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Why are large amounts of DNA required for analysis?
I know PCR is used to create large amounts of copies of genes and that it's a scientific breakthrough but want to understand why. Why do we need large amounts of DNA to be able to analyse it, to utilise it. Isn't a single DNA molecule enough?

Firstly, A DNA sample obtained from a cell or whatever is never going to contain just the DNA sequence you want but will instead contain the entire genomic DNA, plasmids, RNA sequences and whatnot. By using PCR you can selectively multiply the amount of desired DNA sequence while the undesired sequences do not get copied. Keep the PCR going long enough and the amount of undesirable DNA versus the desired DNA sequence is going to become negligible. At that point you can do whatever experiment you want with your DNA sample and be reasonably sure that whatever result you get is caused entirely by your DNA sequence of interest.
Secondly, even if you could isolate a single DNA molecule what would you do with it? You couldn't determine its length by gel electrophoresis as a single DNA molecule wouldn't make a visible band and building it into a plasmid will most likely fail as you only get 1 chance. You probably wouldn't even be able to tell you had a DNA molecule as machines in your everyday lab aren't sensitive enough to detect a single DNA molecule.
Thirdly, having a large quantity of DNA allows you to perform different experiments from the same sample. Most DNA analysis methods I know of are destructive in that the DNA used cannot be reused for another experiment, so a large enough quantity of DNA to perform all planned experiments without having to obtain a new sample (and introduce all kinds of potential problems) is useful.
So, in summary, PCR allows us to filter the desired DNA sequence from a sample, perform meaningful analysis on this sequence and lets us use one sample for multiple experiments. There might be even more advantages to PCR that I have missed but these the ones that sprung to mind.

Many of the methods used to visualize the presence of DNA, such as gel electrophoresis, rely on visual analysis whether by human eye or machine. A significant amount of DNA beyond what might be extracted directly from a particular source is required for this. This need is exercerbated by the fact that the DNA is typically broken down into fragments for analysis.
Scroll near the bottom of this link to see an example of a gel.
https://en.wikipedia.org/wiki/Gel_electrophoresis


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Why don't phagocytes eliminate mutualistic foregin organisms residing in our body?
Many organisms residing in our body and have a symbiotic mutualistic relationship with our body e.g. organisms in our small intestines. How come our body does not activate an immune response against them? Is it that the organisms have self antigens, or do the immune cells have no antibodies for these organisms? Also, how come our immune system is able to respond to these same organisms if they cause an infection in our body? E.g. Entamoeba histolytica causing amoebic dysentery.

Molecular context is important here. E.coli in your colon is OK with the body, it is taken up by phagocytes as part of normal "surveillance". Your immune system will learn and gain "tolerence" to these mutualistic bacteria as long as they are in the correct environment.
If that same E.coli is a pathogenic strain or finds a way into the blood stream (sepsis), your body will recognize that it does not belong and mount a immune response. There are different classes of antibodies with different properties including where they are predominantly found. For instance IgE is found in mucosa but not in serum.
On top of that there are the 'Danger/Pathogen associated molecular patterns' (DAMPs or PAMPs). Cells can 'sense' general molecular patterns such as LPS, unmethylated CpG DNA, double stranded RNA through a class of molecules called Toll-like receptors (TLRs). Different TLRs are found in different cells or cell surfaces and they are the 'first line' response against inappropriate bacteria or viruses.
Once the TLRs are activated the cells will produce 'Danger Signals' called cytokines which initiates an immune response. In the absence of 'Danger Signals' present in the microenvironment, our immune system won't really begin mounting an immune response but just 'surveys'.
In this 'danger' context, you get robust phagocytic response.
If you'd like to learn more about this Mucosal Immunology is what the topic is called. All in all, the vast majority of our immune system is mucosal, it's just less studied relative to humoral immunity since it's harder to study.

So does this mean that there are certain LPS along with double stranded RNA and unmethylated CpG DNA that are displayed by bacteria (or other flora in the body) when they become pathogenic? These molecules are recognised by immune cells which results in an immune response. Is this what you mean to say?

@Tamur No, these are very broad molecular patterns, almost all bacteria will have them as normal molecules, so both pathogenic and non-pathogenic. What they do do is detect when bacteria is in an inappropriate place in the body, like the blood, muscle tissues, lymphatic system etc... TLRs are expressed in many cells, the most important being epithelial (skin) cells. So the skin is an immune organ. TLRs are not restricted to blood immune cells.

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Why is thrombin time longer than prothrombin time?
Thrombin time (TT) and prothrombin time (PT) are two different clinical measures of blood plasma coagulation.
Both clotting tests end with the conversion of fibrinogen to fibrin; however, the TT skips directly to this conversion by adding thrombin reagent, while PT involves the entire extrinsic pathway. Despite the fact that PT involves the same clotting steps as TT plus several others, the normal range for TT is slightly longer than the normal range for PT.
Why is the normal range for TT longer than the normal range for PT when the former skips several clotting steps? Without background information about the normal ranges, it seems much more logical for the prothrombin clotting test to take longer.

I think the close votes here are a bit premature - this question could be improved a bit but it is actually an excellent question.

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In mitochondria, what is the mechanism by which electrons are transferred between different cytochromes?
And how is the energy gained from the lowering of the "energy level" of the electron used to generate the chemiosmotic gradient?

I think this is a completely reasonable question, why the close votes? Can someone at least comment on what the problem is, and give the OP a chance to edit, before voting to close?

Good question. The common picture of the electron transport chain as a sequence of molecular machines that pass along a "high energy electron" is biochemically rather misleading I think. What is really going on is just a series of energy-releasing (exothermic) redox reactions. The respiratory complexes are enzymes that catalyze these reactions and couple the energy released in each reaction to proton pumping against a gradient.
As an example, lets consider the reaction carried out by Complex I, where NADH is oxidized:
NADH + H$^+$ + CoQ $\iff$ NAD$^+$ + CoQH$_2$
This reaction transfers a hydride ion (H$^-$) carrying two electrons from NADH, which is accepted by CoQ. Since CoQ is a much better electron acceptor than NAD$^+$, this reaction is highly favorable with a $\Delta G$ of about
-85 kJ. So quite a bit of energy is released, and part of this energy is captured by Complex I to pump four protons across the inner memberane.
Note that electrons are not "traveling" on their own through Complex I somehow. The electrons are bound to molecules that participate in a redox reaction. And it doesn't make much sense to say that a specific electron's "energy level" is decreased. Rather, the compounds on the right hand side have a lower free energy $G$ in total than those on the left hand side, and therefore the reaction overall releases energy (the free energy difference $\Delta G$ is negative). Also, if you look at the chemical structures of CoQ and CoQH2 --- and you absolutely should look at structures in biochemistry, the names alone are not very helpful --- you will find that the electrons involved are actually delocalized in CoQH2, so there's no way to figure out which electron goes where.
The same reasoning goes for the other respiratory complexes. Complex III oxidizes CoQH$_2$ back to CoQ by coupling it to reduction of cytochrome C,
CoQH$_2$ + 2 Ferricytochrome-C   $\iff$   CoQ + 2 Ferrocytochrome-C + 2 H$^+$
This reaction is also favorable, and again the energy released is used to pump protons. Finally, Complex IV oxidizes cytochrome C back and transfers electrons to O$_2$, also an energy-releasing redox reaction. The reaction mechanisms are much more complicated of course, involving various chemical groups bound to the enzymes, but this is the net result.
So the "respiratory chain" is not some conveyor belt for electrons; it is a sequence of coupled redox reactions. The net result of the Complex I + III + IV reactions is that NADH has lost electrons and oxygen has gained electrons, but it's not necessarily the same electrons, and it doesn't make sense to speak of "energy level" of electrons in this context. To understand the energetics, we must look at all the compounds and reactions involved.

@tomd,  as I interpreted the question, the OP was aware of the chemoosmotic principle but was unclear about the energetics that provide the energy for proton pumping.

All of the members of the Electron Transport System (ETS) are organized in "complexes", clusters of enzymes and other proteins. These complexes are in proximity to one another such that electrons can be passed between them. The different cytochromes, and other electron handlers, have different affinities (attractions) for electrons. Those at the beginning of the ETS have less affinity for electrons than those at the end. The reason the electrons move through the ETS is due to that greater attraction of electrons by the subsequent complexes in the pathway. These complexes are positioned with respect to one another so that no "short circuits" occur; the electrons skip no steps down the ETS. Finally, the "low energy" electron from the last complex is mopped up by that great electron-hog oxygen.
The energy lost by the electron as it passes between carriers is not directly harvested to pump protons. The importance of this "loss of energy" is that it makes the transfer of the electrons a spontaneous process insuring their passage down the ETS. Typical entry into the ETS involves NADH donating a hydrogen ion to the matrix and a pair of electrons to NADH dehydrogenase. The electrons are eventually transferred to the mobile coenzyme Q. This now attracts a pair of hydrogen ions from the mitochondrial matrix which then induces the operation of a proton pump. This pumps hydrogen ions into the inner-membrane space creating the electrochemical gradient.
So, in general the arrival of electrons, with the attendant hydrogen ions, changes the conformation (shape) of pumps which translocate the protons to build up the gradient. The electrons are ultimately passed on to oxygen, forming water with the help of some spare hydrogen ions. This removal of the electrons allows the ETS members to be receptive to another load of electrons from the NADH.
Reference 2nd paragraph: http://www.physiologymodels.info/metabolism/ETSOXPHOS/ets.htm
This is a good site to read more and view some diagrams, especially focus on the second panel, "Complex I".
Reference 1st paragraph: Molecular Biology of the Cell; Alperts, Watson, et.al.

Thanks for the really detailed answer - the link was very interesting; it's just that I'm in the dark as to how these electrons are transferred between complexes? It seems counter intuitive that they can just hop between molecules when all other electron transfers in biochemistry require some kind of enzyme-mediated redox reaction.

@user30109. These are oxidation-reduction reactions. And some of the members of the complexes are appropriately called enzymes.


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Why is bacterial meningitis worse than viral meningitis?
My field is not biology related, but it is commonly said that bacterial meningitis is far more dangerous to the individual than the viral kind. It seems to be true even with antibiotic treatment. What is the biological reason for this?
If this question has already been addressed or this is the wrong stack exchange, feel free to redirect this question to the more appropriate place.

One needs to be careful making broad generalizations about meningitis. The term simply refers to inflammation of the meninges (the outer layer surrounding the brain and spinal cord). Meningitis can occur due to a number of causes, most notably viral and bacterial infections, but can also also be due to fungi, parasites, toxins, cancer, etc. There is a vast range in severity of meningitis depending on the aetiology.
For example, rabies infection can progress to a fatal meningitis. Rabies is a virus. You therefore cannot say that bacterial meningitis is worse than viral meningitis.
That being said, what you have likely heard is that viral meningitis tends to be less severe than bacterial meningitis. This is true not necessarily because viruses are worse at causing meningitis than bacteria, but because the common causes of viral meningitis are often more easily cleared by the immune system.
Non-polio enteroviruses and herpesviruses are the most common causes of viral meningitis. These are the same groups of viruses that commonly cause mild cold or flu-like signs. Usually, when we have these signs, we don't go to the doctor to be treated with antivirals, because in healthy individuals our bodies are usually good at clearing the virus. The same is true when the virus is affecting the meninges. However, this does not mean that these viral infections cannot be severe in some cases.
The most common bacterial causes of meningitis in people are Neisseria meningitidis, Streptococcus pneumoniae, and Haemophilus influenzae type b. The pathogenesis of disease is broadly speaking similar to that caused by viruses, but the inflammatory response of the immune system tends to be more severe with these bacterial organisms compared to the common viral causes of meningitis. Bacterial meningitis is also typically accompanied by sepsis affecting other organ systems. While antibiotics exist that are effective at treating these bacteria, many antibiotics do not cross the blood-brain barrier, which makes treatment of bacterial meningitis challenging.
Finally, it is worth mentioning that widespread vaccination may have had an effect on our perception of meningitis severity. For example, at one time polio was a major cause of viral meningitis, but vaccination has vastly reduced rates of this disease in many parts of the world. Similarly, mumps and measles used to be more common causes of viral meningitis, however due to widespread use of the MMR vaccine these are now less common causes of viral meningitis. On the bacterial causes, there are now several common vaccines such as meningitis B/C/Hib/pneumococcal vaccines which are effective at reducing rates of infection with these bacterial organisms.

I think the question is fine, though some might find it too broad and it is hard to give a precise answer.
It's really just because they are two different diseases, the only thing that is the same is the tissues that are targeted. Bacterial meningitis is associated with bacteria that destroy tissues, release toxins, and cause a strong immune response - that immune response can sometimes be as dangerous as the infection itself. The blood-brain barrier can limit the effectiveness of some antibiotics because the drugs don't get to the affected tissues, though infection also damages the blood-brain barrier (this reference talks about both of these issues).
Viral meningitis can also damage tissues but typically more slowly, and in most individuals without immune problems the immune system is able to limit the virus before the infection gets out of control.


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How do ants follow each other?
I was observing ants in my house.They all were going in a straight line and also some of the ants were coming back through the the same line.
I took some water and rubbed the line with my finger, then the ants were not able to follow each other. Looks like they were confused.
My assumption is that they may had secreted some chemical .
Am I right ?
If yes, then which chemical is that and how it is secreted?

The chemical we are talking about here is called pheromone, trail pheromone to be specific.

A pheromone is a secreted or excreted chemical factor that triggers a social response in members of the same species. Pheromones are chemicals capable of acting outside the body of the secreting individual to impact the behavior of the receiving individuals.1

Pheromones are of mainly 9 types (13 exactly, but 4 not so common) which are:

Aggregation pheromones
Alarm pheromones
Epideictic pheromones
Releaser pheromones
Signal pheromones
Primer pheromones
Territorial pheromones
Trail pheromones
Sex pheromones
Nasonov pheromones
Royal pheromones
Calming pheromones
Necromones2

Ants, and many other animals, use trail pheromones to mark their trail as a guide for others in their gang. Other ants, catching the signal of trail pheromone, follow the way it goes and reach their gang leader. Trail pheromones are volatile compounds, so it is not very likely that you would see ants following the exactly same path tomorrow or a week later. All ants release trail pheromones, so as long as ants are going through that path, the trail signal will keep getting stronger and will also tell lost ants "Hey, bro! We are going this way. Don't you want to join us?" See, for example, here3:

In the beginning, different ants follow different paths, but as soon as an ant finds the shortest path, all ants join it on that path, due to which pheromones on other paths evaporates and finally, they all walk in straight line.
Of course, trail pheromones are very useful for organisms who have lost their way home, but you know, other organisms, like their predators, are not just sitting and watching them. Some predators can also catch pheromones and find out where the whole team is going, to attack them all at once. Such chemicals are known as kairomones. See this4:

A kairomone is a semiochemical, emitted by an organism, which mediates interspecific interactions in a way that benefits an individual of another species which receives it, and harms the emitter.

Semiochemical is just a type of pheromone which a species X releases, but a species Y can also respond to its presence. Its just like when you walk on road and say "Whoa! Seems like a pizza delivery van just passed by" (obviously, smell of pizza is not by a pheromone ;)
The trail pheromones released by army ants can also be detected by a blind snake or a forest beetle, leading it right inside their nest. Obviously, all semiochemicals are not bad. Chemicals like synomones (helping both species) and allomones (just the opposite of kairomones) are also present5, but they are beyond this question's scope.
References:

 Medical Definition of Pheromone
Types of Pheromones - Wikipedia
Life in Wireframe - Ant Algoithms
Kairomones - Wikipedia
These Pheromones Get The Animals That Secrete Them Killed

Just curious, but why could the smell of pizza not be a pheromone? Smells are just chemicals that get into our nose and are interpreted by the brain. And the smell of pizza can change behavior :)

@DrZ214 It's not a smell generated directly by the human body in order to affect the behavior of other humans.  Being who we are, of course, you could make a case for the pizza parlor that arranges to have the kitchen exhaust vent blow into the sidewalk using the smell of food in the same way that ants use attraction pheromones.

@DrZ214 simple, because its pizza, not Pizzacibus caseus ;)


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What, if any, is the difference between covalently closed circular DNA and plasmids?
Are cccDNA (covalently closed circular DNA) and plasmids the same thing? What about DNA topoisomers?

Please add some indication that you've performed prior research to try to answer your own question. This is a requirement on Bio.SE. Unfortunately, if you do not, your question will remain closed and possibly deleted.

The short answer to this question is no, they are not the same thing.
The long answer, however, is in some cases they can be interchangeable. I would like to make the comparison with the coin-just like you can flip it on one side or the other in some(actually, far from always)cases a cccDNA can become a plasmid and the vice versa. cccDNA isn't an entity on its own right-it isn't a component of the cell like a plasmid can be. It is a phase of the replication cycle of some viruses. It can be found in the group I and VII viruses according to the Baltimore classification. This means viruses containing DNA in their virion(the virion is what you would normally consider to be the virus, it is what you see on all those electron microscope pictures on the Internet and is what exists out of the cell as the virus). Some of the members of those groups of viruses have genomes which once inside the cell can replicate using cccDNA, Here is an example of a virus using its circular DNA to replicate:

It uses this form of its genome, because it makes its replication easier since once the enzyme starts to replicate it can do several circles without stoping. It is a replication strategy viruses use, while a plasmid is a mobile genetic element. It means it always needs a cell by definition. Now, it is true plasmids can become viruses and viruses plasmids if genes coding for the proteins needed to construct their virions are present but from a purely definitial point of view they are different things. In reality however it is possible for a plasmid to acquire the genes it needs to become a virus and for a virus to lose them and become a plasmid. Actually this is process often used in recombinant DNA technology to transfer genes from one bacterium to another by viruses because often these plasmids can get included in the cellular genome and include in it the genes they carry. See 3 This is the big difference between a circular viral genome replicating in the cell and a plasmid. Yes, they can look similar in shape but they are not the same as function.
Topoisomers are different forms of DNA which are the same in sequence but differ in their special structure. DNA can have different forms depending on the particular way it folds in space. These different shapes are what is called topoisomers.

Woah, thanks for the detailed answer, I appreciate your help.

As a descriptive term, we can take covalently closed, circular DNA (cccDNA) at face value: any DNA that is circular, with the ends joined by covalent bonds, can be described as cccDNA. Thus, plasmids are a type of cccDNA, but not all cccDNA are plasmids. Textbooks and lecturers describe plasmids as cccDNA for the purposes of DNA topology. This usage also appears in literature. cccDNA can also refer to circularized viral DNA, which is another type of episome. Note that the linked to papers are merely examples of how the term is used, not authoritative definitions.

What about DNA topoisomers then?

@JewelJohnson I don't follow you completely with that question. cccDNA can have topoisomers, but so can topologically constrained linear DNA.

I'm sorry, I thought DNA topoisomers are a different class. My bad.


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What happens if the Nematode epidermis becomes damaged?
This animal has a hydrostatic skeleton which lets it move. If we damage the epidermis and fluids come out, can the nematode still move ?

Nematodes have external skeleton in the form of a cuticle. Their muscles are attached to this external skeleton and when a muscle cell contracts it moves a segment of the cuticle relatively to the other segments, which in turn allows the pushing of the environment and thus, motility. This is very similar to how we, humans, move.
Damaging the cuticle in nematodes results in motility impairment. For example, some C. elegans strains have a mutation that results in a non-normal cuticle formation which makes the animals roll instead of moving peristaltically (like a snake).
In addition, some muscles are not skeletal muscles, or body wall muscles in the case of nematodes. These muscles affect movement of an organ like the pharynx in nematodes or the heart in humans.
for further reading regarding the body wall muscles and cuticle interaction you can see wormatlas.org
References:

Labouesse, M. 2006. Epithelial junctions and attachments. WormBook, ed. The C. elegans Research Community, WormBook, doi/10.1895/wormbook.1.56.1

Please add some references to your answer.

What type of reference is expected in this site?

peer-reviewed, possibly from a well known journal or site, cited by many others...in short, authentic.


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Tissue identification in vascular bundle sections
I always have trouble differentiating the tissues in a vascular bundle. I specially cannot properly identify the vascular cambium and phloem. I know xylem vessel elements are large cells with thicker cell walls, that makes them clearly different from other cells in the vascular bundle. However, the difference between vascular cambium cells and phloem cells is unclear. I would like to know how I can identify these tissues accurately. A photomicrograph with marked borders would be appreciated along with explanation of cell appearance in these tissues. Thank you a lot.

Here is a single Helianthus (sunflower) vascular bundle, complements "The" Ohio State University. The xylem in a vascular bundle is generally the easiest to discern. The phloem tissues is always exterior to the xylem and the cells are generally more uniform and smaller than most of the xylem. Picking out the phloem is also more complicated by other cell types exterior to the xylem such as the "fibers" shown here. The phloem will always be interior to the sclerenchyma or collenchyma "fibers" when they are present. That is, the phloem is always adjoining, and exterior to, the cambium.
The most difficult to precisly locate is the vascular cambium since it is very thin. Notice in the diagram below, the relatively continuous line that is being pointed to by the dashed line from the label. As you go inward toward xylem and outward toward phloem, the smoothness of trying to trace a line parallel to the vascular cambium becomes much more "bumpy" as the cells are already beginning to differentiate.

To find many more images on the web, search "vascular bundle labeled photo". You should investigate further, appearance of these bundles varies between dicots, monocots, roots, shoots and species.


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Adding the Propionyl-CoA Pathway to E.coli
So I'm trying to simulate the production of 3-Hydroxypropionic Acid with E.coli via the Propionyl-CoA Pathway.
However I'm not really sure how the production in the pathway goes.
I got the following picture:

If I understand it correctly the pathway goes:
Acetyl-Coa--> Propionate --> Propionyl-CoA --> .... --> 3-HP
When adding these reactions in Cobra are the stoichiometric coefficients always just 1?

Source of the figure:
Luo H, Zhou D, Liu X, Nie Z, Quiroga- Sánchez DL, Chang Y (2016) Production of 3- Hydroxypropionic Acid via the Propionyl-CoA Pathway Using Recombinant Escherichia coli Strains. PLoS ONE 11(5): e0156286. doi:10.1371/journal. pone.0156286

If I understand it correctly the pathway goes: Acetyl-CoA --> Propionate --> Proprionyl-CoA --> ... --> 3-HP

Not exactly. The first reaction is:
$propionate + acetyl\textrm-CoA \rightarrow propionyl\textrm-CoA + acetate$
The CoA group is transferred from acetate to propionate. The following reactions are an oxidation to acryloyl-CoA and a subsequent hydration to 3-HP-CoA. Lastly the CoA group is transferred back to acetate.
Propionate is a 3 carbon molecule and so is 3-HP. So stoechiometric coefficients of 1 seem logical.


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Human and chimp genome sequencing
Can someone comment on this article which claims that biologists have been misleading the masses when they compare the genome of humans and chimps
https://yaqeeninstitute.org/daniel-haqiqatjou/can-islam-object-to-evolution/

Welcome to Biology.SE. The article is very long. I doubt anyone will be willing to read it through and comment on every single claim. Can you please try to narrow your question down to a specific claim?

As a side note, you might want to have a look at Understanding Evolution by UC Berkeley for a short easy introduction to evolutionary biology.

Please note the biologists are not so much misleading any public as most biologists don't talk much to the public anyway. Science communicator can potentially mislead the big public. Most of science communicator are journalists and not researchers.

The article makes more than a dozen different claims, so ask them individually. or create a short list of the ones you are actually concerned with. Although the overarching message of the article is "different studies using different methods come up with slightly different answers therefore they are all completely wrong"

One extreme example can help you understand the article. Human have 23 chromosomes while chimps have 24, however it is painfully easy to demonstrate human Chromosome #2 is Chimp chromosomes 2Q and 2P stuck together at the ends. This could happen in a single mutation in a single germ cell. So, is this one difference (one mutation) or ~200 million differences (the number of base pairs on both). Most scientists would argue it counts as one difference(one fusion) while the article would have you believe it must count as ~200million differences.

Well. Science is a funny thing compared to say the Koren, the Bible or any other religious text. As Scientist learn more, the narrative in Science will change. For instance, in the 1800, there were ideas that there was free following water on Mar... channels and ditches and such. In the 1960s, Mars was considered bone dry. No water ever. A desolate waste land. In the 1990s, Mar considered to have water, but only in the distant past 3 billion years ago. No water now. Then in the 2010s it is now considered to have subsurface water ice, that may occasionally turn into free flowing water under rare conditions. And worst yet, until recently... perhaps all those features of recent running water way have been caused by out gassing of CO2... Conflict over basic interpretation.
Now in that time, religion text, while silence on the matter of Mars, has not changed much if at all. Religious text has stayed the same.
So has Science been misleading the masses on Mars? Does Mars have water? Yes or No? Science keeps flip flopping.
In some ways yes, Science has been misleading the public. It has not been on target with a singular message, unlike say a religious text book, which has been delivering the same unchanging message for a thousand years or so.
So if you are looking for a consist message, well Science way not the thing for you. Science tends to tell different stories as scientist learn more, learn new techniques, re-evaluate ideas and generally fight with among themselves. The holy men Science like to review, rewrite their holy text rather often and fight. And the common man may find that dissatisfying and perhaps worrisome. If holy men keep changing the holy text, how will the common people worship? Is the Science real? Given it changes when the holy text of many world religions have not changed in centuries or even millennia.
So back to article... the percentage similarity of human to chimp genome changes as techniques improve. If you look at the actual age of the citations used in said article.. we run from papers in the 1970s, before genome sequencing was available, and the ideas of one gene-one protein was how Science thought DNA worked, and karyotyping and chromosome banding was about the only means to make large scale chromosome comparison... to papers in the  2014. Where we know DNA does more than just encodes proteins, and non DNA coding are not junk but can encode RNA with biochemical activity (gene regulation, transcription factor regulation etc). And whole human genomes can be sequenced for less than USD 1,400 when it originally cost USD 2.7 billion.
This is nearly 50 years of change and development. Going from the time before the internet and calculators were serious business machines worth thousands of dollars to a time you can have a a 1980s super computer as a wrist watch.
So yes... the message changes. Science progresses, techniques that could only be imagined by previous generations of scientist have become routine. We have learned more.. RNA isn't just a middle man between DNA and protein. One gene can give rise to many proteins.
Have the masses been mislead?
Scientist are telling the Masses information that is to the best of their knowledge. And if the current generation of scientist (2014 scientist) say the past generation (1970s scientist) had it wrong or not quite right.... If scientist right now disagree on the best matrix... is that misleading?
A science book is not as safe as a religious text. And one of the worst offenders is biology. A biology text book book from the 1980s looks very different from 2010s, even if they are from the same series. Is that misleading or is that scientific advancement?
PS: Common genes and sequence identity is not the same. There is a bit of confusion in the article. A cat and a human may share many many genes. But those shared genes may have sequence difference between them. So you can say humans and cat share 90% (made up example) of their gene (ie both cat and human have the PTEN gene) but have only 70% (made up example) sequence identity (ie there are several DNA difference between the human PTEN gene and the cat PTEN gene). It is easy to confuse the two.
Also are you only only considering gene coding DNA? Or are you also considering the non coding DNA (which until cheap genome sequencing in the 2010s was extremely difficult to capture and sequence)

Most of your answer has little to do with biology but rather philosophy of biology. And IMO, you miss the point of the paper. The paper says what many fail to understand is that what is found in scientific literature and what is reported to the lay public are sometimes worlds apart. It for example discusses the fact that such percentage of similarity are computed only on what we managed to align. There entire sequence that won't align at all. It also does not make consideration of CNV.

The author also argues that the feeling that is transmitted by this high precentage is misleading if it not presented to the public the percentage of similarity between human and cat for example which is at 90%.

I would like to point out that scientific literature being use in that article range from the 1970s to the 2014s. So obviously over the nearly 50 years of time the results of papers will be different. The techniques used to make the human chimp genome comparison changed from karyotyping/chromosome banding pattern, to cDNA comparison, to whole genome comparison. The answers will be different.

What is reported to the public will change... and if reporters look up old text books of just google a number... they will get different numbers.

I can comment.
From your article:

Is 99% human-chimp genome similarity less impressive in light of the fact that domestic cats share 90% of their genes with humans and yeast share over 30% of their genes with us, etc.? What should we make of these various quantitative comparisons? In reality, it is difficult to make sense of these percentages without a uniform metric to reference. Unfortunately, the biological sciences do not provide one.

The public has not been misled. The fact is that chimps and humans share 99% of their genes. The rest is interpretation. The rest is extrapolation. The rest is philosophy.
As a biologist, it's absolutely no surprise to me that we share a lot of our genome with cats, earthworms and even yeast. We do presumably because successful life on the planet Earth takes particular biological processes which are shared. We live in a Nitrogen-Oxygen atmosphere; we have carbon-based energy sources; we need to have similar enzymes to use oxygen and carbon, etc.
Beyond that, scientists have opinions they share. But no one is forcing you to believe a particular interpretation. I happen to believe in what makes the most sense. You can believe in what makes less sense if you prefer. Have there been misrepresentations? Absolutely, but that is often because journalists sharing the information misunderstand it. One of the most misunderstood papers I've seen is Sex Differences in Brain Gray and White Matter in Healthy Young Adults: Correlations with Cognitive Performance by Ger et al. It has been repeatedly and widely inaccurately represented in the lay press, partly (or perhaps wholly) because it is not a particularly well-written paper though the science in it is sound.
Don't assign blame for any belief to science just because you want it to say something different.


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What kind of creature is this?

I saw this on Facebook today and have tried researching it myself, but I have had no luck.

This actually looks like a Gaudy Sphinx caterpillar (Eumorpha labruscae). It only mimics the appearance of a snake!

You can find more information about this species here.

Range: Argentina north through Central America, Mexico, and the West Indies to Florida, Mississippi, South Texas, and Arizona. Strays to Missouri, southern Michigan, Pennsylvania, Maine, and southern Saskatchewan.

You can find more pictures here or videos here and here. Also the below gif (see whole video here) demonstrates the ability of this caterpillar to vibrate its tail end to -- as far as I can tell -- imitate a snake's rattle:

Below is a picture of an adult moth from UC Berkeley:

Wow that is freaking awesomeness!! That first pic is truly amazing. +1

@AliceD Right?!  Google "snake mimic caterpillar" to see some other really cool species!

Here is one of the cooler examples of snake mimicry! It even has a wiggling tail!!

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


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How does the color of henna fade?
Henna contain lawsone pigment that attaches to the proteins of the skin,hair,etc.But after a few weeks the color fades?
How does the color fade?
Is the pigment volatile or it is degraded by the body?

It doesn't become volatile nor is it degraded. Neither is really possible because the dye (lawsone) forms very strong bonds with protein molecules and also penetrates the skin quite well [source: here].
Henna fades with time via exfoliation. In other words, it fades progressively as additional layers of skin die and fall (or "slough") off.

Is the same for hair and nails

almost certainly....


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Phronima sedentaria anatomy
I would like to know how many appendages the arthropod Phronima sedentaria has, and how they are arranged. It's not hard to find picture references, but Phronima's transparency makes it difficult to tell from live photos, while what drawn diagrams and text descriptions I've been able to find diverge wildly.
From what I've been able to determine, it has a bulbous head which may or may not have antennae, near to which are two to four pairs of limbs. There is a small gap, then a much longer pair of limbs ending in claws, followed potentially by a second longer pair, and then two to four shorter pairs of limbs. The tail is lined by three pairs of swimmerets, possibly tipped with paddles or bristles.
The best possible answer for this would be a picture like this one, with the assurance that it does indeed represent Phronima sedentaria accurately, though I would be happy with a confirmation of appendage count. Additionally, while I would prefer information about Phronima sedentaria specifically, I can make do with such information about any member of the genus so long as it is specific.

After finding some higher-quality images/videos with some views of the creature from the front, I can say that the image I linked is mostly accurate, if lacking in detail. There does appear to be a set of antennae, though they are significantly shorter than the legs, the front two pairs of legs are shorter than the others and end in small claws, and are positioned more 'underneath' than 'to the side of' the body relative to the other legs. The reason for the confusion seems to have been a combination of the different position of the front four legs, some pictures of other Phronima species misnamed as sedentaria, and that the antennae appear to be able to fold in close to the head, making them nearly invisible.


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Why Poisson Process for neural firing?
I am new to the world of neuroscience and I would like to understand how come every paper in neuroscience that I read uses a Poisson process to model neural firing. Do I just have a biased sample of the papers I chose to read, or is it a biological fact that neural firing must follow a Poisson process? Why can't it follow, say, binomial, since it either spikes or it doesn't in a given time period. Also, where can I read more about how such a biological phenomena was discovered?
A small correction: I do appreciate the explanation on the difference between the two distributions but I am a statistician who is trying to understand my neuroscience colleagues and communication is key in statistics. I am just trying to comprehend why everyone in the field is using Poisson as opposed to using Binomial even when the bin size you decided on is sufficiently small. In other words, why would you not use Binomial, the bin size is so small that your data is only 0's and 1's (i.e. the spike happened or did not happen within this bin). Is it because Poisson counts discrete occurrences in a continuous domain? What discipline-specific papers would you recommend to read that justify/discuss/explain the continuous domain on neural spiking?

At the limit of small bin size, there isn't much difference. For large bin size, Poisson works better since you don't need to know the max # of events. Also there are plenty of non-Poisson point process models out there in neuroscience. I tend to use autoregressive point process models.

You can read about the differences between a binomial and poisson distribution at this other question on Math.SE.
First, since spikes are discrete events, it makes most sense to use a probability distribution that is discrete. A Poisson process is a process where an event occurs randomly with no "memory" for how long it has been since the last event. A Poisson distribution is the number of events if you integrate draws above some threshold from an infinitesimally small uniform distribution. Therefore, the Poisson distribution is the distribution you choose if occurrences of an event are only dictated by an underlying rate parameter - this turns out to be a reasonable, if ultimately false, assumption for neurons.
There is definitely no biological fact that neurons must follow a Poisson distribution - in fact, no neuron can be truly Poisson because, if nothing else, the refractory period makes it impossible. Rather, Poisson behavior is sort of the simplest behavior you would expect from neurons in a system where they are firing occasionally due to random noise - sort of a "null hypothesis." For many modeling approaches, this is close enough, and it allows the modeler to avoid making more nuanced assumptions. It turns out to be a decent assumption when you look at individual cells, but if you look at populations the activity deviates a lot from Poisson.
Note that the Poisson distribution is often only valid for spontaneous data; it is possible to use a nonstationary Poisson distribution to model responses to some external stimulus, but the results are likely to deviate more from experimentally derived data.

Thank you for your response. I am a statistician and discreteness and independence are also the features of Binomial distribution, so even in those cases when bin size is small enough that you data is 1's and 0's why would you not use Binomial? Is it because Poisson counts discrete occurrences in a continuous domain?

and wouldn't it make more sense to use Binomial if there is a refractory period between spikes? Sorry, I am just really lost on the whole process of neural spiking even after 1 MOOC course and a ton of Youtube videos (I made sure those are from reputable sources at least)

@Jen A poisson is essentially equivalent to integrating a binomial with infinitely brief windows (and a correspondingly infinitely small probability). Neither can really account for a refractory period. For spike rates in most typical neurons, the rates are low enough that you rarely generate spikes within a refractory period, but an alternative is to generate interspike intervals (ISI) from an exponential distribution (this is exactly the same as drawing Poisson counts), and discard very short intervals (this part deviates from Poisson slightly).

@Jen Poisson and binomial become nearly identical for small enough bins but the larger your bins the more they deviate, and the underlying function of the binomial just doesn't describe spiking processes very well: Poisson distribution works well when you know the underlying rate of events, Binomial works when you know the probability in a given interval. The former is a better description of the way people usually think about spiking neurons.

just a silly clarification: "when you know the probability in a given interval" -i.e., the probability of a spike (within a small bin for example) occurring/not occurring?

@Jen Yes. If you are talking about a single bin then you have the special case of a Bernoulli distribution. If you have a sequence of bins then the two parameters for binomial are a) the probability within each bin, and b) the number of bins. The binomial distribution will describe how many of those bins are occupied (i.e., by a spike).

When trying to look at the firing of a neuron as a way to encode information, a useful trick is to model each spike as a Dirac delta function. What this means is any time point is a "spike" or "no spike." It's binary.
http://www.cns.nyu.edu/~david/handouts/poisson.pdf
It doesn't tell you anything about the internal dynamics of the neuron, that is, its electrotonic properties, but at a "macro-level" looking at spikes as delta function is a good way to look at a rate code.
A Poisson distribution gives you the probability of a given number of spikes in a span of time if you know the average rate and are independent.  Because of this, you can model spike trains of "dummy" cells.
Neurons are very irregular. This has to do a lot with stochastic forces that make the interspike intervals (the time between two spikes) highly unpredictable. For convenience, a random process is used to model them. At the higher "systems" level, patterns emerge and this is how your brain makes sense of it all.
Thus, you can model on three scales:
Individual Cell, dynamical system (e.g. the Hodgkin-Huxley model)
Individual Cell, rate code (e.g. a Poisson distribution model)
Systems Neuroscience
https://www.tu-chemnitz.de/informatik/KI/scripts/ws0910/Neuron_Poisson.pdf


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How, when, and where did the very first life in the universe exist/formed
Do we know about the very first life, how it is formed? or from where it originated in the universe?
How life is fromed in our planet earth??
Life require conditions for survival or it can create favorable conditions

To answer all your question: no.

We've never found life except on earth,  so as far as we know, it originated here. However, there are numerous theories about how.


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What if our whole body is made up of cancer cells?
Today I learnt in my biology class that cancer cells are immortal.  That left me wondering what if our whole body is made up of cancer cells?  Will that make us immortal? Is it possible or why is it not possible?

Many cancers are deadly for a reason you know. Vote to close being pob

I'm voting to close this question as off-topic because it lacks research.

This question shouldn't be closed; it's a good question and has an objective answer which @JayCkat gives. There is a difference between immortality as seen in stem cells and immortality as seen in cancer cells. There is tons of research on this kind of thing as well; you can discuss stem cell transplantation vs teratoma formation assays.

@Artem Thank you XD I really wish they don't remove my question.

No.
One aspect of cancer cells is that they no longer follow their programming, ie they stop doing all the work that a normal cell in that particular part of your body would do.
The next aspect is that cancer cells keep growing even when they are told to stop, even when there is no more space to grow.
Cancer cells also tend to destroy surrounding extracellular matrix in the quest for more nutrient. SO stuff like bone get deformed or just broken down leaving holes.
So if your entire body were made of cancer cells... well it would fall apart as cell stop doing their assigned job in the body, start growing without care and break down existing structure for better access to more nutrients.
What you want are immortal cells that still do their job.. stem cells.


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What is the Shine–Dalgarno sequence?
I am trying to understand the Shine–Dalgarno sequence. I currently know it is related to ribosomal binding sites, it is only found in prokaryote cells and it is in front of the initial codon. Also, how do you recognize a Shine-Dalgarno sequence?

According to this Wikipedia article:

"The Shine-Dalgarno (SD) sequence is a ribosomal binding site in
  bacterial and archaeal messenger RNA, generally located around 8 bases
  upstream of the start codon AUG.1 The RNA sequence helps recruit the
  ribosome to the messenger RNA (mRNA) to initiate protein synthesis by
  aligning the ribosome with the start codon.
The Shine-Dalgarno sequence exists both in bacteria and archaea. It is
  also present in some chloroplast and mitochondrial transcripts. The
  six-base consensus sequence is AGGAGG; in Escherichia coli, for
  example, the sequence is AGGAGGU..."

I hope this gives the insight that you needed.


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Calvin cycle:synthesis of glucose
For synthesis of one molecule of glucose,six turns of calvin cycle are required.
One molecule of carbon dioxide combines with ribulose bisphosphate (RuBP) to form a stable product of two molecules of phosphoglycerate (PGA). This is called carboxylation. Then 2 molecules of PGA undergoes reduction to form 2 molecules of phosphoglyceraldehyde (PGAL).
My question is whether there 2 molecules of PGAL goes in the regeneration of RuBP or in the synthesis of glucose.

Your question is not clear. "is the reaction stopped at PGAL ... till 12 moleules of it are not produced" --- what do you mean? Which reaction, there are several reactions in the cycle?  Where does your number 12 molecules of PGAL come from?  What do you mean by "are not produced"? Please elaborate and explain.

I have edited the question.

@AliceD@canadianer@James@another'Homo sapien'@Chris. I have edited the question.Please can u specify which part u all have not understood.And a good answer is also given by Roland which answered my question.So I don't get it what u all have not understood

Moderators, I also think this question was closed too quickly. Initially it was unclear, but I think it is now perfectly valid. I'm voting to reopen.

The quick answer is "both", but the stoichiometry is not 1-to-1. The stoichiometry of the calvin cycle doesn't add up when thinking about a single molecules making one "turn" of the cycle. There is only one carbon (CO2) added, but three carbons (in PGAL) leave, which obviously cannot work.
What's happening is that multiple molecules are processed at the same time. The cycle is of course just a set of enzymes that continually catalyze their reactions, so there are always lots of molecules available for enzymes act on, and the cycle doesn't "get stuck" just because things don't add up in a single turn. The "regenerating" steps between PGAL and RuBP produce 3 molecules of RuBP from 5 molecules of PGAL (15 carbons total). Carboxylating these 3 RuBP molecules adds 3 carbons, so that one PGAL molecule can leave the cycle.
The reason for this odd stoichiometry is that the cycle needs to turn 3-carbon sugars (PGAL) into 5-carbon sugars (RuBP), which is rather complicated. Several enzymes work together in a complicated series of reactions to achieve this. A good resource for learning about the details is the MetaCyc database, where you can explore all the molecular details of the pathway.


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How many cyclic and non-cyclic photo-phosphorylation is required to produce one molecule of glucose?
In non-cyclic photophosphorylation 1 ATP and 2 $NADPH_2$ molecules are produced.
In cyclic photophosphorylation 2 ATP molecules are produced.
For production of one molecule of Glucose 18 ATP and 12 $NADPH_2$ molecules are reqiured.
According to my understanding,6 turns of cyclic and non-cyclic photophosphorylation is required to produce one molecule of glucose.
Because 6 turns of non cyclic photophosphorylation will produce 12  $NADPH_2$ and 6 ATP molecules.
And cyclic photophosphorylation will produce 12 ATP molecules.
Total=12 $NADPH_2$ and 18 ATP.
I think Iam missing something , Please answer me if I am correct or not.

You seem to have mixed up cyclic and noncyclic, as you're first saying that noncyclic produces NADPH (correct) but then that cyclic produces NADPH (wrong). But the overall stoichiometry seems right, assuming the numbers you give at the top.  What is it exactly that you have trouble with?

Yeah!!A mistake while writing but now I have edited.I just want to know if I have said it correct

Well, your conclusion is just plain addition, so not much to say about that. The ATP:NADPH ratio of photorespiration varies though -- since it is a chemoosmotic process, the stoichiometry is not fixed, and it might differ between species, conditions etc. Where did you get your numbers from?

The cyclic and non cyclic part was given in the textbook.but the 6 turns part was a conclusion from myself. So that means there can't be a fixed ratio.

In non-cyclic photophosphorylation the stoichiometry of ATP:NADPH is predicted as 3:2, i.e, for every two NADPH formed, a total of three ATP are produced.
Source: Cyclic, pseudocyclic and noncyclic photophosphorylation: New links in
the chain. John F. Allen. TRENDS in Plant Science Vol.8 No.1 January 2003.
Cyclic photophosporylation, does not occur under normal conditions in higher plants. It is believed to occur only when either light intensity is low (lower frequency so as only PS1 can function) or when carbon fixation is not at par with light irradiance (i.e, too much light).
And hence it is not advisable to come to this generalization "Six Turns of non cyclic photophosphorylation will produce 12 NADPH2 and six ATP molecule"

In non-cyclic photophosphorylation the stoichiometry of ATP:NADPH is predicted as 3:2, i.e, for every two NADPH formed, a total of three ATP are produced.I don't understand what u said . Can u elaborate a little more or provide a link.

Kindly read this: http://jfallen.org/~john/webstar/john/pdf/32775.pdf

I will add the link to the answer

The numbering of 1ATP from noncyclic photophosphorylation and 2ATP from cyclic is little too much to be right. However, the formation of 2NADPH + H+ out of noncyclic photophosphorylation is correct.
Because according to the Chemiosmotic Hypothesis (Mitchell), the number of protons accumulating in the lumen of the granal thylakoid during noncyclic transport of 4e- from P680 towards Ctyb6f complex is 12 (8H+ transferring from stroma by Q-cycle + 4H+ from photolysis of 2H2O at Oxygen-evolving Complex). And at every 5th e- transport, the cyclic electron transport occurs and helps in transporting 2H+(protons) from stroma region towards the lumen of granum. So, a total of 14 H+ accumulates per an O2 release by photolysis of water. These 14H+ find its way to stroma region through CF particle and 3ATP are synthesized.
Therefore, H+/ATP = 4.67, e-/NADPH + H+ = 2, Total ATP release in both photphosphorylation during evolution of an oxygen molecule = 3, total NADPH + H+ during evolution of an oxygen molecule at PS-II = 2
Therefore, ATP/NADPH formation from cyclic photophosrylation at P680 = 7/9 (instead of the expected 3/2) and
ATP alone = 1.29 (instead of 3).

Yes.

One cycle produces 1 ATP and 2 NADPH2.

Cyclic photophosphorylation produces 2ATP in each cycle.

The C3 cycle uses 3ATP and 2NADPH2 in each cycle.

So if if C3 cycle runs one time then both non-cyclic photophosphorylation and cyclic photophosphorylation run 1 time.
For synthesis of one glucose molecule in the C3 cycle, non cyclic photophosphorylation and cyclic photophosphorylation each runs 6 times.

Welcome to Biology.SE! Your answer is much more likely to receive a favorable response if you [edit] it to be clearer (e.g. complete sentences) and include supporting references (primary literature is best). Without that support, your answer is indistinguishable from opinion. In addition, it isn't clear that you've added anything to the other answers. ——— Please take the [tour] and then consult the [help] pages for additional advice on [Answer] effectively on this site and then edit or delete your answer accordingly. Thanks!


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Homework problem:Introductory genetics
The problem is as following:
Primary Ciliary Dyskinesia (PCD) is caused by an autosomal recessive gene. 50% of patients with PCD also have Kartagener Syndrome. Josh has Kartagener Syndrome. What is the chance his brother or sister also have this syndrome?
A  0%
B  6.3%
C  12.5%
D  25%
E  50%

Is this problem actually solvable without knowing the alleles combination of the parents? The answer states C, but perhaps I´m missing something here.

You must be expected to assume that both parents are heterozygous. Then there is a 25% chance each offspring would have PCD and half of those offspring would also have Kartenger (ie 12.5%).

Why should I expect something like that, is that a rule?

@Jarry if any parent is homozygous dominant then all of the offsprings will not express recessive allele.

I didn't say you should expect it…

You can only solve this problem if you know that 100% of people with Kartengers also have PCD.  The question, at least this portion of it, doesn't say that.  You also have to know that the parents are not affected with PCD; the problem doesn't state that either.

Ok, Josh has PCD. That gives three possible genotypes for parents:- ( let the alleles be P and p)
1) Pp x Pp
2) Pp x pp
3) pp x pp
In (1), the probability for next child to be pp is 25% and to have the disease is 12.5%.
In (2) and (3), the probability of any parent to be pp is rare as the p allele is quite rare (discussions with swbarnes2 in comments). So the real probability will be only slightly higher than that of case 1 i.e. 12.5%

Reduced fertility doesn't mean zero fertility, and they already have a child.

@swbarnes2 that's the point! They have a child. So the mother even can't have the disease.

@swbarnes2 I edited the question. Please see if it satisfies the question. Also in such genetic question, it is always yes or no. If there is a "maybe" then its probability will be given.

In the scenarios with pp parents, the odds of a parent being infertile are 0%.  Because they already have a child.  So the odds for scenarios 1,2 and 3 are 12.5%, 25%, and 50%.  But without knowing the proportion of the p allele in the population, you have no idea how likely each scenario is, so you can't work out the overall percentage.  The problem is only solvable if you assume that both parents are carriers, not affecteds.  It's a poorly written question, because you can't actually solve it from the info given.  You have to make some assumptions.

@swbarnes2 can we say then that lack of information in question would lead to assumption that only case 1 is considered as pp genotype would be rare in population as compared to Pp?

The problem is not solvable unless you assume that 1 is what's happening.  And when you make that assumption, the answer is present.  Realistically, the p allele would be likely be quite rare, so scenarios 2 and 3 would be extremely rare, so the real percentage counting all three would just be a bit higher than 12.5%.

Since the answer is C it means both parents are heterozygous.
There are two possible alternatives:

Both parents are homozygous to the recessive allele
One is homozygous to the recessive allele and the other is heterozygous

In the first case the answer will be 50%, and in the second case it will be 37.5%
So yes, the question is missing crucial information.

No, in the second case, Pp x pp, 50% of the kids have pp, and 50% of the pp offspring have the syndrome, so 25% total.


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How did the moray eel evolve a pharyngeal jaw?
I am referring to the retractable second set of jaws in the moray eel.
How can one imagine such an evolutionary step to have occurred? Just by chance an eel grew a second internal jaw and it was luckily attached to some muscles which made it useful for swallowing prey?

What have you found so far? I got a number of hits when I search for moray eel jaw evolution on google or google scholar.

Possible duplicate of Why do some bad traits evolve, and good ones don't?

well considering jaws originally evolved from the first set of gill arches and eels still have gill arches, so it's not that much of a stretch. Most fish gill arches already have muscle attachments that aid in swallowing and breathing. Many bony fish already have  pharyngeal teeth to aid in swallowing (they teeth prevent the prey from being pushed back out of the mouth by water pressure. Moray eels have a much more direct mechanism becasue they live in burrows and can't fold the gill arches out to generate suction and pull food down the mouth as other fish do. So instead the muscles pull the arches backwards and the shape pulls them together pulling food down the gullet.
it has actually happened independently in cichlids and something similar happened in Snakes and Mosasaurs


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Strain vs. Species
What is the convention between setting that this organism is a strain of a specific species and what are the considerations in saying that this organism is just a strain and not a separate species entirely?

Generally strain is equivalent to sub-species or lower. but the exact usage varies depending on the type of organism.  in plants or unicellular organisms it indicated all the descendants of a single specific organism, usually becasue it possesses some unique feature. Basically it is just a clade. In animals it tends to be reserved for a group of organisms that have been interbred to the point of genetic uniformity.
Almost always a strain can still interbreed with the parent population it just has identifiable feature that unites it.
Consider an example, let's say I find or manufacture a mutant wheat plant that produces much larger seeds, and all of its offspring retain those giant seeds. But I can still crossbreed it with normal wheat. That would be an example of a strain.


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DNA topology Linking number vs twist?
Background

Linking number: the linking number represents the number of times that
  each curve winds around the other.
Twist, called "twist", refers to the number of Watson-Crick twists in the
  chromosome when it is not constrained to lie in a plane

 I read these explanations on Wikipedia and I understand the concept of this (supercoils have to form to compensate the "tension" etc..) however I'm not able to discriminate between these terms while looking at a picture.

 (source)

Based on the formula I can easily calculate the twists in the right image. But I'm searching for a way to see/count the twists.

Question
What is the difference between the linking number and the twists (not from a formula perspective)?

This article (DNA Topology: Fundamentals by Mirkin SM) probably defines and describes linking number better than I ever could:

The fundamental topological parameter of a covalently closed circular DNA is called the linking number (Lk). Assume that one DNA strand is the edge of an imaginary surface and count the number of times that the other DNA strand crosses this surface (Figure 3). The algebraic sum of all intersections (which accounts for a sign of every intersection) is the Lk. Two important features of the Lk are evident from Figure 3. First, Lk is always an integer. Second, Lk cannot be changed by any deformation of the DNA strands, i.e. it is topologically invariant. The only way to change Lk is to introduce a break in one or both DNA strands, rotate the two DNA strands relative to each other and seal the break... Another characteristic of a circular DNA is called twist, or Tw. Tw is the total number of helical turns in circular DNA under given conditions. Since DNA is a right handed helix with 10.5 base pairs (bp) per turn, Tw is a large positive number for any natural DNA. Take a planar, circular DNA and try to locally separate the two DNA strands, i.e. to decrease the Tw. Since Lk cannot change, a decrease in Tw will be compensated by several positive writhes of the double helix (Figure 4). Writhing (Wr) is the third important characteristic of circular DNA, describing the spatial pass of the double helix axis, i.e. the shape of the DNA molecule as a whole. Wr can be of any sign, and usually its absolute value is much smaller than that of Tw. The above consideration can be formalized by the following equation: Lk = Tw + Wr. Note, that while Lk is an integer, neither Tw nor Wr should be such. Also, neither Tw nor Wr are topological invariants and their values easily change...

Linking number is simply the number of times one strand of DNA passes over the other. Compare this to:

Twist - the number of helical turns
Writhe - the number of superhelical turns

You can, perhaps, think of twist as the passing over of strands within the helix and writhe as the passing over of strands when the entire helix crosses itself. Both twist and writhe involve strands of DNA passing over the other and so both contribute to the linking number. In the absence of writhe, linking number and twist are equal and both describe the same thing: the number of helical turns. However, in the presence of writhe, twist alone is insufficient to describe the topology of DNA because it doesn't account for the passing of the entire helix over itself.
Since twist is the number of helical turns, actually counting it in your image is not necessarily difficult, just time consuming. The image already has the twists numbered, and I've put a red do at every turn of the double helix. I've also circled, in blue, every point where the double helix passes over itself (writhe):

In that image, in may be difficult to visualize (and even understand!) that the strands only cross over each other 36 times (Lk), even though there are 42 helical turns (Tw). While twist and writhe are different modes of strand crossing, it is important to realize that they are interchangeable without breaking the strands. Let's consider a simpler example, where Lk = -1 (Wikipedia: DNA Supercoil):

In the lower image, the strands do not form a helical structure (Tw = 0) but they do both pass over each other together (Wr = -1). Can you imagine that if you were to "unfold" the superhelix (Wr = 0), the two individual strands would still be linked together in a helical structure (Tw = -1)? Neither could I, so I made a video with my shoelaces:
https://www.youtube.com/watch?v=rI3LWIvptf0

I hope that answers your question. Let me know if I misunderstood what you were asking or if anything needs clarification. You may also find my shoelace video on the topology of helicase-mediated DNA unwinding informative.

Would this: "the two individual strands would still be linked together in a helical structure (Tw = -1)? " mean that  even in the relaxed state of DNA (b DNA) there is a twist of -1? @canadianer

@RickBeeloo I'm not sure I understand your question, but in relaxed DNA with one helical turn, twist would be -1 (or 1).

I have one question: DNA is generally underwound in most cells so this means that the linking number is less than in the relaxed state and we have negative supercoils but what causes the lower linking number as in the relaxed state. I see a lot of videos in which people twist a string to lower the linking number but what is the cause of this in the cell? topoisomerases?

@RickBeeloo Yes, topoisomerases. The reasons for maintaining underwound DNA are transcription and replication, which requires ssDNA, and chromatin structure.

For ds DNA
Twist is the number of times a ss DNA turns around another ss DNA in a helix, i.e. simply the number of turns in the ds DNA helix.
Writhe is the number of time a ds DNA wraps around itself.
From the diagram on the right, Writhe= - 6, you'll find 6 times the DNA crosses itself making 7 loops.
[In negative writhe the upper stand moves from right to left around the lower strand (as in canadianer's diagram) and the opposite is positive writhe]
Linking number is a mathematical parameter, i.e. Tw + Wr which defines the topology of DNA. It is a tool to study the change in the topology of DNA.
Reference and Further Reading: Lehninger Principles of Biochemistry


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Violation of the law of energy conservation between photosynthesis and respiration?
For the production of one glucose molecule in the Calvin cycle a plant uses 18 molecules ATP, but when the same glucose molecule is oxidised — first in the cytoplasm and then in the mitochondrion — it can obtain approximately 36-38 molecules ATP. How is the theory of conservation of energy maintained here?

Please add references for the numbers you cite. Wikipedia or Berg et al. (NCBI Bookshelf online) would be suitable.

@sreekara plant uses 18atp to fix light energy which is more than energy released during respiration.

@JM97 — When you open a comment box to a question you see the following: "Use comments to ask for more information or suggest improvements. Avoid answering questions in comments." Please do what it says, otherwise you are breaking the Stack Exchange system. In the present case your answer is contentious (I contend that it is incorrect), but unless it is formulated into an answer I cannot vote it down or comment on it (without compounding your behaviour). If the poster thinks it correct, he cannot accept it as an answer and the question would appear unanswered.

@David, I studied it in our text book and even our teachers taught the same.

@David: But if you put a simple & obvious answer into an actual 'answer', you will get numerous complaints about it not being supported by references &c.  As to 'breaking' the SE system, the only thing that breaks it are the over-officious moderators who insist on short-circuiting good discussions.

@jamesqf — Stack Exchange is not a discussion site. Please read http://biology.stackexchange.com/tour to  understand its philosophy and how it works. If you use this site you should abide by the rules. You have paid no subscription — someone else has covered the expenses of setting it up. If you don't like the rules, go elsewhere or build your own site.

The Fallacies in the argument
The question contains two main fallacies (some would say sleights of hand) in the energetic comparison of glucose synthesis from CO2 in the Calvin cycle and glucose oxidation via glycolysis, the tricarboxylic acid cycle and the electron transport chain:

The descriptions of the two reactions are incomplete — important co-substrates are ignored.
The formulation of the question seems to assume that the energetics of a biochemical reaction series is reflected solely in the
  interconversion of ATP and ADP, rather than the free energy changes
  that occur in all associated reactions.

Detailed explanation
To make a valid comparison of the thermodynamics of glucose oxidation to CO2 with its synthesis form CO2 we have to consider the single reversible reaction:

 (The ‘6H’ may appear rather odd, but it is accounted for in the reduction of cofactors etc.. We cannot include oxygen in the equation because it is not involved chemically in the synthesis of glucose. Therefore for this treatment the electron transport chain is not included, although it is discussed later.)
The reaction from left to right is associated with a certain decrease in Gibbs free energy (ΔG) and that from right to left in a corresponding increase of the same value. In a non-biological context this might involve the evolution and use of heat energy, but in the cell it involves the chemical energy of bonds between atoms. We therefore have to consider all the chemical reactions to which the reaction above is coupled, i.e. which receive or transfer free energy. The additional reactions and the free energy changes they involve can be found in the chapters on glycolysis, the tricarboxylic acid cycle and the Calvin cycle in Berg et al. and are (omitting water, hydrogen ions and inorganic phosphate):

From which it can be seen that the chemical energy input required for synthesis is greater than that obtained, contrary to what is asserted in the question
What about the ATP?
Yes, the cell oxidizes NADH and FADH2 and uses the free energy change to build an electrochemical gradient, the dissipation of which generates ATP (30 molecules per glucose molecule is the current estimate). However that is separate process, with no counterpart in the Calvin Cycle, where the NADPH is generated from photosynthetic reduction and not from ATP. However, if you perform a naive ‘currency conversion’ at the rate of 3ATP per NAD(P)H and 2ATP per FADH2, the balance is: input for synthesis 54 ATP, output from oxidation 38 ATP, i.e. the same general result as above.
Popularizing science is not easy, and those who make the effort can be excused for equating energy with ATP (often as clip-art lightening flashes). However if you wish to study metabolism you need to think scientifically about chemical thermodynamics and free energy. The fact that the hydrolysis of ATP to ADP is accompanied by a decrease in Gibbs free energy is not particularly chemically remarkable in the context of the free energy changes of other chemical conversions in the cell (including NAD(P) oxido-reductions). What is remarkable is that the cell has evolved enzyme that catalyse reactions in which the free energy change from this conversion is not lost as  heat, but can be used to offset the +ve ΔG of a reaction to which it is coupled. Reactions involving NAD(P)H do the same thing, but they are limited to reductions, and the free energy change is inconveniently large.
Why the accepted answer to this question is a red herring
The accepted answer addresses a different question to that posed. It cites a calculation of the photon energy required for converting carbon dioxide to glucose. This is irrelevant to the thermodynamics of the Calvin Cycle, which can occur in the dark. It is relevant only to the efficiency of the use of photon energy in phosphorylating ADP and reducing NADP+ (incidentally in an open system) — a distinct reaction. The thermodynamics of the reactions the question refers to — glucose / carbon dioxide interconversion processes — do not involve the generation of their co-substrates.

Thank you@David, I wasn't considering the NADPH if we consider them and then equate 12 NADPH produces approximately 12×3= 36 ATPs, and adding 18ATPs it gives 54 ATPs ,which are more than that produced in oxidising it that is 36ATPs.

@ David I have another doubt, the mechanism of ATP synthesis in mitochondria and chloroplast are almost the same, but there is a big difference in mitochondria the f1 particle uses 2 H+ ions to synthesis one ATP and whereas in chloroplast it uses 3H+ ions for the same, shall I post it as a separate question?

@sreekara — I'd definitely post that as a separate question. (And a small linguistic point. I realise that 'doubt' is used in Indian English to introduce a question. However in British and US English it is never used that way. 'Doubt' only conveys the idea of disbelief or uncertainty.)

I will post the question tomorrow because I have posted one today.

I have now revised my answer as I thought it important to address the misaprehensions about ATP and "energy" clearly with a table of free energy changes. The gist is the same as before.

Background: Law of conservation of energy states that energy in a  closed  system remains constant.
So the amount of energy in a molecule remains same when its annihilated( also consider law of energy mass equivalence).
Before answering this I would like to point that in the formation of glucose not only energy from ATP is utilised to fix carbon but also light energy is also utilised, which is about :

It takes eight (or perhaps 10 or more) photons to utilize one molecule of CO2. The Gibbs free energy for converting a mole of CO2 to glucose is 114 kcal, whereas eight moles of photons of wavelength 600 nm contains 381 kcal, giving a nominal efficiency of 30%. $^{(1)}$

So, how is the light energy utilised in Calvin cycle?
This light energy is used for formation of NADPH which used in Calvin cycle. Therefore not only ATP but also NADPH are required for generation of energy.
So after considering the above facts one can argue quantitatively that law conservation of energy is not violated in case of oxidation of glucose by mitochondria.

I do not think this answers the question posed, as it relates to the energetics of the generation of ATP and NADPH by light in a thermodynamically open system. The Calvin cycle does not involve light. I believe my own answer is correct in addressing the failure to consider the energetics of anything other than the hydrolysis of ATP.

@David  I never said that Calvin cycle directly utilises light energy. The OP asked broadly about violation of law of energy conservation between photosynthesis and respiration. My answer too says that the NADPH is the entity which the OP has forgotten. Just to have a broad perspective I highlighted the fact that a lot more of light energy is used to form glucose than the energy released on oxidation. How is my answer misleading?

I am sorry, but the poster did not ask broadly about the violation of energy conservation, he argued specifically from figures for ATP involvement in glucose synthesis and oxidation. By answering in terms of the energetics of a different reaction (the light reaction) you were implying that it was relevant to the thermodynamics of the dark reaction. It isn't.

I can't force OP to accept your answer as accepted.

That's not the point. The accepted answer need not be the best answer. It is valid to comment with diagreement, however. I am just copying the practice common of the original SE StackOverflow, which I was familiar with before joining this SE.


text:
Effect of transpiration on plant growth
It is said that only about 1-5% of water used by plants is used in photosynthesis while the rest is transpired. Suppose that a plant grows in an environment where the temperature is not too high but humidity is very high, e.g. in the shadow of a forest. Would the plant grow faster if the humidity was lower? To what extent is the photosynthesis limited by reduced transpiration?

Simple Answer: There is no simple answer, because transpiration is just one of many factors that affect plant growth, and even in controlled experiments, the conclusions deviate according to different species.
Background: First of all, we know that increase in atmospheric humidity leads to less transpiration. A graph between transpiration and humidity, as given by Wikipedia, is as:

There have been some experiments regarding effect of transpiration on growth of plants. In an experiment, Mishra et al and team tried to get answers by reducing transpiration of Lycopersicon esculentum (tomato). They sprayed chemicals like 2-chloroethyl trimethylammonium chloride and 8-hydroxyquinoline 7 times a week and observed a reduction of as much as 80% in stomatal opening, early flowering, but no overall reduction in yield. Also, wilting was delayed for up to 8 days. Apart from this, TNAU concludes that very high and very low relative humidity severely affects grain yield. They reported reduction of 144 kg/ha yield by 1% increase in mean monthly RH.
Though it is quite common knowledge about what role transpiration plays in plant's metabolism, yet I want to include this part from University of Nebraska for the sake of convenience:

Plant growth and development relies on water for transpiration, photosynthesis, and respiration. The unique ability of water to regulate temperatures, dissolve molecules of life, and allow gas exchange, is essential for all life on earth. Transpiration is essential for evaporative cooling, CO2 acquisition, maintaining plant turgor, and mineral nutrient uptake.

Now, when we talk about transpiration along with photosynthesis, then we see formation of a positive feedback loop. When plant starts photosynthesis, it opens up stomata for exchange of CO2 and O2 with atmosphere. This also allows water to evaporate through stomata and causes transpiration, which slowly dries up the cells. To overcome this, the plant takes up more water from roots to maintain turgor pressure inside cells, which in turn leads to more transpiration. Thus, a continuous loop is formed by which photosynthesis enhances transpiration4. Also, when we talk about how photosynthesis is dependent on transpiration, then again we have no simple answer as it depends on many other factors too. For example, in a research, Graham et al concluded that the answer to this question also depends on whether the plant is grown hydroponically on in soil.
From the above examples, we can conclude that high humidity indeed causes reduction in growth. So how did I conclude that there is no simple answer? Well, there are counterexamples also present. In their research, Ford et al and colleagues found an overall increase in plant growth on increasing humidity. They found that when external humidity was high, then there was overall increase in growth in sugar beet, kale and wheat. However, water loss per plant depended on  vapor pressure deficit of air, leaf area and species. Also, water loss per unit leaf area was less for wheat than sugar beet and kale.
Thus, in short, plant growth involves so many factors, along with transpiration, that it is almost impossible to give a simple answer to this question, and it might even take a booklet to just list all the factors involved!
EDIT: As you asked in comments, I searched for more research papers on the relation between cultivation method and transpiration rate, and came up with two conclusions. First, as I am saying already, there has not been reported a straight forward relation between the two, and second, there has not been much research too on this subject. However, I succeeded in finding a couple of papers. One paper has indicated the presence of a direct relation between transpiration rate and the amount of water present in soil, be it irrigation or any other process7. On the other hand, another paper has concluded that in comparison to plants grown hydroponically, plants grown in soil require a larger root surface area to maintain the same transpiration rate and growth rate as that of plants grown hyrdropoincally8. Again, its quite difficult to draw any conclusion from these papers. So, I'll try to add some more papers as I find them.
References:

Mishra D, Pradhan GC. Effect of Transpiration-reducing Chemicals on Growth, Flowering, and Stomatal Opening of Tomato Plants . Plant Physiology. 1972;50(2):271-274
Agrometeorology - Relative Humidity and Plant Growth - TNAU Agritech Portal
Plant Growth Processes: Transpiration, Photosynthesis, and Respiration; David R. Holding, Anne M. Streich
Transpiration - Kimball's Biology Pages
The effect of increased transpiration on photosynthesis of corn part II. Comparisons between hydroponically and soil-grown plants; M.E.D Graham
Effects of Atmospheric Humidity on Plant Growth; Margaret A. Ford,  Gillian N. Thorne
Silvestre, J. and Ferreira, M.I. 2000. EFFECTS OF IRRIGATION ON TRANSPIRATION AND WATER RELATIONS OF VINEYARDS, IN THE TEJO VALLEY (CENTRAL PORTUGAL). Acta Hort. (ISHS) 537:305-312
The effect of root surface area on the water uptake and transpiration rate of maize (Zea mays) plants  (1998)
He, W.S. Nakayama, K. Yu, G.R.

The references you provided are very good. I especially like the reference about the difference between hydroponically and soil-grown plants. I don't have access to the full paper though. Do you think reduction of photosynthesis as reaction to reduced transpiration is less for hydroponically grown plants because of the increased water availability in hydroponics? If you had any further references about interactions between cultivation methods and transpiration that would be very helpful. In other words which cultivation methods are relatively unaffected by high humidity and its consequences.

Actually my former comment is wrong. Increased transpiration was associated by REDUCED photosynthesis in the paper by Graham. Still, does this have to do with higher water availability in hydroponics?

@L-Theanine I've added a couple more papers. Are those satisfactory?

You seriously made an effort to elaborate on all the facets of this question. Thank you!

Mineral nutrients are conveyed up the tree via the xylem by transpiration. The phytohormone cytokinin that releases buds/shoots is synthesized in the root tips and is also conveyed via the transpiration stream. Transpiration is driven by the water potential of the air --> ln(rH); transpiration stops when the relative humidity is 100%.
Even though some species are able to generate root pressure that will force water plus minerals plus cytokinin up the xylem, growth must, nevertheless, be faster at moderate relative humidity than when rH is near 100% (because of the reduced availability of minerals for tissue synthesis in the lateral and apical shoot meristems).
Fertilizing will make minimal or no difference at 100% rH as there is not transport up the plant by transpiration. However, mineral nutrition could be via 'foliar feeding' wherein a fertilizer solution is applied to the leaves could be partially effective in overcoming the mineral nutrition issue of 100% rH. Minerals are then distributed by being actively loaded into/out of the phloem tubes.
Photosynthesis would be unaffected at 100% rH since all tissues would be hydrated. The consumption of water by PhotoSystem II, however, is the only mechanism that could cause some transport of water and minerals through the xylem when rH = 100% aside from root/stem pressure generated by osmosis.
REFERENCES:

Wikipedia - Mineral
Adsorption
Water ascent in plants: do ongoing controversies have a sound basis?
Chunfang Wei, Ernst Steudle and Melvin T. Tyree, trends in plant
science, September 1999, Vol. 4, No.
9
biology-pages: Transport of Water and Minerals in
Plants

Thanks for your answer. But when humidity is high the stomata are more open than when humidity is low, therefore enabling more CO2 to be acquired. Combine this with the fact that plants are mostly composed of carbon from CO2 one might wonder how large the effect of reduced mineral availability really is. Can you provide a scientific reference?

Acquiring more CO2 is pointless if you don't have the light energy to convert it to sugars, so if high humidity is associated with shade (as you explicitly said in your example) that's probably going to be the main block to growth. Add to that that trees that grow in the shade don't want to grow fast; growing fast is useful for the competition for light, and shade-tolerant trees have usually sacrificed that in favor of resilience/durability, so their carbon allocation scheme may be different (in favor of denser wood for example).

IIRC, potassium is required to keep the stomata open, but if they are already in the leaf it is not an issue. The energy currency of 'all' plants is ATP. If no more phosphorous is acquired then the metabolic capacity remains fixed. More chlorophyll cannot be made without more nitrogen and a dab of magnesium. Photosystem 2 requires iron as well. New leaves require lots of nitrogen, potassium, and phosphorous. Without more, the carbon fixing capacity stays fixed. While it may be that the plant can keep growing by simply fixing CO2, the rate of growth is less at 100% rH than at lower humidity.


text:
Which biological process causes the feeling of having "Butterflies in the body"?
If someone is under stress, he or she may feel a strange feeling in the belly; it can be said that he or she feels that butterflies spread through the belly.
For other emotional reactions like being in love, similar, but different feelings can be caused.
What causes this symptoms? Is it because of the muscle tension varies, is it an electric current through the nerves?

"Butterflies" are caused by adrenaline (or nor-epinephrine) released by stress. It is one of the first stress hormones released. Love is a bit different. This question is very broad, and you can easily google part of it and show your research. If you narrow this down, and add your research, I'd be happy to withdraw mt close vote.

Why we can feel the adrenalin or nor-epinephrine release?

Do some research. I wasn't writing for nothing.

These sorts of behaviors are mediated through activation of the sympathetic pathway of the autonomic nervous system.

it would greatly strengthen your answer if you could expand it a bit...FYI


text:
When can helices form coiled-coils?
The other day, my teacher suggested we find out whether a chain of the following amino acid sequence would be able to form a coiled-coil:
N-KIAEVRAQYEDVANKVRLIVE-C

Now, I can see that the chain is not amphiphilic as it does not alternate between polar and non polar amino acids. But when I come across an exercise of this type, how do I determine if it can actually form coiled coils? I can feel this will be a question on the final test.
All help is deeply appreciated.

http://onlinelibrary.wiley.com/doi/10.1002/cbic.200300781/full

Thank you so much!! I still have the same question. In every article I read, it says: A and G positions are typically hydrophobic. Why typically? Can positions that are not A and G be hydrophobic and still make up a coiled coil?

I don't know, but I expect that exceptions to the rule can be tolerated. You should ask your instructor what they are expecting from you.

Okay, thank you anyway for trying to help me. I, too, think that exceptions can be tolerated just by looking at alpha-keratin sequences that have so many exceptions and yet they form coiled coils! But it is hard to translate to simple cases as the one I proposed above. Thanks again!