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Is a single cell "irreducibly complex"?
(sorry if the title seems like flame-bait - but it's a real question).
I'm trying to understand what could have come before the first cell (What are the "minimum requirements" for a single cell?)
From what I've seen, the presented chemical evolution (aka abiogenesis) process centers around self-replicating RNA that gets trapped inside a lipid-based protocell and then somehow turns into a functioning cell.  But it seems like a giant leap to go from that situation to the most basic cell we know about.
Instead of starting from basic molecule and trying to get more complex, what if we take a simple cell (which is actually really complicated) and try to get more simple - try to take out some of the pieces. Work our way backwards. The problem is, I don't know what pieces you can take out. It seems there are several molecular systems that need to be functioning for cell to be viable.  Once you start to imagine a cell without them, it seems the cell will not be able to survive or replicate.
My question is, what would the step just before a "minimum cell" look like?  Are there pieces we can take away and it would still be able to survive and replicate?
** Edit **
Based on some of the discussions in the comments, I wanted to clarify what I'm asking. This is a bit long - but hopefully it will help.
Evolution is a process in which replicating systems transfer beneficial permutations to 'offspring'.  Usually the term is applied to "biological evolution) (meaning something living - from a cell to more complex organism) but I've also heard people refer to "chemical evolution" which is the process in which atoms combine to make molecules and amino acids and the amino acids combine to make RNA which can replicate.  Or fatty molecules combine to make a lipid membrane, etc.
In this process to get to something more complex, you have to have gone through a simpler stage.  To arrive at RNA, you had to have a system that would first produce nucleic acids.  If the first life was in the oceans, you needed something that could survive in and out of water before you now have creatures on dry land.  Each stage has to have a predecessor.
Generally question of the origin of life start at the raw materials and work their way towards the more complicated.  Most of the discussion I've seen basically end with RNA in lipid cells + billions of years = a prokaryote.  The difference between RNA in a protocell and a working basic cell is vast and I haven't seen an explanation on how to bridge that gap.
I'm approaching the question from the opposite direction.  If we take the most basic, simple prokaryote cell - what came before it? Even such a simple cell is in actually very very complicated (semi-permeable membrane, nucleoid, ribosomes, cytoplasm, etc..) There are so many interconnected pieces that it seems are only valuable when working as a whole. Eg, could I have had a cell without ribosomes and then some how it mutated to have ribosomes?  It seem not, because a cell without ribosomes would never have survived/replicated.  The same with other components.. if I have some precursors without that piece, it would never have survived long enough to mutate to now have that component.
So my question is what could the predecessor to a basic cell have been, considering its complexity and the seeming interdependence on the pieces for the cells survival?
I hope that helps explain the question better - thanks for any insight you can provide!

Comments are not for extended discussion; this conversation has been moved to chat.

ribosomes are made of RNA, Ribozymes are strands of RNA that act like enzymes ribosomes among them. So you have a smoother transition from RNA that catalyzes itself to RNA that catalyzes other strands of RNA, to RNA that translates other RNA into proteins.  The human classification systems get in the way of your imagination, at the chemical level there is very little difference between many "essential" molecules many are in fact the same just arranged in slightly different ways.

This is not a question in terms of SE Biology, but an attempt to start a discussion.  This explains the latest rant it has provoked (Nov 2019). Surprised? Just vote to close.

Part of the issue you are having is cell is not the simplest thing that can reproduce, replication does not require a cell. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3943892/

This question has too many false assumptions to be clear.

@David and others - this is absolutely a real question and the fact that someone started a "rant" has nothing to do with it.  Unless you want to revive the beliefs of the Church and unquestionable dogma - we are allowed to ask questions about how the process works and we can ask hard questions.  This is physics and chemistry, not magic.  If we started with RNA and end with a complete cell, there have to be steps in the middle.

@John - I understand that other things can replicate.  I say it in my question.  The problem is that an RNA molecule has no other dependencies - it just is.  If you have it, it can replicate and make more of the same thing.  But a simple cell is so much more complicated and multiple dependent systems (as I understand it).

I encourage people unclear about this question to read https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2926753/ to understand that it is a valid question.  If people have specific criticism of the question other than inferences about my motives or vague issues ("This question has too many false assumptions to be clear"), please let me know and I'll be happy to try to answer.

@Yehosef sure but they survive better with more complex things like the ability to sequester material and protect them selves from other RNA (cell membrane) or with a way to store the information in RNA in a way that is not so easy to degrade/mutate, (DNA)  the fact that all these things are produced by RNA or the direct product of RNA (proteins) means there is no missing step. Even in modern cells RNA is the basis of basically every process. A simple step up would be a an RNA that catalyses itself but also makes a protein that breaks down other RNA.

the source list for this video will provide a plethora of papers about modeling the origin of life. https://www.youtube.com/watch?v=KvGdllx9pJU also the simplest cell lack many of the things you mentioned, https://pubmed.ncbi.nlm.nih.gov/27013737/ try these out so you can ask a better question.

There is no straightforward answer as to whether a "single cell" is irreducibly complex. Which cell are we talking about? Human mitochondria do not survive without their genome, but those of Cryptosporidium do persist without it. The Minimal Genome Project, led by biotechnologist Craig Venter, concluded with the creation of Mycoplasma laboratorium, the result of removing non-essential genes from Mycoplasma genitalium. This minimum cell had 382 genes.
Are 382 genes the minimum number of genes required for life then? No. That number refers to the total number of genes necessary for a particular organism, which happened to be Mycoplasma. Iterative trials of removing genes will reveal different numbers of essential genes for different organisms. Primates will require a high number of essential genes, whilst archaea could survive with fewer genes.
Regarding the transition from RNA-only to RNA-protein world, peptides function as cofactors for some ribozymes. Amino acids and peptides are known to have existed in the prebiotic environment and have been found in space (glycine has been found in comets, along with other 70 amino acids).
Regarding the formation of nucleotides, from Scientific American.

A New Route
  In the presence of phosphate, the raw materials for nucleobases and ribose first form 2-aminooxazole, a molecule that contains part of a sugar and part of a C or U nucleobase. Further reactions yield a full ribose-base block and then a
  full nucleotide. The reactions also produce “wrong” combinations of the original molecules, but after exposure to ultraviolet rays, only the “right” versions—the nucleotides—survive.

This answer is not complete, I will add more information and provide citations in the future.

"try to take out some of the pieces. Work our way backwards."
Backwards in what, time? Does what you're doing work for any other natural system? No, it doesn't. That is not how scientists infer the history of any process given snapshots, transitional forms, etc. To discover history, they apply validated physical models and processes to the snapshots, they don't remove arbitrary parts.
"The problem is, I don't know what pieces you can take out."
No, the problem is the method you're using is invalid. I'm pretty sure it was a religious fundamentalist that seeded your idea in the first place. You're using a complexity/function-based "reverse-evolution" which may seem reasonable but never worked anywhere else, in any other part of science, for any natural process. How would you apply your method successfully to stellar evolution?
Both complexity and function are not measured, they are assessed subjectively and depend on the size of the system of interest and surrounding environment. They are philosophical concepts and are not good guides or a valid basis for inferring the history of a natural process. They are useful for communication between biologists or as a guide for planning experiments, but have no simple quantifiable relationship to any natural system.
Complexity is superficially related but entirely irrelevant to existence of a particular form of life or anything else. What's relevant, says the laws of physics, is prior conditions, surrounding environment and natural laws that act on those conditions.
To say whether something is functional one must know the environment it exists in. Even if you identify a function relevant to life, it still has other functions. Everything is made of atoms which function as the building blocks for both life and non-life, therefore there is no such thing as objective or fundamental function.
Irreducible complexity (IC) isn't even a coherent philosophical concept let alone a scientifically valid concept. It's a philosophical thought-experiment with no empirical, scientific or observational justification. Basically, IC does the following:
1) Breaks something into parts[1], philosophically, inside the mind.
2) Remove one of those parts [2].
3) Assert with no supporting evidence that the incomplete thing in step #2:
a) actually existed at some time in the past, and
b) was part of some chain of modifications or changes that led to the complete thing in step #1.
4) Assert without evidence that since the incomplete object had no obvious purpose or function [3], then it couldn't have been a step in evolution because evolution requires all parts to be functional[4].
One key blunder and reason why IC fails is step (3). In order for IC to be valid and relevant to this universe, or anything in it including evolution, step 3 must be supported by empirical evidence.
One can't just randomly choose some arbitrary division an object, however relevant to biology it may seem, then choose a random part, remove that part and claim the incomplete object once existed in the real universe. One must demonstrate with evidence that it really existed.
Another key blunder is step #4 that is just plain wrong, evolution allows for non-functional and even functions that hurt survival.
Part 3b is actually another straw-man or misrepresentation of evolution because evolution does not say that the incomplete object in step #2 ever existed or must have existed.
It is a false assumption to think that any combination of parts an object is made of, minus one part, must have existed or been an actual step in the formation process. That doesn't even hold true for designed things.
For example, take a house. Remove its roof. (By the way a house without a roof still functions as a barrier suitable for keeping non-flying and bad-at-climbing things outside the house.) It is a false assumption to say that the house without a roof must have existed at sometime in the past.
It might happen that the typical order for building a house is bottom to top; foundation, walls, roof. But that is not the necessary order. You could easily build the house from left to right using scaffolding, instead of bottom to top. This is how additions or extensions of completed homes are done.
Another false assumption of IC is that removal of one part of something completely destroys ALL functions relevant to survival. See footnote [4] for more details.
[1] Breaking something into parts is completely subjective because there are always multiple ways to do that, and multiple sub-parts in each part down to sub-atomic particles. Even if you somehow had something with indivisible parts, there are still many ways to do that.
[2] The part removed is chosen carefully by the creationist to achieve the conclusion of the argument they want. It is not based on any empirical observation or scientific evidence. There is no evidence that the removed part was once not part of the whole object at sometime in history.
[3] Purpose and function is again subjective and depends on the person assessing the thing in question. If the person sees no obvious purpose or function, that does not mean there is none.
[4] This is false. Evolution does not require all parts being functional. There can be non-functional parts and even parts that hurt survival. What matters is the TOTAL survival ability of the individual, species, or greater group as a whole, not just the function of one part.

Welcome to Biology.SE! This is an impressive rant, but an ideal answer will contain supporting references. ——— You may also want to take the [tour] and then go through the help pages starting with [Answer] questions effectively on this site and edit your post accordingly. Thanks!

I see you didn't even take the time to read my answer, or you would not be classifying it as a "rant". As I explained, the OP's question is due to a philosophical misunderstanding, not any real empirical, scientific, substantial facts. The entire enterprise of philosophically breaking into parts, removing a part, and pretending that object existed is bogus. I responded to philosophy with philosophy. The experts on this site should have immediately identified it as such. How do you expect me to give supporting references for basic logical errors?

Thanks, I was just trying to address the topic in the most philosophically complete and detailed manner. I will add that irreducible complexity exists for one singular purpose: to stifle, retard, and even halt scientific progress that has been utterly devastating to religion in the last 400 years. IC was designed solely for that purpose by fundamentalist lawyers and philosophers at the ultra-conservative christian think-tank, the discovery institute. Micheal Behe is their pawn.

I think you comprehensive answer suffers due to the numerous problems in the question.

@user6552 - thanks for the strawman argument!  I pointed out at the beginning of my question that I was using a loaded, flame-baity title.  Maybe a bad idea - I thought this was a place that rational adults could look past it and focus on the content of the question.  You basically took the "bait", unfortunately, - and built an entire argument refuting my question by trying to refute "irreducible complexity".  Maybe you should look at this article https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2926753/ and let me know how it's different from what they are trying to solve.

"I thought this was a place that rational adult" Why would a rational adult use a word to describe an approach, then do something completely different? Did you mean "let me know how [irreducible complexity is] different from what NIH is trying to solve"? IC is completely different from that article, which is not a thought experiment and doesn't assert or conclude that something is philosophically non-functional, therefore can't exist by natural mechanisms. Again, your entire approach is bogus. Guessing a part to remove based on complexity or function will not yield any insight into history.

"what could the predecessor to a basic cell have been" is a valid question. "considering its complexity and the seeming interdependence on the pieces for the cell's survival" is NOT a valid approach to answering it. Complexity and function are subjective and superficially related but irrelevant to existence. The proper approach is to apply a validated scientific model on reasonably certain prior conditions. I disagree with everyone here who says my response is a straw man or rant (it is a valid philosophical argument against IC), but agree that IC should not appear in any scientific context.

"Again, your entire approach is bogus. Guessing a part to remove based on complexity or function will not yield any insight into history". It's nice that you've decided what's valid science or not.  Try searching for "reverse engineering biology" - I have no idea what is unscientific about this approach.

I wrote, "considering its complexity and the seeming interdependence on the pieces for the cell's survival" and you said this "is NOT a valid approach to answering it." It was never meant to be a valid approach - It's just framing the difficulty of the question.  Asking hard questions is a part of science - ignoring them or trying to label them as religious and anti-science is itself anti-science.

I didn't decide it was invalid, I proved it. Neither complexity nor function are scientifically measurable or have anything to do with existence. Asking philosophical questions is a part of pre-science, before you can even start doing science, which is executing the hypothesis/test/refine process of the scientific method. Nothing was ignored. You presented your philosophical method , I proved it isn't even testable. My question of how your method can be applied anywhere else, like in stellar evolution, was 100% serious. I'm genuinely interested if you can give any successful example.

Searching for "reverse engineering biology" I got this: http://philsci-archive.pitt.edu/12168/1/Can%20biological%20complexity%20be%20reverse%20engineered.pdf published in Studies in History and Philosophy of Biological and Biomedical Sciences. It's all perfectly good philosophy of mind, that may lead somewhere in the far future, once we have empirical substance to back up the imaginary reverse engineered system. But right now there is nothing reliable or scientific about IC or reverse engineering to discover history. Prior states determine history. Complexity and function does not.

@user6552 you are correct about IC. however, 1) simply leaving out "I'm pretty sure it was a religious fundamentalist that seeded your idea in the first place" could have made this much more cordial and productive. 2) OP probably meant to validly ask "what could the predecessor to a basic cell have been" as you said, yet you provided no answer to that.

“Irreducible complexity” is, as you seem to realise, a weasel term used to imply that a thing (like a cell) cannot have arisen from something simpler (or at least “different”). In that sense the answer to the question in the title is a clear “no”, unless we accept supernatural explanations for the origin of life.
You go on to state that the heart of your question is “what could the predecessor to a basic cell have been, given its complexity...”. I can strongly recommend the classic text of A.I. Oparin, “Origin of Life”, published in an English translation  in 1938(!).
This remarkable book contains a general exposition of the notion that living cells were preceded by “a gradual evolution of carbon and nitrogen compounds”, to quote the blurb of my personal copy.
The book is all the more remarkable in that its insights preceded the modern understanding of the nature of RNA and DNA - the type of “inheritance” with which the book is primarily concerned is not one of nucleic acid replication, but the relative abundance of specific chemical reactions - specifically, the so-called coacervates (spelt "coazervates" in the referenced book) and other manifestations of colloidal chemistry.

Eg, could I have had a cell without ribosomes and then some how it mutated to have ribosomes? It seem not, because a cell without ribosomes would never have survived/replicated.

The premise in the chain of reasoning that "we could hypothetically remove parts until we reach the bare minimum, but we can't so the cell came to be in its entirety is flawed". As populations evolve the organisms can gain and lose components. As an analogy consider the question of how humans can develop mouths. Our diet consists of chewing food which gives us energy to build structures like teeth and jaws, but we need teeth and jaws to chew food. A similar paradox. But of course we develop in the womb with an umbilical cord that we used to draw nutrients from our mothers that bypasses the mouth. This structure is not present in us after birth so we can't tell from looking at an adult human.

My question is, what would the step just before a "minimum cell" look
  like? Are there pieces we can take away and it would still be able to
  survive and replicate?

A very interesting question I think, but I also don't think it can be answered by looking at a modern cell and removing parts. The ancestor to cells may have lived through a very different system for example utilizing RNA to both catalyze essential reactions and store replication information as opposed to using proteins and DNA to do the same thing.


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Were Neandertals as Hairy as We Are?
What I mean to say regards facial and androgenic hairs.  There are many theories as to why some people have both kinds of hairs, while others have one or the same and others still have neither.  The best and most popular guess is that those hairs were secondary sexual organs, meaning that they just make the boys more attractive to the girls.
It's a well-known fact that hair provides insulation, and in the last ice age, Europe was dominated by a hominid built specifically to deal with the cold.  I am talking about, of course, the Neandertal.  Is there any evidence that the Neandertals, as a means of adaptations against the cold, were equipped with body hair?  If not, then would it be safe to speculate on such?

It is a good question (+1). You may want to have a look at this webpage for a quick summary of the discussion and different arguments about how hairy was H. neanderthalis. There are other threads online that explain more or less that there is no definitive answer but I failed to find a review in a peer-reviewed journal.

Just a detail about the form of the post: When you say There are many theories, (1) the correct term is "hypothesis", not "theory" and (2) you should link to a detailed explanation for hypothesis (or evidence if there is any in the post) that you talk about, especially when these aren't well known.

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

sort: votes


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What happened to the gypsy moth epidemics in the Northeast US?
I remember that back in the 1980s, 1980-1984, gypsy moths were a veritable plague in the Northeast United States. They were literally everywhere. Sidewalks were covered with their squashed bodies (of the caterpillar). You would drive through areas and every single tree would have dozens of nests. Every summer would be gypsy-moth-a-geddon.
By the late 1980s this completely ended for some reason. I sometimes see a gypsy moth caterpillar here or there, but it is a rarity.
What happened? Did a predator proliferate? Was there a pathogen or disease that wiped them out?

It appears that the gypsy moths were controlled by pesticide spraying by the US Forestry Service.
The defoliation areas measured peaked at 12 million acres in 1981 and again at 7 million acres in 1990.

In response, there was significant spraying of various insecticides starting from 1982 through 1996, peaking in 1990. This spraying managed to keep gypsy moth defoliation areas under 2 million acres since 1993.

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


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Co-dependency between carbohydrates, fats and protein in the mammalian diet?
Following up from the question Are carbohydrates an essential component of human diet? I am interested in knowing more specifically how carbohydrates, fats and proteins are linked in the mammalian diet.
For example, cats and other obligate carnivores eat mostly protein, so I imagine that protein has to be converted first to fat and then to glucose and other carbohydrates that the body needs. Does that mean cats are in a state of ketosis constantly? Do cats have special metabolic tuning to optimize on this metabolic pathway?
Human variations seem to suggest that such tuning exists. For example, (historic) eskimoes when fed carbohydrates tend to be especially likely to suffer from obesity and diabetes. This would suggest that their bodies are tuned to exist on protein and fat. What is this tuning?

What makes you think that cats consume mainly protein?

@AlexDeLarge The way that my cats growl at me if I try to take meat away from them.

But meat does not mainly consist of protein. Adult cats have a 26% (dry weight) protein maintenance minimum.

@AlexDeLarge Did you read the web site you just linked? It says a typical steak has 36g of protein and 7g of fat and 0 carbs. If we exclude bones, the typical mouse is made of 85%-95% protein and 15%-5% fat (depending how fat/starving the mouse is). Human athletes have less than 5% body fat, sometimes as little as 2%. All the rest is bone and protein.

Oh, yeah, you might be right. I actually did not think about that the non-protein parts could mainly have zero nutritional value. ;)

Or maybe Inuit are just prone to obesity if they overeat like all Asians

@GrahamChiu First of all, I was referring to all arctic Eskimoes, not just Inuits. Second of all, a lot of Inuits aren't Eskimoes. Third of all, Inuit tribes are located in Canada and Greenland, neither of which is in Asia.

I should have said Mongoloid


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Is blunt end repair and A-tailing necessary when adaptors can be custom made?
I'm planning on creating a RADseq library, which naturally involves digesting genomic DNA following P1 adaptor ligation. I've read a few protocols that require any over-hangs resulting from restriction enzyme activity (e.g MspI or Nlaiii) need to be repaired (blunt-end repair) followed by adding a single A nucleotide at the end so as to make the DNA fragments "sticky". But is this really necessary? Wouldn't it be more efficient to custom make P1 adaptors so that they have a complimentary 3 or 4 bp overhang specific to the restriction enzyme used instead?
What I want to ask is what are the practical advantages of having a single nucleotide overhang vs. 3 or 4 nucleotides?
Thanks in advance.


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What is the percentage of true bugs compared to all animal species on the plant?
Also, what is the percentage of True Bugs compared to the insect population?
I’m writing a children’s book on bugs and I’m comparing the true bug to the insect. All population info seems to combine the two. Please list sources.

Wellcome to Biology SE. Please could you explain what you mean by "bug" and "true bug". I'm no entomologist so I can only go on my Chambers dictionary, which defines bug as "a name loosely applied to certain insects…and specific to one (Cimex lectularis) that infests houses and beds". Is this what you mean? But it has nothing to do with plants. Or do you mean "on the planet"? Unless you clarify your question, I'm afraid you are not going to get the answer you are after.

@David I think "True Bugs" are usually defined as Hemiptera. Also, that article lists an estimate of 50,000 - 80,000 species of hemiptera. If you find estimates for total insect species and total animal species, you could get your own estimated percentages for each.

@user137 — Many thanks for providing this information. I'm sure many others besides myself will have been enlightened.


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How do neurons find each other?
Neurons form complicated networks in brains, but their connections can't be random (at least not entirely). Brains function similarly among all members of individual species, and that functionality is largely dependent on neuron organization. Furthermore, various brain regions have predictable functions, and there are even parts of the brain where specific cells carry out specialized functions (place cells are an interesting example).
Great! We know neurons can organize into very complex networks, but how? They need to find each other, somehow.
The best I can guess is that either:

Neurons find other target neurons with specific chemical signals.
Neurons don't "find" each other, exactly, but grow in predetermined shapes from from set locations. In this case, the connections would simply be due to neurons bumping into each other as they grow in their predetermined paths.
Or both.

In the first case, there would be a mechanism for searching each other out. In the second, there would be a mechanism for staying in one spot (and growing from there). What are the names of said mechanisms? How do I find out more about them?

I would add another mechanism: Neurons grow more or less randomly, and there is a mechanism eliminating those that formed "wrong" synapses.

Q: We know neurons can organize into very complex networks, but how?
The answer is your first guess: Neurons find other target neurons with specific chemical signals.
Q: What are the names of said mechanisms?
This process is called axon guidance, by which the growth cones of developing axons are directed to reach their targets. This process depends upon a slew of cellular and molecular cues. The first axons to grow in any particular brain region are called pioneer axons and are the most dependent upon these cues. Later axons are able to follow (and diverge from) previous axons by the interaction of cell adhesion molecules on their surfaces. Dendritic development is also important for your question, but dendrites tend not to travel as far.
Here are some of the molecules that we know to participate in axon guidance:

Cell adhesion molecules and substrate adhesion molecules, including IgSF CAMs and cadherins
Some chemokines, e.g. CXCL12
Netrins, ephrins, and semaphorins
Slits, via the Slit-Robo cell signaling pathway
Developmental morphogens, e.g. Wnts and Hedgehog

The list goes on, and this is an area of active research. Each of these cues is recognized by one or more specific receptors on the developing neuron, which upon recognition of the ligand molecule either attracts or repels the axon from (or both, depending on the context). Recognition can function either short-range (by direct contact with a ligand) or long-range (e.g. by detection of a concentration gradient), depending on the molecular cue.
For more information, you may want to read Sanes et al., Development of the Nervous System.

This is a very good question.
There are specific chemical signals, for instance:
1.) LRR proteins, which help signal neurons to each other. These are transmembrane proteins which are characterised by their leucine-rich repeat. They serve as some kind of protein labels for other neurons. These proteins are also known in pathogen recognition in our immune system.
2.) We also have Neurexins. This is a presynaptic protein that helps connect neurons in the synapse. They are known binding a family of proteins, the Neuroligins. Neurexins have actually also previously been implicated in autism/shizophrenia. The failure of the right connections likely lead to an incorrect balance of excitatory and inhibitory connections, which result in dysfunctions in neural circuits and consequently to such maladies.
https://en.wikipedia.org/wiki/Neurexin (wikipedia)
http://www.ncbi.nlm.nih.gov/pubmed/23931994 (research)
(http://) books.google.nl/books?id=qMe5BgAAQBAJ&pg=PA152&lpg=PA152&dq=neurons+predetermined+paths&source=bl&ots=LsYBkr431V&sig=ewc2geKBL1QUYogPXPh21tGC5Ww&hl=nl&sa=X&ved=0ahUKEwiTqJ3Z-YHOAhWLVxQKHcN2DI84ChDoAQgrMAI#v=onepage&q=neurons%20predetermined%20paths&f=false (book)
(http://) www.ncbi.nlm.nih.gov/pubmed/17868438 (research)
These sites could help out in further research (apparently I cant post more than 2).
There are probably many more proteins involved, but these are the main ones I know of, and the ones I have studied in my education. Scientists also often state that there is no predetermined path, but rather a rearrangement of neural pathways (I´d suggest visiting the third website link, philosophy of psychology page 152).
I hope this helped you out with your question, and if you've got more questions on how these molecules work with signaling in depth, I´d be glad to answer them.


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What is DNA-cellulose chromatography?
I am going through a paper where they have done DNA-cellulose chromatography to study the interaction between protein and DNA. They are adding the protein to the column and eluting with high salt concentration.

DNA-cellulose chromatography is used to purify proteins that bind DNA (Potuzak and Dean 1978, Abdullah et al., 1985).
The idea behind it is quite simple: you attach DNA to a cellulose matrix and keep conditions so that the DNA does not dissociate from the cellulose. This stationary phase is then used as a bait for DNA-binding proteins from the mobile phase. The purified DNA-binding proteins can subsequently be dissociated from the column with high salt concentrations.
The method was (as far as I know) first described by Litnam (1968) who used it to extract a DNA polymerase from Micrococcus luteus.


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Optimum pH of Catalase
I am aware that certain organs in the body have specific pH environments to increase the activity of their enzymes. I'm also aware that enzymes only work at certain pHs due to the configuration of the amino acid in their active site and the way this is altered as the pH is changed. What I want to know, however, is why their amino acids are as they are to begin with - has it got to do with the substrate molecules they react with? Particular reference to catalase would be helpful.

Are you asking about how the amino acids of an enzyme interact with the substrate molecule with particular reference to catalase?

It would be helpful if you could answer this for me but, in particular, I was asking whether there is any reasoning behind why the amino acids of an enzyme's active site are arranged in a specific way.

The optimum pH for catalase can be found be a simple search. According to the Wikipedia entry for catalase it is approximately 7.
With the exception of extreme pHs, which can cause denaturation, the pH optimum of enzymes is often related to the ionization of the amino acid residues that participate in the reaction (and hence their pKa). Often what happens is that the reaction mechanism requires a residue to alternate between an ionized and non-ionized form, so that the optimum pH approximates to the pH of half-ionization. (This may not be the same as the pKa of the amino acid in solution, as the environment at the active site can alter this greatly.)
You need to understand ionization chemistry to appreciate this. If you do not, you could try this section from Berg et al. first. If you do, look at the mechanism of action of well-established enzymes like lysozyme and the serine proteases.
I cannot help you further with catalase. Apparently it is not well understood.

Do you have any recommendations for what to read to understand the mechanisms as how reactants reach the Transition state without a catalyst? I'm finding all sorts of information but all are unrefrenced.

@Tytoalba — Heat. But you could post on SE Chemistry (or check previous questions there) for a more comprehensive answer.

I don't prefer asking there the answers are often not backed with references. (This isn't the right place to ask unrelated questions, I just don't know how we may discuss if you are interested).

@Tytoalba — I make a point of not doing discussions on this list. In any case my chemistry is rusty. However the Wikipedia entry on activation energy — https://en.wikipedia.org/wiki/Activation_energy  seems reasonable to me. In general, if you want some of the reacting molecules to be able to adopt the transition state without a catalyst, you need to put in the energy in the form of heat. (For particular reactions there may be other factors such as pH that would help.)

From your comment:

I was asking whether there is any reasoning behind why the amino acids of an enzyme's active site are arranged in a specific way.

After the binding of a substrate to the active site of an enzyme a series of chemical reactions occur at the active site. These reactions in turn convert the substrate into product. So for these reactions to occur a specific arrangement of amino acids at the active site is necessary.
Here's an example:
In the $6th$ step of Glycolysis Glyceraldehyde-3-phosphate is oxidised and phosphorylated to form 1,3-Bisphosphoglycerate.

This reaction is cataysed by the enzyme Glycealdehyde-3-phosphate dehydrogenase. The active site of this enzyme has two amino acids; Cysteine and Histidine. The side chains of these two amino acids participate in the conversion of Glyceraldehyde-3-phosphate into 1,3-Bisphosphoglycerate.
Mechanism:

The thiol group(-SH) of the Cysteine residue reacts with the aldehyde group of the Glycealdehyde-3-phosphate to form a Hemithioacetal.Its a nucleophilic addition reaction.
Then a H+ (proton) and a H- (hydride) from the Hemithioacetal moves to the imidazole group of His and the benzene ring of NAD+ respectively oxidising the Hemithioacetal to a Thioester.
The reduced NAD+ (NADH) then leaves the active site and is replaced by another NAD+ molecule.
Finally, a molecule of inorganic phosphate attacks the thioester and forms a tetrahedral intermediate, which then collapses to release 1,3-bisphosphoglycerate.

Thus after the completion of 1,3-bisphosphoglycerate formation the active site of the enzyme gets back to its original state. By state I mean that the H+ from the imidazole group returns to the Cys forming the thiol group of Cys.

So you can see that the specific arrangement of amino acids (Cys and His) at the active site was necessary for the conversion of Glyceraldehyde-3-phosphate to 1,3-Bisphosphoglycerate, had there been some other amino acids the reaction wouldn't be possible.Even if the amino acids had a different arrangement than what is present in the diagram, the enzyme would not be able to catalyse the reaction.
References:

Wikipedia
Biochemistry, 5th edition-Jeremy M Berg

Interesting answer, but you leave out catalase completely.

Yeah actually after seeing the question I was overjoyed as I found something on this site for the first time that I could answer and cited the enzyme from which I had understood the concept. I'll add catalase to the answer soon.

@Biology Student
I found two links that explain the chemical reactions taking place at the active site of catalase. I couldn't fully understand the mechanism so could not add it to my answer. Expecting you can comprehend here are the links:
[1]: https://en.wikipedia.org/wiki/Catalase#Molecular_mechanism
[2]: https://www.researchgate.net/figure/232700780_fig1_Figure-1-The-catalytic-reaction-and-HRG-mechanism-Active-site-of-catalase-the-haem


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How do centrioles auto-locate to opposite sides of cell during mitosis?
I realize that centrioles are made of 9 triplets of microtubulin wound together with a hollow core, and that they are responsible for the configuration of the spindle during mitosis. The spindle fibers attach to the kinetochores of the sister chromatids and pull, ultimately separating them in preparation for cytokinesis.
How do the centrioles recognize where to go in the cell, such that they are oppositely positioned with one another? Is the mechanism similar to how neurons "find their way" during development to forge the correct connections that give us sight, etc, but on a subcellular scale?

relevant paper http://www.nature.com/ncb/journal/v6/n7/full/ncb0704-581.html

During cell-division centrioles move towards opposite 'poles' and finally get attached to cell-membrane. Different factors influence & drives this process, most still not discovered. So this mechanism is largely unknown. From the scientific literatures published on this  matter till recently we can say that this process should include:

A structure along which the centrioles can migrate,
Molecules associated with the movement of centrioles,
Signal molecules triggering this process,
Signal molecules determining the direction of migration.

To answer 1., Microtubules form a intra & inter-cellular network along which subcellular structures can move. Actin & Myosin are also involved in some cells. For reference read Ganong's review of Medical Physiology. (the example you stated in your question about neurons is a substantially different process. But neurotransmitters are carried with the help of Microtubules. Chromosomal structures also are arranged with the help of them.)
For points 2,3 & 4 read this paper, these parts are very clearly described there.
Thank you.


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Can cell division be stopped during prophase?
There are three known checkpoints which ensure proper division of the cell.

These are: the G1 checkpoint, also known as the restriction or start checkpoint or (Major Checkpoint); the G2/M checkpoint; and the metaphase checkpoint, also known as the spindle checkpoint.

I wanted to know that is there any way cell division can be stopped during prophase(once it has started).

I'm unaware of such stop occurring at a mitotic prophase, but if your definition of "cell division" includes meiosis, the answer is yes: in several species, the oocyte stops at the first prophase (prophase I), in a resting phase called "dictyotene": https://en.m.wikipedia.org/wiki/Dictyate

Yes exactly right.


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What factors make a sequence evolve non-randomly?
On the wikipedia page about Fay and Wu's H, it talks about a non-randomly evolving sequence may be due to some selection acting or a selective sweep or population expanding/contracting. My questions about these factors that affect non-random sequence evolution are:

Does negative selection differ from a selective sweep because a sweep is a form of positive selection?
After a selective sweep, any rare mutations you see must have come after the selective sweep. Is it because they can't have come during it else they'd 'be diluted' by the positively selected alleles?
Population contraction can create a bottleneck, which makes all individuals come from a common ancestor. But how does population expansion make a sequence evolve non-randomly?

Fay and Wu test is a test that compare expected sequences under a standard coalescent theory model, that is a single panmictic population with non-overlapping generation of constant size $N$ and effective population $Ne=N$, that is the variance in allele frequency at any following generation is $\frac{p(1-p)}{2N}$, where $p$ is the frequency of a given allele. As such Fay and Wu (as well as Tajima's D and other tests) are not only test of selective neutrality but also tests of demographic neutrality as underlined in Nielsen 2001.
It may be hard to make good predictions about the extend and direction at which a given selective or demographic event will affect a given statistic such as Fay and Wu's H. Therefore, in answering the following questions, I am not specific to Fay and Wu's H. Also, answering the questions fully would require making an introduction to coalescent theory which is subject to a whole book rather than a simple post. To fully understand such test, you will need to follow an introduction to coalescent theory. You can have a look at the books recommended in the paragraph General Entry Books to Population Genetics of this answer.

Does negative selection differ from a selective sweep because a sweep is a form of positive selection?

Let's first clarify the terms just in case. Reduction in polymorphism at linked loci due to positive selection is called "selective sweep" while when due to negative selection it is called "background selection".
Generally speaking, selective sweep is much stronger than background selection. Also, selective sweep has a higher impact on Tajima's D, then background selection.
To my knowledge, methods trying to disentangle the two processes of selective sweep and background selection mainly use inter-species comparisons to infer what types of sequences are concerned. If The loss of polymorphism is adjacent to a highly conserved sequences and is found in related species, then it is probably background selection at play. If there is a fixed mutation that isn't found in related species and loss of polymorphism isn't found in these related species, then it is probably selective sweep.

After a selective sweep, any rare mutations you see must have come after the selective sweep. Is it because they can't have come during it else they'd 'be diluted' by the positively selected alleles?

A selective sweep indeed modifies the Site Frequency Spectrum (SFS, distribution of allele frequencies) to create an excess of high frequency variants (or a relative lack of low frequency variants). See wikipedia > Tajima's D

Population contraction can create a bottleneck, which makes all individuals come from a common ancestor. But how does population expansion make a sequence evolve non-randomly?

Population expansion yield to longer coalescent times and therefore lack of rare alleles. See the introduction of Excoffier et al. 2009 for nice explanation and figure.

Thanks! To clarify on the reasoning behind: "If The loss of polymorphism is adjacent to a highly conserved sequences and is found in related species, then it is probably background selection at play. If there is a fixed mutation that isn't found in related species and loss of polymorphism isn't found in these related species, then it is probably selective sweep." Is this because positive selection is an event that may occur in 1 species but not others, while negative selection would occur in all related species?

Yes, I think you got it. Background selection is a thing that is constantly occuring and therefore you would expect to see it in many related species. A selective sweep is a single event that is happen relatively fast in time (esp. in panmictic population) and therefore a loss of polymorphism is necessarily due to a relatively recent sweep and can therefore be witness in only few (if more than just one) related species.

I was thinking about the 3rd question again; my interpretation of population expansion is that longer coalescent times means less new mutations come up that stick around, plus the majority alleles 'dilute out' the rarer ones. Is this the case?

Population growth actually yield to an excess of rare allele (typically an excess of singletons; see Fu and Li test) (Eldon et al. 2015) and beneficial mutations have higher probability of fixation in expanding populations (Otto and Whitlock 1997)

Note understanding the consequences of different selection regime and different demographic events on the site-frequency-spectrum (SFS) is not an easy task. I do not have a perfect intuition either and people are still working out on understanding the impact on the SFS of particular events.


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Wouldn't it be more efficient to let the kidneys flow into the intestines?
So I was thinking about how much fluids we lose when we pee. Then I realised that it would be much more efficient to remove the bladder and let it flow into the intestines so that the fluids can be reabsorbed.
What probles would arise from letting pee flow into the intestines? Also, where would be the optimal place to let the pee arrive? In the small intestine or closer to the anus?

You want continuous diarrhoea, and kidney infections?

Then I realised that it would be much more efficient to remove the bladder and let it flow into the intestines so that the fluids can be reabsorbed.

No. This would be very, very bad.
First, the kidney is very good at water conservation when necessary. If you're peeing up a storm, then you're drinking up a storm.
It is much more efficient to flush out waste products through the kidneys, and simply drink when thirsty. So you pee a lot. That's ok. It all ends up in the water cycle.
But emptying the ureters in any part of the digestive tract would mean terrible diarrhea, the kind that your bottom would burn like crazy every time you went (and you would hardly be able to control it, meaning large laundry bills) unless you used a protective ointment barrier between your skin and your diarrhea. To keep that skin from breaking down (yes, breaking down), you would need to bathe your bottom after every bowel movement. And it just would not be as good for fluid and electrolyte balance.
Also, the urinary tract is relatively sterile, protecting the kidneys from infection. The GI tract is anything but. The result would likely be so many ascending bacterial infections that your poor kidneys would be scarred and useless at a young age.
Nope, nope, nope.

Urine is acidic. It would irritate the bowels. It would also react with and spoil chemicals in the intestines that the body wants to recover like thyroxine. In general, the intestinal pathway is for fat-soluble materials and the urinary pathway is for water-soluble waste.
The body can absorb water from urine. For example, camels have very thick urine. Thicker urine is more acidic, so the camel's bladder has to be tougher.


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Are these spider eggs?
I was pulling weeds in my backyard in Southern California, when I saw a spider over a white area on the underside of one of the leaves. It's staying right near the white spot. Are those spider eggs? Also, what kind of spider is this?

Yes, those are definitely eggs.  And I believe that is a female grass spider (Genus: Agelenopsis).

Eggs are typically laid in late summer or fall and spiderlings emerge
the following spring....A female that has mated with a male can produce more
than one egg sac. For some species,  it’s common to see two sacs at a
time, side by side, attached to a surface (such as the underside of a
rock, piece of wood in a wood pile, or in a rolled up leaf, for
example). Each different species of Agelenopsis may create a slightly
different egg sac, but typically each one contains anywhere from 50 to
200 individual eggs. The mother spider will remain near her eggs,
dutifully guarding them, until she dies around the onset of winter.

This seems to fit the picture to a T.  I'm not 100% about the species, but I believe it is either A. aperta or A. oregonensis.
Edit:
As user Xan pointed out, this could likely be a lynx spider (Genus: Oxyopes; likely species: Oxyopes salticus - female).  This would explain the defined setae (bristles) on the legs.  To really decide, you would need to check the following characteristics:

Eye pattern: Lynx spider eyes form an octoganal pattern, while grass spider eyes form two, parallel, curved rows.
Spinnerets: You would have to search for spinnerets on a lynx spider, while grass spiders have two very prominent hind spinnerets that you can visibly see from above.

I originally thought those were spinnerets in picture 3, but upon closer inspection it looks like one of the hind legs folded underneath.

Yes, that does seem to be about right. But the pattern on the spider doesn't quite match those species.

Can't say the species, but it seems to be a lynx spider (genus Oxyopes)


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What constitutes FDA's First in Class designation for New Molecular Entities?
What constitutes a First in Class designation for new molecular entities? I've seen this term on FDA documents, as well as in databases (Chembl for example), but I was curious if there are any set criteria for First in Class drugs? The easy definition, in my mind, would be a drug that hits a novel target given its indication. However, if you look at antifungal drugs, you see that drugs with the same target for the same general indication (anti-fungal) treat completely different fungal infections because of their pharmacokinetics.
Are there discrete criteria for the FDA's first-in-class designation for New Molecular Entities?

This page on the FDA website gives a rather terse definition: "Drugs with a new and unique mechanism for treating a medical condition". I'm not sure how that's applied in practice, though.

What is FDA? What is the biological problem regarding this molecule?

@David the FDA is the Food and Drug Administration in the US. Among other things, they are charged with regulating and approving pharmaceuticals.

@MattDMo — So the question is about public health policy in one particular country, and not about a problem in biology of the type defined in the [Tour].

"First-in-class drugs are ones that use a new and unique mechanism of action for treating a medical condition. These products are often referred to as innovative and cited as offering new treatment options for patients."
Lanthier, M. et al. (2013) "An improved approach to measuring drug innovation finds steady rates of first-in-class pharmaceuticals, 1987-2011." J.Health Aff. (Millwood) 32:1433-9;
Pharmaceutical Research and Manufacturers of America. 2015b. Innovative Oncology Medicines Have Led to Impressive Gains in Patient Survivorship. Retrieved August 26, 2015. <www.phrma.org/innovative-oncology-medicines-have-led-to-impressive-gains-in-survivorship>."
From: Lexchin, J. (2016) "How Safe and Innovative Are First-in-Class Drugs Approved by Health Canada: A Cohort Study" Healthc. Policy 12:65-7.

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How diverse are species in remote, isolated areas on Earth?
If we consider land areas that have been largely isolated from each other from a human point of view, but with a similar climate – for example, a part of Europe and a part of Americas with a similar climate before the time of Columbus – generally how different can one expect the flora and fauna to be between the places?
I realize there can be quite different approaches to measuring the biological differences. Not being a biologist, I probably miss some quite important metrics. Some ideas that come to my mind:

How distinct are the species in each environment? For example, can we expect to see the same ant species? Same grass species? Same bacteria?
DNA difference based approaches: How much of the DNA material in each environment does not exist in the other one? How large a proportion of organisms in one environment does not have a close relative on the other, given some threshold closeness value?
Historical approach (probably overlaps the DNA approach quite a bit): How long ago (alternatively: how many generations ago) did the common ancestor of similar organisms in each environment live? Do the organisms share this number, i.e. is the common ancestor of, say, humans in Europe and America as ancient as that of ants and grasses?

You might narrow this down a bit. There are q number of questions, and to answer them all, the answer would need to be quite long.

The concept that you hint at, has been studied at the example of the island of Australia, where marsupials often look quite similar as their counterparts in the same ecological niche, which live outside Australia and have a placenta, and are less related on the DNA level (e.g.: squirrel-like animals, wolf-like, and the now everywhere extinct saber-toothed tiger-like...).
If you are interested to learn more, I would highly recommend to read Jerry Coyne's "Why evolution is True" ( http://jerrycoyne.uchicago.edu/index.html )
The specific example of Europe and Americas (which does not fully capture the complexity of your question), also is quite interesting - although it is very short on an evolutionary time-scale. E.g.: American squirrels, which lack predators in Europe, and only arrived in Europe because of human journeys following the rediscovery of Americas, are partially outcompeting the beloved red squirrels ( https://en.wikipedia.org/wiki/Eastern_grey_squirrels_in_Europe )


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How to use Transect-based sampling to select sample trees
I was wondering if you help me how to use Transect-based sampling to select sample trees

More detail on what your studying, the question you want to answer, and how you want to go about doing it would be very helpful. But I can answer this basic question of how to select tree's with a transect.
You will need:

Forms to fill out for data.
A compass.
A transect tape (really a very long tape measure, about 100 yards or meters).
A sampling design that fits your study. (I'm assuming you already have this, but if you want to talk more about it see above.)
A wooden meter stick.

Once you are in your 1st area and ready to select a random subset of trees.

Pick a random spot. (Usually done by throwing a stick or water bottle over the back of your head and going wherever it lands).
Pick a random number between 0-360. This will be the random direction you go in from your random spot. Find north on your compass, then which way your random number points. In your mind mark a way point in that distance you can walk to (a mountain peak, a distinct tree, anything).
Stick the beginning of your transect tape in the ground and start walking. The length that you walk should be predetermined from your study design.

Now you'll select trees to perform whatever measurement that you've decided on. But how? Most forests are not so dense that a straight transect tape will touch many of them. This is where the meter stick comes in. Walk back down the transect and choose any tree that comes within 1 meter of the tape on either side. Is the forest not dense enough to include enough trees that way? Then simply increase the length of your transect, or length that you measure out from the transect (ie. 2 meters, or 3 meters).
This is technically called a "belt transect". And it used in natural resources to measure things that are abundant, but not very dense. Such as trees in a forest or shrubs in the desert. It is essentially a giant quadrat.
Why all the randomness? Humans are naturally bias. Even if you think you are not being bias, you could subconsciously be choosing a starting point in a dense patch of trees, or a direction that will let you measure your favorite species. A rigorous study relies on a random sample of a population of interest, and small non-random decisions like this means it is not a random sample, but a bias sample.

Thanks for the prompt reply. Some detail about my study I want to investigate the effect of browsing on above ground carbon-stock in boreal forest. I have two treatments browsed and unbrowsed. 20 x20 meters plots are randomly selected to exclosure or unexclosed plot on the site. Each plot has four subplots measure a radius of 2 meters. To measure the carbon stock I need to transfer sample trees to the laboratory. I want to select a total of 80 sample trees. I found out Transect-based sampling will easy method to select my tree sample. let me know if you need more detail.

Hmm, based on what you said you should do it a bit differently. Within each 20x20 meter plot the 4 subplots should be placed either randomly or at equal intervals.
If you will have enough tree's with this will depend on the tree density. You can increase the radius or number of subplots to account for this.


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Viruses affecting transmission capability of mosquitoes
I've read about bacteria affecting the transmission capability of mosquitoes. For example:

Wolbachia suppresses dengue transmission
When mosquitoes were given antibiotics that decreased their gut microbiota diversity, they became more susceptible to malaria infection

Have there been any studies to show that the presence of certain viruses/viral diversity (rather than bacteria) has an effect on the tranmission of other viruses/pathogens?

There have been some studies looking at this, but not many. One is this study which reported an interaction between Aedes densovirus (AeDNV) and dengue virus (DENV) in Aedes albopictus: mosquitoes already infected with AeDNV were more resistant to infection with DENV, although DENV infection appeared to accelerate the replication of the existing AeDNV infection. A similar interaction was not seen with chikungunya virus (CHIKV).
In addition there are indirect interactions between pathogens of all kinds - viruses such as AeDNV which kill a high proportion of the mosquitoes they infect reduce the average survival and population density of the vector and therefore the ability of the local population to transmit disease (ref).


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How do red blood cells survive without a nucleus?
I was reading this question
Why do mammalian red blood cells lack a nucleus?
According to my understanding, a nucleus is the cell's control center (like the brain). All the functions in the cell are carried out according to  the nucleus's command.
Then how can a red cell survive without a nucleus? Why does it still perform all the functions correctly without the nucleus?

I think the loss of nucleous renders the structural protein synthesis of Rbcs but their further survial depends upon the ir initial metabolic process which help them to survive till their periods.

As explained in the previous answer, the RBC loses its nucleus only at maturity. The nucleus contains the DNA and which can in turn produce protein. No nucleus means - no protein/ mRNA synthesis. Also, obviously, the cell loses its capability to divide.
Hemoglobin too is a protein. Knowing that it would lose its nucleus, hemoglobin is synthesized in the precursor stages of RBC. A mature RBC can not synthesize new Hb. Hence, the RBC keeps ready its store of enzymes and structural proteins (not only Hb, all proteins it would need for normal functioning) since it can not form new stuff once it has lost its nuclues.
The lack of a nucleus also limits the cell's repair capabilities. So human RBCs are cleared from circulation once they are about 4 months old. Damage (mostly from oxidative stress) to their structural proteins leads to loss in membrane flexibility. Since, the RBC can't replace the stuff, it gets gulped in by macrophages.
It is not surprising that the cell doesn't have a nucleus. The loss of a nucleus renders it better oxygen carrying capability. Even platelets donot have a nucleus. There too, enzymes are prepared and stored beforehand.
Hope that helps!

Probably worth mentioning that RBCs don't hang around that long - about four months in adults.

@arboviral, I thought so, but then, there are WBCs too which last for just a week! But I'll add in something like that!

True - I guess 'not that long' is subjective...

@Polisetty so the nucleus only produces proteins to help the cell in fuctioning properly? And if the cell already has those proteins then will it function properly and won't need a nucleus?

@Adi Technically yes. At least for cells like RBCs which can be thought of just as a truck carrying around oxygen. For other cells, which need to perform more complex functions and modify their protein synthesis in response to stimuli/hormones, the nucleus is required. And since almost all cells do, RBCs and platelets are considered an exception.

"No nucleus means no protein/mRNA synthesis." Just a technical note: this is not generalizable. No nucleus means no transcription, but translation of (e.g. stored or previously made) mRNA can occur, and this happens elsewhere. RBCs actually lose their ribosomes (translation machinery) later than their nuclei (when they are reticulocytes), and only completely mature RBCs lack both. This suggests that translation, especially of hemoglobin subunits, might be occuring after denucleation - which makes logical sense.

I feel like a fair analogy could be made between a mature red blood cell and a space satellite. Satellites are launched with all the structure and consumable resources (fuel) they're ever going to have. In that state, they can operate for quite a long time, but eventually fuel runs out or key components wear out from radiation damage or micro-meteroid collision, and the satellite is commanded to leave its operational orbit (sometimes, to burn up in the atmosphere).

How are "too-old" RBCs recognized for destruction? I.e. what are the mechanics and what is different about an old RBC versus a new one that other bodily systems could use to distinguish the two?

Frankly, I find 100+ days to be quite long. It's surprising that a lipid bi-layer could be stable for that long, without needing repair. Quick searches show that the RBCs have a lot of actin in the membrane, so presumably this adds strength and longevity.

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text:
Quantifying the number of fragments from RAD library
I have a series of single-end reads from a RAD library of 48 uniquely tagged individuals in fastaq format. The data comes from a small MiSeq run. I want to know the number of unique fragments per individual/barcode, but I'm not sure how to go about getting that number. I'm new to bioinformatics, but I was able to use Stacks to demultiplex the library using the process_radtags function.
Could someone help? Thanks!

Do you mean the barcode in the FASTQ header?


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Kinetics and de novo protein prediction

De novo conformation predictors usually function by producing candidate conformations (decoys) and then choosing amongst them based on their thermodynamic stability and energy state. Most successful predictors will have the following three factors in common:
1) An accurate energy function that corresponds the most thermodynamically stable state to the native structure of a protein

This is an excerpt from Wikipedia. I have a very, very limited understanding about de novo protein prediction so here goes.
I asked the post-doc I'm working with about whether there are kinetic barriers to protein folding. Yes, everything wants to be at an energy minimum, but sometimes that just can't happen due to kinetic barriers (the reason your diamond ring doesn't turn into graphite/pencil "lead"). So, why does protein prediction software look for energy minimums? Do they also consider activation energy barriers? Do they take into account the presence of chaperonins? Are there examples where the thermodynamically most stable protein conformation is not the biologically active protein? The post-doc told me that perhaps most proteins do reach their thermodynamically most stable state. True?

Generally speaking, structure prediction programs look only at the thermodynamic minimum, without consideration of the kinetic trajectory of folding.
The main reason for this is mostly time considerations. It's very difficult to accurately model the true folding pathway of even a moderately sized protein. With special tricks and a bunch of computing power, we're barely able to simulate a folding trajectory of small, simple proteins. We aren't (yet) able to do so with anything of reasonable size.
Instead, what protein structure prediction programs do is take a shortcut, skip the physically-realistic folding simulation, and instead look for low energy models, with the assumption that these low energy states will look like the natively folded proteins.
(One such program I'm familiar with - Rosetta - effectively takes small backbone structures already seen in crystallized proteins, stitches them together and asks if that looks like a reasonable structure for the sequence. If not, it tweaks which backbone fragments it uses, repeating until it gets something it thinks looks good.)
This assumption - that the native structure of the protein is the global energy minimum - is called Anfinsen's hypothesis. One rationale is related to Levinthal's paradox: unlike simple chemical reactions, a protein folding trajectory has too many degrees of freedom for even nature to exhaustively sample all conformations. This implies that stably folded proteins evolved with well defined "energy funnels" - that is, the energy landscape of well-folded proteins is such that the folded form is "downhill" from a large number of potential states. Since a large number of potential states need to point toward the folded form, this implies that the local minimum of energy which is the folded form is also likely the global minimum of folding.
The energy differences in protein folding also tend to be small - it's relatively easy for proteins to climb back up of local minimums and go elsewhere. Without the strong, global energy funnel to direct them toward a stable state, it's difficult to keep proteins from unfolding and refolding. This is why kinetic considerations like controlling the trajectory of folding from a ribosome, or having special chaperonins don't really work. Because chaperonins are catalysists, they change the rate of the reaction they're involved in, but not the equilibrium. Microscopic reversibility means that any protein which randomly collect enough energy can use the chaperonin to escape the dead end it was put in: it's not a one-way gate.
Now having the kinetic minimum be the thermodynamic minimum doesn't have to be the case - it's just the case for the vast majority of proteins we've seen. There are certain systems where we're pretty sure the normal folded form is in a local kinetic trap, and with time it can escape into a more stably folded version. Amyloid fibrils and prion proteins are thought to be one such instance. The normally produced version is in a low-energy kinetic minimum, but over time or through various interactions with amyloid or other prion proteins those proteins can relax into an alternative, lower energy conformation.
The keyword here for future literature searches is "kinetic trap". Some kinetic traps are very short lived (microseconds), but other may be longer.
Finally, I'll point you to the paper "The Protein Folding Problem" by Dill et al., which is a good review on the topic of protein folding.


text:
Why do we have wrinkly fingers after swimming?
I found an explanation for my question here http://www.pitara.com/science-for-kids/5ws-and-h/why-do-we-have-wrinkly-fingers-after-swimming/, which suggests that water washes out sebum (special oil, which covers our skin) and water gets into outer layer of now unprotected skin by osmosis. This article also suggests that fingers are not really shriveled - they are water-logged. But is this right? I think I observed many times my wrinkly fingers after swimming, but I never felt that they are water-logged. Any thought on this matter would be highly appreciated.

One more paper to add: https://www.scientificamerican.com/article/why-do-our-fingers-and-toes-wrinkle-during-a-bath/

Great question, for which still no definite answer is known despite ~100 years of research.
A simple physical basis for the wrinkling however seems unlikely as glabrous skin without sweat glands does not wrinkle, and as wrinkling requires the activity of specific nerves.
Moreover plausible evolutionary ideas, which used to be popular, such an anticipated improved ability to grab, don't appear that clear in newer experiments.
For the information above, and an even more detailed answer, please see Haseleu, Omerbasic et al. 2014 http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0084949


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why do overweight individuals sweat more than ordinary people?
A common phenomenon that I have noticed while traveling in buses is that overweight individuals seem to sweat a lot more than people with ordinary weight. Is this a coincidence or is there some science behind this?

This study found that only 2.3% of the variation in whole body sweat loss was explained by body fat. However, body size had greater effect. Could you update your question to include a link to reputable evidence that overweight individuals do sweat more?

@Michael_A The study is about exercise and is not ceteris paribus with the study of obesity on sweat.

The question is based on an anecdotal observation of obese people sweating a lot on buses.  So no the study is not an equal comparison, the study is superior; they specifically isolate the effects of body fat on sweating. It is specific to exercise but what would be equal evidence, does the study need to involve buses?

Well there are some overall, simplified answers, but every individual is ..well.. individual.
First there is the ratio of volume to area. As interaction between two mediums normally is depended on their common/shared surface. If we state, that an overweight person A has more volume than a skinny person B of same height, A also has a larger surface as B, but not in the same scale the volume is increased.
The easiest way to describe is with spheres, let's assume bellies are kind of spherical ;-) . A sphere with diameter 2r=1d (hint: one dimension) has a surface of π4r²=πd² (hint: 2dimensions; 2nd power 2²=4; d²=(2r)²=4r²) and a volume of $$\pi\frac{4}{3}r^3=\pi\frac{8}{6}r^3=\pi\frac{1}{6}d^3$$ (hint: 3dimensions; 3rd power 2³=8).
So, if we manipulate r it's manipulated to the 2nd power for surface and to the 3rd power for volume.
So, if we double the radius, we have 4 times the surface, but 8 times the volume.
Humans are biochemical machines, we take an energyform we can exploit to fuel our processes keeping us alive. These processes also produce heat, which is kind of a nice sideeffect allowing us to operate in cold climate. But in hot climate we need to get rid of the heat.
As I stated before, interaction is surface based. Person A has a lot more heat producing volume than B, but the surface isn't that much bigger, so A's surface has a higher urgency to interact with the medium around than B's surface (so more sweat for example). Also more tissue produces more heat. But again disclaimer: different tissues have different activities.
Furthermore fatty tissue has an insulating effect, which reduce interaction even more. Other way round the heatloss of an overweight person isn't as dramatic as for a skinny person in sudden cold.
But these are simplified answers, there's much more to it. Like bloodpressure, thyroid, biological activity. Which can be influenced by so many more things.

Great answer! It would be great to get more about primary and secondary factors of sweating.

It would be great to get sources here.


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Role of the Hypothalmus in the control of Blood Sugar
In homeostatic regulation of blood glucose, the receptor and effector is the Pancreas, but how does the control centre — the Hypothalamus — connect and link into this process?

Welcome to Biology Stack Exchange. At the moment, this question risks being closed for not showing an attempt at prior research, and possibly for being 'too broad'. https://en.wikipedia.org/wiki/Blood_sugar_regulation describes blood sugar homeostasis in some detail. You could improve this question by pointing out why you think something important is missing in Wikipedia's description of the system, and asking specifically about the missing part.

I've made your title more specific (and hence more useful), although I tend to agree with @bshane. I don't like, but refrained from altering, your references to "receptor" and "effector", as in the field of endocrinology they have different connotations at the molecular level. You might consider a simpler statement like "In homeostatic regulation of blood glucose, the pancreas plays a major part. Is the hypothalmus also involved and, if so, how?" or "…the hypothalmus is also involved, but how does it influence the pancreas" if that is what you mean.

Your question doesn’t make it clear whether you think that the pancreas must be under the control of the hypothalmus, or whether you are asking whether it has an influence on the pancreas in relation to the secretion of insulin and glucagon, which control the concentration of blood glucose.
First, it has been long known that secretion of insulin can be influenced by the concentration of glucose in isolated pancreatic islets in vitro, so it can not be true that the effects must involve the hypothalmus. This is implicit in most book or general information articles you might find on the web, but for an original reference a review by W.J. Malaisse in Diabetologia 9, 167–173 (1973) seems highly cited.
I know almost nothing about physiology, but on searching the web for the role of the hypothalmus in glucose homeostasis, found a most readable prize-winning postgraduate essay on the topic by Syed Hussein of Imperial College London. I trust that it is in order to append an edited extract of this:

How does your brain control sugar?
  …altered delivery of glucose to specific parts of the hypothalamus can change insulin, glucagon and glucose levels [2]. …alterations in hormones and nutrient sensing by the brain in rodents leads to marked changes in glucose control. Evidence suggests that distinct regions of the brain have roles in controlling blood glucose in response to changes in glucose, insulin and fatty acids [ref]. These discrete brain nuclei regulate glucose output from the liver, insulin resistance, counter-regulatory responses to hypoglycaemia, glucose-stimulated insulin and glucagon release from the pancreas.
How does your brain tell the pancreas and liver what to do?
  …blood glucose levels and hormones, such as insulin and glucagon, are influenced by the autonomic nervous system [ref]. This system …consists of two parts: a sympathetic nervous system which deals with ‘fight or flight’ responses such as stress and a parasympathetic nervous system which deals with ‘rest and digest’ and ‘feed and breed’ responses. This system arises in the brainstem of the brain and is under the control of the hypothalamus. Nerves from the autonomic nervous system innervate almost every organ in the body including the cells and blood vessels of the pancreas and liver. The ‘wandering’ vagal nerve, a key component of the parasympathetic nervous system, is shown to play an important role in this. This nerve is necessary for the brain to influence blood glucose. The autonomic nervous system can influence insulin release, glucagon release, liver glucose output and even the size and number of insulin producing cells in the pancreas [ref]. …Exactly how these nerve fibres regulate hormone release is still being slowly unravelled [ref].

The essay cites references which you may wish to follow up for further information.


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Mitochodria's Role For Neuron Regrowth
Recently an interesting study has reported.  Zhou et al., 2016. J. Cell Biol. http://dx.doi.org/10...3/jcb.201605101
According to this study, enhancing anterograde axon transport of mitochondria is essential for regeneration of injured axons.
Neurons need a large amount of energy provided by ATP to extend their axons when they are injured. Mitochondria transported to axons produces
ATP which is necessary for that.
This study shows that in mature neurons, the motility of mitochondria is reduced and the reduced mitochondrial motility might
be the cause of the deficit in regrowth capacity of mature neurons. Moreover, this study found that enhancing mitochondria transport enables mature neurons to recover their regrowth capacity.
It is said that mature neurons typically arrest their cell cycle and fail to proliferate and regrow. However, considering the fact that
only enhancing mitochondria transport enables mature neuron to recover their regrowth capacity, I can't help but doubt the commonly accepted theory.
Do mature neurons actually not arrest their cell cycle？
What do you think of this finding ？

Why do you think this contradicts the fact that neurons are cell cycle arrested? There is no DNA replication or cell division, and mitochondria can proliferate independent of cell cycle as well.

Sorry that I couldn't convey to you what I wanted to tell.

Sorry that I couldn't convey to you what I wanted to tell. What proliferates isn't mitochondria but axons are. Moreover, only enhancing mitochondria transport to axons enables even the mature neurons to regrow. So, I doubt if the mature neurons actually don't arrest their cell cycle.

Axons grow but that is not same as cell is proceeding through cell cycle. Cell grows in size but there is no cell division. It is still arrested. However during this process some growth related genes are upregulated which are also upregulated in actively dividing cells.

I got it !! This report doesn't  observe whether some growth related genes are upregulated  or not. Thanks!!

Okay. Does this answer your question? I shall post this as answer, in that case.

ok, please post this as answer

Axons grow but that is not same as cell is proceeding through cell cycle. Cell grows in size but there is no cell division. It is still arrested. However during this process some growth related genes are upregulated which are also upregulated in actively dividing cells.


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Contradiction to evolution
It is said that evolution occurs according to requirement ..if it is true then women who really needs safety should be strong and men who don't should not be strong...isn't it contradictory?

Why don't men need safety? Evolutionary men were supposed to protect the woman while they are weak (pregnancy, caring for small children).

It is not.
The result of an evolutive adaptation depends on different kinds of selective pressures. So, the solution can be more complex that you may expect and there can be more than one solution to the same problem as well.
To stick with the example you made. One possible solution could be to have stronger females (note that this is true for many species of insects for example) another solution could be to have cooperation among the two genders and have for example stronger males that protect the females.
Also, you have to take a broader look at the effect of one particular trait because its evolution doesn't need to answer only a single problem but to fit in a context. For example to have a bigger and stronger body can be a problem if you don't have enough food to sustain it, so that particular solution, that looks obvious at first, can lead to a suboptimal result in a determinate context and can be counter-selected in the long run.
Moreover, especially in the case of social animals, the social context affect the evolution as well. For example, you may have a society in which strong woman are less likely to have children because of some social rule rather than because of some strictly-environmental reason. If we as a society, again just an example, decide that only girls taller than 190cm shall reproduce, then after a few generations you will have selected that trait.
Finally, remember that evolution doesn't propose the only "good" new traits, it proposes "random" ones, you never know in advance whether they will be useful in future or not.


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What is this - nest, eggs, fungus?
Anyone know what these are? I found them in our local park today attached to a wooden earth-retaining wall.I was thinking some kind of insect nest/egg sac (spider?) They're about the size of a medium egg (hen's egg!)

Welcome to Biology Stack Exchange. It would help if this question had a few more details: where was this photo taken (country / state is probably enough)? What season was it taken in? What was the weather like? What's the vegetation like in the local area?

A Google Image search for "wasp nest" returns a lot of similar looking photos.

It looks like you've opened it up, did you see anything inside it?

@C_Z_ Wasp nests and some similar things already have openings on the bottom or side. Would be safer to keep a distance and watch if anything goes in or out. Or maybe poke it with a long stick and be prepared to run away.

@AL Good point, I was thinking it was probably an egg sac but if there's a possibility that it's a wasp nest you definitely don't want to go poking around in there.

Thanks for all your comments. Some more info: Location is in Oxfordshire, UK - inland, not near any water. Photos taken in a local childrens' play park so lots of grass and some trees etc around. I haven't touched the nests/egg sac! I did notice one looks like it's got a hole in the bottom but on closer inspection it's actually covered over so I'm not sure that anything has left it. Sorry the pictures are a bit blurry - it wouldn't let me upload the originals - files too large.

Updated Answer:
Why it's not the egg sac of Argiope aurantia:
Upon knowing your location to UK, we can rule out quite a few spiders, especially the Argiope aurantia since it is endemic to Northern and Central America.  The spider's egg sacs are also noticeably smaller than "a hen's egg" as this post describes.
Why it's not a gall:
We can rule this out since it appears to be located on a wooden fence post.  Galls require living plant matter to grow.
Why it's not a wasp nest:
There are not wasps that produce threadlike materials. Wasp nests are made from fibers of dead wood and plant stems mixed with saliva of the wasps, and no webbing or threadlike material.  In the picture, we can clearly see some white 'webbing' between the gap of the fence posts directly underneath the mass.
So I really think it is an...
Aethalium of a slime mold:
Given the location, described area, spreading pattern in the picture, and apparent spongy texture of the mass, this looks to be the aethalium (or fruiting body) of a slime mold.  My guess would be in the genus Reticularia or Enteridium, which are typically seen in its reproductive phase as a white 'swelling' on standing dead trees in the spring, or on large pieces of fallen wood.  For example, Enteridium lycoperdon are common throughout the UK and are commonly associated with pine trees, the most common wood used to make fences in the UK.

*This post was edited from my original response.  Please refer to the edit history concerning the previous answer.

There is no web in the photo in the question though, wouldn't that rule out the spider?

There appears to be some webbing directly below the mass (in between the fence posts).

To me that looks more like the building material of the best than it does a spider web.

There are not wasps that produce threadlike materials.  Wasp nests are made from fibers of dead wood and plant stems mixed with saliva of the wasps, and no threadlike material.  My vote still stands as a spider egg sac or a fungi of some sort, such as a puffball.

I agree. This looks lika a slime mold to me


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A and AB blood types from B and O?
My grandma is O- blood type, my grandpa is B+, but my mother is A+ and my aunt is AB+.
Is that possible?
I've just looked at different sources like this and all of them are saying that from O and B, comes only B or 0, and A and AB are forbidden.
How can my mother be a child of my grandparents and how my aunt can be a child of my grandma at all? Or can we 100% say that they are not the real children of those parents, assuming that all blood types are correct?

maybe your grandmother is not really O negative or your grandfather is not B positive

Maybe, but I doubt so. Because my grandma was hospitalized (including surgeries) multiple times, and my grandpa was tested for his driving license.

It is correct that O- and B+ parents cannot produce biological children with A+ and AB+ blood groups, with the exception of a few rare edge cases.
Firstly, as noted in the other answer, your grandmother may have the Bombay phenotype. However, this is unlikely, due to the fact that she has been previously hospitalised and it was not noted.
Another unlikely possibility is that your grandmother is a genetic chimera. This means she would have two sets of genes, and her bone marrow hematopoietic cells had the O- genotype and phenotype, while her reproductive cells had an A allele.
If we exclude the rare edge cases, then it is strong evidence that your mother and aunt are not the biological children of your grandparents, and you should consider performing genetic testing to verify this if you wish.

Wouldn't a wikipedia link to genetic chimera be better than a link to a clickbait site?

@Pyritie I thought the "clickbait" site had more detail and was better as a case study, but the wikipedia page works too.

Assuming true paternity and correct ABO blood type detection, your grandma could likely have a Bombay phenotype (h/h blood group), which would make her blood look like the O type: http://www.ncbi.nlm.nih.gov/books/NBK2268/
This means that she would be double recessive to (and therefore lack) the H antigen, which is a precursor to A and B antigens. She would actually be AO or AA (genetically speaking) when it comes to the ABO group.
EDIT: As noted in the comments, this is indeed an extremely rare blood type, troublesome for transfusions, and should have been noticed prior to surgery. Other hypotheses are of course entirely plausible (another father, chimerism, etc.). But I think we can't discard it yet until the OP does some more extensive testing, as the transfusion issue could be handled by autologous blood transfusion or a very well stocked blood bank. Alternatively, the phenotype could be Para-Bombay, meaning that a little H antigen is produced and turned into A/B; this could be slightly more manageable for transfusions.
Sources:

http://www.bloodjournal.org/content/90/2/839.long
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3658345/
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3658345/
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2652237/
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3159258/
http://www.jcbsonline.ac.in/Articles/jcbs%20-%201%20(3)_39-42.pdf
http://www.ijbti.com/archive/2016-archive/100023IJBTINS2016-suraci/100023IJBTINS2016-suraci-full-text.php

Maybe unlikely since, the OP mentions surgeries and Bombay blood is difficult to procure.

Isn't that actually like to say that my grandma group wasn't correctly determined? Or you meant that in the case of Bombay phenotype it's not possible at all to be correctly determined according to the ABO group?

@lalamer Someone with Bombay phenotype will appear as O in standard ABO testing regardless of their actual genotype. This is known as epistasis

Is there any other way except this Bombay phenotype?

@lalamer (and expanding on the comment by March Ho) ABO typing is firstly done with specific antibodies for A and B antigens (anti-A and anti-B), which induce clumping of the blood accordingly; i.e., A blood is clumped by anti-A, B by anti-B, AB by both, and O by none. If there is no H, then neither A nor B are produced or detected by the basic test; you would have to verify this by adding anti-H. An additional note: ABO and H are synthesized by two different enzymes encoded by separate genes (http://www.ncbi.nlm.nih.gov/gene/28 and http://www.ncbi.nlm.nih.gov/gene/2523).


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Validation by PCR of a lowly expressed gene in microarray
I am interested in validating the precence of a gene (FETUB) whose expression is in the lower quartile of the microarray (see figure in link).
https://drive.google.com/open?id=0B82aQne0d_mYWlFiMjRlb05CUVU
Do you think this gene would be detectable by PCR?
Thanks

If your lab is lacking specific expertise on qPCR, and you need a sensitive and quantitative readout of transcripts, branched DNA single-molecule FISH may be less work than PCR ( while also being more sensitive and quantitative than RNAseq etc. )

If it was detectable in a microarray, the odds are very good for RT-rtPCR. If you are designing your own primers, make sure they span an exon junction, or if the gene is intronless, then span the UTR to exon junction to avoid amplifying DNA.


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Does the body have a mechanism for cleaning plaque buildup in arteries?
Is there a self synthesized substance in the body, or a mechanism that can break down plaque in arteries ?

Could you elaborate the question and make it more specific? There is a mechanism of thrombolysis and fibrinolysis if that i what you are asking for. https://en.wikipedia.org/wiki/Fibrinolysis and https://en.wikipedia.org/wiki/Thrombolysis

@Polisetty , I mean a mechanism to clean plaque buildup on arteries, i will edit the question.

@Polisetty The links were helpful too, but i understand that it only deals with blood clots.

Unlike the clots, plaques are a part of the pathological endothelium and actually cant be cleaned as such. Though, the cholesterol can be drained out by HDLs. By intervention, balloon angioplasty and the like can clean it up partially. So, again the answer differs based on what you're looking for.

@Polisetty  So in that case, i guess the answer could be an elaboration on the "cholesterol can be drained out by HDLs" part.

Yes, ldl can be removed once the level falls low enough I.e. Below 1.7 mmol/l.

Atherosclerosis can be reversed to some extent by certain diets and change in life style that result in decrease of excessive weight, blood pressure and cholesterol levels.
Studies
1) Dietary Intervention to Reverse Carotid Atherosclerosis (Circulation, 2010)
In a study in Israel, in 140 participants, who were mostly age 40-65 and overweight, they observed an average of 5% reduction of the the volume of the carotid artery wall, which reflects the reduction of the plaque.

Two-year weight loss diets can induce a significant regression of
  measurable carotid VWV [vessel wall volume]. The effect is similar
  in low-fat, Mediterranean, or low-carbohydrate strategies and appears
  to be mediated mainly by the weight loss–induced decline in blood
  pressure.

2) Intensive Lifestyle Changes for Reversal of Coronary Heart Disease (JAMA, 1998)
Forty-eight patients with moderate to severe coronary heart disease were randomized to an intensive lifestyle change group (10% fat whole foods vegetarian diet, aerobic exercise, stress management training, smoking cessation, group psychosocial support) or to a usual-care control group, and 35 completed the 5-year follow-up quantitative coronary arteriography.

Experimental group patients (20 [71%] of 28 patients completed 5-year
  follow-up) made and maintained comprehensive lifestyle changes for 5
  years, whereas control group patients (15 [75%] of 20 patients
  completed 5-year follow-up) made more moderate changes. In the
  experimental group, the average percent diameter stenosis at
  baseline decreased 1.75 absolute percentage points after 1 year (a
  4.5% relative improvement) and by 3.1 absolute percentage points after 5 years (a 7.9% relative improvement). In contrast, the
  average percent diameter stenosis in the control group increased by
  2.3 percentage points after 1 year (a 5.4% relative worsening) and by 11.8 percentage points after 5 years (a 27.7% relative worsening) (P=.001 between groups. Twenty-five cardiac events occurred in 28
  experimental group patients vs 45 events in 20 control group patients
  during the 5-year follow-up (risk ratio for any event for the control
  group, 2.47 [95% confidence interval, 1.48-4.20]).
The experimental group reduced LDL cholesterol levels by 40% at 1 year
  and by 20% after 5 years.
When we began this study, we believed that the younger patients with
  milder disease would be more likely to show regression, but we did not
  find this to be true. Instead, we found that the primary determinant
  of change in percent diameter stenosis in the experimental group was
  neither age nor disease severity but adherence to the recommended
  changes in diet and lifestyle.
those who gained weight were more likely to show progression of atherosclerosis.
Experimental group patients had a 91% reduction in reported frequency
  of angina after 1 year and a 72% reduction after 5 years (Table 5). In
  contrast, control group patients had a 186% increase in reported
  frequency of angina after 1 year and a 36% decrease in frequency after
  5 years.

Mechanisms
Reversal of atherosclerotic plaques can be achieved by removing the causes. According to Atherosclerosis: Process, Indicators, Risk Factors and New Hopes, (Int J Prev Med, 2014), decreasing excessive body weight + exercise + cholesterol-lowering diet + cessation of smoking can result in:

Less damage to the arterial intima
Higher HDL/LDL ratio, meaning adequate removal of LDL (by HDL) from the blood into the liver and thus less deposition of cholesterol into the arteries
Less inflammation in the arterial intima


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Rules of motif forming
I want to understand how a motif is present or not, can be deduced from a PDB file. Are there any rule of thumb for forming 3D motifs? Like a series of helices and sheets in some direction will lead to a particular 3D motif? Are there any such rules? If so, any resources that you can provide me with?

For example, beta-hairpin. What should be the sequence of amino acids or helix/sheet that would result in the formation of beta-hairpin motif?

A motif is a pattern that you discover in a structure by analysis. For example, common sequence motifs are short sequence fragments with parts similar to a regular expression. So, if you have a motif like "A*C" this matches to the sequences "AAC" and "ACC" but not to "ACA". You can reverse the process to discover the motif from the sequences.
Similarly with structural motifs in proteins. A beta-hairpin is :

The motif consists of two strands that are adjacent in primary
  structure, oriented in an antiparallel direction ... and linked by a
  short loop of two to five amino acids.

So first you have to determine where the strands and loops are, then how the strands are connected into sheets, and finally recognise the hairpins. It is the definition of the motif itself that determines how you discover it.
Some resources that might be helpful are:

Motivated proteins (Small h-bonded motifs)
The protein topology graph library (Larger motifs)
The protein geometry database (Not really motifs, but interesting)
PDBeMotif (define and search for motifs in the PDB)

How do I derive from PDB where the strands and loops are and how the strands are connected into sheets?

@Rishika That's a big topic. There are tools out there to do this, DSSP for example. In addition, the PDB file often has secondary structure information provided by the authors. Or you could even just view it in a structure viewer, which will generally show you the strands and loops. Jmol has a DSSP implemention. It depends what you want to do, exactly.


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Can dead scorpions still sting?
I found a dead scorpion on the sidewalk today, and brought it home, being careful not to touch its stinger. Bees can sting even after they are dead, if you step on them in such a way that it pushes their stinger out.
Does the same apply to scorpions?  Do I need to be careful not to touch its stinger?

Yes, the bark scorpion can still sting after death. I learned this myself after stepping on one. As I make a nightly habit of patrolling inside my home for their presence, I can conclude the offender had died within 12 hours of my stepping on it. When they die their tails stretch straight behind their bodies, this was the position I found it in.