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Anti-parallel DNA code operons
Coming from a software engineering standpoint, suppose I have a string of code like so:
... 5'-ATAGAC-3' ...
... 3'-TATCTG-5' ...
Assume the above code is part of a larger segment. Now, reading from 3' to 5', the promoter and operator would be somewhere before the structural gene on the 2nd stand:
(Promoter) (Operator) ... 3'-TATCTG-5' ...
Where would it be on the first strand? From what it looks like, the first strand codes for a completely different protein than the second stand:
... 5'-ATAGAC-3' ... (Operator) (Promoter)
Yet, the two strands are complementary.

You make one mistake: DNA is always read in 5'->3' direction. So when you promoter is before the gene, it is on its 5' site. So it would be 3'-TATCTG-retomorp-5' or in the right reading direction: 5'promoter-GTCTAT-3'.

related: http://biology.stackexchange.com/questions/14299/on-which-strand-does-the-promoter-sit

DNA is built 5'-3' but the template strand is read 3'-5'.

In your example, yes the two strands do code for different proteins. However, biologically this generally doesn't occur. I say generally because I don't want to rule it out definitively but I don't know of an instance where both strands at a given locus code for a protein and, where it does occur, it is often used as a criterion for annotating one of the elements as dubious. Along with that, there would be no promoter immediately 5' to one of the strands. Even if it does occur biologically, each strand would code for a different protein and would be a different gene.
In any gene, one of the strands is identical to the RNA transcript (before processing and with T instead of U). This is called the coding or sense strand and runs 5' -> 3'. The other strand is used as a template by RNA polymerase (RNAP) to polymerize the RNA transcript. It runs 3' -> 5' and is called the template or antisense strand.
Also, a note on promoters: promoter consensus sequences by convention are given on the sense strand. However, as far as I know, transcription initiation factors recognize the base pairing between both strands in the major groove of dsDNA because they must bind before promoter melting occurs. Thus, I wouldn't say that a promoter exists only on the template strand.

So would both DNA stands code for the same protein at a given locus? How is this possible, given that the bases are different when reading one strand vs. the other?

No, they would code for two different proteins and in opposite directions…

Thanks. How does the cell "know" which strand to read? What I mean is, you mentioned that "transcription initiation factors recognize the base pairing between both strands in the major groove of dsDNA". How does it know which strand to read? The promoter strand?

The strand is determined by the promoter location. Since promoters are directional and transcripts are only polymerized 5' -> 3', there is only one choice for sense and antisense strands from a given promoter.


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A photosynthesizing mouse?
N. Shubin's Your Inner Fish makes the point several times that there is a lot of functional similarity between some seemingly remote gene cousins. If that needed reinforcing we have the spider-goat, whose milk contains spider's silk, and a knock-in mouse whose vision resembles that of humans.
The last two examples are interesting because, as I recall, nothing beyond the gene insertion (already a feat) had to be done to confer the extra/new capability. The machinery at the cellular level (for the mouse to perceive a new color or for the goat to somehow process the milk) already existed.
My question is whether it might not be possible in theory to create a mammal with the ability to photosynthesize? If this is a polygenic trait perhaps it would be accomplished in multiple stages. I realize an answer here would be highly speculative but a careful answer might cast some light on the process of conferring new traits/abilities in this way.
While I see no obvious benefit of creating a photosynthesizing mouse, at least the food bills for their maintenance might be low. This sounds like a joke but it's not a trivial benefit.
Thanks for any insights.

Maybe the answer is, "This is not possible because..." That would also be interesting to me.

also read about kleptoplasty

It is almost impossible for following reasons:

For photosynthesis you need chloroplasts
To maintain chloroplasts you need many genes in the nucleus that will support its endosymbiosis

I said almost impossible because there are some natural examples of what you are asking. A sea slug called Elysia  acquires choloplasts from green algae on which it feeds. However, it cannot maintain the chloroplasts and pass them on to the next generation but it acquires enough to appear green and survive on photosynthesis when there is no food.
Another example is that of the protist, Rhopalodia gibba, which acquired a cyanobacteria like organism. This protist already had a red alga derived secondary plastid before it acquired a "green" cyanobacteria. This acquisition gave the host the ability to fix nitrogen in the presence of light.
The case of Paulinella chromatophora is very interesting because the acquisition of an endosymbiont happened very recently. The endosymbiont is close to Synechococcus clade of cyanobacteria.
Intuitively, it can be understood that these kinds of acquisitions would be quite difficult for a multicellular organism.
ADDENDUM
Photosynthesis is a complex reaction which requires a dedicated compartment which not only harvests light and produces ATP but also has enzyme complexes required for anabolism (carbon fixation etc).
For now we can accept the hypothesis that it would not be possible for a huge eukaryotic cell to perform these functions in absence of a dedicated organelle. For a discussion on why this is so, you can refer this post.
Having said that, there is an easy way to impart partial photosynthetic ability to a eukaryotic cell. Some archaea and bacteria employ rhodopsin to pump out protons against its gradient, in the presence of light; this is coupled with ATP-synthase just like the complexes of ETC in mitochondria. In this study, Hara et al have expressed delta-rhodopsin in mammalian mitochondia which now makes the mitochondria generate ATP in presence of light. Furthermore, these cells were immune to mitochondrial toxins that affect complex-I activity.
PS: thanks biogirl. I almost forgot about this and I just remembered when I was reading about something else

Chloroplast isn't a necessity for photosynthesis. It takes place without it in many prokaryotes. So although I agree with most of your answer, if someone does try to make photosynthesizing mammals I don't think it would be necessary to make chloroplast.

A question : Would it be easier to incorporate so many genes for all the photosynthesis procedures or to try to insert a chloroplast and then maintain it ?

yes I agree that there are other mechanisms of photosynthesis (non cyanobacterial like) but i was referring to the one that is most common in eukaryotes. Having said so there are different kinds of chloroplasts in eukaryotes too (red algae vs green algae). Plus prokaryotes cannot have chloroplasts- no explanation required. In short plastids are more diverse than mitochondria and chloroplast is just a term for an organelle which can have diverse evolutionary origins.

@biogirl see the edit.. I have added some more information. Nonetheless, chloroplast (and its ancestral free living cyanobacteria) with its light harvesting photosystems, is still one of the most efficient photosynthetic apparatus in nature.

Wow the last study cited sounds really cool ! And yes the original photosynthesizing organisms are very efficient...afterall they are products of millions of years of evolution ! Humans will have to work really hard to replicate them..

Also chloroplast photosystem has higher efficiency than rhodopsin based systems

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Bad Eyesight and Evolution
Why do many humans have bad eyesight, such as near-sightedness, which hampers performance in a wide variety of tasks? Shouldn't there be evolutionary pressure towards better eyesight?

Remi.b and Potterbond007 have put forward excellent answers. Would like to add something..
One of the reasons that Myopia (near sightedness) happens is because of use of eye in work like reading, which requires working with close objects. I don't think there was much working with close objects in the past. So very few people with myopia might have been present (and of course, they may have had disadvantages in catching prey.)
Other common disease is hypermetropia which generally occurs during old age, past the reproductive prime, so it could not have much evolutionary impact.

Maintenance of Polymorphism and Mutation Load
There are many possible reasons why some amount of deleterious alleles are maintained in the population. One of which is the mutation-selection-drift balance. In short: Because mutations always occur, there is continually an input of deleterious mutations in populations genome resulting in some fitness decay (called mutation load). While mutations create this polymorphism, processes of selection and genetic drift cause a decrease in polymorphism. At equilibrium there is a balance between mutations, selection and drift called the mutation-selection-drift balance. You may also want to consider various population structure related concepts such as migration between patches. Haldane first explored this mutation load theoretically and estimated that the fitness of an existing individual in a population of perfect (deleteterious-mutations-free) individual is about 80% lower, which is huge! Such mechanism can explain various disease found in a population.
Age-specific intensity of selection
Also, for the question of disease appearing late in life (which is often the case of eyesight related disease), it is important to realize that those genes which are expressed late in life undergoes a lower selection resulting in a higher mutation-selection-drift balance. See this post for more info.
Impact of Medicine and social helping on the intensity of selection
As pointed out by @potterbond007 modern medicine allows to diminish the deleterious effect of some mutations. For example, one that has clubfoot may be operated and is likely to survive and reproduce and therefore propagating its deleterious alleles. This would be different in some past. Therefore, medicine diminish the selection pressure on deleterious alleles. However, modern medicine probably has a very low effect on our genomes because it is so modern. 100 years ago we could not operate clubfoot and 500 years ago (almost) nobody had glasses to correct for eyesight deficiency. We may go a bit further in the past and also consider that social interactions such as helping weak individuals in a tribe may also have decreases the selection pressure against deleterious alleles (more info in @theBIOguy 's answer). Of course, if selection is diminished the mutation-selcetion-drift balance is increased and deleterious alleles are more common and mutation load is greater.
Further investigations will be needed in Epidemiology
Assuming that eyesights disease are particularly common and deleterious, we should have a closer look to the epidemiology of the diseases of interests. If it seems to you that eyesight-related diseases are more common and more important in terms of their effects on fitness than diseases on other traits then, you may want to seek into some physiological and developmental explanations that may tell you why eyes are so likely to be impacted by genetic and/or environmental factors. I personally have absolutely no knowledge about the epidemiology and developmental mechanisms of any eyesight disease! Also considerations of the impact of modern environment should be considered such as the impact of TV and computer screens on our eyes (more info in @biogirl 's answer)

Your answer was technical, but I understood it.

With nearly 40,000 years of natural selection on eyesight, prior to the invention of eye glasses, there needs to be a better explanation than the effects of 'modern' technology. There are two likely reasons for the persistence of "poor" eyesight in humans. First, humans are social animals and live in groups. Within groups there is frequently a division of labor. This division of labor deemphasized the importance of vision. Individuals with "poor" eyesight could easily maintain a high fitness (reproductive success) in this social structure. Second, humans have long term parental care (both within and among families - again a function of social living). Most human offspring maintain close familial connections up to and including the age of reproduction. The strength of selection on eyesight diminishes past reproductive age, allowing individual with poor eyesight to have relatively high fitness.

Mainly because we haven't been forced to remove the bad genes that cause these defects from our gene pool. In ancient times, a bad gene that causes poor eyesight would have made it difficult for a person to spot prey or escape from a predator. However, we have glasses now which gives the bad eyesight gene as much a chance to propagate as any other gene. it also doesn't really matter since poor eyesight is never a factor for survival in present times. The same with poor hearing which we correct with hearing aid. Please read this for an article in the guardian and this article in the orlando sentinel. You could also read this discussion on reddit to see a few fun arguments.

Does is then indicate that if humans stop using artificial aids to overcome their shortcomings, then there is a chance that advantageous evolutionary traits would be observed in the future?

@rudstar no it does not since the existence of excellent eyesight is not such a limiting factor in present times is it. Even if we stopped using artificial aids, every individual with the defective gene is still going to survive and have kids. Would be significant if there was a defective hypothetical gene which lead to infertility and we did not have present day advances like IVF.

Yes, I get it. Reproductive fitness is what matters.

Glasses and hearing aids are very new inventions, only a few hundred years old.  There were hundreds of thousands of years of evolutionary pressure towards better eyesight, yet many people still have bad eyesight.

@Tiberia But human being's evolution to be at the head of the food chain is not a recent occurrence.. There is no pressure on the bad gene to disappear from the gene pool even less with the present advances in science.

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The parameter for setting the number of mismatches in standalone blast
In a standalone blast search, is there a parameter that could be specified to fix the number of mismatches allowed in an alignment. I went through the parameters and I could only find parameters to set score.
-q => Penalty for a nucleotide mismatch (blastn only) [Integer] default = -3
-r => Reward for a nucleotide match (blastn only) [Integer] default = 1
What do I do if I only require hits with a maximum allowed mismatch or gap of 2 per alignment.

There is no direct option like that but you can set percentage identity filter with -perc_identity
However, this is only for reporting. BLAST will still perform all the alignments. That is why I suggested you to use bowtie.
EDIT-1 (getting long for comment)
If you want a word type of search then use the -n option. But it always starts from the 5'end which is quite justified in case of miRNA because the seed region is in the 5'.
Setting -n to 0 means no mismatch in seed region. -l option defines the seed length; I would advise that you use something like 10. -e refers to maximum mismatches in the non seed region but it is not the number of mismatches; it means maximum tolerated sum of phred score of mismatches (fasta files are assigned a default phred score of 40 at all residues. So, for 2 mismatches you have to mention -e 80).
EDIT-2
Yes. Increasing mismatch and gap penalties would make the search more stringent if you have already specified a cutoff on score.

got it.. gonna go for bowtie.. I guess it would be -v 2 for the maximum number of mismatches set to 2, and -e 0.01 for the quality score, --norc for the plus strand and which parameter would be the equivalent of the word match limit.

and one last question for future reference, do you think increasing the mismatch penalty from -3 (default value) to maybe -5 or -6 would serve this purpose?


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Calculation of water potential
For a mesophyte growing in a moist soil, water potential of its root sap is -3 atm, then how to find the water potential of moist soil and leaf respectively?

I don't know if we can calculate the exact values. The only thing I can say is that the potential of the soil will be less negative than -3 while that of the leaf will be more negative.
You know that water travels from higher potential to lower potential. So, it will travel from a region of less negative water potential to a region of more negative water potential.

Could you please explain the reason behind your answer?

@Rudstar Yeah sure.. You know that water travels from higher potential to lower potential. So, it will travel from less negative to more negative.


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Conclusions from hybridization results
A double stranded DNA was denatured in a mixture that included mRNA from a gene in the segment. The mixture was then cooled to promote RNA and DNA hybridization. The following figure the results.

Which strand is DNA/RNA?
What is source of the genetic material (Prokaryotic/Eukaryotic)?
Which segment is exon/intron?

Give us at least a try of your thoughts. The answer is not very complicated.

I thought P is exon and Q is intron. I is RNA and II is DNA from bacterial cell

You are almost right. I modified you picture a little bit to answer it:

Structure I is indeed DNA, structure II is processed RNA.
This is because in I you see loop structures which have no complementary part in the RNA anymore, these are introns (structure Q and the flanking loop regions to P). P is an exon flanked by two introns.
The end of the RNA is not complementary to the DNA because the poly-A tail has been added here.
The DNA is eukaryotic since you have introns and exons (which are not present in bacteria) and since the processed RNA contains a poly-A tail (which is also not present in bacteria).

Everything is fine except that from this figure you cannot conclusively say that RNA is poly-A tailed.

This is the 3' region in which DNA and RNA can not hybridize. Additionally you could also think about a 3' untranslated region there.


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What do viruses do during incubation period?
For example, there is an incubation period of around 1 to 3 days for common cold, and that of AIDS can range over to decades.
What do viruses do actually do during the incubation period?
What triggers them to turn active again?

In the incubation period the virus replicates, infects more cells and prepare for the outbreak.

during the incubation period the virus is typically increasing in numbers and spreading between cells. It takes a while for symptoms to become obvious because it takes time for enough damage to be built up in the tissue to become noticeable.
Take for instance the Rhinovirus which causes the common cold, once you become infected it is a day or so before enough damage has been caused to the tissue at at the back of the throat to give you a cough.
In addition some of the symptoms of infection are caused by your own immune system as a way of fighting the infection. For instance inflammation is often a sign of infection but is typically caused by the immune system to allow the movement of plasma and leukocytes into the infected tissue. As the immune system requires time to recognise and respond to a pathogen this leads to the delayed onset in symptoms.
AIDS is actually a syndrome caused by the HIV virus. the HIV lifecycle occurs CD4+ T-Cells, after infection occurs the immune system tries to cope by destroying the infected cells but over long time the infected population increases. The immune system becomes more and more compromised until the CD4+ cell count drops to a level where the patient is diagnosed with AIDS. At this point the immune system is compromised and the chance of a secondary infection by a different organism increases which the patient can no longer fight off. The actual cause of death for someone infected with HIV is rarely the HIV itself but is quite often a different agent.

Some of the viruses also stay as proviruses..

Very good practical examples to answer this question! I like the way you use acute inflammation. AIDS is well explained from the general to the specific.


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What are some examples of evolving networks in biology?
I'm a master student working on networks analysis in general. A network is something that has nodes and there are links between the nodes. Nodes and links could have attributes. An evolving network is one that changes overtime (new nodes and links are added..etc). An example of that is Facebook. Nodes are users and links represent the friendship relationship. Users have attributes (gender, age, etc.). A Facebook network as you know is an example of a social network.
The issue is that so many people studied traditional evolving networks like social networks, the web, or transportation networks. Currently I'm looking for novel examples of evolving networks to study them. So I thought there might be some examples in biology that could represent some kind of an evolving network.
So my question: Can you give me examples in biology for evolving networks? I'm aware of metabolic networks, but that is also heavily studied, I need something else.

I don't know if you can call them networks : Ecological relationships between organisms

@biogirl My copy of 'Ecological Networks' by Pascual and Dunne would suggest you can :)

Others have nicely summarized to different types of biological networks and how they can evolve. I would like to make a fine distinction between evolution and dynamic adaptation and add some comments about relative evolvabilities of different biological networks.
Given an architecture, a network can respond dynamically to different inputs. The preferred paths may change and the output characteristics can vary. Example cases include the effect of environment on metabolism. Personally, I would not consider this as network evolution because the architecture remains the same. Network evolution refers to rewiring or addition of new connections.
It would be apt to classify the biological networks like this:

molecular networks

Gene regulatory networks (GRN)
Molecular (protein-protein) interaction networks (PPI)
Cell signaling networks

cellular networks

Neural networks
Biofilms (?)

organismal networks

Ecological networks (food webs etc)

There are several ways in which a network can evolve: Edge addition, edge deletion, edge modification, node addition, node deletion and node duplication.
In molecular networks edge modification happens when the chemical interaction is affected. For e.g. in a gene regulatory network a promoter-Transcription Factor (TF) interaction can change if there is a mutation in promoter sequence or in the DNA binding domain of TF. Similar situation exists in the cases of PPI and ligand-receptor interactions (Though concept of mutation doesn't apply to ligands).
Gene (node) duplications are also common mechanism of evolution of GRN. Gene deletions/inactivations also change the network and in some cases result in complex diseases. Metabolic networks evolve if an enzyme mutates and a new pathway is created.
Usually node additions rarely happen; node duplications and edge modifications are more common in molecular networks.
In neural networks the plasticity is higher than molecular networks. There is a basic architecture that is essential to support life but the connections keep changing, nonetheless, in the non-core regions. Since active neurogenesis stops after a certain point, we can assume that number of nodes remains unchanged but edge addition (new synapse), edge deletion (synaptic pruning) and edge modification (long term potentiation/depression) is quite rampant and widespread. In neurodegenerative diseases neurons die and therefore nodes are lost.
Ecological networks are affected by environment and geological barriers. So there are several subnetworks (ecosystems) that are weakly or strongly connected with each other. Introduction of foreign species (node addition) causes immediate perturbation of the local network architecture. Long term effects arise because of extinction (node deletions), speciation (node evolution leading to edge modification i.e feeding habits etc).
It is also to be noted that in all the cases the effect of a change on a network depends on which node/edge is affected; hubs are under tight scrutiny and are protected from perturbations because any dysregulation can lead to network collapse. Some networks also follow the preferential attachment behavior (which appears contradictory to hub preservation as a mechanism). I guess that molecular networks do not employ preferential attachment whereas ecological networks do.

Not sure if this meets your definition of a network, but there are several kinase cascades which transmit signals. For example, the basic MAPK cascade has evolved to serve different roles via the ERK, JNK, and p38 cascades
The evolution of the MAP kinase pathways: coduplication of interacting proteins leads to new signaling cascades. Caffrey et al., Journal of molecular evolution, 1997. Link here
Ancient signals: comparative genomics of plant MAPK and MAPKK gene families. Link here. Manning et al., Trends in Biochemical Sciences, 2002.

Can you please add some references?

added a couple of references -- reading wikipedia articles on MAPK would be very useful as well; these proteins are extremely important for a very wide range of cellular function

The following does not answer the question! It only gives some ideas of where I personnaly found some work involving network analysis in biology.
Most of the networks I've heard about in biology concern

network of species interactions
network of individual interactions within a population
network of subpopulation interactions within a metapopulation
neuronal network
anatomy network (blood vessels, skelleton, etc..)
network of metabolic pathways.

I give you below a bunch of article title that discuss networks in biology. I'll probably add the links later $ \ddot\smile$ but if you just copy-paste these titles on scholar.google or on WebOfKnowledge you will easily find the articles.

Evolution of a vertebrate social decision-making network
climate change, human impacts coral reefs
architecture of mutualistic increase biodiviversity
variation in migration propensity among individuals maintained by landscape structure
skeleton and fractal scaling in complex networks
Habitat modification alters the structure of tropical host-parasitoid food webs

This last article concerns the impact of various environment on the network of interactions between host and parasites. Fairly interesting for a biologist.
I would expect that most evolving networks in biology concerns the impact of environmental changes on the network of species, subpopulations and species interactions. You may have expected some stuff that are more related to evolutionary biology. I think most of this work concers evolutionary ecology and evolutionary processes in metapopulations. Here is a very interesting and very theoretical article (by stuart kauffmann) on evolutionary biology though that has nothing to do with ecology.

antichaos and adaptation

1-actually what I need is to construct a dataset of an evolving network (which is recorded overtime) so I can study the data. My university has a great biology department, so is it possible to get the data of something that you mentioned? Or are the examples theoritical? I'm not good in biology at all, that's why I found them a bit difficult to understand. 2- I'm only concerned in evolving networks. So please can you remove the examples that don't concern evolving networks?

Re-reading the only article I considered to offer evolving network I realize it does actually not give an evolving networks. It is only a comparison of networks between different ecosystems. Hum…so I don't know about any article that report the analysis of an evolving network in biology. There probably exist on though. I guess I won't delete my answer because it gives an idea of where we can find networks in biology which is always informative.

It is going to be even harder if you have to find a good dataset I guess. Once you'll find an article that presents an evolving network, you may always ask the authors if you can use their data for your project and of course don't forget to tell them you will cite their work.

I find this a very interesting question as I personally work with networks very frequently!
Based on your definition of evolving networks, it is feasible to consider protein-protein interaction networks as evolving since over time more and more interactions between different proteins are discovered and more novel proteins (nodes) are tested for their interaction with other proteins.
If this meets your definition, then you can use PP interaction databases such as BioGRID and look at the different releases and see what proteins are added over time and what new interactions have been added between different releases. Here is the archives page for BioGRID (http://thebiogrid.org/download.php). BioGRID has also a Cytoscape plugin which you can use, although I have never worked with dynamic networks in Cytoscape so perhaps have a look at Pavlopoulos et al 2008 BioData Min, which is a survey of visualisation tools for biological network analysis.
Hope this helps!

mmhh interesting. And nice that the data are freely available with your example. But analyzing this evolving network would tell more about the history of discovery of new proteins than about the real biological underlying mechanisms. I am not sure though. It maight tell about how close we are to have a good definition of how the network of protein interactions looks like I guess. This data might indeed interest the OP.

Yes, this dataset analysed in a dynamic sense can tell us how close we are to a good estimation of global PP interactions in a given organism, given the techniques/equipments used and what the progression rate of finding PP interactions has been over time, but non the less it is more of a historical account as opposed to a biological underlying. The data should more appropriately be correlated to equipments/techniques, although there are many other hidden variables such as the number of people that engaged in PP interaction discovery between the data releases etc.

Ants, slime molds, and brains.
Ants and slime molds use simple rules to generate pretty good transportation networks in an emergent way, and brains wire and rewire themselves constantly(adding/removing edges, but not usually nodes).
Evolutionary networks, metabolic networks, and ecological networks are much harder to get concrete data sets from, because of the time and space scales involved. (I mean the time scale over which node addition/deletion and edge modification takes place, which is in evolutionary time)
Slime mold shapes, ant paths, and neuron traces are all reproducible in the lab, however. Antlike algorithms are pretty common, so you could run one of those and then examine the graph it puts out as it works. Those aren't precisely biological networks, but certainly biomimetic. If the subtleties are likely to be important, you might have to physically get some ants.
If you're looking for premade databases of slime mold or ant experiments, you might try contacting the authors of the PNAS paper, but I don't think anyone is looking to model slime mold behavior as a graph. You could be the first!

Could you provide some databases and references which have the evolution of these networks recorded overtime? Also neuronal rewiring/wiring is a static but dynamic network but it does not evolve in a sense that the number of neurons hence the nodes increases over time after birth as stated in WYSIWYG response but as stated, it can be only used as a deconstructive evolving networks in neurodegenerative conditions. Still some references would be great!

I'm not sure that the databases that you're asking for exist. They would definitely be useful for studies like this, though. I added some references to people working in relevant fields and some biomimetic approaches, which may work for you.


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How does the MMR vaccine affect lymph nodes in preventing measles?
I am trying to understand this statement about the Measles part of the MMR (Mumps, Measles and Rubella) vaccine

Measles prevention: MMR (AB protect during primary and secondary viremia)

Measles enters from respiratory tract, through mucosa of the upper respiratory tract. The virus passes into cervical lymph nodes. Now, starts first viremia (MMR somehow helping here) which lasts about 5 days. Then antibodies are secreted during 15 days which leads to rash lasting about 3 days.
I think this second viremia refers to the possible dissemination of the virus to other lymph nodes by blood.
This suggests me that the vaccine primarily have a mechanism that affects in the lymph nodes or generally in the lymphatic circulation.
How MMR vaccine affect lymph nodes in preventing measles?

Lets define viremia first: The primary viremia occurs in the cells which the virus enters first in the body. There it replicates to high titers before it leaves this cells, spreads through the body and infects other cells. This is then the second viremia.
For measles the primary viremia occurs in the respiratory epithelium and in the local lymph nodes. The second viremia then occurs in skin, conjunctiva, respiratory tract, and other distant organs. In this phase also the characteristic rash occurs due to a hypersensitivity reaction of the skin. For details see here and here.
The measles vaccine works like any other vaccine: By raising an immune response against the vaccination virus. This leads to a normal immune response which leads to the production of specific antibodies against the measles virus and also to immunologic memory. These antibodies are available to fight the virus when it enters the body of a vaccinated person. This also triggers the proliferation of virus specific memory B cells which then differentiate into plasma cells and produce vast amounts of protective antibodies. So there is no special mechanism involved here beyond immunologic memory.

Thank you for your answer with appropriate sources! I think similar immunopathology exist also for Rubella (German measles); the MMR vaccine seems to affect similarly as for measles.

You're always welcome. It is the same for rubella, the antibodies protect effectively against the virus.


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downloading a reference genome for alignment
I am currently working through the code example on the MATLAB website. It requires me to download the reference genome of Arabidopsis thaliana (thale cress) so I can use BowTie2 to align the Chip-Seq experiment data. I need it in a .fa file.
Since I am very very new to this, what is the database where I can use to download this reference genome? How do I search for something like this? Thanks
EDIT: spoke too soon. I think the NCBI website did it for me. Under the Representitive -> Reference genome section. Is this correct?
EDIT2: The answer was in the MATLAB page also. The bioinformatics toolbox provides a function:
% getgenbank('NC_003070','FileFormat','fasta','tofile','ach1.fasta');
% getgenbank('NC_003071','FileFormat','fasta','tofile','ach2.fasta');
% getgenbank('NC_003074','FileFormat','fasta','tofile','ach3.fasta');
% getgenbank('NC_003075','FileFormat','fasta','tofile','ach4.fasta');
% getgenbank('NC_003076','FileFormat','fasta','tofile','ach5.fasta');

Yes, NCBI is fine. So is http://genome.ucsc.edu or http://ensembl.org or genomes online.

Some organisms have special repositories like Drosophila has flybase.

Since you are using Bowtie, you want the indexed genome, see if that's not available here, instead of downloading the fasta and indexing it yourself.
http://support.illumina.com/sequencing/sequencing_software/igenome.ilmn


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Are Night Parrots (Pezoporus occidentalis) really extinct?
This incredibly rare animal has been reported to be extinct since 1990, however several cases has been raised that night parrot was spotted in the areas of Australia. What is the cause of their extinction, or in the first place, are they really extinct?

As per Wikipedia it is listed as endangered having been downgraded from critically endangered due to the spread in sightings over the years over a large area. Sightings have been rare with a reported sighting on 12th April 2005 and a dead specimen found in 2006 The first photos and a 17 second video of the bird was taken by a wildlife photographer John Young in 2013. Details can be found in this link.
According to Birdlife.org the reason for its population to decrease significantly include predation by feral cats and foxes, altered fire regimes, competition for food, degradation of habitat near water by stock or rabbits, and reduced availability of water as a result of over-use by feral camels.

At least they are not extinct.. That solves!


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Why don't warts caused by HPV spread to the whole body?
My son had a plantar wart on his foot, which (as I understand it) is caused by a virus which only infects skin cells. Once in the skin cell the virus replicates, but when attacked by the immune system prompts the growth of a hard, thick layer of skin (callus). Warts are caused by a HPV.
Given the wart has infected a skin cell, and skin cells are next to each other in a great big sheet covering the entire human body, why is it that we don't become completely covered in wart?  I assume that it's not the immune system keeping the wart at bay, because the original wart isn't defeated and we can get other spot infections elsewhere.

The Wikipedia page you link to says that they are self-limiting, although it doesn't say why.

actually there is a person who was completely covered with warts; not as a homogeneous sheet, though. Watched the video on youtube.

Plantar warts grow deep into the skin and slowly [1]. It is a common thing for warts to multiply [1], but because of the slow growth speed, their symptoms [2] and the self clear-up [1] they can't end up by covering the entire skin surface of a previously healthy person.
There are cases of generalized warts in patients with immune deficiency like hypogammaglobulinaemia, impairment of cell mediated immunity [3]. The immune system plays an important role in limiting warts. There is also a case of generalized facial warts in a patient with no other known medical condition [4].
References:

American College of Foot and Ankle Surgeons, Plantar Wart (Verruca Plantaris)
MAYO Clinic, Diseases and Conditions - Plantar warts.
Reid TM, Fraser NG, Kernohan IR. Generalized warts and immune deficiency. Br. J. Dermatol. 1976 Nov;95(5):559-64. PubMed PMID: 1086679.
Semon H. Papillomatosis: Generalized Facial Warts. Proc. R. Soc. Med. 1935 Dec;29(2):90. PubMed PMID: 19990539.

Your reference for "self clear-up" only indicates that this is a possibility, not a certainty, and doesn't discuss the mechanism. "Generalized warts and immune deficiency" was informative, and suggests that https://en.wikipedia.org/wiki/Antigenic_variation is the cause of subsequent infections.


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Blood consumption
Is consumption of blood more "dangerous" compared to meat?
There was a news-article about unnatural chemicals found in the blood of mothers. This reminded me about a question I have pondered upon from time to time. Now, I am not a vampire, but curious as to the nature of blood vs meat in animals. More specifically unhealthy components.
There are various examples of viruses being in danger of spreading by consumption of raw blood like ebola, H5N1 etc. (But then also meat etc.)
Perhaps easier if I throw out some questions to show what I am asking:

Are there more of such in blood then meat?
Are there other things that can be worse in blood even after preparing? Like cooking, conservation etc.
Are parasites etc. more frequently found in blood?
Are there organisms that are highly resilient to heat treatment found in blood?
Are there more heavy metals in blood then meat? (Which I assume cooking does not give much of a difference.)
Other toxins?

Some references:

http://www.eufic.org/article/en/food-safety-quality/animal-health/expid/review-animal-diseases/
http://www.fao.org/avianflu/en/qanda.html

can you reference the news article you have mentioned please.

@potterbond007: I did not include it as it is not in English. Also, I have thought / wondered about this before, the article simply reminded me about the question. The article itself is a tabloid chock piece: http://www.vg.no/nyheter/innenriks/forskere-du-har-gift-i-blodet-ditt/a/10124215/ The particular subject at hand I have read about before and seen some docus etc. about, but my question is in regards to animal-meat/blood, not human ;), and more in general.

The (only) answer is actually irrelevant with the question and very ambiguous. What is high dosage of blood...? You can eat a few blood sausages and you will not get iron overload (which is more often an inherited condition). Although everything is digested in the stomach, raw blood could be dangerous if somehow the hypothetical viruses make it to your blood system.

Is consumption of blood more "dangerous" compared to meat?

Actually yes, a simple high dose of blood is enough to kill. The cause is, though it is most important thing to live when flowing the vessel, it's highly toxic when consumed. There are high chances of getting haemochromatosis or Iron overload.
Source and More on this:
http://www.livescience.com/15899-drinking-blood-safe.html
Composition of Blood

(source: snmjournals.org)

It's the same for menstrual blood?

My question, at least in my mind, was more in the realm of toxins etc. But as there still are no more answers I'll accept yours as it points out a valid point :)

I'm highly dubious of the claim, and I'm not sure livescience.com should be accepted as a definitive source. Haemochromatosis is a real thing, but it seems to be associated with multiple blood transfusions and transfusion reactions, rather than consumption of blood as food. Many cultures include significant amounts of (animal) blood in their cuisine, with no obvious problems.


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Properties of Satellite Chromosomes
I have some questions regarding Satellite chromsomes which could not be resolved by a google search.

Does the satellite consist of telomeric sequences ?
If not, What is the function of a satellite ? And where will the telomeric sequences be present - in the main body ? On the secondary constriction ?
Satellite chromosomes are also known as SAT chromosome which stands for Sino Acid Thymidine. I read in some sources that SAT means without thymidine. But how is that possible, if there is A then obviously there has to be T ? ( in dsDNA)

I'm no expert but as far as I understand it, satellite sequences such as micro satellites are just repeating sequences of DNA (http://en.wikipedia.org/wiki/Satellite_DNA), which seems to satisfy telomere sequence repeats (http://en.wikipedia.org/wiki/Telomere). Satellite DNA is the main component of functional centromeres, and form the main structural constituent of heterochromatin (ref above). SAT chromosomes and presumably their sequences play a vital role in the formation of the nucleolus after cell division is completed (http://en.wikipedia.org/wiki/Satellite_chromosome). Not sure about 3

If by "satellite chromosomes" you mean "satellite repeats", then:

Not always. There many types of satellites, such as telomeric, centromeric (like gamma, alpha, beta satellites), simple repeats (CT)n.
It is still an open question. Some say they are important for chromosome structure (e.g., centromeres). Sometimes satellites get transcribed as might act as lncRNAs. And of course, most of them are just junk DNA.
If there is T then there is A too.

Edit

Satellites contain telomeric repeats at their ends as all chromosomes do. But they are more about NOR repeats.
They are important for the nucleolus functioning. But shorts arms of acrocentric chromosomes are not crucial, take Robertsonian translocation as an example.

satellite chromesome and satellite dna are different. I mean satellite chromosome

I edited my answer.


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Can Alzheimer's disease be caused by Slow Prion infection?
I found this claim in my study materials with explanation of amyloi plaques, in comparison to CJD (Creutzfeldt-Jakob Disease).
Its characteristic are

Long doubling time of at least 5.2 days (I think this means the time it takes to double the amount of prions in the target organ)
NO Cypopathic Effect (CPE) in vitro
Long incubation period (about 30 years)
Vacuolation of neurons, amyloid-like plaques
Deficient immunity
Deficient immunoresponse
Deficient Interferen (IFN) production

so this suggests me that the person with infection at a young age can have the disease then at an old age.
Other possible agent could be virus, but it seems that prion is the major one.
Can Alzheimer's disease be caused primarily by Slow Prion infection?

Dr Yong in the paper titled Prion, The unconventional slow Infectious agent states that the formation of amyloid plaque which is a major contributor to Alzheimer's disease is a unconventionally slow infectious disease (Prion). Some papers have also pointed out the similarities between Alzheimers and prion disorders (reference) Cerebral amyloid plaques have also been identified in scrapie which is caused by a Prion. Discovery of a novel prion disorder (reference) with peripheral symptoms have led researchers to believe that protein misfolding, is the basis for most neuro-degenerative diseases, including Alzheimer's disease and Parkinson's disease.
With regard to your question, Alzheimer's has not been completely classified as a prion disorder as of now, but seeing that amyloid plaque formation (reference) and Creutzfeldt-Jakob disease (CJD) (a form of dementia) (reference) have been identified as being part of Prion disorders, it is highly likely that Alzheimer's is too.

I recall that Alzheimer is linked with demyelination or degeneration of motor neurons, particularly. So the target area can be different in Alzheimer than in Parkinson's disease. Intuatively, the main mechanism can be the same in both diseases but the patient's genetic material i.e. processes creating special environments around neurons in different parts of the brain determine where the degeneration is occurring thus determining which disease. It is also possible that there are different types of virion which cause the difference. But I have intuition that both host and virion are players.


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How long does it take for memory to disperse after death?
1: There seem to be cases where coma patients with a non-active brain (i.e. flat EEG) have regained full consciousness. => Apparently memory and knowledge are stored independent of brain activity.
2: There seem to be animals (e.g. hamsters) that can be frozen to complete organic inactivity and will regain full functionality after being thawed. => Apparently the stored memory does not depend on blood flow and other support.
3: From this I assume that quickly cooling a human brain to a temperature low enough to avoid decomposition would preserve the state of that brain that corresponds to that human's memories, knowledge, cogntivie abilities, and maybe consciousness at the time of cooling. => With the proper technology that "content" is theoretically retrievable.
Q: How long would that state remain after death in a brain left at room temperature?
Or in other words: How long does it take for decomposition to destroy memory?

Addendum:
The fact that the stored memory may not be accessible with current means is not relevant to my question. We cannot access the information stored in Linear A, but this unretrievability does not delete the information.

I think your premise is off.  If someone recovered from a flat EEG, I think the simpler conclusion to draw is that a flat EEG doesn't equal NO brain activity.  The brain was still working; but its activity was not detected.

looks like this deals with cryopreservation which is still a field in its infancy

@potterbond007 The actual question (in bold) does not pertain to cryopreservation. I used the premises only to deduce that (long term) memory is indepentent of brain activity, so it should still exist after death (unlike consciousness, which probably depends on the brain's activity). The question is: for how long does memory persist without cryopreservation?

Old question, but case 2 (hamsters can be frozen to complete organic inactivity and thawed) doesn't seem to have anything to do with memory. I'd also be interested to see whether this is true of an adult organism, or simply for sperm and/or egg. Hibernation certainly isn't complete organic inactivity, so this must be referring to something else if it is true.

Note that this point of no return is called information theoretic death.

There are multiple levels of memory, some of which would die immediately, some of which would take some time. So the answer is: it depends; some immediately, some only very slowly.
At the highest level, the current neuronal firing state of the brain encodes memory on a very short scale - working memory. The memory held on this level does not have a clear anatomical counterpart (but for the potential encoded in the synapses). It equals very short-term memory/STM sequences, such as the words you read just before you read the words you're reading right now. This memory is lost immediately when you lose consciousness, at least to some degree; as this memory is hard to even strictly distinguish from consciousness and attention (though see Jonides et al. 2008).
Other forms of short-term memory/STM are stored in a slightly different form: short-term potentation, the adaption of neuronal responses following brief and intense stimulation. Spike Frequency Adaption/SFA is at an intermediate stage between this and the previous level. Short-term potentation and SFA decay within minutes or even seconds if they are not transferred into some more durable form of memory.
Long-term memory (/LTM) stores have specific anatomical correlates; they are stored in, amongst others, the synaptic weights (i.e. the amount of influence the firing of one neuron has on another). Some forms of LTM are best located in cortical synapses, others in the hippocampus. An even more fundamental, long-term, durable storage form is the wiring itself; not just the weights, but the existence of a synapse between two points, or not. For example, an important part of early learning is synaptic pruning, where synapses which do not play a meaningful role die off, whereas those which connect functionally related brain areas remain.
This pruning instantiates one form of learning, and the non-existence of a synapse is a form of memory. Synapses are comparatively stable. Even if the corresponding neurons die, in principle, the synapses still exist - and more importantly, the nonexistence of a synapse is even more durable. This form of memory can be observed in slice preparations of animals long dead.
For a simple example, consider any experiment on the neuronal responses in slice preparations, which can be considered a form of (decontextualised) memory access.
On the most extreme end, epigenetic adaptions and large-scale brain anatomy (which shows developmental traces) can be considered a form of memory that will remain intact until the whole structure rots away.
However, the more direct answer to the question the OP is asking is that once a large amount of neurons have died (brain death), there is currently no power on earth that can access a non-trivial amount of memory. As long as this is averted, nontrivial amounts of memory can be recovered.
For the parts that are lost immediately, see the source by Jonides et al. For more durable memory, you could look at for example Purves et al, Neuroscience.

In some of the founding works of modern neuroscience, Hubel & Wiesel (1977, Phil Trac Royal Soc B) show that plasticity in the domain of ocular dominance induced by partial sensory deprivation results in gross anatomical changes, such as cell shrinkage. This can be seen as the result of a certain kind of information the animal received during its lifetime; and stored information equals memory. Arguably, "one eye was closed off for most of this animal's life" is trivial, but it's recoverable well past death. Contemporary neuroscience of course goes well past that.

I also fail to see how a tattoo would be relevant to the OP, and consequently do not discuss tattoos in my answer.

You have given the OP the answer he wanted. That is what matters.

Once the thermodynamically irreversible processes we call brain-death have occurred both memories and the machinery to retrieve them are lost.
This is not an answer but a cavil with the premise of the question. Challenges that do not destroy the brain itself are different from those that do. In particular there may be a big difference between hypoxia during periods of low metabolic rate$^1$ and hypoxia at room temperature without lowering of metabolic rates, which by most accounts leads to brain death in about 6-8 minutes.$^2$ The assumption underlying the title of the question is unsupported and opinion-based.
$^1$ See the pretty well-known case of Mitsutaka Uchikoshi, and see News Physiol. Sci. 13: 149-153, 1998, detailing case of a meditation adept who was able to drastically lower metabolic levels.
$^2$ See the Wiki page on apnea. Sources avoid putting a time after which brain death is certain, and the definition is not uniform. The one thing they agree on is that it is irreversible; so if someone (or, say, a hamster) recovers from putative brain-death, they were neither factually nor legally dead.

That frozen hamster, whose btain was "dead" by the definition of human brain death, showed no sign of having lost the memory of his habitat after reanimation. Quite obviously memory is stored physically and independent of brain activity.

The brain is unlike a current computer in many ways (e.g. neurons don' t have binary on/off states), and the relevant difference in the context of this question is that the brain stores info in its neuronal structure, i.e. by changing the hardware.

Guyton, Arthur C. (1986). "The Cerebral Cortex and Intellectual Functions of the Brain". Textbook of Medical Physiology (7th ed.). W. B. Saunders Company. p. 658. ISBN 0-7216-1260-1. "We know that secondary memory does not depend on continued activity of the nervous system, [contd.]

[contd.] because the brain can be totally inactivated by cooling, by general anesthesia, by hypoxia, by ischemia, or by any method, and yet secondary memories that have been previously stored are still retained when the brain becomes active once again. Therefore, secondary memory must result from some actual alterations of the synapses, either physical or chemical."

"No activity detectable with this or that instrument" does not equal "no activity", neither is equal to "dead".  Your deduction is flawed.

So you mean to imply that there must be activity in a frozen brain, because otherwise that hamster should have been revived to a brain state similar to a newborn? That is quite obviously nonsense. The childhood development of the human brain has been studied in detail, and learning has been shown to lead to a change in neural structure. What do you think the purpose of that change is, if not the storing of information?

Technically the main limiting factor for recovery from anoxia is actually that the brain goes into starvation mode and the cells self destruct. There are ways to mitigate this, one idea I had in 2013 is to flood the circulatory system with essentially high concentration glucose and barbiturates mixed with very cold (4C) water and irradiate the brain-to-be-preserved with NIR radiation at two key wavelengths. This is known to improve survival in damaged retinal cells (similar to CNS) and in fact Prof. Canavero (aka the head transplant doctor) is using a very similar method to help spinal neurons reconnect in addition to the use of transverse electrical fields and modulated oxygen flow so as to keep the cells in hibernation but not too high as to damage them.
The idea of the barbiturates is to stop the neurons firing out of control therefore "burning out" before the structure can be preserved for later readout.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5820829/
https://link.springer.com/chapter/10.1007/978-3-642-69175-1_17
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5364001/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4768515/

What size of a machine are we talking, if we wanted this solution as an "emergency pack" to carry around always?

This answer is pure hypothesis unsupported by evidence. To say what works on retinal cells will work on brain cells is somewhat like saying what works on thyroid cells will work on pancreatic cells (both similar as exocrine gland with an interrelationship.) Hypotheses are not answers. Much better to give a factual answer that only partly supports your hope.


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Human female chest model or data representation?
I am looking for professionally used representation of female chest (I know how it sounds ;). Generally - a model comprehensive enough to effectively represent human chest, with focus on breasts.
The data it needs to represent are at least: width, height, depth, distance between cardinal points, so on. I do know there's a questionnaire for patients willing to undergo an implant operation - I'm looking around for something similiar. Optimally the model would be directed towards computer represenation.
With that in mind, I've checked some computer implementations:

SOFA (seems promising, but somewhat generic),
MakeHuman (nice
customization, but again, pretty general).

I do not know whether this question is in scope of this site. If it's too specific, then consider the simplified: what are the methods used to describe female chests OR what would be a good source of information about these methods?

What is the purpose for (ostensibly) a breast model? These are commonly used in radiotherapy models but I am not familiar enough to point you to a data source.

@leonardo, for exactly that - to export it to DICOM for radiotherapists.


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Pharmacology Half Life Calculation
I'm really stuck on this question. I'm being asked to find the half life of a drug.
The Vd is 50L/kg. The clearance is 0.1 L/hr/kg. The patient weighs 70 kg.
Equation is:
T1/2 (halflife) = 0.693 * Vd / Cl.
I keep getting 0.693 * 50 / 0.1
               = 346.5
The right answer is 14.4 days but I can't figure it out.
Thanks in advance

You have done the calculation correctly it is just the answer you have is in hours, try dividing by 24.
A  good method of checking answers is to use a trick which is horribly called "Dimensional Analysis". This basically means writing out your equations but use the units of each value rather than the value itself
so in this case you have T1/2 = Vd/Cl      (removing the unitless 0.693)
the units for this are then ? = (L/kg)/(L/hr/kg)
in this case the litres and the kilos cancel to 1/(1/hr) or just hours, comparing this with the correct answer which is in days should then be a little more obvious


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Can Rubella virus pass into brain stem?
B19 virus (about 20 nm) can; which I think is partially because of its small size; not sure of genomics has something to do with the passing. Rubella's (also called German measles) size is then again minimum 45 nm.
So I started to think if this virus can pass into the brain stem.
Can Rubella pass into the brain stem?
Some studies are made about Rubella associated hemolysis.
I think it is not related with this question at all.
Rubella is diffused along carbon dioxide from capillaries into the brain stem, this is my hypothesis.

What makes you think there is a connection between hemolysis (the breakdown of red blood cells) is connected to an infection of the brain?

@Chris Thank you for pointing out my not clear point out! I do not know what is the role of hemolysis with rubella in diffusion to brain stem. I cleared the confusion in the body.

It obviously can do that, causing a rubella encephalitis. A specialized form seems to be the "Progressive rubella panencephalitis", which is very rare with only 20 cases described since its first description in 1974.
About rubella encephalitis more papers are available, see these for a start:

Neurological aspects of rubella virus infection.
Mumps encephalitis: return with a vengeance.
Neurological Aspects of Rubella Virus Infection

Exactly! I have this disease also in my notes. I think it can be caused also by Measles encephalitis. I think Mumps encephalitis cannot cause the disease because it is too big. The disease is only caused by some Measles virus variant and rubella. Both lead to demyelination in CNS progressive degeneratively and ending in exitus letalis.


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Do Noroviruses include many families?
Wikipedia says Caliciviridae Family.
My notes say that Norovirus includes the following
Noroviruses

Norwalk-like viruses
Caliciviruses
Astroviruses and some small gastroenteroviruses

which is a larger definition including at least two families than the Wikipedia definition.
I think

Caliciviruses $\subset$ Caliciviridae
Astroviruses and some small gastroenteroviruses $\subset$ astroviridae

so the note is taking subsets among different families and classifying them into abstract class called Noroviruses.
Extension based by Chris' excellent answer.
Criteria of Noroviruses

(+)sense ssRNA viruses
Structure and replication:

1) only (+)sense ssRNA,
2) simple nucleocapsid viruses,
3) only viruses transmitted by fecal-oral route,
4) size about 30 nm in diameter.

and then final classification of Noroviruses by these criteria
Noroviruses

Noroviruses $\subset$ Norwalk-like viruses ($\subset$ F. Caliciviruses)
Some Astroviruses ($\subset$ F. astroviridae) and some small gastroenteroviruses (what?)

which, however, does not make sense since Caliciviridae $\not\subset$ Astroviridae.
I do not understand what is the point of referring to the viruses by the sentence

Astroviruses and some other round/small gastroenteris viruses

which are not part of Astroviridae.
Which viruses of Caliciviridae are similar to Astroviruses that are apparently round and small gastroenteritis viruses?

I don't understand your new question. What do you mean with understand? What is the purpose of your work?

@Chris Thank you for your comment! I included the criteria of classification for Noroviruses.

You want to know how the Norovirus was selected taxonomically?

@Chris Yes, I think so. In above definition, noroviruses include some viruses from Caliciviruses, Astroviruses and some other small gastroenteroviruses.

Which doesn't make sense. Ciliciviruses include Noroviruses, but not Astroviruses. The only belong to the same group.

@Chris Thank you for your comment! I added the criticism to the body. I think the last point is trying to refer to some viruses in Caliciviridae that have some characteristics of Astroviruses that are small/round gastroenteris viruses.

You are mixing different things here: Virus are grouped based on their genetic material (dsDNA, ssDNA ssRNA and so on) into several groups (see here for details), then grouped into families, subgrouped into a genus and then into species.
So it is: Group > Family > Genus > Species.
What you have here are are different positions in this classification.
The names you mention belong all to the same tree:
Group: IV ((+)ssRNA-Viruses) > Family (Caliciviridae) > Genus (Norovirus) > Species (Norwalk Virus).
The Astrovirus belongs into the same group, but then form an own family.
To answer your question: No, since the Norovirus forms its own genus in the caliciviridae family.

Last sentence - do you mean genus (not family)?

Thank you, Chris, for your excellent answer! I have been completely confused by different naming systems that have been used. Besides those two systems, there seems to be also some conventions. I am trying to understand what is the initial point of making a abstract entity "Noroviruses" and including some viruses from different families into it.

I take NCBI's taxonomy any day over what wikipedia says. According to NCBI Caliciviridae includes Lagovirus, Nebovirus, Norovirus, Recovirus, Sapovirus, Vesivirus, Secalivirus, etc. For example:
Viruses; ssRNA viruses; ssRNA positive-strand viruses, no DNA stage; Caliciviridae; Norovirus; Norwalk virus; Chiba virus
Anyway, due to the absence of universal phylogenetic marker genes, viral taxonomy is mostly based on capsid shape and isn't thus very accurate..


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Why digest proteins into peptides for Liquid Chromatography - Mass Spectrometry?
Digesting (trypsin or whatever other proteolytic enzyme) proteins generates multiple peptides  so the degree of complexity of the sample, at the peptide level, increases a lot. In addition there is the problem of infering the original protein from its constituent peptides.
Why is this digestion step needed when you have to go back to protein level ? Is it just technological limitation?

As you rightly put, it is a technological limitation. Mass spectrometry based studies require proteins to be fragmented into smaller peptides for the ease of analysis.

It seems though, that intact proteins (even protein complexes) can also be analysed by MS. I just knew that

See pg no. 33 and 35 of this pdf. It says that Reversed Phase HPLC can be used both for studying protein digests and intact proteins.

Yes, LC works on separating large macromolecules, but my guess is that the limitation is on analyzing them by MS. Why can't you just do high throughput proteomics by LC-MS/MS as you would with digested protein mixture but with intact proteins?

I found the answer to my own question
It was formulated in a Nature publication by Mathias Mann (Title: The ABC's (and XYZ's) of peptide sequencing), a pope in Proteomics:

Why are peptides, and not proteins, sequenced?
After protein purification, the first step is to convert proteins to a
set of peptides using a sequence-specific protease. Even though mass
spectrometers can measure the mass of intact proteins, there are a
number of reasons why peptides, and not proteins, are analysed in
proteomics. Proteins can be difficult to handle and might not all be
soluble under the same conditions (it should be noted here that many
detergents interfere with MS, because they ionize well and are in a
huge excess relative to the proteins). In addition, the sensitivity of
the mass spectrometer for proteins is much lower than for peptides,
and the protein might be processed and modified such that the
combinatorial effect makes determining the masses of the numerous
resulting isoforms impossible. Furthermore, it is not easy to predict
from the sequence what the mass of a mature, correctly modified
protein will be or, conversely, which protein might have given rise to
a measured protein mass. Most importantly, if the purpose is to
identify the protein, sequence information is needed and the mass
spectrometer is most efficient at obtaining sequence information from
peptides that are up to approx20 residues long, rather than from whole
proteins. Nevertheless, with very specialized equipment, it is
becoming possible to derive partial sequence information from intact
proteins, which can then be used for identification purposes or the
analysis of protein modifications in an approach called 'top-down'
protein sequencing

This is going to be a very long answer but to give a short response.
You have to consider that MS for peptide detection works on the bases/principle of mass to charge (m/z) to detect an AA molecule, which is then normalised and analysed etc etc (http://en.wikipedia.org/wiki/Mass_spectrometry). Once you have the amino acids, then you just look at the order in which they get through and then you have your peptide sequence. Please read about the B, A and Y-type ions although this page is slightly technical (http://www.matrixscience.com/help/fragmentation_help.html). If the proteins was not digested then it would be far too big to be analysed since it would be read as one massive blob of m/z, which could be anything! So once you have your spectra from a peptide, you need to compare it to a model spectra, and based on that you predict what the sequence is as fragmentations peaks can be anything. Look at SEQUEST (http://en.wikipedia.org/wiki/List_of_mass_spectrometry_software). Now there are tons of correction algorithms that are applied, which you can look up.
Now RP-LC is carried out before MS to prevent all the sample rushing into the MS machine all at once as the machine can not cope if too much sample is inserted hence the flow rate is controlled. What I think you are thinking in terms of the set machine limit, is the (digested) peptide fragment that enters the machine, before undergoing electrospray. Now the experts that run the MS machines do set a peptide mass upper and lower limit, for what size/mass of fragment to accept and what size/mass to ignore. Look at this theoretical digest example (http://prospector.ucsf.edu/prospector/cgi-bin/msform.cgi?form=msdigest). This happens frequently with trypsin digest as it recognises specific AA before cleavage (http://en.wikipedia.org/wiki/Trypsin). Now a days, MS has advanced so much that we have machines such as Orbitrap (http://en.wikipedia.org/wiki/Orbitrap), which can cope with peptides, digested with elastase, which cleaves non specifically, which means you are less likely to get peptides that are far too big for analysis, hence increasing the protein coverage.
Hope this helps!


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Identify a bird
I have taken this picture of a bird in university zoo in Tel Aviv. It was approximately 25 cm high and seemed to be a flightless species. Can somebody help me identify it?

They fly rather well when they want to.

It's a Black Crowned Night Heron, Nycticorax nycticorax, in my opinion - you can read more about it here. Key to it's identification is the shape of the body and bill, it's characteristic of species from the heron family such as the green heron. The range is right and the red eye is a good clue too.

Thank you, it seems to be a Black Crowned Night Heron indeed. The photographs on wikipedia page helped me to conform this http://en.wikipedia.org/wiki/Black-crowned_night_heron .


text:
Error in textbook
This must be an error

Just as proteins have a polarity defined by the amino and carboxyl
  termini, oligosaccharides have a polarity defined by their reducing
  and nonreducing ends. The carbohydrate unit at the reducing end has a
  free anomeric carbon atom that has reducing activity because it can
  form the open-chain form, as discussed earlier (p. 325). By
  convention, this end of the oligosaccharide is still called the
  nonreducing end even when it is bound to another molecule such as a
  protein and thus no longer has reducing properties.

In my opinion, this sentence only makes sense if it would read reducing. Can anyone confirm?

Just a quick comment. You would have better to write a title that is a bit more explicit than "Error in textbook". I could not have any idea of whether I'd have the skills to answer your question. (Hopefully you use one tag that is slightly more informative).

I agree that, purely from the point of view of the language used in the last sentence, it must mean 'reducing'.

In case of oligosaccharides, only the final ends matter and not the ends of the individual monosaccharides involved in glycosidic linkage. As a consequence, most oligosaccharides have only one reducing and one non-reducing ends.

I am not sure what the textbook means by the last line but the following two possibilities seem to be consistent with the understanding of oligosaccharide structure.

There is no mistake and the end being talked about is the left end of the monosaccharide on left in the diagram . This monosaccharide has both its ends non-reducing, but only one of these ends will be called the non-reducing end even though the other end(formerly reducing end) is now involved in glycosidic linkage and is hence non-reducing. The it in the last line in this case refers to the entire monosaccharide (and not the end of concern), which has lost its reducing ability.
There is a mistake. And the end being talked about is the right end of the monosaccharide on the left. It is usually not referred to as the reducing end (which is the rightmost end), but for the case of explaining the polarity of the monosaccharide, it can be referred to as the reducing end.

+1 for admirable attempt to give the author the benefit of the doubt. I agree with OP it's just a slip, your (2).


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Why can't intermediate filaments be used as tracks by motor proteins?
A motor protein like kinesin-1 cannot use an IF as a track because it lacks polarity.
Can someone elaborate on this answer?

Just a guess: the IF doesn't have directionality. It would be like a single-lane, but two-way road.

Polarity essentially means a plus end (growing/polymerising) and a minus end (depolymerising). Look at microtubule (MT) (http://en.wikipedia.org/wiki/Microtubule). So molecules such as Kinesin-1 (http://en.wikipedia.org/wiki/Kinesin) use the hetero-dimeric nature of MT (alpha and beta subunits) and its polarity to orient themselves and move directionally along MT in an energy dependent manner.


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Implications of what the discovery of Naia means
Recently a discovery was made of a ~12,000 year old girl in Hoyo Negro in Mexico.
This has been covered by many different news agencies.
I'm confused however by many of the reports.  Does it strengthen the hypothesis that the ancestors to the Native Americans came over the Bering Strait?  Or is there still some doubt on the matter?
Additionally, what are the arguments against the Bering Strait migration?

As far as I can remember from skimming the published paper, it does provide support to the hypothesis that the first Americans probably migrated over a Bering Strait land bridge sometime during the last ice age. Remember, individual scientific findings rarely "prove" anything, they just support or refute a certain hypothesis (what a layman would call a "theory", a word which has a rather different meaning when used by scientists).

I would rather call it hypothesis for this reason instead of theory.

@MattDMo, updated to reflect your and Chris' suggestions.

The discovery strengthens the bering strait land bridge hypothesis because if I remember right they did genetic analysis and her ancestors were almost certainly east asian. As for opposing migration models, they involve boats. Some evidence exists for polynesians reaching the west coast of south america, but probably in small numbers and not before humans walked in from the north. There is more information here: https://en.wikipedia.org/wiki/Models_of_migration_to_the_New_World


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What is this spider?
I took the following picture of this spider in northern Switzerland (alt: ~700m) with macro flash (then it is not so big: probably around 2-3 cm, including the legs)

This spider made its web on the house and it goes out only during night.
In this region we have many Araneus diadematus, but this one looks totally different.
Is it the same family or another? Does anybody have a clue for the real name?
UPDATE: I saw it this afternoon (gave a fly to the web to make it go out), the body is probably around 7-8 mm wide and 9-11 mm long). And now I am sure the colors are more or less right.

My guess is that it is a spider from the Tegenaria genus. There are a lot of spiders in this genus, a lot of them are only active at night. And they are common in europe.

We also have this tegenaria species here but they all look thinner than this one. This one have a big fat body like the Araneus genus (even I guess it can be probably another genus)

Maybe Badumna longinqua (grey house spider)

@TheLastWord Is it not Australian species? do you think it can live in Europe? I have to mention it was taken in a natural environment.

@ruffp According to this article (http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/26406) it is capable of establishing itself in Europe but I would not go as far as to say that this is Badumna longinqua. I went through pictures of some native spiders in Switzerland but could not find a match. Just venturing a guess based on some morphological features like the colour.

I'd guess it's Nuctenea umbratica, or otherwise similar in appearance and coloration pattern, but less frequent Nuctenea silvicultrix.
At least Nuctenea umbratica was recorded in Switzerland.

It look it was a Nuctenea umbratica by all the pictures on Google.
And according to the Bern university site, the distribution of Nuctenea silvicultix does not include Switzerland,
but Nuctenea umbratica does.

@ruffp: I also tend to think it's Nuctenea umbratica. It could be that Nuctenea silvicultrix avoids high altitudes, but it's presence in Germany and Italy makes it very possible to occur in Switzerland as well, so I'd not rule it out completely, but the chances are much lower.

authors: Сергей Лобанов


text:
What is this spider hunting in the tree in the night?
I took the following picture of this spider in northern Switzerland (alt: ~700m) with macro flash/lense.

The picture was taken during the night in a cedar tree (Thuja occidentalis).

Nice picture :)

That is a really well taken picture.

Thanks for the comments, it was taken without tripod, then I was a bit lucky to got it in the focus range.

It's look like Sac Spider (Clubiona lutescens) to me.

Source: http://ednieuw.home.xs4all.nl/Spiders/Clubionidae/Clubionidae.htm

Nice catch, I am wondering how you could find this. I tried to browse many spider database but did'nt find anything.


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Question about what the liver does NOT do
Which of the following functions is NOT performed by the liver?
a) Storage of vitamins and minerals
b) converts glucose to glycogen
c) converts toxins to harmless chemicals
d) produces bile
I chose b and got it wrong, any help?

I'm pretty sure the liver can do all of those things…

A is actually arguable. The other three are perfectly true for liver but I am not sure about option A.

If you are asking a homework question, you must show what attempt you have made to answer it.

Liver does all those functions as far as I know. The liver hepatocyctes are stimulated to create the enzyme glycogen synthase which promotes the conversion of glucose to glycogen in the presence of insulin. Glycogen is stored in the liver after its production for further use. The whole process is explained in detail in this page. Regarding the storage of vitamins and minerals, I have a paper which details the absorption and storage of Vitamin A in rat liver.  I am also linking another paper that details the presence of Vitamin B12 in the human liver.

Even if the liver does store some vitamins, this would not make statement (a) true - there would have to be storage of minerals as well. The liver can store iron as ferritin (along with lots of other tissues).

@AlanBoyd yeah, support both claims to make the statement true which u have done. Reference for the statement is http://library.med.utah.edu/NetBiochem/hi11b.htm Thanks for pointing that out.

animal liver is very rich in vitamin A and iron.

answer a) is definitely the 'least true' and is the right answer for sure. However, the question is iffy and should probably be made a bonus question :)


text:
dsDNA translation
Since DNA is double stranded and each strand is complementary to the other, the codons on each strand will come out to be different after transcription(depending on the reading frame). Does this mean "each strand of DNA" codes for different set of proteins?

Related: http://biology.stackexchange.com/questions/17674/anti-parallel-dna-code-operons/17675#17675

Since DNA is not translated you should think about a different title for your question.

My understanding is that the antisense DNA strand (3'-5') makes the (sense) mRNA hence protein coding DNA strand where as the sense DNA strand (5'-3') is the non-proteins coding DNA strand. Hence the sense DNA produces antisense non-coding RNA, which ultimately acts as a translational regulator (http://en.wikipedia.org/wiki/Antisense_strand). The only reason sense DNA strand is called the the sense strand is because it is complementary to the sense RNA or mRNA.

There are a few confusions here, I will try to get them resolved without adding more:
First, a gene is always read in the 5' -> 3' direction, no matter on what strand of the double helix is is located. In the traditional way of writing down DNA the forward (or +) strand is written from left to right, the reverse (or -) strand from right to left. So even is you draw a gene map like the one below, the genes which run on the reverse strand.

For the transcription the reverse strand (it doesn't matter if it is the + or - strand) is not important. You can even have different genes on forward and reverse. In many cases the reverse strand doesn't code for any genes though.

Can there be opposed directions of read on one and the same strand (determined by the promoter's choic of *3 or 5')?
I recently learnt that promoters bring along a row of nucleotides that anneal and "determine the direction" of reading. In your opinion, isn't it the choice, or fact, that a  promoter sits on either of both strands that determines the direction of read, which, as it occurs, is downstream. Would that make up some different question?

I am not sure if I understand your comment. Do you want to know if transcription from a promoter can run in both directions?

DNA is not always double stranded. Anyway, typically, you have islands of protein-coding genes in both strands in all six frames, i.e. a set of genes in the forward strand, then a set of genes in the reverse strand, then again a set of genes in the forward strand, etc.

I might be misunderstanding you, but this doesn't sound like an accurate description at all.

Care to mention some genome that doesn't conform to the description?

I'm saying that protein-coding genes typically occur as islands on both strands. For example, you might have five protein-coding genes in the 5'-3' strand and then downstream ten protein-coding genes in the 3'-5' strand and then downstream twenty protein-coding genes in the 5'-3' strand again, and within these islands, the genes occur typically in all three strand-specific frames.

Doesn't only the sense strand have its code forming the  protein at the end while the antisense strand serves as a template?

So basically each strand of DNA does code for different protein set?

Yes, but protein-coding genes hardly ever overlap in opposing strands

Are there any references supporting sense DNA strand making proteins?

The sense strand is the strand that has the same sequence as the transcribed mRNA. Antisense strand is the template. Which strand is sense strand and which strand is antisense strand varies by genomic region.

.to put it simply: what you call as sense/antisense strand depends on the gene you are studying. If the gene you study changes, the strand that was called sense for another gene might be the antisense strand for this gene.

I think there’s confusion here about scale. Yes, at the genome or chromosome level, you will find protein-coding sequences in all 6 reading frames. For a specific stretch of DNA designated a protein-coding gene, you will typically only get one protein from that sequence. Notable exceptions are viral genes that encode alternative proteins by ribosomal frame shifting


text:
Why do veins look blue?
I know that veins carry oxygen.
Veins look blue because the oxygen-depleted blood in them is blue.
Is this true??

It's not because the blood is blue. You can easily confirm this by noticing that when the nurse draws blood from your vein for a test, it looks quite red, and neither does it turn blue inside a sealed test tube even though the living cells would presumably use up the oxygen. Furthermore, even if you hold your breath and blow it on blood, it does not turn blue (and even pure CO2 won't make it blue).

If you have "the flying circus of physics by walker", it has a very good explanation of this phenomena.

Well, even though most people presume that it appears blue (reference) is due to the blood being deoxygenated, it is actually not the truth because blood is never blue whether it is deoxygenated or not. In a paper by Dr Alwin Kienle titled Why do veins appear blue? A new look at an old question, the authors measured how much light of various wavelengths was reflected from both real blood vessels in skin and imitation vessels in a skin-like environment. The synthetic vessel (which was a capillary tube filled with blood and placed in a milky substance with optical properties similar to skin) allowed the authors to experiment with a variety of parameters (particularly vessel depth and diameter), and they were then able to validate their results by taking measurements on actual vessels in skin. They eventually came to the conclusion that the optical properties of skin and blood is what makes the veins appear blue.
I quote from the paper as to the reason of blood appearing blue.

"Blue light does not penetrate as deeply into tissue as red light.
  Therefore, if the vessel is sufficiently deep, the reflectance in the
  blue will be affected to a lesser extent. Deoxygenated venous blood
  has a greater absorption coefficient than oxygenated arterial blood in
  the red spectral region, and this difference of two, rather small,
  values is amplified because of the long path length of red light in
  scattering tissue. As a result, veins are more likely to look blue
  than arteries at the same diameter and depth. Often arteries are not
  seen at all because they are generally smaller than veins and have
  thicker vessel walls. It has been shown that a small vessel will look
  red when close to the surface. However, if a superficial vessel is
  large it can still look bluish, particularly in the case of the vein.
  On the other hand, if the depth of a vessel is large, even red
  remitted light will not be influenced by the vessel, and it will not
  be seen."

So in short, the blue appearance could be attributed more to the location of the vein than just the deoxygenation.


text:
Plateletpheresis for hemophilia
Plateletpheresis is seperation of platelets from whole blood and putting the leukocytes and erythrocytes back into the blood.
If the person donating platelets does not have hemophilia than could a hemophilia patient get a periodic transfusion of platelets from a non-hemophiliac platelet donor so that his hemophilia is less severe whether it is hemophilia A or hemophilia B?

Wikipedia has a nice page on clotting disorders  - it shows Hemophilia isn't a defect/deficiency of platelets, but rather due to defective clotting factors in the plasma.  When platelets are transfused, they have a very short half-life and are used for acute support in  disorders like Bernard-Soulier syndrome

but platelets are transfused along with plasma aren't they since platelets and plasma are hard to separate? If so than if someone gets a plasma transfusion with platelets which still qualifies as plateletpheresis from someone without hemophilia and the person getting the transfusion has hemophilia it should lower the bleeding from something as simple as bumping on something.

Indeed, under US standards, an apheresis platelet product contains platelets in donor plasma.   But hemophilliacs are typically treated using plasma-derived or manufactured ("recombinant") clotting factors since that addresses the actual underlying basis of their condition.

yes I know but clotting factors are in the plasma so wouldn't it make sense that a non-hemophiliac donor of plasma if it donates blood to a hemophiliac that the clotting factors within the donor plasma would lower the risk of bleeding for much longer than those manufactured clotting factors?

Plasma contains antibodies that can cause transfusion reactions, so giving bulk  plasma requires cross-matching.  Instead, the fraction of the plasma enriched in the clotting factor needed to complement the deficiency in hemophilia, or recombinant factor is used.   Re duration of effect, in plasma the factor is at x1 concentration.  A plasma fraction could be x1,000 and recombinant x100,000. In the 80s hemophiliacs in Canada got HIV from plasma fractions.  Since it contains no pathogens, recombinant therapy is best.


text:
Are there any organisms that lack ATP synthase?
ATP synthase is used by cells to synthesise ATP from ADP using energy from a proton gradient. Depending on which sites I look at, this is either a universal feature of living cells, or it's "almost universal", used by the vast majority of organisms.
As Superbeast points out in a comment, ATP can also be synthesised on the substrate level via the Krebs cycle. However, I would like to know if there are any organisms that only synthesise ATP this way. In other words, are there any known organisms that entirely lack the ability to produce ATP synthase, and produce ATP entirely through the Krebs cycle, or through some other mechanism not related to ATP synthase?
If there are, I would like some information about them. Are there many such species or just a few? Are they all prokaryotes or all eucaryotes, or some of each? What kind of environments do they live in?

https://en.wikipedia.org/wiki/Substrate-level_phosphorylation

Right, Krebs cycle, that was kind of obvious I guess. Thanks! But are there organisms that only produce ATP that way?

As Superbest mentioned, substrate level phosphorylation (SLP) is alternative pathway by which ADP is phosphorylated to ATP. In SLP, phosphorylation is coupled with a highly exergonic chemical reaction. Fermentative organisms (both fully and temporally fermentative) organisms depend on SLP for ATP.
Note: fermentative $\neq$  anaerobic
Fermentation can either be a temporary situation, depending on the growth substrate (for e.g. yeast) or the only option as in the case of amitochondriate organisms like Entamoeba. You can refer this book if it is available to you. See this article too.
You can also see the wikipedia page on fermentation; it mentions the SLP steps.

If you can add a convincing citation (for the lack of ATP synthase in fermentative organisms) or a link to more information, I will accept this answer.

i added some info. see if it is fine

The linked article appears to be referring to organelles within eucaryotic cells, rather than to the cell as a whole. I'm specifically interested in whether there are any cells that entirely lack ATP synthase, not just in the organelles, but in the outer membrane as well.

Eukaryotic cells don't have ATP synthase on their membrane.. It is always expressed in an organelle. There are reasons to have an organelle. I have given some explanation for this on this post. It is energetically unfavorable for a eukaryotic cell to behave like a huge mitochondria.


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Does a reduction in stem cells mean possible earlier death?
The basis of this question relies on my understanding of these 2 facts:
1) A person has a certain number of stem cells from birth
2) Stem cells are the basis of all cells and are used to repair and replenish

I read an article about stem cells being found in fat removed by lipsuction and that the trials that has been done on using these stem cells for repair elsewhere in the body.
My question is, if stem cells are used for repair in the body and you have a certain amount of them, if you "lose" some via liposuction, does this then mean you have less stem cells and therefore less chance of repair and could then theoretically die sooner?
It's more than likely my lack of knowledge on the subject but I would like to understand why.

yes. problems with stem cell function can lead to many diseases like leukemia which is why we have stem cell transplants.

So if you have liposuction, you have an increased risk of leukemia - is it really that straightforward?

I did not say liposuction can lead to leukemia, I said problems with stem cell function which is a very general observation. Please go through this paper (http://www.nature.com/ncb/journal/v16/n3/full/ncb2928.html). As far as your question about the impact of loss of stem cells through liposuction is concerned, I have to say I am unsure and would have to do some research first before I speculate.

I think the question should be edited to say "does liposuction increase leukemia risk by removing stem cells". This is what you are really asking, and the more general current form is arguably unanswerable.

Stem cells persist because they have the capacity to self-renew.  At birth you will have a finite number of each stem cell type (e.g. hematopoietic stem cells that make blood, gut epithelium stem cells that make gut lining etc).  The general picture is that as tissues require replenishment, a stem cell divides. One daughter cell starts to differentiate (and divide) into mature cells required by the tissue, whereas the other daughter cell retains stem cell function.
So a stem cell is typically defined as a cell with the capacity to: (i) self-renew and  (ii) to give rise to one or more cell types in a tissue. A hematopoietic stem cell can give rise to T-cells, B-cells, neutrophils, red blood cells, platelets etc.  The ability to self-renew means that, in general, stem cells don't 'run out' during a lifetime.
[ Its important to note that to define a cell as a stem cell, scientists use strange hybrid of: in vitro or animal assays + cell surface markers + location in the tissue + measures of 'having the capacity to make continued contribution to new cells'.  So lets just say that stem cells are only ever as well defined as our choice of assays combined with the interpretation of those results. ]
I mention the challenge of defining stem cells because, in recent years as assays and technologies improved, cells such a oocytes (eggs) or adult neurons, which were once thought to be finite, have been shown to have be replaced/renewed, presumably by some 'stem cell like' cell(s).
As noted above, stem cells are usually involved in the replenishment of a particular tissue type.  So liposuction, which will remove fat cells, should not affect the numbers of hematopoietic or neural stem cells and so on.
Any claim of clinical benefit of a 'stem cell treatment' using liposuction should be backed by clear data.
A longer answer would get into:
(i) the concept of 'plasticity' where the classical view - a fixed pathway between a stem cell giving rise to one daughter cell that  gives rise to mature cells and the other returns to a stem cell state - is open for debate, and
(ii) the idea that since stem cell definitions are only as good as our assays, there may be potential plasticity even among stem cells that we cannot 'detect' yet.

Death is caused by a variety of factors, our ability to heal is among them. However, it is possible to die from causes other than a deficiency in healing ability. Most people in the world die from cardiovascular disease and cancer.
The role of stem cells in the heart is an area of intense investigation. Vascular clogging is a more likely cause of cardiovascular failure than a disease of the heart muscle itself. In the case of clogged vessels, no biological mechanism exists to heal clogged arteries. Stem cells are irrelevant here.
Stem cells are most applicable to cancer in the immune system for the recognition of cancer cells. A decrease in actively dividing immune stem cells would correlate with an increased progression of cancer. This is exactly what happens with people undergoing chemotherapy. Chemotherapy kills actively dividing cells, including stem cells in the immune system. This is why they often suffer increased infections. It is rare to die from an infectious disease today. Decreased immune response from chemotherapy is a manageable side effect of treating cancer.
If you recreationally took chemotherapy drugs, this would inhibit the activity of stem cells. Your body would rapidly accumulate genetic mutations and systemic damage resulting in eventual death. This is why people coming in contact with individuals on chemotherapy should be careful not to touch any surface contaminated with the drugs. This especially applies to pregnant woman, where the danger is primarily with the fetus. In development, stem cells are vital in organ formation, not healing.
In different circumstances, to different individuals, during different life stages, destroying or preserving stem cells may be therapeutic, or devastating.

Theoretically, yes. Although, to my knowledge it has not been proven. As far as I'm aware there is no known link between liposuction and leukemia, liposuction would most likely not remove enough stem cells to produce such an effect. I've been doing a lot of research into stem cells lately and from what I have found there have not been many, if any, in depth studies on the impact of stem cell removal as the implantation of stem cells is usually the main focus.

theoretically yes to what?

Theoretically it could inhibit the body's ability to repair itself and cause an earlier death. Although the replication of stem cells to form other stem cells would prevent this from occurring. All stem cells in the region would have to be removed along with a life-threatening condition for stem cell removal to have this effect. Sorry this wasn't clear above.