text:
peptide MHC microarray

"The recent technology is peptide–MHC microarray or artificial antigen-presenting chip.
  In this technique, recombinant peptide–MHC complexes and co-stimulatory molecules are immobilized on a surface, and population of T cells is incubated with the microarray. The T cell spots act as artificial antigen-presenting cells containing a defined MHC-restricted peptides. The advantage of using peptide–MHC is that it can map MHC-restricted T cell epitope."

These few lines are from Chapter 3 of Immunoinformatics, De, Rajat K., Tomar, Namrata (Eds.).
What is recombinant peptide MHC? What is MHC restricted peptide? How did the advantage get derived?

you might need to clarify what you are struggling with here

The entire paragraph. What is MHC peptide complex?  What is MHC restricted peptide?

Have you tried Google searches? You've already asked similar questions to this before, did you learn anything from those answers? I highly recommend obtaining a good introductory immunology textbook and reading it.

@MattDMo completely agree about reading good immunology books. But I doubt peptide:MHCs are covered in any general immunology book.

@ddiez they were in mine...

Please refer me a good immunology textbook

@MattDMo yes peptide:MHCs are covered, sorry. I meant to say peptide:MHC microarrays, which is the question asked by the OP.

@user3237995 what about Janeway's immunobiology?

According to this paper (Yoav Soen et al. PLoS Biology 2003), peptide:MHC microarrays are a type of cellular microarray (a microarray designed to identify cell types; Wikipedia). These microarrays have attached a MHC molecule bound to a peptide, which allows them to work as artificial antigen presenting cells (APCs) that activate specific subpopulations of T cells.
Another recent paper is here where they specifically use the word recombinant peptide:MHC.
The expression MHC restricted refers to the positive selection (in the thymus) of T cells that recognize MHC molecules of the host but not other self-antigens (Wikipedia).

T cells grows in thymus. So what does "in the thymus of T-cells" mean??

@user3237995 sorry about that sentence, not very clear. I added some parenthesis that hopefully improve readability. Let me know if it is still unclear.

This is an important topic in immunology, especially for vaccine development.
MHC or HLA is a molecule expressed by some cells of the immune system which acts like a "catcher's mitt" and "presents" short snippets of protein to other immune cells. Other molecules act alongside MHC to provide co-signals which promote or suppress immune attack against the peptides that MHC presents.
Basically, it's a protein that holds out chunks of other proteins in order to educate the rest of the immune system. Here's the catch: different people have different genes for MHC which do a better or worse job of presenting certain peptides. This is one reason why different people can respond to different vaccines or different pathogens or cancers: they have different MHCs which may or may not present peptides from the relevant targets.
Thus, one big challenge in medicine right now is to develop good models for which peptides are best to include in a vaccine. The right answer depends on the genetics of the vaccine target (ebola, a tumor, e. coli etc) and also on the genetics of the person being vaccinated (does this person's MHC gene properly present this vaccine?)
So, to datafy this, people sometimes make arrays which allow us to quantify which peptides bind to which MHC genes in high throughput. Then we can use that data to learn which factors are most important for P:MHC binding. "MHC restricted" means that we are talking about a specific genetic subtype of these molecules.
Hope that helps.
Bion Alex Howard


text:
Immunomic Microarray

"One can measure two or more signals simultaneously determined by a single feature, i.e.,
  epitope in immunomic microarray DNA microarrays measure one response value for each gene per sample; that is, mRNA concentration produced by the gene but a single epitope
  can generate different response values corresponding to different epitopes in peptide–MHC chips. In case of B cell epitope, it can be recognized by different isotypes of immunoglobulins, so here, one can measure both intensity and quality of antibody response."

These few lines are from the book:
http://www.springer.com/biomed/immunology/book/978-1-4939-1114-1
Chapter 3
What does measure of one response value for each gene per sample mean?
Different response value means??
how is intensity and quality both are being measured??

epitope in immunomic microarray DNA microarrays measure one response
  value for each gene per sample; that is, mRNA concentration produced
  by the gene but a single epitope can generate different response
  values corresponding to different epitopes in peptide–MHC chips.

The excerpt looks grammatically incorrect and is therefore confusing. I guess what it tries to convey is — like there can be several probes for a single mRNA in a normal gene-expression microarray, there can be several antibodies binding to different epitopes in the same protein. Different antibodies will bind to their cognate epitopes with different affinities. This is what is referred to as "response value"
By quality I guess what the authors mean is that for the same epitope it is possible to quantify the binding interactions between that epitope and antibodies of different classes (but same antigen binding site).
Having looked at this excerpt, I would not recommend this book to anyone.
You can also have a look at these two articles:

From Functional Genomics to Functional Immunomics: New Challenges, Old Problems, Big Rewards
Prospects for the Future Using Genomics and Proteomics in Clinical Microbiology

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BLASTn vs ORF tools
Sequencing projects sequence one strand and call that the + strand and then extrapolate the sequence of the - strand. This means that sometimes the genomic sequence that you download from a database might be the complement of the actual sequence you are looking for.ORF tools like exonerate and genewise takes this into account and thereby look for six possible reading frames.Do sequence similarity tools like blastn take this into account and do pairwise alignment for complement of the actual sequence also?

It depends on the flavor of BLAST you are using. Some do, some don't. Specifically, the classic BLAST flavors are:

blastp :
compares an amino acid query sequence against a protein sequence database
blastn :
compares a nucleotide query sequence against a nucleotide sequence database
blastx :
compares the six-frame conceptual translation products of a nucleotide query sequence (both strands) against a protein sequence database
tblastn :
compares a protein query sequence against a nucleotide sequence database dynamically translated in all six reading frames (both strands).
tblastx :
compares the six-frame translations of a nucleotide query sequence against the six-frame translations of a nucleotide sequence database. (Due to the nature of tblastx, gapped alignments are not available with this option)

Of these, tblastn, tblastx and blastx all check the 6 possible reading frames (both strands). This only makes sense for protein searches since that's the only case where the reading frame is relevant. The simple blastn does not deal with reading frames but it does deal with hits against the reverse strand. The matching strand is highlighted in the output and the numbers in the HSP reflect that.
For example, these are the first and last lines of one of the hits when blasting the reverse complement of the human tP53 gene against the human sequences of the nr database:
Range 1: 1 to 2591GenBankGraphics Next Match Previous Match
Alignment statistics for match #1 Score Expect  Identities  Gaps    Strand
4673 bits(5182)     0.0     2591/2591(100%)     0/2591(0%)  Plus/Minus

Query  1     CACCCCTCAGACACACAGGTGGCAGCAAAGTTTTATTGTAAAATAAGAGATCGATATAAA  60
             ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Sbjct  2591  CACCCCTCAGACACACAGGTGGCAGCAAAGTTTTATTGTAAAATAAGAGATCGATATAAA  2532

[...]

Query  2521  AGACTTTTGAGAAGCTCAAAACTTTTAGCGCCAGTCTTGAGCACATGGGAGGGGAAAACC  2580
             ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Sbjct  71    AGACTTTTGAGAAGCTCAAAACTTTTAGCGCCAGTCTTGAGCACATGGGAGGGGAAAACC  12

Query  2581  CCAATCCCATC  2591
             |||||||||||
Sbjct  11    CCAATCCCATC  1

Note that 1) the strands are given as "Plus/Minus" which means that the query sequence is aligned against the - strand of the target and 2) that the coordinates of the subject sequence start from the end (2591) and go to the beginning (1).
So yes, even simple tools like untranslated BLAST take the two strands into account.

Sometimes the hits could also be "false positives" if the sequence is aligned against the - strand.In that case,what is the solution?

@Raghavakrishna why would they be false positives because they align against the - strand?

If the negative strand sequence is not the actual sequence that codes for,sometimes it might be equivalent to some other sequence(false positive?)

@Raghavakrishna I'm sorry but I still don't understand. The details always depend on what you're actually doing. If BLAST gives you a hit, then that's a hit. Whether or not that is biologically relevant is another question and I can't answer that unless I know what question you are asking.

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Books for beginners
I want to study biology. I have zero previous knowledge of biology but I know Physics, Chemistry and Maths. From which book should I start? I have heard about Campbell Biology, but it is very costly in India(more than my 1 month's earning). So please suggest books that:

 Are cheap OR  could be found on internet
Require no previous knowledge of biology
Contain no technical mistakes
Adequately explain the topics which they deal with
and also mention some history of the topics

Edit
I am not looking for online videos. I want books; my internet is slow and there are some other problems. You can also tell costly books--Perhaps I could find them in the library or could print it somehow. If Campbell Biology book is available online then please give me the download link.

Many previous editions of textbooks are available for free online. I don't have any recommendations though. Is there a specific area of biology you want to focus on?

@canadianer Once I read a school book, it says everything is made up of cells and various cells combine to form an organ or something like that. So in particular I want to know everything about cell, how they were made, how they combine etc etc. I want to study historically, i.e. how scientist discovered this and that etc etc.

@canadianer Once I was reading Nervous system, the book said that there is some kind of sodium impluse which sends the electrical signal to our brain. But I could not understand the sodium impulse. So I want to learn about that. But at first I want to make a solid background in biology so I will first read some introductory book.

@metacompactness thankyou very much for the link.

As @metacompactness said in the comments, the campbell (9th edition) is available and free in pdf online (here). This book is a classic that most undergraduate students know quite well.
Online resources
There are some very good online resources to get an introduction to biology. I think that online resources might have the drawback that they may miss the big picture that a whole book can give you and it may be complicated to really understand in what order you should look at the videos particularly if you jump from one website to another. Otherwise, it is often quicker to learn from someone speaking in a video than from reading a book. I learned lots in various field thanks to free online courses. I appreciate a lot reading books but I think that free online resource is the best option for you.
As I did my undergrad in biology, I never really needed this kind of resource but generally speaking I find Khan Academy to be very good for introducing students to new fields of knowledge. And there is a whole biology section on Khan Academy. The MIT courseware is also a very good free resource. Education portail might be a good starting point as well.
If you google "free introductory course biology" you will find many other resources.

Here is a ted talk by Salman Khan (from Khan Academy) for the fun.

Khan academy is amazing! That would be a wonderful place to start!

Sal Khan from Khan Academy teaches good physics, chemistry, and mathematics, but he doesn't teach good biology.

This is a low price edition available in India on flipkart.com, it covers all topics extensively. It costs around ₹ 570.
Biological Science (English) 3rd Edition by Taylor

Is this book for absolute beginners or for BS as many people wrote in reviews?

This book is equivalent book to Campbell Biology.Taking into account the prize of Campbell biology,this book is relatively cheap.

I didn't read this book, I can't judge but Campbell biology is available online for free and I am currently enjoying it :)

A great place to start is Khan academy. It is free and very easy to understand.

Also, another thing you could try would be Bob Jones Biology (books A&B). I don't know how much those cost in India. But, they explain things in great detail starting at the bottom and working upward. I  will let you know that they have a strong Christian influence which some people would disagree with. However, if you can look past that, they are excellent, well-written books!

https://www.khanacademy.org/youcanlearnanything?video=main

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Determining and Differentiating specific ATPases

In respects to this certain ATPase transporter. What do i look for in respects to determining what specific kind it is out of:

F-ATPases
V-ATPases
A-ATPases
P-ATPases
E-ATPases

Im assuming that analyzation of the gradients dealt with will guide me to the answer. With that logic, i can assume that this is an F-ATPase since i know this membrane protein can synthesize ATP using a H+ gradient, and work in the reverse to create a H+ gradient using the energy gained from the hydrolysis of ATP.( I see 2H+ cations being expelled) Is this a correct method in differentiating ATPases ?

Can you please rephrase your question, as I don't understand it? You want to know if you identified the ATPase in the image as the F0-ATPase? Or do you want to know what is different between the different subtypes?

Sorry for the confusion. My question is, am I going about determining what sort of ATPase this is in the correct way? I determined that this photo depicts a F-ATPase by analyzing the 2H+ cations going through it. And is this an F-ATPase at all? You seem to be "the guy" in molec bio, I appreciate it.

First of all, I think you need to research the subunit structures of the various ATPase classes in the list because I am pretty sure that several of them are not as complex as this.
Although this superficially looks like the F-ATPase responsible for synthesising ATP by using the proton gradient generated by the electron chain, there is a clue in that diagram that this may actually be a V-ATPase. The V-ATPases use ATP hydrolysis to move protons from the cytoplasm into the lumen of acidic organelles like lysosomes. The diagram in the question depicts a process like that (ATP is being hydrolysed). Now, you can drive the F ATPase in reverse to achieve this situation, so that isn't definitive.
The labelling of the two compartments is also consistent with the idea that it is a V-ATPase since 'lumen' isn't a word that is usually used in the context of the mitochondrion (it would normally be 'matrix').
So I would suggest that you find out if the subunit labelling is like that used in F-ATPase or V-ATPase (or both). A Google image search will help you to find cartoons of ATPases.
My guess, before doing the suggested research, is that this is a V-ATPAse.

I think that, too. Have a look at the direction in which the ATPase is working, this should give the final clue. It pumps from the cytosol into the lumen.

Yes, but as I said in my answer, you can artificially get F-ATPase to do that, although probably not in the context of cellular compartments.

The F-ATPases are locared in the inner mitochondrial membrane and are not in contact with the cytoplasm if I remember correct.

Thank you for the insight. With further research i've found that this is indeed a V-ATPase.(Learning that the V stands for Vacuole surely helps). Also, V-ATPases hydrolyze, ATP which is clearly seen in the illustration. While F-ATPases only synthesize ATP using a H+ gradient.

http://www.bio.davidson.edu/courses/molbio/molstudents/spring2010/sween/V%20vs.%20F%20ATPases.jpg


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How is it possible to even hope for an ebola epidemic of this current size to remain contained to a relatively small part of Africa?
As of 2014-09-14 at least 5347 cases of ebola have been identitied. Some estimates are much higher. While experts are sounding the alarm to try to get sufficient resources to contain the outbreak, some people are also speaking very hopefully about containment to roughly the current affected area. This article puts the risk of the outbreak reaching the United States as low as 3%. I'm not an expert in the field, but it seems like there are almost countless ways in which an increased number of cases increases the risk of further exponential growth. It's encouraging to hear that in countries with better healthcare, death rates would likely be much lower, but at this point, isn't it inevitable that the outbreak will run its course as a global pandemic?
For example, which of these possibilities is just my imagination, or likely so improbable that we don't need to worry about it?

Scared carriers not yet showing symptoms sneak or force their way across boarders to unaffected regions.
Objects, food, or water touched by the infected go unnoticed until they end up leaving the containment zone.
If it can jump from bats or monkeys, thousands of infected humans increase points of contact to create vectors into other species, perhaps one that will travel unnoticed far beyond the containment zone.
After months of the same security precautions day in and day out, airport checkpoints, and other points of entry become lazy, and let infected through.

With numbers as high as they are, and possibly higher than we even know, is this really containable at all?

The thing to know about Ebola is that it really is not that contagious - you need to be in direct contact with someone else's blood. While this may occur in undeveloped countries, it is very unlikely to occur often in the US. Any cases in the US would be immediately dealt with, and would any deaths. This is true for most of Europe etc., as well.
Countries strongly affected (like Sierra Leone) have also not been using the most effective epidemiological policies, and perhaps even causing harm by, e.g., enforcing quarantines.

The key is "you are not getting contagious unless you show symptoms" so it is unlikely in the west that we will get more then small scale outbreaks.

This is too long for a comment, so my thoughts about this here. The CDC Director said a few days ago after a visit in Africa "The window of opportunity is closing".

This can happen. However, you are not getting contagious unless you show symptoms. This is different in other diseases like chicken pox or measles where you spread the virus before showing symptoms. So there has to be a lot of awareness. Also doctors need to be very careful with patients showing these symptoms. This is most likely one of the main reasons for the wide spreading of the disease.
Same problem as in 1. Theoretically this is easy to prevent, but in a situation of chaos this can cause problems. But since infected people which show symptoms will not handle large amounts of food, this is most likely less of a problem.
Every crossing of a species-barrier is a rare event. Double-crossings are even less likely. So I don't think this is a problem. Besides this, we already have to independent Ebola outbreaks which has never happened before. One is the one in West-Africa, the other one is happening in the Democratic Republic of Congo. Both are independent cross-overs.
This can cause problems. The advantage of the first world is that we have functional health care systems. They allow better care for the persons and also better isolation of contact persons. I think it is unlikely that it would spread widely. The perspective will be different, if the virus makes the jump into the densely populated regions in South-East Asia. There a lot of people live closely together, this can cause real problems. Fortunately for us the virus is not highly contagious. To infect yourself you need unprotected contact to the body fluids (blood, stool, feces, sweat etc.) of infected persons.

"Not highly contagious" is encouraging. It seems easy enough to avoid infected person's blood, feces, vomit, etc. But sweat... We sweat all the time even if we aren't particularly hot. An infected person must sweat a lot more. Doesn't that get the virus all over everything?

Yes, this is one of the problems. This is also the reason why peope of the isolation wards are dress up like they do.

@MarkBailey, yet but UV light kills it.   And infected people do not feel well, so in the west are unlikely to travel much.

I'm not an expert in the field, but it seems like there are almost
  countless ways in which an increased number of cases increases the
  risk of further exponential growth. It's encouraging to hear that in
  countries with better healthcare, death rates would likely be much
  lower, but at this point, isn't it inevitable that the outbreak will
  run its course as a global pandemic?

I don't think it is inevitable. The current strain has a high virulency, high mortality, but low transmissibility. It does not infect until the patient shows symptoms, but by most of that time she/he will be unable to move and spread the infection because of the 39°C degree fever. Only the people nursing the patient, e.g. family members, workers in the healthcare system, are in danger. So it spreads slowly compared to other diseases and that's why it is easy to quarantine and prevent. If it does not change attitude due to a mutation or anything else, I think we can avoid a more serious pandemic, at least I hope so.
There is an already existing model for an older strain available here: Understanding the dynamics of Ebola epidemics.

Scared carriers not yet showing symptoms sneak or force their way
  across boarders to unaffected regions.

I have the impression by listening and reading news, that most of the people know nothing about ebola in Africa, or they don't really care, because they cannot read, or they have bigger problems e.g. starving. For example Sierra Leone is one of the poorest countries in the world. They cannot move so easily, because travel requires money. So I think this is possible, but unlikely. If it happens, the infected person cannot spread the disease fast, because she/he will be unable to move after showing the symptoms. So she/he can be quarantined.

Objects, food, or water touched by the infected go unnoticed until
  they end up leaving the containment zone.

I think in the current case this is unlikely either. But if a food contains virions, it does not necessary cause disease, e.g. microwave oven, or long shipment - usual by fruits like banana - can inactivate it.

If it can jump from bats or monkeys, thousands of infected humans
  increase points of contact to create vectors into other species,
  perhaps one that will travel unnoticed far beyond the containment
  zone.

Well, it needed 8 changes to fully adapt to guinea pigs. (It was possible to infect these animals, but the outcome was not lethal.) The virions contain 19kb of RNA, and the mutation rate is 2.0 x 10^-3 substitutions per site per year. Now I am not an expert of genetics (I always hated it), but as far as I understand it is possible to rougly estimate the risk based on this data. I guess it would take decades to adapt to another species, so it is not a fast process.

2013 - Animal models for Ebola and Marburg virus infections

Comparative sequence analysis of the complete genomes of the GP-adapted
  EBOV and wild-type virus showed 8 nucleotide differences, which led to
  5 amino acid substitutions; single amino acid mutations in NP and L
  and 3 mutations in VP24 (Volchkov et al., 2000). Using a reverse
  genetics approach, it was shown that VP24 had a critical role in the
  pathogenesis and the amino acid changes in VP24 were essential to
  achieve EBOV virulence in guinea pigs.

2013 - Ebola virus infection inversely correlates with the overall expression levels of promyelocytic leukaemia (PML) protein in cultured cells

Ebola virus belongs to the family of negative strand RNA viruses
  (Mononegavirales) and together with the Marburg virus are the two
  known species of the Filoviridae family 1. Electron microscopy of
  Ebola virions produced in cell culture have shown them to be
  pleomorphic, appearing as either 6-shaped, circular or as long
  filamentous (and sometimes branched) forms with a length up to 14,000
  nm and a uniform diameter of 80 nm 2. The 19 kb single-stranded RNA
  genome encodes seven viral proteins: the membrane associated (matrix)
  proteins VP24 and VP40, the viral glycoproteins, GP (that forms the 10
  nm long peplomers) and sGP (non-structural secreted form), the
  characteristic helical ribonucleocapsid that consists of the
  nucleoprotein (NP), VP30, VP35 and the L-protein that forms a
  RNA-dependent RNA polymerase 1.

wikipedia - Ebola virus

Sequencing of 99 different Ebola isolates from patients in the 2014
  West African outbreak of Ebola showed the virus to be rapidly
  mutating,[15] with a mutation rate of 2.0 x 10-3 substitutions per
  site per year making it as fast changing as seasonal influenza.[16]
  This is likely to represent rapid adaptation to human hosts as the
  virus is repeatedly passed from human to human (as opposed to usually
  being passed between fruit bats and only occasionally crossing over
  into humans), and may pose challenges for the development of a vaccine
  to the virus.[17][18]

After months of the same security precautions day in and day out,
  airport checkpoints, and other points of entry become lazy, and let
  infected through.

I don't think security works this way. Btw currently we have the technique to filter out people showing symptoms, for instance with IR detectors looking for elevated body temperature. We have e.g. ELISA for checking IgM or the presence of the virus itself in blood tests. So if these measures are needed, I think we will apply them. Currently they are not needed, according to CDC there were only 5 cases outside Africa.


text:
How can I determine the purity of cells isolated from rat brains if I cannot use FACS, Immunohistochemistry or SEM anaysis?
Please help.
I know how to isolate the different cells (astrocytes, other glial cells, neurons and synaptosomes) from brain tissue using a Ficoll-based separation but how do I determine the purity of the fractions that I have isolated if I cannot use immunological techniques, FACS or SEM analysis.

You can do qPCR for certain markers from the extract. GFAP for astrocytes, Tuj1 for neurons, Myelin for oligodendrocytes etc and calculate their percentages to have an estimate of the relative populations. If you are quite used to microscopy and studying these cells then you can identify the different populations of cells with normal light microscopy as well; this is not quantitative and is susceptible to bias.

q-PCR would be the most accurate PCR technique if you wanted a breakdown of the population by percentage. Simple optical techniques are quantitative if you abide by stereology techniques.

I guess that a Western would count as an example of an immunological technique (excluded in the question).

yeah I meant qPCR only.. @AlanBoyd.. yeah true 'ill correct it

@leonardo.. they are quantitative if there is an automated algorithm for scanning and classification of cells based on the images.

@WYSIWYG - I agree, but that means the technique is not only qualitative. Automated imaging and segmentation is the modern successor to random fields + stereology.


text:
How the conjunctivitis virus spread just by seeing a person's eye who is infected

Conjunctivitis or 'pink eye'.
I have a few questions on conjunctivitis. When I was suffering from conjunctivitis, my doctor advised me to wear sunglasses so that no one else gets infected.
I wonder how it happens that if someone looks into an infected eye, then there is a chance for that person to also get infected. Specifically, why does this apparently happen only when we see an infected eye?.
Another question I have is why does our eye get watery when we see the eyes of an infected person?.

The sunglasses are worn because eyes that are infected are more sensitive to light.  It has nothing to do with infecting other people, and has absolutely nothing to do with someone catching the infection while looking at the eye.

Then why did you provide us that image!?

@HarshalGajjar I have provided the image firstly because I was to make sure what I am asking, I mean, many of us has suffered this but only few are there who know its real name secondly to support my second question that why does our eye get watery when we see the eyes of an infected person?.

I'm affected now! //sarcasm :D anyways nice question.

Also sunglasses prevent dust and wind from irritating the eye..

You can't catch infections just by looking at the infected area but you can catch infections through touching, breathing of person, etc.

Why just repeat what was already stated in an answer that was voted on 17 times by the community; notwithstanding the fact that this is a question that is 2 and a half year old?

You can't catch conjunctivitis by looking at someone, but you can spread it around by touching your eye and touching something else, which then can pass the virus to someone else (viral conjunctivitis can be highly contagious). There are no hard facts, but one estimate is that people touch their faces an average of 3.6 times per hour, more if your eyes are itchy. Wearing sunglasses can not only help the possibly increased sensitivity of eyes with conjunctivitis, but they may also cut down on the number of times you touch your eye (thus spreading the virus).
There is no evidence to support that our eye get watery when we see the eyes of an infected person.
Conjunctivitis (Pink Eye) - CDC
Stop Touching Yourself, Flu Researchers Say

I have been old that door handles, armrests and other shared things are likely to transfer infected tears to uninfected eyes. Is this true?

Yes, it is. Hard surfaced like door handles and pencils can transfer the virus. That's why it's important that the person with conjunctivitis avoid touching his eyes, and should wash his hands frequently.


text:
What is the context in which a species gets the name "elegans"
Quite a lot of Latin binomials from different genera contain the same species name. For example, there are a number that reflect the physical properties of the species (Tables have the latin name, a translation, and the number of European species according to the European Nature Information System).
nigr[a|o|um]    black        545
minim[us|a]     small        325
alb[us|um|a]    white        264
maxim[us|a]     big          166

and some which reflect the way in which they become apparent to us humans
vulgar[is|e]    common       691
sativa          cultivated   70
domesticus      domesticated 19

as well as reduplication for particularly salient/familiar species (e.g. Gallus gallus, Mephitis mephitis)
So, I'm wondering why there are so many elegans (471 European species on the database). It's particularly widespread, but meaning "elegant" or "refined", it's a rather nondescript name to give. Maybe someone might describe a species like this if they were really running thin on defining characteristics, but if this is the reason, why would the name occur so often?
So I'm fairly sure I'm missing something important about how species get named. What is/was the reason for naming so many species "elegans"? Does it have perhaps have something to do with type species?

elegans -> handsome, fastidious (Latin).  maybe neatness or clean as well.

Since "meaningfulness" is not listed among the requirements for new names, any author is free in his choice of name derivation. [There are nevertheless some natural restrictions, such that new names are to be treated as Latin irrespective of the etymology and should follow Latin grammar (with botanical nomenclature being much more meticulous in this respect).]
There are indeed some cases when the name of the species may be meaningful for the purpose of the choice of type species (the "typicus/a/um" names and tautonomous names like "Glis glis"), but "elegans" doesn't belong here.

So, the high frequency of "elegans" has nothing to do with typification and reflects nothing else than the will of authors to reflect their emotions. One recurrent cause of "elegans"-names among paleontologists, for example, is good preservation of the respective fossil material. [By the way, there are even more emotionally loaded (but less frequent) names like "mirabilis/e" or "enigmatica/us/um".]
Since providing etymologies for names alongside formal descriptions of new species at a certain moment became an official recommendation, you can make your own collection of causes people provide to justify their choice of "elegans" as species names.
EDIT: I've just found this revelation: (Oxytomoides elegans, fossil bivalve) "Etymology. Elegans, Latin for choice or select, referring to what we regard as esthetically pleasing appearance of the species".

I've put your numbers into the table above. I was quite lazy and haphazard about searching for all genders, though I realise now that the database a handy regex option. Do you know an accessible source  where the etymologies might be listed?

There is a very nice collection by Mark Isaac available here, but he is mainly interested in specially curious names - you will not find "elegans" there. In general, as said, it is now strongly recommended to provide etymologies in the original publications, so the some kind of semi-manual search is required. The relevant section is called "Etymology" or "Derivation of name", e.g. here.

I'd guess that elegans is mainly used as the common choice for "beautiful."


text:
What bird species is this? (Heron-like waterfowl from China)
I need help identifying this bird.  (Some sort of heron?)
It was seen in Wuhan, Hubei, China, in September.
It is very common there.  It can also swim like a duck, but I've only seen it do this once (it's not something they commonly do).  I can supply more photos upon request.
These are two different individuals:

I'd also be grateful for tips on websites I could use to look up these birds.  Most of what I can find is for North-America only, and I'm having a hard time finding Chinese birds.

My two guesses were Striated heron or Night heron, as the juveniles of both look similar to this.  But I haven't seen any birds that would look like the adults of either species.

juvenile night heron (Nycticorax nycticorax) INDEED good pics, cheers

Based on some external advice, I believe it might be a juvenile night heron (Nycticorax nycticorax), the only remaining question being why I didn't see any adults.
Link to Google Image search results
Update: I went back to the same location today and saw some adult night herons, which convinced me that these were juveniles of the same species.

I'd go with juvenile striated heron. I ruled out others such as the chinese pond heron because of the spotted wing plumage and slightly different shape of the patch around the eye. The night heron seems to have a more red eye than the striated heron and appears to have a stubbier beak.
Arkive is a good place to see a lot of pictures of birds, this is a good birding site, and otherwise I use generic google searching (e.g. start with "herons china" or "herons asia") - this at least helps narrow down the search quite substantially and is considerably cheaper than having a library of the worlds bird books!

It does look very similar to the juvenile of the striated heron (so +1), but how would you explain that all the birds I saw were like this?  (I have tens of photos of several individuals so I don't have to rely on my memory.) Could they all be juveniles, with no adults around?


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What is the difference between osmotic potential and osmotic pressure?
Which term is used to calculate water potential? Does osmotic potential mean the same as solute potential?

Welcome on biology.stackexhchange. This is a pretty broad question, so it would be nice if you could start on these topics yourself (either with a good biology book or the Wikipedia) and then ask specific questions.

Please donot comment if u cannot help me .I know about these term but I need deeper explanation not your criticism .

Then you need to edit your question so people can answer specific questions. There are certain rules about questions, if you choose to not pay attention to them, questions can be closed, as this has already happened here. You can still edit the question and it can be nominated for reopening.

Does it meet the site rules now?

sometimes a question is just a question

Osmotic potential is the concentration of solute molecules in a solution while osmotic pressure is the pressure acting outward on the cell walls and internal membrane in plants

Osmotic pressure: pressure applied by a solution to prevent the inward flow of water across a semi-permeable membrane.
Osmotic potential: the potential of water molecules to move from a hypotonic solution to a hypertonic solution across a semi-permeable membrane.
Osmotic pressure can be calculated using the following formula:
$$Π = iMRT$$
where
$Π$ is the osmotic pressure in atm
$i$ = van 't Hoff factor of the solute.
$M$ = molar concentration in mol/L
$R$ = universal gas constant = 0.08206 L·atm/mol·K
$T$ = absolute temperature in K
The following page has a worked out example.
As for your question on solute potential vs osmotic potential, the answer is that they are indeed the same. You can compare the formula for $\Psi_{\pi}$ on the wikipedia page and the page of this pearson textbook. These formulas are the same:
$\Psi_{\pi} = -Π =-iMRT$
So there's a simple relationship between osmotic pressure and osmotic potential.


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Why do some cuts leave scars, while others do not?
Last year I got a moderately-deep cut on my finger, and it left a scar. Six months later, the scar is still there. On the other hand, I've had lots of other cuts on my fingers, though none have left scars. Why is this? Is scarring related to the severity of the cut, or something else?

Similar question: http://biology.stackexchange.com/q/20129/6422

This depends on a number of factors. Here are the first two that come to mind:
1) Is the cut deep enough to reach the dermis (this is the layer below the epidermis) where scar tissue will form?
2) What is your general state of health, and was there an infection at the site of the cut, which would have altered the normal healing process.
Basically, not all cuts are created equal, especially if some are deeper than others and become infected.
This article studied scratch depth
http://www.ncbi.nlm.nih.gov/pubmed/17440346


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Can you disconnect sensation from the brain without destroying muscle functions?
I want to know if it would be possible for a surgeon to "shut off" a person's senses without causing paralysis of any kind. The person would have to maintain their ability to speak and move, but not be able to hear their own voice or sense the physical world around them at all.

It's possible to block hearing, or sight (especially sight- just block the optic nerve), but destroying feeling in the body would be neigh-on impossible without completely paralyzing someone. The nerves for muscle control and sensation are bundled very close to each other the farther up the extremity you go, and by the time you get to the spinal cord they're all mashed in there together.

I don't know about that. Leprosy often causes numbness in the extremities. When victims don't feel pain they get injuries that can lead to infections and loss of tissue. But the limbs usually still work, suffering from weakness, until they get injured. Of course that weakness could be interpreted as partial paralysis.

@user137 Leprosy is a disease primarily of the peripheral nerves, while nerves responsible for motion are often deeper. However, like I said the two tend to become bundled closer together the closer to the trunk (and spine) you get. I just don't think it would be plausible to selectively block sensory neurons without affecting motor neurons as well.

Even if it were possible to selectively destroy sensory (afferent) nerves alone, the individual would not be able to walk/move normally immediately afterwards, because there would be no environmental stimuli with which to orient one's actions.
Two of the senses people often overlook are balance (or spatial orientation) and proprioception (where the body parts are with respect to each other and the physical world). (Some people lump the two; it's easier to think of them independently, because they really do quite different things.)
Proprioception (and closely associated kinesthetics) is possible because of nerve signals from skin, tendons, muscles, and joints. This gives us the senses of limb position and movement, the sense of tension or force, the sense of effort, the sense of gravity.[1]

Patients (lacking proprioceptive feedback) made large directional and amplitude errors when performing a reaching task without visual feedback....The errors were associated with differences in velocity and acceleration for movements in different directions.[2]

Basically, without proprioception, you could not touch your little finger to your thumb without visual input, let alone actually perform more complex voluntary movements successfully.
The vestibular system exists through input from three semicircular canals located in the inner ear on each side. The canals are oriented at (basically) 90° angles to each other so that we can maintain our balance no matter which position our head is in. These are also connected to one's ocular reflexes. Together they're called the vestibolo-occular system, which functions as a reflex (VOR).

Three sensory systems, vestibular, visual, and somatosensory/proprioceptive, serve our sense of balance. Each of these systems provides unique sensory information to the brain where it is integrated (often in complex ways) to produce a final motor output to muscle groups for maintaining gaze, head and body posture, and controlling static and dynamic balance.[3]

Without these systems, we would be completely unable to get or stay in a standing position. We certainly could not walk.
So, long story short, the answer is no. Not only is it surgically impossible, but if it were, you would not have a coordinated, working body left. Eventually even speech would be affected (as proprioceptors on the mouth are involved in speaking).
[1] Proprioception From a Spinocerebellar Perspective
[2] mpairments of reaching movements in patients without proprioception. I. Spatial errors
[3] Anatomical and Physiological Considerations in Vestibular Dysfunction and Compensation

The nerves for sensation do travel intimately close to motor nerves outsides the spinal cord. In these locations only disease processes can preferentially target a particular class of nerves. Diabetic neuropathy is a common condition causing this kind of peripheral nerve injury resulting in sensory loss. In the spinal cord, afferent (incoming) and efferent (outgoing) conduction pathways are segregated into bundles so a traumatic event can cause a selective deficit of sensation or movement of a region. Further up the chain (brain) entire functions are segregated so it is possible to create not only deficits of physical regions but of specific complex motor functions or sensory processes. Interestingly most of our senses are handled by cranial nerves that are not in the spinal cord. These nerves are generally purely sensory.

While the information is welcome, this doesn't really address the OP's question: can a body without sensation work "properly"?


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Why don't mammals have more than 4 limbs?
Arthropods have 6 or more limbs and arthropods with 6 limbs appear to move faster than arthropods with 8 limbs so I wonder whether this might have something to do with fast and efficient locomotion. But, this is just a guess. I wonder what the official explanation is, if it exists.

Basically because mammals and arthropods evolved separately. If we evolved from a four-legged, fish-like ancestor, then mammals never got to choose how to evolve more efficiently (if it is).

@anongoodnurse What does "efficiency" have to do with anything? If the theory that everything evolved from single-celled organisms is correct, then that argument holds little water.

@b1nary.atr0phy - how so?

Are prehensile tails not considered limbs in this case? Common definitions seem to include them as limbs, giving many mammals 5 limbs instead of 4.

I think that if mammals had 6 limbs, you could ask why don't mammals have 8 limbs. Or if they had 8 limbs, you could ask why wouldn't they have 6 limbs. Evolution had to act a certain way, and it worked in the way so that present day mammals don't have more than 4 limbs.

It is also worth considering that mammals have an upright posture and 2 extra limbs would not be helpful, they would tend to get in the way. So even is my by some anomaly such a mutation occurred it would be selected against.

Before I find myself paraphrasing multiple times, many essentially duplicate answers, to many relevant questions being asked on SB, about selection-based adaptive evolutionary explanations about observed traits. I will link this alternative answer here: http://biology.stackexchange.com/a/57315/5005, perhaps @Remi.b could consider such an answer in future answers, some form of Neutralist evolutionary perspectives... in addition to selection-based perspectives.

Number of legs in terrestrial vertebrates
Not only do mammals have four legs but actually all terrestrial vertebrates (which include mammals) have four legs. There are slight exceptions though as some lineages have lost their legs. Typically snakes have no legs anymore. Apesteguia and Zaher (2006) discuss the evolution of snakes legs reduction and report a fossil of snakes with a robust sacrum. Cetaecea (whales and friends) have lost their hind legs but we can still spot them on the skeleton. See for example the orca (killer whale, easily recognizable to its teeth) on the picture below. Pay attention to the small bones below its vertebral column at the level on the left side of the picture.
I also want to draw attention to the importance of the definition of legs. I guess that we would call something a pair of legs if it is constructed using a similar developmental pathway than current existing legs. If we are using some broader definition, then a prehensile tail as found in some new world monkeys, for example, could be considered as a leg (but only a single leg, not a pair of legs obviously). A list of animals having a prehensile tail can be found here (Wikipedia).
Did you say Natural Selection?
I think (might be wrong) that you have too selectionist a view of evolution. What I mean is that you are wondering why mammals have four legs and you're looking for an explanation of the kind "because mammal have this kind of need of locomotion and for this purpose four is the most optimal number of legs". Consider the following sentence: "If there is a need, natural selection will find a way!". This sentence is wrong! Evolution is not that easy. This false view of evolution is sometimes referred to as panselectionist.
The reality is that it is not easy to evolve such a developmental pathway as drastic as having an extra pair of legs that are well integrated into the body of the carrier of this new trait. Such an individual would need a brain, a nerve code, a heart and some other features that are adapted to have extra legs. Also, assuming such a thing came to existence it is rather complicated to imagine how it could be selected for. To go slightly further, you have to realize that there are many stochastic processes in evolution (including mutation and random variation in reproductive success) and an organism is a piece of complex machinery and is not necessarily easily transformable to some other form that would be more efficient (have higher reproductive success). Often going from one form to another may involve a "valley crossing" meaning that if several mutations are needed, intermediate forms may have low reproductive success and therefore a high amount of genetic drift (stochasticity in reproductive success) to cross such valley of low reproductive success. See shifting balance theory. Finally, even if there is selection for another trait, it may take time for the mean trait in the population to shift especially if there is only little genetic variance. A complete discussion on why the sentence "If there is a need, natural selection will find a way!" is wrong would fill up a whole book.
Gould (1979) is a classic article on the subject and is very easy to read even for a layperson.
Why 4 legs?
Terrestrial vertebrates have four legs because they evolved from a fish ancestor that had four members that were not too far from actual legs (members that could "easily" evolve into legs). This is what we call a phylogenetic signal. The explanation is as simple and basic as that. You can have a look at the diversity of terrestrial vertebrates here (click on the branches).
Number of legs in invertebrates
Arthropoda (Spiders (and other chelicerata), insects (and other hexapods), crustaceans (crabs, shrimps…) and Myriapoda (millipedes) and Trilobite as well)) evolved from a common ancestor who had a highly segmented body. From this ancestor, many groups have fused some segments. In these taxa, each pair of legs is attached to a particular segment (I don't think the segments are still visible in spiders today). In insects, for example, all 6 legs are attached to the thorax but to 3 different segments of the thorax, the pro- meso and meta-thorax (see below).
As a side note, it is interesting to know that the wings in insects did not evolve from the legs (as it is the case in birds and bats). There are two competing hypotheses for the origin of insect wings. Wings either developed from gills or from sclerite (chitine plate, the hard part of the insect). When insect first wings, they actually evolved three pairs of wings (one on each segment of the thorax). At least one pair has then been lost in all modern species. In the diptera, a second pair of wings have been lost and are replaced by halteres, particularly easy to spot in craneflies (see below picture). In millipedes, the link between segmentation and legs is even more obvious (see picture below). You can have a look at the diversity of Arthropoda here (click on the branches).
Pictures

Update 1
Asking how likely it is for a given population to evolve a given trait is extremely hard to answer. There are two main issues: 1) a definition of the question issue and 2) a knowledge issue. When asking for a probability one always needs to state the a priori knowledge. If everything is known a priori, then there is nothing stochastic (outside quantum physics). So to answer the question one has to decide what we take for granted and what we don't. The second issue is a knowledge issue. We are far from having enough knowledge in protein biophysics (and many other fields)  to answer that question. There are so many parameters to take into account. I would expect that creating a third pair of legs would need major changes and therefore one mutation will never be enough in order to develop a third pair of legs. But, no I cannot cite you any reference for this, I am just guessing!
Following the wings example in insects. Insects have had three pairs of wings. While some mutation(s) prevented the expression of the third (the first actually) pair many of the genetic information for this third pair remain in the genotype of insects as they still use it for the two other pairs. Taking advantage of that, Membracidae (treehoppers) developed some features using a similar biochemical pathway than the one used to develop wings. Those structures are used as protection or batesian mimicry.
Update 2
Let's imagine that an extremely unlikely series of mutations occur that create some rodent with 6-legs. Let's imagine this rodent with six legs has a larger heart in order to pump blood to these extra legs and it has a brain that is adapted to using six legs and some changes in its nerve cord so that it can control its 3rd pair of legs. Will this rodent have higher reproductive success than other individuals in the population? Well… let's imagine that with its six legs, it can run faster or whatever and has a very high fitness. How would the offspring of a six-leg mother (or father) and a four-leg father (or mother) look like? Will it be able to reproduce? See the issue is that it is hard for such trait to come to existence because 1) it needs many steps (mutations) and 2) it is hard to imagine how it could be selected for. For those reasons, there exist no vertebrates with 6 fully functional legs.
Well, let's assume it does and in consequence, after 200 generations or so, the whole population is only made of 6-legged individuals. Maybe the species got extinct then and no fossil record has ever been found. This is possible. It is not because something has existed that we necessarily find something in the fossil record.

"all terrestrial vertebrates have four legs". What about snakes? Are they an exceptional exception, or somehow not counted on this?

@BoppreH Good point! Snake lost their legs. I'll give a word about cetacean as well which back legs are only visible on some small bones in the skeleton. If you can think of other exceptions, please let me know.

@Remi.b - I like your edit, but will maintain that there has never been such a creature. The mutations required would take many, many millions of years to produce such a creature, and the body plan would have descendants for far more than 200 generations. Fossils will never be found because it never happened. There is a reason all vertebrates have the same body plan - that's what crawled out of the ocean onto land, and populated the earth and (for some) then back. It's almost as bad as asking why we didn't evolve a set of wings on our backs to escape predation and amke is better hunters.

@anongoodnurse: Depending on your definitions, conjoined twins might provide a counterexample to your assertion.  And of course, some mammals have evolved wings, so it seems reasonable to ask why our particular species did not.

@NateEldredge - you're not reading my comments properly. Conjoined twins are a developmental, not genetic, defect, and bat wings are not from a third pair of limbs.

Nate I encourage you to lookup pictures of bat skeletons. Their skeleton looks like a person with really big hands, because that's basically what bat wings ARE: really long fingers with skin stretched between them. In fact, bats are one of the best illustrations of how all mammals evolved from a common ancestor and thus have basically the same body structure (ie. the answer to this question).

@anongoodnurse a mutation in the Hox genes can cause formation of additional limb buds

I thought I did acknowledge that extra limbs can form, but they are not usually fully functional. For a fully functional six-limbed vertebrate to form would take an enormous number of mutations.

Regarding update 2: A more likely scenario would probably be development of ornamental limbs (maybe due to sexual selection) which then become more and more functional.

I think having an additional limb isn't that rare in mammals. Having one which is usable to a degree that it increases fitness (i.e. chances of reproduction) is apparently much rarer. People who solder or cook for a living would love to have another arm... @anongoodnurse: Beauty is in the eye of the beholder; what some call a "defect in embryonic development" may be an enhancement to others. And don't tell me embryonic development is not dependent on the genes...

While I understand the answer, the final conclusion "Terrestrial vertebrates have four legs because they evolved from a fish ancestor that had four members that were not too far from actual legs", seems to imply that all vertebrates evolved from a common ancestor species. -- Isn't that highly unlikely? If the traits of vertebrates are "positive", wouldn't parallel evolution take place? Why did only 4 legged "proto vertebrates" evolve to have a spinal chord?

Vertebrates (Vertebrata) is a monophyletic taxon (see this post for intro to phylogenetics; see here on tolweb for the node vertebrata). In other words, all vertebrates share a common ancestor who already was a vertebrate and not descendant of this ancestor is not a vertebrate. It does not mean that there are not non-vertebrates that evolve some kind of a skeleton, such as insects with their exoskeleton.

I also think its worth pointing out those vertebrates who have evolved extra limbs. For mammals, this usually comes in the form of an additional prehensile limb, either the tail or the nose, but we have at least one example of a vertebrate evolving wings as well - had it and its ancestors not gone extinct, it's easy to imagine how Weigeltisauridae (notable Coelurosauravus) would have had an evolutionary path towards a six limbed animal like a dragon. They managed to evolve a couple dozen extra bones for their wings!

I think I might interpret your question as asking, not just why don't mammals have more than four limbs, but why arthropods have more variety.  Insects have six, but others have eight, ten, or more.
Partly there are just many more species of arthropods.  80% of animal species are some sort of arthropod, and some lineages of arthropods are distantly related to each other because arthropods as a group have existed since the Cambrian period.  With so many more species, it's no surprise that they've managed to tack on some extra variety.
Although it might seem that insects and spiders are more closely related than, say, humans and fish, the reverse is actually true.  In fact, insects split off from other arthropods at approximately the same time that fish were diversifying into the three main lineages that would eventually become cartilaginous fish (sharks & rays), ray-finned ("regular") fish, and lobe-finned fish (coelacanths and lungfish).  All of these things happened at approximately the same time, geologically speaking, at around 400 million years ago.  Some ancient lungfish crawled up onto land a short while after, giving rise to land animals.  So in light of this, it's not really surprising that arthropods would have so much diversity in body plan - you don't look much like a leafy sea dragon (I hope).
But perhaps another way of looking at it is in the difficulty involved in adapting the body plans of these different types of animals.  Arthropods have segmented bodies.  In some arthropods, especially the myriapoda (centipedes, millipedes and so on), there's a pretty straightforward arrangement of one segment to one pair of legs (excluding the head).  Vertebrates have a segmented body plan too, but our segments aren't quite so well-separated.  In vertebrates, a "segment" is approximately equal to one vertebra.  So since vertebrates aren't in the habit of attaching a pair of legs to each vertebra, it's harder to grow more legs.  Instead, vertebrates have internal skeletons, with the familiar hips and shoulders in land animals.  Vertebrates do have good luck adapting the internal structure when they need to.  Most use the traditional four-leg layout, but humans, birds, whales, and snakes have all made pretty significant changes to it.  But internally, it's still the familiar hips and shoulders - even snakes still have the necessary bones.  Given another few hundred million years, they might disappear entirely, but it seems like the basic bone structure is tough to change.  Who knows, in a hundred million years, the far future descendants of snakes might end up with legs again, and grow six or eight instead of four!
So, overall, I'd say that the two main reasons are that the arthropod body plan is just a little more flexible due to its higher degree of modularity, and that different kinds of arthropods are actually more distantly related than you might expect.

needs references

The answer by Remi.B is excellent, I'll just attempt an explanation by way of gene networks:
In genetics we see new genes "linking" to the older genome by regulation pathways and by being "fit" only in the context of the existing genome. This has the effect of making the older genes indispensable. Change them and you rupture the whole mesh. If you want to increase the number of limbs, you'd have to take that up with the HOX genes, that control the basic body plan. These are awfully ancient, originating in the common ancestor of flies and humans [1]. So as a rule of thumb, these genes will also be awfully hard to mutate without ruining everything.
Another line of reasoning is that the HOX genes not only appeared early in evolution, but they are also expressed early in the development of the embryo. When anything that goes on in development depends on what has preceded it, mutations in HOX genes has a bigger chance of ruining something than mutations that are only expressed late in development.
I'm going out on a ledge here, but consider that the color of hair, skin and eyes of a human baby are often not fully expressed until months after its birth and consider also the range of harmless variations in these colors.
These superficial colors don't affect anything else, so the corresponding genes are free to mutate into a great variety.
[1] http://www.nature.com/nrg/journal/v2/n1/box/nrg0101_033a_BX1.html

Here is a more morphologic, less genetic answer:
According to Sansom 2013, the 2 sets of paired appandages (shoulder and pelvic) was set in stone when agnathans transitioned into gnathostomes (ie. when the first vertebrate organisms began to evolve jaws, an anatomic change that allows for classification of different stages of history found in the fossil record). They found variations where an agnathan had a paired set of anal fins (sort of the 3rd set of paired appendage, since anal fins are typically unpaired).
Now, moving forward millions of years, the Sarcopterygii (lobe fin fish) evolved into the tetrapods (4 limbed land vertebrate including amphibians, reptiles, birds, and mammals), this pattern (2 sets of paired limbs) became immutable, though much less fundamental variation throughout the phylogenesis of the various tetrapods.
Sansom RS,Gabbott SE, Purnell MA. 2013 Unusual anal fin in a Devonian jawless vertebrate reveals complex origins of paired appendages. Biol Lett 9: 20130002.


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What is the mechanism responsible for the 'delay' in delayed rectifier potassium channels?
I've been trying to find a comprehensive explanation concerning the nature of the 'delay' in neurons' delayed rectifier potassium channels. As it's written in my intro to neuroscience textbook, these channels are voltage gated and become activated when the typical neuronal membrane reaches an electrical potential of approx. -40mV. While the channel is activated at this point, it only opens up after a delayed period of approx 1ms.
I'm mostly trying to clarify that this isn't an confusion in wording and that delayed rectifiers aren't actually activated when the inner membrane reaches a charge of approx +40mV which would be correlated (at least in textbook examples) with the '1ms delay', but caused by the actually typical charge observed at approx 1 ms of delay during an action potential.
Thanks so much. Let me know if I can clarify something. I know this wasn't necessarily so well asked

These channels are slow to respond. After depolarization they are activated, but only after a relatively long time. Their closing kinetics are also relatively slow. A definition is give here.


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About animal ecology and one view of this in science fiction
In the movie the Matrix Agent Smith said something like, 'all animals strive to find a natural 'equilibrium' with there environment ,... a harmonious existence with their ecosystem', ( forgive misquoting). Is this true that each animal 'does' a lot of activity whether by instinct or an ad-hoc form of 'simple' planning to 'cooperate' with it's environment ,or exist 'harmoniously with it?

There is a purely philosophical issue behind your question. What does trying mean? Does trying doing A means that an individual is aware of how to achieve A and will behave so to achieve it?
The likely correct answer (it really depends on you definition) is "No" (with some eventual exception among those that have high cognitive abilities such as humans). No, animals don't try to create a nice ecosystem. Animals (just like any living things) just evolve in response to their environment and this ends up creating ecosystems. The ecosystemic balance is just the result of the non-cooperative actions of the different species at play in the ecosystem. For example, animals reject nitrogen not in order to help plants to grow but only because nitrogen is a waste and is toxic for them. You may want to make you understand how evolution works.
For those who have a good enough knowledge in evolutionary biology, I have to admit that the above answer might be slightly wrong if we consider some special kinds of selection such as kin selection, species selection or even ecosystem selection. I think the answer to the question remains "no" given the "conscious" side of the definition of trying that the OP was probably using.
Update
Cooperation is easy to explain, real altruism is more complicated. Real altruism is when one individual makes an action that benefits to the others lifespan reproductive success but decreases the lifetime reproductive success of the one producing the action.
Within population real altruism can be explained by kin selection. see this post for more info.
Between species real altruism is much more complicated to explain. It would need to use concepts such as species selection. But does between species real altruism even exist (beside some behaviour from species with high cognitive abilities)? I don't think so.
What you are interested in is inter/species cooperation. Very often the individual that offers something to the other also directly gain something. For example, the animal excrete nitrogen because it is toxic and the plant take advantage of this. But sometimes an individual (actor) pay a cost for producing something to the benefit of the other individual (recipient). In return, the actor will receive something back from the recipient. For example, in the lichen, the algae offers energy while the fungi offers shelter. If one stops the other will die and both will lose. There are known cases also where individual A stops offering goods t individual B if individual B stops offering goods to individual A. This kind of traits are best studies with the tools of game theory.

I agree that the question is formulated very badly, has a strong philosophical bent, and could be interpreted in different ways. But there is a surprisingly simple answer: all interpretations I can think of are false. Animals do not strive towards maintaining environmental balance, neither consciously or unconsciously. The existing balance is a byproduct of the sum of their independent non-cooperative actions.

I didn't dare being so radical because it keeps kin selection, ecosystem selection and species selection aside. But I updated my question now to clarify my point using your comment. Please let me know if you have other suggestions.

There is some cooperation in nature; like a 'social order' in a group of animals , or symbiosis. How can these things develope if all animals are exerting their independent non-cooperating actions?

see update in my answer.

The answer to the question as stated is, certainly: No. Neither on a conscious level, nor at the level of instinct does an animal have the goal of keeping the ecological balance of its environment intact. Quite the opposite: it is constantly trying to overturn that balance, attempting to change the system and bring it to a new situation, one in which it (the animal) and its children have a higher survival and procreation chance than the current one. Whether the new situation will be stable (= a balance) or not is not a criterion, and cannot be predicted by any animal acting on the environment (including the humans).
To use an example: As the news outlets have been warning us in recent years, if all bees were to die, our whole ecosystem could collapse. Yet no bee is pollinating flowers because it somehow feels that this will prevent the collapse of the current ecosystem. It gathers pollen because its swarm is hungry.
There is also nothing "natural" about the equilibrium our ecosystem is in, at least not in the sense implying that "this is how it should be, and everything else is so bad that it goes against the very laws of nature". It is just one random equilibrium of many possible states of our planet, some including an ecosystem in equilibrium, others including self-destruction of the ecosystem. All of these states are equally natural, and the planet has passed through several of them before establishing the current one (which isn't about to stay here forever either).

By the way I didn't say animals were 'doing' things to be in a state of better 'equilibrium' with their environment ,I just took this as a paraphrase from the movie the MATRIX. I , myself was wondering if the statement FROM THE MOVIE had any truth. I didn't say I believe it.

No
There are many, many examples of species in their native environment accidentally destroying their ecosystem when external factors constraining their ability to reproduce are removed. For example when wolves and other large predators were removed from most of the American west ungulates like deer and elk nearly stripped the environment bare, to the point that riparian lowlands were completely stripped of vegetation and native willow populations were severely effected.
Similarly, invasive species, when introduced, aren't intentionally trying to drive other species to extinction, it's just that their adaptations are so mismatched the invasive species succeeds disproportionately often allowing for a population boom. For example, sea lamprey weren't trying to wipe out lake whitefish and lake trout when they got into the Great Lakes, they were just too good at what they did.
Even in humans "living in balance with ones environment" is a rare idea, and generally only occurs in populations that have the resources to spare and don't have to worry about their own survival.


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Why do we suddenly forget things, like PIN or phone numbers, that we've known for years?
Is it common to forget a 4 or 5 numeric code which has been used extensively for months and well remembered?
There's an article on the guardian describing this phenomenon and by the number of comments it seems quite common yet no scientific aspect trying to solve the mistery.
Is it some common phenomenon of the brain? Some erasing of irrelevant numeric things happening during sleep?

Forgetfulness is a common phenomenon that tends to increase with age. It usually affects short term memories but it can affect long term ones too. Here are some possible causes which I quote from Healthline (the full list available at that link):

sleep deprivation
use of alcohol or drugs and some prescription medications
lack of oxygen to the brain
migraine

It can happen at any age and it is normal if (quoting Deane Alban, Memory Loss: When It’s Normal and When It’s Serious):

Are you overworked and stressed out? Are you eating poorly? Are you on a low-fat diet or skipping meals to lose weight?  Do you struggle with insomnia? Do you drink too much?
If you answer “yes” to any of these questions, it’s likely you are losing your memory because your lifestyle is catching up with you.

You mention loss during sleep in your question. Sleep affects memories (see WebMD and Wikipedia):

deprivation of sleep leads to memory loss
during sleep brain selects relevant information gathered during the day and turns it into memories
certain stages of sleep improve memories


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Does a bigger breast give creamier milk?
It is fairly common for a woman to have one breast larger than the other.  I have also heard that, for a breastfeeding mother it is common for one of the breasts to yield a creamier milk whilst the other is more watery and has less nutritional value.
Is there any correlation between the larger of the two breasts and the one which yields the fattier milk?

Can you please supply a link to support your claim of breast milk production differentiation?

The only reason I know of that gives a nursing mother a breast size discrepancy is that the infant favors one breast over the other. Naturally, production will be different between the two, but probably only related to volume, while fat/protein/water proportions would be very close to the same. I've read in a number of places that the milk that comes out first is high calorie, low nutrition, while the milk that follows is low calorie, high nutrition, but that is off the same breast and a different thing.

Because mammary glands define us (mammals), the genetics of the ability to make milk has been of interest.[1] Because we consume milk, we have a dairy industry. Because the industry places a monetary value to certain milk constituents, the genetics of milk component production has been a viable area of study[2]. Since you are talking of cream production, we'll stick to that.
The effect of nutrition and the environment (e.g. temperature) on milk fat production has long been known, and the ability to selectively breed for higher fat content has been exercised for decades if not longer[3][4], But the molecular genetics of milk fat production is only recently starting to be understood.
Mammals with the highest fat content are those in cold environments where an insulating layer of fat is required, such as gray seal milk (53.2% fat), whale milk (34.8%), and polar bear (31%). Humans and cows have approximately the same milk fat percentage (~4.5% fat).[5]  The gene most studied to date is the DTAG1 allele[6] on chromosome 14.[7]
It is very clear that genetically milkfat production is under the governance of part of chromosome 14.[7][8] Since this chromosome is identical in both breasts, genetically one breast cannot make milk with a higher fat content than the other. Environmental and nutritional factors affect both breasts equally, so those can be ruled out as a source of fat percentage differences. The only factors left that can be variables are 1) fat content of one breast over the other, and 2) demand from one breast over the other.
In cows, more frequent milking increased milk production but decreased fat percentage; in the end, the effect on fat in milk was the least influenced by frequency of milking (significance questionable).[9]
Triglycerides in milk are synthesized in the smooth endoplasmic reticulum of the mammary alveolar cell from precursor fatty acids and glycerol (obtained from blood nutrients), and while other cell types are involved in milk let down, etc., there is no known function of interstitial adipocytes (fat cells).[10]
That was the long answer. The short answer is: no[11].
[1] The origin and evolution of lactation
[2] Milk Components: Understanding the Causes and Importance of Milk Fat and Protein Variation in Your Dairy Herd
[3] A review of nutritional and physiological factors affecting goat milk lipid synthesis and lipolysis
[4] Factors affecting milk composition
[5] The Highest Percentage of Fat in the Milk of an Animal
[6] Evidence for multiple alleles at the DGAT1 locus better explains a quantitative trait locus with major effect on milk fat content in cattle.
[7] Identification of novel single nucleotide polymorphisms in the DGAT1 gene of buffaloes by PCR-SSCP
[8] Scientists pinpoint gene linked to fat in cow’s milk
[9] Covariance among milking frequency, milk yield, and milk
composition from automatically milked cows
[10] MILK SECRETION: AN OVERVIEW
[11] Does a bigger breast give creamier milk?

Please add a reference link to support your short answer. :D

You should move your tl;dr to the top.

There's some link recursion here. I better not click source 11 or I'll get stuck in a loop.

"Since this chromosome is identical in both breasts, genetically one breast cannot make milk with a higher fat content than the other. Environmental and nutritional factors affect both breasts equally, so those can be ruled out as a source of fat percentage differences.".. I don't think so. Environment, which also includes artificial environments such as clothing can affect "symmetric" parts asymmetrically. There is an inherent asymmetry as well. All these can result in different tissue efficiency- just like vision or hearing or muscle strength in limbs etc

However, I cannot comment on correlation of breast size and milk composition.

+1, but I partially agree with @WYSIWYG: fluctuating asymmetry should have its own component in the differences in fat content (although, seemingly less important than that of the main factor).

@WYSIWYG - I don't think that even extreme differences, such as keeping one breast bared to the winds, would affect milk composition. Lots of other things, God help the poor woman, but I disagree with you. I didn't say different breast sizes don't result in different amounts of milk; the amount of milk would vary based on the number of alveolar units in each breast, which, judging from the size discrepancies in women's breasts (as opposed to their eyes or their ears) varies considerably. Quantity, yes. Composition, no. All those alveolar cells are under the same governance.

@anongoodnurse I didn't mean such subtle effects.. I meant things like exposure to heat, mechanical stress etc. What I meant is that it is possible that environment can have assymetric effects. Or some other factor that causes assymetric development. These can affect the composition of the milk.

@WYSIWYG - I might be more convinced if I hadn't read so much about what governs fat composition in milk. To get more fat, you need to feed optimally and breed optimally. None of the papers discuss "bag size" as a factor. The increased bloodflow to, and increased adiposity/insulation around, alveolar units would mitigate most any natural effect, I would think. If you don't think keeping one breast exposed to the wind is too subtle, please tell me exactly what effects you're referring to. I'm open to considering them.

@WYSIWYG - Finally, I had milk goats for many years, which I hand milked twice a day while they were lactating. Bag size varies considerably. I could not see a difference between the milk from each udder.

@anongoodnurse true then, perhaps.. As I said I am not too sure about it.. and I didn't know really that wind exposure does have any effect

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


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How long does a signal from the brain take to reach the limbs?
If the brain sends a signal to move what's the time it takes the signal to travel via neurons to motor neurons in hands, arms and legs?
How fast do those signals travel?

Speed of transmission is going to vary depending on the neuron fiber subtype.
Specifically, the biggest gains will be seen with cross-sectional area (feel free to ask why on physics.stackexchange.com) and neurons with myelin sheathes (fat wrappings which affect saltatory conduction rates).
You're specifically asking about Efferent neuron transmission rates, but here's a general idea:

Keep in mind that the entire circuit (from pre-motor cortex to muscle spindles) will involve several different types. In-general, your central nervous system (brain, brain-stem, spinal chord) are A-alpha, and if I recall correctly - the somatic nervous system (the voluntarily-activated neurons throughout the rest of your body in the PNS [peripheral nervous system]) are A-delta. If I'm wrong, somebody please correct me.
On average non-voluntary reflexes (which is actually information going to the CNS, being processed, and then going out to the motor neurons) take about 0.3 seconds. However, the average human can blink in about 0.1 seconds, which is probably a better measure.

how well are these functions really dedicated to the specific fiber types?

@shigeta - They're some overlap (the Vagus is a good example), but the function maps to the fiber type fairly well since space is the primary limiting factor for the peripheral system. However, I'll admit I haven't refreshed myself of the topic for a while, so it's possible the ratios are less strict than I believe.

How much about that 0.3 is transmission of the signal to the limb? Is there a reason to believe that the difference between the normal reflex of 0.3 and the blink of 0.1 is do to time it takes to transmit the signal?

@Christian - Roughly half, I'd assume. A full reflex arc is from a sensory neuron to the spinal column and back out to the muscles. The difference is probably due to length and the added junctions.

It is generally not a one-way process. The lag also depends on which frequencies you look at (the brain and limbs kind of speak using several channels at the same time). Near 10 Hz the lag is few dozen milliseconds.
Look for articles about EMG and EEG (or MEG) coupling for more precise info.
Use the paper http://homes.mpimf-heidelberg.mpg.de/~mhelmsta/pdf/2002%2520MEG%2520muscle%2520Review.pdf as a starting point.
PS. There is no neurons in limbs

Can you add some references?


text:
5,6-dihydrouracil and 5,6-dihydroxyuracil - how they arise in DNA?
5,6-dihydrouracil can be formed from cytosine after exposure of DNA to ionizing radiation under anoxic conditions [Ref]. What are other ways by which 5,6-dihydrouracil is formed in DNA? What about 5,6-dihydroxyuracil?

Here is the pubmed link to the paper. I couldn't think of an appropriate way to edit the question to incorporate the link.

@WYSIWYG Correction: 5,6-dihydroxyuracil does in fact exist. http://www.chemindustry.com/chemicals/0930310.html

@MarchHo Thanks. I nominated the post for reopen.

Dihydrouracil oxidase can catalyse the reduction of uracil to dihydrouracil in the presence of hydrogen peroxide. The reduction of uracil to dihydrouracil can also be catalysed by dihydrouracil dehydrogenase using NADH.
According to this paper, 5,6-dihydroxycytosine can be formed by treating cytosine or DNA with osmium tetroxide, an extremely strong oxidising agent. Since they are both pyrimidines (and in fact cytosine often spontaneously hydrolyses to uracil), uracil will also be affected by the same oxidation. 5,6-dihydroxyuracil was also detected within the oxidised DNA sample as a result of oxidation and demethylation of thymine.

The presence of 5,6-dihydroxyuracil (peak 11 in
  Fig. 1) can be explained analogously to the formation
  of 5-hydroxy-5-methylbarbituric acid from thymine on
  permanganate oxidation (lida & Hayatsu, 1970, 1971)
  (Scheme 2). The actual oxidation products ofcytosine, i.e.
  structures (I) and (II), were not observed in DNA. As the
  calf thymus DNA used in this work did not contain uracil,
  the uracil derivatives discussed above could not have been
  formed from uracil in DNA.


text:
Which types of blood vessels can regenerate in humans/mammals?
Which types of blood vessels can regenerate in humans/mammals?
From what I understand, arteries and arterioles can be created later in life, while this is not necessarily the case with veins. However I don't understand why damaged blood vessels in an eye recover, while this is not the case for other body parts. Also, I don't understand how angiogenic agents work.
The types of blood vessels I've been thinking about include:

Arteries
Arterioles
Capillaries
Venules
Veins

Also, does the capability vary in different organs (e.g. blood vessels in a hand vs blood vessels in an eye)?

Is this by chance a homework question? If so, please read our homework policy. Essentially, we ask you to try and answer as much of the question yourself as you can, and put down your thinking on the parts you're not sure about.

@MattDMo - no, this is not a homework question. I did some research, and it seems that arteries and arterioles can be created later in life, while this is not necessarily the case with veins. However I don't understand why damaged blood vessels in an eye recover, while this is not the case for other body parts. I don't understand how angiogenic agents work. I mean I could spend a month researching the topic and reading every scientific article, but what is the point of this community?


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How can I find a complete human genome file?
I'm trying to figure out how I can download a file that represents the complete human DNA sequence. I don't care too much about the format – I'm able to write C++ code to parse it. FASTA seems like a simple format though. What I haven't figured out yet is where I can find a complete file – I have found what appear to be subsets of genes or other sequences or single chromosomes but aren't there 46 chromosomes to include or are some of those duplicates (i.e. 22 chromosomes + 2 sex chromosomes)?
On this page, I have found this list of files under "Human > Genome assembly: GRCh38" but it appears to be broken up by chromosome or something? If so, would I merge these? My goal is to display all the letters via projector onto a wall and I want to be able to point at it and tell someone, that's all the DNA for a human (not a subset). Also, to double check, it is a "genome assembly" I want right? By the way, I don't care about allele variants right now.
Please consider in your response that I am not familiar with much of the lingo, thank you.

Thanks for all the great answers! They were actually ALL helpful to me.

The National Centre for Biotechnology Information has a link to a genomes FTP site - on that page, there is a file labelled .../genomes/H_sapiens (this a direct link to that directory).
There are numerous files therein.  From the README file:

Sequence data include chromosomes, contigs, RNAs, and proteins
  generated through the NCBI Reference Sequence and NCBI Genome
  Annotation projects. Map data presented in the Map Viewer resource are
  also provided here.

Only about 770M?  I expected it to be bigger

Non-biologist here stepping in.
@swbarnes2 has a good point pinning the fact that (approx) 3Giga nucleotides to display "on a wall" (as you state) even with a good projector is gonna be a hard task.
You'll need several projectors and a hell of a big wall.
(say you take the smallest readable police setting you'll have each letter take a space of 4*6 pixels which for the whole will bring you to ~[227k x 342k] pixels so around 35k HD-projectors)
Which led me to think of why you would want to do such a thing.
The most plausible of which is : it is for some sort of artistic/cultural intent.
In such case, rather than showing letters (ATGC) I recommend to encode it in binary (00,01,10,11) and make this value code for a colored pixel.
That will leave you with a square matrix of around 57k pixels edge (which remains humongous) of shaded in 4 tones black to white dots.
If you want to go even farther, trichromia stands to the rescue, don't make pixels code for just one nucleotide each.
Make them code for one "pseudo-codon" (triplet) each.
First nucleotide defining the red shade,
Second nucleotide defining the green shade,
last nucleotide defining the blue shade.
(plain and simple Additive color RGB stuff).
-EDIT-
Knowing that the notion of codon is invalid and that any nucleotide (except the leading and trailing 2 of each chromosome) could be part of three distinct codon (depending on wether they are in an intron, exon or even alternatively spliced) we see that this grouping by 3 is not THAT right.
In such case why not take even more liberties ?
Group your nucletides by 12 (3 groups of 4) giving you more depths in the color shades.
-END OF EDITED SECTION-
you'll get a much nicer and significantly smaller matrix of [30k x 30k] (which is still gonna take you a big wall and a few HD-projectors ~150 but at this point you can compress the output with several methods and get merged pixels, yet 150 is far less than 35000).
I know I don't bring actual solutions to the asked question (but I really think @Omen did it pretty well) but I sensed that there maybe here some insight worth handing (at the risk of making a fool of myself)

id think a dynamic display might work, showing segments at a time...

I also considered advising to have a dynamic display (to save even more money on projectors ;p) but it seemed either self-evident or out of what I understand to be the required scope.
Yet it IS probably the smartest way of displaying it all.
It's like displaying a whole book, one should consider displaying it page by page not all of it in a bloated block.

A small niggle...we generally don't call three nucleotides together a codon unless they are actually in the coding region of a gene, and are in the frame that's actually being translated.  Most of the genome would not be in "codons".

As I stated in my message, I'm not a biologist, at most I am a bio-enthusiast.
But that is true indeed. If nucleotides are in an intron (that is not interpreted in alternative splicing) then yes it is not part of a codon.
I'll amend my post.
Yet for the purpose that I described, it can still be part of a non-semantic triplet. After all, if the assumption I stated is right, then grouping nucletides by any numbers, in any way (as long as they are consecutive) would not really matter as it won't be anymore relevant. The DNA in itself is not THAT relevant, it's the way it's gonna be transcripted.

Thank you, this is my favourite answer as it gets to the heart of how I want to use the data. I marked another one as the most direct answer for what I asked. I guess I had a few questions in one.

No problem, glad I could be of any (even vague) help.

but aren't there 46 chromosomes to include or are some of those
  duplicates

First of all, while each person has 2 copies of each chromosome, those copies are 99% identical.  So it would be a waste to repeat the whole thing twice.
Second, the technology is such that it's not easy to generate, say, the whole sequence of a chromosome that came from their mother.  You either get sanger traces which show the two sequences superimposed on each other, or very short reads that are not mixed, but you can't tell which parent generated which fragment.
So in general, a reference genome will just have one consensus letter at every position, even though that's not biologically realistic.  It doesn't much matter what the reference is, as long as everyone knows that it's just a reference.

My goal is to display all the letters via projector onto a wall and I
  want to be able to point at it and tell someone, that's all the DNA
  for a human (not a subset).

Can you really display 3 billion characters like that?

Can you really display 3 billion characters like that? No: assuming a character is ~0.03 sq. in. (about 12pt), it would take 14.35 acres of wall to display 3 billion characters.

For us "metric" readers who wonder, 14.35 acres ~= 58072m² which in turn is a bit more than 5 "large" (internationnal cups) soccer fields.

If I understand your question correctly, you want a single file, i.e. a single string, which represents the sequence of an entire human genome.  However, there is no such thing.  The human genome is stored in 46 different strings (chromosome), and these strings have no natural order.
The numbers used to refer to the genomes are based on their order when arranged by size.
All operations on the genome (such as copying it before mitosis) happen in parallel, with proteins operating on each chromosome individually.
If you want to represent an entire human genome "honestly", I would say your best bet is to put 46 separate strings on the projector, perhaps running parallel to one another like the code in the Matrix.
If you want to display one big long string, any sequence of concatenation is as (in)correct as any other, so just open the files in alphabetical order and concatenate them all.

If you want to merge all the sequences as a single sequence then download the sequence of all the chromosomes and then concatenate them. Simple command for that if you use linux:
grep -v ">" chromosome*.fa > entire_genome.txt
Now it makes sense to separate the genome chromosome-wise because there is no physical connection between one chromosome and the other. Moreover there are many orders by which you can concatenate the chromosomes together which will give you 23! number of genome sequences.
Now you should note that all of this can give you serious errors if you are trying to do study genomic context of any gene. So better go chromosome wise.
If I have interpreted you wrong and what you meant is to have all the chromosome fasta sequences in a single file, yet not merge the sequences then it is a pretty straightforward command.
cat chromosome*.fa > genome.fa
Now, what you download is a reference sequence. You have to find variants etc for your data by controlling your alignment parameters.
And I really don't understand why you want to project it on the wall. There are easier and better ways of analyzing the genome.


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Evolutionary reasoning behind redundancy of CST and RuST
According to my neuro-anatomy class, both the Corsticospinal Tract (CST) and the Rubrospinal Tract (RuST) control upper limb movement. What the evolutionary reasoning behind this redundancy and the fact that the RuST is much more important in non-human primates when compared to humans?

@Susan thanks for the suggestion, I've edited my question


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Can I use grayscale images when working with ImageJ?
I am using ImageJ to analyze Western Blots. I have scanned films in as grayscale images because this is how we did it in my old lab. People in my current lab are not satisfied with that explanation and think I should consider using color images. I've been searching for protocols but they all seem to address how to use the program once you have some films scanned.
Can anyone help me figure out what considerations go into choosing how I scan my films?

You are using film, so the resulting image is black-white anyway, right? ImageJ can of course also deal with grayscale images.

I've never used films in imageJ, but I have done fluorescent microscopy images, which come as black and white images, 1 image per channel. Then I have to go and set each image to a particular color channel, red, green, blue, etc, to create the final colored image. I don't know how to get colored images of western blots since most gel imaging cameras I've used have a black and white camera with multiple filters, creating a situation similar to the fluorescent microscopy images I've worked with. Of course I have no clue how film and scanners would work with this.

There is no evidence that one is better than the other, most likely because it differs from case to case. Neither you, nor your critics, are right. There is a tiny bit of science in a paper on digitizing blots, generalizing from blots of a specific protein (PMID: 19517440), and they use grayscale for no given reason. Come to think, that is the best paper in the field of immunoblot quantification., and it still lacks evidence.
Immunoblot is semiquantitative, meaning it may sort and order bands (and protein amounts), but it fails often at estimating differences and ratios, and may even fail to see differences. Just try your best to find a difference, in the knowledge that if there is no difference in protein amounts, any fiddling with contrast won't create a difference in bands quantitation.
There is almost no difference between color and black-and-white digitized images of an immunoblot. The parts of the blot that are black will still appear in the computer as White = 0, even though a tri-color image file will detail it to Red = 0, Green = 0, Blue = 0. The parts that are nearly black will still be very close to zero.
The only thing that changes a lot between RGB and color is the background.  The background may change, for example, from White = 200, to Red = 190, Green = 190, Blue = 220. There is one consequence of such switching between values for background. (These changes may be induced by switching between grayscale and RGB, but also by altering exposure time etc.) When you use a method where the background gets too close to the blots, the "amplitude" of the blots, the height of the peaks in ImageJ, will be reduced. This loss of contrast should wash out some of the differences between blot bands and lessen support for differences between bands (i.e., for the alternative hypothesis), making you miss a genuine protein difference.
Again, if your blot bands are different enough so that your percent increase / decrease is huge, and your p value is small, you are all set, regardless of the method you chose. Ask your critics to explain your observed differences other than by differences in protein. But if your quantification fails the p test, I think it will be a honest effort, to change the color from grayscale to RGB, or the other way around, just in case your first choice had been the one that dampens contrast.