text:
To what extent is Ebola airborne? (aerosols)
Recently, CIDRAP at the University of Minnesota announced that Ebola may be more transmissible through aerosols than previously thought.
I lack the familiarity with the field to critically evaluate this release. They also seem to more interested in making the point that there is a risk of aerosol transmission, not to settle whether it does transmit by air or not.

What is the simple answer? Can Ebola really be transmitted by aerosols?
If so, how come nobody realized this before? Is this a general phenomenon allowing any pathogen to become airborne? I don't see why you couldn't aerosolize a great many pathogenic objects, not just Ebola virus.
How does the number of virions necessary for successful infection compare to what you could get from aerosols?

Related: http://biology.stackexchange.com/questions/21481/how-is-it-possible-to-even-hope-for-an-ebola-epidemic-of-this-current-size-to-re

Interesting question and hard to answer definitively. First of all: It seems still pretty clear that the major (and by far most important) infection route comes from direct contact with infected people or their body fluids and that aerosol transmission is of far less significance. Ebola is infecting cells of the immune system (mostly macrophages and dendritic cells) which are located in the skin which makes the route through the respiratory organs pretty uneffecient, but it is possible.
However, there are reports for Ebola transmissions (or at least unclear cases in which a direct contact could be excluded), which suggest that the aerosl transmission is possible. There are reports of Ebola infections which spread among experimental animals between infected and non-infected (and without direct contact) control groups. This has been observed between rhesus monkeys and pigs. It was also possible for the pigs to infect non-human primates (see references 1-4 for details).
This results should be seen with some caution: At least for pigs an Ebola infection seems to be pretty much different than one in humans. There it looks more like a respiratory disease with all what comes along with it: Extended sneezing and coughing - which makes a lot of aerosol droplets. See reference 3 for the original paper and 5 and 6 for a summary and a classification. I think it is also possible that anatomical differences to the humans make such an infection route easier or harder.
Finally there are some reports of infected people which had no direct contact to people (see reference 7). However, this is rare and mostly restricted to people which where involved in health care for infected persons. These people come in close contact to the infected people which raises their chance of getting infected by aerosols. This underlines the importance for health care workers to get the right protective equipment.
References:

Transmission of Ebola virus (Zaire strain) to uninfected control
monkeys in a biocontainment laboratory.
Replication, Pathogenicity, Shedding, and Transmission of Zaire
ebolavirus in Pigs
Transmission of Ebola virus from pigs to non-human primates
Aerosol exposure to Zaire ebolavirus in three nonhuman primate
species: differences in disease course and clinical pathology
Pig-to-monkey Ebola: is there something in the air?
New paper on Ebola–no primate-to-primate transmission seen
Ebola Hemorrhagic Fever, Kikwit, Democratic Republic of the Congo,
1995: Risk Factors for Patients without a Reported Exposure

Nice answer but I think "spreaded" isn't a word and should be just "spread".

@Mew You're right. It's an irregular verb. BTW: If you spot errors like these, click on the edit function below an answer or question and correct it. Your edit will undergo a review until you have a certain number of credit points. This is a perfectly accepted way of improving answers.

It is not airborne, because if it had be we would have a really big problem.

Normal immunocompetent mice are not susceptible to non-adapted
  filoviruses. There are therefore two strategies available to establish
  a murine model of filovirus infection: adaptation of the virus to the
  host or the use of genetically modified mice that are susceptible to
  the virus. A number of knockout (KO) strains of mice with defects in
  either their adaptive or innate immunity are susceptible to
  non-adapted filoviruses. In this study, A129 α/β −/− interferon
  receptor-deficient KO mice, strain A129 IFN-α/β −/−, were used to
  determine the lethality of a range of filoviruses, including Lake
  Victoria marburgvirus (MARV), Zaire ebolavirus (ZEBOV), Sudan
  ebolavirus (SEBOV), Reston ebolavirus (REBOV) and Côte d’Ivoire
  ebolavirus (CIEBOV), administered by using intraperitoneal (IP) or
  aerosol routes of infection. One hundred percent mortality was
  observed in all groups of KO mice that were administered with a range
  of challenge doses of MARV and ZEBOV by either IP or aerosol routes.

2011 - Lethality and pathogenesis of airborne infection with filoviruses in A129 α/β −/− interferon receptor-deficient mice

Ebola virus disease is not an airborne infection. Airborne spread
  among humans implies inhalation of an infectious dose of virus from a
  suspended cloud of small dried droplets.
This mode of transmission has not been observed during extensive
  studies of the Ebola virus over several decades.

2014 - WHO - What we know about transmission of the Ebola virus among humans

The virulence (ID50, LD50) is unkown for humans, but ebola is considered a highly virulent disease with low LD50 based on the studies with animals.

INFECTIOUS DOSE: Viral hemorrhagic fevers have an infectious dose of 1
  - 10 organisms by aerosol in non-human primates Footnote 41.

1997 - EBOLAVIRUS - PATHOGEN SAFETY DATA SHEET - INFECTIOUS SUBSTANCES

Although outbreaks of Ebola virus have largely been confined to
  endemic regions, their high fatality rate, ability to transmit
  person-to-person, and low lethal infectious dose make Ebola virus a
  dangerous threat to public health and pose a great risk for
  researchers working with these viruses as well as health care
  personnel treating patients during outbreaks. Furthermore, their
  potential to be developed into aerosolized biological weapons also
  causes grave concern for their use as a bioterrorism agent ( Bray,
  2003).

2008 - Protection against lethal challenge by Ebola virus-like particles produced in insect cells

Ebola virus is a highly virulent pathogen capable of inducing a
  frequently lethal hemorrhagic fever syndrome. Accumulating evidence
  indicates that the virus actively subverts both innate and adaptive
  immune responses and triggers harmful inflammatory responses as it
  inflicts direct tissue damage. The host immune system is ultimately
  overwhelmed by a combination of inflammatory factors and virus-induced
  cell damage, particularly in the liver and vasculature, often leading
  to death from septic shock. We summarize the mechanisms of immune
  dysregulation and virus-mediated cell damage in Ebola virus–infected
  patients. Future approaches to prevention and treatment of infection
  will be guided by answers to unresolved questions about interspecies
  transmission, molecular mechanisms of pathogenesis, and protective
  adaptive and innate immune responses to Ebola virus.

2007 - Immunopathology of highly virulent pathogens: insights from Ebola virus

The LD50 of mouse-adapted EBO-Z virus inoculated into the peritoneal
  cavity was ~1 virion. Mice were resistant to large doses of the same
  virus inoculated subcutaneously, intradermally, or intramuscularly.
  Mice injected peripherally with mouse-adapted or intraperitoneally
  with non-adapted EBO-Z virus resisted subsequent challenge with
  mouse-adapted virus.

1998 - A Mouse Model for Evaluation of Prophylaxis and Therapy of Ebola Hemorrhagic Fever

The high virulency is compensated by low transmissibility, that's why it is not a real threat currently for western countries (it is easy to quarantine). The current strain seems to be special, because it has about 100 times higher mutation rate than the old ones. It may mutate into a more transmissable strain, but I think there is not enough data and knowledge available to calculate the risk of such an event.

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

wikipedia - Ebola virus

Molecular evolutionary analyses for Ebola and Marburg viruses were
  conducted with the aim of elucidating evolutionary features of these
  viruses. In particular, the rate of nonsynonymous substitutions for
  the glycoprotein gene of Ebola virus was estimated to be, on the
  average, 3.6 x 10(-5) per site per year. Marburg virus was also
  suggested to be evolving at a similar rate. Those rates were a hundred
  times slower than those of retroviruses and human influenza A virus,
  but were of the same order of magnitude as that of the hepatitis B
  virus. When these rates were applied to the degree of sequence
  divergence, the divergence time between Ebola and Marburg viruses was
  estimated to be more than several thousand years ago.

1997 - The origin and evolution of Ebola and Marburg viruses.

Thinking that ebola can evolve to become airborne is kind of like thinking horses can evolve to fly. It's not that kind of virus. What it can do, though, is very dangerous, akin to a horse learning to run faster.

@anongoodnurse I don't know whether airborne ebola is possible, but it certainly can become a more transmissible disease, e.g. it can become more stable in vitro, more resistant to UV light, heat, etc...

But it won't learn to float on dust particles. Probably the most dangerous mutations would involve a decreased virulence, such that people will not feel as sick early on (while maintaining transmissibility) so that quarantines are rendered less effective. But it's all speculative.

@anongoodnurse Then why are we talking about it? "I think there is not enough data to calculate the risk or say something about it is possible or not."

Just trying to counter a common but unfounded fear. Is there a reason we should not?

@anongoodnurse Do you have any evidence that it is unfounded?

@anongoodnurse I don't think the current level of life science and technology is enough to decide this question. We know too few about the ebola virus and viral evolution. I will remove the airborne ebola from the post, because there is no evidence about whether it is possible.

Me personally? No. But I quote Dr. Eric Lander, geneticist, molecular biologist, mathematician, and computational biologist (among other stellar qualifications) the founding director of the Broad Institute of MIT and Harvard, a principal leader of the Human Genome Project, a professor of biology at MIT and professor of Systems Biology at Harvard Medical School who is also Co-Chair of the President’s Council of Advisors on Science and Technology. That's good enough for me to give credence to his opinion that it won't happen.

@anongoodnurse Quoting somebodies personal opinion is not an evidence. We need a viral evolutional model with all of the possible (or at least the closest) more transmissible outcomes which we can use to calculate the risk. Currently no such model is available as far as I know, and I think there won't be such a model for many decades, because we know so few.

I thought earlier you said we needed a "life scientist." Key phrase: as far as (you) know.

@anongoodnurse I don't know what you are talking about.

Although the chance of Ebola getting airborne is bigger than zero and thus be possible, it is highly unlikely. The reason for this is quite simple: To act like this it needs to change the cells it infects. For viruses which are transmitted by aerosols these are commonly the (epithelial) cells of the respiratory tract. See the flu for example. To do so ebola most likely has to change the receptors it uses to invade cells and also the way it transmit. Both has never been observed before and would probably be a new virus afterwards.

@Chris It already infects epithelial cells using NPC1 and TIM1 receptors. So the only barrier it has to break down is the new way of transmission. I don't know how hard that is, we will see in the next few years I guess. (There were several studies on animal models, in which it was proven that it is possible to infect with a small dosage of aerosol. LD50 was around 1 virion.)


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If human eyes watch an area, what's the shape of its capturing shape? Rectangular? Half spherical?
A normal camera can capture a rectangular image. If human eyes watch an area, what's the shape of the captured region? Rectangular? Half-spherical?

Mapping the output of a camera's photon sensors as a rectangular grid of pixels is an explicit and arbitrary decision made by the designer of the camera (and driver/firmware architects). Because the output of a human eye is not visualized on a monitor, and consciousness itself is a very controversial phenomenon, I think this question is ill-posed. A better question would be, "how does human visual acuity change over the FOV?".

@Superbest On the other hand, regardless of how the sensory input is used, the eye still, physically, has a definite viewing volume (i.e. a definite range of angles such that photons passing through the lens at those angles interact with the retina). E.g. no matter how you feel about consciousness, a ray of light arriving at the back of your head will not strike your retina.

The capture area of the eye is a bit fuzzier and harder to define than that of a camera.
A camera captures consistent, fully detailed data right up to the edge of its sensor, and no data at all beyond it. Captured data is clipped by an ideally uniform sensor, augmented a bit by the lens, and is well-defined during design and manufacturing.
The eye can capture higher "resolution" near the center of its capture area and also has very little information about color near the edges (see also Peripheral Vision); so it's not quite as clean cut depending on your goal of "capture area". The eye also has a bit of a "blind spot" near the middle, which our brains basically Photoshop out. Additionally, it varies from person to person.
The effective capture area would really depend on your application (e.g. the "capture area" for, say, reading text, would be narrower than the area for, say, detecting motion).
Here is a typical diagram for a single eye, showing just the ability to see something in that area (does not show details related to peripheral vision quality):

Here is a typical diagram for both eyes combined, the solid white area is the overlap:

Both of those images are from a 1964 NASA report detailing aspects of the human visual field. If you want the detailed answer to your question and more, you probably want to take a look at that.
Note that our field of vision is very wide, those diagrams may not do it justice. As an experiment, close one eye, stare straight ahead and hold your arms straight out to the sides. Wiggle your fingers and slowly bring your arms forward until you can just see your wiggling fingers in your peripheral vision, and you will get an idea. As an added experiment, hold a piece of paper with text on it, and repeat the same experiment until you can read the text - this region will be extremely narrow and will give you an idea of how the quality of vision changes across the field. Also try with a colored object and bring it in until you can clearly identify the color.
There are also some simplified mentions of it in wikipedia:

http://en.wikipedia.org/wiki/Field_of_view#Humans_and_animals
http://en.wikipedia.org/wiki/Human_eye#Field_of_view
http://en.wikipedia.org/wiki/Visual_field#Normal_limits

A good set of search keywords is "human field of vision". There is also a nice related article entitled The Camera Versus the Human Eye.

Great answer, but the illustrations hide (as you say in the text) the order of magnitude difference in resolution between the middle of the field and the sides. For a camera, all of the pixels are almost equal, for an eye they are not.

@Peteris Yeah... I added the bit about doing an added experiment to try to make up for inadequacies in the diagrams. When I have a better internet connection I'll try to find better diagrams.

Perhaps add a reference to how the brain makes you feel you have a more cinematic and even visual field (more Photoshopping) e.g. http://en.wikipedia.org/wiki/Saccade - this depends a little on what the OP means by "watch an area". Unless effort is made to keep eyes still, watching is naturally and unconsciously an active scanning process. Edit: Scratch that, that is very nicely covered in your last link (The Camera Versus the Human Eye).

The link to the 1964 NASA report is now broken; if someone can find a better link (or a real citation) that would be a nice update. I tried but failed.

@eclarkso Thanks. I've replace it with an archive.org link.

I don't know why I didn't think of the Wayback!  For posterity, the citation is to Webb, P., Ed.  Bioastronautics Data Book: NASA SP-3006.  NASA Special Publication: Washington D. C., 1964.  An updated and more recent citation for the diagram is also in Parker Jr, J.F. and West, V.R., Eds. Bioastronautics Data Book: NASA SP-3006. NASA Special Publication, 2nd Ed., 1973, p. 631.

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How does the ebola virus attack?
How does the ebola virus attack and how do some people get away with it? Normally any virus would attack a cell with some kind of receptors and some kind of lock and key mechanism entering the cell and then multiplying.
What happens to the virus if a person manages to live through it, does the virus die and is thrown out or still remains inside the host?
I am not sure about a normal virus attack i tried to explain please correct on that also.

It is known that Ebola uses at least one cholesterol transporter called "Niemann-Pick C1" (NPC1) to enter its host cells. Cells with a mutated form of this transporter were not infected by the virus (this extends to other viruses from the Filovirus group as well), which seems like a proof that this can make people "immune" to the virus. However, these are only experiments in cell culture. Other experiments show that a small molecule inhibitor that mimics the transporter can inhibit Ebola from entering cells and infecting them.
There are two papers on this topic:

Ebola virus entry requires the cholesterol transporter Niemann-Pick
C1
Small molecule inhibitors reveal Niemann-Pick C1 is essential for
Ebola virus infection

If a person manages to survive an Ebola infection the immune system fights the virus by making highly specific antibodies against it. These antibodies bind to the viruses and mark them for the immune system (mainly through mast cells) for take-up and degradation while inhibiting them from infecting other cells. Serum from Ebola survivors has been used as experimental treatment for infected people (here mainly the antibodies can be helpful). People who survive the infection are immune against another infection of the same virus strain.

Ebola enters the cells most probably using the NPC1 receptor, which is expressed by all cells. That receptor is important by other viruses as well e.g. by Marburg virus entry, HIV release, arenavirus entry, etc...
Coreceptors are not necessary required, but they can enhance ebola virus entry. Such coreceptors are:

TIM-1 (or HAVcr-1) - expressed mostly by epithelial cells,
C-type lectins,
β1 integrins,
Tyro3 (TAM) family tyrosine kinase receptors - expressed by lymphoid cells,
Rab7

It totally confuses the immune system with moves you can see only in Bruce Lee films e.g. by stimulate the expression of proinflammatory cytokines in the infected cells, so it can cause hemorrhagic fever.
By fighting the virus the adaptive immune system selects and proliferates the B- and T-cells which are specific to the virus and so B-cells can label the cell-free virus in the blood with antibodies for destruction, while T-cells can kill already infected cells. So if somebody manages to live through the symptoms her/his body will destroy the remaining virus after a few days maybe weeks.

2012 - Filovirus entry into cells – new insights
2012 - Filovirus Entry: A Novelty in the Viral Fusion World
2010 - T-cell immunoglobulin and mucin domain 1 (TIM-1) is a receptor for Zaire Ebolavirus and Lake Victoria Marburgvirus

The gene is part of a 3-member transmembrane receptor kinase receptor
  family with a processed pseudogene distal on chromosome 15. The
  encoded protein is activated by the products of the growth
  arrest-specific gene 6 and protein S genes and is involved in
  controlling cell survival and proliferation, spermatogenesis,
  immunoregulation and phagocytosis. The encoded protein has also been
  identified as a cell entry factor for Ebola and Marburg viruses.
  [provided by RefSeq, May 2010]

2014 - TYRO3 protein tyrosine kinase

Recent studies have revealed that the TAM receptor protein tyrosine
  kinases — TYRO3, AXL and MER — have pivotal roles in innate immunity.
  They inhibit inflammation in dendritic cells and macrophages, promote
  the phagocytosis of apoptotic cells and membranous organelles, and
  stimulate the maturation of natural killer cells. Each of these
  phenomena may depend on a cooperative interaction between TAM receptor
  and cytokine receptor signalling systems. Although its importance was
  previously unrecognized, TAM signalling promises to have an
  increasingly prominent role in studies of innate immune regulation.

2008 - Immunobiology of the TAM receptors
2006 - Tyro3 Family-Mediated Cell Entry of Ebola and Marburg Viruses

We showed previously that Niemann-Pick C1 (NPC1), a lysosomal
  cholesterol transporter, is required for filovirus entry. Here, we
  demonstrate that NPC1 is a critical filovirus receptor. Human NPC1
  fulfills a cardinal property of viral receptors: it confers
  susceptibility to filovirus infection when expressed in non-permissive
  reptilian cells.

2012 - Ebola virus entry requires the host-programmed recognition of an intracellular receptor.

Ebolaviruses cause a severe hemorrhagic fever syndrome that is rapidly
  fatal to humans and nonhuman primates. Ebola protein interactions with
  host cellular proteins disrupt type I and type II interferon
  responses, RNAi antiviral responses, antigen presentation,
  T-cell-dependent B cell responses, humoral antibodies, and
  cell-mediated immunity. This multifaceted approach to evasion and
  suppression of innate and adaptive immune responses in their target
  hosts leads to the severe immune dysregulation and “cytokine storm”
  that is characteristic of fatal ebolavirus infection. Here, we
  highlight some of the processes by which Ebola interacts with its
  mammalian hosts to evade antiviral defenses.

2014 - Camouflage and Misdirection: The Full-On Assault of Ebola Virus Disease
2011 - Mouse LSECtin as a model for a human Ebola virus receptor
2013 - Ebola Virus-Like Particles Stimulate Type I Interferons and Proinflammatory Cytokine Expression Through the Toll-Like Receptor and Interferon Signaling Pathways

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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.

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.

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.


text:
Why do bacteria need messenger RNA?
Why do bacteria need mRNA? Isn't the DNA free floating without nuclear membrane so why doesn't the tRNA read the code directly off of the split DNA strands? (ofcourse after helicase splits them). Wouldn't this be more efficient?

Ribosomes don't read DNA.
Transcription adds several layers of regulation tactics: you can control transcription itself, you can control mRNA.
mRNA amplifies genetic information that you need at the moment. Having many copies of a matrix really helps.
Some prokaryotes have splicing. It's not a good idea to splice your DNA.

EDIT per your request of some elaboration.

Why did they evolve to read RNA in the first place as they are primal
  to all other organisms, why did they develop this

The "RNA world" hypothesis (which is the most realistic early life model, considering the ever-growing body of evidence) postulates that RNA had been the main thing long before DNA was introduced into cells. The ribosome (being an RNA enzyme that doesn't require any proteins to bind amino acids together), along with many other RNA enzymes and regulators, is believed to be a relic of that world. Wiki has a good page with all the references you might want to read.

Also, the regulation tactics, isn't DNA free floating and so are all
  the replication enzymes like Helicase, primase and RNA primer etc. So
  how do they regulate the action of these enzymes as they are just free
  floating?

First of all, it's a common misconception that prokaryotic cells are mere bags stuffed with enzymes and whatever. Prokaryotes posses highly complicated compartmentalisation systems (some even possess nucleus-like compartments). Second of all, DNA is not "free floating": it's located at a specific site with a special molecular environment. If you want details, ask a separate question, or better a series of questions with narrow scope, because bacterial regulation is too diverse, bizarre and sophisticated to cover here (we had a 3 years-long course on this matter when I was a student).

Could you explain a bit of how the extra copy helps as is it not just
  more data to deal with?

When you have many copies of a matrix, many ribosomes can synthesise a protein at once. This comes in handy when you need to make tons of something as fast as possible. Remember, ribosomes are quite ubiquitous in all active cells for this very reason: to facilitate fast protein synthesis (at least as far as copiotrophic organisms are concerned).

What exactly do you mean by splicing?

I mean splicing: a group of processes by which introns are excised from primary transcription products.

Why did they evolve to read RNA in the first place as they are primal to all other organisms, why did they develop this? Wouldn't it have been more convenient to just have the the tRNA in ribosomes to just read the DNA? Also, the regulation tactics, isn't DNA free floating and so are all the replication enzymes like Helicase, primase and RNA primer etc. So how do they regulate the action of these enzymes as they are just free floating? Could you explain a bit of how the extra copy helps as is it not just more data to deal with? What exactly do you mean by splicing? @Eli

@SarthakGarg you're welcome

I find most of these arguments unconvincing and undermine the only reasonable argument, i.e. that the translation system developed in organisms with an RNA genome, with ribosomes and tRNAs already tuned to work with RNA messages. For reasons that we cannot know, a transcription system evolved rather than a DNA translation system.

@David I see your point, yet I believe you are approaching this question from a different perspective. From my perspective, the original question was about mRNA's utility in modern cells and not about the process that had resulted in this functional separation between RNA and DNA. Only later (in the comments above), this additional question had been raised and later addressed in the Edit section.


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How does this diagram illustrate carbon cycling in lakes?
Could someone please explain the following process to me:

This process refers to carbon cycling in lakes and is described in the context of $CO_2$ flux from lakes into the atmosphere. GPP is gross primary production, $CO_2$ is carbon dioxide, R is respiration, and OM is organic matter. I realize that this question may be rather simplistic to some but my basic knowledge of any biological/ecological processes is rather limited. So, basically what I am asking is

have I written this process correctly?
how can this process be described?

This shows the major biological transformations of carbon in any system (not just lakes).
On the Left Side:

$GPP$ (Gross Primary Production) is the total amount of $C$ from atmospheric $CO_2$† that is reduced into organic molecules during the calvin cycle of photosynthesis.  This is the process performed by photosynthetic organisms like green plants and algae.

† atmospheric $CO_2$ diffuses into water and develops into several species of inorganic carbon molecules that plants and algae can use but in general you can think of this carbon as being very closely related to atmospheric $CO_2$

$OM$ is a pool of organic matter, which is a general term for reduced carbon molecules.  $OM$ can be living organism tissues (e.g., a fish), dead tissues (e.g., senescent leaves) or biologically generated organic molecules (e.g., sugar that leached from a plant).  $OM$ is the principle pool of energy and raw materials for all living things on Earth so this is a really important pool of stuff.

Since $GPP$ is taking $CO_2$ and converting it to $OM$ as the left side progresses, the amount of $CO_2$ in the atmosphere goes down and the amount of $OM$ in the biosphere goes up.
On the Right Side:

$R$ (respiration) is the oxidation of reduced carbon-containing molecules for the purpose of extracting usable energy.  This may be familiar as "cellular respiration" but there are other metabolic pathways that accomplish the same goal.  In the end when the $C$ in the $OM$ is oxidized and the energy released the $C$ that was in the $OM$ gets converted into $CO_2$.

Note that this is the opposite of the Left Side, so as this occurs, the amount of $OM$ in the biosphere goes down and the amount of $CO_2$ in the atmosphere goes up.
If the Left and Right sides are balanced, then there is no net change in the size of the $OM$ pool or the amount of $CO_2$ in the atmosphere.  However, note that over relatively short time scales these can be very out of balance.  Any time plants or algae are growing (i.e., gaining mass as $OM$) the Left Side > the Right Side or $GPP$ > $R$.  Once those plants die, they accumulate in the system as dead $OM$.  The decomposition of accumulated dead $OM$ by microbes will generally make the Right Side > Left Side or $R$ > $GPP$.
This picture from Wikicommons shows the same cycle in a more realistic setting.


text:
A good book for history of biology/biotechnology for lay people
I have many friends who are interested in Biology and want to know more about the subject in general (like a history of biology, from Darwin's theory, to DNA structure discovery, to the human genome project). Of course, I cannot suggest to them to read Alberts or Lenninger. Do you know whether such a book exist? I guess that a book that covers most fields of biology cannot be compiled, but even more focused book would do.
Let me try to narrow it down: something like the greatest discoveries in the field of biology (like this article) would be an interesting book to read.
I am not sure how appropriate this question is for SE, but I am sure that I will get the best answer here. Besides, it would be great if lay people can be more excited about biology and contribute to the site growth.

I think that this question is too broad, book recommendations about very specific questions are fine, but these very broad ones tend not to work all that well on SE sites. This is really something that chat would be good for, though our chat is somewhat deserted right now.

@Mad Scientist: pretty much any SE site I've been on has a few questions like this. And they are generally CW.

@Mad Scientist Didn't editing my question make it more specific?

It doesn't have very many reviews, but The Epic History of Biology sounds like it's perfect.
Flipping through the first chapter in the preview, it doesn't seem overly technical in any way, so secondary school-level knowledge is probably enough.  If your associates have absolutely no biology experience, perhaps a run through a popular press book would provide all of the background necessary.

I don't think the accepted answer should be a book that no one has actually read. I appreciate the "flipping through" that was done, but can anyone who has read the full book weigh in? If not, I'm uncomfortable that the community's best recommendation is based on a skim of the first chapter on Amazon.

@yamad I accepted this answer because the content of this book was the closest to what I was initially looking for. But the votes to the other answers should give you an idea of how good or well known the other books are.

@GerganaVandova, I understand. But isn't the critical question how good this book is? I'm interested to know if any of the upvotes know more about this book and could give their thoughts.

@yamad Her operative question here was: "Do you know whether such a book exist?"  I offered this based on the diverse list of topics it contains, I never claimed to have read it, and I was quite clear about that.

@yamad Unfortunately, I haven't read any of the recommended books, so it would be nice if people upvoted because they did. I am also happy to change my accepted answer as soon as someone recommends something else. I also recommended a book which fits what I was looking for but I haven't read it as well.

Some that just come to mind, in random order:
One cannot skip reading:

Richard Dawkins - The selfish gene

And, obviously:

Charles Darwin - The Origin of Species

And, for those interested in the evolution of the brain (and its quirks):

David J Linden - The Accidental Mind
Oliver Sacks - The Man Who Mistook His Wife for a Hat

Not very DNA/evolution-oriented, but wonderful science books nonetheless:

Primo Levi - The Periodic table
And the neveraging must-read:
Isaac Asimov - A Short History of Chemistry

Most if not all of Sacks's books also appeal to lay people.  "Island of the Colorblind" is particularly good.

I agree that Sacks is a great author to dig into. Such great first-hand experiences. I am a big fan of Dawkins, and think his 'Selfish Gene' is excellent, although, I think his rigor might turn casual readers off in this volume. However, I find The Greatest Show on Earth  much more readable - and available as an audiobook read by himself. (Selfish gene is also on audible, but I can't imagine it translating as well)

A good recollection of the early days of micro and molecular biology is "The Eighth day of Creation"
It covers the early use of e. coli, the discovery of phage, transcriptional elements and the impact that DNA structure had.  It's very comprehensive and really useful if you are doing molecular biology today.

I had not heard of this - thanks for the recommendation.

I don't know about useful, but it certainly brought things into perspective - it was required reading for our first year in the molecular biology PhD program.

I think somewhere in your PhD you can stop and try to figure out how we know things and how the process of discovery happens in a broader sense which is really useful and fun.

A fantastic book that covers the evolution of modern science since the Renaissance (including a great deal of biology) is The Scientists by John Gribbin. I found that by focusing on the people doing the science in the context of the society in which they lived, I got a much better understanding for why early scientists thought the way they did and researched the questions that they did.
Here's the blurb from the publisher:

In this ambitious new book, John Gribbin tells the stories of the
  people who have made science, and of the times in which they lived and
  worked. He begins with Copernicus, during the Renaissance, when
  science replaced mysticism as a means of explaining the workings of
  the world, and he continues through the centuries, creating an
  unbroken genealogy of not only the greatest but also the more obscure
  names of Western science, a dot-to-dot line linking amateur to genius,
  and accidental discovery to brilliant deduction.

I just came across Understanding Biotechnology. There is one very positive and one very negative review. I haven't read the book myself, but it looks that it is exactly what I was looking for: the table of content includes topics like small history overview, genetic engineering, gene therapy, pharmacogenomics, etc. It might be even useful for people with biology background.
Has anyone heard about this book?

I don't know very many books that might be referred to as the Grand History of Biology or anything like that. That's...a big topic. Really big. How about some suggestions for good Biology/Medical History books accessible to lay people:

And the Band Played On, by Randy Shilts, an account of the beginning of the AIDS epidemic in the U.S.
The Great Influenza, by John Berry, which is about the 1918 influenza pandemic.
The Demon Under the Microscope, by Thomas Hager, which is about sulfa and the development of early antibiotics.

Finally, I believe James Watson wrote a somewhat popular science-oriented account of the discovery of DNA, which would no doubt be interesting, though likely somewhat skewed in favor of his own awesomeness.

Hmm, thanks but I was mostly thinking about Cell Biology or Molecular Biology oriented books. Watson wrote "The Double Helix", but this book is focused only on the discovery of DNA, which, although very appealing to me, is too narrow-scope.

All of Watson's books are mostly about how many pretty girls he saw or met, and then secondarily about how he worked with lots of famous people. At some point he usually mentions a bit of biology, but it's tangential to the main theme of pretty girls.

By far the best book I've read on the history of biology is A Guinea Pig's History of Biology, by Jim Endersby. It tells the history of the field by focusing on experimental organisms and the contributions which were made by studying them. It has an engaging narrative style and the idea of focussing on organisms' stories is an excellent and original one.
However, the best resource there is on the history of science is the TTC History of Science lecture series. It comes in two parts:

Antiquity to 1700 by Lawrence M Principe of Johns Hopkins University
1700-1900 by Professor Frederick Gregory of Harvard

The lecture series are VERY expensive - around $200 each. However, most good libraries will have them, and I strongly recommend getting hold of them if you can.

My two favorite books are Molecular Biology made simple and fun and Biotechnology for Beginners. Both are well written and fun to read. As their names suggest, the former covers the basics of biology and the latter covers the basics of biotechnology.

This book, although a little dated, has given me an incredible appreciation of biology that I never gained in school:

What is Life? by Erwin Shrodinger

I am not a biologist, but I occasionally work on mathematical-biology and have training in physics and theoretical computer science. This book was much more accessible to me that other books on biology. Before reading the book I perceived biology as a collection of fun facts (what Rutherford would call "stamp collecting"). Shrodinger's presentation was well tailored to the typical reductionist and "everything must have a reason" thinking of a theoretical physicists.
I think the book does a good job of explaining the basics and providing intuition and grounding. The excited reader can then move on to more orthodox treatments.

There is a free video course "Modern Biology" at Carnegie-Mellon University's Open learning initiative. This is very technical and does not cover history of biology.
I quite liked D.A. Sadava's non-free video course Understanding Genetics: DNA, Genes, and Their Real-World Applications. This is Genetics and Molecular Biology oriented, but also not a book. It is suitable for a reader with high-school knowledge of chemistry. Maybe it contains too few basics, so it is also not for the absolute layperson. He starts with Mendel and mentions many other 20th-century researchers.
The author has co-authored one of those thick, expensive college-level biology textbooks as well.


text:
Did dinosaurs have more than one brain? If so, why?
I once remember reading (15 years ago) that dinosaurs had two brains. One for their head and another one for their digestive functions. What is the current opinion on this theory? Has more evidence become available?

the enteric nervous system (which humans also have) has been called "second brain" http://en.wikipedia.org/wiki/Enteric_nervous_system , but of course doesn't form an actual brain

It would appear that at one time it was thought that a "gap" in the skeleton of a Stegosaurus was a space for another brain. This is now thought to be a storage space for extra food.
Googling your question brings up a number of answers along these lines:

https://en.wikipedia.org/wiki/Stegosaurus#%22Second_brain%22
https://dinosaurs.about.com/od/dinosaurdiscovery/tp/dinoblunders.htm
https://wiki.answers.com/Q/Did_a_dinosaur_have_two_brains

Oh so it was a stegosaurus. Any current scientific findings that you are aware of?

nice question - another childhood myth dispelled!

This is a myth based on comments about the stegosaurus from a paleontologist in the 1800s. How it managed to persist is really beyond all logical reason but for a time it somehow managed to be accepted enough by the mainstream that it was even taught in school! You can still find this ‘fact’ online- just another reminder not to believe everything you read on the internet. Dinosaurs did not have 2 brains. There is an enlarged space that is likely to have housed glycogen- a characteristic shared by many birds. There is also a possibility that this area simply housed increased muscle and nerve mass, as in other living creatures signifying there back limbs were stronger and used more often than their front. Either way-no 2nd brain here.
Google dinosaur 2 brain myth for a quick jump to the Smithsonian, a reputable source covering the myth, it’s origins, pervasiveness, and both possibilities mentioned above. Cheers!

It would be great if you can add the Smithsonian link in your answer. Cuts short one googling step :) Can you also please add a reference for the glycogen storage?

I saw that some big dinosaurs got a second neuron group near their back legs to overcome some nerves signal delay problems. Not sure about that.

Could you add some citations or references to substantiate your answer?

I can't. I saw that on TV, it was a documentary from the BBC i guess.

A small talk about nerves delay in dinosaurs. Not talking about brains, but still interesting.


text:
Why Do Nerve Signals Get Crossed?
First off, I don't know if this is a normal healthy thing to occur. There have been many times where I have an itch on say my arm and I scratch it, only to feel the scratching elsewhere on my body. I assume somewhere along the transit of the touch signals to my brain the signal gets mixed up and is processed incorrectly.
So my questions are:

Why does this mixup happen? (chemical imbalance, damaged nerves, etc..)
How does my brain correspond the touch to somewhere else? (what is the process behind it)

You might be interested in this. And this.

@terdon: Thanks for the links, but interesting as they are they don't answer why the touch signals get crossed =o(. Irregardless if it is an itch or another form of touch, the brain should not be interpreting a touch on one part of the body as coming from another part. My question is why this mixup occurs and how the brain is incorrectly processing it.

I know, that's why I posted a comment and not an answer. Just thought you might be interested.

Could you clarify exactly how the sensation is wrong for you? You are supposed to have an itch for whatever reason, and when you scratch it it's supposed to go away and you get the touch sensation of your fingers instead. All in the same place of course. Are you saying that the actual touch sensation of your fingers on your skin is mislocated? If so, is there a regularity to where it is mislocated (e.g. symmetrical to body axis)? And does this only occur on skin that was itching before, or any part at any time?

@Armatus well the last time it happened I got an itch on the back of my arm and scratched it only to feel the scratching on my lower back. I don't recall which body axis they were at, I'll have to note that next time it happens, but it's rare. No, it does not occur on skin that was itching before.

What I meant was things like, if it was mislocated on the same spot but opposite side of the body for example; but it seems to be random. The other question was what exactly causes it to happen - does it only occur when you are scratching yourself after you were itching or also in other situations?

@Armatus I've only observed it happening when there is a random itch, but no prior itching, but not all itches have it happen. That's why it is so rare, I've only experienced it around two dozen times in the past ~15yrs. I'm 23, I'm assuming it may have happened when I was younger, but I never thought much of it since was just a kid.

How clear is that sensation? Does it correspond to your finger movement, i.e. are you certain that it is a misprojection of the sensation (onto the wrong part of your body)? With such a rare occurrence it could just be a random error.

@Armatus yes, it does correspond. If I stop scratching the itch, the touch sensation on other area of body stops, and if I start again it starts. I can't reproduce it later on, maybe because I can't find the exact spot the itch was, which is where the error is being triggered. If it is a random error, how and why would such a thing occur?

I get a similar weird nerve sensation happen to me. I can run my fingers down or up the outside of my leg and i feel the sensation on the inner side of my leg? Its weird and i have had it happen in different places on my legs. I would like to know WHY this confusion of sensation happens? I do suffer from multiple level high grade thoracic (T5 to T10) cord compression from herniations onto a tethered thoracic spinal cord (stuck to the bone) peripheral neruopaphy and autonomic nervous system dysfunction, (ideopathic Hypersomnia, Gastroparesis, swallowing difficulty, heart palpatations and low BP

Well nerve crossing or misinterpretation of nerve signal by the brain does not happen all the time. In case it happens frequently then I guess it would be Multiple Sclerosis or might be Fibromyalgia syndrome. In multiple sclerosis, the Myelin sheath surrounding neuron when gets damaged causes certain problem with nerve signal transmission to the brain. But that is not the main cause. The main cause can be found in Neuropathy:

When nerve cells are damaged, perhaps by a temporary restriction in their access to oxygen, they too atrophy or shrink a little, thus the synaptic junctions widens.  Just like with a spark plug in your car or lawn mower, if this gap gets too wide, the spark cannot make the jump. A normal sized nerve signal cannot jump this enlarged gap either, so the signal either does not get through or it gets misdirected to another part of the body and is misinterpreted as pain.

So I can say that the nerve cells in the place where you feel real pain fails to transmit the signal to brain via its neighboring nerve cell instead that signal passes through some other node randomly (or it might take the same path every time you touch the pain area) and signal the brain which gets misinterpreted and make you feel that you have pain in the misinterpreted region.

This is part of a neuro issue...like seeing numbers in color, or touching something but feeling it in another part of your body. The sensations are processed in the brains communication area and ifeas/sensations get mixed or crossed. 4% of the population has these experiences. You aren't odd; you're exceptional.

Welcome to SE Biology. Because this is a straight Q & A site rather than a chat site, our expectations of answers are perhaps different from other sites. You can read the help on writing good answers here. In particular, we expect you to provide evidence of some sort in support of opinions or information you provide. This is best done by a reference to a scientific paper or a reputable source on the internet, such as Wikipedia or one of the text books on NCBI bookshelf. I suggest you might consider editing your answer with this in mind.


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Is iodised salt harmful to the lactofermentation process?
I was discussing sauerkraut recipes with someone on IRC a minute ago, and they warned me not to use iodised salt in the process. My first (and so far, the only successful) batch is one I made with iodised salt - I think it's pretty much the default here. Searching the Internet shows roughly equal numbers of answers going either way, from "it doesn't matter" to "it discolours the vegetables" to "it kills the bacteria you want".
Clearly elemental iodine is nasty, as are any of the halogens. But is the iodide ion similarly harmful to the bacteria (and yeasts?) involved in lactofermentation, in the low quantities in which it's present in supermarket salt?

I think it may make a difference depending on which vegetable you're pickling...

This study found no difference in the outcome of sauerkraut fermentation with or without iodized salt:

There was no clear influence of iodized salt on microbial populations.
Stable fermentations were achieved using iodized as well as non-iodized salt.

Welcome to Bio.SE! This is a great contribution. Clear, concise, referenced. Thanks for contributing :)

from wikipedia:

No-additive salts for canning and pickling
In contrast to table salt, which often has iodide as well as
anticaking ingredients,
special canning and pickling salt is made for producing the brine to
be used in pickling vegetables and other food-stuffs. This salt has no
iodine added because the iodide can be oxidised by the foods and
darken them—a harmless but aesthetically undesirable effect.

I have been looking for a concentration, but I suspect it is below the threshold that would harm microflora, as it typically has to be visibly yellow (~6ppm if i remember correctly) to be effective as a contact antimicrobial agent...

The FDA states that for chemical sanitization, "An iodine solution shall have a … [c]oncentration between 12.5 mg/L and 25 mg/L" Food Code 2009 4-501.114(B)(3)
The main concern in pickling seems to be the aesthetic.  "Fermented and non-fermented pickles may be safely made using either iodized or non-iodized table salt. However, non-caking materials added to table salts may make the brine cloudy." National Center for Home Food Preservation


text:
Is episome a plasmid or a virus?
A plasmid is a small DNA molecule that is physically separate from, and can replicate independently of, chromosomal DNA within a cell.
In general, in eukaryotes, episomes are closed circular DNA molecules that are replicated in the nucleus. Viruses are the most common examples of this, such as herpesviruses, adenoviruses, and polyomaviruses. Episomes in eukaryotes behave similarly to plasmids in prokaryotes in that the DNA is stably maintained and replicated with the host cell.
Source is wikipedia.

A DNA molecule that replicates independently of chromosomal DNA is an episome. By this definition a plasmid is (usually) an episome. If a plasmid integrates into a chromosome by some mechanism (as for example in Hfr strains of E coli where the F plasmid is integrated) the plasmid loses its episomal status. Is this what you are asking?

this was exactly what I asked. Thank you very much.

I'll have to disagree with Alan. If the plasmid is integrated into a chromosome it doesn't lose its episomal status. Actually the integration of the plasmid is a characteristic of an episome.
This is a quote from this article: http://www.qub.ac.uk/mlpage/courses/level3/plasmidhistoryreview.pdf

"... For a decade or more it was confused with ‘‘episome,’’ although that was carefully
  crafted (F. Jacob and E. L. Wollman, 1958, C. R. Acad. Sci. 247, 154–156) to mean agents with
  traffic in and out of chromosomes.

Also this book (https://books.google.pt/books?id=YnXB54RtrR8C&pg=PA132&dq=episome&hl=pt-PT&sa=X&ei=oKZgVd3HEZOu7AaeoYPABQ&ved=0CCoQ6AEwAg#v=snippet&q=episome&f=false) clearly mentions that an episome is a genetic element able to exist in an integrated form (associated with the chromosome) but also with it's  own origin of replication (autonomous form). So in fact an episome can be a plasmid or a viral genome, but not all genetic elements have this ability.

(Reposting my comment as an answer since it seems to be what was required.)
A DNA molecule that replicates independently of chromosomal DNA is an episome. By this definition a plasmid is (usually) an episome. If a plasmid integrates into a chromosome by some mechanism (as for example in Hfr strains of E. coli where the F plasmid is integrated) the plasmid loses its episomal status.
The term "episome" was first coined by Joshua Lederberg to describe the nature of the F element in E. coli.


text:
Number of reading frames in nucleotide sequence
In class of molecular biology was posed this question:
"How many reading frames start in sequence of nucleotides 5' ... ATATGAATGATGACAT... 3' ?"

Please edit your post to 1) reflect your question (I assume it is "How many reading frames begin in the following sequence?") and 2) show what work you have done so far, or your thoughts on the topic.

Every nucleotide sequence has six possible reading frames, because each codon (determining one amino acid) consists of a base triplet (3 frames), and there is a complementary strand which could be coding (3 reverse frames).
To find the possible open reading frames contained in your sequence, you have to look for start codons. That is: ATG. But, as said the complementary strand could be coding. So if your known sequence contains CAT, that would be ATG on the opposite strand and might also be an open reading frame.
Count them now and then read on to compare answers.

Your specific sequence contains four start codons (3x ATG and 1x CAT, which makes ATG on the complementary reverse).
5' ... AT ATG A ATG ATG A CAT ... 3'
3' ... TA TAC T TAC TAC T GTA ... 5'


text:
Is there a link between autoimmune diseases and X-chromosome inactivation?
I was reading about the necessity of niche formations to adequate development of blood progenitors and this idea reminded me of the patchy inactivation of the X chromosome which followed that maybe, if some of these pathways passed through X coded proteins, this might make women have different niches, that could account for the seemingly greater occurrence of auto-immune diseases in women.
Is there any sense to this idea? Was this ever researched?

Yes, here is an article on it: "The role of X-chromosome inactivation in female predisposition to autoimmunity"
Below see the method and results summarised.

Using a DNA methylation assay, we have examined the X-chromosome
  inactivation patterns in peripheral blood from normal females (n =
  30), female patients with a variety of autoimmune diseases (n = 167).
  No differences between patients and controls were observed. However,
  locally skewed X-chromsome inactivation may exist in the thymus, and
  therefore the underlying hypothesis remains to be disproved.

Not very assuring finding, but the size of sample and the heterogeneity of diseases maybe influenced the results. I have to read it again with more attention, but thanks.


text:
Is there a DNA test to identify dog mixes?
We adopted a dog at the age of two. Our vet said it was a mix of an Australian Shepherd and Border Collie, which we've told everyone. Based on markings, I think it's likely. I am wondering, however, if there are any tests or other ways to know the mix of a dog if you don't know the specific parentage.
Does each dog breed have specific genetic markers that can be used to identify the breed? If so, has a dog breed test been developed or is there no commercial demand for such a test?

There are many commercially available mixed breed ID tests, as a quick Google search will tell you.  However, I cannot vouch for their accuracy: this news article may be of interest. Also this.
The genetic markers used to identify breeds in a mixed-breed are microsatellite markers (sometimes SNPs): you can read more here, but from the abstract:

We used molecular markers to study genetic relationships in a diverse collection of 85 domestic dog breeds. Differences among breeds accounted for ∼30% of genetic variation. Microsatellite genotypes were used to correctly assign 99% of individual dogs to breeds.

If you're interested in dog genetics, I encourage you to check out Elaine Ostrander's work.  She's written at least one book for laypeople, in addition to her numerous journal publications.

@leonardo: The paper managed to separate breeds by genotyping only 5 unrelated dogs of each breed, but yes, I agree that the commercial tests are at a disadvantage because of the lack of a common repository (also they might be using SNPs instead of microsatellites) -- this is probably a significant source of the variation between tests.

Another point that follows from the point made by @leonardo: if in the Parker et al paper, if breeds were separated on the basis of groups of microsatellites rather than microsatellites that were unique to each breed, you'd need a lot more markers to identify the heritage of a MBD with any reasonable certainty, so that you'd have clusters of linked markers (the idea being that each cluster was inherited from a single purebred dog).


text:
Why do red blood cells contain haemoglobin and not myoglobin?
So I am reading about muscles and I come across myoglobin. It has a much higher affinity for oxygen than haemoglobin. So why have animals evolved to have haemoglobin in red blood cells, rather than myoglobin, which would be much more advantageous?

Just to expand slightly on the answer by Jack Aidley:
Have a look at this section from Stryer's Biochemistry text book, particularly Fig 10.17, where you can see that haemoglobin has evolved to have a high affinity for oxygen at the O2 concentrations present in the lungs, but a low affinity at the O2 concentrations present in the peripheral tissues. This is achieved by binding oxygen co-operatively. This means that haemoglobin can release 60-70% of its bound oxygen. Under the same conditions myoglobin, were it be used in red blood cells as an oxygen carrier, would release much less.
Incidentally the Figure linked to shows a comparison between haemoglobin and a hypothetical protein which shows 50% saturation at the same concentration of oxygen but which binds oxygen non-cooperatively (like myoglobin).
A more direct comparison of haemoglobin and myoglobin  - found here -  is shown below:

edit added to respond to shigeta's response
I don't understand some of the statements from shigeta so here are my views - if I am wrong, I would (genuinely) like to be corrected, since I have to teach this stuff.

..."what is particularly useful about Hb's cooperativity is that the last oxygen is harder to pull off the Hb tetramer than the first."

This statement contradicts my understanding of the oxygen-binding behaviour of haemoglobin. In the deoxygenated state the protein is in the conformation known as the T (for tense) state, and this is a low affinity state. The binding of an oxygen molecule to one of the haem groups in one of the globin subunits of the tetramer increases the affinity, so that subsequent binding of oxygen becomes easier. The details of how this happens are still debated, but I think what I have said so far is accepted by everyone.
Here is an equation to represent the binding of the first oxygen molecule to the haemoglobin tetramer:
O2 + [Hb]4 <--> [Hb4]O2
If deoxygenated Hb has a low affinity for oxygen then that equilibrium must lie to the left hand side - in other words the right to left reaction (release) is faster than the right to left reaction (binding). This is not consistent with the idea that haemoglobin hangs on to its last oxygen.

"The heart, which is the first organ in the blood cycle after the lungs uses a lot of oxygen - if hemoglobin were not cooperative, it might take all the oxygen from hemoglobin just after the beat when it uses oxygen when in distress, creating a block of hemoglobin which is completely without bound oxygen."

This is based on an erroneous view of the circulation - it implies that all of the blood passes through the coronary artery before getting to the rest of the body. Oxygenated blood leaves the heart via the aorta. Although it is true that the first branch off the aorta is the coronary artery, most of the blood doesn't enter this branch, but proceeds into the remainder of the circulation. In this sense the coronary circulation (by which I mean coronary artery>coronary veins - the heart's own blood supply) is in parallel with the rest of the circulatory system, not in series with it. At rest, just 5% of the heart's output goes into the coronary circulation.
According to this review, Regulation of Coronary Blood Flow During Exercise, (I am simplifying a lot here, but this statement does appear in the review and is not taken out of context): "Increased myocardial oxygen demands during exercise are met principally by augmenting coronary blood flow." At rest the heart is already extracting most of the oxygen from its blood supply (see here for some interesting data) so again there is no question of the heart extracting much more - it simply needs more blood, and of course the increased heart rate will contribute to this. There is also scope for directing a greater proportion of heart output through the coronary circulation, but I have been unable to find any quantitative statements about that. Interestingly, if you take a look at the data in the 1st table of the data here you will see that, at rest, 22% of the heart's output goes into the renal circulation, but that much less oxygen is extracted from that blood (about one ninth of how much is extracted from the blood going through the cardiac circulation). This represents a source of potential increased blood to be diverted to the heart at the expense of a reduction in renal filtration.

"Also - Hemoglobin is pretty clearly an evolutionary adaptation where four myoglobins came together to form a cooperative oxygen binder, so at one time probably myoglobin was the oxygen carrier. There are some primitive animals which have no distinct hemoglobin, just myoglobin like carriers."

I agree it is clear that haemoglobin and myoglobin evolved from a monomeric myoglobin-like ancestor, and that the appearance of a tetrameric molecule created the potential for co-operative oxygen binding. I am not as convinced by the rest of the sentence. I think we have to agree first on what we mean by an oxygen carrier. What I mean is a protein that is a component of a circulatory system. I know of no evidence that a myoglobin like molecule could perform this function. This arises directly from the shape of a simple binding curve (a rectangular hyperbola). For the protein to be saturable at atmospheric oxygen concentrations it has to have a certain Kd, and this precludes significant release of oxygen at physiologically useful concentrations. You either have a protein which can unload effectively but will not ever become saturated with oxygen, or you have a molecule that is able to become saturated but cannot ever unload except at every low oxygen concentrations. That is the remarkable thing about haemoglobin - the appearance of cooperative binding allowed for a more switch-like interconversion between a high affinity state, for loading up, and a low-affinity state, for unloading.
Now, if you wish to include intracellular oxygen transport in your definition of "carrier" then we enter a whole other debate about the role of myoglobin, but I have gone on for far too long already, so I'll stop there.

See that's a much better answer.

Seems like you have focused on different points than I, which is why I felt I should feel free to pot.  "The oxygen affinity of 3-oxy-hemoglobin is ~300 times greater than that of deoxy-hemoglobin."  Coopertivity creates the shape of the affinity curve, but does not make myoglobin intrinsically higher affinity than Hemoglobin.  The shape of the curve is important adaptation to deal with circulation.  You could define oxygen storage any way you like, I am merely pointing out that the evolutionary history of the molecule.  No need to make a contradictory statement out of it by reinterpreting.

@shigeta Apologies if you think I have reinterpreted something - not sure what you mean by that. As a starting point for comparing affinities of the two proteins for oxygen, if someone didn't know anything about the binding curves they would compare the P50 values and conclude that myoglobin has a higher affinity -if both proteins start off "empty" in the absence of oxygen then, as we raise the oxygen concentration, when myoglobin has reached 50% saturation, haemoglobin is just 2-3% saturated. So I'm not sure what you mean by "intrinsic" affinity.

Just wanted to supplement to the other two answers... I was trying to use comments but ran out of space.
@AlanBoyd s figure tells you a lot - you can see that myoglobin (Mb) has a much higher affinity for oxygen, so it will sit in the muscle and take the oxygen the tissue needs from the hemoglobin (Hb) as the blood flows through the tissue.
But what is particularly useful about Hb's cooperativity is that the last oxygen is harder to pull off the Hb tetramer than the first. As a result, Hb will tend to hold onto some oxygen as it flows through the body, retaining some of its oxygen on each Hb molecule until later in the oxygenation cycle.  This keeps the oxygen concentration in the blood consistent.  The heart, which is the first organ in the blood cycle after the lungs uses a lot of oxygen - if hemoglobin were not cooperative, it might take all the oxygen from hemoglobin just after the beat when it uses oxygen when in distress, creating a block of hemoglobin which is completely without bound oxygen.  As this lot of hemoglobin circulates into the capillaries, you could get some parts of the body with no oxygen at all.
Also - Hemoglobin is pretty clearly an evolutionary adaptation where four myoglobins came together to form a cooperative oxygen binder, so at one time probably myoglobin was the oxygen carrier.  There are some primitive animals which have no distinct hemoglobin, just myoglobin like carriers.  Also some hemoglobins are not tetrameric, but with many subunits, so the cooperativity curves have sometimes been tuned by evolution for different organisms.

Figure above: "Rendering of Hb tetramer and monomeric Mb. Hb is composed of four subunits, two α-subunits and two β-subunits, each highly homologous to Mb" ( from figure in reference )

I have responded to this by editing my answer, since I also needed lots of space.

Blood needs to be able to lose oxygen as well as capture it, the whole point is to take in oxygen in the lungs and then release it throughout the body. Blood that is simply really good at absorbing oxygen would only be an oxygen trap. Myoglobin, having more affinity for oxygen, can take oxygen from hemoglobin and store it in the muscle for the near future use.


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What's the use of RNA editing in kinetoplast?
The genes of the mitochondrion (kinetoplast) of some Kinetoplastida - e.g. Trypanosoma brucei, the parasite which causes African sleeping sickness - are "encoded" in a way that the pre mRNA requiries partially heavy editing (insertion and deletion of Uridines) by the editosome (a RNA/Protein complex) until it can be translated to the correct proteins.
The information where to insert and remove Uridines is contained in small gRNA also part of the mitochondrial genome.
However this whole thing seems kind of unnecessary to me. Why did evolution not get rid of the surplus/missing Thymidines in those Genes? What's the use of this?

Parsimony is not the prevailing paradigm of biology - rather it might be opacity

You could have asked a similar question about splicing. The function of RNA editing seems to be similar: it's one of the ways to trigger production of alternative transcripts and proteins given the same DNA sequence.
The question is discussed, for example, in this review. The authors describe different known effects of alternative RNA editing:

Amino-acid substitutions
ORF extension
New unique ORFs
Alternative UTRs

Alternative editing is correlated with developmental stage, which is not surprising, given the fact that the parasites switch their energy metabolism in different hosts (1,2,3), with the mitochondria changing their structure accordingly.
The authors seem to be astonished as well and conclude: "RNA editing in kinetoplastid mitochondria is a beautiful example how evolution favors diversifying mechanisms even if they seem to be extremely wasteful from a
human perspective."

Haha, I read that last quote just the second before I read your answer. I find this answer much more satisfying than the neutral model proposed in 10.1016/0168-9525(93)90011-6. I like how you point out the different oxygen concentrations[source would be nice] as one would usually think of the mitochondrial genes as almost perfect and thus less variable. However, some (healthy?) doubt is left...

I've replaced the oxygen part of the answer with a more cautious and correct phrase. Sources are provided :)

One important point in my opinion, which opposes the neutrality hypothesis is that the minimal number of gRNAs potentially required for RNA editing (~150) is much less than the observed variability (~1000) (see p. 230), which again hints at adjustability of the system and at the biological relevance of this adjustability.

Thanks! I kinda agree on that last point through I don't think that this really challenges the neutral hypothesis ("see we have 850 neutral gRNA developed by chance. Now if a mutation in a gene occurs that can be rescued by one of those gRNA this change will also be neutral but will lead to a fixation of that gRNA"). Is Neutrality even the basis of diversity and thus adjustability?(and thus not neutral, hah)

If in this system a new gRNA emerges and gains no function in the nearest future, its destiny is to be lost within several generations. It's like a plasmid in bacteria: if you don't create a selective pressure (e.g., antibiotic with its respective antidote coded by the plasmid), the plasmid is quickly lost. And in this case we have a large pool of gRNAs, which are at first glance redundant.


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Why is Sanger sequencing inferior for detecting SNPs in cancer cells?
I am familiar with Sanger sequencing, but at the level of an undergraduate. A lecturer of mine tried to describe Sanger sequencing as losing the sequence information in noise when used to detect cancer. This paper also says "lacks sufﬁcient sensitivity for detecting mutant alleles in tumor biopsies,"(Thomas et al., 2006). What is it about Sanger that makes it too insensitive for SNP analysis?
Thomas, R.,K., et al. (2006) Sensitive mutation detection in heterogeneous cancer specimens
by massively parallel picoliter reactor sequencing. Nat. Med. 12, 852–855

As I understand, Sanger sequencing has low error rates compared to the NGS. But high throughput and whole genome coverage is difficult.

In the Sanger approach, DNA would be isolated from the biopsy and would contain both normal alleles and mutant alleles of genes associated with the development of the tumour. If, for example, PCR amplification was then used to derive a sample of a target template region, this material would end up being sequenced as a mixed population: the derived sequence would be an average of that population of sequences, and rare alleles would be masked.
The key difference in most next generation approaches is that the template DNA is "cloned" physically (e.g. by sequestering individual molecules into droplets, or by binding them to a surface) so that the sequences of these individual molecules can be determined in parallel. This approach would reveal tumour-associated polymorphisms when the sequences of the individual template molecules were compared.
Added later as supplementary information.
I have now looked at the paper cited in the question. This quotation from the Introduction bears out my main point about sequencing a mixture of templates differing at just a few key positions.

Although commonly used in many clinical settings, dideoxynucleotide chain termination (or ‘Sanger’) sequencing of PCR products often lacks sufficient sensitivity for detecting mutant alleles in tumor biopsies, where the failure rate has reached 75% in some cases. Gain-of-function oncogenic mutations are frequently heterozygous events or may represent a single allele of an amplified gene; thus, the signal for mutated residues is typically reduced relative to neighboring bases. Moreover, the ability to detect single base mutations or small insertions or deletions in biopsy material by Sanger sequencing depends heavily on sample purity (for example, the extent of contaminating stromal DNA) and genomic DNA integrity. Furthermore, resistance to kinase inhibitors may correlate with low-frequency second-site mutations. These observations underscore the challenges for accurate mutation detection in cancer specimens.
A massively parallel sequencing-by-synthesis approach, ‘picotiter plate pyrosequencing,’ provides a new alternative to Sanger sequencing. This approach relies on emulsion PCR-based clonal amplification of a DNA library adapted onto micron-sized beads and subsequent pyrosequencing-by-synthesis of each clonally amplified template in a picotiter plate, generating over 200,000 unique clonal sequencing reads per experiment. Sequence variants that represent a fraction of a complex sample can be vastly oversampled, thus enabling statistically meaningful quantification of low-abundance variants.

Sample issue would be with both sequencing strategies. Sanger sequencing is still used to confirm the de-novo sequences because of its low error rate. Cloning is also involved in both techniques but in Sanger you may need to prepare BAC libraries. The problem of Sanger is only with respect to its amenability to high throughput. [NGS wasn't there when most of the human genome got sequenced]. PS: Sanger is also relatively cheaper.

This is a recent paper in which two unicellular algae were sequenced using Sanger.

@WYSIWYG I'm not sure what either of these comments is adding. There is no question that Sanger sequencing can be used to derive genome sequences, since as you say it  has been so used. My interpretation of this question was that it relates to a scenario in which a mixed sample is to be sequenced, which creates problems for using Sanger sequencing, as I have tried to explain.

I understood the point of this paper. In this paper, I think the comparison is not between the technologies. Genomes from each cell can be separated using the picolitre plate(or other nanofluidic devices) and parallely sequenced. As Sanger sequencing fails to handle high throughput, the choice is sequencing by synthesis.

@AlanBoyd Your answer summarised the information in the paper very nicely. The paper makes sense after reading your answer! I still don't quite understand "Furthermore, resistance to kinase inhibitors may correlate with low-frequency second-site mutations."


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What is the evolutionary rationale for palm sweating?
Sweaty palms seems to be a reaction to stress, anxiety, etc. For our forest-inhabiting primate ancestors sweaty palms could cause unwanted side-effects such as slipping off tree branches under stressful conditions, like when being chased by a predator.
Why did palm sweating became a reaction to fear, worry, anxiety etc in the course of human evolution? What is the benefit of sweaty palms?

Sweat in response to stress is not limited to palms. Sweat glands just happen to be there I guess.

I guess the question is why do our palms sweat at all(?) because the OP has given an example of when sweaty palms are (possibly) a disadvantage (maybe slightly moist hands grip better). I am not sure of the advantage myself, perhaps because of the absence of hair on the palms they are useful for rapid heat loss which would be further increased if the palm is sweaty.

Many animals use palm or sole-derived sweat for scent marking, so there may have been an evolutionary pressure for retaining sweat glands on the palms. If the negative selective pressure wasn't large enough in primates, then there wouldn't be any reason to lose palmar sweat glands.

When the sympathetic nervous system is aroused, it has historically been for life threat situations, and in those situations historically there have not been a lot of slick things to grip or run on, but rather porous things. Those things, like sticks or rocks, were easier to grip or push off of or climb upon with a little moisture. Think of when you were a kid and you climbed a pole. You wanted your shoes off for that, didn’t you? And you wanted a little sweat because dry feet would slip. Same for if you’re wielding a branch or a bone or a rock as a weapon. That seems, to me, to be the primary

Do the top parts of our hands sweat? I can imagine that sweating palms gave a better grip on certain surfaces that were abundant.

I remember watching a documentary about person with arm transplant. He was complaining about the fact his transplanted arm did not produce any sweat and as result daily objects were often sliping from his fingers. I will try to find the reference.

As @Ben states, every theory of 'why' we evolve a trait is just a guess and never more than part of the story.   But there are theories.
The palms of our hands are a major source of heat transfer out of our body.  For bears it is the nose and pads of their feet, for dogs it is their toungue, for us a major portal for heat out of our body is the palms of the hands.

Black bears are extremely well-insulated animals, equipped with a heavy coat of fur and a thick layer of subcutaneous fat that help them maintain their body temperature as they hibernate through winter. But once spring arrives and temperatures rise, these same bears face a greater risk of overheating than of hypothermia. How do they dump heat without changing insulation layers?
Heller and Grahn discovered that bears and, in fact, nearly all mammals have built-in radiators: hairless areas of the body that feature extensive networks of veins very close to the surface of the skin.
Rabbits have them in their ears, rats have them in their tails, dogs have them in their tongues. Heat transfer with the environment overwhelmingly occurs on these relatively small patches of skin. When you look at a thermal scan of a bear, the animal is mostly indistinguishable from the background. But the pads of the bear's feet and the tip of the nose look like they're on fire.
These networks of veins, known as AVAs (arteriovenous anastomoses) seem exclusively devoted to rapid temperature management. They don't supply nutrition to the skin, and they have highly variable blood flow, ranging from negligible in cold weather to as much as 60 percent of total cardiac output during hot weather or exercise.

Given this, one could see how the palms of our hands are more likely to react to emotional situations where the heart rate elevates and sometimes we get hot under the collar.  The AVAs will
I am not physiologist, but the quote above comes from an article I stumbled upon a few months ago.  They use the AVAs to reduce the swelling associated with exercise and got some amazing results.  I guess that's another story though.

There isn't necessarily a nice neat evolutionary rationale or advantage behind all of the observable traits found in all organisms.
It's perhaps more likely that there simply was not enough selection pressure against having sweaty palms to eradicate it from the gene pool entirely.

I think this should be posted as a comment on all questions that have the title "why does X evolve?" - too often people assume there is some great reason for something to evolve and persist and reason that redundant traits should disappear immediately via selection. However, I don't think this answers the question, there are theories out there such as the answer by @shigeta

It is almost certainly to improve grip.  There is a different type of sweat gland (eccrine sweat glands) in the palms and soles.  The sympathetic nervous system (one feature of which is epinephrine / adrenaline) feeds those glands, so if something is scary or tense they kick in.
Our ancestors were in trees.  Our close relatives still are.  Scary situations often means moving fast through the trees.  Or it is scary because you are about to fall!  Either way you need your good grip: hands and feet both back in those days, or for our great ape cousins.
A little bit of moisture makes hands much more grippy.  Especially if your hands are not very clean.  People sometimes spit on their hands to improve grip.

Because feet and hands touch so many things, I would think that sweat would help act as a protector from various pathogens as well as scent marking, heat transfer, or stress symptoms.  Both the salt and fluid in sweat might wash some pathogens away.

you need to add some background and rationale for your answer - see comment above... otherwise this is not reasonable for this site.

It was advantageous for our ancestor's grip while tree climbing millions of years ago, so the best current theory claims.

Welcome to Biology.SE! It isn't clear that this adds anything to the existing answers. In addition, answers are much more likely to receive a favorable response if you include supporting references (primary literature is best). Without that support, your answer is indistinguishable from opinion. ——— Please take the [tour] and then consult the help pages for additional advice on [Answer] effectively on this site and then [edit] your answer accordingly. Thanks!


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Papers linking telomeres and aging
I'm currently writing a piece of work about telomeres and aging, and wondered if you could share some good papers you've either read or know of.

This question is not really a good fit for the Q&A format, the topic is rather broad, there is a nearly endless list of possible responses with no real criteria on what is a better answer. If you have any specific questions you encounter in your research you are certainly welcome to ask them.

the editors are kind of a pain here.  a good example would be why do we believe that telomeres are related to ageing? or What is the evidence that telomeres are related to aging.

http://biology.stackexchange.com/questions/186/is-telomere-length-a-reliable-measure-of-health-lifespan?rq=1  did you look at this one?

also take a look at this link: http://learn.genetics.utah.edu/content/begin/traits/telomeres/