Comparison between Transmission Electron Microscope (TEM) to Scanning Electron Microscope (SEM)

Well, the main difference between them is that with SEM you get information about the surface using scattered electrons whereas with TEM you get information about the inner structure with transmitted electrons. TEM has higher resolution, but SEM is simpler because you do not need a thin sample.

I recommend these videos about SEM and TEM. Short description of both can be also found at this webpage and in the material for students by ThermoFisher Scientific.


Are there genetic causes underlying the difference in circumference of the upper arm and foream?

The first answer explains that proximal limb segments do more "work" * using quotes to be careful w.r.t. technical definitions of work. Genetically, this is correct--it's the ancestral condition for tetrapods. It is also worthwhile to answer why it's beneficial for why proximal segments get bulky to do this work, instead of their distal counterparts -- i.e. why did natural selection favor this arrangement in the first place.

There is a biomechanical reason for distal limb segments to be less massive than proximal limb segments, especially in tetrapods: That moving masses farther away from the center of rotation, when force is applied between the center of rotation and the mass, takes a LOT more force.

Let's consider the arm from your example. We'll treat the forearm as a "load" which is supported by the upper arm and shoulder.

In this case, the whole arm is a Type 3 lever, with the force applied (by upper arm and shoulder) inbetween the load center of mass and the fulcrum (joint). Image from https://alexeinstein.wordpress.com/2014/09/03/lever-of-human-body/:

 In the picture, it's showing the hand (could be a weight in the hand, too) as the load, but for an empty hand the center of mass of the lower arm is probably slightly more proximal (but not more proximal than the muscle insertion).

In order to support the load that is the lower arm, the torques about the joint need to be balanced. So the torque produced by the muscles (by force AF in the diagram), needs to equal (or for bicep curls, exceed) the opposing torque produced by the mass of the load.

Torque is the product of the rotational force acting perpendicular to the lever and the distance along the lever to the fulcrum. (Reference is Wikipedia, but there's no argument about the definition of torque.)

Lets make up some numbers, and work through the example. Say that the weight of the lower arm (R in the diagram) is 10. And the distance from the center of mass to the elbow is also 10. Then, the biceps in this image needs to produce an opposing torque of at least 100. But the insertion of the biceps is very near the fulcrum, say at a distance of 1. So it needs to produce 100 times the weight of the load to create a balancing torque. For most joints in the body, the muscle insertion is nearer to the joint than the load--so the muscle will ALWAYS need to produce more than the load. So you can see how having a lighter forearm would be of benefit.

Now let's consider the whole arm, relative to the shoulder. I drew a picture for us. Suppose we only need 10 muscle mass to do day to day moving of things. Let's imagine a world where that 10 muscle mass is in the lower arm. If we have an upper arm of length 10, and a lower arm of length 10, and we hold our arm perpendicularly in front of us (so the center of mass of the 10 muscle mass is approximately at the middle of the lower arm(15 length from the shoulder), the weight of the arm is generating a torque of 150. This needs to be matched by the rotator cuff muscles, and it's a lot. The shoulder girdle insertion is quite close to the joint (let's say 2 length from the shoulder), so these muscles must produce 150 Torque / 2 length = 75 force perpendicular to the arm -- which means even more force overall, because the muscle is not acting perpendicular to the arm. That's a lot of force. (PS: red is showing lines of action of forces)

Now, suppose instead we put the 10 required muscle in the upper arm. (Another drawing for you.  We'll say the center of mass of the whole arm is now probably just before the elbow, at length 9 from the shoulder. The whole arm is producing a torque of 10 * 9 = 90 at the shoulder. The shoulder girdle muscles (with the same insertion distance of 2) must produce 90 Torque / 2 length = 45 force perpendicular -- much less. This holds in general--for a type 3 lever, the muscles will always have to do more work if the load is farther away from the joint.

Thus, placing muscle mass distally means the center of mass of the entire limb s farther from the body -- which means the body must produce a lot more force to support the mass than if the load is closer to the body. This is the same reason why it is easier to carry a heavy backpack in your arms than at the end of your arms. On an evolutionary time scale, it makes sense that the bulk of muscle mass has been placed closer to the center of mass.


What evolutionary pressures pushed Galápagos tortoises to mature so slowly and live so long?

This isn't so precisely focused on tortoises, but a general theory in evolutionary biology for why some animals live longer is K vs r selection theory.

The idea here is that animals will make a sort of evolutionary 'choice' and configure themselves to breed as numerously and quickly as they can.  This is called 'r' selection, named after the constant that is proportional to the rate or speed of breeding.  r selected animals adapt quickly to a rapidly changing environment and their lives are pretty cheap.  Many insects that lay hundreds or thousands of eggs every few weeks are examples of r selection. They do not care for their offspring (and may even eat them!).

K selected animals breed to be highly competitive in the environment.  They tend to be highly optimized for success and this often means they are larger, they live longer and require more investment as newborns.

By this theory the galapagos tortioises live longer because their environment changes very slowly and the tortoises are so optimized for that particular way of life that they have no predation or any competition at all.  Islands like the Galapagos are studied in fact because they are so isolated by the water that new species rarely ever arrive.  Such new arrivals may cause drastic changes in their ecosystems because islands are stable environments because migration happens so rarely.

There are other theories that emphasize other factors in the evolution of larger, longer lived animals, but I think r/K selection may describe the environmental pressure on the Galapagos tortoise.


Effect of pupil responses on the electroretinogram

Answer version1 (read the comments, I leave v1 for the those who can make the same assumptions in the future)

To answer the question we should clarify some general concepts and processes mentioned it the clause:

EMG is performed by means of direct placement of the electrode (the are two types here - surface-EMG and needle-EMG) on/into the skeletal muscles, this is why there is no such thing  "iris-sphincter-related EMG": the sphincter is inside the eye and there is no way to contact it without eyewall penetration somewhere. Thus, this part of the question is hypothetical.
ERG is performed after pharmacological mydriasis (pupil dilation to ensure retinal mass response or to perform multifocal ERG), so in the standard settings there is no substantial pupils reaction during the test. Thus, this part of the question is hypothetical too.
ERG measures electrical changes when one of the electrodes is directly attached to the cornea - here we should stress "to one cornea", and "reads" the current from only one side. This is why, the reaction of contralateral pupil, skeletal muscles, heart/defibrillator activity are irrelevant since they are out of the electrical loop existing between the electrodes (the second electrode is on the forehead).
ERG measures electrical activity only - there is no muscle contractions in the process, while EMG involves the time needed to acetylcholine to be released and muscle contraction to begin. This means that the time scopes of these tests are different. In addition, as stated, pupils react as an efferent organ (III nerve, mediator related), while retinal photoreceptors react directly to the light stimulation, so there is a clear delay between these two processes. Theoretically, one can perform full cut of the optic nerve with the resultant loss of afferent signal and consequent loss of efferent pupil reaction, but the ERG will still detect the normal curves if the photoreceptors are intact.

Back to question itself: according to the mentioned facts we should state that the question is more hypothetical and theoretical, thus answering it directly is problematic and the answer should not be assessed without facts mentioned above.

So, the final answer - 1+2: No, pupil reaction does not affect the ERG in the real and standard settings and should not be counted as an interfering factor.

Version2

I've found an interesting patent claiming that pupillary responses can contribute to eERG (electrical stimulus instead of light). These influences stated to be artifacts, thus the authors raise the question how to diminish/filter them out.

They say

  Eye movements and pupil responses may contribute to the eERG;

  Pharmacologic dilation abolished these pupil responses;

  Bilateral artifacts, such as pupil responses, in the corneal eERG
  cannot be sufficiently reduced by using dilation drops; Even after
  dilation, a residual, but substantial electrical response persisted in
  the contralateral eye.

So, I should convert my answer to yes/yes. Taking into account the obscure nature of the subject, I hope you will agree that by making mistakes we can learn something new. I personally learnt a lot trying to answer this excellent question.

Patent application number: 20120143080 (if the link will be broken in future, one can find the patent by this number).

Direct link
http://www.faqs.org/patents/app/20120143080


Is it easier to burn a calorie of fat or a calorie of a carbohydrate?

It isn't burning of the calorie you should consider as once digested different calories are stored in the same manner, it is actually the digestion itself.

Proteins are by far the most energy requiring foods to digest such that around 20% of the calories in proteins are used in extracting them. In comparison carbohydrates are much easier at around 5-10% whilst fats are even easier to digest.

But think of it in simple terms, chewing a vegetable and digesting it down and the relatively sheer quantity of mass you need to make it calorifically the same value as chocolate means that yes 100 calories isn't 100 calories.

All then in terms of real life application, our bodies respond to how much we eat. If we eat a large volume of low calorie food we will eat less calories in total. This also plays an important role.

Source: http://www.ncbi.nlm.nih.gov/pubmed/20613890


This paper seems relevant. I just found it and don't have access, so I haven't read it. It does seem to suggest that there is evidence for eukaryotic genes being taken up by a prokaryote.

I would imagine this is rare, though. Eukaryotic cells don't tend to just spew their genetic material everywhere. Most death pathways involve breaking down any genetic material in the cell, I believe.


In short: Not completely, but more than you would expect.

The project to clone a mammoth considered using an adult female elephant as a surrogate mother, so in theory closely related species can do this.


Caspase do not directly kill the cell, but rather activate a process known as apoptosis, or programmed cell death. The programmed part is there to distinguish it from other types of cell death, such as necrosis, which are more aspecific death processes.

Coming back to caspases, they are a series of proteasis, that can activate in cascade in response to a pro-apoptotic signal.

To simplify matters a lot, the pro-apoptotic signal first activates initiator caspases, such as caspase 8, 9, 10 (plus a series of other proteins).

These, in turn, cleave other effector caspases, which are the ones who effectively do the dirty job: caspase 3, 6, and 7.

Now there are many things happening at the same time (see this PDF from AbCam to get an idea of the complexity of the system).

At the nuclear level you have, for instance:

activation of DNA cleaving enzymes, such as CAD (caspase-activable DNAse), which is normally inactive, due to binding to its inhibitor I-CAD. The latter is a target of effector caspases and its degradation causes CAD to go in the nucleus and starting fragmenting DNA.
cleavage of PARP (Poly(ADP-ribose) polymerase), a nuclear enzyme involved in finding and repairing single-strand breaks on DNA.
cleavage of lamins (by effector caspases + other proteases), proteins that are important for the formation of nuclear lamina, and stability of the cell nucleus
cleavage of U1, a nuclear protein necessary for processing of mRNA.

Very complex events also happen at the mitochondria level: here you have a series of protein, which belong to the Bcl-2 family that control apoptosis mostly by regulating the levels of Ca2+ in the cell. There are 25 members of this family, that can be divided into two "sides": pro-apoptotic proteins such as Bax, Bak, and BAD and anti-apoptotic proteins such as Bcl-2, Bcl-xL, and Bcl-w.

The functioning of the Blc-2 proteins is very complex and I am not up-to-date with the last literature but to simplify, essentially what happens is that when the balance between anti-apoptotic and pro-apoptotic proteins is shifted towards the pro-, there is:

liberation of cytochrome c from the mytochondria into the cytoplasm, which can activate effector caspases.
induction of MPTPs (Mitochondrial Permeability Transition Pores), proteins which increases mitochondrial permeability which causes all sorts of trouble, eventually leading to swelling of mitochondria and loss of their function

Different events also bring to an increase in cytoplasmic calcium concentration, which can, for instance, induce the activity of calcium-activated endonuclease or other pro-apoptotic calcium-dependent proteins.

This is far from being an exaustive list of what happens, but it gives you the idea of the complexity of the system.


The trouble with questions like this--"is this disease genetic?"--is that diseases are complicated phenotypes that arise from interactions with both individuals' genetic makeup and also the changes in gene expression that happen as a result of the environment of that individual over their lifetime.

To put it another way: neither nature without nurture nor nurture without nature are particularly interesting, because the first amounts to a little vial of DNA in a microcentrifuge tube and the second amounts to, uh, a whole lot of nothing.

In the case of Type II diabetes, there is both a strong environmental component--persistent obesity in humans is so likely to lead to diabetes that one of the two original mouse obesity model strains was named 'db' for diabetes--and also a genetic component that affects the likelihood of developing Type II diabetes in a number of ways. Some genetic variants may be less likely to develop obesity even under the high-fat diets that typically are used to create obese phenotypes in mice. Some variants may be more or less likely to develop insulin resistance even in the presence of high levels of adipose tissue. Both of these variations would affect your likelihood of getting Type II diabetes... depending on your environment and the level of body fat you carry, and that last one is going to be dependent on not only your genetic makeup but also your environment and (almost certainly) epigenetic influences from your parents.

With respect to Type II diabetes and actual specific genetic variations that have been identified, there's the twin study cited in another answer here, which was done in Danish twins and really just looked at whether there was a genetic component done at all. GWAS studies have, predictably, resulted in several candidate loci, all with relatively small effects on risk--which makes sense, because metabolism is a complex thing and many players are probably involved in competing roles. (I'd link more, but I'm new here--hitting up a Google Scholar search for "type ii diabetes genetic variance" nets you a whole bunch more GWAS studies talking about specific types of variation noted.)


What type of Interspecific relationship does this graph depict?

Competition makes the most sense, IMO.

For every other type of relationship, A and B should be dependent and roughly proportional: If parasites kill their host, they die in proportion. If predators eat all their prey, they drop in numbers due to food scarcity until food repopulates, the graph would almost look like a double helix. Mutual/commensals also share a dependent and proportional graph. The inverse proportionality of the sample chart, to me, gives away competition: one organism is flat out winning against another through some method.


The definition of a leg from Merriam-Webster is

  "One of the rather generalized segmental appendages of an arthropod used in walking and crawling"

As Gerardo Furtado has already stated, the front pair of appendages are called palpi and are not used for walking, but for mating and manipulating objects. By this definition, palpi are not legs and therefore trap door spiders have 8 legs, not 10. More information on the rather large pali found on trap door spiders can be found in P.D. Hillyard's The Private Life of Spiders.

Image from Biodiversityexplorer.org.


How do point mutations arise from mistakes in DNA replication?

Source of your misunderstanding

Your misunderstanding is very comprehensible as the figure is misleading.

The figure only shows a single event of replication. What you see as a second replication resulting into two double stranded molecules is NOT an event of replication. It actually represents the two possible outcomes from a 'mismatch repair mechanism'. The term DNA replication written on the figure should be replaced by Possible outcomes of DNA repair. The molecule that contains the G-T mismatch is therefore just a temporary state that will very quickly be changed to either the T-A state (bottom right of your figure) or to the G-C state (upper right of your figure). More information below.

DNA repair

  DNA repair is a collection of processes by which a cell identifies and corrects damage to the DNA molecules that encode its genome.

The type of DNA repair that is of interest on the figure is called "DNA mismatch repair"

DNA mismatch repair

  DNA mismatch repair is a system for recognizing and repairing erroneous insertion, deletion, and mis-incorporation of bases that can arise during DNA replication and recombination, as well as repairing some forms of DNA damage.

There are specific enzymes to repair a mismatch such as the G-T mismatch represented on your figure. These enzymes can either repair G-T into G-C or into A-T. If the repair is A-T (lower outcome in the figure) then a mutation would have occurred. If the repair is G-C (upper outcome in the figure) then we are back to the original sequence and no mutation would have occurred.

Note that the probability of the two possible outcomes is different from 0.5 as these enzymes have ways to try to figure out which was the original strand and which was the newly replicated strand. You can learn much more about the mechanism of DNA mismatch repair on the wikipedia > DNA mismatch repair.


What is the most difficult feature to explain evolutionarily?

To answer your question directly, there are a number of examples which creationists like to bring up, such as woodpecker's tongue which is wrapped around its brain or the archer fish which shoots down insects with water and has to adjust it's aim for refractive difference between water and air. These features supposedly 'couldn't have evolved' but of course one's disbelief doesn't make anything true or untrue. This is what Dawkins calls 'argument from personal incredulity'.

Let me also point out a few evolutionary counter arguments to such reasoning.

The presence of selection radically changes what is 'likely' or 'possible' to happen. For example, you wouldn't argue that it's highly improbable that the stones on the beach are ordered by size, if you know that the action of waves orders them in a certain way. Dawkins' weasel (http://en.wikipedia.org/wiki/Weasel_program) also demonstrates this principle.

Another Dawkins' argument is that, contrary to what creationists claim, complex features such as eye don't have to be completely functional to be useful. In the early history of life, when no organism had eyes, any simple system which could distinguish light from darkness could provide a huge advantage to its owner. The simple system can then evolve to a more complex one to provide a competitive edge etc.

Finally, evolution happens over time scales we cannot grasp. We don't have a good feeling of what billions of years of small changes which are selected for can add up to.


What is the advantage of indirect ELISA over direct one?

You are correct, the selectivity advantage of an indirect or sandwich ELISA comes from the fact that two antibodies are employed - one to capture the analyte, the other to detect it.

Here is the classic illustration of how this type of ELISA works. First ([1]), the capture antibody is coated onto the plate and bound via one of a number of different types of chemistry. The plate is then washed (this occurs between all steps). [2], the analyte is added, sometimes in a homogenous solution (i.e., pure recombinant protein), other times in a matrix like serum, cell lysate, etc. The plate-bound antibody has a certain specificity for the analyte — let's say it binds the wrong epitope one time in 1000. [3] The detection antibody is added, and let's say it has the same specificity of 1/1000. Finally, [4] the secondary antibody (with the enzyme linked to it) is added, and [5] the enzyme's substrate is added, producing the color or light output.

From Wikimedia

If we were to use a direct ELISA, the error rate would be 1/1000. However, by combining two antibodies, our error rate is now 1000 times lower — 1 in 1 million. Since both antibodies are required to bind properly in order to get a signal, this makes the results much more reliable.


Are the transverse septum in sharks and the diaphragm in mammals homologous structures?

A beginning of answer here below, I hope. Please first consider that many structures are involved in the question here, the diaphragm (UBERON:0001103), the diaphragmaticus muscle (UBERON:0036071) and the septum transversum (UBERON:0004161). At Bgee (bgee.org) we aim annotating relations of similarity between anatomical structures, please have a look at our GitHub
https://github.com/BgeeDB/anatomical-similarity-annotations

We already annotated 'diaphragm' as a mammalian structure, not homologous in Amniota (please see https://raw.githubusercontent.com/BgeeDB/anatomical-similarity-annotations/master/release/similarity.tsv). In our next release, you will see the annotation for the 'diaphragmaticus muscle' which is an analog organ in Crocodylians (and Turtles) but not homologous to the mammalian diaphragm either. See here for more details about this new Uberon class:
https://github.com/obophenotype/uberon/issues/1229.

Based on the comments here above, I would say that currently we can argue that there is no evidence for a homologous relationship between the 'septum transversum' in sharks and the mammalian diaphragm. Please note that UBERON:0004161 septum transversum describes the (mammalian) embryonic structure that will give rise to the central tendon of the diaphragm, while here you are talking about a adult structure closer to a 'diaphragmaticus muscle'-like septum, as far as I understand.
But anyway thank you for your interesting question that points out a very exciting and rapidly evolving evo-devo field, as this recent paper also suggests
https://www.ncbi.nlm.nih.gov/pubmed/?term=27859325


Why do OX5034 GM mosquitos require the presence of tetracycline to survive? What does the drug do in this case?

They don't go into any detail on the sites you link to and I don't have time to look into patents, but from the context it sounds like they may be using a tetracycline repressible promoter. This is often referred to as a Tet-Off promoter.
The core elements of these promoters were discovered in the bacterium Escherichia coli1 and several variations have been developed. These types of promoters work in organisms from bacteria to yeast to mammals1-3.
References
1: Gossen, M., & Bujard, H. (1992). Tight control of gene expression in mammalian cells by tetracycline-responsive promoters. Proceedings of the National Academy of Sciences, 89(12), 5547-5551.
2: Baron, U., & Bujard, H. (2000). Tet repressor-based system for regulated gene expression in eukaryotic cells: principles and advances. Methods in enzymology, 327, 401-421.
3: Orth, P., Schnappinger, D., Hillen, W., Saenger, W., & Hinrichs, W. (2000). Structural basis of gene regulation by the tetracycline inducible Tet repressor–operator system. Nature structural biology, 7(3), 215-219.


Why does muscle blood flow decrease during exercise?

I think there might be some missing context here leading to confusion of which muscles are being referred to in that passage.

During exercise, blood flow increases in active muscle due to local vasodilation. Cardiac output also increases, which ensures that total blood flow in the body is sufficient to meet the increased demand.

At higher levels of exercise, there is also systemic vasoconstriction. Systemic vasoconstriction acts to maintain blood pressure. You simply have too much total muscle for maximum cardiac output to supply all the muscle with full vasodilation plus the rest of the body without a loss of pressure. For an athlete with greater maximum cardiac output, it would be possible to fully perfuse more muscles at high effort than for someone untrained.

  At maximum exercise, some vasoconstriction occurs in active muscle in order to maintain blood pressure

Because vasoconstriction is systemic, it has an influence on all the muscles, including the active ones. You should think of this vasoconstriction as relative to already dilated vessels, not necessarily compared to rest.

  Maximum muscle blood flow is largely determined by the amount of active muscle.

This sentence could be rewritten as:

  Maximum blood flow through a given muscle is largely determined by how much muscle is active in the rest of the body.

That is, the maximum blood flow through an arm muscle would be greatest if your legs are resting.

  The larger the portion of active muscle mass, the less total muscle blood flow.

This is I think the most confusing sentence...I believe what they are referring to is the total muscle blood flow for a given muscle (total meaning over time rather than over space), which will be maximum when fewer other muscles are active at the same time.

Joyner and Casey 2015 explain all this in more detail; their Figure 8 is most directly related to the question but the rest of the background is also useful.

Joyner, M. J., & Casey, D. P. (2015). Regulation of increased blood flow (hyperemia) to muscles during exercise: a hierarchy of competing physiological needs. Physiological reviews, 95(2), 549-601.


Could bone marrow transplants help make xenotransplants viable?

I feel I've enough sources & data to venture an answer on this one myself now, so here goes.
Step one: Can we produce the pig in the first place?

Fetal Inoculation With Donor Cells in Cardiac
Xenotransplantation 1996
Perinatal induction of immunotolerance to cardiac and pulmonary allografts July 1997
Induction of donor-specific tolerance to cardiac xenografts in utero: 1998 Sep
Cell Transplantation January 1 2003
IMMUNO-INTERVENTION FOR THE INDUCTION OF TRANSPLANTATION TOLERANCE THROUGH MIXED CHIMERISM: 2011 Aug 11
In utero hematopoietic cell transplantation: induction of donor specific immune tolerance and postnatal transplants: 2014 Nov 12

another link to the same article
In utero hematopoietic cell transplantation: induction of donor specific immune tolerance and postnatal transplants 12 November 2014

First human-pig 'chimera' created in milestone study 26 Jan 2017
Interspecies Chimerism with Mammalian Pluripotent Stem Cells 2018 Jan 26
Interspecies Chimeras and the Generation of Humanized Organs 3 Jan 2019

Yes, an animal can be produced with donor specific tolerance to the patients organs, it's a known procedure & observed effect that has been replicated numerous times in experiments, its immune system would not attack either the patients cells or its own.
Step two : Can we transplant this animals bone marrow to the patient?

Stem cell and bone marrow transplants

Yes, bone marrow transplants involving the complete removal of the original bone marrow is a long established procedure for the treatment of leukaemia.

And now being used for treatment of other severe autoimmune diseases in a way which may make this idea moot, I'll have to look into that further, not read that article in full yet.

Step three : Will we then be able to transplant other organs from this (or a genetically identical) animal to the patient without tissue rejection?
The immune system isn't seated entirely in the bone marrow & its products (the thymus, spleen & lymphatic system also have roles) so for best results some of these may also need to be replaced.
If so it must be hopped the lymph nodes play no role in in the development & tuning of the immune system, there are 500-600 of them around the body so replacing them all would be no small task.
Conclusion :
Still in progress / just saving work so far


What restriction enzyme was used in cutting this DNA piece?

In order to keep this on topic, I will try and give a more general answer.

The most widely used restriction enzymes, and the ones typically taught first, all cut within their recognition sequences, however, this is not necessarily so as most Type I and Type III enzymes cut at a distance from their site, sometimes this is a fixed distance, sometimes it is not. It is only Type II enzymes that cut symmetrically within their sites, and even then, not all of them. However, cutting within the site is usually the most useful kind of cut for molecular genetics and thus these are the most common enzymes to encounter in the lab (see here for more).

For a particular enzyme, the best way to find the cut site is simply to google it or search directly on the NEB site (where you will likely find the top Google hit anyway), doing this for XhoI would get you a page containing information like this:

Where the little arrows in the given recognition sequence indicate where each strand will be cut, whereas as for enzymes that cut outside the recognition site you will get something like this (for AlwI) where the $(N)_4$ part tells you that the enzyme cuts four bases away on the 5'-3' strand, and the $(N)_5$ part tells you it cuts one base further away on the opposite strand.

In order to identify which of a number of enzymes cut a certain sequence you need only find the appropriate information for the relevant enzymes so you can compare these cut diagrams for the relevant enzymes.


Is there any evidence for secondarily poikilothermic vertebrate?

What do you mean by cold-blooded?

There's an issue with what you mean when saying "cold blooded". The correct words you may want to use are homeotherm, poikilothermic, ectotherm, and endotherm. In short…

Source of heat

endo = inside
exo = outside

Variance in warmth

Poikilo = varies
homeo = does not vary

Any combination of these two axes exist. For example: If the temperature in the environment never varies you can be homeotherm without needing to be endotherm. A fun example also are the large dinosaurs that are thought to be homeotherms because their metabolism produce some heat and they are so large that they remain warm thanks to this heat source. However, they were probably not able to regulate actively their temperature. Therefore, I would tend to qualify dinosaurs as homeo-exo-therm but I wouldn't be surprised if someone prefers to call large dinosaur home-endo-therm individuals. Hope that makes sense to you.

Note that the terminology might be a bit more complicated in reality as the diversity of mechanisms of body temperature regulation is important.

What did you mean in your question when talking about "cold blooded" species?

Transition from endothermy to ectotherm

Thanks to @tchrist. naked mole rat is ectotherm while its ancestors where endotherm.


Can dietary monosodium glutamate intake induce restlestness?

There is no strong evidence for MSG having any kind of neurotoxic/neuromodulatory effect.

However, A 2010 article says that, in a double blind trial, it was found that the people who consumed MSG containing soda, reported headache in significantly more numbers compared to the placebo subjects [1]. The concentration of MSG used in this study was 75-150 mg/kg. Assuming that one serving of soda would be 300ml i.e 300g, the amount of MSG consumed would be maximally 45mg, which is much less than glutamate concentration in some natural food stuffs such as tomatoes (~2000mg/kg [2,3]; a tomato that weighs 6oz/~170g contains ~340mg of glutamate). Therefore, I would doubt the findings of this article. The results could have possibly been observed because of some hidden dependent variable (such as the soda formulation).

In general, the USFDA considers MSG as GRAS (generally regarded as safe) [4].

Finally, a 2014 article concludes that dietary MSG would not lead to increase in either blood or brain levels of glutamate [5].

From the Abstract:

  The sodium salt of glutamate (monosodium glutamate; MSG) imparts a
  savory/meaty taste to foods, and has been used as a flavoring agent
  for millennia. Past research on MSG/glutamate has evaluated its
  physiologic, metabolic and behavioral actions, and its safety.
  Ingested MSG has been found to be safe, and to produce no remarkable
  effects, except on taste. However, some recent epidemiologic and
  animal studies have associated MSG use with obesity and aberrations in
  fat metabolism. Reported effects are usually attributed to direct
  actions of ingested MSG in brain. As these observations conflict with
  past MSG research findings, a symposium was convened at the 13th
  International Congress on Amino Acids, Peptides and Proteins to
  discuss them. The principal conclusions were: (1) the proposed link
  between MSG intake and weight gain is likely explained by co-varying
  environmental factors (e.g., diet, physical activity) linked to the
  "nutrition transition" in developing Asian countries. (2) Controlled
  intervention studies adding MSG to the diet of animals and humans show
  no effect on body weight. (3) Hypotheses positing dietary MSG effects
  on body weight involve results from rodent MSG injection studies that
  link MSG to actions in brain not applicable to MSG ingestion studies.
  The fundamental reason is that glutamate is metabolically
  compartmentalized in the body, and generally does not passively cross
  biologic membranes. Hence, almost no ingested glutamate/MSG passes
  from gut into blood, and essentially none transits placenta from
  maternal to fetal circulation, or crosses the blood-brain barrier.
  Dietary MSG, therefore, does not gain access to brain. Overall, it
  appears that normal dietary MSG use is unlikely to influence energy
  intake, body weight or fat metabolism.


How are Maggots Sterilized (Disinfected)?

History
Ambroise Paré is credited with being the first to note his observations on Maggot Debridement Therapy (MDT) in the 1500 though it is a technology that has been used for centuries (reference). It wasn't until the 1920's that therapeutic experimentation with maggots was instigated by William Baer, a clinical professor in orthopaedic surgery at the Johns Hopkins University in Baltimore, Maryland, whose unorthodox methods were successful in the treatment of osteomyelitis and pyogenic wounds. He is also considered the father of modern MDT since he was the first to devise a way to sterilize maggots (reference).
Procedure
In addition to removing necrotic tissue from the wound (a procedure known as debridement) maggots have also been proven to disinfect wounds, promote healing, and inhibit a pesky substance known as biofilm from forming on the wound bed. Maggots are nature’s cleansers, showing up to remove dead tissue and promote healing (reference).
Currently Lucilia sericata, or the greenbottle blowfly larvae is preferred for MDT because

Firstly, larvae have been shown to debride wounds with extremely low
probability of myiasis upon clinical application. Larval secretions
have been shown to help in tissue regeneration. L. sericata have also
been shown to lower bacteremia levels in patients infected with MRSA (reference).

Sterilizing maggots
In early applications, sterilizing the larvae was a major problem. Doctors had to first bathe the eggs in bleach and then soak them in mercuric chloride or formaldehyde. The bandages, gaudy and cumbersome for the patients, were held in place with either surgical tape or Unna’s paste—made of zinc oxide, gelatin, glycerine, and water. Other problems that doctors faced included the maggots escaping during the application process and the leakage of toxic waste secreted by the maggots into the wound, which led to infections such as tetanus. Today, commercial and research laboratories produce sterile larvae. And instead of the bulky gauze bandage, a form-fitting cast with a nylon net to corral the larvae is placed over the wound. An absorbent pad put on top of the netting soaks up the larvae’s toxic waste products. The number of larvae used has also changed. Early prescriptions ranged from 5–6 maggots for a fingertip injury to 500–600 for a more serious wound. Today, the scientific standard of 10 larvae/cm2 is used (reference).
William Baer proposed a method to produce sterilized maggots and it is understood that sterilization has to start from the egg stage in itself (reference). The sterilization solution that he proposed was.

Stock Solution of bichloride of mercury, strength one in 1,000 parts.
Stock Solution of fifty per cent. ethyl alcohol. Take equal volume of
each Solution, mix, and add one-half of one per cent. chemically pure
hydrochloric acid. The final Solution will contain bichloride of
mercury, strength one in 2,000 parts, twenty-five per cent. alcohol,
and one-half of one per cent. hydrochloric acid.

He did not sterilize the maggots as such but took care to feed it sterile food. His work can be read here. Another solution used for sterilization was  5 per cent solution of formalin plus 1 per cent sodium hydroxide (reference).  Sterilization of maggot larvae in itself was found to be hard with some success being reported (reference). Current maggot sterilization techniques include.

UV Sterilization
Rapid washer sterilization
Egg to maggot sterilization (reference)

There is no first generation that has been detailed as such. Mostly sterilization starts from the egg stage. As far as bacteria in the gut is concerned, if sterilization is carried out well, it has been found that there is a significant decrease in any harmful bacteria present (reference). Most details of sterilizing maggot larvae is given in this paper. Consider reading this paper as well.


It seems like you may be thinking along the lines of DNA, where adenine pairs only with thymine and guanine with cytosine.

Unlike DNA, amino acid chains are single-stranded...

...so there is no pairing of compatible types like there is in DNA. Neighboring amino acids in the chain can be in any combination (as you say, because each has a carboxyl group and an amino acid group), just as neighboring nucleotides in DNA (ie those next to, not across from, each other) can come in any order.

In practical terms, the functional groups of amino acids have different chemical properties (hydrophobic, hydrophilic, aromatic), therefore some pairings are probably more commonly found than others. But in principle there is no restriction on who is next to who.


how much can changing light enter the eye shap what you see?

I'm interpreting your question to be: "How much can changing the light entering the eye change the shape of/how objects are seen? Would manipulating that light just stop you from seeing certain things?"

Manipulating the light entering the eye is the exact premise of a virtual retinal display (VRD):

  From Wikipedia –  A VRD is a display technology that draws a raster display (like a television) directly onto the retina of the eye. The user sees what appears to be a conventional display floating in space in front of them.

Google Glass and other technologies (virtual reality headsets, heads-up displays) operate through relatively similar projection mechanisms. Light defines everything the eye sees (outside of hallucinations, and even those can be induced by flickering light). Also, the way your brain processes visual information (photons received by your eyes) can be "tricked," which is discussed in this BBC article. Finally, your brain's ability to process visual information can be altered by external forces (e.g. drugs, motion, or even strong magnetic fields).


The passage:

  To test these samples, the only materials she has at her disposal are
  a sample of type A red cell suspension and the serum from type A
  blood.

means, I take it, that she has available two containers: One has red blood cells from a known blood-type A individual suspended in a neutral fluid such as saline solution.  The other container has blood plasma (without red blood cells or fibrinogen) also from a known blood-type A individual.

These should be enough to determine the blood types of four individuals  from the unknown test tubes (four pairs of test tubes, each pair being one with cell suspensions and one with plasma, coming from four individuals having different blood types).


What kind of spider is this?(Rajasthan, India)

That's neither a spider nor a scorpion (and, of course, not an insect). That's a solifuge, a different group of Arachnida.

The most common Genus of solifugae in India is Galeodes, which resembles the specimen in your photo:

Genus Galeodes

However, narrowing it down to the Genus may be a little bit more complicated.

It's worth mentioning that, despite their frightening appearance, they are not dangerous to humans.


What's the simplest set-up to demonstrate soiless plant growth to middle school students?

You can take a glass mason jar, a bean seed, and a moist paper towel. Place the seed between the paper towel and the glass. If you press the paper towel so that it lines the inside of the glass jar, the seed with grow and the students can see this process through the glass.


Why is the 3'UTR region highly methylated in most of the human genes?

According to Choi et al. Genome Biology 2009, 10:R89, DNA methylation at both coding boundaries may regulate transcription elongation and stabilize splicing by reducing the occurrences of exon skipping.

From the abstract:

  Here we report a genome-wide observation of distinct peaks of
  nucleosomes and methylation at both ends of a protein coding unit.
  Elongating polymerases tend to pause near both coding ends immediately
  upstream of the epigenetic peaks, causing a significant reduction in
  elongation efficiency. Conserved features in underlying protein coding
  sequences seem to dictate their evolutionary conservation across
  multiple species. The nucleosomal and methylation marks are commonly
  associated with high sequence-encoded DNA-bending propensity but
  differentially with CpG density. As the gene grows longer, the
  epigenetic codes seem to be shifted from variable inner sequences
  toward boundary regions, rendering the peaks more prominent in higher
  organisms.

Their data (figures 1 and S2), however, do not support a generalized increase in the 3' UTR regions in either human T cells, mouse liver, yeast or flies.


Difference between going against and going down a concentration gradient

"Concentration" is "how much stuff is there someplace?" "Concentration gradient" is "how much is concentration changing from point A to point B?"

Imagine a terrain where concentration is represented by height.

"Down" a concentration gradient means from high concentration to low concentration - this is the direction things would move via simple diffusion.

"Up" or "against" a concentration gradient means from low concentration to high concentration. Moving in this direction requires some sort of energy input, such as active transport using ATP, or an electrical gradient, or something else.


How did genome duplication in jawed vertebrates allow gene specialization?

With a single copy gene, mutations may affect some vital function and are therefore often deleterious and negatively selected. Immediately after a duplication event, there is a level of redundancy in gene function and mutations in one copy giving rise to novel phenotypes are more easily tolerated since the ancestral function is retained by the paralogous gene.

Some reading material, if you feel so inclined:

Wikipedia:

Functional Divergence

  Functional divergence is the process by which genes, after gene duplication, shift in function from an ancestral function. Functional divergence can result in either subfunctionalization, where a paralog specializes one of several ancestral functions, or neofunctionalization, where a totally new functional capability evolves.

Neofunctionalization

  Following the gene duplication event there are two identical copies of the ancestral gene performing exactly the same function. This redundancy allows one the copies to take on a new function.

Subfunctionalization

  Specialization is a unique model of subfunctionalization, in which paralogs divide into various areas of specialty rather than function. In this model both gene copies perform exactly the same ancestral function. For instance, while the ancestral gene may have performed its function in all tissues, developmental stage, and environmental conditions, the paralogous genes become specialists, dividing themselves among different tissues, developmental stages, and environmental conditions.

Kryuchkova-Mostacci N, Robinson-Rechavi M. 2016. Tissue-Specificity of Gene Expression Diverges Slowly between Orthologs, and Rapidly between Paralogs. PLoS Comput Biol 12:e1005274.

  The most widely accepted model is that orthologs diverge slower, and that the generation of paralogs through duplication leads to strong divergence and even change of function.

Soria PS, McGary KL, Rokas A. 2014. Functional divergence for every paralog. Mol Biol Evol 31:984-992.

  Because genes can be constrained by selection at more than one phenotypic level, the relaxation of constraints following gene duplication allows for functional divergence (FD) along multiple phenotypic axes.


Why do some fruits have a much wider range of acceptable sizes than others?

Pumpkins, squashes in general, grow on vines, while apples grow on trees. Vines are fast growing and trees are not. Zucchini can be quite large; cucumbers, too. Pears, plums, peaches and other tree fruits do have a reduced variation in fruit size. While I do not know the answer to your question, my background in plant biology tells me that this is an important part of the reason. For example, a watermelon or pumpkin rests on the earth, but a tree fruit hangs. If that fruit is too heavy it falls from the ground before it is ripe - before the seeds are fully differentiated that is. So, while "evolution" might be an answer, it is important to discuss what aspects are at play.

I think it has to do with vine vs tree, and how the fruit is attached and hangs/lays.


Is there an 'opposite' neurotransmitter to dopamine?

The release of dopamine has a positive effect on the reward center in the nucleus accumbens. The neuron that releases the dopamine can be inhibited by other neurons, so there gets less dopamine released.
The response elicited by a neurotransmitter, either excitatory or inhibitory, is determined by its receptor on the postsynaptic cell. ~https://www.ncbi.nlm.nih.gov/books/NBK21607/def-item/A7678/


Does the use of "var", "x", and/or "ssp" in a scientific name provide specific information?

Let me clarify my answer since it is lower quality than people may like.  To answer the question, my friend is a horticulist and has given a more detailed answer.

Subspecies is the most generic, taxonomically-defined term one rank order lower than species. The subspecies (either an individual subspecies, or collective group of subspecies) are defined to be genetically or morphologically distinct among other subspecies belonging to the same species, yet still produce viable offspring from interbreeding. For example, every type of dog is a sub-species of Canis familiaris, and all dogs are capable of breeding with each other. Subspecies, abbreviated Ssp, may refer to an individual subspecies type, or a collective group of related subspecies when a distinct subset is difficult to define or unknown.

There are a variety of terms that are analogous to subspecies, when the strict definition does not apply, or a different term has been used historically. For example, a varietal is the botanical term, and refers to a named subspecies. For example, grapes are a family of species, divided into the various subspecies, and a varietal is a specific subspecies that we refer to by a more common or familiar name, such as Riesling, Chardonnay, etc. (Grapes are a slightly different case in which most grapes are produced from hybrids or crosses for reasons of withstanding environmental conditions avoiding insect prey and fungal infections.) Microbiology has yet another distinction, called a strain. Strains are often genetically different, and yet all belong to a species. For example, several E. coli strains exist. In contrast, viruses are also given strain/subspecies names which don't technically fit the ICZN definition of interbreeding. Cultivar is a similar term, also from the field of botany. Cultivar is specifically applied to plants that are grown for some agricultural benefit, and have been bred or altered by humans for some reason.

In short, there is a zoological definition of subspecies set out in ICZN. This definition requires viable interbreeding among subspecies belonging to the same species. The term applies to individuals, or groups, as the context dictates. Analogous terms of subspecies are applied (adapted?) to other realms of biology, such as botany, microbiology and virology, but the definitions are slightly different, but consistent within the branch of biology (eg, viruses can't breed so they don't fit the ICZN definition, but the term applies). Ssp can also be qualitatively used to describe an unknown subset of a species (I've seen this used in microbiology mostly).

Crosses/hybrids are indicated with the "x" in the nomenclature. Since I found this confusing, I'm copying from Wikipedia.

  From a taxonomic perspective, hybrid refers to offspring resulting
  from the interbreeding between two animals or plants of different
  species.

  Hybrids between different subspecies within a species
  (such as between the Bengal tiger and Siberian tiger) are known as
  intra-specific hybrids. Hybrids between different species within the
  same genus (such as between lions and tigers) are sometimes known as
  interspecific hybrids or crosses. Hybrids between different genera
  (such as between sheep and goats) are known as intergeneric hybrids.
  The second type of hybrid consists of crosses between populations,
  breeds or cultivars within a single species. This meaning is often
  used in plant and animal breeding, where hybrids are commonly produced
  and selected because they have desirable characteristics not found or
  inconsistently present in the parent individuals or populations. This
  flow of genetic material between populations or races is often called
  hybridization.

There are some horticultural examples of crosses in which an example of interspecific and intergeneric hybrids, and others, are shown.


What is the lipid membrane of SARS-CoV-2 made of?

I don't know if this questions has been studied in detail even for SARS, let alone SARS-CoV-2. As noted in a comment by reuns, the virus lipid envelope is most likely derived from that of the endoplasmic reticulum.

What we know however from from some studies on influenza viruses, that's hardly the end of the story though:

  Using rigorous virus purification, marked differences between virions and host were observed. Over 125 phospholipid species have been quantitated for three strains of influenza (HKx31- H3N2, PR8- H1N1, and VN1203- H5N1) grown in eggs. The glycerophospholipid composition of purified virions differs from that of the host or that of typical mammalian cells. Phosphatidylcholine is the major component in most mammalian cell membranes, while in purified virions phosphatidylethanolamine dominates. Due to its effects on membrane curvature, it is likely that the variations in its content are important to viral processing during infection.

And this part is a bit of a "reverse answer", but lipid rafts on the membrane of the target cells are thought to be important for the entry of coronaviruses, including SARS. One experiment found that depleting cholesterol from the cell membranes dramatically slowed SARS virus' ability to enter them.

(Regarding how SARS-CoV-2 might come out [with different envelopes] from different cells: we only had confirmation very recently that it substantially infects intestinal enterocytes. So expecting a lot of extra details on that is a bit premature right now.)


Gene transfer between Gram positive and Gram negative bacteria?

Have a look at this two links:

Exchange of genetic information
and
Gene transfer between distantly related bacteria

Especially the second should answer a lot of questions.


Why do bird sing?

The main reason, male bird sing to attract mates (often, only males sing). Birds may also sing to communicate to their peers. For example a song can mean "This is my territory, you'd better not approach!". There are other reasons birds can sing (although I think I cited the two most important ones); you'll find much more information if you just google why do birds sing?, there are plenty of very accessible online articles on the subject. Here is one such article that you may like reading

Talking about emotions is always difficult due to the absence of a good definition of what an emotion is. But anyway... yes, if females are attracted to the mates that sing well, it probably (depending on your definition) means it cause them to feel some emotions (sexual excitement for example).

Evolution of music in birds and humans

Bird song to attract mate (sexual selection). Humans, on the other hand, have evolved music production for different reasons (or at least this is what we think). The field of evolutionary musicology is a field in the junction between evolutionary psychology and biomusicology. In evolutionary musicology (and in evolutionary psychology) empirical testing is very complicated and therefore, today we can only think and make hypotheses but we can't test them. So always take with a grain of salt what you read in those fields.


Does the existence of one species imply the existence of many other?

I am not sure I'm providing the kind of answer you would expect.

Your question is very conceptual. For such question it is important to very well define the concepts you're using. For example, the concept of species is not well defined (and will certainly never be well defined as it does not represent a natural category to my point of view). Also, the separation you do between complex and non-complex species might not be obvious. For example, you create two categories which are bacteria/virus and multicellular. But you kind of forget the many of the eukaryotes which belong to non of these two categories. Or some bacteria that might almost be considered as multicellular.

I think it would help answering your question if we had the arguments of Sir Arthur Clark for saying such things. Below are two arguments I could use to defend your statement.

Speciation:

If you consider than one population rarely (or virtually never) go under sufficiently major changes before undergoing speciation, then you would never have only one species which is very different from the others.

Ecology:

One might consider that one species cannot by itself be responsible of a whole cycle of elements. Therefore, if the species we observe can theoretically live forever (equilibrium), then, it implies that other species must exist to recycle their wastes. But this hypothesis has nothing to do with the separation of species per complexity that you do.

Update:

Following your comment: So what you had in mind seem roughly the same than my "Ecology" argument. The difference is that I emphasized on the fact that one species alone cannot live for ever because they degrade their resources through time. I did not want to say that one individual of one species cannot live without the presence of another individual of another species. This individual would need the presence of the other species not for himself but rather but its great-great-grand-children when one resource would have been totally consumed by the ancestors.

For your curiosity, here is base of the tree of life. What is eukarotic but not plants, animals or fungi are called protista and are all (or almost all?!) unicellular. You'll notice that viruses/viroid and prions does not belong to this tree. It would be a bit long to explain why they are no represented and it would have nothing to do with your question :D


Do trees grow from the bottom or the top, or is that oversimplifying?

It appears you are mostly interested in the vertical growth of trees. As @Joe Healy points out, this is done only by cells in the apical meristem. This region always remains at the top tip of the tree, that is where the upward growth occurs. The apical meristem, as it continues upward with growth, will leave portions of itself behind that may result in branches (axillary merristems). So yes, unless you carve at the very tip of the tree, your initials will remain at the same height you carved them.

A very simple experiment that I've done many times with students demonstrates this. Germinate some corn seeds until the shoot and the root are about 2 cm long. With a fine Sharpie, mark each with lines every 4 mm or so. Continue the germination. After a few more days you'll note that the line spacings nearest the kernal are the same as when you drew them. But on the very outboard end, near the tips of shoot and root, the spacing will appear stretched out.

Another type of meristem, the vascular cambium, is responsible for the increase in diameter of a tree. It is a sheath that lies between the bark and wood producing new wood to the inside and new bark to the outside.


Is the ratio Brain Mass/Total Mass still considered a valid indicator of intelligence?

I don't know about brain mass to body size, but ratio of neocortex to brain volume is correlated with primate evolution (Figure 3, here). If you subscribe to the view that humans and more closely related primates are more intelligent than more distantly related primates, then that is an important correlate.
I think the issue with this question is that we're still having trouble defining intelligence.


What are the positive and negative effects of insulin on cognitive function?

Diabetes

I've not read about any conclusive evidence for a link between insulin and differential cognitive function, but I have read studies that link type-2 diabetes and impaired cognition (1). I will point out now that this is cross-sectional, so the study only reports associations (i.e. diabetes may not necessarily cause the cognitive impairment).

The study I have mentioned does not conclude that this is caused by raised insulin, but rather the effects on the vascular system (specifically microvascular). They also find a significant interaction between diabetes and smoking status, in the context of cognitive impairment. Again, this seems likely to be the vascular system, rather than insulin levels.

A recent review paper also refers to the links between diabetes and executive function (2), but again makes no reference to insulin as the cause, but rather microvascular changes, hypertension, and other associated traits (again, the causes are not known, these are speculative based on the evidence).

Diabetes may not be the best model for studying this though, as it can be characterized by either high insulin (tolerance), or low insulin (impairment) - therefore the association may not be found this way.

Insulin

In a separate review (this may be the best one for you if you only read one of the papers I've referenced) the author posits that whilst insulin may have a neuroprotective role, it also increases amyloid-Beta metabolism and tau phosphorylation, possibly contributing to Alzheimer's-like pathologies (3). Studies have found that insulin directly improves cognitive performance (4) after infusion of insulin, but the long term effects are less certain - it is unlikely to improve overall health having constantly raised insulin serum levels!

However the link between IGF-1 and improved cognition is less disputed, so you may well be right in thinking that the 'overall' effect of insulin on cognition may be protective, but this may just be a marker of good health overall, which is certainly protective!


Unknown plant, can anybody identify this plant?

This is Phytolacca esculenta, Asian pokeweed. Because the flower stalks (berry) are standing upright, and not hanging. The berries are also closer together compared to P. americana.

Despite the name 'esculenta', this plant is also poisonous.

https://m.wikidata.org/wiki/Q17244662


Vegetation Monitoring - Why permanent plots

The answer boils down to statistics rather than anything particular about this type of experiment.

If you have a sample of plots, and then take repeated measurements in that same sample over time, the variance in the values you record is a function of the variance of the time-dependent process causing changes.

If you take future measurements from a new sample of plots, you have additional variance to account for due to choosing a new sample. That is, even if you would have measured no change at all in the same plots, you expect the second sample will be different from the first just because of sampling. Because of this additional variance, you have less ability to detect smaller changes over time: less statistical power.


What do the the different arrowheads mean in a cell signalling diagram?

Arrowhead interpretation
As I said in my comment and to add to @AlwaysConfused's answer, the arrowhead is a promotion, and flathead is an inhibition.
Typically, any other notation such as dotted lines would be explained in the figure legend of the illustration.
The below definitions are generally accepted and widely used.
But don't take these definitions for granted; there are no strict usage policies for these diagrams.
Different groups may use different nomenclature and symbols.

These definitions were taken from a legend in cellsignal.com.
Upstream and downstream
The arrowheads are not necessarily linked to up and downstream signalling.
Generally, the direction of the arrow indicates upstream/downstream.
However, at a glance, this has even less standardisation than the arrowheads.
Sometimes, like in the example in the question, upstream is generally at the top, and downstream is at the bottom.
Other times it is from left to right, or right to left.
There are many examples of cyclical events which the only way to tell is by following each arrow "path" for a particular signal.


Why is menstruation in wild animals not a disadvantage to organismal survival?

Thanks to the other answer for pointing me in the right direction with some references. It seems that two biologists in the early 1990s had a back-and-forth over this topic in The Quarterly Review of Biology.1,2

A statement of the problem:

  The function of menstruation is a central enigma of mammalian, and especially primate, reproductive physiology. Each cycle the uterus builds a glandular epithelium with a high secretory capacity and an elaborate microvasculature, only to reabsorb or void it with the menses if implantation does not oc-cur. Why does the endometrium not maintain a steady state of readiness for implantation by the blastocyst? What is the selective advantage of cyclical regeneration and regression?1

One hypothesis2

In  1993, Margie Profet hypothesized that menstruation is primarily advantageous as a defense against pathogens transported by sperm. During mammalian insemination, she stated, bacteria from the male and female genitalia cling to sperm tails and are transported to the uterus. Menstruation, triggered by the abrupt constriction (causing necrosis of endometrial lining) followed by dilation (causing shedding of said necrotic tissue), forces loose not only the endometrial lining but sperm-borne pathogens contained therein. In addition to shedding the uterine tissue harboring these bacteria, menstruation delivers immune cells to the uterine cavity, triggered by the mechanical pressure exerted via the shedding of endometrial lining.

In this 50 page (!) article, Profet also points out that other mammals with covert menstruation take advantage of some of these same benefits, as the immunological stimulation includes phagocytosis of pathogens by cells that may be expelled in cervical/vaginal mucous. Further, proestrous  bleeding (i.e. that preceding ovulation, 180 degrees off from the human cycle), which occurs in some mammals (domestic dog, coyote, etc), seems to serve a similar function.

  If not eliminated prior to estrus, these tenacious pathogens might otherwise attach to incoming sperm during estrus and ascend the oviducts.

As to why humans and other primates are subject to overt bleeding in contrast to other mammals, she lays out a theoretical argument that selection pressure to menstruate should increase with decreasing per-cycle “fecundability” (the probability of pregnancy) because copulation not followed by bleeding risks infection. In contrast to, e.g., mice (98% fecundability), humans have some of the lowest fecundability rates, primarily due to “concealed” ovulation which de-couples copulation and ovulation. (Contrast this to most mammals whose females have a defined estrous period during which they are receptive to male sexual advances; the data for the existence of such a period in humans are controversial, and sexual behavior is driven primarily by “higher” social, environmental, and cognitive cues.)

A different view1

In response/objection to this paper, Beverly Strassman in the same journal published an article outlining an alternative hypothesis about the potential adaptive value of menstruation. She proposed a hypothesis based on energy conservation:

  [T]he uterine endometrium is shed/resorbed whenever implantation fails because cyclical regression and renewal is energetically less costly than maintaining the endometrium in the metabolically active state required for implantation.

Her research determined that, in its regressed state (i.e. s/p endometrial shedding), oxygen consumption in the endometrial tissue is markedly declined, nearly sevenfold. Although this would seem to be a trivial component of whole-body metabolism, she argues otherwise:

  Metabolic rate is at least 7% lower, on average, during the follicular phase than during the luteal phase in women, which signifies an estimated energy savings of 53 MJ over four cycles, or nearly six days worth of food.

Her argument shares with Profer’s the implication that mammals with lower fecundability are more likely to menstruate. In those with high probability of pregnancy at every cycle, the energetic benefits of ridding the body of the need to support endometrial lining (relevant only in the absence of pregnancy), are decreased. Her hypothesis also predicts the larger volume of menstrual shedding in humans and chimps in contrast to other mammals related to the increased uterine size relative to the female body (a ratio that is largely determined by the especially large head of the human fetus).

Conclusion

As noted in the comments, only primates have overt menstrual bleeding. The adaptive benefits have been variously explained, and it is probable that there is more than one operative explanatory model. Whatever the small decrement in survivalship incurred by the intermittent and uncontrolled depositing of blood in the wild, it is apparently outweighed in these species by the processes described above.

References and Notes

1. Strassmann, Beverly I.  The Evolution of Endometrial Cycles and Menstruation The Quarterly Review of Biology, June 1996; Vol. 71, No. 2 pp 181-220.

2. Profet, Margie. Menstruation as a Defense Against Pathogens Transported by Sperm. The Quarterly Review of Biology, Sept 1993; Vol. 68, No. 3  pp. 335-386.

Note: Your comparison to urine and feces is an interesting one. Perhaps a vaginal sphincter would be a good idea…..were it not for men and babies….


Can bacteria be reservoirs for animal viruses?

The Answer is No

There are no examples of animal viruses infecting bacteria or incorporating themselves into bacterial genomes. Nor is it a theoretical possibility, given our knowledge of bacteria, eukaryotes, eukaryotic viruses and bacteriophages.

Why is it not a possibility?

As the questioner admits, the replication, transcription and translational systems of eukaryotes and prokaryotes are quite different. None of the known viral genomes could replicate and their genes be expressed in cells of the other kingdom. Why, the questioner may ask, could not a virus evolve to have signals recognized in both types of cell — at least in theory. Perhaps it could, but there is another factor to be considered, and this is the question of how viruses interact with the cells they infect. This is relevant to how other species can harbour human viruses and why there would be nothing driving a virus to acquire the means to replicated and be expressed in both system.

Receptors for Viruses on Host Cells

The point the question fails to take into account is that entry of both eukaryotic and bacterial viruses is a specific process involving interaction between protein or carbohydrate components of the virus and those in the membrane of the host cell. The host components are called virus receptors, and generally differ for different viruses. There are many reviews of this topic in the literature, so I cite a couple of examples freely available on the internet: Grove and Marsh on animal viruses and Rakhuba et al. on bacteriophages.

Viruses evolve to exploit one particular host species, and tend to be specific to that species because, although there may be a functionally similar protein in other species, differences in amino acids in the proteins (or sugars in carbohydrates) preclude recognition. When viruses cross the species barrier, this is due to mutations that allow recognition of the receptor protein in another species. If the change still permits recognition of the receptor in the original species then even if the virus is eliminated from the second (e.g. human species) it will still be present in the original species. Subsequent contact between humans and the species can therefore lead to a reappearance of the virus in humans.

This is how the original species acts as a reservoir. There is no question of a virus ‘hiding’ in bats by some sort of evolutionary pressure to allow it to return later to humans. Understanding this you will see that:

The differences between the membranes of bacteria and humans are so great that there is little likelihood of an animal virus finding a receptor on a bacterial cell.
Even if it managed to do so, it would not be able to replicate in the bacterium.
There is no evolutionary pressure that would select for the series of mutations that could convey the ability for such replication.

Footnote: ‘Dormant’ Viruses

There is another quite different phenomenon in which certain bacterial or animal viruses ‘hide’ within the species they normally cause a lytic infection. This involves incorporation in the genome and later release. In bacteriophages it is called lysogeny and in animal viruses examples include retroviruses and herpes viruses. This has no relevance to the question.


Why aren't all infections immune-system resistant?

First of, not all infections are mediated by bacteria and not all bacteria are infectious. Also, not all parasitic bacteria lead to a strong infection or important health problem that cause any non-negligible selection pressure. Following the implicit logic of your post I will talk about infectious bacteria which cause "noticeable harm".

The mistake in your thinking is in the sentence

  bacteria evolve much faster than humans do

While it is true that the mutation rate of base pair is higher and that the generation time is lower, the statement bacteria evolve much faster than humans do is made way too general and lead to your mistake here.

Infectious bacteria are selected to deal with the host immune system and the host is also selected to deal with the the parasite. Both virulence and penetrance evolve in this evolutionary arms race.

The evolution of host-parasite interaction is a very large field of study and it would take several books (and several books have been written on the subject; see this Amazon search) to summarize it. For some theoretical insights into the evolution of host and parasites, you might be interested in the book by Martin Nowak Evolutionary Dynamics: Exploring the equations of life

You will also note that a parasite does not have any "direct interest" in killing (or even harming) its host (thanks @jamesqf for his comment). You might want to have a look at the post Why do parasites sometimes kill their hosts?


A microelectrode is quite literally a small electrode and they come in a variety of shapes.

The glass pipette electrode you are specifically referring to is mostly used for patch clamp experiments. Patch clamp experiments are performed using various configurations:

Source: Leica

So basically there is the cell-attached configuration, where a patch of cell membrane is sucked slightly into the pipette. Upon stronger suction the membrane is ruptured and the whole-cell patch clamp configuration is obtained. Here, access is gained to the cell, but a high-impedance seal is maintained between pipette and cell membrane. Lastly, there is a configuration where the patch is broken off the cell to exclude effects of the entire cell. This patch configuration is often used to obtain single-channel recordings. Dependent on the exact technique an inside-out or outside-out patch configuration is reached (see the picture above).

Hence, the glass pipette is basically only there to obtain a proper seal (cell-attached), to gain access to the cell (whole-cell), or to break off a piece of membrane. Notably, in whole-cell mode the pipette provides a means to administer compounds into the cell (think ions or drugs).

The recording electrode is situated inside the pipette and is a simple metal wire (platinum or platinum/iridium) and nothing different from any microelectrode as you rightfully state in your question. The electrode wire simply picks up a voltage difference (or current flow) between the interior of the cell (in whole-cell mode) and the exterior. The exterior is measured using a reference electrode outside the cell.

Furthermore, current can be injected to stimulate the cell, or to current-clamp the cell at a specific current. Likewise, voltage can be applied to voltage-clamp the cell. Therefore, an inert material is often chosen such as platinum or platinum/iridium to maintain integrity and prevent electrolytic breakdown. Electrodes are made out of metal to provide a low-resistance means to pick up currents or voltage-differences.

Voltage differences or currents can be amplified with an amplifier, registered and analyzed. See the following picture for the basic recording setup:

Source: Robinson et al. (2013)

Reference
 - Robinson et al. Front Neur Circuits 2013; 7: 1-7


mRNA Sequencing Basepair from Polyadenylation Site?

50-75 bp could be achieved.

Refrencing TruSeq® RNA Sample Preparation v2 Guide. My lab used random primers and read lengths were an average of 75 bp in length for an RNA seq project. But controlling distance from polyA wasn't considered in out project.

Using oglio(dT) primers you could try and control a specific length from the polyA tail.Two basic variations use either random primers or oligo(dT) primers for this reaction. Oligo(dT) primers are highly 3’ biased and mostly
suitable for mRNA abundance (expression) analysis. Random primers also result in some bias, which can be reduced by fragmentation of the input RNA.

Source: RNA Sequencing Methods Collection - Illumina, Page 8.

Different lengths can also be achieved for different needs.
Gene expression / RNA Profiling – Quantifying the coding transcriptome typically requires a short single read (often 50–75 bp) to minimize reading across splice junctions while counting all RNAs in the pool.

Transcriptome Analysis – Novel transcriptome assembly and annotation projects tend to benefit from longer, paired-end reads (such as 2 x 75 bp) to enable more complete coverage of the transcripts and identification of novel variants or splice sites. Paired-end reads are required to get information from both 5’ and 3’ ends of RNA species with Stranded RNA-Seq library preparation kits.

Small RNA Analysis – Due to the short length of small RNA, a single read (usually a 50 bp read) usually covers the entire sequence. A read length of 50 bp sequences most small RNAs, plus enough of the adapter to be accurately identified and trimmed during data analysis.

Source: Illumina (Considerations for RNA-Seq read length and coverage)


Paracetamol is a pain killer, it does not treat the cause of your illness, it only alleviates the symptoms. From its wikipedia page:

Paracetamol [...], chemically named
N-acetyl-p-aminophenol, is a widely used over-the-counter analgesic
(pain reliever) and antipyretic (fever reducer).

So, paracetamol does not make you better. Your immune system makes you better. Paracetamol just makes you feel better while you are waiting for your immune system to get an infection under control.
You should be aware that it is only safe in small doses and a toxic dose is not that much more than the recommended one (source):

Risk of severe liver damage (ie a peak ALT more than 1000 IU/L)
Based on the dose of paracetamol ingested (mg/kg body weight):
Less than 150 mg/kg - unlikely
More than 250 mg/kg - likely
More than 12 g total - potentially fatal

Again from wikipedia:

While generally safe for use at recommended doses (1,000 mg per single
dose and up to 4,000 mg per day for adults),[6] acute overdoses of
paracetamol can cause potentially fatal liver damage and, in rare
individuals, a normal dose can do the same; the risk may be heightened
by chronic alcohol abuse, though it is lessened by contemporary
alcohol consumption. Paracetamol toxicity is the foremost cause of
acute liver failure in the Western world, and accounts for most drug
overdoses in the United States, the United Kingdom, Australia and New
Zealand.

I am sure someone else can explain the pharmacokinetics and details of action of paracetamol. I just wanted to point out that paracetamol can be dangerous and should be treated with respect.


What happens to eyeball when you push your eye muscles harder?

Do you mean squinting? Any sort of tension on the eyes would result in changing of the shape of the eye. A change in shape will bend light differently. The perceived effects you're describing are most likely from you changing the shape of your eyeball to take in more light.
In terms of squinting, eye strain like that won't lead to blindness or worse vision. There's more danger with UV from the sunlight (cataracts) or getting wrinkles from squinting too much in the long-run.


How long can the brain survive during ongoing cardiac arrest?

From Boron and Boulpaep textbook of Medical Physiology, second edition, p.289:

  Because of falling ATP levels in the brain, consciousness is lost within 10 seconds of a blockade in cerebral blood flow. Irreversible nerve cell injury can occur after only 5 minutes of interrupted blood flow.

If conscious is lost within 10 seconds of blockade in cerebral blood flow, I guess a person will not be conscious to do any action in only 10 seconds!

Brain ischemia is divided into

Focal ischemia which signifies stroke.
Global ischemia which occurs in cardiac arrest.

Permanent neural injury means that once perfusion is restored, the symptoms don't relieve as the part of brain which caused those symptoms becomes dead irreversibly.

For a list of symptoms check this page.


How does boiling water revive cut flowers?

I could not find any scientific papers that have done research into this phenomenon but the general reason given for wilted flowers to being resuscitated is given as the hot water being absorbed faster and I quote

  Florists use warm water only for resuscitating wilted flowers, because
  warm water is absorbed quickly. For restoring wilted stems, hot water
  (110 degrees Fahrenheit) is recommended. For woody or badly wilted
  stems, very hot water (180 to 200 degrees) is better. Florists then
  move them into a refrigerator (reference).

The reason for absorbtion faster is given as

luke warm water in a vase arrangement because warm water is “thinner” (has fewer air
bubbles) and moves up the stem faster than cold water (reference) and Warm water molecules move faster than cold water molecules and so can be absorbed by flowers with greater ease (reference).


Answer in brief

  Heteroduplex called patch does not have double-stranded recombinant regions, there is a new fragment in a single strand only. It means that the two strands are not complementary at that regions and as soon as DNA repair systems detects it, the mistake will be corrected. In case of heteroduplex called splice, there are double-stranded changes, which do not go against the complementarity principle and thus, they will not be removed or corrected in any way.

Diagrammatic Explanation

After horizontal and vertical resolution patch and splice are formed respectively.

A better version of this diagram with complimentary base pairing is shown below $-$

In patch the heteroduplexes formed have only a single stranded middle recombinant region which is not complimentary to the other strand when this is detected by the DNA repair system and corrected the duplexes formed are same as the original duplexes (before crossing over) so the products of horizontal resolution is called non-recombinant products.

In splice the heteroduplexes formed have double stranded recombinant segments with middle non complementary region which when detected and fixed by the cell's DNA repair system two duplexes are formed having recombinant DNA segments, so they are together called recombinant products. The recombination in splice is well represented by the reversal of terminal genes.


Cyclin dependent kinase is the answer for the first question. Cyclin concentration increases during m phase and falls in g1 s and g2 phase as it is degraded. Cdk is always present in the cell but gets activated during m phase, when cyclin is present. (cyclin dependent)

Cancer cells do not require growth factors to stimulate cell division. They have mutations which disrupts the normal cell cycle regulation. Now can you think what should be the answer ?


No, this is not a Brown Recluse.  There are several reasons for saying that, among them the fact that it's outside; it's hanging on a screen, and it doesn't look at all like a Brown Recluse - (Recluses don't have a rectangular cephalothorax "head end", and they have a bulbous abdomen, not that pointy-ended one this spider has).
As for what it is, there are some good clues - first that rectangular-looking cephalothporax.  That's pretty unusual in spiders, although it's not actually rectangular; it's just the central dark pattern is very blocky.  Then, look at that color - kind of a creamy light mahogany rather than a real brown, and no darker/lighter patterns that the bigger wandering spiders that look like this would have.  Finally, look how it's holding its legs - both the front pairs are close together.  That's something you tend to see in two sorts of spiders - the big Argiope orbweavers, and the big Fishing Spiders and their relatives.  Argiopes have a different body shape, pattern and color than this, and it would be a little unusual to find one this size hanging around not in a web.  Fishing Spiders are generally dark-colored, and with more patterning than this, but there is a close relative that fits this image:  the Nursery-web Spider, Pisaurina mira.  Here's the Bug Guide page, and a representative photo:

https://bugguide.net/node/view/2919


A maggot typically feeds on carrion. A maggot is the larva of a fly and usually  particular to the larvae of Brachyceran flies, such as houseflies, cheese flies, and blowflies.

Interestingly decomposition from maggots has a lot of use in forensic science as the presence or development of maggots on a corpse can be useful to a forensic entomologists to determine the approximate time of death. Depending on the species and the conditions, maggots may be observed on a body within 24 hours. The eggs are laid on the body and when the eggs hatch, the maggots move towards their preferred conditions and begin to feed. Insects are usually useful  25–80 hours post mortem and is contingent on temp humidity and oxygen availability. After 80 hours, this method becomes less reliable.


Plant cell question in age 12 science test Part II

So, to go through the question in total:

(a) Part A nucleus is correct, but Part B ist the cytosol/cytoplasm, as the line does not stop at the border, but goes through it and ends in the gray part of the cell.

(b) For part C, it is the same problem as in your first question. Yes, the picture may be a plant cell, however, upon this drawing one cannot differentiate a mitochondrium from a chloroplast. In my opinion, a good teacher should have marked this answer as correct, even if he/she wanted to hear the other possibility. Part D is correct.

(c) 'Photosynthesis takes place here': Photosynthesis takes place in the chloroplasts. Mitochondria would have been correct, if the teacher would have asked for the respiratory chain or for the often in school simplified powerhouses of the cell.
'Many of the cell's chemical reactions take place here': I think, the teacher wanted to hear the cytosol as answer.


What is an simple way to burn glucose for visible effect?

You could combine the demonstration that glucose can be burned with the principle of catalysis: a sugar cube won't burn by itself if you hold a match at it. Using a bit of MnO2 or even simple ash on the cube will make it inflammable through catalysis: the MnO2 acts as catalysator (is not used up).

MnO2 (manganese(IV) oxide), a dark powder, is a safe chemical that only reacts with acids, and is insoluble in water.


Differences between Heracleum mantegazzianum and H. sphondylium

Yes, the species can be identified by the shape of the leaves. The leaves of H. sphondylium are more or less flat (in one plane); the leaves of H. manteggazianum are more crisped and much more pointed.

Here are two pictures from the Dutch wikipedia (h. sphondylium last):


Measuring depolarizations over the membrane

It is extremely important where you put your electrode when measuring such delicate structures as dendrites (which is when you want to compare voltage changes between two parts of a neuron). That is why you put your electrode inside the dendrite. Each recording electrode has its own ground that goes inside the bath, i.e. outside the neural tissue. Alternatively, you can observe fluorescence changes of a calcium or voltage dependent indicator that you have introduced inside them.

https://www.janelia.org/sites/default/files/Labs/Spruston%20Lab/Stuart_Spruston_2015.pdf


How to do a whole genome analysis of Multidrug-resistant Mycobacterium tuberculosis

You've picked a fascinating and very important organism to study. Unfortunately there are many many steps with many software packages that you'll need and each next step will depend on what you find making any particular tutorial nigh on pointless. I'm sorry to say that I don't think anyone will dump an entire project proposal or workflow as an answer. I'll give you an answer to get you started on your research.

Example

An excellent example of such a study is Fellay et al., 2007 and you can find their materials and methods supplement here.

An introduction to this kind of research

First you need to find the sequences of proteins that you think are significant. There are a bunch of ways of doing this, but I suggest standing on the shoulders of giants and scouring the literature (regardless, find an example where this has been done elsewhere). If there isn't much out there or for an entirely new viewpoint on something, this answer might help for finding proteins in the DNA sequence.

Sequence alignments against other strains is your best bet of identifying mutations (and possibly an indicator of resistance, which is what I guess you're after). There are plenty to choose from, but BLAST is a good tool to start with. You should compare your resistant strain with non resistant strains. Be very careful when analysing the data, not every mutation will be significant.


What is the reason behind more severe proteinuria in nephrotic syndrome than in nephritic syndrome?

It is to do with the extend of the damage to the glomerulus. In nephrotic syndromes the glomerulus is damaged so that there is death of the podocytes. This happens to sufficiently high number of podocytes so that large proteins such as albumin and clotting factors can leak out causing large proteinuria. Damage to the basement membrane may also occur, such as in minimal change, where there is a loss of charge on the basement membrane.

In nephritic syndrome the damage is as a result of inflammation which does not lead to the same structural damage as in nephrotic syndrome, therefore there is not leakage of protein to the same degree.


Which part of the reflex arc takes the longest time?

The answer to this question depends which reflex arc was activated, without knowing the exact reflex arc one should assume the answer as multifactorial and relate to this (or similar) table:

(Source: Fundamental Neuroscience for Basic and Clinical Applications,  by Duane E. Haines)


Is there a feasible way to create a large number of long random DNA strands?

Chemical DNA synthesis has you covered for short DNA strands.

It's possible to just use an equimolar mixture of all 4 bases when you do chemical synthesis, which results in random sequences. (This is most often used to generate barcoded primers).
The main problem with this approach is that:

chemical synthesis is not super efficient, anything above ~1-2kb will likely not be possible
If you work with a fully randomised sequence it becomes much harder to do quality control of the product (you can't sequence it).

You can also easily even calculate the probability of generating all possible sequences for a given strand length and yield.


Question regarding research project on indigenous ants during Eastern European winter

Do you have any specific reason for using a wild species? If not, you would have better using a lab lineage (or any ant farm). Breeding a wild species by yourself might be very tricky.

Taking care of an ant colony might not be as easy as you may expect. Your best chance is to target a species of interest based on past studies and visit a lab that is breeding this specific species.


Is the transcription starting site located before or after the promoter?

Just in addition to David's answer, there are examples of internal promoters (those which have elements 3' of the transcription start site). As an example, internal promoter elements of tRNA genes direct binding of and transcription by eukaryotic RNAP III:

White RJ. 2011. Transcription by RNA polymerase III: more complex than we thought. Nature Rev Genet 12:459-463.

Many class I retrotransposons also contain internal promoters which allows them to be transposed along with the other elements:

LINE - internal RNAP II promoter
SINE - internal RNAP III promoter


What is this rather large insect in northwestern USA?

This is a Jerusalem cricket, an insect from the Genus Stenopelmatus.

Here is an image of Stenopelmatus fuscus for comparison:


Are drones from one honey bee queen all clones?

The queen is diploid; the drones are haploid. Meaning the queen has two copies of each chromosome, and the drones have only one. So for each gene, the queen has two copies and passes one of those copies on to the drone.

This means the drones are different for exactly the same reason female bee siblings, or human siblings, are different: because every parent has two copies of a gene, that are often different, and passes only one of those to their offspring.

If the queen were homozygous for every allele, i.e. the two copies of all her genes were identical, then the drones would indeed be genetically identical. But this is true as well of the children of two completely homozygous parents.

See this page on inbred laboratory strains of animals (animals which are inbred to the point they and their offspring are genetically identical to each other):
http://isogenic.info/html/inbreeding___it_s_effects.html

  F1 hybrids, i.e.  the first-generation cross between two inbred strains, are isogenic but not homozygous.

In other words, if you have two parents who are genetically different, but have two identical copies for all of their chromosomes, their children will be isogenic (have exactly the same genes); they all have two copies of their genes, got one copy from their father and one from their mother, and those two copies might be different from each other (their mother and father have different alleles), but all the children got those same two copies because they're the only copies their mother and father have.


Is there a publically available database of microbes that details what their wastes and food sources are

You could try to look into the kegg database. It's main purpose is to describe biochemical pathways, but it also has information on which species actually have these pathways (not sure how well this annotation is for bacteria though).

You should be able to pinpoint a few key pathways that start on free ammonia or have sulphuric acid as a sink/endpoint and then check for all annotated species. I wouldnt expect such lists to be comprehensive, but it should give you at least a starting point.

As an example the Nitrification and Anammox sub-pathways of the Nitrogen-metabolism page show direct usage/incorporation of free ammonia. If you click on some of the enzymes/genes (the boxes with numbers) and follow through to the 'taxonomy' box under genes, you'll get a list of some bacteria species each.


What would you choose when your treating physician gives you the option: leukemia or antiviral treatment? HIV is not lethal anymore these days, at the least life expectancy can be substantially prolonged. Admittedly, treatment is life long and not a cure, but you'll live.

Leukemia on the other hand, is life threatening and needs immediate treatment. Treatments for leukemia are primarily chemotherapy, and perhaps radiation therapy, biological therapy, targeted therapy, and stem cell transplant, all of which are by no means guaranteed to be curative.

But interestingly: a Berlin leukemia patient with HIV was actually cured after receiving chemotherapy and having received HIV-resistant stem cells to repopulate his white blood cells (Source: Medicine Net). The donor carried the relatively rare mutation called CCR5delta32. People with this mutation lack functional CCR5, the protein that HIV most often uses to enter cells.

Why is this not a standard treatment? The Berlin patient serves as a good example, because the patient suffered intestinal and neurological symptoms due to the chemotherapy. And besides being dangerous in itself, chemo is truly a grueling experience to go through. And in fact, this patient was the only instance in which this approach was followed (Source: Medicine Net).


What do you see when your eyes are closed?

This is called a phosphene — the experience of perceiving light in the visual cortex without light actually entering the eye. This commonly happens due to stimulation of the retinal ganglion cells by something else. The most frequent source in normal individuals is pressure to the retina (e.g. rubbing a closed eye.) It is also possible for phosphenes to occur due to neuronal stimulation at the cortical level. Most people have had the experience of “seeing stars” when you stand up too quickly. This happens because orthostatic hypotension results in transiently decreased cerebral perfusion; it is the metabolic shift in oxygenation and/or glucose delivery to cortical neurons that causes the perception of light. Something similar occurs with brief rises in intracranial pressure that occurs with sneezing or coughing.* Magnetic stimuli can also induce this phenomenon.

Phosphenes can also be pathologic (i.e. disease-associated). Migraine headache sufferers may experience a visual “aura” prior to a headache, which is a type of phosphene, likely mediated at the cortical level. There is some evidence to suggest that preventing the phosphene may also reduce headache frequency. Other conditions associated with phosphenes include abnormalities of the optic nerve** and retina — just as stimulation of a peripheral somatic sensory nerve might cause a pain signal to arrive in the brain in the absence of true tactile stimulation, disorders of the optic nerve can generate disorganized signals that the brain perceives as light.

*Increased intracranial pressure leads to decreased perfusion due to the differential between peripheral and cerebral pressures.

**If you read nothing else linked to this question, take a look at that paper (free in PMC). It describes optic neuropathy associated with auditory-evoked phosphenes. The patients perceived sound as light!