text:
Why do people perceive blood pressure as the force that moves the blood forwards (see details)?
For example "Veins contain a lot of valves because the blood pressure inside them is low.". This wouldn't make any sense unless if blood pressure was perceived as the force that drives the blood forwards. But in reality blood pressure is the force exerted by the blood on the inner walls of the blood vessels so can someone explain to me why low blood pressure results in increased likelihood of back flow of blood ?

In the vascular system, pressure is what moves blood forwards, at least in an analogous manner to voltage...just like voltage, pressure itself doesn't move things, but a pressure gradient does. You are correct that the pressure applies in all directions, but the resistance of the blood vessels means that the pressure can only be relieved by flowing in one direction: down the pressure gradient.
Although blood pressure is often medically reported at a single site(i.e., 120/80mmHg), this is only the pressure in the larger vessels. The pressure originates from the heart forcing blood out into the major arteries, and the compliance/elasticity of those vessels keeps a sort of "reservoir" just like a capacitor would in an electrical circuit. The pressure drops over time from systolic to diastolic as that reservoir drains out into the body.
Importantly, and most relevant to your question, blood pressure also drops significantly through space, through the arterioles and capillaries, down to near zero in the venous system:

(from https://legacy.owensboro.kctcs.edu/gcaplan/anat2/notes/APIINotes5%20cardiac_equations.htm)
This pressure drop occurs for the same reason that you get a voltage drop over a resistance in an electrical circuit: the rules of Ohm's law for electricity are analogous to the Poiseuille's Law for fluids.
Sidenote: there are some exceptions to the pressure drop over space in the arterial system because of hydrostatic pressure (i.e., the pressure from gravity, for example see this question, though the better answer is definitely not the accepted one or the one with the most up-votes). However, that hydrostatic pressure difference is offset by gravity in the same direction, so you can effectively ignore it. It is also much less significant once you get to the smallest vessels.
I'm not sure where you got the quote in your example:

Veins contain a lot of valves because the blood pressure inside them is low.

..but I would say this statement isn't really false, though it could be stated better and the full causation is missing. Veins use valves because a lot of the pressure in the veins is coming from muscle contractions that squeeze the vessels from the outside, not from a pressure wave caused by forced blood volume from the heart. Venous valves ensure that the flow caused by this external pressure travels in one direction.
The Wikipedia page on hemodynamics may be helpful, though I noticed some poor wording in a couple places; any physiology textbook from a major publisher should be a good reference as well.
For a more "ELI5" answer, if the concepts I discussed so far are foreign, try this: In the arteries, blood is moved because the heart fills the big vessels with lots of blood, and the only place it can go is through the vessels into the capillaries. However, because the capillaries are all so thin and skinny, it takes a lot of pressure to push through them, and all the pressure is lost by the time you get to the veins.
So how do we get blood back to the heart? Well, we could try a vacuum, and have the heart "suck" blood back the way it "pushes" out the other side. However, this would collapse the veins. You can suck through a plastic straw because its rigid, but if you make it less rigid, such as by crushing a section, when you suck it will collapse, and sucking harder won't help the situation. Not good!
Okay so it's better to pump, but all the vessels are so small it would be hard to have them each have their own pump. So instead, the veins go through and around various muscles, and when those muscles move, the veins get smushed. Imagine you have a hose full of water, and you jump in the center...oops! Water goes out both ends! Okay, what if you put your hand over one side? Now it only goes out the end you want. That's essentially what a valve does: only lets the flow go one way when things are squeezed. Then the blood stays in the next compartment and over time works its way back to the heart.

I am sorry to say this now ; I am just a high school student so there are some things which you mentioned that i have never heard of before. Hydrostatic pressure is an example. Also i never understood electricity so i wasnt able to understand your analogy. I was also supposed to write my quote in a better way ; "Veins contain lots of valves to prevent the back flow of blood. Blood is liable to flow back due to the low pressure inside the veins." So here it is. I am not understanding how  low pressure in a vein can cause a back flow of blood

I understood the pressure gradient thing but that itself raised another question. If the pressure in the capillaries is higher than the pressure in the veins and blood flows from areas of high pressure to areas of low pressure, why isnt the pressure difference alone enough to make the blood flow towards the heart ? Sorry for wasting your time.

@Sam19KY Try reading over my edits and see if that clarifies things at all. No problem being a high school student, your question is a good question for even college-level physiology. For your question about why the blood doesn't just flow back to the heart, it actually isn't as much of a problem to get blood back to the heart from things at it's level and above: the vein valves are most important in your legs and lower body, and in your arms if they are at your sides, but of course this all depends on posture so there are valves other places too.

@Sam19KY There is also the issue of flow rate with pressure; if you look in the graph, about 80% of the pressure is lost by the time you get to the venous side. At those pressures, you would need really big veins to move the same amount of blood that moved through the earlier stages (in fact, veins are bigger than related arteries), otherwise you would get pooling of blood in the veins. You can't get around this problem by just pressurizing the veins either, because that would slow the flow through the capillaries, so then you need more arterial pressure - hello hypertension!

@Sam19KY And about hydrostatic pressure... sounds fancy but it's all in the roots of the words: hydro, as in water, and static, as in not moving: the pressure that would be there if everything just held still, ignoring the flow. Hydrostatic pressure is the pressure you would feel at the bottom of a swimming pool or lake just from the weight of water above you. The blood in your legs feels the hydrostatic pressure of all the blood on top of it.

SO here is the thing : I got it but what i want to say is that the whole problem arose because i was overthinking it. I literally lost my reasoning skills as i did that and that was making me look stupid. I really should start dealing with my real problem which is overthinking everything. Thank you a lot for helping me.

@Sam19KY I am glad you are understanding better now, and yes sometimes it is possible to "overthink" something and miss a simpler solution, but please don't be so hard on yourself: you haven't lost any reasoning skills, you don't look stupid, and you don't have a problem. My advice is to try to enjoy learning and the complexities that come with it: the things I read in a textbook and "got" right away aren't the things that stick with me; instead, the problems that didn't make sense, were hard, or needed explanation are the opportunities to really understand something better.


text:
What are internal and external osmotic pressures when referring to a cell?
I've seen the term used but cannot find a clear answer:
What are internal and external osmotic pressures when referring to a cell?

The internal osmotic pressure is the osmotic pressure inside the cell. The external osmotic pressure is the osmotic pressure outside the cell. Osmotic pressure is proportional to the concentration of solutes.
Wikipedia has a perfectly reasonable page about this.

source: Stack Exchange

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text:
Why is the hexose monophosphate shunt called a direct oxidative pathway?
Why is the hexose monophosphate shunt (pentose phosphate pathway) called a direct oxidative pathway( Ref. Biochemistry by Satyanarayana , 4th edition, pg.no: 244) , even though oxygen molecule is not used for oxidation? It uses NADP for its oxidation. So if utilisation of NADP is direct oxidation then what will be indirect oxidation?
How can I differentiate direct and indirect oxidation? Is the use of Electron transport chain considered as secondary oxidation?

You should avoid using abbreviations in titles and always repeat the question and define any abbreviations in the text. HMP is not a standard abbreviation anyway, as most biochemistry texts refer to the pentose phosphate pathway. I have corrected this and the use of direct when you meant indirect in the penultimate sentence. Finally, please provide a reference to the use of the term "direct oxidative pathway". It's not one I have heard of and, though it's not my field, I used to lecture on the subject.

@David please view question again , I have added the reference.

OK. Satyanarayana is not a text I am familiar with, but as my comment to @AnubhavGoel indicates, the term seems to have been current in the 1950s, but has fallen out of use in US texts. I think it would require some effort to track down. All I can suggest (and as I don't know if it is correct I am doing that as a comment rather than in an answer) is that complete oxidation of one glucose molecule is achieved in the pathway, whereas glycolysis produces pyruvate, which requires further metabolism for complete oxidation (PDH and TCA cycle), and this seemed important at the time (if no longer).

I had a try at tracking it down and have now posted an answer.

This answer is based on a 2002 autobiographical account of the work of Bernard L. Horecker entitled The Pentose Phosphate Pathway. Here he refers to “direct oxidative pathway” but does not unambiguously explain this, so I shall summarize my interpretation and then provide evidence in terms of quotations.
Summary of my interpretion of Horecker’s account
When what I shall initially refer to as the hexose monophosphate shunt (HMS) was being elucidated in the late 1930s and the 1940s it was thought that its main purpose was the same as that was envisaged for aerobic glycolysis — to oxidize glucose to provide energy — and was merely an alternative way of doing this. The term ‘direct oxidative pathway’ was used to distinguish it from the glycolytic pathway (then refered to as the Embden–Meyerhof–Parnas pathway), presumably because six cycles of the oxidative phase e could completely oxidize one molecule of glucose 6-phosphate to carbon dioxide, whereas glycolysis only oxidized it to pyruvate. Presumably this was regarded as ‘indirect oxidation’ because complete oxidation required the further metabolism of pyruvate using the tricarboxylic acid cycle.
The term ‘direct oxidative pathway’ fell out of use as it was realized that the main functions of the pathway were to provide pentoses for nucleic acid synthesis and NADPH for synthesis of fatty acids, steroids, and reduction of oxidized glutathione. It was for this reason also that the name most commonly used for the pathway changed to the pentose phosphate pathway, transfering the emphasis to one of the products.
Quotations from Horecker

…Haas arrived from Warburg’s laboratory in 1939. Haas asked me to join
  him in the search for an enzyme that would catalyze the reduction of
  cytochrome c by reduced TPN (now NADP). This reaction was thought to
  be the missing link in the electron transport chain from substrate to
  oxygen and marked the beginning of my interest in what was then
  thought to function as a direct oxidative pathway for the metabolism
  of carbohydrate but is now known as the pentose phosphate pathway…
…These observations gave rise to the hypothesis that the oxidative
  pathway was really a cyclic mechanism for the direct oxidation of
  carbohydrate. With each turn of the cycle one molecule of carbon
  dioxide would be produced, and the pentose phosphates formed would be
  metabolized back to hexose phosphates to start another cycle. Six
  turns of the cycle would result in the complete oxidation of one
  molecule of glucose…
…The function(s) of the new
  pathway, however, turned out to be quite different from the pathway
  for the direct oxidation of carbohydrate that we had expected. It
  provides two mechanisms for the production of ribose 5-phosphate. One
  is the “oxidative branch” of the pathway, which also generates 2 eq of
  TPNH (NADPH). Ribose 5-phosphate can also be formed directly from
  hexose and triose phosphates by the non-oxidative rearrangements
  catalyzed by transketolase and transaldolase. Where large quantities
  of NADPH are required, as in the synthesis of fatty acids or sterols,
  the excess pentose phosphates produced would be recycled back to
  hexose monophosphates.

[My emphasis]
Google Books ngrams of term usage

Addition of $O_2$ or removal of H means oxidation.
In this process H is removed from sugar, added to NADP as well
C is oxidised to $CO_2$.
Hence , it is oxidation reaction.
HMP pathway is used to produce NADPH. The process directly oxidise glucose to $CO_2$ and $H_2O$. It does not require TCA cycle or ETC. Hence is called direct oxidative pathway.
Glycolysis on other hand does not produce any $CO_2$ and $H_2O$.Hence, is indirect, as it needs TCA and ETC for complete oxidation.
Source: Biochemistry
U. Satyanarayan
Edition: 2013
Pg: 244 and 245(written in brackets on Pg 245)

This sounds nonsense. How can the fact that ATP is generated make a pathway indirect? The papers I find in which this term are used date from  the 1950s. Please cite a reference supporting this explanation. If it is true it certainly explains why it is no longer used (e.g. Berg et al.section on pentose phosphate pathway.)

@Anubhav Goel could you please cite a reference  for further information?

@David Removed nonsense. Added relevant source as backup.

@JM97 Maan gya bhai ko?  I use Vasudevan. But, teri hi book me dhoond diya.

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text:
Can bacteria or other microorganisms be killed by applying pressure?
Can you smash a bacteria (or any microorganism) and kill it?
Let's say there is millions of microorganisms on a table. When you put your finger on the table, will or can you kill at least some of them ?

I'm voting to close this question as off-topic because it is just too silly.

Good physics oriented question. According to @JayCkat 's answer; the bacteria require 40 k psi; whereas human beings die after 43.5 to 58 psi So the question could be improved as, "why bacteria would need so huge pressure to die whereas larger organism die at much less pressure".

Yes, you can kill bacteria using pressure. The devised used is called a French press
https://en.wikipedia.org/wiki/French_pressure_cell_press
http://www.glenmills.com/cell-disruption/high-pressure-homogenizer/french-press-gm/
However the pressure use is about 40k psi.... which is a lot higher pressure than anything a human body can generate.
Other methods to kill bacteria include,
heat, gamma radiation, oxidative chemicals, antibiotics, dehydration, salt, oxygen exclusion, freezing.
However bacteria are a very diverse group, so it might take one or more methods in combination to kill all bacteria (and their spores) in a sample.

I'm probably being overly pedantic here, but a human can certainly easily generate 40,000 psi, if merely by standing on something pointy (a surface of up to a few sq mm, depending on your mass). Of course, clearly not as OP is suggesting by pushing your finger on a table without the aid of something like a pin.

Well if you get a 70kg person to stand and balance his complete weight on a pin (2 mm2),... then yes, 40k psi can be achieved by a human body. But if we start factoring aids, a human can do a lot of things.


text:
Can mRNA be used by ribosomes more than once?
Can mRNA be used by ribosomes more than once? I mean can mRNA be translated more than one time? If not what will happen to it after translation?

Have you looked for an answer on your own?

Welcome to SE Biology. Before asking a question we expect you to have done some work yourself. This is a very basic question the answer to which you can find in Wikipedia or in the online editions of textbooks like Berg on NCBI Bookshelf.

There are a few cases in translation that I can think of where an mRNA is translated more than once: the closed loop model of mRNA translation, translation reinitiation, and translation by polysomes.
Closed-loop model
Here's an interesting paper to get you started: ncbi
Essentially, the theory is that mRNA can form a closed loop with the 3' end held to the 5' end by various factors. The ribosome assembles near the start, runs through the mRNA, translating the polypeptide sequence, then dissociates at the STOP codon. Since the "end" of the mRNA is near the "start" of the mRNA, the ribosome can reassemble soon after dissociation.
Translation reinitiation
See this.
The ribosome dissociates incompletely at the STOP codon, the small subunit keeps moving on the mRNA, then the large subunit reattaches at a downstream start site. This happens when the mRNA has multiple ORFs.
Polysomes
(See the wikipedia article on Polysomes for more details)
This basically means that you have a ribosome train moving along an mRNA. The same protein is being translated multiple times, but by different ribosomes. One really cool thing about this is that it's actually been observed by electron microscopy!

(source: bioninja.com.au)
To answer the 2nd part of your question...
wikipedia
mRNA gets degraded in a process called RNA interference (RNAi). Small interfering RNAs (siRNAs) are also transcribed that are incorporated into a ribonucleoprotein complex (RISC) that has an mRNA cleaving activity. The siRNAs are complementary to segments of mRNAs in order to give specificity to RISC.

You should not have answered this question but waited until the poster had shown some evidence of effort himself. As it happens your answer is unduly complicated for a novice and incorrect as regards RNA degradation.

I agree with everything @David said. I'd also add that translation reinitiation is not "reusing" the mRNA, it's simply translating multiple ORFs in succession. The closed loop model is interesting, but the authors say directly in the abstract that it's a part of polysome processing, which is the section you should have focused on. Additionally, as David said, this question should not have been answered. From How do I write a good answer? in the [help], Answer well-asked questions. Not all questions can or should be answered here.

Since you are new here, I strongly suggest you take the [tour] and carefully read through the entire [help] to learn more about the site, including what is on-topic and what is not.

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text:
What is the difference between Crossbreeding, Outbreeding and Outcrossing?
I only found one book which isn't a textbook  named Storey's Illustrated Guide to 96 Horse Breeds of North America By Judith Dutson (not sure if it is good enough to follow) that defined these terms.

Outbreeding/ outcrossing is deliberately crossing one line of horse within a breed to a very distant or unrelated line. The term is also occasionally used as a synonym for crossbreeding.
Crossbreeding is the deliberate crossing of horses of different breeds.

My understanding:
Outbreeding or Outcrossing is the mating between two individuals of a  breed but different varieties/sub-varieties.
Crossbreeding is the mating between two individuals of different breeds (could be intraspecific or interspecific as well).
Are these definitions correct?

The term cross breeding is a bit broader term , whereas outbreeding is more specific.

Answer in keywords
Inbreeding : related individual,same breed
Outbreeding

Cross breeding : between different breeds
Outcrossing : unrelated individual,same breed,no common ancestor

Detailed answer
Inbreeding it is a mating within the same breed between different superior male and superior female. Inbreeding between close relatives can cause inbreeding depression like decreased Vigour , fertility and productivity. It is therefore advisable to mte superior animals of different population of the same breed .
Outbreeding is mating between unrelated animals of same or different breeds.
Outcrossing is mating between unrelated animals of same breed with no common ancestor for at least 4 to 6 generation. Offspring formed from such a cross is called out cross .
Cross breeding is mating between superior animals of different breeds for raising new breeds for improving local breeds.
Please note: Outcrossing and
cross breeding are two types of Outbreeding.
If you have any further doubts please ask .
Hope it helps!!

Welcome. If you can add the definition of Outcrossing, and add appropriate resources (wikipedia would suffice here I guess, given the textbook-question-like-nature of this post) this would make a great answer (imho - I'm not an expert on this topic). For now, no upvote and just a banner.

The link is broken. Also, please do not post a link only answer. Link only should better be posted as comments.

I have updated my answer as suggested.


text:
DNA fingerprinting
About a month ago i performed a DNA fingerprinting lab and now i have a small lab report due in about two weeks.
Questions:
What are some possible errors that can happen during the process of DNA fingerprinting?(non-human errors)
My research:
One of the errors that can happen during the process of making DNA fingerprint is when the microcentrifuge tubes are open air particles can get inside it. The air itself has many things especially bacteria that can possible get into the microcentrifuge and can cause false results.(Can someone confirm this)
Thank you

This should be a comment

The most common causes of failures related to the laboratory process
were contamination and human error. Most human errors could be
corrected, whereas gross contamination in crime samples often resulted
in irreversible consequences. (article)
In DNA fingerprinting work, it is well known that, although fragment
lengths of a sample are uncorrelated, measurement errors of fragment
lengths are correlated. Unless the fragment length is very large, the
measurement errors are directly proportional to fragment lengths. In
the currently practiced matching procedures for forensic
identification, these facts are ignored or inadequately used. Some of
these issues are addressed in this study. (article)

You should provide more information about the method(s) you used. Further you found:

One of the errors that can happen during the process of making DNA
fingerprint is when the microcentrifuge tubes are open air particles
can get inside it.

This is error is not a specific DNA fingerprinting error, based on this I would suggest to read something about "DNA extraction/purification errors" like:

foreign DNA in your sample
Wrong phenol-chloroform ratio (I don't know if you used this --> reason why you should tell something about your methods)
PCR errors
etc..


text:
What determines the efficiency of electron production in photosynthetic bacteria?
Is there a specific gene involved, perhaps? Would one be able to genetically engineer a bacterium to oxidize water and generate electrons quicker? I am speaking about this biological problem in terms of an application to solar cells.
Edit: I am not inquiring to the existence of a gene responsible for photosynthesis, I am inquiring as to why some exoelectrogenic bacteria can produce electrons in electron transport more efficiently than others. Is there a reason for this that can be traced to a certain gene that makes certain exoelectrogens superior to others?

Electrons aren't actually generated during photosynthesis. Instead, they are excited (brought to a higher energy state) when they absorb light. The decay back to the original energy state is coupled to chemical reactions, which is how the cell uses the light to make compounds that would otherwise be unfavorable.

Nothing. Electron transfer (not production) has been found to be about 100% efficient and involving quantum phenomena.

The question is a bit unclear to me. What do you mean by "oxidize water and generate electrons"? does than not take place in case of photosynthesis? (as well reduction take place there. Whenever oxidation take place, reduction take place at same time). And why only 1 gene would contribute to water splitting?

Are you looking for a physics-based answer? The main reason kind of boils down to the fact that the structures of the photosystems affect the physics in such a way that the efficiency is greatly increased. Also, it must be noted that the dynamics are different in plants compared to photosynthetic bacteria. The energy transfer mechanisms are slightly different.

You may or may not consider this an actual answer to your entire question, but it's interesting nonetheless.
A physicist friend of mine did some work recently modelling the quantum dynamics of photosynthetic complexes, and their coupling constants for passing energy throughout the photosystem. His results showed that, (and I believe this is in agreement with the literature), that photosynthetic systems are actually about as efficient as it is possible to be (not only this, but they are the most efficient energetic systems known to man I believe - over something like ~90% efficient).
If you begin altering positions of chromophores and so on, the photosystems exhibit remarkable robustness and you get a more or less logistic decay in efficiency (i.e. removing one or 2 chromophores results in marginal reductions in efficiency, more still in considerably more severe debilitation, until ultimately it's efficiency is markedly lessened, but further manipulation has a plateau in efficacy reduction).
Much of the work that's been done on the quantum biology of photosystems has concerned the FMO Complex (Fenna-Matthews-Olson) which is a simplified model system from photosynthetic algae - you might find more detailed answers to your queries by reading up in this area.
As for discrepancies seen in photosynthetic effectiveness bought about genetically, there are theories that suggest that the organisms are actually protecting themselves. E.g. to avoid over-production of ROS species. I can't offer you much in the way of a well evidenced case for this though, it's just a conversation I had with a post-doc at work recently, who completed his PhD on photosynthetic cyanobacteria.
EDIT Here's one of the papers about optimality in the FMO:
http://aip.scitation.org/doi/pdf/10.1063/1.4930110

May I know who this post-doc is? I have been researching this field for quite some time, and I am pretty interested in the modeling of the system, in particular the FMO complex

The guy who did the FMO complex modelling was a fellow PhD student - Lewis Baker. There is some information at his university page here. I'm sure he wouldn't mind you getting in touch directly. http://www2.warwick.ac.uk/fac/sci/moac/people/students/2013/lewis_baker/msc_year/mp3/

@Joe Healey's answer is great, but I would like to expand on the subject, having done a thorough literature review on the subject before.
Before we do that, I would like to clear up some misunderstandings that you seem to have about the electron transfer.
Just like @stords said, electrons aren't generated during photosynthesis. Where it comes from is from the oxidation of water mediated by the reaction center. The reaction center is part of the photosystem,  which contains all the light-dependent parts of the reactions. The oxidation is performed by the oxygen-evolving complex. This process of oxidation isn't very well understood. However, most photosynthetic bacteria contain similar complexes. Note that green sulfur bacteria doesn't use H2O for oxidation, but instead H2S.
Reaction center
Now, in the light-dependent reactions, we have what's known as a light-harvesting complex, which contains many pigments that absorb light and get excited. The pigments then transfer the energy to the reaction center, which also gets the electrons from the oxidation. So when the energy from the antenna reaches the reaction center, the energy excites the electron to a higher energy level. This higher energy electron is transferred to the electron transport chain, where it reduces various electron acceptors, and while doing so, using the energy released to pump electrons to make a proton gradient. This proton gradient is used to make ATP. Even in bacteria, the process is very similar. The exact details can be read here
Excitation efficiency
Now, answering your question, what really determines the efficiency of the electron transfer is actually the energy transfer occurring in the light-harvesting complex (LHC). Now, different organisms have different mechanisms, but all scientists agree that there is some quantum mechanics behind this. In the following discussion, I will be referring to the dynamics of the FMO complex, the antenna complex found the green sulfur bacteria, and commonly used to study the quantum mechanical interactions of energy transfer.
Now when we have this transfer of energy from one pigment molecule (chlorophyll in plants, bacteriochlorophyll a in green sullfur bacteria), we call it an exciton. This exciton is a quantum mechanical state. Now, in quantum mechanics, there is a concept called superposition. Basically, superposition means that a single quantum mechanical state is composed of multiple states. In the case of the light-harvesting complex, when we say that the exciton is in a superposition, what this means is that the energy can travel in all possible pathways from a pigment to reaction center, and when the best pathway is found, the interactions in the complex causes the state to collapse into the best state. This is how the transfer of energy occurs in less than 1 ns!
This dynamics is very complicated, and very surprising, since this quantum mechanical dynamics is occurring in an open system. Typically, it is very hard to observe quantum mechanical dynamics because of something known as decoherence. This is when a mixed (superposition) state collapses into one state. However, interestingly, the complex uses this decoherence to collapse into the best path for the exciton to reach the reaction center.
This field is very interesting. If you have any questions, please leave a comment. I am a little rusty on this subject, but I am very interested in this subject. If you want to see more examples of quantum mechanics in biology, look up "quantum biology". Quantum biology is a new field studying the intersection of quantum mechanics and biology.
References:

https://en.wikipedia.org/wiki/Light-dependent_reactions
http://rsif.royalsocietypublishing.org/content/11/92/20130901
https://en.wikipedia.org/wiki/Fenna-Matthews-Olson_complex

Vibrational-electronic coupling: Vos et al. is most likely, but some have suggested quantum entanglement which would be great if photosynthetic organisms grew at cryogenic temperatures.

We're looking for long answers that provide some explanation and context. Please don't just give a one-line answer; explain why your answer is right, ideally with citations. Answers that don't include explanations may be removed.


text:
The colour of aquatic plants found deep under oceans
I have read that many aquatic plants found in deep oceans are red in colour, however, I do not understand why. As red is the color which gets the least scattered it should be the only light available to them. Thus reflecting red light would deprive them of any light. Yet they appear to be in red color. Why is this so?

Would there even BE plants in the deep oceans, since there isn't enough light for photosynthesis below 100-200 meters?  NOAA explains why many deep ocean animals are red: http://oceanexplorer.noaa.gov/facts/red-color.html

@Deepakms you say I have read that [...] Can you please link to your source (even if it is not a peer-review paper)?

Is the red Colour the physical appearance or satellite imagery?

@Remi.b I read it in Class 12 NCERT Biology book, chapter on ecology.

Certainly,it was from NCERT. Also it is not just any plant ,but the algae.

You're right that certain wavelengths of light are more capable of penetrating deeper depths of water. However, it turns out, blue light typically travels to deeper depths than all other visible wavelengths of light (and red light does not travel deeply at all).

See my previous SE answer for more details about plant coloration due to this phenomenon.

So that leaves the question of why are these plants red?
Plant life itself cannot exist without the ability to photosynthesize, so actually no plants exist beyond a few hundred meters down. And in fact, many of these plants are still green (e.g., see here and here).
However, some red algae represent an example of a red "plant" (not actually a plant, but quite closely related) that can live fairly deep. According to the University of California-Berkeley:

red algae are red, "because of the presence of the pigment phycoerythrin; this pigment reflects red light and absorbs blue light. Because blue light penetrates water to a greater depth than light of longer wavelengths, these pigments allow red algae to photosynthesize.

Interestingly, this 'reddening' phenomenon is shared by many deep sea organisms, though more often for the sake of protection from predation.
Red light does not reach ocean depths, so deep-sea animals that are red actually appear black and thus are less visible to predators and prey.
See this NOAA page for more:

All objects that are not transparent or translucent either absorb or reflect nearly all of the light that strikes them. When struck by white light (containing all colors), a red fish reflects red light and absorbs all other colors.
The deeper you and the fish go, the less red the fish will appear, because there is less and less red light to reflect off of the fish. At 100 meters, red light does not penetrate and, at this depth, a red fish is difficult, if not impossible to see. Instead, the fish appears blackish because there is no red light to reflect at that depth and the fish absorbs all other wavelengths of color.

Nice answer. Just a correction: algae, specifically Rhodophyta, are not plants.

@theforestecologistTHANKS,for the answer;but I didn't understand why blue is able to penetrate better.Could you please explain it?

@Gerardo right, though it's actually more complicated than that. The taxonomy of red algae is still debated.  See here for a brief explanation. Regardless, I just simplified that discrepency here and just said "plant." I'll edit my answer to add a link to something to address  this,  though.

Thanks. I know it's more complicated than that, I taught phylogenetic systematics for 20 years... We can always create a bigger monophyletic group by adding sister groups but, if we take this trend too far away, Plantae becomes the same of Eukaryota! I like to keep Plantae as synonym of Embryophyta, I particularly don't like Viridiplantae, let alone including the Rodophyta...

BTW, if you want to explain to OP why blue is able to better penetrate water, the reason is water absorbs light at 605, 660 and 760 nm: http://www.dartmouth.edu/~etrnsfer/water.htm

@Gerardo fair. And I tend to side with you. I've updated my answer to at least aknowledge this :p. I'll let these comments serve the purpose  of further acknowledging  this point  so as not to distract  from my answer (which extends beyond plants anyway).  And thanks for the dartmouth link.

To be honest, I should just go down the hall and ask  Max H. Hommersand his pinion about it :p


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How can a powernap boost memeroy and cheerfulness?
Background

A power nap is a short sleep which terminates before the occurrence of
  deep sleep or slow-wave sleep (SWS), intended to quickly revitalize
  the subject. (wiki)

The results of powernapping are described in An ultra short episode of sleep is sufficient to promote declarative memory performance

In the first experiment we assessed free recall of a list of 30 words
  after a 60 min retention interval that was either filled with daytime
  napping or waking activity. Memory performance was significantly
  enhanced after napping as opposed to waking but was not correlated
  with time spent in slow wave sleep or total sleep time within the
  napping condition. The second experiment was designed to clarify the
  role of total sleep time and therefore included an additional third
  group, which was allowed to nap for no longer than 6 min on average.
  In comparing word recall after conditions of no napping (waking),
  short napping, and long napping, we found superior recall for both nap
  conditions in contrast to waking as well as for long naps in contrast
  to short naps. These results demonstrate that even an ultra short
  period of sleep is sufficient to enhance memory processing

Question
I'm wondering how it's possible that such a short napping period can boost cheerfulness and memory (thus in a biological sense).

Perhaps better asked on CogSci?


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How does horse extract the energy to needs from a relatively small digestive system?
Recently I saw Inside nature's gaints episode on horse, and was fascinated about its internal organisation. And my question is that they have a very large lungs to accommodate, but a relatively smaller stomach. But other herbivores like the hippopotamus have a very large digestive system even though they need less energy than horse. How does horse manage this problem? How do they get that much of energy even though it had small digestive system and more over it is an herbivore?

Horses (and rhinoceri) are hindgut fermenters unlike cows which are foregut (stomach) fermenters. I don't know about hippos, but the hindgut fermentation in horses allows it to eat more frequently.

So, the horses eat a lot frequently.

The digestive system of a horse is by no means small:

They have 15 to 21 m (50 to 70 ft) of small intestine, with a capacity of 38 to 45 L.
They have a 1.2 m (4 ft) long caecum that holds 26 to 30 L.
They have 3.0 to 3.7 m (10 to 12 ft) of colon, capacity up to 76 L.
(Figures sourced from Equine Anatomy (Wikipedia))

Certainly horse stomachs are comparatively small as they are hindgut fermenters, but that is not where most energy and nutrients are absorbed. Some food passes from the stomach to the small intestines before it is fully digested, which enables more continuous eating to keep up with their energy and nutrition requirements. Most proteins, carbohydrates, and fats are absorbed in the horse's small intestine. Some nutrients are absorbed in the large intestine as well, see Is there nutrient absorption in the large intestine of hindgut fermenters?.
The hippopotamus is a pseudoruminant, having a 3 chambered stomach (unlike the 4 chambers of a cow). Hippos are therefore considered to be foregut fermenters, and are not comparable to horses. In terms its digestive tract, the hippo is much more similar to a cow than a horse.


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Did cyanobacteria commit evolutionary suicide by producing oxygen?
I heard this story from one of my friends:

Cyanobacteria can convert carbon dioxide into oxygen through
  photosynthesis, so the concentration of oxygen in the atmosphere kept
  going up over a long period after their appearance. Finally, those
  oxygen poisoned cyanobacteria through some mechanism, which
  effectively killed many of them. As a side effect, the oxygen produced
  lead to the evolution of fishes and other fantastic creatures,
  including human beings.

I wonder whether it is true. After some searching, I found that cyanobacteria can perform photosynthesis. However, I can't tell whether oxygen is poisonous to them.

By the term "suicide", one generally refers to the decision of a single individual to self-detrsuct (which you realized I suppose as you put the term in quotation marks). The kind of process you are referring to (where a population pollutes its environment to the point of threatening the persistence of the clade) is called an evolutionary suicide.

@Remi.b Thank you! I've edited the title to make it more scientific.

Oxygen is inherently a toxic substance as it is the second most reactive non-metal. However, most organisms have evolved mechanisms to counter the toxicity caused by oxygen.

@WYSIWYG Since cyanobacteria is such a primitive creature, I guess they don't know how to protect themselves from oxygen. Also, there wasn't much oxygen in the atmosphere before their existence, so I think the resistance to oxygen hasn't been vital by the time they evolved.

@SunQingyao Organisms don't think and implement strategies. They evolve to acquire traits that allow them to survive. Please read more about evolution. Understanding evolution is a good place to start.

@WYSIWYG In fact, I meant an individual cyanobacteria could still survive that environment even if it isn't equipped with resistance to oxygen, so those born with oxygen resistance (by accident) didn't have advantage over those who haven't. As a result, oxygen resistance failed to be passed to the next generation. When the oxygen in the atmosphere became poisonous/fatal, everything was too late (There wasn't enough time for another useful mutation to occur). Anyway, I'll read the materials in the link you provided :)

Oxygen is, indeed, highly toxic to cells, due to its oxidizing power, i.e., the ability to remove electrons from another substances. Since the first carbon-reducing organisms started to increase the amount of molecular oxygen in the atmosphere, more than 2 billion years ago, life on earth has been dramatically changed by this compound: you can even consider that aerobic respiration appeared originally as a mechanism of reducing the toxic molecular oxygen to the innocuous water.
Today, organisms that use water to reduce carbon dioxide, releasing oxygen as a by-product, have molecular mechanisms (as aerobic respiration, for instance) to protect them from the very oxygen they produce.
But your question is quite interesting: how did the first photosynthetic organisms protected themselves against the oxygen they started producing?
This is a catch 22. An interesting solution was proposed by a team of geobiologists from Caltech: There was a little amount of molecular oxygen in the ocean's water before the appearance of photosynthesis. This small amount of oxygen was able to promote the evolution of biochemical mechanisms protecting organisms from its toxicity. Some of those organisms, then, were capable to develop photosynthesis and protect themselves against the huge amount of oxygen that they started releasing. According to the team:

Low levels of peroxides and molecular oxygen generated during Archean and earliest Proterozoic non-Snowball glacial intervals could have driven the evolution of oxygen-mediating and -using enzymes and thereby paved the way for the eventual appearance of oxygenic photosynthesis.

Source: Liang, M., Hartman, H., Kopp, R.E., Kirschvink, J.L. and Yung, Y.L. (2006) "Production of hydrogen peroxide in the atmosphere of a snowball earth and the origin of oxygenic photosynthesis", Proceedings of the National Academy of Sciences, 103(50), pp. 18896–18899. doi: 10.1073/pnas.0608839103.
EDIT: according to your comment, all you want to know is "whether cyanobacteria is able to survive oxygen". Well, that's even easier to answer:
Cyanobacteria can perform aerobic respiration. That means that they can easily use protons and electrons obtained from organic matter to reduce molecular oxygen to H2O:

Cyanobacteria... are among the very few groups that can perform oxygenic photosynthesis and respiration simultaneously in the same compartment,and many cyanobacterial species are able to fix nitrogen. Therefore, they can survive and prosper under a wide range of environmental conditions.

Source: Photosynthesis and Respiration in Cyanobacteria

Firstly, please let me thank you for your complete answer, from which I learnt that cyanobacteria know how to protect themselves from the toxic oxygen, due to the small amount of oxygen in ocean from the very beginning, along with other interesting knowledge. However, what I want to know is whether cyanobacteria is able to survive oxygen, or which level of oxygen can cyanobacteria survive. I would appreciate it very much if you could answer it and/or find some reference s.

@SunQingyao check my edit.


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Location of t tubule in muscle
Why do mammalian skeletal muscles have t-tubules at the junction of the anisotropic and isotropic band, whereas non-mammalian muscles and cardiac muscles have it at Z-line? What could have been the functional significance?
If skeletal muscle would have it at the Z-line then I think it would have been more effective in contraction of muscle fibre. So which arrangement is more efficient?
Also, why is a common arrangement (the more efficient one) not seen in all those muscle types?

Interesting question. Indeed it is related to the working of cardiac muscles. First of all, lets have a look at the structure of a sarcomere of a cardiac muscle from here:

Here, what we can see is that the t-tubule is a depression formed in myocyte. It is important to know this fact here. Why? See this:

In contrast to skeletal muscle, cardiac muscle requires extracellular calcium ions for contraction to occur. Like skeletal muscle, the initiation and upshoot of the action potential in ventricular cardiomyocytes is derived from the entry of sodium ions across the sarcolemma in a regenerative process. However, an inward flux of extracellular calcium ions through L-type calcium channels sustains the depolarization of cardiac muscle cells for a longer duration. The reason for the calcium dependence is due to the mechanism of calcium-induced calcium release (CICR) from the sarcoplasmic reticulum that must occur during normal excitation-contraction (EC) coupling to cause contraction.

First, cardiac muscles don't work by external action potentials, they work on a cycle governed by themselves, known as the cardiac cell cycle.

Second, as is clear from above paragraph, these cells depend on extracellular Ca2+ ions for initiating contraction, a clear difference from skeletal muscles which need Ca2+ stored in SR. Hence, they require t-tubule at a place where a sarcomere ends. Obviously, having a depression in the middle of a sarcomere (i.e. between I- and A-band) would not work here.
Also, the structure of t-tubules is also different between the two. Compare my first image with the image below from here:

In the second one (from skeletal muscle), t-tubule seems like a mere little pit covering the muscle cell in 360° like a duct tape. In the first image, the t-tubule is more like a double wall dividing 2 sarcomeres. It is so because in skeletal muscles, t-tubules have to just transfer the action potential to SR while in cardiac muscle, they have to transfer calcium ions into the cell. So, at the end, the difference is not in efficiency, but in function.
If we look at non-mammalian muscles, then the cause of presence of t-tubules at z-lines couls be associated with presence of large amount of sarcoplasmic reticulum at z-lines. See this article:

Electron microscopic examination of developing myofibrils in regenerating skeletal muscle of Rana pipiens tadpole tails reveals that SR is in regular and close association with Z-lines of young sarcomeres before t-tubules have formed alongside the myofibrils. SR is also associated with M-lines of young sarcomeres but on a less regular basis than with Z-lines...This suggests the formation of a specific bond between SR and Z- and M-lines...These observations support the conclusion that SR does not initiate formation of Z-line precursor elements, but rather associates with Z-lines as they condense from more diffuse Z-bodies.

Since SR is thought to be bonded with z-lines during their formation from z-bodies, hence large amount of SR should be present at the site of association. Hence, it might be beneficial for t-tubules to be present at z-lines to efficiently transfer action potential to SR. However, such association might be absent in mammalian muscles, which can partly answer your next question.
EDIT 1: As you asked in comments
what it would have been if duct like to tubules of skeletal muscle would were present at z line instead of a-i junction?
Now we head towards evolution aspect. Yes, it might have been more effective for skeletal muscles to have t-tubules at z-line instead of A-I junction, but it would not be effective enough to create an evolutionary pressure. Both of these could have same effectiveness too, but during the course of evolution, only those traits which have much greater and direct benefit to an organism's survival and fitness are selected. There is no specific answer for 'why we have 5 fingers instead of 6 or 4', the answer is just that there is no such benefit in having 6 or 4 fingers which would cause it to be selected against 5 fingers.
EDIT 2: Obviously, its exact cause can never be known, but following might also be partly helpful. In mammalian muscles, close communication between SR and mitochondria has been observed. Such so- called "through-space" communication is an important feedback system for effiecient muscle functioning. See this article:

the SR and mitochondrial function in muscle are not independent as calcium uptake into the mitochondria increases ATP production by stimulating oxidative phosphorylation and mitochondrial ATP production and production/detoxification of ROS/RNS, in turn modulates SR calcium release and reuptake...The resultant anchoring of mitochondria to the Calcium Release Units provides a structural basis for maintaining bi-directional SR-mitochondrial “through-space” communication during vigorous contraction.

Now, for such critical communication, SR, t-tubule and mitochondrion need to be as close as possible for fastest & direct communication. Hence, SR & t-tubules need to be as near mitochondrion as possible.

Ogata and Yamasaki used electron microscopy to provide the first detailed description of mitochondrial localization in adult mammalian skeletal muscle (Ogata and Yamasaki, 1985). These studies revealed that mitochondria are located within the I-band, adjacent to the CRU on either side of the Z-line. Precise localization of mitochondria adjacent to the CRU at the A-I band junction was subsequently confirmed in non-fixed rat skeletal and cardiac muscle (Vendelin et al., 2005). Juxtapositioning of mitochondria adjacent to sites of Ca2+ release that occur during EC coupling provides a structural basis for potential local or privileged communication between these two organelles (Rossi et al., 2009).

Thus, presence of mitochondrion at A-I junction and of a "through-space" communication also tend to answer this question.

Yes, I do understand that tubules are different, but what it would have been if duct like to tubules of skeletal muscle would were present at z line instead of a-i junction? Wouldn't that be more effective in contracting two adjacent sarcomeres simultaneously? So why not that configuration?

Why only a-i junction? What's the speciality in that?


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Why is the total length of Introns greater than the total length of exons?
I have just been reading that typically the total length of the Exons of a split gene is very much smaller than to total number of its Introns.
Could anyone please explain why this is the case if its correct, why are some genes composed of more non coding DNA(intron) than coding DNA.
Thanks

[..] if [it is] correct [..] Yes it is correct. Please note that a gene is made of other things than just introns and exons (see wiki > gene # structure_and_function).


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Validity of comparing gene expression levels between alive and <24h postmortem cohort
There is a recent paper about assessment of a suicidal risk in psychotic patients https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4759104/
One of the important points is that the authors compare gene expression levels between alive patients and post-mortem suicidal completers (RNA extracted from blood <24h post-mortem).
In result, they identify suicide-specific blood biomarkers that also have "biological roles in immune and inflammatory response, growth factor regulation, mTOR signaling, stress, and overall the switch between cell survival and proliferation vs apoptosis".
Do you think that one may really perform this type analysis if we know that post-mortem biochemistry is very different? Plus they killed themselves via different means (gunshot, hanging, electrocution, slit wrist etc.)


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Why are interneurons needed in the spinal cord for polysynaptic reflexes and somatosensory tracts to the brain?
The single explanation I found for the polysynaptic reflex is that the interneuron diverges into more pathways, such as the efferent motor neuron, the inhibitory neuron to the opposite extensor muscle, and a ramification that goes to the brain. But why couldn't the afferent neuron axon solve for these ramifications? Furthermore, it is counterintuitive for a nociceptive reflex, that must save the damaging tissue as fast as possible, to be slowed down by an additional synapse.


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Insect identification request
I live in France. I've just found several (8) of these in my living room, close to an oak cupboard and my Christmas tree, a cut Abies nordmanniana (supposedly grown in France).
Their body is around 5 mm (1/5 in) long. On the tissue they walk easily (1st picture), but on the glass of the jar they can't even stay upright and fall upside down (2nd picture).
(At first I was afraid they would be woodboring insects, which I've never seen, but WP taught me the latter are beetles, and these beasts aren't beetles, right?)

I found 6 more today. Hoping these aren't "pests"!

EDIT -- I think this is actually a black stem aphid (Cinara confinis) [see below]

I think these are Hemiptera, and I doubt they are pests. They probably came from the christmas tree (which usually brings hundreds of arthropods into your house). It is a bit hard to see from your pictures (blurry, no clear underside), but my initial guess would be a nymph from Hemiptera (True bug), for instance from the Coreidae family (look at a google picture search at nymphs for some examples). An alternative could be nymphs from Psocoptera), which can look a bit similar. A clear difference between them is in the mouthparts, where Hemiptera have a rostrum (a "straw", sucking mouthparts), which should be seen from the ventral side, while Psocoptera has biting mouthparts. Your second ventral picture seems to show a long rostrum along the underside, which would point directly at Hemiptera. I don't know of any indoor Hemiptera pests (except ones that might attack house plants), but I might be mistaken.
This is just shown as an example, and is not likely to be the correct species, but here are the nymph stages of the common Coreus marginatus, just for comparison:

(from http://www.ukwildlife.net/heteroptera/coreidae/coreus_marginatus.html)
Here is a picture clearly showing the rostrum (see arrow):

(from http://www.fao.org)
Another possibility could be that they are aphids. This is still within Hemiptera (but not Heteroptera), and they also have a rostrum. Aphids have a pair of "tubes" (cornicles) coming out of their backs where they can extrude defensive compounds, and your first picture shows something that might be cornicles (the pointy things towards the back). However, to me, they seem to lie towards the side and look like the type of spikes or thorny sides that many Heteroptera have (a suborder of Hemiptera). Your individual also seems to have flattened edges of the hind body, which e.g. many Coreidae have. Again, clearer pictures would separate these possibilities. It would also be useful to see the number of antennal segments clearly.

EDIT
That said, I looked at some pictures of aphids living on coniferous trees and they can be fairly similar to your specimen. I actually think Cinara confinis is very likely (or another species in the same genus). This species is circumpolar, found in France, and often lives on Abies:

(source: free.fr)

(Cinara confinis, both pictures from http://aesgsf.free.fr/V5/hemipteres-divers-de-picardie-hemiptera-cinara-confinis.html)

Many thanks! The pictures were the best I could do without a macro lens and relying on the camera autofocus. I'll try to look for a rostrum with a magnifying glass. From this I guess they are not final instars, so I'm not going to find tens of shield bugs flying around when I'm back home this evening, phew! :-) (written before your edit:) I searched WP and found the most familiar (to laymen) bugs are pentatomidae, maybe likely candidates?

@L.Levrel Yes, Pentatomidae are probably the most well-known by laymen (due to their size), but I think other subgroups of Hemiptera are more likely. Most Pentatomidae live on herbaceous plant (but some on trees though). On second though, the time of year might indicate that these are not nymphs but adults (most Heteroptera I know of have their nymph stages during spring/summer), and together with the number of individuals could point towards aphids (they are usually found a larger numbers).

@L.Levrel Somebody more knowledgeable in Hemiptera could probably give you a direct answer from your pictures though. They are not my speciality, and I only have a general familiarity (I've mostly looked at  Pentatomidae and Gerridae).

I've added a few more pictures I had in stock and they are most similar to your last two (Cinara confinis)! I learned much with your answer, thanks again! (I cannot award the bounty yet, but will do.)

@L.Levrel You new pictures also show the cornicles more clearly, and these definitely look like aphids. The Cinara genus seems very likely. I'm glad you found the answer useful.

This is what I have found...
Phylum: Animal (animal - obviously)
Subphylum: Hexapoda (wingless - six legs)
Class: Insecta (insects)
Subclass: Collembola (springtails)
Order: Symphypleona (more or less globular - long antenna - live in Northern Hemisphere)
Superfamily: Sminthuridoidea
Family: Sminthuridae (globular springtails - longer antenna than head - often has scale-like skin - roughly 3-5mm long)
The genus is Ptenothrix, but that may be incorrect. I found a photo of a species (Ptenothrix renateae) that looks similar to yours, but almost definitely not it (http://bugguide.net/node/view/610295/bgpage). In comparison it does have the same: ovular body, number of legs, thinness of legs, stripes on legs and antenna. However, the differences (and the reason that I believe this is not the same species as yours) are; though your insect has long anntena in comparison to its head it is not quite as long or thick as this species; the hind legs of your insect seems to be slightly longer; your insect is a different shade (which of course can happen amongst the same species).
Consequently, I believe that the Ptenothrix renateae species is located in a similar location to your insect; I am confident they are in the same order and probably family too, though I am not sure about genus.

Thanks for your effort. However fileunderwater clearly found the exact species and it's not a collembola.


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Structure of phosphates in nucleotides
Nucleotides are made up of a heterocyclic nitrogenous base, a sugar (only ribose or deoxyribose), and a phosphate. In nucleotides, obviously the nitrogenous base matters as its variations dictate the production of certain amino acids, and the sugar can only be ribose (in RNA) or deoxyribose (in DNA), but does the type of phosphate matter? I've seen that a nucleoside describes the nitrogenous base and the sugar alone, and there are nucleoside monophosphates, nucleoside diphosphates and nucleoside triphosphates.
Do these three variations differentiate; when it dictating the production of amino acids; when looking at any sort physical variation; in any sort of way; or are all three just the same as each other??
Also, do all of the phosphates have to look like this?
(https://en.wikipedia.org/wiki/File:Phosphate-group.png). Or can they look like this (https://en.wikipedia.org/wiki/File:Phosphodiester-group.png). If they can look like the second image, then similarly to the question above, does it make any difference?

Hi, welcome to the Biology Stack Exchange! Interesting question, do you think you could try and distill it down to one question? I'm not sure if you're trying to ask about phosphate (of which there is only one: PO4) or asking about nucleotides.

I have cleaned up your title and removed irrelevant tags. You are asking a very basic chemical question about chemical structures, the only complication of which is the ionization of the phosphate at physiological pH.  Read and understand the WIkipedia or Berg et al (NCBI Bookshelf) pages about the structure of  nuceotides, phosphate, and nucleic acids and you will be able to answer your own question, which will no doubt be put on hold shortly.

Do the differentiations of possible phosphates (e.g. mono-,di-,tri-, isomers) as components of a nucleotide affect the function of that nucleotide?

Is it often that nucleotides are found with more than one regular phosphate group (first link in question) as a component?

@LucasDyson-Diaz please do not ping everyone every time you respond. This is exactly why you can only ping one person per comment. You now have two very basic chemistry questions, which (again) can be answered by reading the relevant Wikipedia pages. The answer to both of your questions is yes.

@MattDMo (to the first question) How so? How does the phosphate group(s) it affect the nucleotide?

@LucasDyson-Diaz you'll have to read the resources we've all suggested to learn more about nucleotide mono-, di-, and tri-phosphates.

Well it turns out that when nucleotides are bonded together in a strand of DNA/RNA (nucleic acid) they ALWAYS HAVE only one phosphate group attached to their nucleoside (nucleoside = sugar + nitrogenous base (without phosphate)).
However, when they are by themselves, they are more often found with two or three phosphate groups as oppose to just the one. For this reason, the definition of a nucleotide is often misunderstood as it refers to containing one OR MORE phosphates, in reality, the official definition of a nucleotide states that only one phosphate group is present...
An example of a (so-called) "nucleotide" is ATP (adenosine triphosphate); it follows all of the rules that the misunderstood definition of a nucleotide states (these are; a nitrogenous base (adenine); a pentose sugar (ribose); and one "OR MORE" phosphate groups (triphosphate)). However, according to the official definition of a nucleotide, it is not, in fact, a nucleotide! It is instead considered a 'nucleoside triphosphate', since it is a nucleoside. with three phosphate groups (it is also a nucleotide with two additional phosphate groups, but I guess 'nucleotide-with-a-diphosphate' attachment doesn't roll off the tongue so well as nucleoside triphosphate).
Finally, as in nucleic acids and indeed anywhere else (according to the official definition of the nucleotide), there is only one phosphate group allowed to attached to each nucleoside (regular phosphate group) to form a nucleotide (officially). Therefore there is no variation allowed in the phosphate groups (since there's only one and they bond to other nucleotides, in the same way, every time (in nucleic acids)), furthermore in the pentose sugar the only variation allowed is whether it is a ribose (in RNA) or a deoxyribose (in DNA). So the phosphate-sugar backbone of the DNA strands and the RNA strands (nucleic acids) are consistent throughout the entire strand (and each strand of its type; differentiating only in the type of pentose sugar it consists of (ribose/deoxyribose)). Consequently, there is no phosphate-sugar backbone variation within DNA strands or RNA strands, for the phosphate or the pentose sugar to make any genetic difference to genetic material (those strands); only the nitrogenous bases and their sequences can make a difference to the genetic material...


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Claim: Cat litter with different colors each son, could have different fathers
I'm newbie in biology. I can't look this in the internet and distinguish reliable sources because of this. I want to know if it's normal that a cat mother litter normally has multiple fathers, and that is the cause of cats looking very differently colored. Now, I imagine difference in coloring of the fur could happen with the same father, because sons are not necessarily genetically identical, however there are many claims in google when searching:

http://pets.thenest.com/can-cats-litter-two-different-fathers-8341.html
http://pets.thenest.com/possible-kittens-one-father-8061.html
http://www.drjeffnichol.com/?p=2277
http://animalcarebasics.com/each-kitten-different-father/

If the claim is true, does all the kids start developing at different starting times? Does that mean they could be born some more premature than others? How big is the window for female cats to be fecundated?

This might be better suited to [skeptics.se].

@MattDMo I though the same. I decided randomly.


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Why does a stomach come before the gizzard in birds?
Since the gizzard is for mechanical digestion, shouldn't that happen before the stomach digests the food with acids? (to make the morsels smaller)

The gizzard appears to be a structure that bird inherited from a distant ancestor, as the structure is found in dinosaurs (which birds are derived from) and crocodilians.  https://en.wikipedia.org/wiki/Gastrolith
As to why, the bird gizzard is not in a better position, (like say the grasshopper gizzard which is located in front of its stomach), the best reply I think off is evolution is blind.  The innovations that appear, are random and further constrained by the features that the animal already has.
It is probably the same reason why rabbit eat their own poop to better digest their food, even though cows have evolved a four chamber stomach to handle the same problem of digesting grass. Or why no animal has evolved a second set limbs to fly even though it would be super useful to keep arms to catch prey and not sacrifice said arms to be made into wings.
In a sense these questions of why didn't evolution design it better is evidence that the concept of intelligent design is rubbish. Designs in animals (and bacteria) can be really really dumb.

"...found in dinosaurs (which birds are derived from)" This is incorrect. Birds are dinosaurs.

Birds are a derived species of theropod. And theropod are only one of two members of Saurischia. And there is deep divide between Saurischia and Ornithischia. Secondly Birds are a derived species....while they have many features of theropods... the evolution of flight has cause birds to gain many features not shared by most member of theropods. Birds have no teeth, reduced jaws, no grasping fore limbs,a truncated tail, a bird hip, an arrangement found in Ornithischia. Birds are a derived species, avian dinosaurs.


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Why isn't meiosis II called mitosis (as the chromosome number doesn't half)?

Meiosis: a type of cell division that results in four daughter cells each with half the number of chromosomes of the parent cell, as in the production of gametes and plant spores.
Mitosis: a type of cell division that results in two daughter cells each having the same number and kind of chromosomes as the parent nucleus, typical of ordinary tissue growth.

After meosis II we have the same number of chromosomes as before. So why isn't meiosis II called mitosis instead?

Well, in my opinion, the entirety of the meiosis is a process (reproduction of sex cell) in which two levels of division occur, it's all kind of one process. Though meiosis II may seem to have many similarities with mitosis, meiosis II can only occur with sex cells, to my understanding that is the main factor which differentiates meiosis I and II from mitosis. Furthermore, regardless of the similarities, to call meiosis II the same as 'mitosis' (whilst meiosis II is still in the entirety of the meiosis process) is not only confusing but impractical. I'm sure, though, that somewhere along the line there are several detailed differences between the technicality behind the cellular division in mitosis as in meiosis II. But, don't listen solely to my answer, that's just my opinion since your question is subjective to my personal opinion...


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What is the point of Meiosis II, considering Meiosis I already produced haploid cells?
Meiosis I is required so that the 2N cells become 1N, and so a 1N sperm and 1N egg can fuse to become 2N again.
But why is meiosis II required? Why does our body need to go from  2 1N cells to 4 1N cells? Can't it just use one of the 2N cells after Meiosis 1?

Source

Please visit this question

After meiosis I, those n=23 chromosomes have two chromatides. Meiosis II just separates them into single chromatides.

befor a cell enters its division its heridity material is in a form of a coilled and condensed material called chromatin whose amount is 2N and is diploid 2n However when the cell enters its interphase  its chromatin dobbles but its no of chromosomes remain 46 so  when cell enters meiosis 1 it produces two daughter  haploid cells 2n having 2  same   sister chromatids attach to same centeromere as cells at the end of meiosis 1 are  haploid 1n but amount still remains 2N to half the amount of chromatin meiosis 2 occur so that 4 daughter cells with haploid no of chomosomes 1n as well as halfed amount of chromatin 1N o can be produced

Welcome to Biology.SE! Please add some references to your answer.


text:
Do allergens have structural similarities to pathogens?
The conventional popular explanation of allergies is that the immune system confuses allergens with pathogens and reacts to them as such.  Is there any merit to this explanation?  If so, I would expect it to be possible to predict which proteins would be allergens by their structural similarity to pathogens.  Is it?  If not, how else could we explain which proteins are allergens and which aren't?

Have you done any basic research?The wikipedia article is a good read to start with. I think you should go through this to finf out What should you do before you ask the question?.

Allergens are antigens. Please do some research on what each term refers to. Wikipedia is an excellent resource.

@MattDMo Sorry, I think I meant "pathogen" instead of "antigen".  I will change my question.

@SanjuktaGhosh You seem to have linked to the page on homework questions.  This is not a homework question.  Is this the page that you meant to link to?  And I have done research to try to answer this question myself.

Low effort questions are closed under the tag 'homework question' and I meant to link it to the 'What should I do before I ask the question? ' paragraph. You have to share your research (mentioned in a paragraph below it).

@SanjuktaGhosh no, not all low-effort questions are to be closed as homework. See the recent discussions on meta. Homework is for homework, low-effort can be closed as too broad, unclear, or using a custom close reason.


text:
Recommendation of Ecology books
What are some of the standard books to study :

Biological Interactions: Symbiosis, Mutualism...etc
Concept of Limiting factors
Niche concept
Resource partitioning
Concepts of community change
Theories of climax
Models of Succession

P.S. I am looking for a book for beginners for studying ecology at UG level.

You must know by now that this question is going to be closed as too broad and/or primarily opinion based.

Related: https://biology.stackexchange.com/questions/45716/guide-to-learning-about-population-biology-ecology-dynamics-for-a-non-biolog

Nobody else ever did vote to close. Tyto Alba (second reincarnation of another name) is unfortunately long gone. So I've voted to close.

A classic standard textbook that I've used a lot myself (earlier editions) is Begon, Harper & Townsend. This book is very broad and comprehensive, but I know that some students dislike it's back-and-forth discussion style (fewer definite answers). I see this as a strength though.
Another good choice, that is much shorter, is Gotelli's A Primer of Ecology. This one has a slight theoretical leaning (many standard mathematical models), but can work well in a  introductory course. I don't have the book in front of me, but, looking at your list of topics, I suspect that A Primer... might be weak in some of them (e.g. climax, succession).

How good will Fundamentals of ecology be? I found an old copy of the book in my college library, it dates back to 1996.

@SanjuktaGhosh I've only browsed it, so I cannot really say. It's a classic that has gone through numerous editions though. Most well-known textbook has a good coverage though, and you cannot go too wrong for an overview of the major topics. The biggest differences are in writing/presentation style and emphasis. As I mentioned, A Primer.. has a slight theoretical bias (for an overview text) while e.g. Evolutionary Ecology (Pianka) emphasise, well, evolutionary aspects.

@fileunderwater Thanks for mentioning a book for learning basics of the  mathematical theories of ecology (Gotelli). I'll look for this book at library.

 Ecology Textbooks:
Molles, M.C. 2010. Ecology: Concepts and Applications. Fifth edition. McGraw-Hill. New York, NY. p. 572.

I'd say this is the "standard" undergraduate textbook. Those planning on continuing to graduate work should best know this book cover to cover by the end of their 1st year of graduate work.

Tons of pictures, lot's of definitions (with glossary), tons of references, and easy to read (as far as textbooks go).

Begon, M., C.R. Townsend & J.L. Harper. 2006. Ecology: From Individuals to Ecosystems. Fourth edition. Blackwell Publishing Ltd. Malden, MA. 738 pp.

As @fileunderwater said, this is the standard text for ecology. I'd say anyone moving through graduate work should know the concepts in this book front-to-back by the time they finish their graduate degree.

Strengths: Numerous relevant publications; good discussion; most in-depth/comprehensive of those I've read.

That being said, it's not the greatest place to start. There are no colorful pictures, there are no bolded definitions (and no glossary), and the discussion assumes you already have a grasp of simple concepts.

J Gurevitch, S.M. Scheiner & G.A. Fox. 2006. The Ecology of Plants. 2nd ed. Sinauer Associates, Inc Sunderland MA. 574 pp.

This is a great textbook to learn about the ecology of plants (well illustrated, lot's of definitions, fairly easy to read but still fairly comprehensive).

This book would best be read having already taken an intro ecology class.

Smith, R.L. and T.M. Smith. 2001. Ecology & Field Biology. 6th Edition. Benjamin Cummings, USA. 843 pp.

This book is very dated, which results in a number of more recent studies not being mentioned. However, if the goal is to develop a simple understanding of ecological principles, this book could be found very cheap online.

Bush, Mark B. 2003. Ecology of a Changing Planet. 3rd edition. Prentice-Hall, Inc, New Jersey. 477 pp.

This book is likewise very dated, which results in a number of more recent studies not being mentioned. However, again, if the goal is to develop a simple understanding of ecological principles, this book could be found very cheap online.

I would also say that the chapter introductions (as well as copied papers) in Foundations of Ecology (Real & Brown 1991) are great for catching you up on both the history of the field of ecology and the most important classic papers/researchers in the field.
 Books on Communities & Succession:
These are a bit more dated, but here are some of the classic books on these topics.

Bazzaz, F. A. 1996. Plants in Changing Environments: Linking
Physiological, Population, and Community ecology. Cambridge:
Cambridge University Press, 320 pp.

Bormann, F. Herbert, and Gene E. Likens. 1979. Pattern and Process in
a Forested Ecosystem: Disturbance, Development, and the Steady State
Based On the Hubbard Brook Ecosystem Study. Springer-Verlag, New
York. 253 pp.

Glenn-Lewin, David C., R K. Peet, and Thomas T. Veblen, eds. 1992.
Plant Succession: Theory and Prediction. Chapman & Hall, London. 352
pp.

West, D C., Daniel B. Botkin, and Herman H. Shugart, eds. 1981.
Forest Succession: Concepts and Application. Springer-Verlag, New
York. 517pp.

Whittaker, Robert H. 1975. Communities and Ecosystems. 2d ed.
Macmillan, New York. 385 pp.

Let me provide a second answer that summarizes the responses given by a number of ecologists from all over the world. These ecologists gave the below responses to a similar question asked on ECOLOG on Jan 30, 2018. This will hopefully broaden the search for others coming across this post in the future...

Note: The ECOLOG question specifically asked:

I’m looking for recommendations/suggestions of a general ecology book, preferably with at least some plant examples to supplement lectures and field in a brief introductory ecology class for adults who are interested in and often quite knowledgeable about (native) plants

The responses (in ABC order):

Cain, Michael L., William D. Bowman, and Sally D. Hacker. 2013. Ecology. 3rd Ed. (4th Ed. due May, 2018, authors same but start with Bowman). Oxford University Press.

It was fairly easy to consume and had lots of material to draw from...though I believe it was more geared towards theoretical ecology rather than naturalism.

Drury, William H. ed. John G.T. Anderson. 1998. Chance and change: ecology for conservationists. University of California Press, Berkeley.

Bill Drury, who wrote against models like "Classical succession", and after he died his family asked me to edit his manuscript for an "alternative" Ecology text book. It is by no means perfect, but it seems to have held up pretty well & provokes good discussion among students.

Ennos, Roland. 2016. Trees: a complete guide to their biology and structure. Comstock Publishing Associates.

It doesn't cover quite the subject matter you're looking for, but I quite enjoyed "Trees: A Complete Guide to Their Biology and Structure" by Roland Ennos. It's fairly small, but technical, almost like a chapter or two from a broader introductory textbook. It gave me a basic overview of the natural history of, well, trees.

Gurevitch, Jessica, Samuel M. Scheiner, and Gordon A. Fox.  2006.The Ecology of Plants, 2nd Ed. Oxford University Press/Sinauer Associates.

Book intro says it is basic ecology with plant focus. How about The Ecology of Plants?

Gotelli, Nicholas J. 2008. Primer of Ecology 4th Ed. Oxford University Press/ Sinauer Associates.

good and succinct, but might not be right for your audience. [technical with focus on models]

Karban, Richard, Mikaela Huntzinger & Ian S. Pearse. 2014. How to do ecology: a concise handbook 2nd Ed. Princeton University Press.

I also really like “How to do Ecology” by Karban and Hartzinger about the process of developing and conducting ecological research, but again, might not be right for this situation. [looks very useful for planning research projects]

Keddy, Paul A. 2017. Plant Ecology, origins, processes, consequences. 2nd Ed. Cambridge University Press. New York.

Covers basics but book intro suggests reviewing basic ecology text.

Marchetti, Michael P. & Peter B. Moyle. 2010. Protecting Life on Earth: an introduction to the science of conservation. University of California Press, Berkeley.

A short non-majors ecology/conservation biology text.  I think we did a solid job at explaining general ecology to nonscience people.  you might check it out, although it is not plant centered but there are plant examples.

Molles, Manuel C., Jr. 2014. Ecology: Concepts and applications 7th Ed. McGraw-Hill Higher Education.

Manuel Molles book is good. I like the idea that he focuses on students understanding the language of science (figs and table-with helpful annotations-still use some of those in my senior level cons bio class)

Relyea, Rick and Robert E. Ricklefs. 2017. The Economy of Nature 8th Ed. W.H. Freeman Publishers.

Completely redid all of the figures and photos, with lots of plant examples. I am pleased to report that the response from instructors and students has been very positive. [the chapter on line has a terrific discussion of soils, and plants and soil relations]

Stokols, Danel. 2017. Social ecology in the digital age: solving complex problems in a globalized world. Academic Press/Elsevier.

Know you’re interested in identifying a general ecology text, but in case you’re interested in a supplemental text on social and human ecology, this 2018 title might be a relevant resource for you and your students:  Social Ecology in the Digital Age - Solving Complex Problems in a Globalized World.

Apparently a good blog: fredsingerecology.com

Weekly blog that discusses recent papers in Ecology (~75%) and Conservation Biology (~25%).  Each post has background, hypotheses, data and a discussion of why this question is important or of interest. It's designed to be used for instruction at a high school/college level, and should work fine for interested adults, regardless of background. Emphasis on interactions, reflecting author's preferences, but has fair number of posts that focus on plants.


text:
Cannot see images beyond a certain magnification with a microscope
Using a new microscope with my son, we cannot see images beyond a certain magnification:
Eyepiece: 25x - Objective lens: 4x   --> OK
Eyepiece: 25x - Objective lens: 10x  --> OK
Eyepiece: 25x - Objective lens: 40x  --> not focused
Eyepiece: 25x - Objective lens: 100x --> not focused

In the last two cases, we try moving the stage along all its range, without getting anything.
Same issue using a 10x eyepiece.
On the 100x objective lens "OIL" is written; does it mean the observation needs to be done through oil instead of air? Or just that oil is used inside the objective?
We did not prepare the leaf; we just put a small piece of it between two slides.
Are we doing anything wrong?
Observing a leaf at 250x, we can see tiny round structures (I think barely bigger than what can be possibly seen by our eye): are those the cells?

Can you tell us the other writings on the objective lenses ? Do you also have a 10x ocular in your kit ? How are you preparing the leaf for observation ?

Generally speaking, strong objective will focus very close to the sample. (Be careful of lens-sample collision though)

It's been thousands of years since I've used a microscope, but shouldn't 100x be an oil-immersion magnification? Also, looking at a pre-fixed set of slides first should help you to get the hang of things. Looking at cells takes practice. If you have none, buy some. The very thin skin between two layers of an onion needs little preparation, and is a great home-made intro to plant cells. A scraping of the inside of your cheek mixed with saline (easy to make) is also a good home-made intro to animal cells.

Oh, btw, it's possible that the things you're seeing at 250x are chloroplasts. Round and green and very small.

60x has already entered oil immersion range.

I updated my question with more details. Thank you.

Just a guess, but putting the piece of leaf between two slides may not let the objective get close enough to focus at higher magnification.  There are cover slips made of much thinner glass that are used for this purpose.

This is probably the problem: "We did not prepare the leaf; we just put a small piece of it between two slides.".
I suppose you mean you put a leaf fragment between two regular microscope slides, those measuring 26mm * 76mm (1in. * 3in.)?
That won't work. Long story short: microscope optics/objectives are designed with a specific working distance in mind, which is not an entiraly free choice, but dictated by the laws of physics/optics. An average achromat 40/0.65 has a working distance of about 0.6 mm. An average achromat 100/1.25 has a working distance of about 0.2 mm. An average microscope slide has a thickness of about 1 - 1.2 mm...
In the... well... regular microtechnique, a specimen is put on a slide and covered with a very thin coverslip, having a thickness of around 0.15 - 0.17 mm.
Also, as others mentioned, using a 25x eyepiece in combination with a 40/0.65 or a 100/1.25 is kind of overkill. With that combination, you enter the realm of "empty magnification". In short: structures appear larger, but no new structures are revealed and the image becomes more and more fuzzy.
And yes: you need to use immersion oil with the 100x objective, but keep in mind this is a very demanding objective to be used, on the part of the microscopist as well as on the part of the slide preparer.
Using a microscope is not all that simple for novices, but there's an easy way to find out -if no image can be produced-, if it's a microscope problem or an inexperienced user problem: take as a specimen an as thin as possible large object, such as a leaf of cigarette paper, and try to focus on it, using low power and gradually use stronger objectives up to 40/0.65. If an image can be produced, even if it's rather blurred at 40/0.65, the microscope is okay.

"We did not prepare the leaf; we just put a small piece of it between two slides." Nice point... a slide is too thick for a 40x objective.

Sorry. I'm not a native English speaker, but in Dutch and, as far as I know, in French and German as well, any object put on a slide for microscopic examination is considered "prepared" for -, being it as a temporary mount. Ah well, I'm not a linguist, unfortunatly.

Logically it is true...irrespective of language... whether you are preparing 'chemically' or preparing just with a blade and forceps, or just preparing by hand; temporary or semi-permanent or permanent; coverslip or another slide or naked... you are 'preparing it for microscopy'.

Eyepiece: 25x - Objective lens: 40x  ---> not focused

Are you sure it can't be focussed? Objective lens like 40x or 45x normally have very near-focus (can be less than 1 mm) and also a shallow depth-of-field.
To focus the slide at 40X objective; at first focus it with 10X objective. Then rotate the turnstile at nose-piece and bring 10X objective. (In some lower quality microscope with the adjustment screws you may need to bring the main-portion of microscope upwards, distant from the slide. Otherwise the long 40x lens may hit the slide or drag the coverslip. However good-quality microscopes doesn't have this problem). Now it is time to focus the 40X.
To easily do that; at first bring the 40X lens tip just 1 or 2 mm distance from cover-slip. (Just like sometimes while a known-titration we blow the titrant from the burette quite high-rate upto certain value; and subsequently slow-down). Now take only the fine-adjustment screw and bring the objective backwards (and very carefully forwards... so that the lens doesn't hit the cover slip).

Note-1. I didn't worked with 25X eyepiece; but I worked up to 15X eyepiece; that normally gives wonderful clear picture. But in some microscopes having expandable draw tube, higher magnification with similar 15X eyepiece I've seen, but gradually high expansion of drawtube (and refocus of course) makes image gradually more blurry. But focus was not impossible.

You could also try eye-pieces of 10X and 15X values.

Note-2: Use thin and uniform cover-slip (such as Blue-star (trade-name)) and try to make your sections more thin. See if that cause any improvement.
Note-3: Do not use bare specimen (no-coverslip)... it may damage the lens which is very close to specimen.

Eyepiece: 25x - Objective lens: 100x --> not focused.

The 100X objective lense is usually a Oil-immersion lens. I.e. between the coverslip and 100X lens tip; the light pass through a specialized oil instead of air.
What I've seen if I do not use the oil; I do not get the focus even when the lens tip touches the coverslip.

Note-1: Cleaning of oil immersion lens: Do not use xylene (though some protocol says that). It damages the eyepiece, cause blur, and may make it permanently non-functional. Most of our university-teachers forbidden strictly to use xylene for lens cleaning. Use a soft cotton cloth, at first moist, then dry (or alternatively wet and dry for several times). However cotton and xylene to be used to clean the coverslip quickly with minimal damage/friction of the microscopic specimen.
Note-2: If use oil; make its use neat and clean way. Do not contaminate oils to other lense.
Note-3: For common purpose we do not need the oil-immersion lens. It is used only to view very tiny things like chromosomes, bacteria, cell-wall ornamentation, pollen walls, fungal spores and such type of things. Average plant and animal cells' contours (and tissues) could be seen well under the 10X objective and 10X to 15X eyepiece. Sometimes students' microscope come without the 100X objective; the place for it on the turnstile kept closed with a screw-cap.

25X is a mighty strong ocular (eyepiece) lens, certainly for home use. This means with the 40X objective you are already at 1000X overall. It would take a seriously thin, well mounted and well lit specimen for you to see a good image. This assumes the optics are of sufficient quality.
I recommend using a 10X objective. This will give you 400X with the 40X objective. To use the 100X objective, you will need to insert a drop of oil between the objective and the slide. "Immersion oil" is made especially for this purpose.
At the 400X, or higher, magnification you will need to slice tissue very thin. But there are a couple ways to view cells without the knowledge or tools for preparing sections. To view plant cells, do an internet search for "onion cell wet mount". To view some animal cells (your son's), search "cheek cell slide".


text:
What food has the highest calorie per unit price that you can buy and eat regularly?
What food has the highest calorie per unit price that you can buy and eat regularly? The food cannot give you any undesirable health effect due to the sole reason that you eat it regularly (say once daily).

This question is unclear. Calories aren't the same as nutrition; fat is the most calorie dense food. What do you want to know? The most nutritious food for the price? The price where? Or are you trying to gain weight? There are better ways to gain weight than eating cheap calories.

I'm looking for high calorie food, not the most nutritious, but the bottom line is you can eat it regular without causing any health concern....

I honestly do not understand why it would be opinion based (I am entirely amused by the absurdity of people calling a close of this question). At best you can say little research would have been able to provide answer to this question (I am not sure) and me, the author himself does not show enough effort on his own to answer. This question can be entirely answered scientifically, given enough data about price and calorie of food, as well as long-term nutritional and health study of food substances. What kind of reason is that to close a question (do you even think???)? What a shame.

The first part of the question can be answer by simplifying it a bit. Food can be divided into a few base categories
Carbohydrate (eg rice)
Fatty acids (ie fat, butter and oil)
Aminoacids (meat)
What is the cost of rice? It depends on the quality of rice you are willing to eat. Good quality US rice cost  about  = $530 Per Metric Ton. Low quality 100% broken rice cost USD 350 per ton
http://www.riceauthority.com/prices/
Cost of cheap fatty acid (palm old) = ~$650 per ton.
http://www.indexmundi.com/commodities/?commodity=palm-oil
Meat : well it is over $ 1000 USD per ton.
http://www.globalmeatnews.com/Industry-Markets/Meat-prices-to-remain-high-as-demand-increases
IN terms of energy per cost...
Rice 4 cal per g https://www.google.com/?gws_rd=ssl#q=calories+rice+per+gram
Oil 9 cal per gram https://www.google.com/?gws_rd=ssl#q=calories+oil++per+gram
So in terms of highest calorie per unit price, the winner goes to palm oil.
The second requirement.. is a bit difficult to answer.
Genetics can play a role. Specifically the innuit can have a diet were 50% of their calories is derived from fat, without suffering form cardiovascular problem and starvation from lack of carbohydrate (ie the brain only runs on glucose) https://en.wikipedia.org/wiki/Inuit_diet. How this is possible is debated. Idea include, high levels of animal glycogen in their diet where most meat is eaten raw, a miss calculation in anthropological studies on the amount of plant carbohydrate in Inuit diet, and genetic differences.
Traditional asian diets can have upto 70% of calories derived from carbohydrates.
https://hms.harvard.edu/news/lower-diabetes-risk-asian-diet
http://sampan.org/2015/05/follow-traditional-asian-diet-for-asian-american-and-pacific-islander-heritage-month/

Thx for your answer!!

The cheapest source of calories in the world is one that is contributing to global extinction and catastrophic climate change through the destruction of the rainforest (palm oil).  These definitely qualify as undesirable health effects.

Pick the fatty acid of your choice, any fat or oil has the highest calorie to weight than any other food. Most fats are fairly cheap, there is a reason fried foods are so fattening. As long as you are eating an otherwise healthy diet all the health risks associated with fats are from gaining weight.


text:
Cells in tissues
Tissue (biology): In biology, tissue is a cellular organizational level intermediate between cells and a complete organ. A tissue is an ensemble of similar cells from the same origin that together carry out a specific function.(Wikipedia)
Are all the cells of a tissue of a kind?
In the definition Tissue  what is from the same origin?

Welcome to SE Biology. Please read the instructions on constructing good questions. A title should be a one line phrase indicating what the question is about, not an extract from WIkipedia. Also, you are expected to write in standard English and a single question mark after a question is sufficient. I have corrected your question. Please try to do better next time.

What you say is true that most of the cells in a tissue are of the same kind. However, as with most rules in biology, there is almost always an exception to these rules. There are only four types of tissues (can be split up into further subdivisions): muscle, epithelial, connective and nervous. Also, a muscle tissue is made up of an ensemble of myocytes (muscle cells). Therefore, the answer to your question would be yes, the cells in a tissue are (if not all, then) almost all of the same kind.

Many different types/kinds of cells comprise a single tissue.  For instance, the epithelial tissue of mammalian skin can contain cells that produce hair, excrete sweat, or do neither of these things but simply serve as a barrier.  These cells are all epithelial tissue.   Here is another example of the diversity of cell types in a single tissue: the cells of the brain are part of 'nervous tissue', but there are thousands of different kinds of neuronal cells (the precise number is growing actually; see this website, where this image was grabbed).

Blood is technically a tissue, and yet there are many, many different kinds of blood cells.

In reference to your second question, the cells share a common origin in a tissue because they come from a small number of precursor cells, like the depiction in the image above for blood cells.


text:
Reading annotations from a plasmid map
Can anyone explain why inside plasmid mapping software the annotations are layered under each other, I am confused as to why there are essentially two layers within the map, for example in the image below.
The bottom red layer is annotated as "DsRed2" and the top yellow is "LacZ-DsRed2 fusion expressed in E. coli". Does this mean that the red layer is inserted into the original LacZ gene or some sort of mutagensis...? Any explanation would be real helpful.

Second Plasmid design

Third Plasmid

Keep in mind that the plasmid map is made by someone, and probably not perfect. They're also made by programs that let you annotate everything everywhere, even overlapping stuff.
In silico, I assume that the DsRed part and the Lacz parts were present, perhaps copied from some other plasmid map including annotation. After that, someone decided it was a good idea to annotate the complete ORF (in yellow).
What I think this means in reality (just guessing from the map, which is just coarse schematic picture): there's a part of Lacz still present in the plasmid (in pink, second lane) which is fused (in frame) to the DsRed gene (red). Together this gives the fusion gene marked in yellow. Also notice the part (terminator?) in pink that's in the third lane.

Thanks for this, I have added 2 more larger images of plasmids since the original was kinda small. The ORF 2 and ORF 3 (blue) in the second plasmid are under the genes (red), does that mean that simply an insert can be placed there? Also there seems to be a third green layer on top, does that mean the terminator and primer are in the same location? And just a last thing, the third plasmid has arrows in reverse, i.e. lacl and amp', what does this mean? thanks!

ORF2 and 3 are probably just there because of the plasmid / annotation software. There's the Ampicillin resistance gene, which is also just one of the ORFs on the plasmid. The place to insert something new would be in the multiple cloning site at the top (with all the restriction sites). Arrows running in reverse mean the gene is on the other DNA strand, "upside down".

If you want to more about the practicalities of a plasmid I'd suggest to look up the manual for the same (or similar) plasmid. Usually the plasmid in your lab is based on a commercial one, or you use a classic plasmid that's also commercially available.