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Can DNA base pairs go through each other?
Consider the simplified version of the motion one DNA base pair held together by a hydrogen bond:

Use u and v to denote the displacements of the bases from their equilibrium position along the direction of the hydrogen bond that connects them,
Define y = u-v to measure the stretching distance between the bases in a pair of bases.
So, y = 0. u=v. No stretching. When y > 0. Stretching. When y < 0. Compression. u

I would like to say, that physically, it is not possible for u to go through v or vice versa. Meaning that the stretching distance measured by y has a lower bound. In other words and my question, does it make physical sense for two base pairs to go through each other?

What do you mean by going through? Is there any terminology for this?

I do not have any terminology for this. I am trying to visualize what the model implies. I am assuming that if that we have 1 dimensional motion (1 degree of freedom) and if I, say, fix u and let v move towards u (compression), then eventually it will have to go through u if the motion of both bases is along the hydrogen bond.

I'm voting to close this question as off-topic because this is Physics.

Covalent chemical bonds between atoms like C-N, C=N, C-C, C=C etc are actually maintained by electron orbits. It is hard to disturb these orbits. When they are disturbed, the bonds would break, which means some chemical reaction occurs. Then you get different chemicals--they are not u and v anymore. That is what I think. This seems more chemical thing rather than biology.

@243 I think OP is describing a situation where you have 2 bases in a plane, and push 1 towards the other, still in the plane. As the bases moved closer the atoms would begin to repel. We can think of it in terms of Leonard-Jones Potential, where the repulsive force is inversely proportional to the distance to the 12th power. This means that the repulsion gets really high really fast. Since the bases are magically locked in the plane, you'd probably push them close together and stop. In reality, one would pop above or to side of other.

The base pair you are describing is only stable if each base is part of a macromolecular polymer, a polynucleotide. Specifically the DNA strands need to be oriented in an anti parallel alignment, and there will be a chain, or string, of base pairs (imagine the rungs of a ladder).
Remember, individual hydrogen, or H-bonds, are one of the weakest molecular interactions that we can detect. So the scenario you propose, where one single base forms a Watson-Crick base pair with its complementary base, free in solution, is so unstable as to be undetectable.
Once the base pairs are formed in a DNA double helix (think of a flexible ladder where one end is fixed and the other end has been twisted through several clockwise revolutions) then there are many other energetic contributions that stabilize the base pairs. For example, the electrostatic repulsion of the anionic phosphates in the sugar-phosphate backbone drives the two strands apart.  The hydrophobic stacking interactions of the pi bonds of adjacent bases also makes a major contribution to the stability of the helix, and permits the H-bonds to be more stable in this context.
Finally, the fact that base pairs are only stable in polynucleotides means that if you melt a single base pair, the sugar phosphate backbones will topologically prevent any other melted base pair from "passing through" the first one.


text:
Stochastic parameters in population growth equations
I'm more of a mathematician than a biologist, so I had a question about an application of the population growth equation to real-life models, and thus would like to ask biologists for their insights. The equation I'm looking at is the following (in reality, I have n-species but it's just an extension of this two dimensional problem):
$$ \frac{dx_1}{dt} =x_1\Big(b_1-a_{11}x_1-a_{12}x_2 \Big) $$
$$ \frac{dx_2}{dt} =x_2\Big(b_2-a_{21}x_1-a_{22}x_2 \Big) $$
where the $b$ are growth parameters, and the $a$'s are all parameters describing interactions among the species (and carrying capacity). The papers I've looked at for stochastic perturbations with these equations have primarily dealt with stochastically perturbing either the $b$ parameters while holding the others constant, or perturbing the $a$ parameters while holding $b$'s constant. However, these papers are written by mathematicians with no biological experience, so the decision on which sets of parameters to perturb are somewhat arbitrarily decided without any biological basis.
For the biologists, can someone suggest some cases for where it would be more biologically reasonable to perturb the growth parameters and some cases were it would make more biological sense to perturb the interacting parameters? I ask because I'm a part of some interdisciplinary neuroscience project which is using equations of this form to study interacting neuron clusters, but since I'm a math person and not a biologist, I am trying to understand reasonable explanations for what stochastic perturbations mean biologically for these parameters.

This is somewhat similar to the https://en.wikipedia.org/wiki/Lotka%E2%80%93Volterra_equations You can probably find related articles here: https://www.google.com/search?q=Lotka+Volterra+equations+perturb , https://scholar.google.com/scholar?q=Lotka%E2%80%93Volterra+equations+perturb Note: I don't know what "perturb" means in this context.

Since you are asking for the biological interpretations about these parameters, it is important to realize that the model you are presenting is a non-dimensionalized version of this model:
$$ \frac{dx_1}{dt} =b_1x_1\Big(1- \Big(\frac{x_1 + \beta_{12}x_2}{K_1} \Big)\Big) $$
$$ \frac{dx_2}{dt} =b_2x_2\Big(1- \Big(\frac{x_2 + \beta_{21}x_1}{K_2} \Big)\Big), $$
which can also be written as:
$$ \frac{dx_1}{dt} =b_1x_1\Big(1- \frac{x_1}{K_1} - \beta_{12}\frac{x_2}{K_1}\Big) $$
$$ \frac{dx_2}{dt} =b_2x_2\Big(1- \frac{x_2}{K_2} - \beta_{21}\frac{x_1}{K_2}\Big). $$
This clearly shows how this competition model is merely the logistic Verhulst model, with an extra term attached. This extra term is simply describing to what extent each individual in "species" 2 is using up the resources of "species" 1 ($K_1$), where $\beta_{12}$ describes this relationship (~proportion of species 2 that is counted as species 1). The parameters in the model formulations above are also more easily interpreted in ecological/biological terms than the $a_{ij}$s in your model.
To go from this latter formulation to yours you substitute:
$$a_{11} = b_1/K_1$$
$$a_{12} = \frac{b_1\beta_{12}}{K_1}$$
$$a_{22} = b_2/K_2$$
$$a_{21} = \frac{b_2\beta_{21}}{K_2}$$
As you can see, this means that the $a_{ij}$s are composites of other parameters, and perturbing $a_{ij}$s could correspond to either $b_i$, $K_i$ or $\beta_{ij}$ being perturbed. It also means that perturbing e.g. $b_1$ in your model while holding $a_{11}$ fixed means that you are actually also perturbing $K_1$ to offset the change in $b_1$ (since $a_{11} = b_1/K_1$), which will introduce a positive temporal correlation between $K_1$ and $b_1$. This is a strong assumption to make. This also means that $a_{ij}$s are not strictly "interaction parameters" as you call them, but they include other aspects as well.
Since realistic cases and scenarios for perturbations may often be expressed in terms of the parametrization I give above (e.g. random fluctuations in population growth rate or carrying capacity), these relationships are essential to keep in mind.

You just have 6 parameters in this model and you can easily perturb each of them individually while holding the others constant. This will let you know the individual effect of different parameters.
To assess the global sensitivity of the system to "environmental" perturbations, what you can do is to a random multivariate sampling of parameters. You will get different combinations of parameter values. Then you can plot the distribution of any metric that you intend to study.
However, if you intend to perturb a single parameter or a few parameters in combination, the choice of which ones to perturb depends on what you intend to study. System can, in general be insensitive to certain parameters. Local sensitivity analysis can be done to study the effect of parameter on the steady state. This you can do by taking a derivative of the expression for steady state with respect to the parameter. For a simple model such as:
$$\frac{dx}{dt}=x(b-ax)$$
local sensitivity of the steady state $x^*=b/a\ $ to $a$ would be $$\frac{dx^*}{da}=-\frac{b}{a^2}$$.
From here you can see that the effect of perturbation of $a$ on $x^*$ would be higher than that of $b$.
However local sensitivity analysis does not tell anything about dynamics and for complicated systems it may be difficult to guess which parameter would have the strongest effect.
For such cases you may do a random sampling and then run a classification/regression algorithm to determine which parameter had the strongest effect on your metric.
Another approach is to guess which parameters are likely to get perturbed in the natural course of events. This, you would know from prior knowledge of the system. If we assume steady environment, then the carrying capacity is not likely to change much. However, for a population of great phenotypic diversity, the growth rate may vary a lot.

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text:
Can/Have cancer cells be/been used in stem cell culture lines?
Since Cancer cells have unlimited growth potential, can they be induced towards totipotency and pluripotency?
If so, can cancer cells be used in stem cell culture because of similar properties of unlimited replication?
Can they be used in cell lines to culture viruses even?

Some murine embryonic carcinoma cells are pluripotential and can differentiate and develop to mice.

Cancer cells can be and are used in cell culture. HeLa cells were the first human cell line to be grown in culture and they were derived from a cervical tumor.
That being said, Cancer cell lines would not necessarily be used for stem cell work. They have sustained too many mutations to study the type of questions that stem cells are used to study, though as MattDMo points out, teratomas, tumors that originate from stem cells, can be used in stem cell research as a model for Stem Cells in culture. Also, they could never be used for therapeutic purposes.
As for viruses, HeLa cells were used by Jonas Salk to develop the polio vaccine, so cancer cells are used in viral research.
Edits in italics.

This is actually not true. I have used teratoma lines to simulate stem cells in some experimental protocols.

Teratoma lines are from stem cell derived tumors. Can you prove that the cells that formed the stable lines weren't still at the stem cell stage? And would you use those cells therapeutically? Would you make a chimeric line of mice from teratoma derived lines or would you use ESC lines? And what were the assays you ran?

see my answer below for some additional details. No, of course we wouldn't use them therapeutically or for chimeras - we used them purely for in vitro work, alongside "true" iPS and ES lines.

Adding onto AMR's answer, cancer cell lines are used extensively for research. They are typically fast to grow. HeLa Long grow to capacity of a 10cm dish within about 48hours, depending how you split them. Now some lines are different than others and each have their pros/cons but the main thing behind them is they make it possible to view the effects of genes being knocked-down/out in human cells.
As for the use of viruses in cell cultures. They are not only used for viral research but also genomic research.
What is typically done is to introduce a gene into a cell culture line via a retrovirus (called a Retroviral Transfection). It is an extremely effective method of creating a stable cell line with your gene of interest attached to a "fluorescent" gene so you can visualize it in the cell when it gets transcribed. This leads to Immunofluorescence(IF) and many other techniques commonly used today.
You can also introduce a plasmid to cells that contains a shRNA that will "knockdown" the gene you are studying the effects of. This way you can see what happens to cells when this gene is not present (done a lot for study of replication proteins).
The caveat is that sometimes these cell lines can be transient (last only a few passages) or stable. They all also act very differently so typically to "prove your case" that the protein has the function you conclude it to have, you should do experiments with several different cancer cell lines.

Regarding your question about whether cancer cells could be used in studying stem cells:
I have done stem cell work, and we used various teratoma cell lines (which are cancers that resemble germline tissue) in parallel with embryonic stem cells (ES cells) and induced pluripotent stem cells (iPS cells) for various experiments. Of course the choice of experimental system completely depends on what exactly you're studying, but teratomas have proven themselves to be reliable model systems for looking at certain aspects of stem cell structure, function, and differentiation. One of the biggest advantages, at least in the work that I was doing, was that they grew relatively quickly and consistently, while iPS or ES cells can very easily spontaneously differentiate if extreme care is not taken in culturing and passaging them. You don't have to worry about donor-to-donor variation, and they are pretty tolerant to being frozen and thawed.
The work I did was in industry, so unfortunately I can't really get into many details, but I was involved in looking at various transcription factors that are responsible for the maintenance of pluripotency as well as the induction of differentiation, as well as testing various live-cell imaging techniques to track particular differentiation pathways. We made a number of observations using teratomas that directly translated to iPS and ES systems, without all of the overhead that those systems required.

If they do not behave like stem cells, i.e. If you do not need to carefully use inhibitors such as 2i or LIF with fibroblasts in culture to prevent differentiation , then I would question the reliability the results I obtained. Just because a system is easier doesn't always mean it is the choice that will get you completely accurate data. If I read a paper that used teratoma lines instead of SC lines I would read more carefully with a higher than average degree of skepticism over the results.

@AMR the teratoma lines were used as a model system for ES/iPS cells, not in place of them. We used them for assay development and experiments where significant amounts of protein were needed initially, to verify conditions and make some observations. Of course the studies were repeated in actual ES/iPS cells to ensure the model matched. This is exactly the same as performing some immunological studies using Jurkat cells, then repeating the assays using primary human T cells, which are harder and more expensive to obtain and maintain. You can learn a lot about "reality" from a model.

See edit in my answer.

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Why do some trees in California have dead brown leaves but also new green leaves?
It's Autumn 2015, and I just saw a tree that had mainly dead brown leaves but also some new small green leaves growing. Why didn't the tree just keep its old leaves? Does it think we are in spring already?
EDIT: To be clear, I had always thought that in autumn that all the leaves of a tree would fall off together, as a preparation for winter. It seems silly that the tree would then immediately grow some new leaves when it just decided to let all those previous leaves die. Why not just use that same energy to maintain those leaves?
I've taken some photos of the leaves and the trunk for help with identification.

More images of the tree can be seen at this Imgur link

Welcome to Bio. Without a picture or species identification any answer is mere guessing.

I don't think it would be localized to just California but a picture would definetly help. There could be so many reasons why the tree hasn't dropped it's dead foliage .

I've edited the original post with a link to some photos! Tell me if you need more.

What is your question? Are you asking why there are dead leaves and green leaves, are you asking why trees don't have their leaves last forever, or are you asking why the dead leaves didn't fall off?

I'm wondering why the tree seems to be growing new green leaves while it has many dying leaves. Why didn't it just use that energy to maintain the existing leaves?

Whether trees are deciduous or evergreen, their leaves don't last forever; they need to be replaced at intervals.  The process of photosynthesis depletes the chlorophyll in the leaves, so that needs to be replaced and this is a significant metabolic cost to the tree.  Therefore, whenever a tree is experiencing metabolic stress, it will slow down the chlorophyll replacement, and let the leaves die to save energy. It's metabolically cheaper to simply let the leaves die -- after removing the most precious nutrients -- and then regrow new leaves as needed, than to keep repairing the leaves that aren't needed because the tree is resting for other reasons.
In temperate areas, where there are well-defined seasons, this typically happens in the fall, and deciduous trees let their leaves die all at once in the fall.  In tropical or subtropical regions, where trees could photosynthesize all year, leaves may drop all year round (as with evergreen trees, like conifers, in temperate regions).  Often, though, their leaves will reflect metabolic stresses on the tree, such as drought.
(The Wikipedia article on "Deciduous" makes the point that this can be very localized, related to very local environmental differences that could only affect a single tree.)
Much of California is a subtropical region, and it has been experiencing severe drought for some time, so it wouldn't be surprising for a tree to have reached a point where its leaves have all had their chlorophyll removed.  On the other hand, as the El Nino event of 2015 increases, rainfall in California is returning, so it would also not be surprising for a tree to have recovered from drought enough to start making new leaves.
If your question is why the old leaves didn't fall off before the new ones started to regrow, it is probably simply a matter of timing.  The tree doesn't really "care" if the leaves fall or not, so long as they're not using up its resources, so there's no reason to force them off.  The new water supply may have arrived fairly shortly after the degree of drought that caused the tree to shut down the leaves.

Ah, I assumed that all the leaves were browning and falling off together because of the season. In this scenario, it seemed silly to start growing leaves again after letting them all die. If I'm understanding you correctly, in California this may be a continuous leaf dying/growing cycle throughout the year? And the recent rain (indeed, it rained for the first time in a few months last week) allowed the growth of some fresh new leaves?

Exactly right.  In fact, drought is functionally why leaves drop even in temperate zones -- in winter, all the water is locked up in the form of snow and ice that plants can't take advantage of, so they drop their leaves in preparation for this predictable period of drought.

Depending on the part of California, most deciduous trees will go through the customary winter-dormancy cycle as is seen throughout the rest of the planet, albeit often majorly abbreviated. Even as far south as Needles many "eastern hardwoods" that had been planted by landowners will dutifully drop their leaves as winter approaches, renewing their greenery he following spring.
The problem you mentioned is not restricted to California: Deciduous trees and shrubs facing severe and/or prolonged drought conditions will "go dormant" earlier than would be normal. This is a simple "survival strategy," in which the plant reduces the potential for long-term injury or harm by---in effect---hibernating. Nature has built this survival strategy into a wide range of life-forms; periods of crisis-dormancy allows the subjects to "weather" adverse conditions and, "hopefully," revive when the previously-experienced problems had passed.
I've noted deciduous plants going through leaf-drop as early as July, in New York State. Recently-planted deciduous trees and shrubs do not have the extensive root-systems of established plants, and will quite often go through early leaf-drop because they will feel the effects of a drought far more keenly than established plants. That is not to suggest that your trees or shrubs were recent plantings: It is merely a statement of fact.
A curious thing about early-dormancy is that plants will "rebound" and set new leaves---essentially, sending forth some of the leaves that had been grown for next year's spring and summer cycle.
This will come about when there has been a very recent period of increased rainfall, coupled with cooler ambient temperatures.
If you will check the recent weather-tables for California, you will note this is exactly what happened: A long, hot, period of zero precipitation and arid humidity was broken by an interval of cooler and more-moist weather, going into late-summer and fall.
The California hardwoods had "rebounded," setting a reduced number of new leaves and, essentially, tried to make up for the brutal conditions of the previous spring and summer by getting a few more weeks of photosynthesis and growth before Autumn arrived without doubt, and the cycles of shorter days and reduced temperatures obliged the plants to enter "true" dormancy.
My 12-15 hours of "Dendrology" (the study of trees) were taken nearly five decades ago, although I'd striven to maintain a B+, even in "Science electives." Besides, I'd really enjoyed "woodsy" courses as it allowed me another valid excuse to "prowl the pines & ramble the brambles!"


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What does uniprot consider "unambiguous" evidence for the subcellular domain of a protein?
Uniprot has annotation for subcellular location of protein domains. This topological domain information of proteins is under the TOPO_DOM flag.
In most cases the subcellular location is assigned by rigorous sequence analysis both for the experimentally verified and predicted subcellular locations. Sometimes more reliable information is available...

... when the experimental technique used allows the unambiguous
  assignment of the transmembrane boundary to a particular position
  (X-ray crystallography, etc.), the ‘Sequence analysis’ qualifier is
  not added in the topological domain annotation. In this case, the
  positions of the topological domains can be propagated ‘By
  similarity’.

What evidence is available that constitutes "unambiguous assignment" so that the by similarity qualifier can be used?

Following your question, we have updated the documentation for topological domains in UniProtKB:
http://www.uniprot.org/help/topo_dom
I hope you will find it more informative now. Please don't hesitate to contact the UniProt helpdesk if you have any additional questions (or, if you prefer to discuss here, a short note to the helpdesk would help us spot your posting more reliably, since we cannot closely monitor all forums as you may understand).


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How can I find the mRNA sequence for a specific prokaryotic gene?
What I want to find out is the start of the transcription for a specific gene, how long the UTR is before the actual coding sequence starts.
I've looked at various databases like NCBI Gene, Refseq or a specialized one like PRODORIC. But none of them actually contain the mRNA sequence or any information about the untranslated parts of the mRNA. Just the coding sequence itself.
Is that kind of information simply not annotated for many bacteria? I'm not looking at model organisms like E. Coli or B. subtilis, but I would have expected some information to be available.
Is there a database where I can find the actual transcript sequences for prokaryotic genes?

I haven't been able to find that kind of information anywhere. Finding the genomic context is "fairly easy" but the transcription information is much harder to find. You'll probably will have to find transcription elements yourself.

mRNA specific queries
Add this to your NCBI query: AND mrna[filter]
If it's not available in major databases it may not be known.
However mRNA data can be obscure to find even in those major databases but it should be there. I would be surprised if that is the case, however since you're not working with model organisms there may well be nothing available.
When looking for a transcript gene, NCBI have some tips that you can see here for searching their database. #8 might be relevant to you as it's a way of filtering exclusively mRNA records.

If there is no UniGene cluster for this gene and organism, perform a
  search in the Nucleotide database with the gene name, product name, or
  symbol. Include the organism in the search to find the most relevant
  results and filter for transcript sequences, for example: Cytochrome c
  AND bullfrog[orgn] AND mrna[filter].

Predicting mRNA
Basic: ExPasy DNA translation tool
Advanced: regrna 2
Assuming that advanced querying doesn't reveal what you need you might be able to make some useful predictions before taking it to the lab. There are a handful of other predictive tools that can maybe help you out if that's the only option available. I can't get my head around exactly what information you have as an input. Assuming you have the DNA sequence, I would start with the obvious choice: the ExPasy DNA translation tool.
I would then say that regrna 2 might be able to steer you in the right direction regarding more subtle translational elements.


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Getting PCR amplification at annealing higher than Tm!
I am amplifying a gene where in a gradient pcr i am getting amplification at an annealing temperature about 5 degrees (67) higher than Tm (62.5)? What is wrong here? Also, I am getting a very strong intense band at wrong size for all the temperatures tried below Tm. Pls help

Are you calculating Tm bioinformatically, because that is just an estimate? If you have a lot of GC content, your melt temp will be higher. It could also be the salt concentration of your buffer. If they are old reagents, you might of had some evaporation and your salt content could be higher than normal... You also do not mention whether the wrong size is smaller or larger. Could be primer dimers or you could have off target annealing. primers do not need to be completely complementary to anneal properly and if you have a primer and a sequence with a lot of GC it could anneal preferentially.

Possible duplicate of Does an annealing temp higher than primer's Tm contribute to primer dimer?

It is very common to get annealing at higher than predicted Tm.  If it's a problem in your case, especially if you're getting mis-annealing at lower temperatures, consider using touchdown PCR to find an optimal temperature.  Or, pragmatically, if you have any flexibility in primer design, simply order a set of primers and try them all.  Primers are cheap today, and you'll often find a set that work even where the design programs claim they won't.

Tm of primers would not tell much about PCR conditions. When you get non-specific bands, it is worth to try higher temperature.
Your temp trying is already close to the temp to extend, so that shuttle PCR is available. Shuttle PCR has just 2 steps: 94 to 96 degrees for melting DNA and 68 to 74 degrees for annealing and extension together.
You might want to add DMSO or betain. They could help to reduce mis-annealing.
If the non-specific bands are smaller and longer than bands you expect, longer and shorter extension times may give you better results, respectively.
And remember, primer design is also important. Check you have sequences repeating in your template and avoid to design primers from such sequences.

Regarding higher annealing temp than Tm, I often use T7 primer of which Tm is 48.3 degrees. The primer works well at 55 degrees of annealing temp. Usually, primers are excess in PCR reaction tubes, pushing the chemical equilibrium toward annealing. That is what I speculate.

The TM of the primer is also influnced of the salt concentration of your mix. Do you try the PCR gradient? Or you try the calculation of Tm and take in consideration the salt concentration.
http://www.biophp.org/minitools/melting_temperature/demo.php

Welcome to SE Biology. It is a good idea to look at the date of posts — easy to miss, especially on a phone — because if you are asking a question of the poster or making practical suggestions in your answer you may be wasting your time. Of course if the question is scientific and you feel it has not been properly answered go ahead. (But not in this case, I think.)

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Is this a spider caught on video floating its web between trees?
I live in the US and have trail cameras on my property to capture wildlife, visitors, stray animals, etc.  Several are equipped with infrared and I have watched hundreds of hours of video. Many videos feature a large amount of insects flying so I know what a bug looks like on infrared.
What I captured yesterday is completely different. It is a perfectly round sphere floating from one side of my driveway to the other and back again. It appears to me to be on convection currents passing between the trees that line my driveway.
I uploaded this video to Youtube and would be very grateful if you could take a look and tell me if you think it is indeed a spider floating its web between trees. Additionally, are you aware if this phenomenon has ever been captured on video before?  I searched the web looking for other videos but am unable to find any.
The 'orb' appears at 10 seconds into this video.

If you're saying you think this is a spider riding air currents to travel from tree to tree, sorry, but I don't see it. If it's actually moving from one side of the drive to the other, it would have to be moving relatively quickly to cover that distance (about 20 feet according to the video) in only a second or so. If it's just being blown by the air, it seems to me like it would have to have been fairly windy to have moved that quickly, or be capable of directed flight.
It seems more likely to me that's it's just a particle of dust or similar material floating close to the camera. The reflection of the IR light causes it to appear much larger and causes the shape to appear more regular than it truly is. If it's actually a much closer to the camera, only light breeze would be required to show this behavior. There's a strand of web clearly visible near the camera, and perhaps this is indeed something caught in another strand web and dangling down in front of the camera—heck, it could actually be a small spider, but it appears dangling from a web near the camera rather than floating between trees.
I couldn't tell you exactly what it is, but it seems more likely to me that be a trick of light and perspective than a spider floating from one side of the drive to the other.
Disclaimer: I'm not an expert in arachnology or videography. These are just my thoughts on the video.

OK, so I posed the question in the wrong location.  This IS how spiders build webs between trees .. they DO float on convection currents that don't even have to be breezy but more made up of heat rising.  I submitted this to the international arachnid institute and they have verified that it is not only a spiders kiting bubble but at second 18 you can see the spider.

@user3037683 - Why posting a question where the answer is already given by a seemingly credible source?

@user3037683 To be clear, I'm sure that some spiders make their webs in this manner, I'm just skeptical that this is what's being shown here, given the speed at which the object would be moving. I've watched the video closely, and tried to look at each frame around the 18s mark as you suggest and I still can't see anything that can clearly be distinguished as something other than compression artifacts around the orb. You very well might have captured just what you say here, the video just isn't clear enough to say for certain.


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Why do specifically bananas go brown quicker in the fridge?
Perhaps the title should be: Why don't all fruits containing phenol residues go brown quickly when left in the fridge?
Bananas go brown over time because of the oxidation of phenol residues.
Bananas go brown quicker in the fridge than left at room temperature. This seems to contradict the first point since the reaction should be slower at colder temperatures. Dialogue from the naked scientists briefly explains why my line of thinking might be wrong.

Emily: Well it’s a good question and the answer is that they will
  brown faster in the fridge.  It’s mainly due to the formation of ice
  crystals, so if you put your banana in the fridge, the ice crystals
  grow, and they actually rupture the cells of the banana skin. This
  releases an enzyme called polyphenol oxidase and as the name suggests
  it acts to oxygenate phenols, which have a ring-like structure, into
  quinones, and these quinones can then all join together or polymerise
  and produce a black, brown, or red pigment called polyphenol and this
  is what gives it the brown colour. So, if you have your banana in the
  fridge, this will occur and you'll get a brown banana.  But another
  interesting thing about bananas is that if you have them in the fruit
  bowl, they'll release ethene and this will make the other fruits in
  the bowl ripen faster because it’s a ripening hormone.
Chris:   So, the question is though, if this is a chemical reaction
  making this brown pigment, if you slow down the reaction by lowering
  the temperature, then it should happen more slowly, therefore, going
  in the fridge should make the bananas go black slower?
Emily:   I can see why you're thinking that but actually, it’s more
  the rupturing of the cells.  So if you have a banana on your table,
  the cells are going to be intact, the enzymes contained, and the
  reaction is not happening at all whereas if you put in the fridge, the
  enzyme is released and the reaction can happen – although yes, it
  might happen slower.

At the risk of channeling people into a yes or no answer, could someone clarify for me if the following statement is true maybe with a peer-reviewed source, which I've had no luck finding:

TLDR Bananas go brown quickly in the fridge because cell lysis, caused by ice crystal formation at cold temperatures in the fridge, releases Polyphenol oxidase (PPO) into the surrounding area which freely causes more browning.

This leads me to another seeming paradox and the question I would like answered: Why doesn't this rapid browning in cool temperatures happen for other fruits and vegetables? What is special about bananas?

That is a good question indeed, but funding bodies are likely to be industrial, and they generally don't care much about writing papers, and often choose to go for patents instead.

@AliceD... I am going to flag you for using the There is no money in basic research argument. I don't know that I buy Emily's argument completely. Most fridges will not go below 4°C. I have actually observed this phenomena in my freezer and seen the brown bananas (Makes really good banana bread that way), but I just don't see ice crystals forming before you get to 0°C. There has to be something else going on. Maybe the enzyme is more stable at colder temperatures? Seems counter intuitive, but maybe it is an adaptive response to frost.

@AMR Not even microcrystals? Also, I don't think bananas originate from countries that have frost, so perhaps that's the key. Other vegetation can withstand or cope with microcrystals, bananas can't.

You are aware that we have had ice ages... While domestication is only about 7,000 years it is likely the plants that they were selected from had to endure periods of cold. As for microcrystals, they have cell walls which should provide a decent amount of structural support before you hit the freezing point, and you get significant expansion in volume.

@AMR Perhaps bananas are particularly vulnerable to microcystal formation somehow... I meant to say that whilst some plants like potatotoes were agriculturally selected for hardiness and yield through colder seasons, banana farmers never had to worry about that and cold resistance could have gone 7000 years without being selected for. It could have taken perhaps a handful of bottlenecks and frost resitance could be diminished. I'm not sure I agree with what I just said, but it's a possibility!

We also have had frosts in Florida that wiped out citrus crops, My thought was that maybe it hastens the decomposition of the fruit so that nutrients can go to maintaining the plant and when the fruit rots and falls off it can go back into feeding the plant. That was my line of thinking in how it may be an adaptation to frost. Protection for the plant to survive, the fruit is expendable.

If you freeze and thaw a tomato, it is pretty awful, there the ice definitely breaks down the fruit. I can't say I have tried other fruit that were frozen... But I think you have the same problem with berry.

@AMR I agree that there are a lot of foods that taste, feel, and look different after freezing (even carrots, which I would expect  to be very resistant to frosty conditions, taste powdery almost). But with bananas this happens well above freezing point. We have a relatively warm fridge at 7+ degrees and the bananas were completely brown and mushy overnight. I think there is something unusual about bananas, although I bet it's not limited to bananas.

Maybe it is the confined space, Ethene concentration is allowed to build up to higher concentrations in the enclosed space of the fridge. Try this experiment. Seal a banana in an airtight plastic bag at room temp in the dark, maybe with a slightly damp sponge to simulate the humidity in the fridge, leave one out, put one in the fridge, and one in the freezer and compare after 24 hours.

@AMR- I may have been unclear. What I meant was that I think chances are slim basic scientists have bothered with it. Food industries may have.

@AliceD NIH is sponsoring programs for scientist to learn to market their science to industry... The US thought we lost a lot of ground when we defunded stem cell research... Wait until they see the kind of science we start to do when we are expected to sell it.

+1. It can also be added that banana skins go completely black when frozen, even though freezing them will stop the enzymes from catalysing the reactions. The same does not happen for cut apples, despite the same explanation (polyphenol oxidases) being put forward for the browning of both fruits.

Banana fruit is very susceptible to chilling injury (CI) and this can occur at relatively high temperatures: CI may occur at  12oC and under. Typically the banana skin turns brown, but in addition there may be pitting and the fruit may not soften (Wang et al., 2013).
Oxidative Stress & ROS
One generally accepted theory it that oxidative stress, due to the accumulation of reactive oxygen species (ROS) such as H$_2$O$_2$ (hydrogen peroxide), O$_2$$^−$ (superoxide) and OH$^{\bullet}$( the hydroxyl radical), is a primary cause of  CI in bananas. (Wang et al, 2003, 2016; Pongprasert et al., 2011).
ROS may give rise to lipid peroxidation, enzyme inactivation, membrane rupture and, ultimately, cell death.
One possibility is that the effect of lowering the temperature is to decrease the activity of key enzymes involved in the 'normal' plant response to ROS.  In other words,  it is postulated that low temperatures cause key enzymes involved in the stress response to ROS to become sluggish, allowing the build-up of  reactive oxygen species that (indirectly) lead to cell death and browning (Wang et al., 2013).
However, plants also respond to cold-induced stress and a key player is the amino-acid proline (Verbruggen & Hermans, 2008; Chen et al., 2008).
Proline has a  key role in maintaining plant cellular integrity in times of stress, and it has been proposed that it does this by acting as an osmolyte, by scavenging ROS, by maintaining protein structure, and by buffering pH (see Verbruggen & Hermans, 2008).
Two key biosynthetic enzymes (starting with glutamate) are pyrroline-5-carboxylate synthase and pyrroline-5-carboxylate reductase (Verbruggen & Hermans, 2008).  A key degradative enzyme is proline dehydrogenase.  Although an aside to this answer, it is nevertheless interesting that proline biosynthesis occurs in the cytoplasm, but proline degradation occurs in the mitochondrion (Verbruggen & Hermans, 2008)
Biochemical Aspects of Stress Response
Plants have an intricate antioxidant defense mechanism to counter the dangers of ROS.
Non-enzymatic antioxidants include ascorbic acid (Vitamin C), polyphenols, the reduced form of glutathione, and α-tocopherols (Pongprasert  et al., 2011). Key enzymes of the antioxidant response include superoxide  dismutase (SOD), glutathione reductase (GR), catalase, peroxidase,  and ascorbate peroxidase
In addition, another important enzyme is phenylalanine ammonia-lyase (PAL).  This enzyme catalyzes the conversion of phenylalanine to trans-cinnamic acid, a key intermediate in the biosynthesis of polyphenols and (many) other plant secondary metabolites (Chen et al., 2008)
As will be seen below, many of the strategies employed to counteract CI involve  pretreatments designed to increase the levels of non-enzymic oxidants and to  increase the expression/activity of key enzymes involved in the stress response to ROS.
The Browning Reaction
It is almost universally accepted that the browning reaction is the result of the action of (the copper-containing) polyphenol oxidase (PPO). This enzyme oxidises mono-phenols and di-phenols to ortho-quinones that  non-enzymically polymerize, via  a free radical mechanism, to give a dark brown or black compound(s).
In normal undamaged tissue the enzyme is latent and, furthermore, does not have physical access to its phenolic substrates due to subcellular compartmentalization (Promyou et al., 2008; Hind et al., 1995).  In damaged tissues, however, the enzyme is activated and comes in contact with its substrates, perhaps through membrane rupture. The resulting  brown, structurally complex polyphenol product is thought to protect plants from pathogens and herbivores (Hind et al., 1995).
Thus the brown color is the response of the plant to irreversible tissue damage as a defense mechanism against further degeneracy.
(Polyphenol oxidase is sometimes referred to as tyrosinase and catechol oxidase, and the reaction catalyzed by PPO is similar to that catalyzed by tyrosinase in the (human) formation of melanin from tyrosine).
Prevention
A number of innovative methods have been used to prevent low-temperature browning. Many attempt to induce an increased stress response to ROS  prior to storage at low temperatures.
UV-C Irradiation

Pongprasert and co-workers have shown that  irradiation with UV-C light increases the expression of phenylalanine ammonia-lyase and other key ROS stress-response enzymes, and pretreatment with UV-C seems be a very effective method in reducing CI (Pongprasert et al., 2011).

Heat Pretreatment

Chen and colleagues demonstrated that heat pretreatment (38oC for 3 days) induces chilling tolerance, and they attribute the effect (at least in part) to an increase in both the activity and expression of phenylalanine ammonia-lyase (PAL).  (Chen et al., 2008)

Hot water

Promyou and associates have shown that hot water pretreatment is a practical method for preventing CI, and they attribute the effect to decreased polyphenol oxidase activity (which they call catechol oxidase)  (Promyou et al., 2008).

Modified Atmosphere packaging

It has been shown that  modified atmosphere packaging, where ethylene and CO$_2$ levels are lowered, alleviates the problem (Nguyen et al., 2004). The effect is attributed to  a lowering of polyphenol oxidase and phenylalanine ammonia lyase activities in the peel of bananas packaged in the modified atmosphere.

Nitric Oxide (NO)

In a detailed an innovative study, Wang and co-workers have shown that pretreatment with nitric oxide (NO), itself a free radical, greatly diminishes CI in bananas.  They demonstrated that key enzymes of ROS metabolism are elevated by NO treatment. In addition, the activity of phenylalanine ammonia-lyase (PAL) is increased as is the activity of a key proline biosynthetic enzyme (pyrroline-5-carboxylate synthase), but the activity of a key enzyme of proline degradation (proline dehydrogenase), decreased in activity.

Summary

The browning of banana skin is due to polymer formation by the catalytic action of polyphenol oxidase on mono- and di-phenols in response to irreversible tissue damage by reactive oxygen species (ROS)
ROS accumulate at low temperature due to a lowering of plant defense mechanisms.
The brown polyphenol product is formed only when tissue damage occurs as a plant defense mechanism against further abasement by pathogen and herbivore attack.

Key References
Chen, J.Y., He, L.H., Jiang, Y.M., Wang, Y., Joyce, D.C., Ji, Z.L. and Lu, W.J. (2008). Role of phenylalanine ammonia‐lyase in heat pretreatment‐induced chilling tolerance in banana fruit. Physiologia Plantarum, 132, pp.318-328. [PMID: 18275463]
Hind, G., Marshak, D.R. and Coughlan, S.J. (1995). Spinach thylakoid polyphenol oxidase: cloning, characterization, and relation to a putative protein kinase. Biochemistry, 34, pp.8157-8164 [First page]
Nguyen, T.B.T., Ketsa, S. and van Doorn, W.G., 2004. Effect of modified atmosphere packaging on chilling-induced peel browning in banana. Postharvest Biology and Technology, 31, pp.313-317. [pdf]
Pongprasert, N., Sekozawa, Y., Sugaya, S. and Gemma, H. (2011) The role and mode of action of UV-C hormesis in reducing cellular oxidative stress and the consequential chilling injury of banana fruit peel International Food Research Journal 18, pp 741-749   [pdf]
Promyou, S., Ketsa, S. and van Doorn, W.G. (2008). Hot water treatments delay cold-induced banana peel blackening. Postharvest Biology and Technology, 48, pp.132-138. [pdf]
Verbruggen, N. & Hermans, C. (2008). Proline accumulation in plants: a review. Amino acids, 35, pp.753-759. [pdf]
Wang, Y.,  Luo, Z., Du, R., Liu, Y.,Ying, T. & Mao, L. (2013)
Effect of Nitric Oxide on Antioxidative Response and Proline Metabolism in Banana during Cold Storage,
Journal of Agricultural and Food Chemistry,61, pp 8880-8887. [PMID: 23952496]
Wang, Y., Luo, Z., Mao, L. & Ying,T. (2016) Contribution of polyamines metabolism and GABA shunt to chilling tolerance induced by nitric oxide in cold-stored banana fruit.  Food Chemistry 197, pp 333-339. [PMID: 26616957]

Really interesting thorough answer! Thanks.

What's interesting with this one is we don't really know very well the mechanism behind what's called chilling injury. It happens to a range of fruits, like bananas, peaches, avocado, or apples. The belief is that the chilling alters membrane permeability to storage vacuoles inside the plant cells. Try On Food and Cooking, pp.269, and Puig et al. (2015) for references here.
Now the membrane permeability to the storage vacuole changes (it gets leaky), and inside these vacuoles are phenolic compounds. In the cytoplasm of the plant cell, there's an active enzyme called polyphenol oxidase (PO). The reactions it catalyzes end up with a compound called melanin, a brown/black pigment:

Fig A. An overview of what a PO might do.
So the phenolic compounds leak out and PO goes to work catalyzing reactions that start building up the dark pigments associated with browning. Being said, I can't at this moment find a good paper that says "look, this is how the entire process happens," but I'll be attempting to read a little deeper into the matter.
Keywords: flesh browning, enzymatic browning, chilling injury, polyphenol oxidase, storage quality, storage conditions

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


text:
Textbook Recommendations Covering The Adaptive Immune System
I will soon begin work on a project about immunology. I would like to read more about the main mechanisms of the immune system.
What books or articles could you recommend to me? In particular I am interested in the adaptive immune system.
I would appreciate if some of the recommendations are at an undergraduate level as I do not have a background in biology.
Thanks a lot.

@MattDMo 's answer is a great starting point. You probably also want to look through Nature Reviews: Immunology to get an overview of what is  currently occurring in the field today. From there, you can look at the referenced articles in more specialized journals for topics related to your project.

echoing @AMR 's sentiment, Annual Reviews of Immunology is also a great resource if you're looking to go deeper than textbook-level, although Nature Reviews in general has better pictures :)

There are two books that I see as "standards" in the field:

Cellular and Molecular Immunology, 8th Ed. by Abbas et al.
Immunobiology previously by Charlie Janeway, who unfortunately has passed, so it is now authored by Kenneth Murphy. Many people just refer to it as "Janeway".

These texts can be used both at an undergraduate and graduate level (I used them in both), and are updated every few years. The latest edition of Immunobiology is from 2011, while CMI is from 2014, so you may want to start with that one first.
An earlier version of Immunobiology is also available for free on NCBI's Bookshelf, but unfortunately you can't read directly through it, you'll need to search for what you're interested in.

+1 for Cellular and Molecular Immunology. My undergrad immuno course used Parham's The Immune System and I really didn't like it. There are very good figures in Abbas' text, and I think it's also more in-depth for those of us who want to know more without multiple textbooks.

The Immunobiology book (previously by Janeway) - is awesome! Used it for my graduate school course on immunology. Great pictures and explanations - even for someone who didn't have a strong background in immunology. I would recommend that to anyone interested in learning more about immunology.


text:
What neurons make up the CNS?
I generally see it written that there are three types of neurons, classified by projection: (1) sensory neurons, (2) interneurons, and (3) motor neurons. Now, in the CNS, I don’t think there would be sensory or motor neurons, seeing as they connect the PNS to the CNS. Does that mean, then, that all the neurons in the CNS are interneurons? I remember my biology teacher telling me not all neural pathways involve interneurons, so that suggests to me that the CNS consists of other neurons as well. What neurons would these be, if they are existent?

There are probably thousands if not more neuron (cell) types in CNS...this 3 level classification is very simplifying. What level of biology are you learning?

Short answer
Sensory neurons are invariably considered to be located in the periphery. Interneurons and motor neurons are part of the CNS.
Background
There are various classifications possible to categorize neurons.
One classification is the one you mention (Furness, 2000), which is a broad classification based on where the neuron projects to. It divides all neurons in:

Sensory neurons (feed information to the central nervous system (CNS));
Interneurons (are stimulated by sensory neurons and/or other interneurons);
Motor neurons (feed information from the CNS to the periphery).

Sensory neurons are invariably considered to be part of the peripheral nervous system. Their cell bodies are located in the periphery. Their projections may feed directly into the brain. For example, olfactory sensory neurons directly project onto the olfactory bulb in the brain.
Motor neurons include the motor neurons controlling muscles. Their cell bodies are located in the spinal cord, which is the CNS, but not the brain. Here the terminology becomes confusing, as this functional classification uses overlapping terminology with the projectional classification. That's why I, personally, prefer to talk about efferent fibers (away from CNS) and afferent fibers (to the CNS). Especially because motor neuron implies something motoric. In case of neurons driving glandular secretion this is counter intuitive. Efferent and afferent fibers are essentially the same names for motor neurons and sensory neurons. One way or another, motor neurons controlling muscles have their cell bodies in the spinal cord and hence are part of the CNS.
Interneurons are invariably located only within the CNS. Interneuron is also a confusing term, because often they are implicitly considered to be inhibitory. Often they are, but they don't have to be. In the classification scheme discussed, most CNS neurons can indeed be classified as interneurons. For example in the neocortex, 70–80% of the neurons are excitatory pyramidal cells, while the remaining 20–30% are inhibitory interneurons (Markram, 2004). The spinal cord also contains interneurons.
In all, most interneurons are located in the CNS, but not all CNS neurons are interneurons, because motor neurons are part of the CNS too. I agree with 243's answer that the classification scheme is most appropriate for the relatively simple neuronal circuitry characteristic of the spinal cord.
References
- Furness, J Autonom Nervous Syst (2000); 81: 87–96
- Markram, Nature Rev Neurosci (2004); 5: 793-807

For example, interneurons account for 20% of neurons in neocortex (1)(2). I think that the classification, mortar-, sensory- and inter-nerons, comes from the simplest neuron circuits like spinal reflex.
In human brain, their thoughts and experiences modify such simple neuron circuits, suggesting existence of other neurons affecting the simple circuits. It should be noted that many neurons in CNS spontaneously fire(3). If interneurons spontaineously fire, your leg spontaineously move unconsciously. Some other neurons secrete hormones in brain, called neurosecretory cells cells(4).

Inhibitory interneurons make up 20-30% of the cortex see your ref 2


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Difference between the inactivation of neurotransmitters and hormones
Neurotransmitters must be somehow removed from the synapse once they’ve produced a post-synaptic potential, whether it be through enzymatic breakdown, diffusion, reuptake or another mechanism. However, I rarely see such mechanisms mentioned when discussing hormonal communication. I assume hormones just diffuse away from their receptor and do not continually stimulate the cell. However, there does not seem to be an urgency in breaking it down. Why is there this urgency, then, in the case of neurotransmitters, but not with other first messengers, like hormones?

I don't quite understand what you're saying. Neurotransmitters and hormones alike are ligands. Dissociation from the receptor is a stochastic process. One ligand can activate a receptor multiple times. Many neurotransmitters are actively removed from the synaptic cleft. What is your question? Why hormones are not removed? Could you limit your question to specific representative example cases?

@AliceD Why are neurotransmitters actively removed but hormones aren’t? Is it not just as imperative to remove the hormone from the binding site?

Does your comment capture the question?

@AliceD I suppose, yes.

I edited the question in response to your comments. If this doesn't reflect your intentions feel free to roll back.

Short answer
Hormones act in the order of minutes or hours. Neurotransmitters in the order of milliseconds. Moreover, hormones are blood-born, neurotransmitters are confined to the synaptic cleft or in the extracelular space directy surrounding the neuron. Hence, their mechanisms of inactivation are different.
Background
The distinguishing feature of hormones and neurotransmitters is the fact that the former are generally released into the blood, while the latter are confined to synapses, or the immediate extracelullar neuronal space. Hence, hormones can be readily cleared by the workhorse of blood clearance: the liver. For example, adrenaline is rapidly (half life 5 - 10 minutes) metabolized mainly by the liver, followed by excretion via the kidneys. Diffusion then will draw adrenaline away from the receptors as blood concentration drops. The relatively slow time course is beneficial, as the effects of epinephrine includes metabolic changes, such as the release of glucose to power up the body (Sherwin & Saccà, 1984). This needs time.
In the synapse, there is no blood flow and inactivation has to occur through other means. Further, epinephrine in the above example is a fast acting hormone. Many hormones work on an even slower time frame. For example, a stress-induced cortisol peak can last for as long as an hour (Kirschbaum & Hellhammer, 2000). Neurotransmitter responses may last for a few milliseconds. For example, some pacemaker neurons may fire at rates of 40-50 Hz (Häusser et al., 2004). Hence, neurotransmitters have to be cleared from the synapse at least within 20 ms. To wait for the released neuroransmitter to passively diffuse out of the synapse is simply too time-consuming. Neurotransmitters act at an entirely different time scale.
References
- Häusser et al., J Neurosci (2004); 24(42): 9215-9
- Kirschbaum & Hellhammer, Encyclopedia of Stress, 3 (2000)
- Sherwin & Saccà, Am J Physiol (1984); 247(2-1): E157-65


text:
Cancer a method for early Earth Evolution?
Something I have been wondering for a while is looking at cancer from an evolutionary standpoint.
It's easy to conclude (from observations today) that cancer is something we would rather avoid. However I kept asking myself what would be the purpose of cancer existing in the first place? In my experience of studying biology if a organism or mechanism in nature exists it is because there was a pressure to create it.
It has led me to think that perhaps early on, when cells were just beginning to clump together forming very very primitive organisms, that cancer was a way for a cell to proliferate very quickly and make their particular genomic sequence more common within what would have been organisms made of a lump of cells. Perhaps the different organs we have today exist not just because there was environmental pressure to have a specific organ with a specific function. Perhaps the cells descended from a "cancer" that proliferated faster over other cells in a primitive ancestor of that organism.
The answer that "cancer exists because our bodies make mistakes" doesn't satisfy me when everything else around us evolved and formed due to a multitude of different pressures.
In an effort to make this question less broad my question is basically this:
Is it plausible that cancer is a phenomenon that began to occur relatively early in Earth's evolutionary history as a form of survival for cells in primitive organisms or am I applying evolutionary theory incorrectly?
(I know there is a better word for "pressure" to describe the variables that guide evolution but right now my brain can't come up with anything better).

The majority of cancers occur around or after the end of reproductive viability of the organism. Therefore there is no selection against it. Had it been a disease that predominately affects embryogenesis or early development, then there would be spontaneous abortions or young dying prior reproduction, thus taking the genes out of the gene pool. That it occurs later in life means that the organism's genes, with all of their strengths and weaknesses get passed to the next generation. Those can then be offset by a more fit mate so that it continues to keep cancer at bay until after reproduction

There is a lot of terminology, semantic and biology to be discussed if one was to fully answer your question and it would take a whole book. Below I am just trying to push you to reading more on the subject.
Evolution of cancer prevalence
The probability of getting a cancer is under selective pressure for sure. Citing cancer.net, here is some information on the genetics of cancer:

Many of the genes that contribute to the development of cancer fall into broad categories:

Tumor suppressor genes are protective genes. Normally, they limit cell growth by monitoring how quickly cells divide into new cells, repairing mismatched DNA, and controlling when a cell dies. When a tumor suppressor gene is mutated, cells grow uncontrollably and may eventually form a mass called a tumor. BRCA1, BRCA2, and p53 are examples of tumor suppressor genes. Germline mutations in BRCA1 or BRCA2 genes increase a woman’s risk of developing hereditary breast or ovarian cancers. The most commonly mutated gene in people who have cancer is p53. In fact, more than 50% of all cancers involve a missing or damaged p53 gene. Most p53 gene mutations are acquired mutations. Germline p53 mutations are rare.
Oncogenes turn a healthy cell into a cancerous cell. Mutations in these genes are not inherited. Two common oncogenes are:

HER2, which is a specialized protein that controls cancer growth and spread, and it is found on some cancer cells, such as breast and ovarian cancer cells
The ras family of genes, which make proteins involved in cell communication pathways, cell growth, and cell death.

DNA repair genes fix mistakes made when DNA is copied. But if a person has an error in a DNA repair gene, these mistakes are not corrected. And then they become mutations, which may eventually lead to cancer. This is especially true if the mutation occurs in a tumor suppressor gene or oncogene. Mutations in DNA repair genes can be inherited, such as with Lynch syndrome, or acquired.

Somatic Evolution in cancer
A cancer is a group of cells that proliferate. In other words a cancer is a group of cells having a higher fitness than other cells.
See Wikipedia > Somatic Evolution in cancer
Can a cancer be beneficial?
I am here attempting to answer your specific question.
We define a cancer based on the fact that it is detrimental to the organism carrying it. If a group of cells divide a lot more than the others and this is beneficial to the organism, then it is not a cancer but an adaptive developmental process.
Let's generalize the definition of cancer
To generalize the definition of cancer, one can say that a cancer is a group of individuals that proliferate to the detriment of the group. In other words, we need a social group of individuals (such as a multicellular organism) to get a cancer. Depending on your definition of a social group, one could consider a criminal organization as a cancer to human society.
If you push the definition a little further by either leaving out the need of a close phylogenetic relatedness between individuals of the group, one could say that "humans are a cancer of the earth". If you google this sentence you will get many hits!

The majority of cancers occur after the age of reproduction, so they are absolutely not under selective pressure. Selective pressure only occurs if it affects getting genes to the next generation. That is why Huntington's disease has survived as long as it has, the onset of the disease isn't until the 40s or later, after people have reproduced.

Just because something is genetically heritable does not automatically mean that it is selective. It is only selective if it helps or hinders the organism from reaching reproductive age and producing offspring.

Yes, absolutely. Prevalence of cancer is a trait that evolve with age-specific effect. See Mutation Accumulation (MA) hypothesis and Antagonist Pleiotropy (AP) hypothesis. Wikipedia > Evolution of Ageing. Do you feel like your comments are contradicting my answer?

Why are you linking to an article that has this warning This article is written like a personal reflection or opinion essay that states the Wikipedia editor's particular feelings about a topic, rather than the opinions of experts. (October 2009)
This article contains weasel words: vague phrasing that often accompanies biased or unverifiable information.

This is what prompted my comments. "The probability of getting a cancer is under selective pressure for sure. "

That is a very insightful question.  In general terms, you're right that cancer is unregulated cell division, which hijacks the mechanism of cell division which is ancestral to all multicellular life.  In early multicellular life, it may well be the case that faster reproduction was selected for, while it has been selected against for most organisms as they became more complex.
The mutations which cause tumors are usually two-fold: first there is a mutation which causes a cell to get genetically switched on.  This might be a mutation causing an overproduction of a protein signalling molecule which tells the cell it is time to grow.  The second is usually a mutation in cancer prevention genes, since a cell going haywire is likely to be spotted and destroyed relatively quickly.  If both of these mutations happen in the same cell, the cell can form a tumor (and if the tumor spreads to other parts of the body, it is called cancer).
Some people have suggested that cancer be thought of as "cell-level selection."  This idea of levels of selection takes a little explanation.  When evolution was first proposed (and the way in which it is introduced still) is individual-level selection.  Individuals compete against other individuals to survive and reproduce.  However George C. Williams suggested (and Dawkins later popularized in "The Selfish Gene") that genes might compete against other genes.  This is called the gene-level view.  In the mid 1980s, Leo Buss suggested that a cell might also be a level of selection, and that cancer represented cells trying to reproduce at the expense of the individual which carried them.
In some cases, such as instances of transmissible tumors (there are only a few such tumors known in the wild, none in humans).  These cancers spread from individual to individual, rather than just within one individual.  In that way, the cancer's evolutionary strategy was successful.  However these are rare, so if we view cancer as an evolutionary strategy, it is not usually a successful one.  As such, thinking of cancer as a cell-level selection has not yielded many interesting ideas so it is not widely used in biology today.  It is not incorrect, but it doesn't further many research projects so it is not commonly taught or studied.
There's one exception to that, however.  Thinking of cancer itself as an evolutionary process, where cells survive and die off according to their mutations, is very useful to understanding the progression of a tumor.  If you're interested in this line of thought, there's a summary paper Merlo et al 2006 which you might want to take a look at.

You are wrong and right. Remi.b's answer is describing the idea is not right and the answer is generally accepted.
The cells in muticellular organisms have to be regulated tightly--some has to differentiate into skin to protect bodies, other, into stomach to secrete digestive enzymes, etc. This regulation was established when multicellular organisms appear.
In other words, unicellular organisms do not care about the regulation. They do not have to be skin, stopping cell growth. Not much problem that they grow as cancer cells do, although you don't call such unicellular cells "cancer" probably because they are not abnormal.


text:
Replicator equation for mixed strategies?
The the replicator equation is usually defined for pure strategies. More specifically, the replicator eqn for $n$ strategies is given by:
\begin{equation}
  \dot x_{i} = x_{i} \left( \sum_{j=1}^{n} a_{ij}x_{j} - \phi \right)
  \qquad i = 1, \ldots, n
\end{equation}
where $x_i$ is the frequency of the strategy $i$, $A=[a_{ij}]$ is the payoff matrix, and $\phi$ is the average fitness of the population. Basically, what the replicator equation is saying is that the per capita rate of increase of the strategy $i$ (i.e., $\dot x_i/ x_i$) is the difference between the fitness of $i$ (i.e., $\sum_{j=1}^{n} a_{ij}x_{j}$) and the average fitness $\phi$ of the whole population.
Question: Does anyone know of a formulation of the replicator eqn for mixed strategies?

When you allow for mixed strategies, you essentially have an infinite strategy set. There is a branch of evolutionary dynamics concerned with infinite strategy spaces. I know of this paper, for example: http://link.springer.com/article/10.1007/PL00004092


text:
Is there any way to make protein pass through cell membrane?
Protein cannot pass cell membrane because it's a large molecule. Until now, is there any technique that can make protein pass through the cell membrane in vivo? I want to create a protein-drug that must be accessible DNA to reach it's site of reaction. How possible can i do it?

Various protein transfection methods are available.
The simplest one is electroporation. By using electric pulses, transient pores can be formed, so that proteins outside can go the inside of membrane.
Several protein transfection reagents are commercially available. I think the mechanism is similar to lipofection of DNA.
http://www.clontech.com/US/Products/Transfection_and_Cell_Culture/Protein_Transfection/Protein_Transfection_Reagent
https://www.neb.com/products/m2563-transpass-p-protein-transfection-reagent
https://www.thermofisher.com/order/catalog/product/89850
Fusion with the transactivating transcription factor (TAT) protein transduction domain from the HIV TAT protein. This 11-amino acid sequence help proteins cross plasma membrane.
http://www.nature.com/mt/journal/v8/n1/full/mt2003155a.html

I am adding a couple of methods here.
Liposomes
Liposomes were designed to deliver drugs to places where the effects are wanted. Drugs are enclosed in liposome vesicles, but when reaching plasma membrane, liposomes could fusion with plasma membrane and release drugs inside of liposomes, although all liposomes are not designed to fuse cellular membrane.  Lipo-fection of DNA is a bit different from this kind of liposomes because DNA is not necessarily enclosed in vesicles.
nanoparticles
This is relatively new. I do not have much knowledge about nanoparticles, but I know they are used to transfect DNA or RNA in vitro and in vivo. I do not know how popular nanoparticles for protein transfection are, but there are publications.
http://www.ncbi.nlm.nih.gov/pubmed/24859743

I don't think they let you electrocute patients these days, even just a little.

electroporation can perform in vivo , however it will make other free protein and free gene fragment outside pass through the cell membrane, what will happen?

@AMR There are clinical studies using electroporation. For example: http://pancreatica.org/electroporation-for-the-treatment-of-locally-advanced-cancer-of-the-pancreas/ , https://clinicaltrials.gov/ct2/show/NCT02079623

@AMR electroporation is unlike electrocution. People have used in-vivo electroporation extensively in animal studies without any significant tissue damage and moreover as 243 said, clinical trials have been conducted using this technique.

@WYSIWYG The examples of electroporation use invasive measures to deliver the electrical charge to the tissue. It would not be practical if the OP is looking at systemic treatments or longer term, maintenance protocols, though the OP doesn't say, and you already are aware of my thoughts on this question.

Another example here. http://www.nature.com/mt/journal/v21/n9/full/mt2013119a.html

https://en.wikipedia.org/wiki/Electroporation . "Scientists from Karolinska Institute and the University of Oxford use electroporation of exosomes to deliver siRNAs, antisense oligonucleotides, chemotherapeutic agents and proteins specifically to neurons after inject them systemically (in blood)."

@DucFabulous Read the prior section. It requires an invasive procedure to target the neurons. The siRNAs are packaged and delivered in the blood, but to get them into the target tissue electrodes need to be inserted into the site. How much do you think it will cost to have all of those brain surgeons operating to get the drug delivered, and do you think that countries with national health care systems would agree to pay for the expense? Just because things are researched, and even proceed to and through clinical trial doesn't necessarily mean that it is good science or even practical.

Adeno-Associated Virus (AAV) vectors.

Every virus is "a protein-rich nano-particle." i can imagine man-made virus-like nano-robots in not so distant future . . .


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When does a chromatid become a chromosome?
When chromosomes lie on the metaphase plate, they have the characteristic X shape. But these are actually two chromatids that are held together at the centromere. If separation fails and both chromatids are pulled in the same direction it leads to trisomy (three homologues chromosomes). So when exactly does a chromatid become a chromosome if it's not after successful separation?

If no centromere split occurs during anaphase and consequently chromatids are pulled to one daughter cell, the possible outcome is during telophase the chromatids uncoils into chromonema which in subsequent divisions become supernumerary chromosomes.

Welcome to Bio. Can you add citations to back up your answer by any chance?

So the two unsuccessfully separated chromatids could become a single B-chromosome?


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Are the ribosomes specific for each organism
If we removed one ribosome from human and we put it inside horse, would the ribosome perform the as it would in humans or it will not work or somewhere inbetween?

Welcome to Bio. It's best to ask one specific targeted question per post. I.e.  You might want to split them up. Second, a ribosome is huge. There's many things that gives it functionality. There is not something as the thing.

This sums it up https://www.quora.com/Do-all-ribosomes-in-the-plant-animal-kingdom-read-and-respond-to-DNA-in-the-same-way

First part is too broad and would essentially be considered a homework in this site. You should start with basic biochemistry and molecular biology (looking at your question I would also recommend you to read some fundamental organic chemistry. There are thousands of chemicals made of same atoms and sometimes even the same number of atoms [isomers] but still they are chemically very different).

One can prepare rabbit ribosomes from reticulocytes (immature red blood cells), and by providing a few cofactors required for an active extract, create an in vitro system that will translate virtually any eukaryotic mRNA that contains the correct sequence determinants. You can purify mRNA from your cells or tissues of choice, or you can synthesize an mRNA in vitro using a DNA template and an RNA polymerase. Either of these will be translated in a nuclease-treated rabbit reticulocyte lysate.
IVT (in vitro translation) extracts can be prepared from virtually any source (e.g., C. elegans shown by Bob Edgar in Cell ~ 1984). So I would predict that horse ribosomes would be happy translating human mRNAs, and human ribosomes would be happy translating horse mRNAs. The experiment you described, placing a human ribosome into a horse cell would be difficult to interpret because the endogenous horse ribosomes would already be translating the endogenous horse mRNAs, and so detecting activity from one additional ribosome could be challenging (even if you could come up with an experimental approach that gets that foreign ribosome in to the cell).
The take home message is that ribosomes, in general, do not care where the mRNA comes from--because ribosomes, as far as we know, do not have a way of distinguishing "self" from "other".

thank you for the valued information, actually my concern is if I want to think about the nature of the Ribosome, it would be chemical interactions at the end of the day right?,now, what is the thing that gives the result of the chemical interactions a behavior and function?

In an abstract sense one can consider the ribosome as an enzyme, an enzyme whose name would be something like polypeptide polymerase (or perhaps polypeptide synthetase). Now it happens that this enzyme has two rather large sub-units, and each sub-unit consists of a large structural RNA, plus dozens of proteins, but to answer your question, the ribosome has a catalytic reaction site, and it consumes substrates, and spits out products, just like every other enzyme. There is nothing magical. So your question becomes: how do enzymes work? You have the answer: chemical interactions.

what is the thing that gives the ribosome its functionality ( to synthesis the protein ).

RNA strands can fold themselves in a sequence specific manner. In fact ribosomes are highly structural being able to hold tRNAs having a hole which a polypeptide goes through during protein sysnthesis.

I do not know, but it could work. I do not know if it works exactly as horse ribosome works, either.


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Acoustic characteristics of thoracic diaphragm
I am looking for any kind of information about the acoustic characteristics of the thoracic diaphragm. In particular, I'm looking for characteristics which will allow to differentiate it from other muscles using ultrasound, MRI, CT, etc.
References to the literature are especially welcome.

One identifies the diaphragm on ultrasound/CT by thinking about the anatomy and appearance (e.g. on ultrasound it's a thin hyperechoic structure between the liver and lungs). I'm a bit unsure what you're asking as unless you get close to the body wall there's not many other muscles in that area to confuse it with.


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Large set of semen microscope images needed
As a course project I have to write an algorithm whose purpose is to analyze a sperm sample (total number, motility etc). In order to do that though, I need to have a sufficient number of images to use during the coding and testing parts.
Do you know if there is any dataset available with semen images? It would also help if the corresponding stats of the images are also given, so that I can use them as a benchmark to see how well my algorithm works.
Thanks in advance

Researchers, male anyway, have tended to collect their own samples.

Yes, check out the methods for library construction used by one of the authors in this classic paper: http://hogness.stanford.edu/PDFs/62_isolation_and_nucleotide.pdf

@AMR Yeah, that's a pretty bright idea..
go ahead and jerk off every single day of the week...

I wasn't kidding. That is actually what researchers in human sperm do. mdperry gave you a paper where the first author was the source shown in the methods. I have also seen a researcher mention it in a documentary on fertility. And I know of a lecturer who gets one of her male students to provide the lab techs with a fresh sample for her lecture on gametogenesis a few hours before. They set up a microscope with a video camera and project it onto a screen in the lecture hall. It is really quite amazing. This is science and sometimes scientists have to be their own test subjects.

Also if you want to be taken seriously as a Biologist, you need to learn to use terms such as "Collect a Sample" in place of "jerk off." The Biologists in the room will know what you mean without needing to be indelicate. If you must refer to the method of sample collection, then masturbation is the more appropriate terminology.


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How is adrenaline (also known as "epinephrine") a ligand?
I keep reading that adrenaline is a ligand, however, from what I understand a ligand is a molecule or ion which donates a pair of electrons to a central transition metal ion in a complex. If this is the correct definition of a "ligand", then how can adrenaline be a ligand?

In biology, ligands are chemicals that attach to receptors on cell membranes, stimulating a cellular response. You’re using the definition of a ligand in chemistry. :)

@lightweaver - that's sufficient for an answer when you include a link to the respective definitions.

The definition of "ligand" in the question, "a molecule or ion which donates a pair of electrons to a central transition metal ion in a complex" is clearly a more technical 'chemistry-type' of definition. Ligands in biology and medicine can be all sorts of molecules, though most of the time we think of them as molecules that bind to a particular receptor. Those receptors can be ion channels, enzymes, transmembrane receptors at the cell surface or within the cell in an organelle, nuclear proteins that control expression of genes in the cell nucleus (i.e. transcription factors), etc...the list could go on and on... In fact, more recently we have come to appreciate that compounds like bile acids - that were previously thought to be important only in fat absorption in the gastrointestinal/digestive tract - are also ligands for receptors that control gene transcription ("Farnesoid X Receptor") as well as increase energy expenditure in brown adipose tissue and skeletal muscle (through receptors like the "TGR5" receptor).
But... back to the question...
If a molecule binds to a receptor, then it's a ligand for that receptor. The ligand doesn't have to donate any electrons specifically to a transition metal. Most of the time in medicine/biology the binding of a specific ligand to its receptor is a reversible process that is dependent on the concentration of the ligand and the availability of the receptor (among other things). The specificity of ligand for the receptor is due to chemical factors like hydrogen bonding, electrostatic interactions (like positive charges attracting negative charges), as well as other chemical interactions beyond the scope of this question. As you can see from the picture below, the hydroxy groups (-OH) that are part of the serine residues on the receptor are hydrogen bonding with the hydroxy groups on the epinephrine molecule itself. Moreover, the carboxy group (-COOH) on the aspartate residue is binding to the positively charged amino (NH3+) on the epinephrine molecule.


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Good model for comparative genomics in relation to temperature adaptation
Can anyone suggest any highly related bacterial or parasitic species which live at very distinct temperatures, which might be a good model for comparison of genomes in regard to temperature adaptation. For example, related pathogens of which one species infects warm blooded animals, and the other infected cold blooded animals? So far I have come up with one possible example: Salmonella enterica is a pathogen which infects warm blooded animals, whilst Salmonella bongori infects mainly reptiles.
Examples for which there are publicly available genomes, and which have been used in previous studies would be preferable.

As a starting point I would suggest you look at genomes of thermophiles and hyperthermophiles (organisms that thrive at upwards of 40 °C and 60 °C respectively), which are often found near underwater volcanos or hot springs.
For instance, one could do a genomic analysis of the archaean Methanocaldococcus jannaschii, comparing it to mesophilic species of Methanocaldococcus or Methanococcus. This organism is well studied, and genomic information for this organism is readily accessible.
Some studies have been done comparing the genomes of mesophiles and thermophiles. For example, Zheng and Wu (2010) found a correlation between GC content in coding/noncoding regions and temperature conditions.
At the other end of the spectrum you could examine psychrophiles (organisms that grow at low temperatures, −20 °C to +10 °C). However, few of these organisms are obligate psychrophiles, meaning many can thrive at higher temperatures as well and thus may not be suitable for your purpose.


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Do the claims in this paper have any degree of validity?
The paper The waiting time problem in a model hominin population talks about a problem of waiting time, etc. Is the methodology of this numerical simulation, and the conclusion right or is it wrong?
(A quick search reveals that the first author is an intelligent design advocate and apparently believes or believed that the earth is less than 10,000 years old)

I had a quick look at the paper and it is quite hard to understand it as they are using a very unusual vocabulary. For example, they are using the term selective elimination in the abstract which is not a defined concept. Also, they build their own model instead of using existing numerical framework which make it harder to understand what they really did.

If you feel like giving a try summarizing their methods, results and interpretation concisely, I'd be happy to consider reading the paper a bit more and expressing my opinion.

Here is a possible pitfalls in their paper. They are calculating time for a specific sequence (what they seem to call string) to fix in the population from an ancestral sequence that is 100% different. Of course it takes time. The fraction of pairwise differences is very low between related species such as chimps and humans.

Does anyone know of a good take down of this paper I can reference? It is appearing more and more as though it has some value!

I have zero interest in giving a click to what looks like a journal of hogwash.  Can you provide a link to the pubmed abstract?  And if you can't, because the paper can't be found in pubmed, that's a pretty good answer to your question right there.

I'm afraid I laughed a bit when reading that paper for the first time.
Why? Well, here's what they essentially did: They tried to model evolution by implementing an algorithm. They had a population of 10000 individuals, represented by their genetic sequence, and had an algorithm do mutations of those sequences and modeled selection and reproduction to get the next generation. They did that for a long time. Why did that make me laugh? I did both my BSc and MSc theses in the field of Evolutionary Bioinformatics. Almost every student there implements something like that when they first start, to learn to write that kind of program. It's not exactly novel. They even cite several other studies doing this kind of analysis.
Now, their result is basically that human evolution from human-chimpanzee ancestors couldn't have happened because it would have taken way too long. Not only would the whole difference between these two species have taken too long, every single difference of more than two nucleotides would have taken too long to get fixed.
Since this goes against established science, this algorithm better be good... The paper is lengthy and much of it isn't all that interesting or related, in my opinion. But here's the big problems, in my opinion:

When natural selection successfully amplified the target string to the point of fixation (i.e., when the allele frequency reached 99–100 %),

Their target is for their target sequence to reach a frequency of at least 99 percent. That's unnecessarily high, and will of course take a long time, especially as they hold their population constant at 10000 individuals. They don't show a figure with how frequency changed over generations - I'd assume that 90 percent is reached a lot earlier than their threshold.
Holding the population size constant is of course also not a realistic model for human evolution. It wasn't at 10000 individuals for millions of years.

initialization : initialize every individual to the same random or user-specified string (e.g., AAAAA)

Humans didn't start with random sequences and then mutated them to make them do something useful, we started with useful genetic material that then changed. If you start at AAAAA, expect a target of TAGGC, don't confer any benefit to intermediate steps (as they did) at a mutation rate of something like 1 per ten million nucleotides per generation, of course you are going to wait a long time. Mutation rate in genomes also isn't uniform, it varies by region. From what I can see, this was neither taken into account nor discussed.
There is also the problem of them only looking at single nucleotide mutation, not gene duplication, insertions, etc. that also make up a lot of the difference between humans and their ancestors.
Then there's random "mate-choosing", which is a valid simplification to make if you are just looking at some mechanisms of evolution, but not valid if you are going to use your model to estimate time needed for speciation.
They also only allow for one beneficial mutation to arise, then wait for it to be fixed, claiming that anything else would have just resulted in even longer times, without, as far as I can see, just implementing this and then testing that assumption.
At some points, their paper is just going to going for some kind of dramatic effect:

waiting time was 500 million years – which is still extremely prohibitive. This amount of time approximates the estimated time required for the evolution of worm-like creatures into people

500 million years ago, we had the first animals emerging on land and the first chordates. Chordata and the "worm-like" phyla had already diverged.
Basically, in my opinion, they took a very simple model and drew sweeping conclusions from it. This kind of analysis is suited for looking at how evolution might result in speciation, what parameters might play a part, etc. but it is not suitable for estimating the time this takes.
But these are just my first thoughts, I hope there'll a more thorough review of this on the internet somewhere soon.

Actually the estimate of the genetic diversity of humans that made it through the genetic bottleneck in human evolution is accepted as being about 10K individuals, give or take. One think that I don't think you mention is the idea that Evolution, through Natural Selection keeps its successes and throws out its mistakes, which is what allows the Cambrian Explosion to make sense. 3 billion years of working out all the kinks and building the foundation, then 500 million years of diversifying on the successful themes.

@AMR yes, I know that estimate. But those 10K individuals didn't randomly interbreed with each other, they probably formed subpopulations pretty soon, and they didn't stay at 10K for the next 5 million years.

It is only 60-70K years since we were down to around 10K humans... I am not agreeing with the paper, just that it points out how they take facts and warp then to their cause. As you said "a mutation rate of something like 1 per ten million nucleotides per generation." That is the mutation rate per cell division as that is the inherent error rate for DNA Pol with DNA Repair Mechanisms in place. Also they do not take into account events like meiotic recombination or as you mention gene duplications. Many of the differences have more to do with amount of gene product, not differences in genes.

A very late comment however, the time frame presented in paper referenced the OP is actually based on external research by Michael Lynch & Adam Abegg Dep't Biology and Dep't Mathematics @ Indiana University. The claim from this research is that it would have taken at least 200 million years for just 2 mutations...and that is based only on 98% similarity. The figure now is that we are only 85% similar...so the 200 million years would need to adjust dramatically to that now accepted figure...which is significantly worse for evolution!


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What are necessary parameters for a tissue scaffold to be biodegradable?`
I am a mechanical engineer with little biological experience, but I have recently been looking at tissue scaffoldings.
My current understanding is as follows, but may be flawed. I would appreciate any feedback: The purpose of tissue scaffolding is to provide a structure where there is none, and to facilitate healing. The tissue scaffolding is typically porous because it must facilitate the transport of cells during the inflammatory phase of healing, while the scaffold also later provides an interface and structure for the growth of new cells. It can essentially replace extracellular matrix.
I understand that these scaffolds need to be made of inert material so that there are no reactions with the body. But I know that some tissue scaffolds are meant to be biodegradable, so that once stronger extracellular matrix is established, the body can go back to doing its job. But, arent biodegradability and inertness mutually exclusive?
I also understand that a major issue with tissue scaffoldings is the compatability of specific scaffold materials with corresponding tissues, and that there are issues with adherence, etc.
I was hoping to gather some more insight as to what types of challenges tissue scaffolds typically encounter, how they are dealt with, and why? I'm also in scaffolding materials' use to deliver drugs, but that may be an issue to discuss on another day.


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How to Determine the Most Conserved Sequence from BLAST Result?
I used BLAST to find the best aligned DNA sequence to my query sequence.  The BLAST result shows a number of sequences that it calculated to be the best aligned sequences to the query sequence that I give.  Each of those aligned sequences have an e-value score representing the best hit by chance.
My question is how can I determine if the query sequence is highly conserved with the aligned sequence, or not?  Can I determine that by saying the sequence with best hit e-value (lower e-value) is the one that is highly conserved? or are there other concepts that I need to consider in this case?
I appreciate your help!

Whats the identity score like?

The identity score is pretty consistent with the e-value score.  I mean the higher the e-value score the higher the identity.  I am curious what the "identity score" tells me about the aligned sequences. @RoverEye

The "best" is the one with the highest ID score, lowest e-value and greatest length. There is no magic bullet, all of these are important. You should always look for the most similar sequence that matches as much as your query as possible with the lowest e-value possible.
Furthermore, it will depend on what you are looking at. If, for example, you are blasting a protein with a specific domain and are looking to find its homolog in another species, it is often more important that the domain be conserved than that the whole sequence be very identical. If you find a sequence with high identity but where the domain is not conserved, that is probably not what you are looking for.