sucking AIDS Virus like snake's poison, will he get cured?

I do not know the answer to this question, nor do I think that there would be any published information regarding the efficacy of trying to suck out HIV infected blood, but given the nature of the virus and how a subcutaneous injection works, I think it is safe to say that it is highly doubtful that attempting to prevent the infection in this way would be an effective treatment option.

Also note, as March Ho stated in the comments, attempting to suck the venom of a snake bite from a wound is an ineffective method of treatment as well.


Well, it seems quite obvious that it was not a single I-eat-you-but-you-survived act but rather a convergence of endosymbiotic and host species into a greater and greater cooperation.
Of course this leaves a question if there was one or more species of endosymbionts involved.

Mitochondria are a very primeval story forced by the oxygen catastrophe, so it is hard to say, although great majority of mitochondria seems to have a single origin.

Plastids are much more divergent, however it seems that they did originated from a single source, diverged into chloroplasts, cyanelles and rhodoplasts and were later mixed up by numerous acts of secondary and even tertiary endosymbiosis (plus a further evolution); this variety can be especially seen within Euglenas, and they are the main group investigated in this manner.


Can threat to survival increase mutation rates in germline cells?

Well... since I can't delete this accepted answer... it's going to be a reverse ferret, to some extent. One 2014 review by Ram and Hadany lists a fair number of SIM occurrences outside of bacteria:

Stress-induced mutagenesis (SIM)—the increase of mutation rates in stressed or maladapted individuals—has been demonstrated in several species, including both prokaryotes and eukaryotes. [...] SIM has also been observed in yeast, algae, nematodes, flies and human cancer cells.

The one for algae (Goho and Bell, 2000) appears/claims to have been the fist:

Cultures of Chlamydomonas were exposed to a range of relatively mild stresses for a period of 24 h. These stresses comprised high and low temperatures, osmotic stress, low pH, starvation and toxic stress. Fitness was then assayed as the rate of division of isolated cells on agar. We found that there was a strong tendency for stressed cultures to have lower mean fitness and greater standardized variance in fitness than the negative controls which had been cultured throughout in unmodified minimal medium. The same tendency was shown, as expected, by positive controls which received mutagenic doses of ultraviolet irradiation. We concluded that the most reasonable interpretation of these observations is that mild stress increases the genomic rate of mutation.  This appears to be the first time that this phenomenon has been noticed in eukaryotes.

The paper cited for Drosophila, Sharp and Agrawal (2012)

Our results show that mutation rates are sensitive to genetic stress, such that individuals with low-quality genotypes will produce offspring of even lower genetic quality, in a mutational positive feedback loop. This type of variation in mutation rate is expected to alter a variety of predictions based on mutation load theory and accelerate adaptation to new environments. Positive mutational feedback could affect human health by increasing the rate of germline mutation, and possibly somatic mutation, in individuals of poor health because of genetic or environmental stress.

Clearly this one is quite bold in extrapolating its findings.
And long story short, the paper on nematodes (Matsuba et al., 2012) finds a temperature dependant mutation rate.
What seems to be the weak point in these paper, and perhaps why a more critical review of Lynch et al., 2016 of SIM doesn't mention them, is that no explicit mediating mechanism appear to have been identified in these studies on eukaryotes. In bacteria (e.g. the paper linked by the OP) how SIM works inside the cell is pretty well understood, there are in fact several mechanisms that all respond (convergently) to various forms of stress.
There's an acknowledgement (in the Drosophila) paper, that such mechanisms in eukaryotes might differ from bacteria

The sources and mechanisms underlying this variation have been best studied in microbes, but the sources of variation in microbes may differ from those in multicellular eukaryotes for several reasons. [...]
In animals, mutation rate varies among genotypes, although the functional sources of this variation are unknown. [...]

It does go on into some theories how it might work.
As for yeast, Rodriguez et al. (2012)

Mismatch repair (MMR) is a major DNA repair pathway in cells from all branches of life that removes replication errors in a strand-specific manner, such that mismatched nucleotides are preferentially removed from the newly replicated strand of DNA. Here we demonstrate a role for MMR in helping create new phenotypes in nondividing cells. We show that mispairs in yeast that escape MMR during replication can later be subject to MMR activity in a replication strand-independent manner in nondividing cells, resulting in either fully wild-type or mutant DNA sequence. In one case, this activity is responsible for what appears to be adaptive mutation. This replication strand-independent MMR activity could contribute to the formation of tumors arising in nondividing cells and could also contribute to mutagenesis observed during somatic hypermutation of Ig genes.

I guess a weak point of this paper vis-a-vis of SIM (which they only mention in passing) is that it's not obvious in their setup what the stress was. Basically they saw (adaptive) mutation-rate change (in response to the environment), but they don't pinpoint what exactly they think the stressor was. So this paper is a way the reverse of the other three I, i.e. the mechanism is clear, but stress is not.


Trying to extract DNA with an incomplete kit

It is the vortex step that is causing you the trouble. But you can vortex manually, by pipetting up and down a few times in the well. Then seal the top of the plate with parafilm for centrifugation.


Restriction enzymes, how are the recognition sequences determined?

This paper describes a simple method to determine restriction sites, which was used to determine the restriction sequence of the previously uncharacterised enzyme from Haemophilus gallinarum.

In short, a known sequence of DNA (from the phage $\phi \text{X174}$) is partially digested with the restriction enzyme, and the various digested fragments can be used to determine the relative distances between each of the restriction sites.

Then, the restriction fragments are extended using T4 polymerase and sequenced using $^{32}\text{P}$ labelled Sanger sequencing.

Once the restriction map of the enzyme on the known DNA sequence is completed, the individual fragments can then be checked for similarities. For example, HgaI has a recognition site outside of the restriction site. Therefore, when the individual restriction sites are compared, it can be seen that all of them have the recognition site GACGC.


number of RNA pol II molecules in a given human nucleus?

it is highly variable even in a single cell type.

Dont know for a human cell but this is the range for ecoli: 1500-11400

check this site out. got this number from there (its quite useful for questions like these):

http://bionumbers.hms.harvard.edu/bionumber.aspx?&id=101440&ver=3&trm=RNA%20polymerase

You can estimate protein copy numbers and there are techniques available for doing so. One of such techniques:

http://www.mcponline.org/content/11/3/O111.009613.long

You can also calculate concentration using traditional techniques like western blot and elisa and calculate approximate copy-numbers (you have to also calculate average cell volume and number of cells for protein extraction.


Is Batesian mimicry more important for females?

In sexually dimorphic ant-mimicking spiders, it depends on the specific species which sex resembles the ant most (Cushing, 2012).

In many cases of sexually dimorphic spider myrmecomorphs, the male is more mimetic than the female, such as in Corinnidae species and the genus Castianeira, Oonopidae and Antoonops.

Such sexual dimorphism may be adaptive if the sexes are exposed to different predation pressures. The spider's mimicry of noxious ant species yields protective benefit from predators who would avoid the ants. However, the mimicry often results in being more conspicuous in their color markings than related spider species that are more camouflaged. Hence, conspicuousness can be considered a cost of Batesian mimicry. A palatable species may be evolutionary maximizing its level of protection for the smallest cost (in terms of conspicuousness). Sexual dimorphism, in which the more active sex (which, in spiders, is typically the males) evolves mimetic resemblance to noxious ants, whereas the other sex remains relatively more concealed and camouflaged behaviorally and morphologically.

Reference
Cushing, psyche (2012); 151989: 1-24


distribution of some injected materials/medicines through blood vessels

It depends on what your target tissue is, as @another 'Homo sapien' stated.

If you want to get something to the hand, for instance, injecting it into the brachial artery will get it there "faster" than injecting it into the cephalic vein.

However,

  Fastest distribution of some injected materials/medicines & with no risk of any kind

does not exist. There are risks with any invasive proceedure, and invading arteries is riskier than invading veins. Unless the risk outweighs the benefit, substances which cannot be administered orally are given intravenously. Arterial lines are usually used for purposes other than injecting substances.

Arterial Line Placement


As the comment by @terdon says, the most likely explanation is that your species identification is mistaken. The superfamily Curculionoidea, which contains the weevils (Curculionidae are the true weevils) is also extremely species rich. Without seeing a picture of what you found, there are many other similar species with long necks in the family Attelabidae, which is the family of Trachelophorus giraffa. For instance, the wikipedia page includes a picture Apoderus longicollis which is very similar to the Giraffe weevil from Madagaskar, and it is supposed to be found in India (see GBIF info):

Paracycnotrachelus is another genus found in Asia where some species have long necks. Another giraffe-necked species is also found in New-Zealand - see Lasiorynchus barbicornis - so the overall body shape is not that unique (note that much of the elongation in this species is of the snout though):

Even if we should never rule out the possibility of range changes/introductions, this must be based on close examinations of the specimen, and it is even more unlikely in this case since Trachelophorus giraffa seems to be a very specialized species.


Do humans have a "dominant" neurotransmitter system/sensitivity within their brain?

Dr. Helen Fisher's conclusions are plain bunkum. What does it even mean when she says associated with a particular neurotransmitter? The sheer work required to even get at this question is vast and difficult so it is unsurprising that she is venturing as much as a guess.There is scientific evidence to support different neurotransmitters systems can go awry in diseases but Fisher is overinterpreting the literature. Take a look at the neurotrasmiter table and you can see what each does and how malfunctions can result in certain diseases.
http://en.wikipedia.org/wiki/Neurotransmitter

Also testosterone and estrogen are thought of primarily as hormones not neurotrasmiters.So Fisher is saying women(who have more estrogen) are better negotiatiors whereas men(more testosterone) are directors. Even these banal conclusions are contentious and debatable.


building intelligent structure with random evolution requires series of non useful steps

What you say is true, but the answer as to how modern evolutionary theory understand this considers other ideas about living things which seem to allow so called 'neutral traits'.

Neutral traits being those phenotypes which seem to have no particular relationship to fitness. Toungue rolling is an often mentioned example.  Some folks argue that there is only adaptive changes and phenotype, others like Gould and Lewontin argue that some traits can be the result of pleiotropy.

So first of all this sort of discussion can tell us that the question is argued both ways in a convincing enough way that it is not resolved in biology - some argue quite confidently that all traits are selected for and things like flagellar motors and upright ambulation and eyeballs evolve because of and experiencing constant evolutionary pressure.  Others argue that these genes that produce these things are doing something else useful while they are becoming these later more useful traits.

The common twist here is plieotropy.  That the genes that are producing the phenotype one is observing is also participating in one or more other biological traits that may is being positively selected for.

A more interesting example of how this works is the domesticated silver fox experiment. Foxes which have had domestication bred into them (just to show that it can be done by selection) lose their red color and their ears are softer and fuzzier.  Nobody tried to select for these traits, but they come associated with each fox that is domesticated.  Are these traits plieotropic or only very tightly linked?  So far they have not been exhibited separately.  In any case I think its fair to say that the experiment didn't care about the color of the fox - only its meekness towards people.  These traits come along for the ride.

So it might be with any other desirable genetic trait.  If a gene becomes closer to producing a lung from a gill, if that gene is sticking around it must be because there is positive selection for that trait, even if the lung like gill is not particularly useful for that fish.

Sorry but I actually disagree that it is obvious that non-useful steps must be had for any such complicated trait.  If that were true then you would have a point, but not every biologist would give that to you.

It might be a bit surprising that such discussions are and continue to be matters of faith in science, but I hope you don't dismiss it because of this either.  All sciences do assume some things that make their view of the world make more sense.  But there are also other components of these theories which are consistently observed and understood that demand them... until they don't.

I don't give really any credence whatsoever when someone says 'this is a widely accepted theory by the scientific community'.  This in itself is not a scientific statement, but more the hope that someone else has one somewhere.  But a refutation must also take under consideration what is being refuted.


There is indeed a repulsive force between the phosphates in the DNA backbone. (The pK of the phosphate is very low so it will be ionised at all physiologically-relevant pH.) This is why DNA behaves like a stiff rod over short distances. However cations in solution will help to shield some of this repulsion. This is why DNA melting temperature decreases as the ionic strength of the buffer is reduced (by increasing the repulsive force relative to the favourable energy term coming from the base-pairing).

When DNA is condensed these repulsive forces are masked by cations like spermine, and of course by histones.


Is synesthesia caused by crossing the circuitry of different sensory inputs?

Short Answer
Synesthesia happens at a point during processing where we are not dealing with "raw visual input" or "raw auditory input" anymore, but already with more abstract constructs such as "colors" or "sounds".
Full Answer
Your question seems to consider sensory perception as a matter of "inputs" and the brain detecting those inputs, such that for example the only difference, from the brain's point of view, between visual inputs and auditory inputs is that one comes from the ear and the other from the eye.
A more accurate way of seeing it is that our sensory perceptions are really the brain constructing a coherent reality from the information it got from our senses. And I do mean "information" in the most abstract, computer-sciency sense possible. It's not like our eye is a photographic plate that contains "what we see", and the brain just has to reconstruct that. The processing of visual information, by which I mean picking out various features from the light received and deriving meaning from them, starts right in the retina. Some examples from the "14.5 Visual Processing in the Retina" section in this page:
http://nba.uth.tmc.edu/neuroscience/s2/chapter14.html
On bipolar cells:

The two bipolar cell types have different functional properties.

The off bipolar cells function to detect dark objects in a lighter background.

The on bipolar cells function to detect light objects in a darker background.

On horizontal cells:

The surround effect, produced by the horizontal cells, enhances brightness contrasts to produce sharper images, to make an object appear brighter or darker depending on the background and to maintain these contrasts under different illumination levels.

On the retinal ganglion cells:

The retinal ganglion cells provide information important for detecting the shape and movement of objects.
Type P retinal ganglion cells are color-sensitive object detectors.
Type M retinal ganglion cells are color-insensitive motion detectors.

On amacrine cells:

There are 20 or more types of amacrine cells based on their morphology and neurochemistry. The roles of three types have been identified. One type

is responsible for producing the movement sensitive (rapidly adapting) response of the Type M ganglion cells.

enhances the center-surround effect in ganglion cell receptive fields.

connects rod bipolar cells to cone bipolar cells, thus allowing ganglion cells to respond to the entire range of light levels, from scotopic to photopic.

Similarly in our ears, the cilia cells that vibrate in response to sound are frequency-dependent, and it is information about those frequencies that gets transmitted to the rest of the brain for processing. In other words the very organ that detects sound also performs a kind of Fourier transform on the sound waves it detects before anything else.
See for example:
https://psychology.stackexchange.com/questions/15274/how-does-the-inner-ear-encode-sound-intensity
This parsing, combining and interpreting of information continues throughout the perceptual circuits of the brain, and not in a straightforward way either - it is hypothesized that there are two independent or semi-independent processing streams for visual information, the ventral and dorsal streams, one which is for identifying objects and the other for guiding actions:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4678292/
There is also information flowing the other way, where more "advanced" brain regions draw conclusions about what's actually there and feed those conclusions back into the more "basic perception" parts to ensure that that's what we see. I.e. perception has both "feedforward" and "feedback" processes, or "bottom-up" and "top-down".
All of this is to say, there is absolutely no way for the brain to confuse information from the retina and information from the ear; the early processing in both of those is too tightly linked to the organ itself, and perception as a whole is inextricably linked to cognition. It's not like a mouse and keyboard that you can plug into different sockets; the retina technically is part of the brain in the first place!
This is not to say visual and auditory senses cannot be confused, obviously synesthesia happens, but it likely happens at a point in the processing where we're not dealing with "raw visual input" or "raw auditory input" anymore, but already more abstract constructs such as "colors" or "sounds".
For example this paper (gotten from the Wikipedia page https://en.wikipedia.org/wiki/Neural_basis_of_synesthesia) :
https://web.archive.org/web/20060527085838/http://psy.ucsd.edu/~edhubbard/papers/JCS.pdf
Hypothesizes that the synaesthetic association of letters with colors is caused by cross-wiring between the area of the visual cortex that processes letters and the one that processes colors.
This paper from the same source:
https://academic.oup.com/brain/article-abstract/118/3/661/321747?redirectedFrom=fulltext
Finds that color-word synaesthetes had, when told words the associated with colors, activation in the language and "advanced" visual processing areas but not in more basic visual processing areas.
Similarly for autism, given that sensory perception happens at every level in the brain, including conscious thought, those perceptions can be blocked or filtered (or not) by the brain at any stage. No need to assume it is at the "raw input" stage.


Are mutations a source of genetic variation?

Going through the possible answers

(A) Rates tend to be very high in most populations.

This is a very unclear statement. What does "high" mean? In humans, the average mutation rate per reproduction per nucleotide is of the order of $10^{-8}$ (Rahbari et al., 2016) (hence of the order of 10 - 100 mutations for the whole genome). Whether someone wants to call that high or low is up to this person original intuition.

(B) generally lethal

No, that's wrong (Robert et al., 2018)

(C) irreversible

It is a little unclear. By "irreversible", do they mean that the function of the gene (or of any other functional element in the genome) cannot be restored or do they mean that a specific mutation cannot be exactly undone by a future mutation. In both cases, however, it would be wrong!
Mutations that restore the function of a gene (or any other genomic functional element) are called reverse mutations (aka. suppressor mutations; I personally don't know of any difference between the concepts of reverse mutation and suppressor mutation). Most reverse mutations are likely to act via a second mutation that restores the function of the gene rather than undoing the previous mutation. It does not mean however that it is impossible a mutation that perfectly undoes a previous mutation. Consider a substitution inverting A into T. A reverse mutation could do just the opposite.

(D) Only certain gene locations are affected.

Mutation rate varies throughout the genome but all of the genome is subject to some non-zero mutation rate.

(E) source of genetic variation

Yes, mutations are the ultimate source of genetic variation in populations, while genetic drift and directional selection removes variation.
As other users have highlighted in their answers, many mutations (incl. synonymous mutations but not only and soma mutations) do not bring up any the underlying genetic variance of phenotypic traits. These details are however mainly irrelevant; what matters is that it still remain true that (some) mutations increase genetic variance.
We could also add the complication as to wonder whether by "genetic variance", they meant "genetic variance underlying phenotypic variance" (which is its standard usage) or "genetic variance where one allele is given an arbitrary value and another (problem arising for loci with more than 2 alleles segregating). More information about the terminology and the math when it comes to quantifying genetic variance in the post Why is a heritability coefficient not an index of how “genetic” something is?
What I would have answered

The correct answer is (C). These recent conclusions about mutations—recall that Darwin did not know of mutations—are all the reverse of those listed in the choices, with the exception of choice (C), the correct answer. Rates, in fact, tend to be below in populations, mutations are generally not lethal, any gene location can be affected, and they are felt to be the source of genetic variation. Darwin felt over-production of offspring was the source of potential variation.

I disagree. To me, B and D are wrong, A is unclear, C is slightly unclear but wrong in both interpretations I can think of and E is correct. I would have answered E.
About the justification given

Rates, in fact, tend to be below in populations [..]

This piece of the sentence is not even grammatically correct. Below what? It highlights that A is unclear.

they are felt to be the source of genetic variation

The term "felt" is poorly chosen here IMO, but this piece of the sentence seems to rather give credit to answer E. I think, whoever wrote this answer mistakenly wrote C instead of E

Darwin felt over-production of offspring was the source of potential variation.

Really, who cares about Darwin thoughts on the subject here?! But in any case, this sounds like a misrepresentation of Darwin's ideas. More info can be found in Charlesworth and Charlesworth (2009) and also maybe this post


What is the cause of "imbalanced" linkage disequilibrium?

This can occur if the Ab genotype is lethal, i.e. you won't observe individuals with a Ab genotype.

Allele lethality is a common mechanisms that can explain non-mendelian inheritance of a trait.

For the question of which LD metric to use, this is tricky. Under the assumption that allele lethality is indeed at play, you observed perfect haplotypes, so D'=1 wouldn't be incorrect. Yet the correlation coefficient is also correct in the sense that SNP A is not a perfect proxy for SNP B.


I think you are correct, but I'm not an expert in Diptera/Drosophila morphology. Since the prothorax (pronotum) and metathorax are greatly reduced in flies, you mostly see the mesonotum in dorsal view, and this includes the scutellum. Personally, I think it would have been more accurate of them to label this structure mesonotum, or at least dorsal mesothorax length, since mesothorax could just as well imply a ventral view (mesosternum).

More information can be found at this webpage: Flies - Morphology and anatomy: Thorax, which state that:

  The mesonotum occupies most of dorsal view of the thorax. In order anteroposterior we can identify four parts, called as follow (McAlpine, 1981): prescutum, scutum, scutellum, and postnotum. The scutum is the most large, condition considered apomorphic for the entire order of Diptera.

Also see this picture of the mesonotum from diptera.net


How can ingesting a prion "infect" someone?

Prions are misfolded proteins with abnormal tertiary or quaternary structures. That grants them resistance (to some extent, at least) to proteases (1).

Also researchers believe that prions are able to replicate (2), by changing the structure of other proteins.

Regarding the gastrointestinal barrier, that isn't exactly true. It has been shown that small quantities of intact proteins do cross the gastrointestinal tract in animals and adult humans (3), and that this is a physiologically normal process required for antigen sampling by subepithelial immune tissue in the gut

So, the resistance to the proteases and the ability to replicate in certain conditions might explain the odds of a prion crossing the gastrointestinal tract and infecting an individual.

References:

http://www.ncbi.nlm.nih.gov/pubmed/24338008
http://www.nejm.org/doi/full/10.1056/NEJM199609193351218
http://www.ncbi.nlm.nih.gov/pubmed/3060169


How does the Endoplasmic Reticulum scale with Cell Volume in Epithelial Cells?

Please consider this "answer" as an enlarged comment. I can't answer your question, but it's possible that my speculations or considerations could be helpful in your particular situation, in the early phase of building a model.
First of all, I doubt that general formulas that link cell-volume to ER-volume of different cell-types can exist. Dependent on the specific cell-type, (dependent of the protein production need in the rough ER), the ER/total ratio can strongly vary (i.e. compare neurons (strongly protruding ER), red-blood cells (no ER), pancreatic cells (large ER), endothelial-cells..). Thus, any correlation may just be chance, without the general meaning that you truly seek.
Therefore, you should focus on such volume-correlations within the same cell-type at different cell-cycle stages.
In this context, I can think of mathematical considerations, that could help your model: When cells divide, they effectively half their membranes (membrane-lipid count). Mathematically, this means that the overall volume of the cell should reduce to around 35%. In contrast, the volume of the ER as a highly condensed structure could scale linear with its surface area, if we see it as a long tube that gets separated. From this, you could build an easy mathematical model, in which ER volumes are relatively bigger, when cells are small.
However, according to cell-size measurements this is not true; cell-volumes get halved [1] when cells divide, which should indicate relative stretching of the membrane. Unfortunately, I could not find any data on how the stretching of the cell-membrane relieves over time. Further, the volume (quite) linearly increases over time until the next division can take place [1].
This means the cell-membrane keeps a constant weight/V before and after cytokinesis, while the surface-area increases by root 2. Given, that the ER-membrane-mass is also halved when the cell divides, and there is no apparent mechanism that should cause swelling, it is still quite difficult to predict how the ER volume would change. Again, the ER is no simple sphere, but has a highly collapsed shape.
However, I found this source, that deals with changes in shape and volume of the ER during the cell-cycle. Apparently, there is a membrane exchange between nucleus and ER and the ratios in volume between ER and nucleus is constant throughout the cell-cycle. You can study this yourself in more detail, but I would take this observation as an indication, that the ER volume behaves as would be inferred from a mathematical standpoint; to the third power of the diameter of the cell.
To sum it up, I initially expected smaller cells seem to have relatively larger ER volumes, and I suspect, that you had a chance to fall for the same trap. However, if the volume-ratios are not constant, they should rather behave the opposite way: ER takes less cell-volume after division, when the cells are small.


What is the biochemical explanation for tingling and burning sensation in brain due to certain food?

You are right the compounds provoking this burning/tingling sensation is called allyl isothiocyanate.

We (human) perceive these compounds in two different ways when ingested, namely via the gustatory and olfactory systems. The molecular receptor sensing isothiocyanates is called the transient receptor channel A1 (TRPA1) [ref].

Here a simplistic view of how ingredients are perceived:

Gustatory sensation

First we get a burning sensation in the buccal cavity due to TRPA1 receptors present on the surface of the sensory neurons of the trigeminal nerve. In essence isothiocyanates dissolved in the saliva will activate those neurons via TRPA1 provoking electrical impulses in the trigeminal nerve which leads to a burning sensation.

Retronasal olfactory sensation

For several food ingredients we also perceived an aroma (taste = gustation, aroma = olfaction, taste + aroma = flavor). The aroma of an ingredient is perceived by olfactory sensory neurons in the nasal cavity and because some of the ingested ingredient will be vaporized inside the buccal cavity and travel through the nasal cavity where they are perceived (retronasal perception).

Not so surprisingly, isothiocyanates will again be perceived by sensory cells of the olfaction system via TRPA1 hence a burning sensation in the nostrils.

How receptor activation leads to a neuronal stimuli

This is a very broad subject and I will only give an overview of what is happening. We first start with the activation of a receptor by an agonist (in your question, isothiocyanates binding and activating TRPA1). Upon binding of the agonist the conformation of the receptor will change from an inactive to an active state. The way the signal is transduced varies according to the type of receptor but for the TRPA1 channel what happens is that the channel opens leading to an influx of calcium ions ($Ca^{2+}$) in the cells which changes its electrical state (as calcium ions are positively charged), a phenomena called depolarization. Depolarization of specific sensory cells (here the one expressing TRPA1) start an electrical signal in the nerve which travels to the brain where it is then decoded. The exact way the brain decodes sensory signals is still under debate but a likely explanation is that only some neurons within the nerve are activated which allows the brain to decode the sensory signal based on the nerve activation pattern. As an analogy, it would be the same as having only specific wires (neurons) turned on within a bundle of wires (nerve).

Further reading

If you want to further extend your knowledge on taste perception at the molecular level read this excellent review Chandrashekar, 2006. For a in-depth review on olfaction refer to this book. For a book on signal transduction refer to this while for TRP channels activation this is a good reading.

The field is quite broad and there are many good references. Sensory perception includes two distinct and broad fields namely neurosciences and cell signalling.


Is numbness the absence of one or all touch sensations?

The definition of numbness has been answered by yourself, and I will focus on the second part of the question.

In terms of the underlying physiological mechanism behind numbness I think it's good to narrow the question down and focus on local anesthetics, which numb a local area of the body for minor surgical procedures. Cocaine and related compounds have been shown to block not only pain, but also warmth, cold and touch perception, as well as blocking motor function. Cocain and related compounds are basically voltage-gated Na+ channel blockers, but also block K+ channels to some extent. Their affinity to various different channels differs, explaining the differential effects. E.g., pain is blocked more effectively than motor functions (Scholz, 2002).

We all know the feeling of numbness when our limbs are asleep due to restriction of blood flow. Likely all neural activity is blocked here too, as the cutting off of oxygen affects all neurons.

Given the broad range of effects of local anesthetics and restriction of blood flow, I would tentatively conclude that numbness can be interpreted as a reduction of sensitivity of all the senses.

Reference
- Scholz, Br J Anaesth (2002); 89; 52-61


Time lapse between fresh blood's exposure to air and that same blood turning darker red-brown

In comments it been discussed that clotting is partial answer to OP. I would say, that is is somewhat tangential to the original question.

If I may re-phrase, OP asks: how one can estimate age of blood that has been exposed to air? Problem is that you will have to have a starting point to solve that backwards, like having an initial condition for solving differential equation.

One example that can be used is measurement of $pCO_2$ content in blood serum. If it is available, someone already collected this data. In 2 hours $pCO_2$drops 30% and total $CO_2$ drops about 6%.

Moreover, it seems that during hemorrhagic shock RBC shape changes, which means that sampling patient you will be able to approximate time since bleeding started. However, you will need an electron microscope at your disposal...

Finally, and I'll leave it like that, cellular death is a powerful process that leaves a lot of traces. Apoptotic cells have mitochondria bursting (except in RBC there are no mitochondria) and releasing, for example, cytochrome C. In case of bleeding probable cause of cellular death is necrosis, so different biochemical changes will occur. Point is that you can measure time since necrosis/apoptosis started by careful measurement.


Need help identifying multi-colored grasshopper

It's what's called a Rainbow or Painted Grasshopper (Dactylotum bicolor).

You can learn more at Bug Guide Species Dactylotum bicolor (where the picture is found) or Wikipedia' article on Dactylotum bicolor. The colour and pattern is very unmistakable.


Why doesn't Fenoxaprop-P-ethyl damage cool season lawns?

A number of studies have been done that investigated resistance to Fenoxaprop-P-ethyl and related compounds. Most of these studies focused on resistance in crops (e.g., maize) or black grass. One of these studies (Kay et al., 1999) was particularly interesting as it focused on several possible mechanisms of herbicide resistance in Alopecurus myosuroides (Black-Grass). I quote from the abstract:

  [...] Resistance at the whole-plant level correlated well with reduced acetyl Co-enzyme A carboxylase sensitivity (target site resistance) in two of the populations (one from the United Kingdom and one from Germany) but enhanced metabolism appeared to be the primary mechanism of resistance in the majority of the other populations. [...] We suggest that resistance in Lincs E1 may be explained by multiple resistance mechanisms—the expression of both insensitive acetyl Co-enzyme A carboxylase and an increased rate of detoxification. However, resistance in the population Clay from the United Kingdom could be explained neither by target site insensitivity nor by an enhanced rate of metabolism. These results provide conclusive evidence that a single resistance mechanism alone cannot explain insensitivity to fenoxaprop-P-ethyl in European resistant black-grass populations and that additional, as yet uncharacterized, mechanisms must also be present.

So based on these data, I think several mechanisms may play a role in the cool season lawn grass resistance (a species name may help to specify my, admittedly, broad answer).

Interestingly, Fenoxaprop-P-ethyl is an acetyl CoA carboxylase (ACC) inhibitor (Kay et al., 1999). Note that Haloxyfop (as mentioned in your question "How does Haloxyfop control young grassy weeds in fields of broadleaved crops?") is also an ACC inhibitor. From the answer on that question it appears that ACC inhibitors inhibit cell membrane formation and that monocots (grasses) are most susceptible and dicots less. Dicots are less sensitive because they have two ACC types at their disposal, one being insensitive to ACC inhibitors. Not surprisingly then, Bermuda grass, being a monocot is killed by this herbicide. Interestingly however, other monocots seem to survive, such as the cool-season lawns you mention.

I was not able to find conclusive evidence as to why some monocots survive ACC inhibitors. An educated guess is that resistance can be conferred by mutations in the ACC enzyme (Letouzé & Gasquez, 2001) that make the enzyme less sensitive to the herbicide. These mutations can be caused by repeated exposure to these herbicides, whereby strains become resistant to the material, much like the way in which (multi-) resistant bacterial strains emerge after repeated exposure to antibiotics.

References
Kay et al. Pesticide Biochem Physiol 1999; 65:169–80
Letouzé & Gasquez, Theoretical Applied Genetics 2001; 103:288-96


Tools that take a kinship matrix for phylogenetic decorrelation

If you willing to do Bayesian model fitting, this is likely possible but will take some tinkering to make sure the models are what you think they are. Stan (via rstan or brms), can fit multinomial logistic regressions (A demo from Thinkinator).

If you can convert these models to pure stan code, then you can incorporate phylogenetic/kinship/arbitrary correlation structure into the model following this example on github (or this one). I have had better luck getting phylogenetic regression to work correctly in pure stan than via convenience functions.


Photolysis in the Light Reactions of Photosynthesis

A catalytic site on a subunit of Photosystem II is responsible for splitting water via photo-oxidation. This site, called the Oxygen-evolving complex (or OEM), uses energy from sunlight (which is converted to electrochemical potential energy in the photosystem's reaction center) to accomplish this task.

 Source: Wikimedia

See Barber (2012)1 for an explanation. The abstract (my emphasis):

  The oxygen in our atmosphere is derived and maintained by the water-splitting process of photosynthesis. The enzyme that facilitates this reaction and therefore underpins virtually all life on our planet is known as photosystem II (PSII), a multisubunit enzyme embedded in the lipid environment of the thylakoid membranes of plants, algae, and cyanobacteria. During the past 10 years, crystal structures of a 700-kDa cyanobacterial dimeric PSII complex have been reported with ever-increasing improvement in resolution--the latest at 1.9 Å. Thus, the organizational and structural details of its many subunits and cofactors are now well understood. The water-splitting site was revealed as a cluster of four Mn ions and one Ca ion surrounded by amino-acid side chains, of which seven provide ligands to the metals. The metal cluster is organized as a cubane-like structure composed of three Mn ions and the one Ca2+ ion linked by oxo bonds. The fourth Mn is attached to the cubane via one of its bridging oxygens together with another oxo bridge to an Mn ion of the cubane. The overall structure of the catalytic site provides a framework to propose a mechanistic scheme for the water-splitting process and gives a blueprint for the development of catalysts that mimick the reaction in an artificial chemical system as a means to generate solar fuels.

My understanding is that we are still not totally certain how this actually works...

Cady et al. (2008)2 wrote a review in 2008 of various functional models trying to explain the chemistry of the oxygen-evolving complex of photosystem II.

A quick Google Scholar search reveals plenty of proposed mechanisms published since.

Most currently proposed mechanisms do, however, incorporate the 4 oxidation steps proposed by Kok et al. (1970)3 (now referred to as the Kok Cycle, or Kok's S-state cycle).

From Kern et al. (2013)4:

  The oxidation equivalents generated by the absorption of four photons by the PS II reaction center are stored in the four consecutive redox states of a Mn4CaO5 cluster, known as the Si (i=1 to 4) states. The accumulated energy is used in the concerted oxidation of two molecules of water to form dioxygen (1) returning the catalyst to the most reduced S0 state in the Kok cycle (Scheme 1).

 Scheme 1 from Kern et al. (2013) explaining states of Kok Cycle.

You can learn more here.

Works Cited:

1 Barber, J., 2012, January. Photosystem II: the water-splitting enzyme of photosynthesis. In Cold Spring Harbor symposia on quantitative biology (Vol. 77, pp. 295-307). Cold Spring Harbor Laboratory Press.

2 Cady, C.W., Crabtree, R.H. and Brudvig, G.W., 2008. Functional models for the oxygen-evolving complex of photosystem II. Coordination chemistry reviews, 252(3-4), pp.444-455.

3 Kok, B., Forbush, B. and McGloin, M., 1970. Cooperation of charges in photosynthetic O2 evolution–I. A linear four step mechanism. Photochemistry and photobiology, 11(6), pp.457-475.

4 Kern, J., Alonso-Mori, R., Tran, R., Hattne, J., Gildea, R.J., Echols, N., Glöckner, C., Hellmich, J., Laksmono, H., Sierra, R.G. and Lassalle-Kaiser, B., 2013. Simultaneous femtosecond X-ray spectroscopy and diffraction of photosystem II at room temperature. Science, 340(6131), pp.491-495.


Alternative plant taxonomies to Linneaus

The most common alternative to taxonomic classifications are functional classifications. Emphasizing ecological similarities rather than similarities in relatedness, they can be regarded as complementary approach to, but not as a replacement of taxonomy. Why do we need this? Because species often perform very similar tasks, exhibit very similar characteristics and, most importantly, are very, very numerous (there are ~ 300,000 vascular plants). Reducing this redundant complexity is crucial for decision-making in conservation politics or the projection of vegetation change under future climatic conditions (Woodward & Cramer, 1996).

The idea behind this is to use functional traits, such as seed size, height, photosynthetic pathway, root density, etc., as a surrogate of a species' ecological 'role' -- its response to environmental factors and its impact on ecosystems. Seed mass for example (functional trait), is a proxy for the dispersal ability of a plant (function, performance). You should have a look at Lavorel et al. (2007), there is a nice table (too big to include here) that links specific traits to the actual ecological functions they describe. But look at this figure from the same paper:

By applying multivariate statistics like cluster analyses or ordination methods, species can then be classified into functional types. To make up one example, a functional type that might emerge from species with the following traits

height: > 20 m
seed size: > 0.5 cm
woody: yes
Specific leaf area: low

would certainly represent climax forest trees. This classification does not distinguish between individual species, because, from an ecosystem perspective, they all are functionally roughly equivalent.

For further research google 'Functional trait', 'Plant functional type' or have a look at refs 3 and 4.

Citations:

Woodward, F. I. and Cramer, W. (1996): Plant functional types and
climatic change: introduction. Journal of vegetation science, 7(3):
306–308.
Lavorel, S., Díaz, S., Cornelissen, J. H. C., Garnier, E., Harrison, S. P., McIntyre, S., Pausas, J. G., Pérez-Harguindeguy, N., Roumet, C., and Urcelay, C. (2007): Plant
Functional Types: Are We Getting Any Closer to the Holy Grail? In: Canadell,
J. G., Pataki, D. E., and Pitelka, L. F. (editors): Terrestrial Ecosystems in a Changing
World, Global Change—The IGBP Series, pages 149–164. Springer Berlin Heidelberg.
Halloy, S. (1990): A morphological classification of plants, with
special reference to the New Zealand alpine flora. Journal of
vegetation science, 1(3): 291–304.
Leishman, M. R. and Westoby, M. (1992): Classifying plants into groups on the basis
of associations of individual traits–evidence from Australian semi-arid woodlands.
Journal of Ecology, 80: 417–424.


RMSD during conformational transition in proteins

The best way to distinguish "actual conformational transition from thermal fluctuations" in a protein is to (determine and) compare atomic-resolution structures of the ligand-free and ligand-bound protein.

http://www.rcsb.org/pdb/home/home.do


Density of neurons/cells in the mouse brain

The newest and most accurate method (far more accurate than older extrapolating/manual counting methods (Stereology) and yielding some surprising results) to estimate number/density of neurons/cells in brains is Isotropic Fractionator to my knowledge. Using this keyword you find some recent papers, comparing different brain areas (cerebral cortex, cerebellum,...) among rodents:

  Combining our estimates of total cell number and percentage of NeuN-containing nuclei in each brain region, we find that adult rat cortex contains ∼80 million cells, 40% of which (∼30 million) are neurons. In comparison, rat cerebellum contains more than twice as many cells (∼170 million), >80% of which are neurons (Table 1, top). Therefore, the adult rat brain contains almost five times as many neurons in the cerebellum (∼140 million) than in the cerebral cortex. When all of the brain regions are taken into consideration, the cerebellum thus accounts for more than one-half of the cells and ∼70% of all of the neurons of the entire rat brain (Table 1, bottom). Overall, we estimate that of all of the cells in the adult rat brain, 60%, or 200.13 ± 21.17 million, are neurons. Glial cells, therefore, contrary to common belief, are not the most numerous cell type in the rat brain.

Isotropic Fractionator: A Simple, Rapid Method for the Quantification of Total Cell and Neuron Numbers in the Brain
Cellular scaling rules for rodent brains
The Human Brain in Numbers: A Linearly Scaled-up Primate Brain


How straightforward is in vitro compartmentalization?

It is actually surprisingly easy and reproducible to make emulsions with defined components. We do it routinely in our lab:
http://www.sciencemag.org/content/332/6026/209.full - CBT protocols
http://www.sciencemag.org/content/336/6079/341.full - CST protocols


Meiosis 2 can not be called mitosis.

You correctly recognized there are similarities between Meiosis 2 and mitosis. In other contexts, however, there are further differences. For instance Mitosis usually does not recombine genetic material (https://en.wikipedia.org/wiki/Meiosis), and the molecules that regulate Meiosis 2 and Mitosis are different. Calling "Meiosis 2" "mitosis" could lead to miscommunication.


Looks like European Starlings (Sturnus vulgaris).  They are often seen in large numbers and are native to most of Europe, including Serbia.  They were introduced to North America (Central Park, New York City) as a project to introduce species of birds from works of Shakespeare and are now widespread.

Source: https://www.allaboutbirds.org/guide/European_Starling/id