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What is the relationship between W, X, Y and P, M retinal ganglion cells?
In Guyton and Hall Textbook of Medical Physiology (12e) the retinal ganglion cells (RGCs) are classified into W, X, and Y types. However, in Gray's Anatomy (40th ed.), RGS are subdivided into midget and parasol cells. What is the relationship between the W-X-Y versus midget-parasol classifications?
Summary of the WXY classification as in Medical Physiology:
About 40% ganglion cells are W cells. They are the smallest (<10 μm), and the slowest (8 m/s) to transmit signals, but they have the broadest receptive field. They receive signals from rods and detect directional movement.
About 55% are X cells. They have medium size (10~15 μm) and transmission speed (14 m/s). Their fields are small. They transmit color vision.
About 5% are Y cells. They are the largest (<35 μm) and the fastest (35 m/s) to transmit signals. They have broad fields. They respond to rapid changes in the vision.

Short answer
X = P = midget = β
Y = M = parasol = α
W = γ

Background
First off, P and M cells are not equal to parasol and midget cells; on the contrary - P cells are midgets and M cells are considered to be parasols.
X, Y and W cells are used to denote different retinal ganglion cells in cats, as proposed by experiments Enroth-Gubel & Robson (1966). As you already indicate, these cells have different physiological response properties. X and Y cells have the standard center-surround distribution of their receptive field, X cells having linear additive response properties in center and surround and Y cells nonlinear properties. X cells therefore have predictive responses such that responses can be predicted to be maximal (e.g. light shining on the ON center and no light stimulation on the OFF surround). Y cells tend to respond in more complex ways. W cells do not have a center-surround structure (Bruce et al, 1996).
Based on morphology, retinal ganglion cells in the cat have been labelled α, β and γ cells, which are thought to correspond to the physiological classes of Y, X and W cells, respectively (Boycott & H. Wässle, 1974).
The P and M division was introduced by De Monasterio & Gouras (1975) based on monkey experiments. P and M refer to the parvocellular and magnocellular connections retinal ganglion cells in monkeys make in the LGN of the brain. Both types of cells have a center-surround receptive field structure like X and Y cells in the  cat. P cells show color opponency and respond to specific wavelengths of light, and are involved in color vision. P cells respond to a range of wavelengths and respond most vigorous when different light intensities illuminate the center and surround (Bruce et al, 1996).
P cells are considered to be mostly midget ganglion cells, and equivalent to β cells of cat. M cells, on the other hand are considered to be mostly parasol cells and resembling α cells (Kolb, 2001).
References
- Boycott & H. Wässle, J Physiol (1974); 240(2): 397–419
- Bruce et al, Visual Perception (1996); 3rd ed. Psychology Press
- De Monasterio & Gouras, J Physiol (1975); 251(1): 167–95
- Enroth-Gubel & Robson, J Physiol (1966); 187(3): 517–52
- Kolb H. Webvision (2001). Salt Lake City (UT): University of Utah Health Sciences Center

According to Comparative Vertebrate Neuroanatomy, the XYW classfication is used for cat retina. They roughly correspond to the M, P, K cells in primates, respectively.


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best book for a comprehensive introduction to biology for a computer science graduate interested in undertaking research in bioinformatics
I have a postgraduate degree in computer science, and I wish to undertake research in bioinformatics. I had chemistry but no biology in high school. I have read bioinformatics books like "biological sequence analysis" by durbin and "fundamental concepts of bioinformatics" by krane, etc. But I wish to read a comprehensive book on biology (genetics) that will help me undertake research in bioinformatics properly. I have been considering 2 books: "molecular biology of the cell" and "molecular biology of the gene". Are these books comprehensive enough? Please suggest some good books as I have almost no knowledge of biology at highschool or graduate levels.

Molecular biology of the cell is a really nice book..

I concur with biogirl. MBotC was my introduction to molecular biology, and will give you a lot of background information. Of course, it shouldn't be your only resource (you wouldn't read just one book to learn a new programming language, for example), but it's a great place to start.

Molecular Biology of the Gene is a very good textbook.   For molecular genetics, this is an excellent choice. Molecular Biology of the Cell is also a very good textbook (actually, you listed my two favourites) but, as the name suggests, it is more focused on molecular cell biology. That said, is does cover molecular genetics quite comprehensively; you can't really go wrong with either book. However, it's hard to say whether either of these are the best book for you. There's a difference between molecular genetics and, say, population genetics.

Also, if you have no experience with biology at all, you may want to try a more introductory textbook. Molecular Biology of the Cell is good at working its way from the basics to more complicated topics. On the other hand, Molecular Biology of the Gene assumes you have some working knowledge of molecular biology.

Welcome to Biology and welcome to Biology.SE!
It is hard to answer such a question as the domains you describe are very vast.
If you want a book in an introductory book to biology, then you want to read this post and this post.
If you are more interested in population genetics and molecular evolution then this post will interest you. Still talking about evolution I'd like to attract your attention to this post for the second suggestion in the first answer:  Yang, Computational molecular evolution
You'll probably want to have a look at the post A free book/resource for learning genetics?.
Book recommendations for algorithms used in evolutionary biology and Introductory book in genetics might be a post of interest as well.
Unfortunately I don't know any of the two books you cite so I can't quite give you advice for them. molecular biology of the cell is a very common book among first year biology. It sounds like a potential good reading for you. I know nothing about molecular biology of the gene except what I just read about it on Amazon.
I am hoping one will give you a better criticisms about very general books about molecular biology.

Thanks a lot for the info. Do you think I should read books on biochemistry, virology and immunology in addition to the above books you suggested, because I am finding most research in bioinformatics being focussed in these areas?

It very much depend if you're intending to work in those areas. You can't learn everything. I think that a basic understanding in molecular processes of the genetic expression is essential. I think that having a slight understanding of molecular evolution is essential as well (but I am maybe bias as we are getting closer to my field) and then I suppose that it is not necessarily worth knowing much about phylogenetic, immunology or virology if you don't intend working in those fields. There are many existing tools and database in bioinformatics, it is part of the formation to know them I guess.

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Why do Alu repeats form secondary structures?
I've been doing a lot of research on Alu repeats and how they mediate the gene expression. I read the following article "Useful junk: Alu RNAs in the human transcriptome".
And it says that alu repeats embedded in 5'UTR makes stable secondary structure that prevents the assembly of ribosomal subunits, thus blocking the process of translation. I've been reading various articles to find out why Alu repeats form this secondary structure and why only in the 5'UTR and not in the 3'UTR. But haven't been able to find an answer.

Single-stranded RNA can easily form secondary structures, a very important example of this are tRNAs.
From a quick look at the article you read it seems that these Alu repeats work similar to riboswitches in the 5'-UTR. They can form secondary structures that block translation initiation, riboswitches commonly do this by hiding the Shine-Dalgarno sequence in a stable helix.
This kind of regulation of translation can obviously only work in the 5'-UTR as that is the place where the translation starts. The 3'-UTR can't affect translation in this way as the translation starts at the other end of the mRNA.
The Alu repeats still can form secondary structures in the 3'-UTR, and the article suggests that those might have an effect on mRNA stability.

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List of non-native terrestrial molluscs in California?
I'm looking for a list of non-native terrestrial molluscs in California. Ideally, I also need the date each taxon was introduced into California. Can anyone help?

This might be a start: Wikipedia: List of invasive species in North America: Mollusks.


text:
Why do flies leave dirty spots on shiny/glossy surfaces?
I've seen flies leave dark spots on lacquered wood, mirrors, glass and monitors. Why do they do that? Is it some food stash or are they dumping waste in a single spot? Why pick a smooth surface?

House flies (Musca domestica) prefer to rest on light colored surfaces, and what is lighter than windows, windowframes, glossy surfaces that reflect light, etc.? Where they rest (not eat) is where they defecate (or regurgitate), leaving marks politely called "fly specks".

House flies also leave dark fecal and regurgitation spots on wall surfaces where they rest, and with a preference for resting on light colored surfaces, these spots can be quite noticeable when fly numbers are high.

If you ever visit an "open" barn, you'll notice the phenomenon is quite remarkable. If the number of flies is high, there will be specks everywhere, but the windows and other shiny surfaces will be more densely covered.


text:
Plant identification
What plant species is this?
Its stalk looks like a grapevine, but the leaves & flowers not. It bloomed this week (Mid-June). I have found it in Turkey, Amasya.

If you want, I can add more shots of plant.

Welcome to Biology.SE and thanks for your question. I edited the question wording a bit to improve clarity. I substituted "body" for "stalk" (the part you are holding), I hope that fits your description. I also rotated the picture. Feel free to roll back my edits, they are just suggestions.

That is a kind of honeysuckle. The picture below is for Japanese honeysuckle (Lonicera japonica), but your specimen is different in the way the flowers are arranged and that the distal-most paired leaves are clasping the stem.

It might be Lionicera periclymenum, or Lonicera etrusca (there are about 150 species of honeysuckle); L. etrusca is pictured below (the color is irrelevant) which is native to Europe.


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Patterns/Motifs Repository
I am new to this area. I am a researcher working on fast pattern searching in general scenarios (e.g., regex in string matching).
I am curious about the "regular expression (regex)" (pattern/motif) in bioinformatics. Can anyone help point out some repository where I can see some "regex" instances (used by people in real cases)?
So that I can get a sense how complex they are and the possibility to apply our techniques.
Thank you!

There are only a fixed types of characters for DNA or protein sequence. For inexact matches you can use a regex. People do it quite often for general stuff. I don't understand what you mean by a repository.

Prosite (http://prosite.expasy.org/) uses regular expressions to search for protein domains, in contrast with Pfam. If you look at an entry, such as http://prosite.expasy.org/cgi-bin/prosite/prosite-search-ac?PDOC00022, you can see the consensus pattern under the PATTERN section towards the bottom. Prosite does not have the same coverage as Pfam, but the ease of searching means it is updated much more frequently and has tighter integration with UniProt.

Regular expressions are not commonly used for DNA or Protein analysis, but many people use Hidden-Markov-Models (HMMs).
If you are looking at protein domains, you can find many HMMs here:
http://pfam.xfam.org/

You will probably want to read up on Position Frequency Matrices (PFMs) and Position Weight Matrices (PWMs).  These tend to be much more sensitive and useful for pattern recognition in nuclei acid sequences. Two examples of databases with these patterns are TRANSFAC and JASPAR. Regex patterns can be useful in protein sequences sometimes, although PWM have application there as well.


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Any examples of an organism's life cycle where the reproductive stage occur before the 'adult' stage?
Most life cycles we knew of consist of a juvenile stage (e.g. larval for insects, sporozoite for some intracellular parasites), a reproductive stage and an adult stage. Usually the reproductive stage occur when the organism reached the adult stage.
But are their examples of organisms where its natural life cycle involve reproduction at an early stage, and then the parent then went through more distinctive stages after the reproductive stage and then dies off? For example:

The closest thing I can think of is the life cycle of mayflies, which dies a short period after the mating stage. But mayflies has only one adult stage thus it is does not really answer the question

I would guess not, since reproduction is really life's endgame

Yeast cells go around the cell cycle in both haploid and duploid states.

There are two important points here:

The adult phase is defined as the phase during which reproduction occurs. It is therefore impossible for reproduction not to occur during the adult phase as you would immediately call this phase the adult phase. Because of this purely semantic issue (nothing to do with biology) the answer to your question is necessarily "no".
Only kin selection/group selection/lineage selection makes life after the reproductive age possible. It is therefore a pretty rare phenomenon. If this is unclear, you may want to read things about the evolution of ageing such as this post for example.

Maybe a question that would be of higher interest would be something along the lines of: "Can you list species that have non/reproductive phases in between a reproductive phase and death?" or "Are there any species that undergo different reproductive phases during their lives such as being first a sneaker and then territorial (yes) or such reproducing asexually at first and then sexually (probably but can't think of any examples)?".


text:
Can anyone help me identify this plant?
I have a Chamaerops humilis in my apartment and in there is these small plants growing. I live in Denmark, Europe and my palm tree has only been inside my apartment since i got it.
Can anyone identify this plant?
Click on photos for full size

It's a bit early yet, but it looks very much like a weed known in my area as "cleavers" or "clingweed" (Galium aparine) because of it's tiny stiff hairs which make it catch and cling to clothing. The picture below is for a fully mature plant, which is stiffer and stickier than when they first sprout. Note the whorl arrangement of (usually six) leaves, with each leaf having a "point" protruding from the tip, the distrubution of hooked hairs along stem and leaf, and the initially prostrate habit (they grow along the ground initially). The mature stem will be squarish and easily crushed.

Though your plant's leaves are broader, there are ~650 species of Galium, and I believe yours will be either Galium aparine or Galium mollugo. But you'll be able to tell what it truly is when it flowers.

Thanks a lot for the detailed answer. Do you know how this plant got into my palm tree?

@Sova - Usually in a potted plant, they are brought in in the soil, especially if you add soil from outside to top off soil which gets compacted naturally as humus is broken down. If the plant has ever been outside, it will be subject to weed seeds. They are everywhere - carried in the wind, splashed up by hard rain, carried by insects, even dropped by birds.

Wow i didnt know that. My palm tree was standing outside when i bought it some months ago. The funny thing is that there is also some milipedes living in it. Some weeks ago i found a huge milipede in the soil. Then i grabbed him and put him outside. Then a week ago i found a small milipede about 1 cm also living in the soil. If i knock on the vase a couple of time i can get him to surface for a short time and then he returns back into the soil. I wonder how they got there and what they eat.

The millipedes came from outside - definitely not sterilized soil mix. Millipedes eat dead and decaying plant (and sometimes animal) matter - what gardeners call "humus". :-)

Okay, i see. So they do not harm the palm tree in any way? I was thinking of letting him stay there since i like having a small pet.

@Sova - lol! No, it won't harm the plant, unless it multiplies very fruitfully.

These are the worst ... so messy, and spread like wildfire in disturbed areas

@J.Musser - Worse than mile a minute weed? ;-) Or, heaven forbid, Japanese hops... Maybe 7 years ago, the first, single Japanese hops arreared on my property. I was intrigued, and did not kill it. BIG mistake. :-(

Mile a minute is worse.


text:
Best tail for swimming?
I understand that the vertical tails of fish and the horizontal flukes of cetaceans evolved due to the spinal movements of their ancestors but I was just wondering if there has been any investigation into which was the most efficient for swimming (speed, required effort etc...)?

What kind of swimming? Distance efficiency? Speed efficiency? Acceleration? Manueverability? Cheetahs and kangaroos both have extremely efficient legs, but they're extremely efficient at totally different things.

Why would the orientation matter in the first place? The effectiveness will depend on the body shape (other fins, streamlining) and more importantly, cetaceans went back to the oceans, so didn't have as much evolutionary space to develop tuna-like speed and endurance.

Swimming speed is subject to scaling – larger animals generally swim faster in terms of meters per second. One way to deal with this is to measure speed in body lengths. Scaled like this, speed tends to be proportional to tail beat amplitude and frequency. This seems to hold true across all body plans: http://wwwextra.inln.cnrs.fr/argentina/publications/2014NaturePhysics.pdf . One way to get at "efficiency" might be to look at the residuals of that relationship to see whether vertical-tailed or horizontal-tailed animals tend be above or below the general relationship.

If someone want to dg through the supplementary info for the article I posted above to find those residuals here it is: http://www.nature.com.ezproxy.umsl.edu/nphys/journal/v10/n10/extref/nphys3078-s1.pdf

For lift-to-drag ratio (so, hydrodynamic efficiency), high aspect ratio semi-lunate tails are most efficient-- leading edge suction is implicated in their ability to produce lift (which provides the thrust for high economy swimmers) while minimizing drag. Convergence of multiple animals (tunas, swordfishes, jacks, pomfrets, whales, ichthyosaurs, etc.) on that tail shape is considered indirect evidence of it's hydrodynamic benefit. So, for speed and energy economy, a tuna like tail, independent of orientation in the water.
NB: other aspects of morphology and physiology are also very important in predicting performance, and a semi-lunate tuna-like tail has often coevolved with these other traits.
More info:
http://rspb.royalsocietypublishing.org/content/280/1756/20122071.short
http://jeb.biologists.org/content/213/1/89.short
https://academic.oup.com/icb/article/24/1/107/104211/Body-Form-Locomotion-and-Foraging-in-Aquatic


text:
Is the size of the genome across species roughly the same?
Chromosome number differs across species.
Is the amount of DNA comparable between organisms, just being split into smaller chunks in those species with more chromosomes, or do species have different genome sizes? If so, does the genome size correlate roughly with the complexity of the species?

Please clarify your question. As it is written now, you ask multiple, very broad questions.

To briefly answer all four of your questions: no, no, yes, and kind of but not really. If you narrow it down a little more there are great answers to this question.

@Resonating - now, see why comments are bad as answers? I think I can make a good case for "yes, yes, yes, and not really".

There are exactly two questions: do different species have the same genome size and, if they don't, does size relate to complexity. This is pretty straightforward and can be well answered in a paragraph, which is hardly broad.

I guess you're right. I retracted my close vote and removed my comment.

I would call this a homework. It is quite well known that genome sizes are different between different species.  You may edit the question to add more details if you really wanted to ask something more than this. In general what you intend to ask should be clear in the question.

@anongoodnurse Comments are terrible as answers, that's why we have answers. I sometimes can't resist, though :( Too broad questions get too short answers. I'd like to read your case for your first yes though, if you'd like to drop it in chat for my edification?

I'm not voting to close but think it would benefit from a good edit

Chart of C-values (the mass of DNA in a single haploid cell); there is no logical order to the groups:

[source]
Base pairs in haploid genome (some examples):

Escherichia coli (bacterium): ~4.5 million
Caenorhabditis elegans (nematode worm): ~100 million
Homo sapiens (we all know what these are): ~3 billion
Pinus taeda (coniferous tree): ~22 billion
Prorocentrum micans (single-celled algae): ~245 billion

From these data we can conclude:

Different species do not have the same genome size.
Genome size is not correlated with complexity. Organismal complexity can be hard to define but, qualitatively, I think we can all agree that a human is more complex than a single-celled alga. And yet, humans have a genome that is 80 times smaller. This is known as the C-value paradox. Note, however, that this paradox has been resolved after it was found that the genomes of most eukaryotes contain a large proportion of non-coding and repetitive DNA.

Further reading:
The C-value paradox, junk DNA and ENCODE by Eddy SR
Eukaryotic Genome Complexity by Pray L

It is already mentioned by canadianer that genome size differs between organisms. But what about complexity?
First we should define what complexity is: complexity can be defined as number of different cell types that a multicellular organism can produce, with the same genome. Yes complexity does not correlate with genome size. However, it seems to correlate with number of genes. According to Kauffman, the number of cell types i.e. complexity is linearly correlated (direct correlation) with the square root of number of genes.

Though Kauffman says that complexity increases with DNA content, which is not actually true, it is certainly possible that that complexity is correlated with number of genes. The book is a little old and certainly molecular and cell biology has seen a lot of progress in this time. However, theoretically higher number of distinct genes should produce more complex phenotypes which Kauffman justifies using his NK-model. This assumption has again been disproved. The catch would be that exact duplicates/polyploid genes should not be counted as different genes. Moreover metabolic genes should also not be counted (plants/bacteria have a higher number of functional metabolic pathways). Organismal complexity arises because of the complexity of gene regulatory network which in-turn is dependent on the number of regulatory genes. NK model also in a way assumes regulatory genes (i.e. genes that can interact with each other). Surely complexity cannot arise out of nothing. I can't find the data for this at the moment but the theory is quite strongly plausible.
Another point I would like to add is that complexity need not only mean spatial complexity. Complexity can also be temporal.

 Reference:
    Stuart A Kauffman (1993) The Origins of Order, Chapter 12

That graph seems quite outdated. Man, for instance, doesn't have ~600,000 genes (or am I reading it wrong, I can't imagine an estimate that high in the 90s). Also, the selection of organisms isn't exactly inclusive. Plants are conspicuously absent. It would be interesting to see the comparison done with contemporary estimates and a broader range of species. From what I've read, complexity and number of genes don't correlate.

@canadianer I agree and I said that this is outdated. However, number of unique genes can theoretically (perhaps also in real) give rise to complexity. It is also intuitive that with increased functionality, you need a bigger repertoire of genes. The complexity of gene network also matters, though. I must also indicate that metabolic genes would not play a role and it is the regulatory genes that would matter. Complexity cannot just arise from nothing (if it has no connection with genome whatsoever). I'll add this to the answer.

I can show the facts here.
Human:
total length: about 3,000,000,000
coding genes: about 50,000 (included predicted ones)
3,000,000,000/50,000=60,000
Chromosome number: 23
Zebrafish:
total length: about 1,400,000,000
coding genes: about 36,000 (included predicted ones)
1,400,000,000/36,000=38,889
Chromosome number: 25
Fruitfly:
total length: about 1,400,000,000
coding genes: about 19,000 (included predicted ones)
1,400,000,000/19,000=73,684
Chromosome number: 4
Saccharomyces cerevisiae:
total length: about 12,000,000
coding genes: about 7,000 (included predicted ones)
12,000,000/7,000=1,714
Chromosome number: 16
http://useast.ensembl.org/Homo_sapiens/Info/Annotation
http://useast.ensembl.org/Danio_rerio/Info/Annotation
http://useast.ensembl.org/Drosophila_melanogaster/Info/Annotation
http://useast.ensembl.org/Saccharomyces_cerevisiae/Info/Annotation

and how do these numbers answer the question? The answer is in there, but it would be good to end with a concluding few sentences addressing the question.

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text:
LCMS/MS versus Western Blot
I have a general question regarding which method would you recommend me to use if I would like to investigate the difference in the level of several proteins in tissue samples and compare different treatment groups. I could either do an LCMS/MS or a Western blot. Which one would you recommend and would you do both for validation? I am looking for time- and cost-effective techniques.
I'll appreciate any suggestions.
Thanks!

How would you prep the tissue for LCMS/MS? That read out would totally look like garbage. There are all sorts of tricks for western blot that you could get an accurate measure. Personally, I would do ELISA to quantitate how much protein you actually have.

Which quantification do you need, absolute,  relative, or semi? Usually semi-quantification would be enough.

Related post

Western blot, though is a commonly used technique and is relatively simple to do, has some issues:

Low throughput: it is difficult to analyse multiple proteins simultaneously
Limited cross comparability: since antibodies to different proteins can have different affinities, they cannot be compared with each other.
Low sensitivity
Not very quantitative

LCMS addresses all the above limitations of western blot. It is also possible to do targeted proteomics i.e. study just some few proteins instead of the entire proteome.
An LCMS system has a high initial setting up cost but a relatively lower run cost. However, the mass spectrometer has to be maintained and it is not an easy job; you basically need a facility and a dedicated technical staff.

Which one would you recommend and would you do both for validation?

Which technique to use depends on what you really want to see and what resources you have at hand. It is a commonly practised approach to do a western blot for re-validating a few selected genes identified from LCMS experiment, which is just to prove that the result can be obtained using another technique too.

Although quantitative methods using MS have been developed, MS is not inherently quantitative. Quantification with MS could be quite tricky. Therefore, it is not the first choice. But, if you do not know which protein levels change and want to find proteins the expression levels of which are different between your samples you are going to compare, MS is not bad idea. In this case, validation is necessary. In other words, MS is not used to validate WB results in general.
In your case, you know which proteins you want to see. Therefore, I would suggest WB. This is a more direct way. Validation of WB may not be necessary, but it is better to get some supportive data: the protein activities in lysates, mRNA levels, etc.

MS=Mass Spectrometry; the name itself implies quantification. When you say it is not so quantitative, what are you comparing it with?

Peptides are ionized to determine the mass and ionization efficiency is not predictable. It would depend on peptide sequences and probably environments surrounding peptides. I think the word spectrometry in MS is used because you can see spectrum of molecular mass.

Ionization and fragmentation techniques are quite standardized. All quantification techniques suffer from some kind of bias. Western blot also suffers from biases.

Western blotting and mass spec each have their pros and cons. If you're doing a targeted analysis of a particular protein and have antibodies available (especially commercially available antibodies) I would suggest doing a Western blot. This is a much older technique and people are likely more comfortable with it. In my opinion, it's also much more comforting being able to compare relative densities on a blot visually than looking at mass spec output.

@VanceAlbaugh The only advantage of western blot is that it is easier to do and most people are comfortable with it. As you said, it is certainly cost-efficient and easy when only a few proteins are to be studied. However, even in this case cross comparisons are difficult. Antibody-protein interactions for different pairs are not comparable. It can be much more biased than fragmentation/ionization bias in MS.

@ WYSIWYG ionization efficiencies for fragmented peptides also vary very much. I though this makes cross comparisons difficult as well.

@WYSIWYG Although ionization techniques are standardized, comparison of two samples would be difficult when MS is performed in the same way but separately. Even if solution eluted at the same time from LC, ionization efficiency seems to vary. To improve this, mixing both sample to analyze them in same solution is designed. I'll write it in the next comment.

To improve this, mixing both sample to analyze them in same solution is designed. This ways, everything is the same exactly except for from which sample the peptides derived from. To recognize peptides from which sample, samples has to be labeled. Stable isotope labeling metabolically results in several molecular mass shift (or depend on which isotope and how many atoms)mass shift). This makes comparison more reliable. There are other ways to label, but they seem less quantitative.

What I am saying is that, despite all the possible problems you that mention, western blot is much more unreliable than MS. In MS ionization efficiency may vary but there are ways to detect multiply charged species (it also depends on ionization method and IMO only ESI has a high likelihood of producing multiply charged species). In western there is no way to compare two antibodies unless you make a standard curve (which I don't think anyone does).

@WYSIWYG (which I don't think anyone does)>It is because they do not think it is necessary. Because different proteins have different activities. Comparison of the actual amounts between different proteins is less informative unless you are studying stoichemistry of components in some protein complexes. Even if cell lysates has protein complexes and you want to see one of the components, cells may not form the complexes by some regulations.

@WYSIWYG (In MS ionization efficiency may vary but there are ways to detect multiply charged species> Ok, then here is my question. Then why scientists have to desperately develop quantification methods, utilizing stable isotopes etc.

Western blot is an old technique. MS has been relatively recently developed for proteomics so a lot of advancement is still going on. Stable isotope labelling helps in differentiating samples  quantified in the same run (test vs treated). At least I know this is so for SILAC and ITRAQ. I said standard curve is necessary for WB because there is no way you can compare two different antibody labels from the same blot. This is turning into a huge discussion and perhaps we should discuss this in chat.

Thanks for your answers. So I have access to both techniques, for LCMS there is a trained technician that could sort out any problems arising from the procedure. It is not clear yet whether it would be better to use one or the other, or necessarily both. I will need to detect changes in targeted proteins but also it would be nice to see changes in other unknown proteins. So with LCMS I could achieve this, but would it be necessary to confirm it with Western blot? Thanks!

Many people use LCMS for comprehensive, exhaustive  proteome analyses then assess the results with some other ways. Especially WB is popular for this assessment. Various steps are involved in MS data process because coverage of peptides is not 100%, some proteins share the same peptides, and modification disturbs peptide identification. I would say MS is not straightforward. WYSIWYG may know the way using only MS. You could also ask people in the facility you are going to use if the ability of the MS there could achieve satisfactory results to publish only MS.

If you are going to do bioinformatic analyses using whole data, you do not need to assess all proteins. But you might want to pick up several to show the MS is working well.

@Mary It is good to confirm the results using another technique and I guess there is no other technique that is more popular/easy-to-do than westerns. MS is data intensive and doing replicates would be time consuming. You can do multiple replicates in WB. So the general idea is: do LCMS → identify important proteins → Do WB for them.

@243 I am not disagreeing with you. MS analysis has problems and new algorithms are being developed for better reliability. What I am saying is that WB does not necessarily address the issues that MS has. The only advantage is that it is easy to do (sometimes that also can be problematic if you don't have the antibodies).

@Mary If you found your answer then please accept it. In general if you find a post useful then you can upvote it. (Check the buttons on the top left side  of the posts)

The best way is to use FPLC if you know what kind of protein you're looking for.in case you don't know what are you looking for,then you can run a 2D-PAGE and after analyzing spots then use LC MS/MS to identify your proteins and then continue with FPLC ( for record FPLC is a method of HPLC or LC which is protein friendly and even you can use it to isolate and purify your chosen protein )


text:
Does our heart stop when we sneeze?
Is it fact or myth that our heart stops beating for moments when we sneeze? If it is fact, what drives the heart to start beating again?

Both your linked fact from the University of Arkansas

When you sneeze, the intrathoracic pressure in your body momentarily increases. This will decrease the blood flow back to the heart. The heart compensates for this by changing its regular heart beat momentarily to adjust. However, the electrical activity of the heart does not stop during the sneeze.

...as well as your 'myth' from webMD

For instance, it's not true that your heart stops when you sneeze. When your chest contracts because of a sneeze, your blood flow is momentarily constricted as well. As a result, the rhythm of your heart may change, but it definitely doesn't stop.

...come to the same conclusion, namely the heart does not stop during a sneeze.

Isn't the length of a sneeze less than the time between resting heartbeats, at least for most healthy people?  So it seems odd to say that the heart would stop.


text:
What are dreams, biologically?
Falling asleep or states of subconsciousness does not stop the mind from making its own fictional images. These seem like sensations just like those received from human eyes. But, how do we define these visual sensations biologically?

Short answer
In terms of visual function, the low-tier primary visual cortex and high-tier frontal cortex are inactivated. The activity of the intermediate ventral stream and limbic regions are increased, apparently uncoupling low- and high-level vision processing from the system.
Background
The sleep stage where visualizations (dreaming) occur is called the rapid-eye movement (REM) sleep.
Brain imaging studies have shown pronounced effects of REM sleep on the functioning of the visual system.
In the awake state, the primary visual cortex (V1, or striate cortex) is activated, which is mainly concerned with low-level visual processing such as contrast perception. This cortical region in turn projects to higher-level (extrastriate) regions for more complex processing of visual information.
During REM sleep, however, a selective activation of extrastriate visual cortices is observed. Particularly the ventral processing stream is activated, which is associated with perception and recognition in the awake state (Deubel et al., 1998). Also the limbic and paralimbic regions are active (the emotional brain centers).
Interestingly, activity in the primary visual cortex (V1) is attenuated, as well as the frontal association areas of the brain. V1 is the primary, most 'primitive' visual cortex, while the frontal association areas are the highest-tier cortex that integrates complex perceptual information across perceptual modalities (Braun et al., 1998).
Overall, this pattern suggests a model of REM sleep where visual association cortices and their paralimbic projections may operate as a closed system dissociated from the regions at either end of the visual hierarchy that mediate interactions with the external world (Braun et al., 1998).
References
- Braun et al., Science (1998); 279: 91-5
- Deubel et al., Vis Cognition (1998); 5(1/2), 81–107

I need to learn some patience from you. Quite an informative answer for a broad question +1 :)


text:
What does it mean to "map the human genome"
I know some elementary chemistry and biology. I also think I know what a gene is (it's a sequence of DNA which encodes a particular protein). I also know that on a chromosome there are sections of DNA which are kind of junk and do nothing. But being armed with this information, doesn't seem enough for me to understand what it means to "map the human genome".
Some possibilities:

a. It tells me the entire sequences of nucleotides that make up a particular human's chromosomes (it could not possibly do this for humans in general because of course the sequence is different from one human to another).
b. It tells me the entire sequences of nucleotides that make up a human's chromosomes... with some annotations along the lines of "at this point in the molecule, we could optionally have nucleotides A, B or C".
It tells me the start and stop points for each of the genes along the chromosome.
It tells me the function of every gene.
Something completely different!

Suggested edit changing molecules/atoms to nucleotides for accuracy/clarity, DNA is composed of nucleotides, a very specific subset of molecules which are composed of atoms. Molecules are composed of bonded atoms, atomic structure is not of particular interest, but would be inferred from the nucleotide sequence (and could vary for a given Dna sequence depending on pH and DNA modifications).

"Mapping" the genome is ambiguous. Originally it meant making a genetic map, which involved finding the ordering of various genetic markers but not the sequence of nucleotides. Mostly these days people are interested in a genome sequence which is seldom described as "mapping" by researchers.

So, the very first map of the human genome was of a few pooled samples with a single nucleotide called at each position.
This is basically okay, though, because humans are 99.9 (with possibly a few more 9s) % similar to one another. So you can get a lot of broadly-applicable information out of a single individual's DNA.
Further genome-mapping efforts brought data from new individuals and started to give us information about variants, like in your option 1b. At this point, there are projects like the 1000 Genomes Project that are trying to get 1000 full human genomes from a variety of ethnic groups sequenced and to characterize all the common variations.
Your point 2 was a different project, but was also part of mapping the genome. It's mostly complete now-- in that we know almost all of the RNA sequences that are produced by most cell types and mostly where they come from on the genome, with a few mysteries left around the edges.
Point 3-- no. Lots about the genome we still don't know. We're pretty good about where genes are encoded, but how they're regulated, how they interact... and remember that the part of the genome that codes for genes is a very small percentage of the overall sequence. Something like the the ENCODE Project is trying to figure out the various biochemical interactions present at every position of DNA, but even if that data were complete and reliable, which it's not, it still wouldn't tell us the "purpose" of all DNA.
So, when we say we've "mapped" a genome, we generally mean (A) we have (something pretty close to) full sequence of at least one individual's DNA (or a consensus sequence from a pool) and (B) we know where genes are on it. That's a huge step but only the beginning of understanding genetics. In the case of humans, we're adding on to that understanding by learning where variants are and how common they are.

As this answer suggests, mapping the location of known genes to their location in the genomic sequence is a specific (but important) example of genome mapping. More generally, mapping is identifying the location or locations of a sequence or sequences of interest in the genome. This can be genes, transcription factor binding sites, mapping variations in sequences associated with different human populations or with certain diseases, etc.

The sequence from the International Human Genome Sequencing Consortium was actually a mosaic of DNA different donors, not one individual.

Good point, I'll edit. I was thinking of the Celera DNA, which I thought was Venter's, but it turns out that they were using a pool, too. (Venter was just in the pool.)

The Celera genome is indeed mostly from Craig Venter, but this is not true for the HUGO project and today there is more data in it anyways.

InactionPotential raises a very important point. Mapping does not necessarily involve sequencing. There were maps of the human genome long before it was sequenced. There were also maps of other organisms long before sequencing was even invented. Like geographic mapping, genome mapping establishes spatial relationships between "interesting" loci.


text:
What happens in lasik operation?
First of all,I am very bad at biology. So please bear if it sounds elementary.
I heard about lasik operation for reshaping cornea.
Assume the patient is suffering from myopia implying lens is thicker than expected.So if i think logically ,to correct the lens thickness ,lens must be reduced.
In lasik, do they cut the lens's tissue.If yes what happens to the part that is cut and if no then how exactly lens thickness is reduced?

There are two possible ways to perform refractive operation: first,  to perform the procedure on the cornea, the second - to exchange the crystalline lens with the artificial one.
The second approach is extremely rare, because the lens (1) is inside the eye and (2) it allows us to accommodate (=change the focus of vision). Thus, this method is relevant only to extremely high myops and people who have some degree of cataract (the clouding of the lens).
In "classic" myopia the eye is larger than "normal" one, and the lens thickness is less relevant in the terms of treatment.
Back to LASIK - the operation is performed on the cornea: for myopic eye the corneal thickness should be reduced, for hyperopic eye there are other protocols (special thickness reduction).


text:
What biological processes can affect the temperature of the shadow a tree casts?
Assuming two trees have similar shape and leaf coverage, could differences in the biological processes among them lead to differences in the temperature of the shadow they cast?
What biological processes occurring in plants could affect this? I was thinking that transpiration will cause heat loss, and photosynthesis also absorbs energy, so these would contribute. What other processes that occur in a tree could affect the dissipation of heat causing cooler shade?
Has there been any studies specific to rates of transpiration and photosynthesis, and the effect on shade temperature?

please specify what you mean by quality of shade. also, probably, number of leaves in $m^3$ is not good enough: something like total surface of leaves in $m^3$ should be more useful

By quality of shade, do you mean something like $ΔT = T_{unshaded} - T_{shaded}$, the difference in temperature between a shaded and unshaded area?

From personal experience (I don't know that anyone has actually studied this), much depends on the air, not on the tree itself.  In humid lowland climes, shade may not be all that much cooler.  In a dry, high-altitude clime (like the Sierra Nevada, where I live), you can be hot in the sun, but want to put on a sweater when you move into the shade.

Density of leaves, humidity, general temperature, time of day/sun angle... various differences in human experience

@Luigi Yes, that is what I meant. Thanks for the tip. Will edit question to reflect it.

This is more or less a physics/general mathematics question. There may be some effect of transpiration but I think that would be small.

@WYSIWYG I thought transpiration has a major role in regulating temperature around trees

@rg255 thanks for the help. I have cleaned up the comment made by me

I don't think anyone has cared about this question in the literature sorry to say. It's kind of trivial. What may have drawn attention in the literature is why cities are always a few degrees warmer than non-urban areas.

Depending on the purpose of your question, you might get more practical answers by looking in gardening/landscaping sites.

The short answer is NO. A shadow is strictly due to the blocking of sunlight, so the shadow of 2 equally non-transparent (i.e., same density of leaves, both have similar trunk diameter, etc.) trees on the same hillside in the same weather conditions would not have different temperature shadows.
A plant's metabolism can and will affect the temperature surrounding the tree, but this affect is lost almost immediately as you move away from a tree. For example, in a study I did a few years ago measuring spruce tree temperatures (unpublished), we found that even within 5-10cm from the tree, the rise in ambient temperature was no longer measurable.
You're correct that the leaves of plants will absorb sunlight and as a result will increase in temperature. Walter Loomis's (1965) paper, Absorption of radiant energy by leaves (found here), suggests that leaf temperatures can raise to 30 $^\circ$C or more. However, he notes that their study found that even wind speeds of 5mph instantly cooled the leaves via conductive heat transfer. Our study with spruce trees also found this to be true. Transpiration will further help the tree rid itself of that increased temperature fairly quickly. Regardless of these facts, radiant energy from leaves in the canopy will not be felt how-ever many meters below within its shadow.
Finally, yes, transpiration can affect local climate, but this is only on the scale of whole forests. The transpiration of a single tree will likely not impact the ambient temperature around itself in any measurable way, especially at any distance greater than that I've already mentioned.

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


text:
Altruism in viscous (asexual) populations
The viscosity of a population is the tendency of offspring to remain
near their place of birth. Taylor 1992 ("Altruism in viscous populations") provides a model to study how viscosity affects the evolution of altruism in a patch-structured population. In Taylor's model, the marginal inclusive fitness is given by
\begin{equation}
  W = bR -c - s^{2}(b-c)R
\end{equation}
where $R$ is the relatedness of a mother to random offspring born on her breeding patch and $s$ is the probability the offspring will remain on the natal patch. The altruistic act creates $b$ offspring with average relatedness $R$ and $-c$ offspring with relatedness 1.
My question is about the term $s^{2}(b-c)R$. Taylor explains this term as follows:

these b - c extra offspring remain on the natal patch with probability
  s and will therefore displace s(b - c) random individuals competing
  for the next generation breeding spots on that patch, and these will
  be native to that patch with probability s and in this case will have
  average relatedness R to the actor. Thus these displaced individuals
  will have average relatedness sR (p. 353)

My question is: Why is the average relatedness $sR$ (as opposed to $R$)? In other words, why is the term that accounts for competition among relatives $s^2(b-c)R$---as opposed to $s(b-c)R$?

The $sR$ that your looking at is the average relatedness of the next generation.  This assumes that the new immigrants into the the population are completely unrelated. So if the population is completely viscous ($s=1$) the average relatedness of the next generation equals that of the current generation.  On the other hand, if the population is not viscous ($s=0$) the next generation would be entirely unrelated because it would only be made up of unrelated immigrants.
The $s(b-c)$ is the number if individuals that are displaced by new offspring.  Again if all of the new generation sticks around ($s=1$) then the number of displaced individuals equals the number of new individuals.  And if all new progeny leave ($s=0$), there are no displaced individuals.

Thanks for your answer @Adam C. Now I understand that the relatedness after migration has to be a fraction of $R$. But why $sR$ exactly and not, say, $s^2R$ or any other fraction of $R$?

It is specifically $s$ and not some fraction or multiple of $s$ because the model assumes all incoming migrants are entirely unrelated ($R=0$).
For example, if $s=0.5$ and $R=1$, half of the population leaves and is replaced by incoming migrants in the next generation and all that remain are perfectly related.  So, in the following generation, 50% of population has an average relatedness of $R=1$ (those that stayed) and 50% of population has an average relatedness of $R=0$ (those that just arrived). Therefore the average relatedness for the entire population is $sR$ or $0.5$.


text:
Is there a name for this phenomenon described in "Phylogenies and the Comparative Method"?
The figures below are from Felsenstein's paper "Phylogenies and the Comparative Method". I was wondering if there was a specific name for this effect where there is an apparant correlation that is actually the result of the data being structured into two separate groups, where there is no correlation within groups but an apparent correlation between groups. "Phylogenetic non-independence" doesn't seem specific enough.

Is this similar to Simpson's Paradox?

@Oreotrephes Not really, I'm wondering if there is a term for this specific phylogenetic effect

@kmm "Phylogenetic pseudoreplication" is exactly what I was looking for, I just couldn't remember the name of the term. Thanks!

what is X and what is Y? I mean what is plotted against what in the figures? (and no, the answer won't be coming from me ;-)

@AliceD The axes are arbitrary. X and Y don't matter, nor do their units. The point is to show that the apparent moderate positive correlation between X and Y in the upper figure masks underlying structure. When you separate by 2 monophyletic clades (boxes and Xs), there is clear separation and within groups there isn't any correlation.

I've seen this termed "phylogenetic pseudoreplication", but I can't remember offhand where. I'll see if I can find it. Without a tree, the boxes and Xs essentially represent 2 data points. As Remi.b suggests, this is really just high phylogenetic signal.

http://www.biology.ucr.edu/people/faculty/Garland/Phylogenetic_Pseudoreplication.jpg and Garland. 2001. Phylogenetic comparison and artificial selection. Two approaches in evolutionary physiology. I think I've seen it somewhere else as well though.

The fact that species are not independent observations because of their specific phylogenetic relationship is sometimes called phylogenetic dependence (see its use in this paper for example).
Most often though, we talk about the existence of such phylogenetic dependence for a particular trait and we talk about phylogenetic signal for this trait.
I think (correct me if I am wrong) you're searching for a name to describe a situation where two quantitative traits correlate along a phylogeny (when you have one data point per species) but not within any of the species of this phylogeny. If this is the case, I don't think you will actually find a name for this pattern as it it is already quite specific. You could eventually say that there is an inter-species correlation between the two traits but not an intra-species correlation.

Thanks for the response. I'm looking for a term to describe what happens when there appears to be a correlation between two traits when you just look at the extant species, but actually the correlation is a result of having two separate clades, neither of which has a correlation within the clade. "Phylogenetic signal" doesn't really describe this, but it could be that there actually isn't a term for what I'm describing, in which case phylogenetic dependence is probably as close as I'm going to get.

I think I got your question. See edit (which won't be super useful unfortunately).

I think that the answers here are good, and @Remi.b's term is preferable, but the term in the literature appears to most frequently be "phylogenetic non-independence", e.g. here.
I don't care for this term. Why not just "dependence"? But it seems to be what folks use.


text:
Is there an advantage to antibacterial soap?
There are plenty of different hand soaps out there, as well as hand sanitizers. Is there an advantage to soaps that claim that they're antibacterial vs soaps that just say soap?
In particular I'm looking at Softsoap who offers normal soap and antibacterial soap.
Examples:
Normal:

Antibacterial:

Short answer: There is no benefit for their use in households.
Long answer: These soaps (see here for the complete list) contain the so called quaternary ammonium compounds Benzalkonium chloride and Cetrimonium chloride which indeed have antimicrobial properties.
While they do not promote resistance to these compounds (see reference 1), their use is still not recommended, as their permanent use might dry out the skin, can cause contact allergies and the products released into the environment are also problematic.
There are two studies, which compared the use of normal soap (which has some antibacterial properties on its own) to antibacterial soaps in household environments and found no differences. See article linked in reference 2 for a summary and references 3 and 4 for details on the studies.
This doesn't mean that antibacterial soaps are useless at all, they simply make no sense in households. For hospitals or doctors they are an important tool to protect their patients before operations. But here detailed instructions for how long and how the hands have to be washed are provided. Hand washing is also followed by another disinfection step, which helps with efficiency. But this is very much different from the way people wash their hands at home. See reference 5 for some opinions here.
References:

Use of germicides in the home and the healthcare setting: is there a
relationship between germicide use and antibiotic resistance?
Plain soap as effective as antibacterial but without the risk
Consumer antibacterial soaps: effective or just risky?
Effect of antibacterial home cleaning and handwashing products on
infectious disease symptoms: a randomized, double-blind trial.
The Burning Question: Is It Safe to Use Antibacterial Soap?

Thanks for the link, updated my answer to discuss other members of the Softsoap antibacterial series.

If there is no difference between the normal soap and "antibacterial" ones, what benefits do hospitals get by using it?

@zaftcoAgeiha They make no sense in households. I clarified the answer. The thing is different in hospitals with people which have systematically learned how to disinfect their hands.

Chris has correctly identified the antibacterial agent in the hand soap depicted in the image in the question, and therefore his answer is superior as a direct answer.
Nevertheless, other members of the Softsoap series of hand soap uses triclosan, 0.15% as their antibacterial agent, as seen in an image of their ingredient list on the reverse of the bottle.
(click for enlarged image)

Triclosan has been shown to be effective by Webster et al (1992) in reducing the incidence of MRSA infection as well as being milder to the skin as compared to chlorhexidine gluconate in a neonatal ward.

The average number of new cases of MRSA per week was reduced from 3·4 to 0·14 (P < 0·0001) in the experimental ward whilst no significant changes occurred in the control ward.

Triclosan has also been shown by Jones et al (2000) to be effective on a large variety of different bacterial, viral and fungal strains.

Therefore, the usage of triclosan is effective as an antibacterial agent, and would likely result in less bacteria on the hands after washing.

The depicted softsoap product do not contain triclosan but beanzalkonium chloride. See here (you have to scroll down).

@Chris but most antibacterial soaps, these days contain triclosan. Tertiary ammonium salts are a bit harsh.

@WYSIWYG Still they are used in some products.

I'd note that less bacteria on your hands is not necessarily a good thing. The natural microbiome on your hands has noticeable protective effects.

@Jack Aidley Although your comment cannot answer the question, I think it's the best viewpoint that we can have with repect to the matter.

Using triclosane is a very bad idea. Microbes become resistant to it, and there is cross-resistance between triclosane and some antibiotics e.g. chloramphenicol and tetracycline. Here is a summary in the topic: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4295542/ Afaik. most MRSA is already resistant to it and they grow much better with triclosane, because the antibiotics kills competing species. So I think your answer and your references are outdated, a lot of things happened in the last decades...

The sources you cite show triclosan has antibacterial properties.  But this implies neither that it is effective in the context of domestic liquid soap, nor that using hand soap with triclosan confers an actual health advantage.

@augurar At no point did I say that it is effective as hand soap nor that it confers a health advantage, just that it would likely result in there being less bacteria, ceteris paribus, due to the bacteriocidal action.

You may be interested to look into the Old friends hypothesis, since this is related to how the human immune system may respond to reduced biodiversity in the microbiota. The basic idea is that the human immune system is developed by exposture to the microbiota, and without exposture to organisms from our evolutionary past, immune system regulation might fail. This can then lead to poorly regulated inflammatory responses and
maybe allergies or other chronic inflammatory diseases. Since the exposture to our evolutionary Old friends is lower in developed countries and urban areas, this hypothesis might potentially (partially) explain the increased prevalence of allergies in developed countries. Even though it is somewhat tangential to your question, and does not directly answer the question of the pros and cons of antibacterial soap, it should still be relevant for a more general case.
Two good starting points are Rook (2013) and Hanski et al (2012). Rook (2013) is a general overview of the theory with many good references to empirical studies that relate to the hypothesis, by one of the main proponents of the theory. Hanski et al (2012) is an interesting epidemiological paper, where they relate the allergic disposition of individuals to both the general biodiversity in their larger living environment as well as the generic diversity of their skin microbiota. In the paper, they find a positive relationship in healthy individuals between immune responses and the abundance of the gammaproteobacterial genus Acinetobacter on the skin, but they do not find the same pattern in atopic individuals. The study also finds a negative relationship between the environmental biodiversity close to the homes of study subjects and the frequency of atopy (so high biodiversity -> lower levels of atopy).
To be clear, this is still a hypothesis that needs further testing and support. However, there are many interesting case studies that can lend support to it, and indicate plausible mechanisms.
References:

Rook. 2013. Regulation of the immune system by biodiversity from the natural environment: An ecosystem service essential to health. PNAS 110(46)
Hanski et al. 2012. Environmental biodiversity, human microbiota, and allergy are interrelated. PNAS 109(21)
Rook. 2013. Microbial ‘Old Friends’, immunoregulation and stress resilience. Evolution, Medicine, and Public Health
2013(1)

Related - https://en.wikipedia.org/wiki/Hygiene_hypothesis

Probably, it is worth to add some historic (and ironic) "perspective" to this question. It will probably explain that even without scientific research the answer to this question is probably "no" and that real use of bacterial soap should probably be reduced to hospital settings and not expanded to households as suggest promotions and commercials.
The historic perspective I wanted to add relates to the book "The Hermit in the Garden" by Gordon Campbell. Here live hermits are described (there were non-alive as well, this is why I call these "live"). Campbell cites another book -  "Sir William Gell's A Tour in the Lakes Made in 1797":
"the hermit is never to leave the place, or hold conversation with anyone for seven years during which he is neither to wash himself or cleanse himself in any way whatever, but is to let his hair and nails both on hands and feet, grow as long as nature will permit them."
From this "work" description we can speculate that "dangerous" infections were not expected during such a long period of soapless live. This is why we could assume that any soap is probably of limited "antibacterial" value for otherwise healthy person.
(Remark: This "exclamation" not trying to answer the question in a scientific way, but just to add some "color" to the question and the answers posted. I hope, it is worth to place it here instead of a comment).

Remember though, that they are living in isolation, they won't come in contact with as many bacteria or viruses as the general population. It's not like they will come in contact with sick people if they are living more or less in isolation. Besides, what viruses and bacteria are there they will adapt to especially if they are healthy individuals. However, I do appreciate the insite.

@SolarLunix They lived in gardens, their isolation from sick people were not absolute and contact with all the mosquitoes, flies, worms, dogs etc had to increase the exposure to multiple pathogens. I suppose it is interesting point to start with.

Human immune defense response is primed by cell damage products as it does not have prior knowledge about bacterial or viral "malware".
The whole purpose of disinfectant substances is damaging cells and potential organic disease carriers.  As those substances are not discriminating, frequent use of them will prime your immune defense against benign organic matter as well.  In combination with solvents that remove protective layers of fat and thus increase the permeation of this kind of cell waste into top skin layers, this sounds like a recipe for allergies and neurodermitic reactions in the long run.
There is a high correlation of countries (and eras) with high standards of living including household hygiene and autoimmune response problems.  Finding actual causations is work in progress.
While that is still the case, it is my gut feeling that contact with disinfectants should be reserved to cases of tangible risk.

Interesting answer. Can you please add some references to it?

Apart from references, I found your answer a little hard to read, could you please try to add a summery such as "Antibacterial soap doesn't help because..." ?

This is an interesting answer, but this kind of stuff will get you a lot of downvotes. The thing to remember about this site (and it is aggravating, and not very well stated) is that "it is not a forum." Answers are supposed to be very definite with reasons spelled out in detail, and supposition and comments about the question are suppoosed to go in the short comments.

That being said, I was unable to find any studies showing that Benzalkonium chloride caused over-sensitivity of the immune system to benign agents. I think you have generally the right idea, but most of your facts seem to be unfounded theories(?). Like others said, these things need references or clear statements that they're guesswork (in which case they're probably inappropriate for empirical discussions like this).


text:
What is the transmembrane 'Positive-Inside Rule' nowadays? Has the definition changed over time?
First definition.
Two publications by von Heijne in 1989 and 1992 coined the 'Positive-Inside rule' and showed it's practical value in topology prediction of transmembrane helices. It was clearly defined and evidenced that in bacteria the positively charged residues more commonly were found on the "inside" of a membrane (the cytoplasm rather than the periplasm).
Recent Literature.
However it seems the field has moved away from the idea of "inside the compartment" to "inside the cytoplasm" as more data became available. In a 2006 review even von Heijne describes some transmembrane helices as abiding to the positive inside rule because their positively charged residues were inside the cytoplasm, although never explicitly backtracks on the original definition. A similar review in 2007 by von Heijne offers a more definitive refinement of the rule, however removes the concept from being applicable to subcellular membranes.

...the loops connecting the helices differ in amino acid composition, depending on whether they face the inside or outside of the cell (the “positive-inside” rule).

We are now faced with an awkward rule that doesn't account for proteins elsewhere in the secretory pathway or in the other organelles. All those proteins are inside the cell.
More recently still large-scale analysis of transmembrane helices from different biological membrane surfaces, Sharpe et al., 2010 and Baeza-Delgado et al., 2013, show the clustering of positive charge being cytosolic rather than discussing it in terms of the inside of the compartment. Both of these papers still say that they corroborate with the positive inside rule.
Question.
To me it seems that the definition is somewhat sloppy and can broadly be used to say "inside the cytoplasm", despite publications being reluctant to define the rule clearly. Has the definition ever explicitly been changed, or has the field silently changed what "inside" means? ... Or have I completely misinterpreted something? How do the organelles fit into any of these definitions?

I think you have misunderstood the "inside" part of the "positive-inside rule". Perhaps because "inside" is indeed an imprecise term (but now it is history and cannot be changed ;) ). In order to understand it a bit better it helps to think about the topology of the membrane. During synthesis most membrane proteins (ignoring peroxisomal and mitochondrial proteins, which are a whole other topic) are inserted into the ER membrane by the Sec translocon. The parts of the membrane protein that are exposed to the lumen are matured by the ER and Golgi apparatus to be presented on the extracellular surface. Secretory proteins (those that will ultimately be exported from the cell) are made in similar way except they pass entirely through the translocon and end up in the ER lumen. Therefore, the lumen of the ER (and consequently the lumen of other endomembrane compartments) are topologically consistent with the extracellular space, "outside", and not the "inside" of the cell. Perhaps is is easiest to see in a picture (borrowed from here: http://www.bioon.com/book/biology/mboc/chapter12/figure12-4.gif)
Coloured in pink are compartments whose topology is consistent with the "outside" and coloured grey are compartments whose topology is consistent with the "inside". So, for membrane proteins found in the endosome, for example, amino acid residues in the lumen are actually "outside" not "inside". It is true that this may not be immediately clear to those not steeped deeply in the field. As the initial studies used bacteria, which do not have membrane-enclosed subcellular compartments, "inside" was simple and made sense. Perhaps "positive-in-the-cytoplasm rule" would have been more accurate. Hope this helps!


text:
Plant identification in Turkey
What species is this ? It is a stinky, hairy plant. I have found it nearby a river. It had reached a height of 1 meter. Bloomed three weeks ago. Found in Turkey.

I included the correct picture. @Oğuz İsmayil uysal - links to a webpage will not work. You should post the factual images.

Looks like a Hyoscyamus niger also called stinking nightshade.

I knew I knew it! I thought Chelidonium https://en.wikipedia.org/wiki/Chelidonium but that wasn't it! Thanks! +1


text:
Identify this caterpillar

Could anyone try to help identify this caterpillar, there are loads of them all over my garden and I've got three of them in a makeshift caterpillar house. I've had them for about a week and they've grown to about 3 or 4 centimetres in length and I am yet to see any of them form pupae. I am from London by the way.
EDIT: they don't seem to be too fussy about what they eat, I have found them on honeysuckle, rose bushes and even some nibbling on the bind weed I've pulled recently.

@rg255 thanks, once I am home I will take some closer pictures, I believe there were a lot on my honeysuckle but I will give a full list later.

@rg255 I have added new, closer images and a brief description of the plants I've found them on. Two of the ones I have been looking after have seemed to now be staying close to the dirt level I've put in the tank (possibly going to cocoon under ground or in the floor???).

Actually, the animal is not a caterpillar but larva.
The species is Abia lonicerae Sawfly, discovered by Linnaeus 1758.
(Another picture)

Is the sawfly considered a pest? Should I worried about the massive population of them in my garden?

Thanks for the response, that explains why I couldn't find them anywhere on the Internet by searching for caterpillars!

Are you sure that it's that particular species (if so, what characters are you using?), or could it be a related species (Abia sp.)? +1

@fileunderwater I am, actually... the images are related to specific species from the answer.

How do you distinguish it from other species in Abia?

@user16370 With regards to pest status, the larvae will eat the plants in your garden, potentially causing damage.  The adults are relatively harmless.

Larvae of this species do feed on honeysuckle (Lonicera) foliage


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Recommendations for an intro level virology textbook?
I'm a college sophomore, and I was just accepted into a research lab that works with retroviruses. Since I haven't taken any classes on the topic yet, does anyone have recommendations for good, intro-level virology textbooks I could work through to learn some background information?

You can ask the head of the lab or your supervisor, they might have targeted ideas for your research.

Have you taken any molecular biology or biochemistry? They seem like a prereq to virology.

Have a look at the tag wiki on [tag:book-recommendation]. You should provide more details in your question, otherwise it seems broad and tends to generate opinion-based answers.

http://as.wiley.com/WileyCDA/WileyTitle/productCd-EHEP001462.html This book is good enough to guide through the course.

Understanding Viruses, 2nd ED by Shors is the current recommended text at my university for the undergraduate virology course. If you're interested in the area, as suggested in the comments, I'd recommend some reading in cell and molecular biology to really get a sense of the host dynamics. Alberts' Molecular Biology of the Cell, and Watson's Molecular Biology of the Gene are standard core texts. Really, though, the only prereq to our virology course is the upper-level microbiology course.


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Michaelis-Menten equation type - how it is derived?
Can somebody explain how is the following differential equation found? It is about the blood alcohol content.
See this article (pages 3 and 4).
They say the concentration of blood alcohol satisfies (in the drinking phase): $$\dfrac{dC}{dt}=u-\dfrac{\alpha C}{C+\beta}\quad; \quad C(0)=0,$$ where $\alpha, \beta$ are the liver and the kidney parameters. For the Recovery Phase we have: $$\dfrac{dC}{dt}=-\dfrac{\alpha C}{C+\beta}\quad; \quad C=C_{max}.$$
I can't see how they came to these equations. The only thing they say about the origin of this model is that it comes from a continuity argument: the amount of alcohol that is introduced in the body, equals the amount of the alcohol that leave the body.
I wonder if there is a model which takes into account all parameters in the above article plus the amount of food in the stomach.

Are you asking about how the Michaelis-Menten equation is derived or why it was deemed appropriate to model blood alchohol levels? The former is off-topic to BioSE since the Michaelis-Menten equation is used in many fields of science, and its derivation belongs to mathematics (maybe suitable for MathSE).

@fileunderwater really? I always assumed the MM equation was closely related to biochemistry (enzyme-substrate interactions). I was unaware of any other application of the MM equation ?

Given that the two individuals it is named after were noted biochemists Michaelis-Menten, it is difficult to imagine any other SE that would be more relevant than Biology.

Based on the appearance of your source I would caution you about taking it too seriously. I does not seem to be published in a peer-reviewed journal and is just a manuscript (for example the first reference is to another unpublished URL and the second reference does not contain enough information to allow one to find it).

@RoverEye Same thing, different names: the Monod equation is used to model bacterial growth and the Holling disc equation is used to model the functional response of consumers/predators. There are other examples as well. I've seen the Michaelis-Menten equation being used/mentioned many times as a general modelling tool/functional shape.

Microbial growth, Prey-predator ecology, and enzyme-substrate kinetics in protein chemistry, yet you posit that it is off-topic for Biology SE? A better reason might be that there is no mention of any of these versions of the equation in the source our OP cites.

@RoverEye These kind of equations denote saturation kinetics and they are not just applicable for enzyme-substrate reactions but to other kinds of biochemical reactions too. Examples include transcription regulation, ligand-receptor interaction etc.

@mdperry I think that the question is unclear and/or off-topic, given what the OP is actually asking for ("... explain how is the following differential equation found?", "...how it is derived?"), but whether the Q should be closed is up to the community. No close votes have been cast so far, and it is up to the OP to clarify what he/she is actually asking for.

These kind of equations (the Michaelis-Menten [MM] like term) denote  saturation kinetics. The basic mechanistic assumption behind saturation kinetics is this:
A rate (of lets say product formation) is dependent on the concentration of a molecule such that the rate increases linearly with increase in the concentration of the molecule.

Example 1: Substrate in an enzyme catalysed reaction
Example 2: Transcription factor in a transcriptional activation

However at a certain point increasing the concentration of the molecule will have no effect on the rate of reaction. For the above examples this point will arrive when (respectively):

Active sites in all the enzyme molecules are bound and there is no more space to accommodate a new substrate molecule.
All the binding sites in the DNA are occupied by the existing TF molecules and no more can bind.

In other words, the reaction kinetics changes from first order to zeroth order.
We can provide mechanistic explanations for some cases but in many we do not know how exactly the saturation happens. In modelling we just use a function that will mimic this kind of behaviour.

Why functions of the form $\dfrac{X}{K+X}$ ?

In deterministic modelling using differential equations, it would be preferred to use a continuous function (instead of using a piecewise linear function) because:

Numerical integration is better in case of continuous functions
In biochemical systems, operations are always continuous. There is no digital logic.

The MM function can actually be derived using an equilibrium or a quasi-steady state approximation (See the wikipedia page for the explanation).
In the MM function, when $X \gg K$ then the function is almost 1. This multiplied by the maximum rate constant will give you the max catalytic rate. At $X=0$ the rate will also be equal to zero. Note that in this model the catalytic rate will not indefinitely increase with $X$.
There are several functions that have values between 0 and 1 for increasing concentration of the substrate. Hill function and logistic function are common examples. However MM is a simpler model. You can always revise your modelling approach when you have better information of the biological system.
Now back to your question:
In this model $C$ denotes alcohol concentration $\alpha$ denotes maximum clearance rate and $\beta$ denotes half saturation concentration (concentration of alcohol at which the rate of clearance is half the maximum rate). Intuitively you can think about the mechanism like this: rate of clearance of alcohol depends on the level of alcohol i.e. if you have a lot of alcohol the amount of it removed per unit time will be higher. Think of it as water that is pumped through a pipe; more water in the tank will result in higher flow rate. However when the kidney (or pipe) is overloaded or "clogged" with an already excess of alcohol then clearance rate would remain the same (the maximum that the kidneys can excrete).

the amount of alcohol that is introduced in the body, equals the amount of the alcohol that leave the body

That is called mass balance which can be summarized as follows:
Accumulation = Input + Production - (Output + Degradation)

Note that MM kinetics is outdated, currently the unified enzymatic activity modulation equation is the best approach. http://biology.stackexchange.com/a/23561/3703

@inf3rno No it is not outdated. No model is outdated unless it is proven universally incorrect. Your choice of model depends on what you are trying to ask. You can always plug in more parameters to make it precise but the question is what level of precision do you want.

These equations are working, not doubt, but they are the bad approach. Ofc. we can talk about what "outdated" means in your dictionary and in mine, but I think that would be off-topic here.

@inf3rno I have had a huge debate about this elsewhere. A bad approach is, IMO, one where one does not select the method that is suitable for an approach, rationally. Quantum mechanics answers questions that classical mechanics does not. Moreover quantum laws are applicable for macroscopic systems as well- that does not mean that you should study the mileage of your car using quantum mechanics.

I think you got the wrong analogy here. Both the unified and the MM model describe enzyme kinetics on the same level, while classical mechanics and quantum mechanics are very far from each other.

@inf3rno The post that you link to, seems unclear in this context. Also, I am not sure what you are trying to indicate here. Either the link is insufficient or the argument is not valid in this case. There are no inhibitors here. Why should you consider them?

Right my mistake, I only skimmed the text.


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What's read depth in VCF?
There is an attribute defined as DP (Total Depth) in VCF file format. For example, http://www.1000genomes.org/node/101.
What does this attribute mean? If I get a value of like DP=128. How can be that be interpreted?

So the general sequencing analysis pipeline is to generate a bunch of read sequences, figure out how they match to a reference genome and align them, then call any differences between the reference genome and the sequencing reads. The following image, from the Broad Institute's Interactive Genome Viewer, may help you visualize what is happening here. As you can see in the image, the human reference DNA is found at the top of the window, and the sequence of bases for the current selection, at the very bottom of the window. Then each of the gray bars that you see below that is an individual sequencing read that matches to that particular location along the human DNA.

When you use a variant caller like Freebayes, it will list out information about locations along the reference genome that had differences in your actual sequences. For instance, as you bring up, DP or read depth. Looking back at the IGV image, you can see a location that had a lot of 'G' showing in the sequence reads, where the reference DNA has 'A'. Variant callers will pick up on this and list it as a possible variant. They will also tell you the read depth at that location which is the total number of sequence reads overlapping that position. In this case there are 21 gray bars (sequence reads) overlapping at that position, meaning that DP=21.
Even though it is not listed in the VCF example to which you refer, variant callers can also give other data like AO, which is times that a variant was observed, and RO which is the number of times the reference base was observed. This information allows you to decide whether or not an identified variant was a sequencing error, or a real variant.
For instance if DP=1, AO=1, RO=0, that means there was only a single read at that location and it was not what is listed in the reference genome. Because the depth is so low, and the error rate of a next-gen sequencer is somewhere between 0.5-5%, you cannot say that this is a mutation or just a sequencing error. However, as DP increases, you gain more confidence in whatever was called. So if DP=10, AO=10, RO=0 you can be quite confident that the reason you read an alternate base at a given location, it is not just a sequencing error because you read this location 10 times and every time you saw the same variant.
Let me know if I can clarify further.

That number refers to the number of reads that overlap that base pair that has the variant. Sequencing reads in this case almost always refer to next generation sequencing. These metrics and other VCF fields are used to give some indicator of confidence for variant.

The way you phrase this is maybe a bit confusing. A DP of 128 means that base pair locus was read 128 times, not necessarily that variant. If you look in the VCF file, you should have AO=x, RO=y and DP=z for a given locus. Where AO is times that a variant was observed, RO is the number of times the reference base was observed, and DP is total times that base location was read. Such that x + y = z.

I don't see AO or RO in the vcf specs.  Samtools v 0.1.19 returns DP4, which is a breakdown of the number of quality filtered reads showing alternate or reference letters, split by direction.

@TheNightman Maybe you can post a new answer?

No problem I'll post it in a minute.


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Which part of human body sustains most pressure when standing up straight?
Let's suppose a healthy fit barefoot young adult standing comfortably on a flat solid surface.
A reasonable guess is somewhere around the foot.
But is it the ankle, the heel, or the Metatarsus?

ankle seems reasonable. pressure is force/area, but higher you climb, less mass you have to support (neck vs lumbar vertebrae)

the graph here shows that peak pressure is higher at the Metatarsus compared to the heel. however I cannot find a convincing comparison between ankel and Metatarsus.

What about the base of the spinal column? Very small surface area compared to the two feet, bearing a huge fraction of the load of the upper body. I'm not sure at all about this one, just speculating.

It is logically clear that the ankle could only partly be analyzed in the group of joints that are below its height. There is no direct way to measure the pressure on ankle joint (on talus bone), but from the logic it is clear that it should be the point of highest pressure in the group of points lister in the question, however the pressure is distributed through the other joints of the foot.
Below are the graphs of pressure distribution according to surfaces (not joints). From the graph we can conclude that part of the pressure experienced by ankle joint distributed tangentially to metatarsal region and other surfaces.

Indeed the highest pressure in standing person in on feets. The term you are asking about is foot pressure distribution (FPD).
In we assess the FPD dynamically, in younger persons the FPD is nearly equivalent between calcaneus region and metatarsal region, while in older persons the FDT in calcaneus region is higher than metatarsal pressure.
During stance:

Foot pressure distribution. A. Maximum pressure distribution on all sensors during stance for one subject. B. The nine anatomical masks superimposed on the insole (MC = medial calcaneus, LC = lateral calcaneus, MA = medial arch, LA = lateral arch, MT1 = first metatarse, 3 = second and third metatarse, 4 = fourth and fifth metatarse, H = hallux, and T = toes).

Pressure distribution by anatomical region. Normalized maximum pressure distribution for the young (white bar) and elderly (black bar) group for each anatomical region (medial calcalneus mask p = 0.0001, lateral calcaneus mask p = 0.03):

source article, you can find much more using FPD as a keyword.

Thanks for your answer. It is clear and informaitive. Maybe someone can run a simulator of human foot on computer and get a 3D pressure map? It'll be fantastic.

@GrigoriSun I'd say this simulator is a good candidate for PhD for someone... %)

@Ilan cheers mate!

Note that estimations in this answer are very very crude. I can speak with confidence that the mean pressure of ankel joint is greater than the heel and the metatarsus. However I do not trust that it can pin down the point with most pressure.

@Ilan gave a very good synopsis on foot pressure distribution. However, pressure in ankles was not analyzed in his answer.
Kimizuka et. al. measured contact area of human ankle joints under various load-force configurations. The main results were shown in the graph below.

For a $70kg$ human, the contact area of each ankle is about $3cm^2$, whereas of each foot with ground surface is approximately $37 cm^2$. Please note that we include only the heel ($4cm\times4cm$) and the metatarsus ($7cm\times 3cm$) in above calculation, which sustain most pressure.
We can safely ignore the mass of both feet compared to the whole body. So it seems that ankle pressure is the clear winner here.


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How are the physiological properties of mitochondria measured?
this is my first question on BiologySE. I am a Physics and Mathematics student currently doing a project on cell growth simulation. I am doing literature survey and I have a question about cellular biology experimental methods.
I understand that the membrane potential is a measure of mitochondrial functionality (higher potential means more efficient electron transport chain). Additionally, the mitochondrial volume is also an indicator of mitochondrial efficiency (higher volume, higher area, more places to do electron transport).
I would like to have some points elucidated.
In particular, can these mitochondrial membrane potential and volume...

be measured for a single cell, or only in a population?
be measured non-destructively, leaving the cell alive?
be measured simultaneously, or experiments measuring one necessarily make the other unavailable?

I am thinking mostly of in vitro experiments of course.

Note that mitochondrial shape would also matter.

A simple method would me to express a fluorescent protein in the cell that specifically localizes to mitochondria. mito-dsRed is a Red Fluorescent Protein which has that property; it can be expressed from a plasmid.
Using fluorescent microscopy and image analysis, you would be able to measure the geometric properties of the mitochondria. This can be done at a single cell level too (using confocal microscope) and non-destructively. Volume can be measured by what is known as Z-stacking— an automated technique by which the microscope takes several 2D snaps at different planes and stacks them to construct a 3D image.
You can implement this in live cells too; this method is called live cell imaging.

Could you say something about the membrane potential too?

@AndreaDiBiagio There are some voltage sensitive dyes, that can be used for that purpose but I don't know much about them. I'll have to check.


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What happens to the red blood cell in CaCl₂ solution?
Here's the problem:
One red blood cell is placed in a hypertonic solution of NaCl, another is
placed in a solution of CaCl2 equimolar with the NaCl solution. What
would you expect to happen and why?
My reasoning is that the red blood cell will shrink due to water loss by osmosis when placed in hypertonic NaCl. It will shrink even further due to the larger osmosis gradient due to there being such low concentration of Ca2+ normally in the cell. However, I'm not sure if this is right so could someone please explain the correct answer?

The reason why the cell would shrink more in CaCl2 solution is because it has a higher van't Hoff factor i.e. total number of dissociated ionic species per solute molecule (it is 2 for NaCl whereas it is 3 for CaCl2).
(Nonionic solutes do not dissociate and will therefore have a van't Hoff factor of 1)
Osmotic pressure (and other colligative properties) are proportional to van't Hoff factor. Therefore osmotic pressure in CaCl2 solution will be 3/2 times of that in an equimolar NaCl solution.
Note that the ionic chemical potential is not what drives osmosis; it is the differential concentration of water (or any other solvent) that drives it.

The osmolarity of the CaCl2 solution is higher than of the NaCl solution.


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How to understand relatedness in an infinite island model?
My understanding is that the relatedness coefficient in kin selection models measures positive assortment. That is, altruism is more likely to evolve if altruists tend to interact with other altruists. As an example, consider a general model of kin selection due to Queller (Queller 1992 "A general model of kin selection"). According to this model, relatedness is viewed as the regression coefficient $\beta_{G'G}$, where $G$ is the individual's frequency of the altruism allele and $G'$ is the average value of $G$ of an individual's neighbors. Queller's definition of relatedness is a measure of positive assortment because, by definition,
$$\beta_{G'G} = \frac{E(G'\mid G) - E(G')}{G - E(G)}$$
If relatedness is positive, if the focal individual is more altruist than average ($G-E(G)>0$), then this individual will tend to interact with individuals that are more altruist than average ($E(G'\mid G) - E(G')>0$).
Now, in Taylor's 1992 kin selection model in patch-structured populations with asexual reproduction ("Altruism in viscous populations"), relatedness $R$ is defined as the recursion (p. 354):
$$ R' = \frac{1}{N} + \frac{N-1}{N}s^2R$$
where $N$ is the number of individuals in each patch and $s$ is the probability the offspring will remain on the natal patch (link to a question about $s$). Here $R$ doesn't seem to be a measure of positive assortment, but simply the chance that two alleles picked at random within the patch will be of the same type.
On one hand, $R$ in standard models of kin selection (e.g., Queller's) measures positive assortment. On the other hand, Taylor's kin selection model for patch-structured populations $R$ does not seem to measure positive assortment within a group but the chance that two random individuals share the same allele.
I tended to think of Queller's model as a general formulation of kin selection (accordingly, Taylor's model would be a particular instance of Queller's model). But, as I tried to explain above, my impression is that Taylor's model is an entirely different way of modeling kin selection ($R$ does not measure positive assortment). Am I missing some connection between Queller's and Taylor's models of kin selection? Or is there any way of connecting the two definitions of relatedness mentioned above?


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His Tag location in gene circuit
I am part of an undergraduate research group and we are trying to produce a protease in an E.coli gene circuit. We are not sure where to place the His tag in our circuit. The sequence is
...OmpA(gene)->linker->his tag->protease->Terminator->res site
Should the His tag be in this position, before the linker, or after the protease? OmpA is a outer membrane protein that will allow a protein to be taken to, and linked to, the outer membrane of the E.coli. Our fear is that the protease will not fold correctly and will be nonfunctional.

When you say gene, have you made sure that the stop codon is removed?

Usually the his-tag should be in the terminal. Why don't you express the protease as a separate cistron?

There are advantages and disadvantages to put His-tag both N and C termini. When you put a tag at a C terminus, you can purify the full length easily. If you are lucky, you could get full length products even if you put a tag at the N terminus. An additional sequence at a C-terminus may disturb functions of some proteins, but in most of cases, it would not be predictable.

We have removed the stop codon of the gene. We wanted to have the His tag attached to the protease in some way to use as proof of concept that they protease is being expressed on the outer membrane of the E.coli.

Then what, I think, you should do is put his-tag after the protease. Is the C-terminal of Omp-A on the outside?

OmpA is a outer membrane protein so it will bring the protease to the outside of the cell. I'm not sure I fully understand your question. There are other parts of the sequence before the OmpA. OmpA will be on the outside of the cell.

@KellyEckartt got it. I just wanted to know if the protease would be outside the cell (Can you add this to your question?). C-terminal tag seems safer, in this case, to me. If your objective is just detection then FLAG-tag may be a better idea.

Fusing your protease to the C-terminus of the OmpA will not diplay it on the outside of the bacteria because the C-terminus is facing the periplasm (the space between the outer and the inner E coli membrane)


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Do Blanding's Turtles die of old age?
I have recently found articles and various claims that turtles (Blanding's turtles as an exact example) could possibly live indefinitely. http://discovermagazine.com/2002/jun/featturtle
This is said to be due to the fact that they

don't senesce— deteriorate physically— as they grow old

I am highly skeptical of that claim, and on the other side are links such as this http://www.nature.org/ourinitiatives/regions/northamerica/unitedstates/indiana/journeywithnature/blandings-turtles.xml which say they can live up to 70 years (though in the actual article it says 70+)
I realize in the wild that predation, disease, and other causes other than old age could kill turtles, but my question is:
Can blandings turtles die of old age? If so, around what age would this be?

It looks like as in fishes, the lack of an intrinsic cause of death in turtles in general is seen:

Like in fishes, the reptiles appear to show three types of senescence. The African skink, Mabuya buettneri, shows rapid senescence similar to death at mating observed in Salmon and marsupial mouse. Most of the lizards and snakes undergo gradual senescence comparable to the pattern exhibited by a majority of vertebrates. On the other hand, turtles, tortoises and crocodiles continue to grow throughout life and are thus credited with slow or negligible senescence.
  Patnaik 1994 Gerontology 40(2–4):200–20.

The main article by Congdon, the researcher who the Discover article profiles, also seems to be fairly definitive about this lack of senescence (or negative senescence?) in Blanding's Turtles specifically:

Survivorship, reproductive frequency and size-adjusted mean clutch size were all higher in the Oldest age group compared to the younger age groups.
  Congdon et al 2001 Experimental Gerontology 36(4–6): 813–827