text:
Cooking with sawdust
In a book about post-war Japan (Embracing Defeat, Dower) the author mentions a process for making sawdust at least partially edible, so it could be used in recipes in a 1:4 ratio with flour for cooking. The author says the sawdust was "fermented," as I recall.
My question is whether this is anything more than marginally possible. After all, kimchee, yogurt, beer, and other fermented foods aren't necessarily easier to digest. Is there a fermentation process involving bacteria that break down cellulose that might make wood even slightly nutritious?
My impression is that in forests the process of breaking down wood does not initially involve bacteria but other microorganisms; on the other hand, ruminants such as cows use bacteria to help them metabolize.
Thanks for any insight.

Be careful about wood preservatives, some of which double up as pesticides. For example 2,4-Dinitrophenol, something you definitely don't want to eat. https://en.wikipedia.org/wiki/2,4-Dinitrophenol

Yes. I think it would certainly be possible for raw sawdust to be made digestible by humans through some sort of fermentation process with some kind of microbe or another.
Pickling (as is done with kimchee and cucumbers and lots of other fruits) uses naturally occurring bacteria that are artificially selected for by using a strong brine solution so that most microbes die but the ones that naturally survive in strong brine also convert the organic materials they find (raw cucumber or cabbage) into different organic materials (pickled cucumber or pickled cabbage in the case of kimchee).
If you could find a microbe that could digest wood (there are many I'm sure; the gut bacteria in termites provide evidence of at least one or some), and if you could find a way to select for that particular microbe, then fermenting sawdust for nutritious human consumption becomes feasible. The only remaining problem is finding that particular microbe whose excretions were digestible to humans.

Was hoping for something more particular, but +1 and will accept after decent interval if nothing appears.


text:
How tolerant are ants to cold?
There was a trail of what are commonly known as sugar ants (small, brown, hyperactive) in my kitchen. Three of them walked onto an ice tray placed in their path.
They only walked a short distance on the ice before being immobilized by cold. I put the tray in the freezer beside a very shallow dish of water. When the water in the dish had frozen (about a half hour later) I removed the tray/ants and let them passively drop onto a warm dry surface. After 2-3 minutes they revived, walked in circles a few times, then headed off to forage (they were released outdoors).
There is anecdotal evidence of ants' tolerance of cold but I was a little surprised by this. Do we know the extent of their tolerance of cold?
I guess it would vary with size and conditions. But an obvious question is whether, having survived freezing at (let's say) 22F, they could survive lower temperatures and/or longer periods of cold if properly handled? There may be cell structures that are sensitive to freezing because they break or change shape but it's already amazing to me that ordinary freezing does not distort water-bound structures in a lethal way.
Thanks for any insight.

As an afterthought-- I would not have done this if I was not quite sure the ants would survive. The result was surprising but more or less expected.

Acclimatization increases cold resistance of ants [1]. They have a strong adaptability to different environments [2].
When it comes to the red imported fire ant (Solenopsis invicta) here are some numbers (from [2]):

When the exposure time was 0.5 h, the survival rate of workers was 15.3% at -14°C. At the exposure time of 1, 2 and 4 h, the entire lethal temperatures for S. invicta were -13°C, -9°C and -9°C, respectively. When the exposure temperature was -10°C, all workers died within 240 min; while at -11°C, it took only 120 min.

References:

Modlmeier AP, Pamminger T, Foitzik S, Scharf I. Cold resistance depends on acclimation and behavioral caste in a temperate ant. Naturwissenschaften. 2012 Oct;99(10):811-9. doi: 10.1007/s00114-012-0963-8. PubMed PMID: 22955370.
Xu YiJuan; Lu YongYue; Huang Jun; Zeng Ling; Liang GuangWen. Cold hardiness of natural populations of the red imported fire ant, Solenopsis invicta Buren (Hymenoptera: Formicidae) in Shenzhen, Guangdong. Acta Entomologica Sinica 2009 Vol. 52 No. 9 pp. 974-983.

This answer is helpful +1. I also wondered how they are able to tolerate this degree of cold and what goes wrong at the molecular level if they don't.

@daniel this is about yeast cells frozen to much lower temperatures, but it says what is happening at cellular level http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1392953/

Your answer together with the comment is I think a complete answer to the question. Will accept in a bit. Thanks.

source: Stack Exchange

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

sort: votes


text:
Which are more beneficial: lyophilized or hydrolized collagen peptides?
Looking at two different manufacturing methods for collagen peptides: hydrolyzed vs lyophilized (freeze dried), I read that hydrolyzed results in a hydrophobic biolayer molecule collagen peptide.
Re: https://www.quora.com/What-is-the-difference-between-hydrolyzed-collagen-and-natural-collagen

There is a big difference between types of collagen or natural
  collagen available on the market. The main collagen sold is cheap
  hydroyzed collagen, which is produced by extreme heat. And the
  opposite end of the scale if lyophilized collagen which is freeze
  dried and more delicate expensive processing. The collagen known as
  natural collagen retains its triple helix and is an active collagen
  very similar to that of humans. This natural collagen is derived from
  fish skins of fresh water fish like silver carp.

Lyophilization process:  https://www.rdmag.com/article/2017/03/lyophilization-basics
While this may be quickly absorbed through the GI tract, thus "FASTEST ABSORBENT", does this hydrophobic biolayer hinder hydrolized collagen's ability to be broken down into amino acids - which is what we want out of them, right?  Or is it that lypholization retains its triple helix?
I'm not entirely clear on all the terminology, but essentially I would like to know which one is actually better and used by the body, rather than marketing "fastest absorbed by the body".
Additional reference:

US National Library of Medicine National Institutes of Health - lyophilization vs hydrolyzed collagen
Collagen Type I, salmon

If down-voting, please provide a reason.

Please do not continue reposting the same question. You should instead edit questions to preserve their history.

I changed  the question

Is anyone actually interested in answering the question?

"Hydrophobic bilayer" is not related to collagen supplements but to cell membranes, in this case, apparently to intestinal cell membranes. That part is confusing, so if you do not know where you have read it, I suggest to remove that.

I have found no evidence that lyophylization of collagen "retains its triple helix." And even if it does, this is not important for its effectiveness, because collagen needs to be digested (broken down) into individual amino acids or peptides before absorption, which means that any triple helix would be be gone at that point.

The first step in digestion consists of degradation of hydrolyzed
  collagen to form dipeptides and tripeptides or free amino acids.
  Several proteases (eg, pancreatic proteases, small intestinal
  brush-border proteases, peptidase) are involved in the degradation
  process (Clinical Inteventions In Aging, 2014).

The point of lyophylization colagen is not to improve its digestion or bioavailability, but to extend its shelf life.

Lyophilization enables longer shelf life, often as long as two-five
  years and makes it much easier to transport the product. In addition,
  products can be stored at room temperature  (rdmag.com).

You can also see that "hydrolyzed" and "lyophilized" do not exclude each other, because "Lyophilized Collagen Hydrolysate" is being sold.

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


text:
Why would low complexity regions be linked with relaxed selection?
I'm reading a text (Wagner, 2007) on identifying positive selection. In the paper, the author says that low complexity regions are known to be associated with the relaxed selection. I'm trying to understand why this is true. I get that if the region is under relaxed selection then most mutations would be tolerated but why would that lead to low complexity (other than something like slippage during DNA replication)
It's in the section: "Little overlap between variation clusters and low complexity regions"
Wagner A. 2007. Rapid Detection of Positive Selection in Genes and Genomes Through Variation Clusters. Genetics 176(4): 2451–2463.

can you provide a link to the text that you are reading so that the context of the author is clear

What is complexity?
"Complexity" in this case is derived from the SEG algorithm, which is based on Shannon's information entropy.
This is not necessarily repeated regions, but regions in which a limited pool of characters are used (for example transmembrane regions, in which you are far more likely to see a hydrophobic residue than a polar one).
These scripts can help you calculate sequence complexity if you have specific examples in mind.
This idea asks how "compressible" is the information in the string of characters (think zip files).
Random characters in strings need more information, whereas less variable, more predictable regions can be recorded with less information and are less complex.
So a region in which you can more easily guess the next amino acid is simple, and more random amino acid sequences are complex. Sequences with more complexity are often more functionally important and more useful as functional indicators than low complexity sequences.
Indeed, BLAST used to mask low complexity regions as they were not useful for homology searches.
Why are complex regions more variable?
The question as I understand it is asking about this fourth conclusion from the paper.

Fourth, variation clusters occur in structurally well-defined and functionally important protein domains of high sequence complexity.

This is now not as paradoxical as it seems. Regions that are highly variable with lots more random/unpredictable amino acids such as those with well-defined structures and functions are more likely to occur in areas with high complexity as a result (which is a measure of randomness in a sequence).
There is more to this than meets the eye...
This is of course not the whole story.
In regions of high complexity, there are highly conserved and essential for life residues that cannot be changed.
On the other end of the scale, there are also areas like STRs that have low complexity yet are highly variable in length between individuals and underpin DNA fingerprinting.

Low complexity regions have repeats in nucleotides ( or amino acids ).  E.g.  PPCDPPPPPKDKKKKDDGPP or AAATAAAAAAAATAAAAAAT.  This 2011 article compares 14 individual Plasmodium falciparum genomes and finds that these repeats are highly variable between individuals - some may be short AAAATAAAA  others may be longer AAAATAAAAAAAAATAAAAAAATAAAATAAAA....AATAA even to scores of bases.
I think its not clear what these sequences do, but the mere fact that they can vary so much from one viable individual to another indicates that they are not strongly selective.  *If they were subject to selection, you would be able to see the difference in the variation in the health, fitness, and reproduction that these significant genetic changes have, but in this case the change in sequence would not change the properties of the sequence much if at all. *
I think these are also related to copy number variable (CNV) regions.  which expand and contract in the genome easily even between identical twins.  (sorry for the indirect reference - like many SDN stories, the reference is totally wrong), but I remember this work...

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

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


text:
Is plasma membrane permeable to sucrose
I searched a lot in the net but don't found a clear answer.
I just want to know if plasma membrane is permeable to sucrose.

No, but yes.
Sucrose is a large polar solute.
Because it is polar, it cannot easily pass the hydrophobic core of the membrane.
So, if the lipids of the plasma membrane are mostly impermeable to sucrose, how do cells take in sucrose?
Plants
In biology, membrane-bound proteins are used for efficient transport across the membrane (Brian, 2011 from a review of Suc transport in plant cells).
The specific group of membrane proteins used for sucrose transport are unimaginatively called Suc transporters (SUT).
So in a plant cell, sucrose can be moved across the membrane.
Humans
In mammals, there are no SUTs. Instead, sucrose is broken down into fructose and glucose by the enzyme sucrase.

From there, glucose transporters GLUT proteins carry glucose and fructose across the plasma membrane.

What I don't understand is that in the osmosis experiment, potatoes shrink for a long time in the solution of sucrose. if plant cells were permeable to sucrose the potatoes will gain their initial size

@medmorad it depends on sucrose concentration and whether sucrose transporters are expressed in that particular tissue.


text:
Is there any program or website that allows me to create phylogenetic trees without having to insert an already created dataset?
I asked a similar question on Quora before, but did not get any useful answers as the program the one answerer suggested turned out to have the exact same problems as all others I have found so far.
Most programs for the construction of phylogenetic trees—being made for researchers in various biological disciplines—seem to rely on the input of a dataset that is a formulation of collected genetic and/or anatomical data.
Specifically, I am looking for a program that is like this, but with a GUI that allows tree editing (i.e. you can add and remove new taxa), for example, poorly described/novel theoretical species, dubious species, and subspecies and can be used to create simplified versions of charts like these.

Welcome to Biology.SE! Thank you for taking the [tour], but please also go through the help pages starting with [Ask] questions effectively on this site. Note in particular that this doesn't appear to be a question that is appropriate for this forum — a tree without data is fiction not biology. ——— There is a [worldbuilding.se], perhaps that might be an appropriate venue for this question? Thanks!

@tyersome The reason why I first asked this question on here, rather than the Worldbuilding forum was because I was not sure that anyone on there would have the expertise to answer the question, given the fact that the majority of questions deal with fantasy and (relatively) soft sci-fi concepts, and when hard scientific concepts are brought up, they are not usually in the the fields I am looking for.

@tyersome So, do you think I should still try to ask the question there? Also, now that I look back upon it, I feel that a better way of phrasing the question would be that I am looking for a software where you can directly create and edit phylogenetic trees (through an intuitive graphical interface), rather than having to indirectly edit it through the difficult and gratuitous creation and/or modification of a dataset that one must run through the program.

I can't tell you whether Worldbuilding is the right place, but I can assure you that your question doesn't belong here and won't get an answer even if it isn't closed. The problem is that an expert in phylogenetics is unlikely to have an answer because no one studying biology would need to build a tree that wasn't based on data. Consequently, I doubt that anyone has taken the time to create software for that purpose.

I agree it does not belong here but I don't understand why you can't use some general graphics program like inkscape or photoshop or something? At the end of a day you just want to draw a custom picture of a tree, no?

Maybe SoftwareRecs.SE?

@BagiM Something with similar functionalities to that would be perferred, but the problem with those specific programs is that creating a tree that looks professional with them would require a large amount of advance planning, and I would basically have to rip up and redo the entire thing if I were to want to add or move a taxon.

@BryanKrause Thanks, I'll try there.

I should probably stop talking now, sorry for wasting everyone's time.

if you're comfortable programming in R you could easily define your own phylogenetic tree in the ape package.  Alternatively, if you write down your tree in Newick format, a standard and fairly human-friendly format, you could probably import it into any of a number of phylogenetic tools ...

@Grant I disagree. When using vector graphics program like inkscape or illustrator no advance planning would be necessary while keeping professional look. Seamlessly adding or removing taxon should be quite straightforward.

I'm voting to close this question as off-topic because it is not about biology as defined in the help center.

I think this can be a valuable question in the context of lab techniques. I've tweaked the wording of the question to highlight that this might be a valuable question for people sketching out incomplete or weird trees.

Have you ever tried using Mesquite?
I used it when I taught intro bio lab course as a TA.
Basically you try to come up with yes or no questions, and based on how you answer these questions it will generate a tree similar to your second link.
Can be a little bit complicated, but I am sure there are many tutorials for it on its website.


text:
Why do tears fall from our eyes when we ride a bike too fast?
When we ride a bike too fast why do tears fall from our eyes. What is going on biologically and what may the evolutionary story be behind this?
This quora Q&A gives a few ideas, none of which satisfy my question fully.

This is similar to a response to smoke.

But this is clean air? Why doesn't this happen all the time?

Our eyes always need to be lubricated.

But why the need for excess tears?

Our eyes need to be covered with a thin film of liquid all the time. When riding fast, the wind flow pushes the liquid away from your cornea. Your eye compensates for that by producing more tear.


text:
How do mutations of viruses lead to drug resistance?
For instance, after starting zidovudine monotherapy against HIV, resistance develops against the drug because of a point mutation in the RNA transcriptase enzyme to which the drug binds.
So how does the virus ‘know’ to mutate this particular enzyme?

@David After your edits, the answers no longer make sense. Yes, the question was based on a misunderstanding, but the answers explain why that understanding was wrong.

@Barmar, I've restored the original title question.  I agree the changed title had reduced the value of the answers for little benefit.

@mgkrebbs — I think we can improve the question by improving rather than restoring a bad title. I have had another go. The essence of the misapprehension remains, but it is no longer expresses it as an assertion, which I have reintroduced in the body of the question.

@Barmar I don't think so, because a title is not a question, and the last sentence of the question still encompasses the misapprehension. However, I have had another go at the title and altered the last sentence to explicitly include the "know" that appears in the accepted answer.

Coming in from outside, after having visited this question once before, the new title makes the answers make no sense.

@probably_someone I have edited the title to capture the revised title without destroying the context of the top answers.

@James I regard that as unnecessary (the last sentence in the question includes "know") and retrograde. By retaining the original title you are propagating the non-scientific thinking of a question which should have been closed for the lack of research.

@David I appreciate your point and agree completely that we should not encourage the idea of sentient evolution (or whatever you want to call it). However, when asking a question, it is more helpful if the title is a question rather than a topic/chapter title. What do you think of this one?

This is molecular evolution and is completely undirected.
Mutations happen all the time, most of them disappear without anyone noticing, since they have no evolutionary advantage to permeate.
This is different when you treat the cells and put them under an evolutionary pressure. Under this conditions, mutations which affect the mechanism of the drug (as here with a single point of binding) pose a great advantage for survival and with subsequent generations all carrying this mutation. This mechanism is simply a statistical one as the numbers of viruses produced in the infection is really large. It is not a matter if such a mutation occurs, only when.
Such a selection of specific clones is seen in other diseases too, leaving to the deactivation of the drug or the activation of different signal pathways, avoiding the one which has been targeted.
If you want to read further on viruses and mutation rates/mutations, take one of the following articles.
References:

Mutation—The Engine of Evolution: Studying Mutation and Its Role in
the Evolution of Bacteria
Antiviral drug resistance as an adaptive process
Mechanisms of viral mutation
Why are RNA virus mutation rates so damn high?

It doesn't. Viruses don't "know" anything. Mutations occur at random. Most of them don't do anything, or have a slight negative effect on the ability of the virus to infect and reproduce. However, there are billions and billions of viruses. Once in a while a random mutation will offer a significant advantage like immunity to an anti-viral drug. The viruses that have that beneficial mutation will then massively out-reproduce the viruses that don't have it. Eventually the population of viruses will consist mostly of individual viruses that have that mutation.

Are you suggesting every mutation ever happened is just an accident?

Yes, exactly. It's just that there are billions and billions of them, so sometimes something useful crops up.

@user73023 The same is true for all the mutations in every species of bacteria, plant, animal, etc.

@Jagoe: Well, humans are an accident :-)  And from a strictly linguistic point of view, the changes made to GMOs are not mutations.

@Jagoe Even mutations involved in creating GMOs are random. You try to target a specific piece of DNA, but what will you actually modify is based on chance. Same like throwing the ball on target. You are trying to hit the centre, but you might go off. Most GM process involve stage where you try to look at the thing you created and verify that the change occured at the place you wanted and that there are no side effects.

@Jagoe here's one (crude) way how some  GMOs were developed through random mutations - https://en.wikipedia.org/wiki/Atomic_gardening

@jamesqf Not really, if you look at the big picture. Genes are replicators that create vessels for themselves to spread. As part of those vessels, they managed to build brains, which themselves are capable of supporting their own replicators - cultural information, memes. Those memes hijacked the "plans" of the genes (oops!), just what happened probably a few times before (any parasite in the broad sense does the same thing). When you look at humanity as a whole, much of our progress is through the same mutation-and-selection process, just ridiculously faster than genes could ever do.

@Jagoe Except that GMOs have been created by nature over and over again. We just adopted the same mechanism, and tweaked it for our own purposes. Both selective breeding and "modern" genetic manipulation are things that happen in nature all the time. And it's not like humans are all that special; we've developed thanks to natural selection, just like every living thing on this planet. Retroviruses change genomes of other organisms (including ours) too; bacteria share plasmids; many plants routinely hybridize like crazy (wheat and citrus fruits are probably the most visible crazy hybrids :)).

Billions sound like greatly underestimated when this site claims there are hundred million virus particles in a single cough drop https://www.livescience.com/3686-gross-science-cough-sneeze.html  They wouldn't evolve nearly as fast if there were just billions.

@Jagoe Well, of course. When we talk about natural selection being important, we're talking about adaptive evolution, which is the buildup of complex systems piece by piece. Things like tails becoming longer can easily be due to genetic drift and such. But it still fits the general pattern - genes building machines to spread genes, and those machines not always doing what's best for the spreading of genes. I'm not sure what part of what I'm saying you're disagreeing with. What makes us human still developed through natural selection, even though it's not the only effect at play.

@Colombo Yes and no. The problem with CRISPR-Cas9 is not that it misses its target, but that it introduces unintended changes in the same area in addition. It's certainly not the same kind of random as in atomic gardening.

@Jagoe: You completely misunderstood my comment.  I meant that human beings AS A SPECIES are an accident.  As for individual children... Well, the parents may have intended to produce A child, but until genetic engineering progresses a lot further, the particular child they get is still an accident.

Summary: They Don't.
Long explanation:
Mutations happen at random. A series of factors can lead to the perceived notion that the mutation was intentional.

The mutation can be harmful, beneficial, or neutral.

Harmful: We don't see the harmful mutations as these individuals don't proliferate. The mutant individual just dies off without passing their genetic material forward, or they die out after just a few generations.
Beneficial: To the virus' viewpoint, of course. The mutants gain a competitive advantage over the other strains, and proliferate. This advantage may be noticed (e.g., as in the case of developing drug resistance).
Neutral: Most of the time, the mutation won't affect the individual's performance. Due to the mechanism of codon degeneracy, changes in one base in the DNA code may not even cause a structural change to the codon's amino acid equivalent.

Most viruses are not successful in reproducing. Those that are make millions of copies of themselves. One successful mutant has the potential of creating a whole new strain.
Viruses too are subject to selective forces. In the case of drug resistance, the successful resistant mutant won't have to compete with the other strains as the drug already eliminated them.
Drug resistance is not immunity. However, a resistant strain can very well mutate again to develop a stronger resistance.

We only observe the final effect (a new virus strain that seems to be engineered) but not the intermediate steps. There was a lot of (random) intermediate and unsuccessful mutations in between.

Let me know if this is off topic, but as a developer, my eyes were opened when I learned genetic algorithms. While the mathematics are tangential to actual biology, I think it illustrates the mechanism of an environmentally directed evolution of random mutations. An example I have is here:
https://github.com/Jarrod1937/genetic-algo-example/blob/master/ga/Form1.cs
The mutations are random, but the fitness function defines when the mutation is beneficial. In the case of a virus, the virus successfully propagating is the fitness function, and thus those of a higher fitness are more likely to propagate more, thus you see the increasing adaption against things that prevent propagation. However, this isn't the virus knowing where or how to adapt, rather, it is a case of sample bias. Your sample of viruses are the ones that survived and propagated, you don't see all of the failures that came before.

Hi Jarrod - this is the same way biology works, as described in the existing answers by Charles, Chris, and Mindwin. The mutations are random; what makes certain mutations increase their prevalence in the population is selection (effectively, this is the fitness function), plus other random components like genetic drift (which has most effect for mutations that have no or a small survival cost or benefit). Genetic algorithms sometimes cheat a bit, though, and have non-random mutations or other algorithmic tricks in selection and 'mating' that are not accessible to biology.


text:
How does the OD correlate with the number of algae cells?
My research team and I are using a spectrometer to measure the OD of an algae sample. We are trying to answer the question "Is there a correlation between OD and the number of algae cells?"
What should we consider in our experiment? Is this an established technique?

are there any materials from your instructor that could help you? have you tried use google/web search?

No, we only have a spectrometer. Also, Google shows results for bacteria, not algae.

just to be clear: you were told: "here is spectrometer, here's some algae. Go figure how many cells is there, don't ask me anything"?

No. We are doing a research project that we chose by ourselves. We are trying to find a way to measure the amount/ quantity of algae there is. We have a spectrometer but dont know how to correlate that to the number of cells.

Hi there and welcome to Bio.SE. Although this is a weird way to count cells, I can see your line of thinking. If there is more absorbance, there are probably more algae. You'll need to control against the feed you add for the algae, get as close to uniform distribution of algae as possible, and consider that you are measuring algae per volume rather than a simple cell count that you'll presumably be doing at each OD measurement under a microscope for a tiny volume from the solution. If you could provide more details about your experimental setup and aims then you might get a better answer.

We are trying to find the effect of pH on algae growth. Along the way, we are going to measure the growth with a spectrometer. We need to find a correlation to prove that the correlation is linear, not quadratic or something else.

As with bacterial cells, number of cell and OD are correlated. I am not a specialist, but it seems that you can use microscope to visually count number of cells, then correlate it with optical density of the solution you have. This will allow you to first establish how many cell correspond to 1 unit of OD, then use OD to estimate number of cells quicker than by counting.
Just a few details: counting of cell number is done by dropping given volume of culture on a special slide with grid, then manual counting using microscope.
If we assume that 100 cells/mL (or whatever) solution gives you OD of 1, then OD of 2 will correspond to 1000cells/mL concentration. That us due to logarithmic relationship between OD and light absorption by the cell culture.

What do you mean by 1 unit of OD? Also, how would we count the amount of cells in a liquid.... take a sample?

@AProNoob added some details

Thanks so much! Wait, so the correlation is logarithmic for all cultures?!


text:
Why do some people have symptoms of salmonella and others not?
So I was reading from the Mayo Clinic website and they say that typically people with Salmonella have no symptoms, but why?  Why do some people have symptoms and others not?  Salmonella does after all mutate.
Here is an excerpt from the Mayo Clinic Website

"Typically, people with salmonella infection have no symptoms. Others
  develop diarrhea, fever and abdominal cramps within eight to 72 hours. Most healthy people recover within a few days without specific treatment."

https://www.mayoclinic.org/diseases-conditions/salmonella/symptoms-causes/syc-20355329

I removed the "toxins" tag because salmonella doesn't actually secrete toxins like Clostridium. Anyway, why is this fact difficult for you to understand; people have varying levels of immunity to different pathogens. Can you elaborate more on what you specifically want to know?

Symptoms can also depend on the number and virulence of the Salmonella bacteria you ingest.


text:
Did the Hela cells leave John Hopkins
Did John Hopkins let people outside of the university use the Hela cell-line that was isolated from an immortalised cervical cancer?

Perhaps more biology-inclined people know what those are, but I personally do not... Could you expound a bit on what those are and what they were used for?

The HeLa cell line is fairly famous - I think 'Hela cells' is enough to identify the line. The Wiki is here: https://en.wikipedia.org/wiki/HeLa

If you are interested in learning more about HeLa cells, there is a very nice book : The immortal life of Henrietta Lacks which tells the story of life of Henrietta and also of the cells

Cultures of HeLa cells are used in many labs around the world, and were widely shared from very early on. From the Wiki:

In the spring of 1953, a cell culture factory was established at
  Tuskegee University to supply Salk and other labs with HeLa cells.

It may be worth noting -- since many non-biologists seem very unclear on this point -- that HeLa cells were not the first immortal cell line, and they have not been unique for many decades since there are now tens of thousands of human immortal cell lines

But it should be noted that HeLa cell line is very easy to grow compared to other cell lines. In fact there was a period just after DNA finger printing became affordable, that  researchers realized just how easier it was for HeLa to grow. Many cell lines turned out to be contaminated by HeLa or were HeLa (as the HeLa cell had outgrown the cells of the original cancer line).


text:
Can a miRNA be upregulated and downregulated in the same disease
I am computational guy and hence apologies if the question is silly.
Can the same miRNA show upregulation and downregulation in the same disease? (Not in the same experiment, though). For e.g. can there be a instance of miRNA hsa-miR-21 being upregulated in a disease glioblastoma in 1 study and in another study there is an occurrence of hsa-miR-21 being down-regulated in glioblastoma. Is this possible?
As an example, I found:
hsa-miR-345 -> overexpression in pancreatic cancer (PMID: 16966691) and,
hsa-miR-345 -> downregulation in pancreatic cancer (PMID: 17149698)
Any pointers would be appreciated.

Glioblastoma multiforme? miR-21 is usually upregulated in some cancers. Sometimes there is no real change but I haven't come across a case when it is downregulated. Pancreatic cancer is an even broader term than glioblastoma (glioblastoma usually refers to GBM but there can be others); there are many cells in pancreas and any of these cells could become cancerous. Some of these cells may overexpress miR-21 whereas others may not. But there should not be a downregulation, as far as I know.

Thanks. But as to the notion - 'that a certain miRNA documented as to be shown as upregulated and downregulated in a disease', do you think there is a biological basis for it? There are scientific databases (for e.g. miR2Disease) which have reported these and hence I'm curious.

In the same disease? In that case I would say that the particular miRNA is not a reliable marker for that disease. Usually, these datasets do not have enough replicates to calculate statistical significance. Moreover, the way upregulation/downregulation is usually calculated (fold changes) is not a good idea when the actual concentrations are too low. To attribute a biological significance, a more detailed and precise study is necessary.

Since diseases are frequently complex, it is not surprising to find specific genes (both miRNA coding genes or protein coding genes) being deferentially regulated when different studies of similar-sounding-diseases are compared. In other words, things like glioblastoma or Pacreatic Cancer should be treated as labels describing grossly similar disease states (i.e. excessive proliferation of glia and pancreatic cells, respectively), rather than as labels of specific cellular state associated with a particular gene expression pattern.

It's also worth to note that even the same 'type' of cancer is never really the same disease: but different occurrences but also relapses, metastases or even just different parts of one tumor can (and mostly will) have different mutations and genetic changes, which makes every cancer unique to a certain degree - there are of course similarities, but the differences especially between different patients make cancer treatment very difficult (and are one big reason why 'personalised medicine' is becoming more and more important)


text:
What is the structural difference between beta and gamma globin chains of Hb?
Hemoglobins are tetramers composed of pairs of two different polypeptide subunits. The subunit composition of the principal hemoglobins are α2β2 (HbA; normal adult hemoglobin), α2γ2 (HbF; fetal hemoglobin) and α2δ2 (HbA2; a minor adult hemoglobin)
The total number of amino acids in beta chain and gamma chain is the same-146. The higher affinity of HbF to oxygen is due to presence of serine(in gamma chain) in place of histidine(in beta chain), which inhibits its binding with 2,3-bisphosphoglyceric acid.
Is this the only difference, or are there more such differences in the amino acid sequence?

Here's a pairwise sequence alignment of the human hemoglobin beta (HBB) and gamma (HBG1) chains:
HBB_HUMAN          1 VHLTPEEKSAVTALWGKVNVDEVGGEALGRLLVVYPWTQRFFESFGDLST     50
                     .|.|.|:|:.:|:|||||||::.|||.|||||||||||||||:|||:||:
HBG1_HUMAN         1 GHFTEEDKATITSLWGKVNVEDAGGETLGRLLVVYPWTQRFFDSFGNLSS     50

HBB_HUMAN         51 PDAVMGNPKVKAHGKKVLGAFSDGLAHLDNLKGTFATLSELHCDKLHVDP    100
                     ..|:||||||||||||||.:..|.:.|||:||||||.|||||||||||||
HBG1_HUMAN        51 ASAIMGNPKVKAHGKKVLTSLGDAIKHLDDLKGTFAQLSELHCDKLHVDP    100

HBB_HUMAN        101 ENFRLLGNVLVCVLAHHFGKEFTPPVQAAYQKVVAGVANALAHKYH    146
                     |||:|||||||.|||.||||||||.|||::||:|..||:||:.:||
HBG1_HUMAN       101 ENFKLLGNVLVTVLAIHFGKEFTPEVQASWQKMVTAVASALSSRYH    146

You can see the H143S (or S143H?) substitution, as well as many more.


text:
Do camels have nucleated RBCs or enucleated RBCs?
Most mammals have enucleated RBCs as an adaptation to facilitate the transport of oxygen. My text says that camels and llamas are exceptions to these.
I was wondering why they are exceptions, and the Google search results are confusing. Some sites say that camels have nucleated RBCs to facilitate cell division. Some others state that camels, like all other mammals possess enucleated but different shaped RBCs. So, which is correct?
The links:https://www.quora.com/Why-do-camels-have-nucleated-red-blood-cells
https://in.answers.yahoo.com/question/index?qid=20070702070352AAkfspZ

Camel RBCs are anucleate [1, 2]. The dark structure seen in microscopic images is not nucleus but a network of microtubules called the marginal bands. Marginal bands cause these RBCs to adopt an ellipsoid shape. The unique shape of these RBCs possibly allows them to survive osmotic stress and is probably advantageous to a camel under extreme dehydration.

 References:
[1] Cohen, William D., and N. Barclay Terwilliger. "Marginal bands in camel erythrocytes." Journal of cell science 36.1 (1979): 97-107.
[2] Long, Charles A. "Evolution of function and form in camelid erythrocytes." Actas de The 2007 WSEAS International Conference on Cellular & Molecular Biology, Biophysics & Bioengineering. 2007.

Do other vertebrates also have these marginal bands?

@SnackExchange yes in nucleate/primitive RBCs. See more here https://doi.org/10.1007/BF00519909

Camel erythrocytes are oval in shape and without nucleus. No intracellular organelles were observed with the occasional exception of a small number of mitochondria . are well-adapted to hot arid environment and .The red blood cells of the dromedary camel protect it from dehydration because the oval-shaped cells can circulate even in thick blood and can significantly expand during re hydration

Welcome to SE Biology. Please take the Tour and read about how to answer questions. The poster asked a question because he had found a disagreement or inconsistency in different accounts of camel red cells. To resolve this conflict it is not enough to state what you think the correct situation is, but to cite authoratitive evidence for your point of view. You may well be right, but how can the poster or anyone else (including me) tell?


text:
Global database for patients with rare and important injuries or disease?
I was recently reading Christof Koch's The Quest for Consciousness, and several times he mentioned how important some patients with sad and terrible brain injuries were for the understanding of the working of the brain.
It made me wonder how brain researchers as Koch and others find such patients. I expect that only a small number happen to see an expert-brain researcher who understands that this patient could be important for brain research, especially for such people in less developed countries.
More generally, I wonder the same for patients with very rare injuries or diseases, which could potentially be significant for medicin- and biology-research:

Is there a global database for patients with very rare deseases or injuries, making it possible for medical experts in the field to find them?

Even if the expert can not help the individual person, I imagine that such patients could be very important for future understanding/curing of the injury/disease. I hope to get some literature references or suggestion.

Are you aware of the concept of medical confidentiality? If not, you might find it instructive to read https://www.bma.org.uk/advice/employment/ethics/medical-students-ethics-toolkit/9-confidentiality. Then perhaps you will realize why the answer to your question is no.

@David Thank you, but your answer is not complete I believe. 1., such lists could be created when the patients or their relatives agree. 2., somewhat related lists do certainly exist, such as for organ transplantations. 3. I know that several very rare cases have been well-documented in medical literature, so your argument do you apply there either. But I see your point, and it gives some necessary conditions for what I was wondering about. Thank you.

I guess the closest you can get to this are collections of case reports. Where, if you were extremely interested, you could contact the author of the case report and if you are lucky get in contact with the patient.

The Undiagnosed Diseases Network (https://undiagnosed.hms.harvard.edu) is similar to what you're looking for; it's not for injuries, but rather for rare genetic diseases. @David: there are well-established procedures for getting informed consent.

@RaghuParthasarathy — if you have an answer to a question please post it as an answer. Comments are intended for asking clarification or making  suggestions to the poster, as you will have seen when you clicked in the comment box.

The Undiagnosed Diseases Network is similar to what you're looking for; it's not for injuries, but rather for rare genetic diseases.

The MatchMaker exchange project is a federated approach that allows clinicians to find matching cases based on genetic or phenotypic similarity, retaining patient confidentiality.

I don't know whether there's a global database of the sort you're thinking of, but
Crowdmed.com is a website on which patients post their own obscure medical cases and post a bounty for researchers to try to solve them.


text:
Why does Nature use a 4-level system to encode information in DNA?
First, I am not a biologist, so this question might be naive:
Computer information processing and storage is based on 2-digit system of bits with values 0 and 1. Now, DNA stores the information in a 4-digit system: A, C, G, T. Three base pairs form a codon and can encode 43 amino acids.
Is there a good reason why a 4-level system (which can store 2 bits per encoding entity) evolved rather than a 2-level or a system with a larger number of symbols in the alphabet?
Put differently: Why was a binary system not preferred for storage and processing of data? In computing, binary is much easier, and the very few tests of exotic higher-level data processing have not really been successful.

At an abstract level, both systems perform information storage and processing. My question was not whether living organisms are computers, but why - on the abstract level of information, why a 4-level encoding system has been favoured. Your comment seems to be not constructive - but maybe I misunderstood something?

Why not? There is no inherent drawback in a base 4 system instead of a base 2. In the absence of selection pressure, the precise system evolution ended up with may just be a coincidence.

It's an interesting question but I doubt that it has an answer, only hypotheses. This paper may interest you.

@Roland how do you know there was no selection pressure; i can't imagine that this was the first and only system that was developed - Looking at the complexity, I can't believe that there were no prior steps of more primitive information encoding systems, and not more than one of such systems competing.

@canadianer thanks for this paper, that looks pretty cool! as far as i see, they start already with 4-nary logic. but the structure of the info-encoding, using two nb per codon is great!

Well, we really have no way of knowing, but I for one can't imagine what the selection pressure in favor of a binary system would be. Can you give an example? If anything, since a base 4 system carried more information per base, it seems more economical. But my guess is the chemistry was much more important than any of this.

The basic question perhaps is, "why DNA has 4 bases at all".  Next comes "why use three for a codon".. In any case the answers can only be speculations.

@Roland as a physicist I can only speculate, so that might be naive; but of course i can see reasons favoring binary systems (involved logic is much easier thus error correction might be much easier; maybe with binary only, there is a simpler chemical system to encode information, which might be significantly smaller/more robust than DNA); or higher-level systems (more information in less carriers, so the code might be much smaller). I'm sure there were real biological scientists who asked that questions, and came up with different interesting hypothesis. That's what I'm searching for :-)

My understanding of the information content, and coding capacity is that a single nucleotide site can contain a maximum of 2 bits of information, and therefore a codon triplet can contain a maximum of 6 bits of information. Where did base 4 come in? You may find reading Tom D Schneider's treatment of the ~ 70% efficiency of the genetic code both interesting and germane.

@mdperry If one nb carries 2 bit of information, it is (at least) a 4-level system. the 4 levels in DNA are A,C,G,T. Did you read my question?

When you say 'one nb' is that an abbreviation for 'nucleotide base'? The common abbreviation is 'nt' for 'nucleotide'. Reading back through this thread I see some people are using 'base' as in nb or nt, but some posts use 'base' for a counting system so base 2 is binary, base 10 is decimal. I am ignorant of the term you use '4-level' or '2-level' for that matter. I was probably confused.

"All of our information processing and storing is based on 2-level logic, bits with 0 and 1." You take it as a given that this an organic, long-standing construct, but it is intimately related to the mechanisms by which computers work. Transmission of data and calculations using computers rely on circuits which output either high or low voltage signals based on the voltages of their inputs. Because the exact voltage can vary significantly system to system and circuit to circuit, fidelity is maintained by differentiating only between  high voltage and low voltages (on and off or 1 and 0).

I would argue that in the modern computers the system is not actually just binary. Given that words are 32/64-bit long, the base can be seen as 2^32 or 2^64 (if we draw the parallel with DNA encoding). But at the very least the base is 256 (byte).

The current hypothesis is that RNA came first, DNA and proteins came later. So the reason that four bases are used might be related to the initial RNA world, and then DNA just reused the already existing RNA bases in a slightly modified form. In the RNA world, all functions had to be performed by RNA. Having more bases available than two would likely be important to be able to adopt various structures and create binding pockets or active sites for ribozymes.
You can't really think of the genetic code as an abstract data storage device. There are physical and chemical consequences to the choice of encoding. For example, proteins have to be able to bind to DNA and recognize particular patterns. With your binary code, the recognition sequence would have to be longer, because each basepair contains less information. The tRNA anticodons would have to be larger for protein biosynthesis to work with the binary code. Another issue that plays a role in some processes is that GC base pairs are more stable than AU/AT base pairs.
These are all just hypotheses. Evolution doesn't necessarily choose the best option, sometimes it is just the most convenient one that still works well.
I also found a review titled "Why are there four letters in the genetic alphabet?" that makes a similar point as my first one.

All present models to explain the fact that we have four base types in
  our genetic alphabet hinge, in covert or overt form, on the assumption
  that the genetic alphabet evolved in an RNA world

Another factor I didn't think of that is mentioned there is that while more bases make better ribozymes, more bases also decrease the accuracy of  replication.

In summary, two-dimensional RNA-like structures (and, presumably also
  the three-dimensional structures) become better defined as alphabet
  size increases, whereas the accuracy of replication decreases.

that is a wonderful answere, thank you! there are some insights I haven't thought of - especially the RNA world hypothesis. great! And thanks for the link to the paper!

"You can't really think of the genetic code as an abstract data storage device. There are physical and chemical consequences to the choice of encoding." This is a really good succinct sum-up.

Why does nature use a 4-level system (DNA) to encode information?

Short answer: Ease of manufacture, simplicity of matching, sufficiency for requirements. Fewer simple bases take less effort to create, provide fewer possible matches, yet is complex enough to code what is required while retaining sufficient degeneracy for success. Also it was the coincidence of replicase–alphabet co-evolution, both occurring in the same place at the same time.
Longer answer:

First, I am not a biologist, so this question might be naive:

Beginners and experts are welcome at SE.

All of our information processing and storing is based on 2-level logic, bits with 0 and 1.

Euler's number ($e$) is defined as the sum of an infinite series $\sum_{n=0}^\infty \frac{1}{n!}$ and has the lowest radix economy, but it's not convenient to implement in logic circuits. With the radix economy of $e$ set at 1.000, ternary is 1.0046 and binary is 1.0615.
Ternary computers have been constructed using ternary logic and while they are uncommon ternary logic is used in SQL; even in binary based computers.
Most, but not all of our information processing and storing is based on 2-level logic.

Now, DNA stores the information in a 4-level system: A, C, G, T. Three basepairs form a codon and can encode 4^3 amino acids.

Most, but not all.
The five canonical, or primary, nucleobases are: adenine (A), cytosine (C), guanine (G), thymine (T), and uracil (U). DNA uses A, G, C, and T while RNA uses A, G, C, and U.
In the laboratory DNA has been created with 6 and 8 bases, it is functional.
See the (paywall) report: "Hachimoji DNA and RNA: A genetic system with eight building blocks", Feb 22 2019, by Shuichi Hoshika, Nicole A. Leal, Myong-Jung Kim, Myong-Sang Kim, Nilesh B. Karalkar, Hyo-Joong Kim, Alison M. Bates, Norman E. Watkins Jr., Holly A. SantaLucia, Adam J. Meyer, Saurja DasGupta, Joseph A. Piccirilli, Andrew D. Ellington, John SantaLucia Jr., Millie M. Georgiadis, and Steven A. Benner. (Google Cache version).

"Fig. 4 Structure and fluorescent properties of hachimoji RNA molecules.
  (A) Schematic showing the full hachimoji spinach variant aptamer; additional nucleotide components of the hachimoji system are shown as black letters at positions 8, 10, 76, and 78 (B, Z, P, and S, respectively). The fluor binds in loop L12 (25). (B to E) Fluorescence of various species in equal amounts as determined by UV. Fluorescence was visualized under a blue light (470 nm) with an amber (580 nm) filter.
  (B) Control with fluor only, lacking RNA.
  (C) Hachimoji spinach with the sequence shown in (A).
  (D) Native spinach aptamer with fluor.
  (E) Fluor and spinach aptamer containing Z at position 50, replacing the A:U pair at positions 53:29 with G:C to restore the triple observed in the crystal structure. This places the quenching Z chromophore near the fluor; CD spectra suggest that this variant had the same fold as native spinach (fig. S8).".

Centrifuge tube C contains the spinach with the DNA containing eight bases.

Is there a good reason for why during early evolution, a 4-level system (which can store 2 bits per encoding entity) is favoured over a 2-level system or over larger systems?

Yes.

Copying fidelity decreases roughly exponentially with increasing size (N pairs) of the alphabet (keeping the length of the genome fixed). The reason for this is that as one adds more letters to the alphabet, they will resemble each other more and more, and hence the chance of mispairing and mutagenesis increases.
Overall metabolic efficiency and fitness are determined by the size, we have 20 amino acids to code for (smaller makes 16 or less) and 3 stop codons. So we have a space for 64, and rely on degeneracy to provide a degree of 'error correction' (synonymization) where errors are converted, usually to produce non-fatal errors. While seldom fatal translation errors can still cause rare diseases.

We are already running inefficiently, going to a larger number of pairs introduces unnecessary complexity and going smaller isn't available for the number of amino acids that must be coded for. Increasing the codon length makes DNA larger, as it is it must already be coiled to stuff it into the cells; one third larger DNA would better fit cells that are also one third larger.
In the opinion piece "Why are there four letters in the genetic alphabet?", Nature Reviews Genetics volume 4, pages 995–1001 (2003), by Eörs Szathmáry there are the following observations:
Page 995:

"There are four main constraints on the successful incorporation of a new base pair$^{[6–8]}$:

chemical stability (the base should not readily decompose);
thermodynamic stability (new base pairs should not destabilize nucleic-acid structures);
enzymatic processability (polymerases should accept the base pairs as substrates, catalyse addition to the primer and be able to carry on the process); and
kinetic selectivity (orthogonality to other base pairs).

All four criteria are important but the combination of the last two, which we might call replicability, has received particular attention
  because it is the main obstacle to adding to the genetic alphabet.".

Page 997:

"Theoretical arguments
  The feasibility of alternative base pairs raises the question: why are there four bases in the natural genetic alphabet? As Orgel pointed out, there are two types of answer: either evolution has never experimented with alternative base pairs or four bases ‘were enough’$^{[20]}$. The first option might hold for the hydrophobic base pairs discussed above (an adequate early synthesis might be lacking), but it is unlikely to be true for all of the hydrogen-bonding bases in a prebiotic ‘chemical mayhem’. At any rate, it does not explain why we do not have only two bases$^{[21–24]}$. It therefore seems worthwhile to pursue the second option: why might four bases be enough? If ‘enough’ is understood in terms of evolutionary stability, it means optimality within the frame of the structural constraints that are afforded by natural selection. Here, I describe attempts to show that four bases are optimal under STABILIZING SELECTION, especially when we consider MUTATION–SELECTION EQUILIBRIUM. I then discuss evidence for the optimal size of the genetic code obtained from in silico DIRECTIONAL SELECTION and finally analyse a more abstract contribution from so-called ERROR-CODING THEORY.".

Page 1000:

"Theoretical investigations based on structural, energetic and information-theoretic studies confirm the view that increased alphabet size
  decreases copying fidelity while increasing information density. This indicates that there must be an optimum alphabet size in terms of fitness, whether we assume that the genetic.alphabet was fixed in an RNA world or not.
...
According to the RNA-world-based view, the genetic alphabet became fixed more than 3 billion years ago$^{[31]}$, and the origin of the genetic code and translation happened subsequently$^{[42]}$. This line of reasoning indicates that the informational/operational division of labour between nucleic acids and proteins$^{[43}]$ has uncoupled the genetic alphabet from
  enzymatic functionality constraints. As the genetic code evolved in the context of a certain genetic alphabet, any further change of the alphabet would have been unnecessary and/or extremely unlikely.
If, however, the genetic code originated by the simultaneous co-evolution of nucleic acids and proteins (a much more complicated model), then the fixation of the genetic alphabet must be considered in this complex context. Here, the general insight of Mac Dónaill$^{[38]}$ helps: the information density of the alphabet is a useful concept, whether the exercised function is ribozymic or a messenger function in protein synthesis. In this case, the problem of the size of the ‘catalytic alphabet’ (the number of encoded amino acids) readily arises: why do we have 20 rather than, for example, 16 or 25
  different amino acids? It has been pointed out that some of the considerations discussed in this article (effects on catalytic efficiency and translation fidelity) apply to this related problem$^{[32}]$. However, another crucial factor is likely to be involved: the metabolic cost of producing amino acids. An amino acid that belongs to the same biosynthetic family$^{[43]}$ is expected to increase catalytic efficiency only modestly and its metabolic cost is likely to be small. By contrast, an amino acid from a new biosynthetic family is likely to confer a high enzymatic advantage, but is expected to incur high metabolic costs (for instance, many new ATP-requiring steps).".

References:
$[6.]$ Mathis, G. & Hunziker, J. Towards a DNA-like duplex without hydrogen-bonded base pairs. Angew. Chem. Int. Ed. 41, 3203–3205 (2002).
$[7.]$ Ogawa, A. K., Wu, Y., Berger, M., Schultz, P. G. & Romesberg, F. E. Rational design of an unnatural base pair with increased kinetic selectivity. J. Am. Chem. Soc. 122, 8803–8804 (2000).
$[8.]$ Kool, E. T. Synthetically modified DNAs as substrates for polymerases. Curr. Opin. Chem. Biol. 4, 602–608 (2000).
$[20.]$ Orgel, L. E. Nucleic acids — adding to the genetic alphabet. Nature 343, 18–20 (1990).
$[21.]$ Orgel, L. E. Evolution of the genetic apparatus. J. Mol.
Bio . 38, 381–393 (1968).
$[22.]$ Crick, F. H. C. The origin of the genetic code. J. Mol. Biol. 38, 367–379 (1968).
$[23.]$ Wächtershäuser, G. An all-purine precursor of nucleic acids. Proc. Natl Acad. Sci. USA 85, 1134–1135 (1988).
$[24.]$ Zubay, G. An all-purine precursor of nucleic acids. Chemtracts 2, 439–442 (1991).
$[31.]$ Szathmáry, E. Four letters in the genetic alphabet: a frozen evolutionary optimum? Proc. R. Soc. Lond. B 245, 91–99 (1991).
$[32.]$ Szathmáry, E. What is the optimum size for the genetic alphabet? Proc. Natl Acad. Sci. USA 89, 2614–2618 (1992).
$[38.]$ Mac Dónaill, D. A. Why nature chose A, C, G and U/T: an error-coding perspective of nucleotide alphabet composition. Orig. Life Evol. Biosphere 33, 433–455 (2003).
$[42.]$ Szathmáry, E. The origin of the genetic code: amino acids as cofactors in an RNA world. Trends Genet. 15, 223–229 (1999).
$[43.]$ Wong, J. T. A coevolution theory of the genetic code. Proc. Natl Acad. Sci. USA 72, 1909–1912 (1975).
Further Information:
Eörs Szathmáry’s Wikipedia web page
http://www.colbud.hu/fellows/szathmary.shtml - The Collegium Budapest is closed.
Scripps Research Institute
Steven Benner’s web page
http://www.chem.ufl.edu/benner.html - Dr. Benner left UoF in 2005.

Asked differently: Why did evolution not prefer to have a binary system to store and process data? For us, binary is much easier, and the very few tests of exotic higher-level data processing were not really successful.

Binary has nothing to do with evolution. Few of us can count to 255 in binary, we prefer decimal. Both ternary computers and SQL are "really successful", people prefer the alternatives.
This is intended to be an answer suitable for a layperson. Eörs Szathmáry’s article and it's associated references can be consulted for more details.

Thank you for this very interesting answer, after 3.5years. it gives a quite broader perspective.

@NicoDean You are most welcome. I referred to the newest information available and used it for my answer but ultimately an old opinion article offered a simpler explanation. There exists many theories, not all of them are disproved.

Just came across this post. Nice answer, @Rob. Really great effort. Your answer serves as a superb example of the high quality, well-cited answers we're looking for here. Thanks

General answer
The use of binary in computers arose primarily from practical considerations of how to represent digits using electric current or voltage (i.e. either ‘on’ or ‘off’ is the least equivocal). Such representation was not only — or even primarily — for storing information of different numerical types, but for programming logic using Boolean algebra. Physical storage of data can be in various different formats (magnetic, optical, electrical) but these are functionally equivalent and the retrieval and conversion of binary data into integers real numbers, text or images is predominantly a mathematical rather than a physical concern.
DNA has various functions, but these do not include a concern with programming logic. In  storage of data of different types, there is no problem representing different bases or radixes — sufficient different nucleic acid bases are available to represent base-4 digits. The most pertinent question in storage is one that does not arise in computer memory, that is the physical transformation of the information into other molecules. This can take the form of inverse copying of a genomic nucleic acid (DNA or, perhaps originally, RNA) in replication, the copying of one strand of information in a DNA duplex into a single strand of a related but not identical nucleic acid in the transcription to mRNA (messenger RNA), and ‘reading’ (translation) of the information in the chemical bases of the mRNA to produce a protein composed of amino acids — quite different chemical molecules.

Thus, the electronic or mathematical considerations that lead to the statement “In computing,
  binary is much easier” have no relevance for DNA and the genetic
  code, where chemical and structural molecular considerations are
  paramount. The supposition that there is a need to explain why information
  in DNA is not specifically binary is therefore false.

Speculation on the structural chemistry of the evolution of genetic information
The question of why 4-digit system (rather than 2- or 6- etc.) is still valid, but cannot be answered definitively. However, it is worth discussing to illustrate to numerical scientists the ways in which structural considerations might have determined the choice of information system. I shall consider two early stages in biochemical evolution at which the 4-digit system may have been selected for, after which — one should recognize — there might have been severe barriers to further change. Giving up Java and moving to Python (or even just changing from Java I to Java II) was probably not an option.
THE CHEMISTRY OF THE SELF-REPLICATING GENOME
I shall assume one of the main tenets of the RNA World Hypothesis — that RNA preceded DNA as the cellular genome. Even if the original genome were DNA, the question is the same — why four nucleic acid bases rather than two or six etc. — and the requirements of its chemical constitution are similar: to allow self-replication (hence the need to consider even numbers).
One might consider that an RNA with two bases arose first — let us assume adenine (A) and uracil (U) for the sake of argument. Later the cell acquired the catalytic ability to synthesize guanine (G) and cytosine (C), so that development from a self-replicating AU genome to an AUGC genome became possible. Assuming that this occurred before the amino acid-coding potential of the RNA had arisen, what might have favoured the more complex genome? It might have been something to do with the fact that there are three, rather than two, hydrogen bonds in a GC base-pair, perhaps producing a different RNA:RNA structure which was either more stable or easier to replicate for some reason. Alternatively it may have had nothing to do with the structure of the RNA:RNA helix, but was a side-effect of the acquisition of additional bases the greater chemical versatility of which enhanced the enzymic functions (ribozyme activity) of primaeval RNA.
If more meant better, why not six bases, rather than four? There might be specific chemical reasons like the slower development of the enzyme activities to produce other nucleic acid bases, or that with more bases the possibility of mispairing of bases was higher. (The ‘Goldilocks principle’ takes one a long way.) Or it may have been that the system worked well enough, was followed by the development of a triplet code, at which stage the system was frozen.
THE STRUCTURAL CHEMISTRY OF TRANSLATION
The die may have already been cast in the genome, above, but it would be a shame not to look at the chemistry of the decoding of the genetic information, as it is hardly a consideration for computer systems. So let us consider a competition between closely related organisms, one with a two-base genome and another with a four-base genome (and even a six-base genome). The requirement is to encode the information for a number of amino acids that can give proteins functional versatility — somewhere about the 20 (plus termination signals) we have today. The  size of the codon  (the word size), is 3 in a 4-bit system, accommodating 64 (43) possible codons in a (the standard) genetic code. If a 2-bit system of data storage were used then a word-size of 5 would be required to generate 32 (25) possible codons, whereas a 6-bit system could reduce the word-size to 2 with 36 (62) possible codons.
The physical consequences of such different systems would be seen in the decoding process where an adaptor molecule — transfer RNA (tRNA) — delivers amino acids to the peptidyl transferase centre of the ribosome (at one end) while interacting with the messenger RNA (mRNA) at the other end through codon–anticodon base-pairing. One might argue that the tRNA anticodon of three bases fits into the loop at the end of the helical anticodon stem in a manner that allows it adopt a relatively precise position (yes, I know about wobble) where it can make appropriate contact with the mRNA codon bases (see diagram below).

A quintuplet anticodon and five-base interaction (although not impossible) would appear less naturally adapted to the structural chemistry of RNA. Similar objections would not apply to a  two-base interaction, although one might argue that total energy of interaction between two base-pairs was insufficient to prevent errors. The error consideration also applies to a binary system where the difference in energy between a five-base interaction and a four-base interaction (i.e. a simple mismatch) would be low. Indeed, if the hypothetical competition between 2-bit and 4-bit organisms had occurred, the 2-bit system would also have been more prone to error frequency through slippage during replication.
The Last Word…
…goes to Steven Benner, whose group has constructed 8-base DNA in the laboratory:

“The ability to store information is not very interesting for
  evolution. You have to be able to transfer that information into a
  molecule that does something.”

Just came across this post. Nice answer, @David. Really great effort. I certainly appreciated reading your succinct but detailed response. Always nice to see multiple excellently-written answers to a single question. +1. Thanks


text:
What is the effect of self envenomation on reptiles?
If a venomous lizard bites its own tongue will it die?
I've searched the whole internet and I am unable to find a reliable answer on self envenomation.

Welcome to Biology.SE! We encourage you to do some research on your own and then, informed by what you have learned, ask any questions you might still have (ideally with references to reliable sources). In particular, an internet search with "reptiles immune venom" finds multiple hits as does searching for "venom" on this site. Also, homework questions must be tagged as such. ——— Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!

Sounds like a fun experiment

TL;DR
No, it won't die. Lizards/snakes are usually immune to their own venom.
Since I couldn't find a good answer to this recurring question on this site, I will try to summarize it here. I found more research on snakes than on lizards, but for now we will just assume that similar mechanisms can be found in lizards.
First, the question is how the venom kills the prey. What does it do in the body?
A common mechanism is a block of acetylcholine receptors at the neuromuscular junction. Simplified, these receptors activate muscle contraction upon a neuronal signal. When the receptor is blocked by the toxin, the neuronal signal cannot be transmitted to the muscle, which paralyzes the animal. Research has shown, that some snakes and lizards have evolved different acetylcholine receptors, that can still bind acetylcholine (and activate muscles), but not the toxins (source1, source2). This makes them immune to the most common neurotoxins found in reptile venom.
Another mechanism is hemorrhagic activity of the toxin, which is a disruption of blood vessel integrity resulting in bleeding and death. This was linked to a proteolytic ("destroying proteins") function of venom compounds (source3, source4, source5). The blood serum of snakes can contain factors that block the hemorrhagic function of toxins, possibly by neutralizing the mode of action (inhibiting proteases). This could be specific antibodies/inhibitors or an adaptation of serum proteins (source6, source7, source8).
Further research has implicated phospholipidases (destroying phospholipids like used in cellular membranes) as the mode of action for snake venoms. Again, phospholipidase inhibitors can be found in the blood serum of the snakes themselves. There were also reports, that the expression of these inhibitors changes from younger to older snakes (source9, source10) and can be induced by venom injection (source11). It is therefore hypothesized that venomous snakes or lizards are repeatedly exposed to small amounts of their own venom, building up immunity over their life span.
Other modes of action include myotoxicity (destroying muscles), edema-formation or blood thinning. Again, it depends on the specific mechanism and how snakes and lizards have adapted to be immune to these.
Since similar toxins are found in several species, snakes and lizards are often not only immune to their own venom, but also to bites of other members of the same species or other related species.


text:
What happens to embedded membrane proteins after a vesicle is formed?
When an animal cell is going through endocytosis it cell surrounds a food particle, and the membrane swallows it, creating a vesicle within the cell.
However, what happens to the embedded transmembrane proteins previously in the cell membrane? Do they shut down? Are they degraded? Or do they just not cause a problem that the cell just leaves them be?

Do you have a specific protein in mind? As @ScienceIsGolden points out in their answer, different proteins respond to this situation differently.

Endosome formation.
For the sake of keeping this somewhat brief, I'm going to stay somewhat surface level.
When a vesicle is endocytosed, it is called a primary endocytic vesicle.
When multiple primary endocytic vesicles fuse together, they form a larger entity called an early endosome.
Early endosomes can also be called "sorting endosomes" because different portions of the vesicle are sorted into different destinations, including these things called "recycling endosomes."
Transmembrane proteins in endosomes
In my experience, transmembrane proteins largely get sorted into these recycling endosomes and are then re-inserted into the cell membrane.
To my knowledge and from some cursory review on the topic, this is a common outcome for transmembrane proteins; they are eventually recycled and placed back into the cell membrane via exocytosis after being sorted into a recycling endosome.
Further reading
I'm sure others can add more explanation and some of the alternative routes these proteins can take, but in the interest of brevity and clarity, I thought it best to just stick with what I've come to know as most common.
Also, if you'd like a helpful source, see if you can get access to the following paper through a school or library service: Elkin, S. R., Lakoduk, A. M., & Schmid, S. L. (2016). Endocytic pathways and endosomal trafficking: a primer. Wiener Medizinische Wochenschrift, 166(7-8), 196-204.
In a phenomenon that I think is really cool, some receptors are thought to actually keep functioning after they are endocytosed and form these things called "signalling endosomes" (search "signalling endosomes NGF and TrkA" to read more).

Lovely answer. I've made some superficial edits to make it clearer, but feel free to roll back. Could you point me toward some article explaining the reinsertion process? As far as I am aware, unless it is a post-translationally inserted tail-anchored-TMP or a mitochondrial TMP, TMPs can only be inserted via the Sec61 translocon at the ER. I would be interested to learn more about how this mechanism works.

Hi James!  Thanks for the edits, definitely made the answer more digestible!  I tracked down an article that will hopefully get you the info you're looking for:  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3038567/
The specific section to look at is "From the ERC to the plasma membrane."  This article and others point largely to the protein Arf6 for this process, but this specific paper does the most to explain its role in re-insertion.  Hope that helps!


text:
What technique biologists use in order to determine the function of organs?
How the biologists were able to determine the functions of body organs? Using a specific example organ for an answer would be ideal.

Do you mean historically how were the functions determined or in present day how are they studied? You question is quite broad at the moment.

I mean how biologists collected data which we are provided about functions of organs? Like they determined structure of cell by observing it under the microscope but observing how it works seem difficult out of body because after cell is taken out of body it will no more be able to perform functions.

Yes I mean historically how were the functions determined

Are you asking for the entire history of an organ, the definition of an organ, or a reference that shows some tissue being described as an organ/organ-like structure?

I want to know that how scientists determined function of organ for example it is said that hypothalamus of brain is responsible for controlling blood pressure, homeostasis, body temperature, hunger , thirst etc but how did they know this?

A very common way of getting information on the function of an organ, part of an organ (such as a region of the brain) or a protein is to look at the outcome (symptoms or phenotype) in cases where it is not functional. E.g., a lot has been understood about brain function for speech production by studying aphasia in stroke patients (see wikipedia) and linking the symptoms with the brain region that is damaged.
This is still the way we mostly study living cells or organisms: mutants defective for such or such protein, or in which external disruption (such as ablation) is used and the resulting phenotype or symptoms are studied.
This is indeed very different from what can be done for research in physics e.g., where reduced systems with simpler functions can be studied. The approach in biology is much closer to reverse engineering, where a given system has to be studied as a whole but a rational approach on some subpart allows to build an understanding of that subpart.


text:
What is PDMS used for in microfluid models?
When creating a microfluidic model using polydimethylsiloxane (PDMS), is PDMS used only as a stamp to lay proteins in coverslips or can cells be cultured in the channels or patterns created in PDMS?

can you add some information about PDMS to those users who are not as familiar with it? it would greatly strengthen/clarify your question. Thanks for your contribution!

Well, it's definitely usable for more than just stamps - you can certainly perform experiments on cells within PDMS channels/patterns, etc. Not sure about long-term culture.  (PS: I don't think this question needs information about PDMS - for those who don't know: https://en.wikipedia.org/wiki/Polydimethylsiloxane)

@AJK, it does need more information about PDMS but not much. PDMS is an abbreviation so the full name should be included in the question.

Thank you for your responses. I did include the full name. But I have no problem providing more information about PDMS. So, again, PDMS stands for  Polydimethylsiloxane. it's a bio-material with several applications. the main properties of the material are that it is bio compatible (non toxic), it is very elastic, chemically stable, transparent, so it's perfect for imaging etc. PDMS is used in soft lithography as a stamp to transfer patterns onto glass and then culture cells in those patterns. I was wondering if besides acting as a stamp PDMS structures could also be used to culture cells.

I remember a friend of mine used to make microfluidic devices by pouring it in a cast and allowing for solidification. Basically, it is a building material. It can be used for cell cultures but then the matrix has to be made "bio-compatible" by coating it with appropriate substances.

PDMS in fact is established to be a reliable material for cell culture in many microfluidic devices.
Here are several papers (Titles) including reviews on microfluidic devices using PDMS:

Microfluidic devices for cell cultivation and proliferation Here
Adhesion patterns in the microvasculature are dependent on bifurcation angle Here (Microvascular Research)
Advantages and challenges of microfluidic cell culture in polydimethylsiloxane devices Here
A physiological model of the tumor microenvironment for screening drug delivery systems Here (Cancer Research Proceedings)
A Novel Dynamic Neonatal Blood-Brain Barrier on a Chip Here (Plos One)
A novel microfluidic assay reveals a key role for protein kinase C δ in regulating human neutrophil–endothelium interaction Here(JLB - Journal of Leukocyte Biology)

My research at Temple University is actually based on a microfluidic device to study cell-cell interaction in a real-time fashion.
Majority of established protocols are using fibronectin or collagen, and in the case of tumor cells culture, matrigel for extracellular matrix. Devices are being coated with the ECM protein and then cells can be cultured in the device.
We have shown that in our microfluidic device, human umbilical vein endothelial cells (a.k.a. HUVECs) are forming a complete 3D lumen in the channels.
It is important to note that due to the elasticity of the PDMS, cells are needed to be under physiological flow conditions. Otherwise, it was shown that the cells start to detach from the PDMS. Under such physiological conditions (flow, media, gas exchange), cells can be alive and functional up to a week or two, depending on the design. In our system, the last two publications, cells are functional up to 2 weeks and 1 week respectively.

Could you link the cited papers?As of now the citations are meaningless. +1 for this answer and welcome 2 Bio.


text:
Is a DNA molecule a single strand of polynucleotide or two of them linked together?
Our molecular biology teacher told us that a double helix of DNA was composed of two DNA molecules linked together by hydrogen bonds. The thing is, until now, I always thought a DNA molecule was composed of two strands, those being polynucleotides, both of them being linked together. I can't find a link which is saying the same as my teacher, even if it seems technically correct to call a double helix a dimer of two DNA molecules.
I was curious to know what was the exact terminology.

I have provided an answer to this question, but would stress that there is NO "exact terminology" provided in any of the answers because, as far as I am aware, the terminology in molecular biology is based on usage rather than definition.

Hmm, I think that the teacher is actually correct and that the previous explanation, although very nicely referring to text book diagrams, is a little misleading.
The issue here is the nature of a hydrogen bond within the DNA structure. Within a chemical context, generally a molecule is a collection of atoms primarily bonded together via covalent bonds. Hydrogen bonds, by their very nature are transient - if they weren't then the double stranded DNA wouldn't be able to opened for reading! So, a strand of DNA, from the 5' end to the 3' end is one molecule. The reverse complement strand to this is another molecule of DNA. This is important as if you were carrying out a PCR reaction (for example), you would use single, stranded DNA as primers - so this would be a molecule of DNA. Also, if we were to use hydrogen bonds as a means of defining a molecular species, then water would only be one molecule - all of those H2O molecules interact via hydrogen bonds with each other!
But what about the double helix structure? Well this is a consequence of the chemical structure of each nucleotide (and the chemical properties of those atoms), aided by the hydrogen bonding to tightly pack the atoms together - it's a form taken by the thermodynamics of the inter-molecular interactions between the two molecules of DNA.
So, a strand of DNA is a molecule. Two strands (two molecules) of DNA give us the natural, stable, helical form.

Biologists can be pretty lax when it comes to chemical definitions. Technically it's not a molecule at all but rather a polyatomic ion.

The IUPAC definition of molecule is "An electrically neutral entity consisting of more than one atom (n > 1). Rigorously, a molecule, in which n > 1 must correspond to a depression on the potential energy surface that is deep enough to confine at least one vibrational state. " https://goldbook.iupac.org/html/M/M04002.html So unless the two strands are held together too weakly to confine at least one vibrational state (which is not the case) the two hydrogen-bonded strands are one molecule.

@DavePhD There needs to be more rigourous definition I believe because if we just consider the cited IUPAC definition, liquids and solids can also be possibly considered one single molecule. That is definitely not the case. Moreover, in case of RNA (which has higher structural diversity in nature compared to DNA) can form hairpins, double helices and single strands (and a complex containing all these forms). In such cases we do use the terms intra/inter- molecular interactions/hydrogen bonds to distinguish between the double helices and hairpins/stem-loops.

This has come up again recently, so let me summarize my own arguments on what I believe is a purely semantic question.

In strict chemical terms, according to the IUPAC definition, neither double-stranded DNA (dsDNA) nor its individual separated strands is a molecule but, as stated in the Wikipedia article, a polyatomic ion.

If one extends the term ‘molecule’ to ions and considers only the historical criteria of covalent chemical linkage and indivisibility (as applied to small chemical species) one would conclude that the individual separated strands of DNA were molecules, but dsDNA was not — the complete opposite to the assertion in the accepted answer!

In practice, however, many authors refer to dsDNA as a molecule, presumably because they regard it as conceptually different to the two (different) single stands. I accept this as usage, but emphasize that it is not based on any formal re-definition of the term ‘molecule’ for molecular biology that I am aware of.

Although some text-book authors avoid using the term ‘molecule’ for the individual strands of dsDNA — presumably for clarity in explanation — this use by others is widespread (e.g. in Lakowicz, DNA Technology).

It seems absurd to argue that the single stranded DNA genome of, say, SV40 virus is a molecule, but an individual strand of a circular dsDNA plasmid is not. The situation is compounded in the comparable question for RNA. Consider dsRNA viruses, where one strand is synthesized in large quantities: what is being synthesized if it is not an RNA molecule?

But likewise it would seem to be absurd to argue that dsDNA is not a molecule but becomes one after, say, chemical cross-linking.

In my opinion this question would only be of practical importance if ambiguity could arise from applying the description ‘molecule’ to both dsDNA and its single strands. I see no such ambiguity, per se, and maintain that this is a purely semantic question.

I therefore conclude that assertions that the term ‘molecule’ be restricted to either dsDNA or, conversely, to its individual single strands are both pointless and unjustified.


text:
Are oysters really aphrodisiacs?
Oysters have been thought of as aphrodisiacs for millennia.
Is this a case of the bark of a willow tree as a precursor to modern paracetamol, or some sort of marketing ploy.
Is there any biological evidence that foodstuffs such as lobsters, oysters and other sea delicacies boost our sexual health and desire? If so, what biological mechanism underlies this property?

What research have you done before asking it here?

Positively, a lot of people consider seafood an aphrodisiac for various reasons. I am interested in the scientific point of view.

Welcome to Bio. It feels more like a rumor than anything else. I am unfamiliar with the specific stack, but Skeptics.SE may be more appropriate. The question as it stands may be anecdotal and it is too broad for this site. If you could add a credible source that claims your hypothesis, it would already improve your post. Why and How questions generally fair well here. 'Is X true questions' are generally much less well received.

I'm voting to close this question as off-topic because I think it may be better suited for Skeptics.SE

@LadyFickle To be answered in Skeptics.SE you will need to provide a specific source for the information which has to show that it is a notable claim (for example, something like a major newspaper publication, not a copy of a Facebook post). I am sure you can find such a source but you have to do that work rather than having us do it for you. Second, I somewhat disagree that this question doesn't belong here. I think if you provide a decent source we can answer it as a biology question.

(also note that "notable" doesn't mean you have to find a well-referenced source, just something to show that it isn't just speculation among a group of people but rather a wide-ranging idea, see this meta )

I've heard this before. Apparently, oysters have been thought of as an aphrodisiac for millennia: https://theoystersmyworld.com/tag/casanova-and-oysters/

http://www.telegraph.co.uk/news/uknews/1486054/Raw-oysters-really-are-aphrodisiacs-say-scientists-and-now-is-the-time-to-eat-them.html


text:
How much oxygen does a plant use up at night?
Given the fact that plants cannot do photosynthesis at night but need respiration for their energy needs, they use up oxygen and generate carbon dioxide. But how much is this? If I fill a room with plants thoroughly, what composition will the air in this room be in the morning? Are different plant species vastly different in this regard?

I saw this and thought, "surely this is google-able"! For me, a non-expert in plants, there seem to be different results for different plant types and this makes getting an answer tricky on the scholar, and on regular google, it's hard wading through the basic level material. I'm sure for an expert this is an easy answer.

@James: I first googled it, but I just stumbled upon answers from people not educated in the matter, who just made wild guesses. I hope to find an answer that is more fact backed than what I found out in the wild of the internet.

Roughly, half of the CO2 assimilated annually through photosynthesis
  is released back to the atmosphere by plant respiration (Gifford,
  1994; Amthor, 1995).

Source:
https://academic.oup.com/aob/article/94/5/647/151785/Plant-Respiration-and-Elevated-Atmospheric-CO2
Furthermore, it appears like plant respiration rates do not change much with changing temperature, and that larger plants have higher respiration rates.


text:
General Enhancer Questions (Methylation Patterns, ect.)
I have a biological question(s) for ya'll involving enhancers.
1.) Enhancers work by being the binding sites for TFs. But how does this increase transcription? (Especially when enhancers can be extremely far away from the gene they control.)
2.) Enhancers can become methylated. When they do, does this usually prevent transcription factor binding? And if it does prevent the binding, how does this affect the role of the TF and gene expression.
EDIT:  Here's what I found.
It seems that enhancers can be far away from the gene they act upon, but the binding of TF via their DNA-binding domain can cause looping of DNA to help them reach the promoter region of the gene of interest. Thus, increasing the rate of gene expression.
On the reverse, methylation can sometimes be seen to act as silencing of gene expression. So, if our enhancer region is methylated, this may prevent TF binding and the enhancer from increasing gene expression.
BONUS:  Methylation in promoters can also cause silencing by preventing RNA polymerase II, and the required proteins (ect) from carrying transcription.
If anybody wants to add (or correct anything, let me know!)

Welcome to SE Biology. Please read the Tour and the Help on asking questions. You will see that we expect you to show evidence of the research you have done yourself to try to answer questions. What did you find on Wikipedia or other sources when you did an internet search? How did it fail to answer your question?

Thanks.. I added what I found onto my original post!  Cheers!

Your question is very broad. You can find several reviews on how methylation affects DNA function.

This subject is actually both complicated and incompletely understood. For example, there is evidence that some enhancers don't result in loops at all — instead their influence travels along the chromatin to a nearby promoter.
You can think of enhancers as being staging areas where protein complexes that promote transcription are assembled. In some cases enhancers are where the RNA polymerase complex is first bound.
When loops do form, this allows the proteins at an enhancer to interact directly with the transcriptional start site.
I think you will find this 2015 review to be a helpful introduction.1

As for methylation (which maybe would be better as a separate question), it is generally true that methylation acts to reduce transcription factor binding and thus decreases transcription.2
However, that overall trend disguises some more complex dynamics.3

References:
1: Pennacchio, L. A., Bickmore, W., Dean, A., Nobrega, M. A., & Bejerano, G. (2013). Enhancers: five essential questions. Nature Reviews Genetics, 14(4), 288.
2: Lea, A. J., Vockley, C. M., Johnston, R. A., Del Carpio, C. A., Barreiro, L. B., Reddy, T. E., & Tung, J. (2018). Genome-wide quantification of the effects of DNA methylation on human gene regulation. ELife, 7, e37513.
3: Sharifi-Zarchi, A., Gerovska, D., Adachi, K., Totonchi, M., Pezeshk, H., Taft, R. J., ... & Araúzo-Bravo, M. J. (2017). DNA methylation regulates discrimination of enhancers from promoters through a H3K4me1-H3K4me3 seesaw mechanism. BMC genomics, 18(1), 964.