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Are wild cats the same species as house cats?
I thought that the definition of species is "can interbreed"
From Wikipedia:

The wildcat (Felis silvestris) is a small cat found throughout most of
  Africa, Europe, and southwest and central Asia into India, China, and
  Mongolia. Because of its wide range, it is classed by the IUCN as
  Least Concern. However, crossbreeding with housecats is extensive and
  has occurred throughout almost the entirety of the species' range.[2]

So why does it have a different name than the house cat?
From Species at Wikipedia:

A species is often defined as a group of organisms capable of interbreeding and producing fertile offspring. While in many cases this definition is adequate, the difficulty of defining species is known as the species problem.

While I understand that sometimes problems arise, what makes biologist mark the wild cat as a distinct species from the house cat? If they are genetically different, how different?
Donkeys can breed with horses. The result is sterile. Tigers can breed with lions with lots of complication. Wildcat seems to interbreed with housecat without problem whatsoever. Or does it? That's actually the essence of the question.

There are many definitions of species - look at the wikipedia page for an overview (this is a large and tricky subject). Some hybridization is not uncommon between "proper" species (often in narrow contact zones), also with fully or partially fertile hybrids. Definitions of species in these cases often comes down to genetic similarity/dissimilarity of populations. Even though hybridization is taking place it usually does so at very low rates, so the gene pools stay relatively distinct. The biological species concept (which is what you are referring to) is also problematic when it comes to e.g. ring species.
As for wild cats and domestic cats, my feeling is that modern evidence (e.g. molecular studies and phylogenies) places domesticated cats firmly as a subspecies of wild cats (Driscoll et al. 2007, 2009), with the domesticated cat as Felis silvestris catus. In the study by Driscoll et al. (2009), domesticated cats fall in the same mtDNA clade as F. silvestris lybica. However, domesticated cats were traditionally described as a separate species (by Linnaeus), and this has stuck and some still label them as separate species (as does Mammal Species of the World). I can imagine that some who argue for species status now might use a mixture of ecological, phenetic, and biological species definitions.
From Driscoll et al. (2009):

In contrast, the world's domestic cats carried genotypes that differentiated them from all local wildcats except those from the Near East. Domestic cats show no reduction in genetic diversity compared with the wild subspecies (37), thus giving no indication for a founding genetic bottleneck. Multiple genetic analyses produced concordant results, in each case tracing the maternal origins of cat domestication to at least 5 wildcat lines (A through E, Fig. 2B) originating in the Near East. The domestic cat is referred to as a sixth subspecies, F. silvestris catus, although it is clear that domestic cats derive very recently from F. silvestris lybica (37).

   ... the vast majority of sampled domestic cats fall into the same mtDNA clade, which also includes F. silvestris lybica...

There is also evidence that hybridization can help adaptation by facilitating gene transfer (even though hybrid fertility/viability might be low), so you might want to check out e.g. results from the Heliconius Genome Consortium (2012).

Am I (an Asian) within the same species of whites and blacks? I can interbreed with white or black females though I haven't really tried that. What makes the wild cat a different species?

@JimThio That is not a very useful analogy (for many reasons). For one, genetic differences between human populations are much smaller that within population variability, while wild and domesticated cats have relatively separate gene pools and hybridization is rare. However, hybridization can become a problem in small threatened wild cat populations (e.g. when they have a problem to find mates), which will dilute their gene pool.

@JimThio See the paper by Driscoll et al (2009) for molecular evidence for placing domesticated cats as a subspecies.

@JimThio you are attaching way too much importance to the ability to interbreed. Donkeys can breed with horses, as can zebras, tigers can breed with lions, and various other feline combinations are also possible. The ability to interbreed is not suffiecient to describe a species. In fact, defining what makes a species is still the subject of many PhD theses.

Donkeys can breed with horses. The result is sterile. Tigers can breed with lions with lots of complication. Wildcat seems to interbreed with housecat without problem whatsoever. That's actually the essence of the question.

The "species" concept is an attempt to fit a simple human conceptual category onto a reality that is not that simple.  The reality is a continuum of reproductive compatibility between an individual and any other organism rather than a binary compatible/incompatible relationship which would actually be a basis for defining "species".

@JimThio fileunderwater has given you an answer by the way. He cites a study that shows that they are not different species but one is a subspecies of the other.

@mgkrebbs Agree, and to look for the definition of species is a lost cause if you consider the multitude of modes of life. However, I dont think it is just a human construct - it is essential to understand evolution and biodiversity.

@fileunderwater, Yes, species is useful for thinking about how groups relate and evolve; when you want to look closely, though, it's good to remember the species boundaries are gray, not black-and-white.


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Image Processing Suite for bacterial microscopy: Schnitzcells or MicrobeTracker?
I am looking to start doing some work tracking the size and growth of individual bacterial cells in the microscope. In order to analyze the images I need software that can segment the cells, accurately determine their shape, and track cell lineages on a 'movie' of images collected from one experiment. Given the constraints of my microscope setup, the easiest thing for me to do is to use a strain of bacteria constitutively expressing GFP and segment the cells based on fluorescent intensity. This is functionally equivalent to segmented phase-contrast images of wild-type cells, i.e. I'm not that interested in changes in fluorescence or using fluorescence as a gene expression reporter, though my needs may head in that direction.
I don't want to reinvent the wheel (and I think that it's better if the community consolidates around a few programs that everyone uses so that experiments can be more comparable), so I'm looking for a previously published package that is robust and easy to use. Flexibility at measuring fluorescent tracking is nice, but at this stage is not crucial. The two packages that I have seen are Schnitzcells from the Elowitz lab at CalTech and Microbetracker from the Emonet and Jacobs-Wagner groups at Yale. Unfortunately they were released at the same time and don't provide a good comparison of the pros/cons of each tool.
Finally, my question is

What are your recommendations for an image analysis suite (from the two packages above or another package you have used)?

Let me know if I can make my criteria more clear or anything else. Thanks!

Although I haven't done live image tracking and analysis myself but I know the main method that people use is through Matlab, which means programming/coding so you would have to find someone to help you with some coding if you haven't worked with it before. Otherwise I suggest looking at fiji Image-J since it has a wide variety of open source plug-ins. I personally use image-J very very frequently and I'm very happy with it.

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Measuring algae growth or death
My daughter (10th grade) is doing a science fair project on the toxicity of triclosan for the algae Selenastrum capricornutum. She is wondering the best way to measure the effect, given the limited resources at the school.

Should she use the school’s UV/Vis spectrophotometer or just do low-tech cell counting?
If she uses the UV/Vis, does she have to do a calibration curve where she manually counts the cells for some number of data points?
Or can she just compare %absorbance to the controls and before/after numbers?
Or is it already know for this particular algae at a particular wavelength that a certain %absorbance equals a certain number of cells?
If she uses the UV/Vis, does that indicate the total number of cells, dead or alive, or does it only measure live cells?

The trial is over 96 hours.    Thanks!

I've asked some of my colleagues who work on algae to chip in... hopefully one of them will turn up :)

I don't think it's wise to use a spectrophotometer for this experiment, as it is a total count, i.e. it can't distinguish between dead and alive cells very well, and so she might not see a clear difference between her treated and untreated algae. If she has access to a haemocytometer and a good microscope, then she can count the living cells directly, and calculate the cells/ml using a simple formula.
This paper has a nice overview of how to count algae using a haemocytometer, and if her species of algae can swim, then she would need to use the iodine solution mentioned in here:
http://weis.science.oregonstate.edu/files/weis/Protocols/Symbiodinium/Cell%20Counts.pdf
I hope this helps!

I agree with your answer, but it got me thinking. You could use a spectrophotometer if you took identical samples of algae, treated with different concentrations of agent, then inoculated an aliquot of each into a fresh culture (with a fairly large dilution). By reading the OD of these secondary cultures at some later time you could relate the final OD to how many living cells were inoculated. This could easily be standardised by setting up a calibration with different amounts inoculated from an untreated control.

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Transposons and the net amount of DNA
The retrotransposons and certain DNA-transposons, are "jumping" sequences which may be incorporated elsewhere in the genomic DNA of an organism, through varying mechanisms. This insertion is almost random in case of retrotransposons and most DNA-transposons, but some transposing enzymes show specificity in selection of insertion sites. In either case, the "copy-paste" mechanism of transposition is essentially a random process(considering the frequency and place of transposition) and therefore, the extent of transposition should vary among all individuals, and all cells of a single individual. My question is,

Is the extent of transposition random and varied among the different
  somatic cells of an individual or is there a regulatory mechanism which ensures that
  there is not much difference in the net content of DNA (caused by unequal transposition) by equalizing
  the extent of transposition in different individuals or different
  cells of the same individual? If not, does this unequal c-value in different cell cause any troubles?

I'll have to find a reference before I can post an answer but I am pretty sure these will be independent processes in each cell. I would be fascinated to learn the opposite but I very much doubt it.

@terdon If it isn't equalized, will not the net DNA content(amount i.e. C-value) vary among different cells, and different individuals of the species?

for germ cells, I know that transposition is very tightly controlled.. most of the times transposons are heterochromatinized which reduces the rate of transposition. Will look up if there is any limit for the increased DNA content (or maximum observed expansion)

Transposition may occur at any given time in life, and in any cell. There are several cases known where transposition interests somatic cells (give a look here for reference). However, the frequency of transposition events is low, and the difference in amount of DNA between different cells in an individual is low. When you reason at the level of different individuals, however, the proportion of genome affected by transposable elements may be relatively high (give a look here for a reference)


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Do ants within a colony ever fight or come to conflict?
I'm investigating how hierarchical groups of a larger organization with a common goal tend to come to conflict with one another over time.  As you decompose a large group (for example a corporation), peer groups may compete in an effort to accomplish short-term goals in an effort to further the corporation as a whole.  For example, two groups of software developers might fight for time on the corporations computer system to finish their immediate deadlines.  Though this typically can be resolved through mediation and compromise, there is a human element where one group might inflate the real need to use such a resource.
I was then wondering if the same situation could ever arise in an ant colony.  Are ants truly purely social and never come to conflict within a colony?  Or can they end up fighting internally if food or space is ever scarce?

There has been several major transitions (John Maynard Smith and Eors Szathmary) and systematically there is opportunity for conflict to arise…. and it does! There is conflict along genes within a chromosome (example the Psr gene of Nasonia vitripennis, see R. Trivers and A. Burt Genes in conflict), along chromosome within an individual and along individual within a colony.
Ants has been much studies (see E.O. Wilson, L. Keller, M. Chapuisat) and it has been found that there are tons of different reproduction system in those species. There are conflict between queens, between workers and between queen and workers to reproduce. In some species, a colony have several queens, in others, there are several queens fighting early in life for the right of being the unique queen. In some species, workers can fight to take over the queen and take her function. In some species, workers reproduce sometimes even if there is a queen. There is conflict over who will survive depending on how much related one is to the other one. For example, there is conflict over sex-ratio, the queen is as much related to her sons than to her daughters but the workers are more related to their sisters than to their brothers (because of haplo-diploidy, see Robert Trivers).
There are various factors limiting the conflicts: high relatedness (Hamilton, Trivers), Cost of a fight, absence of information, power asymmetries. Ants evolved various strategy. There is a "police" who kill worker's spawn. We might as well consider lineage selection that select for cooperative colonies (note that L. Lehmann and L. Keller argue that group selection and kin selection are the same concept!)
I basically repeated some stuff I read (or learned in class) but I am personally not sure that all that makes sense! I don't know if really the frequency of conflicts is not simply related to the mutation-selection balance. Criticisms are welcome!
UPDATE:
In reaction to your comment:
Conflicts always have to do with reproduction or survival in evolutionary biology. One might make three categories of conflict:
1)Those involving the right of reproducing
2)those involving the probability of dying (I prefer not to be a forager because forager have a very high mortality)
3) Those that concern the survival of kin individuals. The "purpose" (if I might use this agency way of speaking) of any one to to increase its inclusive fitness (Hamilton, but don't read Hamilton, there is lots of easy source of information on kin selection). Therefore, one will rather help its brother to survive rather than his cousin as it is more closely related to its brother. Similarly, beccause of the haplo-diploidy nature of sex determination system in hymenoptera, workers are more closely related to other workers than to the males while the queen is as much closely related to her daughters and sons. Therefore, we would expect a conflict over the sex ratio, queen trying to have a sex-ratio of 1:1 while the workers are trying to have a sex-ratio of 75:25 (if there is only one father).
Hope this helps!
If you want more specific information about sex-ratio in ants, kin selection, group selection please ask it in another post. Note that there is already some discussions one these subjects on Biology.SE.

So is it safe to say that any conflicts that would arise are centered around the confusion of a queen or general reproductive differences?  I'm a little confused by the answer but you did give a lot of references and subjects to explore so this is good stuff and a much better start than I already had with naive google searches.  :)

@ngramsky See my updated answer


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Difference between CDS and cDNA
What is the difference between Coding Sequences (CDS) and cDNA?
Are Coding sequences the sequences that is transcribed to mRNA and cDNA in contrast DNA obtained by reverse polymerization of matured mRNA?

The difference boils down to UnTranslated Regions. A CDS or coding sequence is the part of a transcript that is actually translated into protein. Therefore a CDS will (almost) always start with an AUG codon and stop at one of the three STOP codons (UAA,UGA,UAG).
The transcript however (note that I am referring to mature transcripts that have already been spliced so introns have been removed) will also contain the UTRs which are not actually translated into protein. A cDNA sequence is derived from the transcript by reverse transcription and will, therefore, also contain the 5' and 3' UTRs. For example, see this schematic diagram of an unspliced transcript:

The CDS of the gene depicted in image above will only contain the ATG, the STOP and the two green regions (exons). The cDNA will contain all that and, in addition, the two UTRs. Of course, both the cDNA and the CDS will not contain the introns.

Actually, exons include 5' UTR, CDS and 3'UTR. And CDS should not include STOP codon as it's not translated into an amino acid.  Your diagram isn't very accurate with where you draw Exon 1 and Exon 2.

@olala that's just a simple diagram to illustrate the existence of UTRs. Yes, of course they are exonic but that is not really relevant here. As for the CDS, no it also includes the stop codon. First because the stops are recognized by specific tRNAs, just like any other codon, and because that's the convention in the field. See, for example, the CDS described here: http://p53.iarc.fr/p53Sequence.aspx

i have to disagree on CDS and stop codon. If you look at at GTF format annotations, they listed stop codon separately from CDS, see an example from this post at the bottom of the page: http://mblab.wustl.edu/GTF22.html, also see this post Istvan's answer https://www.biostars.org/p/65162/

The definition of coding sequence is, to my mind, a little confusing. It is actually the sequence of DNA in the gene which has the same sequence as the corresponding mRNA (except it has T instead of U). Now, you will often see definitions that say that the coding sequence is the DNA that is transcribed, but this isn't really correct because during transcription the RNA polymerase actually copies (transcribes) the other strand of the DNA (i.e. the one that is complementary to the coding sequence). And I would go one step further and say that the coding sequence excludes introns. You could also refer to the coding strand of the DNA, to encompass the entire transcriptional unit including introns as a way of referring to the strand which carries the coding sequence.
You are correct in your definition of cDNA (except its reverse transcription not reverse polymerisation). The the full-length cDNA sequence for a protein-coding gene will encompass the CDS but, as @terdon points out in his comment, will also include untranslated regions at the 5' and 3' ends.

so the difference in sequence to a given gene among its CDS and cDNA would be?

The CDS sequence is not identical to the cDNA sequence. That will only be the case for genes with no UTR regions.

Yes, @terdon is correct - I'm so protein-oriented I overlooked this. So the cDNA sequence will encompass the CDS. Will add a correction to the answer.


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Which is the best way to fix and preserve comet assay slides before staining with Ethidium Bromide?
I want to use the method of Single Cell Gel Electrophoresis (comet assay). I have many samples, but I don't have the appropriate microscope. So I have to preserve my slides until the time comes for staining and microscopic analysis. I've read many different protocols, and I can't decide which is the best. Also, after the staining and the analysis, I might need to reuse the same slide. Is that possible? and if yes, what should I do?

Can you give more information about what protocols you have looked into?

Most of them use either 100% or gradually increasing percentage of ethanol or methanol. Some suggest to hydrate before the staining and some of them don't. Also some use mounting media at the end and others just a coverslip. I suppose that most of these work but it would be very helpful if I had a specific protocol that I know that will work.

This could be of use: http://onlinelibrary.wiley.com/doi/10.1002/cyto.a.20071/full


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At which step should I apply a detection filter when preprocessing microarray data? (Before/After normalization, batch effects removal)
What is the best practice when preprocessing microarray data using a detection filter (on scanner p-value)?
Suppose I have a microarray dataset that I have to normalize with Loess and correct with ComBat. When should I apply a detection filter, relative to the other steps in the process?
In my experimental design, I have two pipelines to test:

Normalize per sample between 0 - 1
ComBat
Loess normalization between samples

and

Loess normalization between samples
ComBat

Is there any best practice for the timing of applying a detection filter?

Why not try applying before and after for all pipes and see which gives you more believable answers?

@virtualxtc how do you decide if an answer is more "believable"? You will get a result eventually.

My guess is that both methods will work equally well, just plot the data and validate by eye. The first rule of biostats (according to Ethan Meyers) is just plot everything & don't add extra thought to it unless l something is broken. That said, I use interquartile normalization (due to the fixed lower bound at 0) then hit call.

did you find an answer to your question? If you did, it would be great if you could post it here for people having similar questions in future

you might also want to ask the bioinformatics.stackexchange.com

My comment above still stands; provided your detection filter doesn't rely on your data being normalized, your detection filter can exist anywhere.
However, since it seems you know that you want to run a PCA, and know all the normalization's you'd like to try already, it is simplest to run all of your normalization first, rather than having to filter out high scoring vectors that appear to be caused by inter-sample variation.

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Index of ecological niche overlap
What is the Pianka's Index?

How does it work?
How can one calculate this index?
How often is it used?
In what context do people usually use it?
Can one infer any statistical significance with this index?

Do you plan to apply it to a particular dataset or problem, or are you asking out of general curiosity? Have you looked at Pianka's paper?

No I haven't had a look to Pianka's paper! I might not have looked thoroughly but I haven't found a paper that only presents such equation. I found some equations without really knowing what was called the Pianka's Index. I might aime to apply it on a dataset but for the moment my question is not specific. I just want to know how it works and why do poeple usually use this index.

Pianka's index of niche overlap is defined in his papers from 1973 and 1974, as:
$O_{kl}=\dfrac{\sum_i^n{p_{il} p_{ik}}}{\sqrt{\sum_i^n{p_{il}^2} \sum_i^n{p_{ik}^2}}}$
where $O_{kl}$ is the resource overlap between species $k$ and $l$, and since the index is symmetric $O_{kj} = O_{lk}$. $p_{ib}$ represents the proportion of resource $i$ that is used by species $b$. The index is a modification of one presented in MacArthur & Levins (1967).
As apparent from the formula, the only thing you need to calculate the index are estimates of resource use from the resources that both species depend on. The tricky part can be to determine how you calculate proportianal use of all resources.
I haven't used the index myself, and cannot really say anything about how common it is. I have seen references to it though. Pianka (1973) use it to study overlap between lizard species, and how the distribution of niche overlaps differ between habitat types. I haven't seen any statistical tests on it, but you should be able to use resampling or bootstrap to determine the uncertainty in the index.

Thank you! Shouldn't $j$ be $l$ in your formula? Or where is $l$ in the right-hand-side and what does $j$ mean?

@Remi.b Yes it should be. Fixed now.

Just to make I understood it correctly. $p_{ij} + p_{ik}$ does not necessarily equal to 1 even if there are no other species (than $j$ and $k$) using the resource $i$ because one should take into account that not all resources are used at 100%. Is it correct? Thank you for your help!

And the index vary between 0 and n/4?

If yes, do you think it would make sense to divide the index by n in order to have comparable indices?


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Definitions and examples of some math-releated ecology branches
I would like to have an example of application and a brief description/definition (two or three lines) of the following fields. I would like to understand the exact differences between them. Other related informations are also extremely appreciated e.g. if these are fields in growth, the name of the best researcher in that field, best institution etc.

Computational Ecology;
Mathematical Ecology;
Numerical Ecology;
Statistical Ecology;
Ecoinformatics.

I will think more about the Q, but generally these are fairly vague descriptions and I think that different researchers use them in different ways. Also common that researchers working on the same topic/field use different labels on their activities.

Although work in those areas is definitely all related, there are some kind of general differences in how those labels tend to be used, and I'll take a stab at defining them:
Mathematical ecology - this is typically the creation of theoretical models composed purely from math (i.e. not stochastic computer models). Examples include a lot of classics from ecological theory, such as Lotka-Volterra models of predation and competition, but there are also people who still do this kind of research, such as Peter Chesson in his research on the storage effect.
Numerical ecology - this is not a term that I've heard used very frequently, but I think it tends to cluster pretty closely with mathematical ecology, perhaps with more of an emphasis on also including and analyzing empirical data. I hear it used more to refer to techniques than actual ongoing areas of research.
Statistical ecology - I think this term gets used more loosely because obviously statistics are important to most ecology research. It can either refer to research that makes heavy use of advanced statistics because the questions that its getting at are hard to untangle from other effects, or research that uses a statistical model to make its point (note that statistical models are generally different from the mathematical models mentioned above in that their goal is generally to determine how likely something is to happen rather than to untangle some fundamental principle of ecology). A lot of studies on neutral vs. niche-based community assembly would probably fall into the category of statistical ecology. Here is one of many examples.
Ecoinformatics - maybe this is just because I study ecoinformatics, but I tend to think that this is the most distinct of the fields that you mentioned, although it certainly still has a great deal of overlap with the others, especially since it's a pretty diverse subfield. In general, ecoinformatics focuses on making use of large datasets in ecology. This involves both research on developing methods for doing this (for example, I study ways to efficiently collect information from ecological wireless sensor networks. Another good example is the development of GIS tools) and research that uses these methods (e.g. a study that uses GIS to synthesize sensor data and observations of a given organism to determine what that organism's range will be as climate change progresses, or that otherwise seeks to pull ecological concepts out of the data).
Computational ecology - I left this until last, because I think it's the vaguest of the labels you listed. It definitely includes ecoinformatics, but it probably also includes a lot of statistical ecology (and perhaps numerical and mathematical ecology too). I think that the main reason that it's a useful label is that it can catch areas of research that don't really fit in to the other labels. For instance, I once saw a study on quantifying niche space using support vector machines. It was really interesting, and maybe it could be classified as ecoinformatics or statistical ecology, but it didn't really quite fit into either of those. So I guess I tend to see computational ecology as a catch-all term.
These are just the impressions that I have gotten - if others chime in too we can probably build a better consensus definition of these labels.

"Numerical Ecology" is the title of a classic text by Legendre and Legendre, with a recent variation applied to R; but it is not clear how the field is different

Well, this goes to show how differently they are perceived. I find Comp ecol, Stat ecol and Math ecol most common. Don't remember seing Numerical ecol, but can imagine that it can be used for e.g. simulation studies of theoretical models. For me Ecoinformatics is fairly vague (but overlapping with Comp ecol), but often dealing with Big data, next-gen sequencing and remote sensing.

I agree that those are the most common labels - just perhaps not the most descriptive. And I also agree about Ecoinformatics involve big data and remote sensing. My one disagreement would be on next-gen sequencing being part of ecoinformatics. I would definitely classify it as bioinformatics, or else systems biology if it's done in a more ecological context.


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mRNA with Pseudouridine and 5-methylcytidine?
I am making mRNA by in vitro transcription for transfection purposes. There is a lot of literature about how protein expression is increased and innate immune activation is decreased by substituting uridine for pseudouridine and cytidine for 5-methylcytidine. I decided to try this, but my yield was lower and the mRNA was shorter than when using natural nucleotides. The papers all say they made the mRNA by simply using the new nucleotides in their in vitro transcription kits, but they never mention any further changes to the protocol. Now I would assume that since pseudouridine and 5-methylcytidine are a little different from the normal substrates for RNA polymerase that they might not be incorporated as quickly and the resulting reaction rate would slow down. It might be possible that the Polyadenylate polymerase that adds the polyA tail doesn't recognize the modified mRNA as well. Both a slower reaction rate and less efficient tailing could make a lower yield of shorter mRNA.
Does anyone here have any experience with IVT using modified nucleotides and can suggest something to improve yields?

After a couple months I got this working. I ordered the psuedouridine and 5 methylcytidine from Trilink. I also switched from the mMessage mMachine kit the the Megascript kit. Megascript has all the nucleotides separated while mMessage mMachine has them pooled. You have to dissolve Trilink nucleotides so that the concentration is the same as the natural nucleotides in your IVT kit. Then you just use the non-natural nucleotides instead of UTP and CTP. Let the IVT reaction run 4 hours. Be careful about RNAse contamination.


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Workflow for batch analysis of ROI in histology samples
This is a pretty big task, and I have several work-arounds, but I am looking for an efficient way to go from PAS stained slides of lung tissue to defined ROI's over the whole slide (presumably via BLOB detection).  I am hoping to get every airway epithelium annotated as an ROI so I can get colorimetric/masking data from the ROI.
That's the simply stated goal, but there are several issues along the way.  The imager we are using produces files in the MRXS format.  Satyanarayanan group's work at OpenSlide has been great in the initial hurtles of exporting the files into very large tiled TIFF files (~2-5GB each, under JPEG compression, generating a few hundred a week).  This has it's own bugs, but the mailing list has been solid.
Given a very large series of very large tiled TIFF files, what is the best way to train a BLOB (or other) detection method to find an ROI?  Using small images, I've gotten acceptable mapping with WIKA, but every time I try on larger images I run into errors and corruptions (when I don't run into memory limits).  Is ImageJ the best choice for this?  If so which plugins would you recommend trying?  I've used what comes FIJI and I've been exploring over others.  LOCI will load ~80% of the image correctly then run into tiling problems.  Given that you can't choose the ROI strictly on color, but human's can quickly ID it, I think a computer will be able to.
I have two systems I'm trying this on:
64-bit Ubuntu, 32GB RAM, FX-9590 processor
64-bit Windows 7, 16GB RAM, 2x E5430 processor

The Win7 machine is the one required for the imager, and I'm trying to do the analysis on the more powerful Ubuntu box.  Deroulers et al produced an interesting work on the subject, however, my group hasn't been able to implement the system as of yet.
I would prefer an open solution, but a proven solution with propitiatory software would also be acceptable.
I thought the over-arching question would fit here, but if people think I should break it up and put smaller questions on SO, I will.  I'm just not sure we're tackling this the best way from slide to graph.

Two general comments: using JPEG compression is lossy, why not use lossless LZW or similar with TIFF? Have a look at Fiji (fiji.sc) the updated brother to ImageJ. It has macro and programming language inputs, a huge user base, is open source, and is designed for image manipulation tasks.

@leonardo As mentioned in the question, I have tried FIJI.  Unfortunately I don't have a method that works to go from MRXS to an LZW compressed TIFF. I can go from MRXS to an uncompressed TIFF (5-10GB), then from that to an LZW compressed file, but that is a huge time hole. If you look at the paper, it's a known problem in the ImageJ world, and I think one that has no coordinated effort to solve. I was wondering if anyone else here has tried to tackle this, and we may end up publishing a methods paper if we figure it out.


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Microarray gene expression matrix format
After scanning the microarray chip we get RAW data with different formats depending on the type of microarray used. However, these RAW data files can be normalized and processed to generate gene expression data matrix.
I've been trying to figure out what exactly is the result of the processed data and what is the format of that data. As I've seen so far, there's no specific format for processed data. Of course most of them agree that columns represent experiments and rows represent genes, but the additional information at the top, they're usually different but I'm not sure based on what. Can anyone suggest me with the most common used formats? Is there any additional information to that processed data file in case I wanted to apply classification on it?

Just to be clear, it sounds like you're asking how microarray data is typically displayed, as in a publication. This would be different from the actual content of the processed data. In the simplest case, processed microarray data consists of a numerical value for each point on the chip, i.e. each gene you are testing. For each point on the chip (i.e. for each gene), the data is the ratio of mRNA abundance from one experimental condition vs another. You can imagine a lot of ways this data might be presented, e.g. a heat map of relative abundance of mRNA for each gene.

@A.Kennard Do you mean it depends on the type of microarray used? Affymetrix has different Array design than illumnia for example

I think I might not be understanding your question. What do you mean by "the additional information at the top"? Could you provide an example of processed microarray data you are having trouble understanding?

The RAW signal values from each microarray are transformed and processed to give you normalized signal values for each microarray. The transformation and processing steps are standard but different for each manufacture. Each manufacture uses a different method/technology to obtain signal values. Thus, signal values are not directly comparable between different microarray technologies.
Experiments using different technologies might get similar RANK of results but the normalized signal values will be different. You can have a look at GEO for a list of datasets and commonly used technologies. I have no clue what you mean by applying classification (are you looking to cluster the results from different microarray technologies run on the same experiment? I'm pretty sure a comparison of microarray technologies has been done before/already)


text:
Why does hypertension occur in obstructive sleep apnea?
What is the physiological mechanism behind systemic hypertension resulting from obstructive sleep apnea?

From Obstructive sleep apnea syndrome and hypertension: mechanism of the linkage and 24-h blood pressure control:

OSAS directly induces negative intrathoracic pressure and decreases pulmonary stretch receptor stimulation, chemoreceptor stimulation, hypoxemia, hypercapnia and microarousal. These changes potentiate various risk factors, including the sympathetic nervous system, renin-angiotensin-aldosterone system and inflammation.

Summary:

Low oxygen levels at night increase oxidative stress to the body inducing inflammatory reactions and damage to the interior of blood vessels
Nitrogen monoxide production is decreased, decreasing flow-mediated dilation of blood vessels
Frequent night-time awakenings bring elevated sympathetic nervous system activity
During episodes of hypoxia, blood pressure and heart rate increase
"Increased sympathetic nervous activity may also cause coronary spasm and induce vasospastic angina pectoris."
"[P]eriodic negative intrathoracic pressure (−80 mm Hg, at most), together with a midnight surge of BP, exerts mechanical stress on the ventricular and atrial walls, resulting in the development of left ventricular hypertrophy and left atrial remodeling and, consequently, an elevated risk of heart failure and atrial fibrillation"


text:
Standardized Selection Ratio (SSR)
In this article the athors used the Standardized Selection Ratio (SSR) in order to infer what is the preferred host (anemone) of anemonefish.
Here is a quotation coming from their methods:
  The “preferred host” of anemonefish was assessed calculating the “Standardized
Selection Ratio (SSR)” (values between 0 and 1) (Manly et al. 1993). Manly’s standardized
selection ratio represents the probability that an individual will use a particular habitat
type, taking into account the different resource availability. For each anemonefish species (i) inhabiting an anemone species (j), SSR was calculated as:

$$SSR = \frac{wi}{\sum{}{wj}} $$
where $wi = \frac{oi}{pj}$
    `Oi` is the relative frequency of the anemonefish species i and `pj` the relative frequency
of the anemone species j. Higher values of SSR indicate a strong preference for the
selected resource. The Log- Likelihood statistic (χ2L) (Manly et al. 1993) was used to
check the significance of the observed distribution under a null hypothesis of a random
host choice.

Here is the book they cite (Manly et al. 1993).
Can you help me understanding basically what they did and how they calculated their SSR and p.values. If $wi = \frac{oi}{pj}$ what does wj equals to?

I can see why you might be confused! The authors chose bad notation, since the way they wrote it $w_i$ clearly depends not just on the choice of anenomefish species $i$ but also on the choice of anenome species $j$. And it is not clear how exactly they are performing their sum in the definition of SSR: sum over all possible anenome-anenomefish species pairs or only over all anenomefish species? The former makes sense but is extremely unclear, and the latter doesn't make sense because there's no way to interpret that as a probability that an anenomefish will choose a particular anenome because the sum of the SSR for all the different anenome species would not necessarily be 1, so the probability of an anenomefish species choosing some species of anenome would not be 1!
NOTE: The reference to Manly 1993 was incorrect (you cited a 1995 paper); they actually cite a book: Manly B, McDonald L, Thomas D (1993) Resource selection by animals. Statistical design and analysis for field studies. Chapman and Hall, London. This would probably be the best place to look to get an exact answer to your question. I think that would be the best place to look first.

Thank you! I fixed the problem with the Manly et al book.


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What is one Botulinum toxin medical unit?
How many Botulinum toxin molecules or grams are contained in one medical unit of Botox?

1 unit is approximately 10 pg
Source

One unit of MYOBLOC (botulinum toxin type b) corresponds to the calculated median lethal intraperitoneal dose (LD50) in mice. The method for performing the assay is specific to Solstice Neurosciences' manufacture of MYOBLOC (botulinum toxin type b) . Due to differences in specific details such as the vehicle, dilution scheme and laboratory protocols for various mouse LD50 assays, units of biological activity of MYOBLOC (botulinum toxin type b) cannot be compared to or converted into units of any other botulinum toxin or any toxin assessed with any other specific assay method. Therefore, differences in species sensitivities to different botulinum neurotoxin serotypes preclude extrapolation of animal dose-activity relationships to human dose estimates. The specific activity of MYOBLOC (botulinum toxin type b) ranges between 70 to 130 Units/ng.

UPDATE
10 pg of toxin (150 kDa) is 4 x 109 molecules

A Botox unit is essentially a measure of a defined amount of biological activity and corresponds to a fixed number of botulinum toxin molecules.
The biological potency of these preparations is expressed in mouse units. One mouse unit is defined as the intraperitoneally injected quantity of each pharmaceutical product required to kill 50 per cent (LD50) of an experimental group of female Swiss-Webster mice, each of 20 g body weight.
A 100 unit of Botox (Onabotulinum toxin A) contains approximately 5ng (nanograms) of toxin. And hence 1 unit of Onabotulinum toxin A contains approximately 0.05ng of active toxin.


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How to define "evolution"?
The standard answer found in intro course to evolutionary biology to the question:

what is evolution?

is:

It is a change in allele frequency over time!

I believe a complete definition should encompass the following concepts:

mutations
copy number variation (CNV)
codon usage
chromosome numbers
phenotypic change (whether heritable or not)
Complex phenotypic trait such as plasticity and developmental noise
maybe some other things...

My questions are:

Would it be worth it to talk about phenotype in a definition of evolution?
What are the alternative definitions that have been proposed?
What is your definition?

Note: I would rather talk about genetic evolution, but if you think it is worth making one definition for genetic and cultural (and some other stuff maybe) evolution, you're free to suggest it!

Asking the what our individual definitions are is too subjective. Also, are you looking for a definition? Or an explanation. You mention "worth"... worth to who?

@Sancho I think a definition is never objective. It is totally arbitrary to decide what is hidden behind the word "evolution". Therefore, I would have expected several suggestions of definition. I guess a good definition is a definition that fits quite well the everybody sense of what is the boarder of a concept. "Worth" to any individual person willing to answer this question.

@Sancho Explanation? Explanation of what? I don't think I'm expecting any explanation about the science of evolutionary biology. I guess my question is close to a question of philosophy but I expected better answer by posting here than on philosophy beta.

@Remi.b Are there "wrong" answers to this question, then?

@Remi.b What is wrong with "It is a change in allele frequency over time". What things does that not include as evolution that it should? What things does it include as evolution that it shouldn't?

@Sancho "It is a change in allele frequency over time" does not encompass some concepts that I listed in my question. No, there might have no True answers but rather useful answers. That makes my question rather a philosophical question but I guess evolutionary biologists are better than philosopher to define "evolution".

@Remi.b The quality of a definition is not whether or not it "encompasses concepts". That's why I thought you were looking for an explanation. The quality of a definition is how well it demarcates. What is an example of an occurence that is evolution, but the definition "change in allele frequency over time" says is not evolution?

let us continue this discussion in chat

I think you are confusing a definition of evolution with a complete description of evolution. the first should be a sentence the second should be  several books worth of information.

What is evolution?
In a non-biological sense, evolution means change:

"a process of [...] change"

Biological evolution (seeing as this is Biology stack exchange) then needs to be tweaked to give a biologically specific context. Many textbooks etc. give definitions of evolution and here are a few good ones from across the history of evolutionary biology:
Charles Darwin:

"Descent with modification".

Mark Ridley1:

"Evolution means change, change in the form and behaviour of organisms between generations. ... When members of a population breed and produce the next generation we can imagine a lineage of populations, made up of a series of populations through time. Each population is ancestral to the descendant population in the next generation: a lineage is an ancestor-descendent series of populations. Evolution is then change between generations within a population lineage."

Brian and Deborah Charlesworth2:

"Evolution means cumulative change over time in the characteristics of a population of living organisms. ... All evolutionary changes require initially rare genetic variants to spread among the members of a population, rising to high frequency..."

All of these have a common theme. Biological information is moving through time, descending with a degree of directionality (e.g. parent $\rightarrow$ offspring), and the information is modified with time.
Personally I would define evolution as:

Evolution is a change in gene frequencies, resulting from four mechanisms (mutation, migration, drift, and selection) which can all affect the transmission of heritable genetic information within populations. Evolution has the potential to cause phenotypic change (when genotype affects phenotype) and has the potential to cause both adaptation (microevolution) and divergence (macroevolution).

This definition captures that biological evolution occurs through changes in heritable genetic information, the prerequisites of evolution, the mechanisms of evolution, and what the consequences of those changes can be.
I think it is important to include mutation (and drift, selection, and migration) because these explicitly state how evolution occurs. I don't think it is necessary to include copy number variation, chromosome numbers, or codon usage as they are not central to the process of evolution (though they can be important).
Whilst only the first sentence of my definition is critical, I think it useful to include the latter part (or something of a similar effect) whenever possible as it helps to clarify evolution and it's relevance.

ISBN: 978-1-4051-0345-9
ISBN: 978-0-9815-1942-5

Nice +1. It is good to have this short review of definitions. I like your definition, I would just note that often when talking about divergence, people are talking about neutral molecular divergence and not phenotypic divergence. Thanks

The problem with defining it as only change from these four sources is when we find other sources of change, like recombination, engineering, or possibly extinction. The entire second sentence of your definition does not belong in a definition, it is accessory information. It is like a inserting a specific reference to kin selection in the definition it does not need ot be there. Worse it tires to define other terms as well, many will disagree that divergence=macroevolution.

@John recombination doesn't change gene frequencies, extinction will either occur through selection or drift, and one could argue that mutation also includes engineering (if you mean changing the genes). The second sentence is there to clarify that phenotypic change and evolution are not synonymous terns.

Also why do you not think that divergence is macroevolution?

Depends on the organisms, in unicellular organisms it can lead to speciation by creating a novel combination of existing genes. divergence does not have to result in speciation speciation while macro evolution is defined by occurring at or above the species level. More importantly not all macroevolution is a result of divergence. Wiping out part of a ring species for instance would create speciation while not creating any new genes or structures. They are closely related but not identical. but more importantly you should not be defining one term in the definition of another.

I'd argue that wiping out the middle of a ring species is not divergence or speciation either, the species remaining at the ends are already diverged from one another prior to removing the connection @John

they had already diverged but they were not separate species until the middle were wiped out,  It is most definitely a speciation event directly caused by the death, without it it is not speciation. But this debate itself shows another problem with the definition by adding unnecessary terms it makes the definition evern more open to interpretation and confusion. The accessory information should not be part of a definition,  A definition is for defining something not listing all the possible outcomes of it.

I really don't understand why you have such a big issue with the answer. I even addressed that the second part is not necessary in the original answer (see the last paragraph). The fact is that the answer defines evolution as it is understood within the field, genetic change by any of the four mechanisms - there are no other mechanisms. Removing the middle of a ring species may be a speciation event, but it's not evolution. @john

debatable, it is essentially an extreme form of genetic drift, but the argument itself is why all the extra stuff should not be part of a definition. The first seven words of your defintion all all that are needed for a definition, the rest of it really adds nothing to it as a  definition. There is no benefit in defining it as only those four mechanisms becasue there could be others, but those new mechanisms would still be evolution.

Well that's is your opinion. Personally I think the extra detail in the answer add to the definition to help make cleat what evolution is not. Perhaps we can just accept that we have different opinions on that. Something that you should note, however, is that it is well accepted in the research community that these are the four possible mechanisms of evolution, there's not much else that could occur - they kind of cover all the bases @John

Theoretical biology spans multiple disciplines and the unaccompanied term evolution is defined differently in each:
As such chemical evolution is different from time evolution in physics and many other systems in theoretical biology that "evolve". These do play a role in theoretical biology.
Also, what standard answer to evolution in the field of theoretical biology are you referring to?
I recall learning that an allele as a special[:species:] gene variant, is defined as such as being present in at least one percent of the population. That definition has broadened meanwhile. A definition that has broadened.
Point in case, I don't believe there to be an evolutionary master-framework to (yet) exist, along the lines of desires for a Theory of Everything in physics.
On the other hand, as soon as you cross the boundaries of biological evolution, like let's say in the most primitive of living, biological entities, you are bound to cross over to cultural evolution as well. ( I am no expert on the subject, there are probably other intermittent steps as well). Synergistic effects in the process of evolution may even be considered in Quorum Sensing's most favorite model: Vibrio fischeri.
A simple search on the subject instantly yielded me:

"Evolution of alkaline phosphatase in marine species of Vibrio". J Bacteriol....

In other words: molecular evolution, as being part of the many evolutiony research focuses.
The idea and gross effects of Darwinian evolution are often rather straightforward at first glance. All the little details, that have to be accounted for -with scientific rigor-, as science itself is evolving, are probably where the team-work starts, as do the discussion.
So the only fixture you can count on is team in science.
The introduction to the evolutionary topic at hand, that you would use in an abstract or introduction would depend on the scientific sub-discipline, and would likely already be readily available through peer-publication.


text:
Will I grow taller? How can i tell?
I'm 17 and I'm about 160 cm and my weight is 47 kg . I just want to know if I will still grow taller ?

Two things might help here... The height of your parents (and possibly any older siblings), and your gender. As the answers below show there is sex specificity in timing of growth spurt, and height (and timing of growth spurt) is heritable from parents. Don't give up hope, I grew 30 cm after turning 18!

By the way this question in it's current format is a personal medical question and is more suited to your GP, not suitable for BiologySE. I suggest you rewrite it in a general biological framework, perhaps along the lines of... "How heritable is height, how does the likelihood of significant growth decrease with age, at what age can someone expect to have achieved their maximum height?"

Simpler answer (although I like Remi.b's):
Probably.
If you want to know for sure go to a doctor and have them look at your Epiphyseal Plates in your long bones (Femur, Tibula, Fibula). If they've fused, you won't grow anymore. If they're still distinct then you'll continue to grow until they fuse.
For males that can happen as late as early-20's. However, depending on genetics, you might not gain that much height.
Here's a graph you might be interested in:

You're at the tail-end of probably your last growth spurt. You have probably 2-3 years' worth of growing left, but don't expect miracles. You've got maybe another 1-2cm.

wow. that is a great find.

I guess there are two main solutions:
1) From the science of antropometry you might find some clues of the probability that you have of growing taller. For example, if your body (hairs and stuff) already look like an adult body, then you would probably not grow much more. See @MCM's answer who gives a solution that will be way more useful to you than my answer!
2) Knowing the size of your parents you can infer your expected size. Below are some comments on this question.
Any phenotypic trait has shows some part of variance. This variance is explained by genetic variance, environmental variance and the variance due to the interaction of genetic and environment. In equation it gives:
$$V_P=V_G+V_E+V_{GxE}$$
Dividing the genetic variance by the phenotypic variance gives the heritability
$$H=\frac{V_G}{V_P}$$
Estimations of heritability (in the narrow sense, see this for more info) can also be realized with selection experiments or parent-offspring.
The heritability of height in humans is around 0.6 (Welcome to anyone who can give an accurate value and a good reference) which is quite high. It means that more than half of the variance in height among humans has to be accounted to genetic variance. If your parents are tall, don't lose hope, you have quite a good probability to grow tall.

I think your answer is perfect but the "asker" seems to be looking for a simpler answer as he does not seem to be from a scientific background.

Wow! Real Good! Is this sentence correct? "Any phenotypic trait has shows some part of variance"

I guess that all phenotypic traits should show some variance in a population (as soon as the population is larger than 1 individual!), just because there is internal noise (proteins degrade a ta given rate for example). However, not all phenotypic traits shows some underlying genetic variance (that is, not all phenotypic traits are heritable).


text:
Why are interspecies hybrids so often larger than either parent species
Recently doing a little reading on interspecies hybrids I noticed that it seems interspecies hybrids are most often much larger than either parent.  Notably, Ligers, Dzo and Savannah Cats, but it seems like all or at least most.
Is there a reason for this genetic expression in hybrids?
If I am incorrectly inferring this to be the case let me know that instead.

While they do not necessarily constitute the majority, it is true that there is a large number of interspecies hybrids whose members are larger in size than the parent species, and there exist explanations that account for this phenomenon.
What you are describing is an example of positive heterosis, or hybrid vigor.  While the rationale for plants is more complex, it commonly arises between related species in mammals as a sort of heterozygote advantage in which the contrast in genetic contribution during conception spawns some phenotypic benefit.  The exact implementation of this varies from species to species, but this link here is a nice, concise explanation for why ligers might be so large.


text:
Body's decomposition
Does a human body decompose in a completely sterile environment ? If yes, what decomposes it ? And how fast ? What happens in vacuum ? Can it remain exactly the same ?
Thanks

In vacuum for example?

In vacuum, exactly.

Does a human body decompose in a completely sterile environment ?

No it wont. Unstable molecules like ATP will quickly degrade spontaneously. The stable ones like many proteins and lipids wont degrade spontaneously. Enzymes are essential to degrade them and are to be supplied extraneously.

What happens in vacuum ?

Body will dry up :P


text:
A weird-looking fish with a shield
I found this photo in a local news page. The page claims that this fish is a new species that was found by a Malaysian fisherman. Is this true or is it a known fish and already has a name?

Can you please add the link to the local news website? It looks like an April Fish ;)

@Remi.b updated the question with the link. It is in Arabic anyway :) hope you can understand the language. You can use google translate if you don't.

BTW, Alarabiya.Net is a well known well trusted news source in the Middle East.

Found a similar article in an English website: http://www.muldersworld.com/photo.asp?id=7644

There are tons of similar article on this fish. Here, here and here

The front part of the fish looks like part of the cranium of a fish. I'd bet that the tusks have been "made" by removing some bones in the middle.
Well, after having looked at the links given by Remi.b, it seems that it's not even necessary to remove bones. This is probably a Peristediidae.
You can find some images on fishbase

blood-mark in mouth-portion

Aww I missed the old answer also contained the taxonomic designation in the second paragraph. sorry for that.

This is a species in the Peristediidae family, commonly called armored searobins or armored gurnards.

found in deep waters around the world, with most species in tropical regions. They are related to the searobins in the family Triglidae, and some authorities classify them in that family,[2][3] but they are encased in heavy scales with prominent spines. They have prominent and often elaborate barbels on their chins.

Characteristics of Peristediidae [Source]:

The scorpaeniform family Peristediidae (armored sea robins) is characterized by (1) a body entirely enclosed by four rows of spinous bony plates (scutes) on each side; (2) a large bony head with spines and ridges; (3) each first infraorbital (lachrymal) anteriorly extending in distinct rostral projections; (4) barbels on the lower jaw, and (5)pectoral fins with the two ventral most fin rays free and enlarged (Miller 1974; Miller & Richards 2002; Richards 1984, 1999; Kawai 2008, 2013)

Specifically, this looks similar to other species in the genus Satyrichthys.

 Satyrichthys welchi (Source: Taiwan Biodiversity Informaiton Facility)
According to Pogoreutz et al. 2013:

The genus Satyrichthys is diagnosed as follows: (1) no teeth in upper and lower jaws; (2) lateral margin of the head smooth; (3) the ventral row of bony plates on caudal peduncle extending posteriorly, separating the posterior bony plates of the lower lateral series; (4) only the posterior lip and chin barbels branched, and (5) fewer than 20 soft rays in dorsal and anal fin (Kawai 2008, 2013).

An important character in separating species of the genus
Satyrichthys is the number of lip and chin barbels (Miller 1964, Kawai 2008, 2013)

One similar looking species is Satyrichthys welchi (the Robust armoured-gurnard) [pictured above] found in the South China sea:

 Source: AquaMaps
According to FishBase, here are some characteristics of Satyrichthys welchi:

Dorsal spines (total): 7
Dorsal soft rays (total): 17
Anal spines: 0
Anal soft rays: 18

@AlwaysConfused thanks a lot for the bounty! Glad you appreciated the answer! You should Youtube the family -- some species walk on barbs like they're tiny legs! :D

I also want to know about the 2 eye-like objects on the head-portion at back  (shown) side. Are the eyes? or nostrils? or something else? And also, is its mouth present at the lower (frontal) portion? and is there any advantage/function of 2 protruding portion beside mouth region.


text:
What makes a DNA sequence motif a DNA sequence motif?
I've read about DNA sequence motifs, but still don't understand what makes some sequence a DNA sequence motif. Is this a well-defined concept? For, example,
What are DNA sequence motifs? says:

Sequence motifs are short, recurring patterns in DNA that are presumed
  to have a biological function. Often they indicate sequence-specific
  binding sites for proteins such as nucleases and transcription factors
  (TF). Others are involved in important processes at the RNA level,
  including ribosome binding, mRNA processing (splicing, editing,
  polyadenylation) and transcription termination.

For example, I've been working with Recombination Signal Sequences (RSS), which are important in immunology. However, from what I can tell, RSS are not themselves motifs, but they do contain motifs. E.g. Conservation of sequence in recombination signal sequence spacers
says

Previously, the RSS has been described as possessing both a conserved heptamer and a conserved nonamer motif.

So, apparently, the heptamer and nonamer component of the RSS are themselves motifs, but the RSS itself is not. Can anyone explain why? Thanks.

Motif means a pattern. For any array of objects to be called a pattern, it has to have at least more than one instance.
To define more precisely, a motif should have significantly (statistical) higher occurrence in a given array compared to what you would obtain in a randomized array of same components (expecting at random).
[Here i use the term array to mean an arranged set such as a genome (array of nucleotides with their position in the sequence) or a protein structure (array of amino acids with their vector positions). A randomized array with same components is generated by shuffling the elements and their values; for e.g. assign the same collection of nucleotides to random positions]
RSS nonamers/heptamers are called a motif because they are a pattern of sequence which a) has more than one occurrence b) the occurrence is significantly higher than a random expectation. Generally in sequence motifs randomization is not usually done because the genome size is too huge. In such conditions if your sequence has >= 2 occurrences throughout the genome it may be considered a motif. Lets assume a 10bp sequence. Its random probability = 1/4¹⁰. Therefore in 1048576 bp (1Gb) there is a likelihood of finding one instance of that sequence on random. So I assumed that if that sequence has >=2 instances it can be called a motif. However, I am not sure about this.
RSS is not a motif because the entire RSS is not conserved; the conserved 'motifs' are interrupted by sequences. This is analogous to lets say a promoter which is a functional region of the DNA. Promoter can have binding sites for different transcription factors and these operator sites (TFBS) can constitute a motif (if they are conserved) but not the entire promoter.

Thanks for the reply. I've read such definitions before, but they have never seemed very precise to me. Does this mean, for example, that the RSS cannot be determined to have "significantly (statistical) higher occurrence in a given array compared to what you would obtain in a randomized array of same components (expecting at random)."?

Edited the answer.. see

I'm confused. So, you are saying that all of the RSS and the included heptamer and nonamer are motifs? I had the impression that the RSS contains motifs but are not themselves motifs.


text:
Why are antibodies so expensive?
The amplification on vector transgenic microorganisms and the subsequent purification does not seem that complicated. Also, what are the processes that biotechnological industries follow, in detail, on their production?

Your question is not very clear - what exactly do you mean by the first sentence? I can answer your second sentence quite easily, as I used to work for a major antibody company, but I'd like to know what you'd like me to focus on, as the subject area is very broad.

Additionally, please read my answer to this question and let me know if you'd like more detail.

Making antibodies is mostly nothing you do with transgenic microorganisms. To make an antibody you first have to immunize an animal with the correct antigen. This includes have an animal facility where you can keep animals under clean conditions. If you are looking for polyclonal antibodies (meaning a whole bunch of different antibodies with different specificities) you will boost the animal before sacrificing them and isolating their blood to purify the antibodies.
If you are aiming for monoclonal antibodies then the animals will be boosted as well, then sacrificed and their spleens isolated. From the spleens you make single cell solutions from which antibody producing cells are isolated and plated one cell per well of 96 or 384 well plates and cultivate them to identify cells which produce antibodies. These cells are fused with immortal cells to produce immortal hybridoma cell lines which secrete a lot of antibodies into the cell media. These antibodies still need to be characterized to make sure the really bind the antigen of choice and not something else (in the spleen a lot a these reactions take place).
Just for estimations: Making one batch of a custom polyclonal antibody in rabbit with a given peptide sequence will cost you at least 5000\$ to 10.000\$ the last time we checked for it. Monoclonals are more expensive. So making an antibody is quite an investment on the first hand.

There are some pretty good articles on Wikipedia about antibody production here and here. My crude understanding is that, you will have to grow and animal and bleed or sacrifice it to extract antibodies. This process along with purification costs a bit of time + money. Additionally, antibodies for humans must be grown under more stringent conditions to avoid contaminants and reacting to human immune system.


text:
Why is the 4.4 kb band barely visible in this HindIII digest of lambda DNA?
Why is the 4.4 kb band barely visible?
Also, what is the mass (ng) of DNA in band X if lane S contains 250 ng of digested lambda phage DNA?

This question is literally impossible to answer with the information given. What samples are run in each lane? How were they prepared? I assume the left lane is a ladder. What ladder is it? What sample are you adding the HindIII-restricted phage DNA to?

First of all, the 4.4 kb HindIII band is derived from the right end of λ DNA, so during storage it anneals to the 23.1 kb left arm fragment via λ's 12 bp cohesive ends. You can solve this problem by preheating the markers to 65°C for a few minutes then cooling rapidly (i.e. on ice).
In a stained gel the intensity of a band is proportional to the amount of DNA in that band. This is why the heavier bands are more intense. The fragment X in lane 2 is similar in intensity to the 0.5 kb λ fragment so DNA content of the two bands is similar.
The amount of DNA in the 0.5 kb band is 250 ng *(0.5/48.5) where 48.5 is the size of wild-type λ DNA. I'll leave it for you to complete the calculation.


text:
explanation of conjugation experiment in bacteria
In this paper (On the expression of a structural gene) I am confused about what is being plotted in Figure 6. The x-axis contains the fraction of radioactive day and y-axis contains the enzyme formation (I assume this is just the concentration of enzyme like Figure 5?). Different point shapes are different times after mating. If so, why are there multiple points of each time? Why are there multiple measurements for say 48 mins past mating? Is the correct interpretation that for each condition, they are showing the fraction of radiolabeled material for each number of day post thaw, like figure 5? It is unclear.

When I tried to access the pdf you cite (or the host webpage ac.els-cdn.com) I get an Access Denied notification. Could you post a full citation so we can look it up, or post a different link to the pdf?

@A.Kennard fixed link

There are three variables being shown here:

The amount of time samples were stored in the freezer to allow $^{32}$P decay (x-axis),
The length of time samples were allowed to grow in a nonradioactive environment before being frozen (points with different symbols), and
The rate of $\beta$-galactosidase production when cells were thawed and grown in the presence of the transcriptional inducer IPTG (y-axis).

Let's break those down a bit more:
The x-axis measures "fraction of $^{32}$P decay." In terms of the experimental protocol, this translates to "length of time left in the freezer." For the $^{32}$P-decay experiments, samples are stored in the freezer for various lengths of time, where metabolic processes, like DNA replication or enzyme production, are shut down or drastically slowed. Although metabolism has been shut down, $^{32}$P can still beta-decay into $^{31}$S (according to Wikipedia), which promotes the breakdown of any DNA containing (formerly) radioactive isotopes. The implication is that the longer you leave samples in the freezer, the more $^{32}$P will decay and the more formerly radioactive DNA will be degraded. So you can read the trend in the x-axis either as "increasing fraction of $^{32}$P decay", "increasing amount of time left in freezer," or "decreasing fraction of intact $z^+$ DNA." The different points corresponding to, say, "48 minutes past mating" correspond to samples that were frozen down 48 minutes past mating but kept in the freezer for different lengths of time.
The y-axis measures "percent survival of enzyme-forming capacity." I think that it's safe to interpret this as the rate of $\beta$-galactosidase production relative to the rate with no $^{32}$P-decay. In other words, if you plot $\beta$-galactosidase production over time (as in Figure 5) for different conditions, you'll measure a slope, the rate of enzyme production. If you normalize all these rates from different conditions by the rate when there was no radioactivity (and thus no degradation of $z^+$ DNA in the freezer), you'll get the values plotted on the y-axis.
The final interpretation of this plot is that the $\beta$-galactosidase production rate is sensitive to the loss of the introduced $z^+$ DNA when the loss occurs soon after mating, but if cells are allowed to grow enough to divide once or twice before DNA degradation, then the loss of the original conjugated $z^+$ DNA does not affect the $\beta$-galactosidase production rate. This data is consistent with the idea that the DNA form of a gene is constantly required for sustained $\beta$-galactosidase production, and after several rounds of division the $z^+$ DNA has been replicated and is no longer radioactive and prone to degradation.
There's a lot of data in this plot (ah, the elegance of 1960s molecular biology!) so it can take a while to digest. Hope this helps!

Great answer - was working on an answer myself, but no need for it now. It's worth adding a historical note that this paper, and especially an earlier (1959) paper from Pardee, Jacob & Monod, formed the basis of the idea of mRNA - an unstable intermediate between gene (DNA) and protein. And this in turn led to the experiments of Nirenberg that are touched upon in this question


text:
Why does caffeine consumption cause one to urinate more?
What is the physiological mechanism behind the diuretic effect of caffeine?

Caffeine inhibits the secretion of the antidiuretic hormone (ADH), so it increases diuresis, but this effect is small and transient.
http://en.citizendium.org/wiki/Vasopressin
Caffeine in amounts up to 400 mg/day (~4 cups of coffee) does not results in net dehydration, since the amount of water lost due to slightly increased diuresis is much smaller than the amount of water in coffee.
http://www.ncbi.nlm.nih.gov/pubmed/19774754
In some people, caffeine may irritate the bladder and thus trigger more frequent urination, but this is not increased diuresis and the total volume of the urine is not increased.


text:
Telomere shortening during replication
It is widely know that each cell cycle during DNA replication some fraction of the telomeres is lost, and this phenomenon is called the end replication problem. Well this is due to the fact that the DNA polymerase only adds nucleotides in 5´--> 3´ direction, thus the synthesis of one of the two DNA strands will need some RNA primers for its polymerization (and DNA polymerase will replicate DNA in a "jumping" pattern). Then, in the very end of the synthesis of this strand (called lagging strand) one last fraction will not be copied from the template as even if the last primer is set in the very end of the chromosome, once this RNA is degraded a void space is going o remain invisible for DNA polymerase.
Well this is all well known, but my question is whether during each DNA replication it is ONLY the telomere of the chromatid whose origin was in the lagging strand  which will be shortened? (Thus chromosome shortening is happening in a truly asymmetrical and stochastic pattern)

Not only one strand is used as lagging strand. In a replication bubble for half the length from the centre one will be used but for the other half other strand will be used.See the wikipedia article for replication.

you sure?? where do you locate the centre?

and you cannot use the same strand one "side" as lagging and the other as leading as the direction of a strand is the same from beginning to end

See this

Welcome!I love telomeres too! I will post this as an answer just for the sake of statistics.

so, when a whole chromosome is replicated, the process is carried out from one point following the two opposite directions always, or is there any other scenario?

let us continue this discussion in chat

If you are talking about prokaryotes - yes, if about eukaryotes - no. Eukaryotes have multiple origins of replication to increase speed. So the telomere problem is going to arise at only the "last" origins of replications at both the ends. (No telomeres in middle as there will a 3'end available from the replicated dna from  either side. Do you understand this ? It's a little tricky. Try to visualise it with the help of the image I linked)

By the way there are no telomeres in prokaryotes.

In replication, both the chromosomal halves (which are simultaneously threaded through the replication complex) have a lagging and a leading strand. A part of the segment will be replicated as leading and a part as lagging.

i think you are a little confused.. the strand that is in the direction of the fork  (5'->3') is leading strand . The other one is lagging. It is so because the DNA polymerase holoenzyme complex has two polymerases in the same orientation. So the 3'->5'strand has to be first bent to make it locally 5'-> 3' and then replicated.

Since replication can be bidirectional, a strand of a chromosome will contain both leading and lagging elements (was that what you were trying to explain ?). If so, you should elaborate in your answer. The concept of leading/lagging strand is confusing because it is just a local structure, not the entire chromosome.

@WYSIWYG Yes I meant the second thing. Please feel free to edit it.


text:
Gliotoxin ingestion and actions needed
what are the "next day" actions that one has to take, when accidentally ingests contaminated drink/food from Aspergillus or Penicillium or Candida fungus?
Is it feasible to take N-acetyl-L-cysteine supplements? What other measures minimize the damage from the mycotoxins?
What kind of supplements and/or treatments reduce the superoxides produced as effect of the mycotoxins?


text:
Which pathways/mechanisms could control some Synaptic clefts in series by Somatic Nervous System?
I listened a talk where the speaker said that this can probably be possible by Weak Quantum Cognition Theory.
I see that there is no evidence at the moment, only theory.
I see no pathways by which this could happen directly such that the quantum entanglement and quantum superposition could happen.
They should happen in a series, but I see no system holding the signal going on.
I think this is a only a hypothesis, without any supportive  evidence.
Probably, some type of synaptic cleft can be controlled, but still I see no evidence or no pathway or pathways.
I do not understand which pathway/pathways this could happen.
What is the target mechanism? Presynaptic membrane or postsynaptic neuron?
Which are possible pathways that could control the secretion of synaptic cleft?


text:
Proportion of amino acids from a random polymer of U and C

A protein synthesis assay was carried out in vitro. A
  polyribonucleotide containing U and C in proportion 1:5 (positions of
  U and C are random) was used as a template. Which amino acids and in
  what proportions will be incorporated into the synthesized polypeptide
  molecules?
А. 1Phe : 5Pro : 3Leu.
B. 1Leu : 1Pro : 1Ser : 1Phe.
C. 1Phe : 5Ser : 5Pro : 5Leu.
D. 1Phe : 25Pro : 5Ser : 5Leu.
E. 5Leu : 5Pro.

First thing I am not sure is whether only U and C is there. I have tried solving this sum taking both the conditions into consideration . I also tried solving it from options but could not succeed.

The first thing to mention is that this is the type of experiment that Marshall Nirenberg performed in order to break the genetic code, and for which he got the Nobel prize in 1968. We stand on the shoulders of giants.
If the ratio is U:C, 1:5, then it is easy to calculate the probability of encountering each of the 8 possible codons composed by just U and C. So for example:
the probability of UUU is (1/6)3
the probability of UUC is (1/6)2*(5/6)
and so on.
Here's a Table that gives all of the values and demonstrates that the answer is (D).


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Basic step by step methods for PCR & Gel electrophoresis class
I'm teaching a class how to do PCR & gel electrophoresis soon and would like it if you could check through my basic step by step instructions - it's a while since I've done one. Is there anything there that is wrong, missing, or should be excluded in the following?

A)    Collect all ingredients from the refrigerator and keep cool (on ice). Leave the TAQ in the freezer until required.
B)    Make master mix by adding all ingredients (ddH20, MgCl2, PCR Buffer, F Primer, R Primer, dNTP) (excl. TAQ)
.......
W)    Take the gel to the UV camera and take a picture. Large DNA molecules move through the gel slowest so will be nearest to the wells.

(The students will use primers they designed to sex 6 DNA samples from 3 species of birds, males should produce 1 band & females 2 bands in the gel)

for the full version see the answer below

for one thing you have to add a stain to the gel to see it on the UV. ethidium bromide requires gloves and is toxic.  GelGreen/GelRed is expensive, but is a lot safer.  also remember to keep the mastermix frozen at -20C until use - aliquot it because you can't refreeze it more than ~6 times or so - it degrades.

Thanks @shigeta useful tip of freezing and aliquot in the mm. I forgot the loading dye is a prepared mix of loading dye and gelred

Might not be necessary for a teaching lab, but a better control might be to have one extra PCR tube without any template (No Template Control) to assess if there are primer-dimers or any other contaminations. If reagent cost/availability is a problem a control run by one student would probably provide enough liquid to run on 2+ gels (since I assume many of these reactions will go in the same thermocycler it's still a reasonable control)

So use the defined amount of Master mix and then add millipore water in the same quantity as the DNA in the samples? @A.Kennard

@GriffinEvo Exactly, and then do PCR on that sample alongside all the others and run it on the gel.

here's a good PCR troubleshooting guide.. https://www.neb.com/tools-and-resources/troubleshooting-guides/pcr-troubleshooting-guide

Looks good to me, with the comments others have shared. I think the most important part of preparing a lab like this is not only make sure you get decent results (although with master mixes and the like these days that's usually pretty straightforward), but to know exactly WHY you're doing each step, and to be able to explain that clearly to the students so they understand. Anybody can follow a protocol, but it takes a special person to connect the "how" with the "why" and explain it all in a unified story. Good luck with your lab!

Thanks @MattDMo I'll keep that in mind, perhaps I could set them up in groups, get them to follow the standard protocol to start with, then have them tweak the PCR reaction mix and thermocycler set up to see what that does, then have them write up the results describing the effect of and explaining why, for example, changing Mg++ concentration affected the end product.

@GriffinEvo I read the article u wrote on wordpress about this and I absolutely loved it ! Learning by teaching. Way to go...

I've run a test following this protocol to the letter...

PCR step by step:

Collect all ingredients (excluding TAQ) from the refrigerator and keep cool (on ice). Leave the TAQ in the freezer until required.
Make master mix by adding all ingredients (excluding TAQ) using fresh pipette tips for each ingredient and using the volume specified
in the PCR reaction mix recipe.
Vortex & lightly spin down on a centrifuge.
Add the required amount of TAQ to master mix (insert in to the liquid) and mix using the pipette to draw some liquid up and down.
Add master mixes to labeled PCR tubes in the required volumes as specified by the protocol.
Add DNA to PCR tubes (using fresh pipette tips for each DNA sample) again using the volume specified in the protocol. Label your tubes
carefully (and on both the lid and tube).
Lightly spin down the PCR tubes on a centrifuge.
Run PCR in the thermocycler according to your protocol.
Collect samples from thermocycler and place in fridge until needed.

Gel Electrophoresis step by step:

Make 1xTAE (enough to make the agarose gel and to place in the electrophoresis apparatus).
Make an agarose gel (about 5 mm thick) by melting agarose and 1xTAE in the microwave; allow the liquid to cool a little before adding it
to the mold.
Once the gel is cool, place it in the electrophoresis apparatus, cover it with 1xTAE (just covering the gel) and then remove the comb.
Collect the PCR products from the fridge/thermocycler.
Make spots of loading dye on parafilm. The loading dye is premixed with GelRed so your samples show under UV light.
Add one sample to a spot, mix it by drawing the liquid in and out of the pipette tip, and then carefully add to a well in the agarose
gel. Take care not to puncture the gel or spill any of the liquid out
of its well. Discard the pipette tip.
Repeat the previous step for each sample and for a negative control (master mix and milli-q water instead of DNA). Use a fresh tip for
every sample.
Load PCR Ladder, also mixed with loading dye, in to a well.
Connect the electrophoresis apparatus to a power supply, with negative electrode (black) nearest to the wells containing the
samples.
Set the power to run 80-120 volts.
Wait until about a finger-width gap appears between the blue and purple bands (approximately 20-30 minutes).
Disconnect the power and collect the gel carefully from the liquid.
Take the gel to the UV camera and take a picture. Large DNA molecules move through the gel slowest so will be nearest to the
wells.

And got a perfect result...

The order is Control, female, male, female, male, female, male, ladder. Males have one band, females have two. The final pair didn't show too well on the picture but were clear enough on the screen in the camera room. Thanks for the tips everyone! Sorry the picture is low quality.
Feel free to recreate these guidelines but remember to credit the Biology Stackexchange Community!

now that's dedication! Thanks for sharing this!


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Homework : Sodium Potassium pump
Why does sodium-potassium pump consume about 2/3 energy of a cell ?
A.maintains appropriate membrane potential
B.helps in co-transport
I think it should be A.

I don't know the answer, but my feeling is that it will be (b). If the cell isn't a neuron then there will be no processes directly collapsing the resting potential. There will however be lots of symporters and antiporters carrying out secondary active transport by tapping into the gradients of sodium and potassium ions.

@AlanBoyd Aren't the "leaky" channels and other free ion channels (on top of secondary transporters) tending towards obliteration of the membrane potential in most cells, so that the pump is required to maintain steady concentrations and hence a steady potential? In the absence of the pump, the channels would allow a steady ion flux completely neutralizing the membrane potential from the active GHK potential to the donnan-equilibrium state This would mean (a) is the answer. But I am not sure on this.

Neither of the options explain the 2/3rd energy consumption. So the question should either be: why is Na/K pump important or How much energy does a single Na/K pump consume in an event of transport. Rest everything is situational. As @AlanBoyd points, Na/K pump performs additional functions in electrically excitable cells.

UNIMPORTANT COMMENT..... I wonder who gives you these homeworks :P

I can't yet comment, so here's a (sort of) answer:
I've only ever heard the "2/3 of cellular expenditure" rule applied to neurons, and frankly, it wouldn't make much sense in any cell other than a neuron.  The Guyton and Hall Textbook of Medical Physiology says, "For some cells, such as electrically active nerve cells, 60 to 70 percent of the cells' energy requirement may be devoted to pumping Na+ out of the cell and K+ into the cell."  A cardiac muscle cell, for example, would probably use more of its energy for contraction than pumping ions.
In a neuron, the bulk of energy expenditures are for electrical signalling done via allowing sodium and potassium ions to temporarily run DOWN their respective gradients.  As such, the "purpose" of a neuron is to pump ions across a membrane and then let them run back when needed.  Since a neuron doesn't really DO much else, it makes sense that the bulk of the energy produced will go towards pumping ions.  A practical example is the use of barbiturate comas to reduce metabolic activity in the brain.  Flat-lining the EEG drops metabolic requirements by ~50% (Source: Medscape).
Please keep in mind that this answer is specific to neurons...other cells perform other functions, and those other functions will take up significant fractions of energy produced.  Further, other cells probably aren't devoting large fractions of their energy towards signalling, and so the fraction of energy devoted to pumping ions will be markedly less.  They'll still be pumping ions to maintain a gradient to perform tasks like membrane transport and osmotic control, but those tasks are ancillary to the "purpose" of those cells.  I can't find any solid numbers for Na/K ATPase energy expenditures in non-neuronal tissue at the moment, but if I do, I'll update appropriately.
UPDATE:
With regards to the question itself, which I apparently forgot to answer:
Can a cell function without an appropriate membrane potential? Can co-transport run without a membrane potential?

Why does sodium-potassium pump consume about 2/3 energy of a cell ?

It's A, assuming we're talking about a cell-type that heavily utilizes the potential.
On to some of the comments...

If the cell isn't a neuron then there will be no processes directly collapsing the resting potential. - Alan Boyd

Incorrect, Pacemaker cells collapse the membrane potential frequently and don't have any resting membrane potential, only hyperpolarization-repolarization cycles.
Neurons are merely the most prominent users and best examples as they're entire existence is dedicated to the membrane potential.

In the absence of the pump, the channels would allow a steady ion flux completely neutralizing the membrane potential from the active GHK potential to the donnan-equilibrium state This would mean (a) is the answer. But I am not sure on this. - Satwik Pasani

Correct to some extent. The leaky ion channels (which are usually K+ channels) would allow the equilibrium to be reached for a handful of ions. This still prevents utilization of the potential, however, and is an easy way to kill something.


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Why can CO₂ be transported dissolved in plasma?
Is it because CO2 is more soluble in water or has it got to do with the alkaline pH of plasma ?I here mean only aqueous CO2 transport from body cells to lungs.

can you cite some support for this?  offhand i would think that CO2 is more soluable in acid - it forms bicarbonate carbonic acid.

At what level do you mean? Are you talking about transporting from a source to a sink? CO2 is soluble in pure water, and as atmospheric partial pressures of CO2 are going to be lower than physiologic levels, any reversible buffering is just going to aid in transporting CO2 "downhill".

By Dissolved state do you mean just the aqueous $\ce{CO2}$ molecules or those that are in form of $\ce{H2CO3}$ and $\ce{HCO3-}$ (free or associated) also?

Edited the question

Solubility of gases is affected by the chemical nature of the gas. Acidic oxides dissolve in water readily because they react to form acids. The high pH can keep the acid dissociated thereby pulling the gas-acid equilibrium towards acid. CO2 is more soluble, in general, than nitrogen and oxygen because it is polar (however it lacks net dipole moment)

The bulk of CO2 is transported as bicarbonate/carbonic acid.  The conversion between CO2 and carbonic acid is catalyzed by carbonic anhydrase in red blood cells, otherwise the conversion would be very slow. The bicarbonate is then shuttled out of the RBCs and into the blood plasma. The CO2 (gas) in blood plasma accounts for <10% of CO2 transport, and the solubility isn't that much different from that in water.
Source: Guyton and Hall Textbook on Medical Physiology

about the same amount of CO2 is transported by hemoglobin...

Hemoglobin actually doesn't carry very much CO2, as it doesn't have a dedicated spot to carry it.  There is a binding site on the protein, but its purpose is to facilitate the release of extra oxygen to metabolically active tissues.

... in fact only 10% of it!  see wikipedia: Hemoglobin.

Haemoglobin cannot bind CO2. It is not a good ligand for metal co-ordination complexes. However carbon monoxide is a strong ligand and can form carbonyls with metals, which accounts for its toxicity.

@shigeta - I thought you were saying hemoglobin carries as much CO2 as bicarbonate transport does...my mistake!

@WYSIWYG Hemoglobin does have a CO2 binding site - its not the haem site though.  LMGTFY: http://en.wikipedia.org/wiki/Hemoglobin#Binding_for_ligands_other_than_oxygen


text:
Is the Michael Jackson skin pigmentation disease realistic?
Quoting wikipedia:

Jackson's skin had been a medium-brown color for the entire duration
  of his youth, but starting in the mid-1980s, it gradually grew paler.
  The change gained widespread media coverage, including rumors that he
  might be bleaching his skin. According to J. Randy Taraborrelli's
  biography, in 1986, Jackson was diagnosed with vitiligo and lupus; the
  vitiligo partially lightened his skin, and the lupus was in remission;
  both illnesses made him sensitive to sunlight. The treatments he used
  for his condition further lightened his skin tone, and, with the
  application of pancake makeup to even out blotches, he could appear
  very pale. Jackson was also diagnosed with vitiligo in his
  autopsy.

1) Is this plausible?
2) Is it likely to be an actual disease, or would there be so many mitigating factors that it is unlikely a person would suffer to the extent he did?

Vitiligo is a real disease, and can absolutely have the effects it did on MJ. I've known people with skin that looked like patchwork quilts, and others where there was more generalized loss of pigmentation. I've met sub-Saharan Africans with skin much lighter than mine (my ancestors are from Northern Europe). I see absolutely no reason to question his appearance from a medical standpoint.

1) Is this plausible?

It is absolutely plausible. His particular condition was called Vitiligo
 (as stated in your quote) and isn't that uncommon, albeit not usually as severe.
Skin pigmentation expression changes over time, sometimes dramatically.

2) Is it likely to be an actual disease, or would there be so many mitigating factors that it is unlikely a person would suffer to the extent he did?

Vitiligo is a very well-documented disease, and like every disease, there's a broad range of affectation. Treatments options are very limited, and so makeup or other methods are often used to disguise the affected skin.
Here's some more pictures of people with Vitiligo at varying stages: