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How are two species with similar phenotypes identified as different?
How are two species with similar phenotypes identified as different? Have two different individuals  that were thought to be different species ever been determined  to be from the same species ( or one a subspecies of the other's species ) ?

More information about the semantic difficulties of the concept of species can be found in this answer.

Species are difficult to define. This is because they form over a gradual continuous spectrum via evolution, one species does not suddenly become two, but lineages diverge (perhaps because there is some kind of barrier - like a mountain range - in the way) eventually reaching a point where we class them as separate species. How we define species is debated but the most generally accepted definition is the Biological Species Concept (BSC). Roughly the BSC defines a species as "a group of individuals that do, or could, successfully breed." Other species concepts do exist, some have their merits, but the BSC is most widely accepted and normally taken with a pinch of salt - it's not always possible to perfectly define a species because evolution and speciation are ongoing processes. Therefore, according to the BSC, two groups can be called different species even if the individuals look identical as long as there is true reproductive isolation.
Reproductive isolation can occur because of physical barriers such as rivers, oceans, mountains, environmental change. This is the cause of allopatric speciation. One species could become split when a subpopulation forms on an island (e.g. if humans take them to an island). If enough time passes without migration they will become reproductively incompatible. Another mechanism is sympatric speciation, when two species form without geographic isolation. This could be by the evolution of new behavioural, morphological or physiological forms which create division within the initial meta-population in to distinct sub-populations which over time become more reproductively isolated. Traits related to reproduction are amongst the fastest evolving and can quickly reinforce speciation (e.g. sperm morphology is extremely varied between species, see Sperm Biology: An evolutionary perspective, chapter 3).
The higher up the tree of biological classification you go the easier it becomes to classify things in to distinct groups, e.g. An oak tree is clearly a plant, and a whale is clearly and animal; further towards species definitions a whale is a mammal and a sparrow is a bird and both are animals; and perhaps less clearly, carrion crows and hooded crows are two different bird species in the Corvus genus. (Formerly these two were considered the same species!)
Obviously problems begin to occur when we consider species that reproduce through means other than sexual reproduction - e.g. bacteria which clonally reproduce. Traditionally this has been done by phenotypic information. We are now in the genomics era which opens new possibilities. This article discusses modern techniques by which utilise genetic similarity & difference between cells to define species and they suggest it to be a good method. However, this article seems to suggest that genomic methods need some refining first before we start classifying species with them.

Currently, it appears more pragmatic and efficient to preserve the current species definition than to replace it, because it is serviceable as a first level of screening and current phylogenetic knowledge is too limited for a universal and sound change in the definition.

As for whether two species have been reclassified in to one I know there are examples but Google is not throwing up anything and there's nothing I can remember off of the top of my head - if I remember correctly the male and female mallard were once considered separate species because they look so different but I can't find anything to back this up. Species formerly described as one have been split in to two as well - gorilla's are one such example.

Genotypes are used to differentiate when phenotypes are identical. In Bacteria the 16S rRNA sequence is particularly useful in helping to identify which population is present in what percentage. In fungal its ITS and in mammals its 18S.

How does this fit with a species concept? There is genetic variation within species. The biological species concept is the widely accepted one and that requires reproductive incompatibility/isolation - that's not entirely dependent on the DNA.

@GriffinEvo Yes, but is a concept of species based upon ability to interbreed of any use when dealing with bacteria?

You're right @alan_boyd it obviously becomes problematic with asexual/clonally reproducing species- in that sense every cell could be considered a different species (which would be plain ridiculous!) it's just the question is not specific to bacteria

@AlanBoyd I've updated my answer to include some about bacteria :)

If one species doesn't suddenly become two species and there is no case of say, two mammels having a fertile offsring that is a different species than it's parents then a confusing problem results. (confusing to me) The problem is a fertile mammel would have had parents from the same species. Each parent which is fertile also would have had their parents from the same species and so on..Where is the divergence? This all seems to follow if there is no sudden change in a species.

Can a fertile individual have two parents of different but similar species? If the parents have slightly different reproductive functions that can't be used as a 'source' of biological info. for just one offspring then how could the individual offsping become fertile?

Is it true a fertile animal had to have it's parents from the same species? And each of them being fertile had to have their parents of the same species , and so on?


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PDB file for Osteopontin (SPP1)
I am looking for PDB file for Osteopontin (SPP1). The entry- 3CXD shows the structure of an Osteopontin antibody, not of the protein itself.
Thanks

Is the structure known?

Apparently osteopontin lacks secondary structures. Only a 4-residue beta strand is reported in Uniprot.

There doesn't seem to be a 3D structure of Osteopontin available, and after looking a bit at the literature about this protein I'm not really surprised.
Osteopontin is hypothesized to assume an elongated and flexible structure (Sodek et al., 2000). Flexible proteins are very hard to impossible to crystallize, typically the flexible parts are either removed or stabilized in some way. I'm not a crystallographer, but this protein doesn't look like it can be crystallized in the full form.
For NMR it is a bit on the large side, a full structure would likely be not feasible.
It also has extensive posttranslational modifications, which makes it much harder to produce in large amounts as needed for crystallography, and extremely expensive for NMR where you would have to isotope-label the protein as well.

Thank Mad Scientist, I wanted to docking OPN with a small molecule. It seems it is impossible.

only a small peptide of Osteopontin is available currently
http://www.rcsb.org/pdb/protein/P10451

source: Stack Exchange

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Can animals make their own unsaturated fatty acids?
I know that animals can't make poly-unsaturated fatty acids (PUFA) and so require them from dietary sources. For eg.Omega -3 and Omega 6 fatty acids.
My questions : Can animals synthesize other unsaturated fatty acids from scratch? If not, does the unsaturated fatty acids in the phospholipids of plasma membrane of animals come only from dietary sources?

At least fish should be able to do this - most Omega-3 and Omega-6 fatty acids used for food supplementation are extracted from fish, namely salmon or cod.

Fish don't make it themselves either, they get it from algae through the food chain.

However, it is very energy-intensive and not at all efficient for heterotrophs to desaturate and elongate LA & ALA to EPA & DHA, so it is better for them to obtain these long-chained fatty acids from their diets. This is true from zooplankton to crustaceans to insects to fish, birds, and mammals (lots of refs for this).

Yes, animals can make their own unsaturated fatty acids.
Mammalian fatty acyl desaturases can introduce double bonds at the Δ5, Δ6 and Δ9 positions (i.e. numbering from the functional group). As shown in the diagram below, this means that we cannot introduce double bonds at the ω3 or ω6 positions (i.e. numbering from the methyl end of the molecule) in fatty acids of a reasonable length (see any Biochemistry textbook for confirmation).
I've illustrated the impossibility of us making α-linolenic acid as an example.

So can the plasma membrane unsaturated phospholipids be made from scratch ?

@biogirl Yes, the unsaturated fatty acids will be incorporated into new phospholipids at the endoplasmic reticulum then transported in vesicles to the plasma membrane.

Only linoleic acid ($\omega 6$) and $\alpha$-linolenic acid ($\omega 3$) are essential. Other PUFAs are synthesized from these by desaturases (as Alan Boyd pointed out).
I haven't come across any study that reports de-novo synthesis of $\alpha$-linolenic acid in animals. However, this study reports that mites can synthesize linoleic acid.

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What happens to human dopaminergic reward system once a teenager becomes adult?
I've recently heard a podcast which explained teenage impulsivity and novelty seeking in part by

"Lowering the baseline dopamine activity in the reward system"
"Increase in dopaminergic reward in response to novelty"

I assume that by reward system the author means mesolimbic and mesocortical dompaminergic pathways in the brain.
Here's an article that seems to state similar findings:

Starting in early adolescence and peaking midway through, this
  enhanced dopamine release causes adolescents to gravitate toward
  thrilling experiences and exhilarating sensations. Research even
  suggests that the baseline level of dopamine is lower—but its release
  in response to experience is higher—which can explain why teens may
  report a feeling of being “bored” unless they are engaging in some
  stimulating and novel activities.

The dopamine system here is being compared to the child's dopamine system. I'm interested in what happens to the dopaminergic system once a teenager/adolescent becomes an adult at around the age of 24-25?
I'm looking for insight along these lines - does the reward system of an adult "settle down" and no longer respond to novelty as strongly? Is the baseline dopamine level higher?

This may shed light on why the teenagers response to dopamine changes. Quote from reuniting website

There's much still to learn, but it looks like a number of reward
  circuitry events occur after climax that have the potential to
  desensitize us for a time. First, androgen receptors decline after
  ejaculation, and take up to seven days to normalize. (That means the
  effects of testosterone on the reward circuitry are probably blunted
  for a while, quite possibly affecting outlook.) In addition, opioids
  released during copulation hang around for a while, apparently causing
  lingering declines in oxytocin, which hamper sexual responsiveness. As
  noted above, there is also likely a drop in responsiveness to a
  neurochemical vital to our sense of well-being: dopamine. In effect,
  the brain has changed. It now requires more stimulation to get the
  same pleasure response as before, and sometimes no amount of
  stimulation will truly satisfy—until it recovers. Anecdotal evidence
  suggests that such changes affect both sexes.

The author further suggests that orgasm and ejaculation increase prolactin levels for up to 14 days, during which the brain is less responsive to pleasure and requires novel entertainment or partners to produce pleasure.
From the info on that site, it seems that the 14 day dopamine-affecting cycle following orgasm continues for as long as a person is sexually active (with orgasms). With this in mind, it appears that the adult response to dopamine release is the same as teenagers who are sexually active.


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Modern alternatives of DNA footprinting
Since DNA footprinting is an old method I thought there may be some more recent and effective methods to identify a DNA sequence, do you know any of them?

You could look into ChIP-Seq

Identify it as what? Guess the species of origin? Guess the individual it came from? Guess its function?

Since he is talking about footprinting, I assume he wants to identify what motif a particular protein binds.

@canadianer ah! DNAse footprinting, OK.

DNAse-seq is the most obvious choice. It uses the same idea as DNAse footprinting but measures output using high-throughput sequencing, so it can be done on a whole genome in one shot.

DNA sequencing, RFLP, IHC, In Situ Hybridization, Southern Blotting.
I think the technique you are looking for (what you are talking about), is an Electro Mobility Shift Assay or EMSA


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What is optical density in Lowry's protein estimation method?
I have a few questions:

What is an OD value?
Why do we use blank solution in Lowry's protein estimation method?
If The OD of a protein is 0.01, what does it mean?

Thanks in advance.

The OD measurement is the output of what the photometer measures. It is actually the amount of light which is scattered or absorbed by your sample - scientifically called extinction.
A blank is used to be able to substract the influence of reagents, light that is scattered on the surfaces of the cuvette (which is probably also not completely clean) and so on. Every of this influences reduces the amount of light which should reach the detector on the other side of the probe and give you false extinction readings. If you are using a colored detection sample (which colors deeper or looses color during the reaction) this is more obvious. The solution already has an extinction on its own which is not of interest. So you make a blank (which basically substracts all these influences from you sample reading) to correct for this. How this is done depends on the photometer. Some make a correction reading at the beginning, while others use a second cuvette (a blank cuvette) which is permanently measured.
It means that the protein gives you this extinction. Without a calibration curve (made from serial dilutions with known protein concentrations) it is impossible to make any further comment on this number.

Thanks a lot for quick response.but can you elaborate ans no. 2 please.

@N00B Sure, I expanded my answer.

You can think of the blank as a way of calibrating the instrument. The blank defines the amount of light that will hit the photodetector when there is none of the species of interest in the cuvette. By setting this as the zero you have prepared the instrument for measuring the samples of interest.


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Viruses: Adaptation to a new host through repeated host jumps
A friend told me, during a 3 minute discussion, that viruses that are endemic in host $A$ and make repeated jumps to host $B$ but can't be transmitted between individuals of species $B$, may slowly adapt (through these repeated jumps) to be able to be transmitted between individuals of host $B$ and become epidemic.
I don't know much about epidemiology. I don't understand how a virus population that is endemic to host $A$ may adapt to host $B$ with repeated jumps while the viruses that jump to host $B$ are dead end because they cannot be transmitted further more. Or Are these viruses able to jump back to host $A$ to bring back their newly acquired adaptations to host $B$?
Also, I might misunderstand the meaning of "repeated host jumps transmission". I first thought it meant repeated jumps from a reservoir population in host $A$ to host $B$, but it is also possible that it describes the dynamic of a virus population that is adapted to jump from species to species and they actually gain this ability by keeping jumping and jumping. But then, how could a virus species get adapted to jump from species to species? I'm a bit confused…. Can you give me some hints about this process of cross-species transmission through repeated jumps?

A friend told me, during a 3 minute discussion, that viruses that are
  endemic in host A and make repeated jumps to host B but can't be
  transmitted between individuals of species B, may slowly adapt
  (through these repeated jumps) to be able to be transmitted between
  individuals of host B and become epidemic.

This is...mostly true. A good example is avian influenza - there are a number of human infections linked to contact with infected poultry, but the virus is not particularly good at sustaining long chains of human-to-human transmission, likely due to differences in the respiratory tract between humans and birds.

I don't know much about epidemiology. I don't understand how a virus
  population that is endemic to host A may adapt to host B with repeated
  jumps while the viruses that jump to host B are dead end because they
  cannot be transmitted further more. Or Are these viruses able to jump
  back to host A to bring back their newly acquired adaptations to host
  B?

What they mean by repeated jumps, or what they should mean, is not a virus hopping back and forth, but a virus going from A to B many times. This is my problem with your friend's statement, it's not so much a "slow adaptation" as, well, random chance.
Imagine that there's a mutation in Virus A, which lives in chickens, that will make it well adapted to live in human beings. It's an extremely rare mutation, so the dominant strain of Virus A is maladapted for human to human transmission. That means most Virus A infections in humans will be the non-productive kind, that will infect a person, but not go on to infect other people. But, with enough rolls of the dice, a human might get the human-favored Virus A, and since there's now intense selective pressure for that strain of the virus within its new human host, it might establish itself and take off.

A quick answer for now (I'll add details as I find):
The infection of B from A would be zoonosis. This transfer may not have followed a classical route of infection. For example the case of hantavirus pulmonary syndrome (HPS), the zoonosis occurs throuch the rodent (primary host) droppings.
Other example is that of avian influenza- the zoonosis doesn't happen via the respiratory route but by contact with body fluids of infected birds.
Also dead end can be achieved in the case of vector borne diseases especially those of Arboviruses. There is no mechanism of spread other than through a vector.
In other cases the virus may not be produced in high titres in the secondary host to cause infections, but enough to cause mild symptoms.
It is interesting to know how the pathogen can propagate in B but cannot infect: I dont have a definitive answer for this. If a receptor/viral adsorption site is similar between the two hosts but interaction with virus is much stronger in A, then B cannot be infected unless there are loads of virions. However once adsorbed, they can propagate within the cell and go from cell to cell with a relative ease, may be by using a different mechanism. For e.g. , in case of plants the viruses can go through plasmodesmata.
Back jump should be possible unless the pathogen has mutated to fit the new host. In such cases a enzootic infection might happen and A will be dead end. For e.g. in influenza.
This article says that dead-end host (dragonfly) behavior can be manipulated by a certain parasite (Acanthocephalus lucii) to increase transmission probability to original host (perch).
PS: influenza is a very unique case as you might be aware of the genetic drifts/shifts that make it highly adaptable.
Refer this article for some details, It has a section on dead-end transmissions.

Thanks a lot for your answer. I am not sure I fully understand: Can you tell me what is usually meant by "repeated host jumps". Does it mean repeated jumps from a reservoir population in host $A$ to another host $B$. Or does it mean that virus lineage jumps repeatedly from host to host, from the bat to the dog, from the dog to the pig, from the pig to the human, etc...

i dont understand that term either.. didn't get any hit on google.. It might mean the case of influenza where the virus has jumped to and from many hosts.


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How would a different solar day affect evolution?
Has anyone theorized how evolution would be affected by a different length of solar day, what were the conclusions?
The thought came from thinking about life on other planets/moons, but I'm initially thinking about it from the frame of "How would life on earth and humans specifically have evolved (or if they would have) if a day were 12 hours or 48 hours?
I imagine the actual effects on evolution and lifestyle would be extensive.
Note: this question How would the human body adjust to sleep times if we were to live in a place with different day lengths? is slightly related, but just to clarify I'm intersted in effect on evolution, not adaptation if an indivdual moved between planets.

Think about places like the arctic circle where there are extended periods of light and dark - that would give some idea. Many plants and animals cope well with long periods of dark, and make use of the co-occurring long days at other times of the year.

True, but I think season variation relates to a different set of effects.  I think things like the study of deep sea life is probably more closely related, just not easily extrapolated humans.

Deep sea is another - seasonally long days and nights were just a starting point for some ideas

its all about adaptation.. we might look different or we might not.. each stage of evolution is basically adapting to changes in the environment to better suit our needs..

This question is a little broad- if you remove the evolution from the question then this is quite answerable.

It depends on how different. Day length affects more than just how long the periods of light and dark are. Let's assume a very slow rotation, and a very long day, maybe 1 month light, 1 month dark. The light side would get much warmer while the dark side would get much cooler. At the border between light and dark sides, you'd expect to see powerful storms as the hot moist expanding air moved into the cooler side and had to lose moisture. Any life on a planet like this would have to adapt to surviving in both hotter and cooler temperatures. We can take this to an even worse extreme and look at a planet like uranus. Uranus's axis is tilted at 97.7 degrees, so even though it rotates, the day/night cycle is controlled by it's rotation around the sun. If the earth were tilted like this, then we would 6 months of light followed by 6 months of darkness. Life would either have to keep moving to stay in the moving temperate twilight zones or adapt to hibernate.
If we assumed a shorter day/night cycle, I think the changes would be less significant. Lets say we had a 4 hour day. ( There has to be a speed where things get thrown off the planet, but I don't think 4 hours per day is fast enough ) A 4 hour day would have 2 hours of light with 2 hours of dark. My guess is that circadian rhythms would be less important. Temperature changes from light to dark would be less significant than currently.
It's an interesting thing to think about because the Earth's day is slowly getting longer as the moon exerts a tidal force on our planet, slowing our rotation and escaping further into space, but this change is so slow I doubt it will ever become a problem for humans.

This answer is good, but you're focusing a lot on how the solar day would affect the environment rather than evolution of humans... or at least not extending those thoughts into evolution.  Would we eat differently? forage differently? have different physical body types..

If it were bad enough we wouldn't be humans. If we had 6 months of darkness and 6 months of light almost every form of life would have to go dormant for half the year, and I don't think humans would develop in an environment like that.

It's an interesting thought, but animals that hibernate (bears / squirrels) are not significantly different from their non-hibernating brethren.

I don't know how cold the dark side of the planet would get, but I'm pretty sure it would be far colder than any winter bears have hibernated through. Wikipedia claims that the polar night lasts about 28 days http://en.wikipedia.org/wiki/Polar_night , which is far shorter than 6 months. And the poles would receive heat from the rest of the planet. If half the planet were dark at any given time, the center of that darkness would get very cold. And while some plants keep photosynthesizing all winter ( conifers ) they only deal with normal nights. 6 months of darkness would challenge them.


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Regarding cancer cells and radio-frequency ablation
Are cancer cells destabilized if near a strong electromagnetic field over a long period of time? I read this technique of using radio-frequency ablation and heat shock to kill cancer cells. I don't know if this is viable but maybe a person could wear a device like a pacemaker right over the area of a tumor that emits  strong E.M. pulses over say a month or a year. Could this destabilize the tumor ?

Can you please add a source for this? To my knowledge electromagnetic fields have no proven effect on humans. Otherwise the use of NMR scanners (which use very strong magnetic fields) wouldn't be a good idea.

a separate device could be designed if viable. Doesn't make sense to get a pacemaker as it has another more specific purpose.

There was a story today on the C.T.V. news (in Canada) , on Saturday August 9/ 2014 about using beams of microwave and an M.R.I scanner to kill a tumor ; the patient improved greatly.

I think you're referring to radio frequency or microwave ablation. It works by heating the tissues up with electromagnetic radiation, just like you'd use to microwave food, but it's heating you instead. Healthy cells have better repair mechanisms and survive these treatments better. Cancer cells tend to have poor repair ability and can be killed more easily. I've heard of injecting metal nanoparticles which collect in the tumor due to the enhanced permeability and retention (EPR) effect. The nanoparticles respond to the microwaves much more powerfully than cells do and get hotter, burning the tumor from the inside out.

User 137 said 'cancer cells tend to have poor repair ability'. Could a mild virus that is not harmful to healthy cells kill a cancer cell?

Do cancer cells have poor repairing ability because most of their 'facilities' are committed to growth and repair?


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Hypothalamic breakdown and effect of temperature on membrane lipids
I'm in my last year of high school and doing a research assignment on thermoregulation. In the excellence level exemplar for the standard, a student made the statement:

Once the body's internal temperature is well above the optimum range, important enzymes start to denature, phospholipids start to destabilise, and cell membrane lipids begin to dissolve. As a result of this, important organs in the trunk of the body are unable to carry out important metabolic processes. If the temperature continues to rise it causes tissue damage which could cause disability depending on its severity. It also causes the hypothalamic thermostat to break down, meaning the body can no longer have control of the core temperature.

However, I have been unable to find any sources which mention destabilisation of phospholipids or the dissolving of membrane lipids. I have also not found anything on tissue damage or the cessation of the hypothalamic thermostat.
Are these things true? And if so, could someone please direct me to a reliable source which states this?

If you supply heat to a system, the entropy increases which results in destabilization of order. This is a general thermodynamic principle and you can refer any basic book on that topic. However, it is not essential that all molecules would be affected equally. There are heat-stable enzymes in thermophiles such as Thermus aquaticus which are resistant to heat. Also the membranes in these organisms are made up of stronger and more rigid isoprenoid lipids.
Even in mesophiles, lipid membranes with higher content of cholesterol are rigid and more resistant to thermal movements.
On Breakdown of thermostat:
The body can regulate the temperature only in a certain range; at higher temperatures these mechanisms will fail as well.


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Parallel Autonomic regulation of Cough and Runny Nose
I describe here the serous inflammation of runny nose.
Cough is mediated by Cough center.
I think Runny nose is also controlled by the autonomic nervous system and probably by some reflex.
Assume you have mild runny nose under Montelukast medication.
You have irritated cough (coughing so much you cannot sleep).
You stop the cough by codeine before sleeping.
You sleep at 30 degree angle.
Sometimes, you also feel that the runny nose stops i.e. complete relieve of runny nose in both nostrils and whole nose for about 30 seconds to a minute - perfectly clear nose and no serous inflammation - no symptoms of imflammation in the nose.
Then, it (serous inflammation) starts again - not like mucose running back - but the feeling of uneasiness in the whole nose starts again - then mucose can also continue to migrate from one nostril to another.
What is causing this kind of behaviour i.e complete relieve of of runny nose for about 30 seconds?
What is causing the stopping of serous inflammation in the nose?
I think the Runny nose can also be controlled by medulla oblongata because Codeine is blocking the cough center there.
I tried to achieve this behaviour by stimulating by lymphatic system in regulating breathing by abdominal muscles - lymphatic drainage massage - breathing inside with abdomen (not with thorax) and deeply exhale with abdomen).
At that time, I did not hear any creaky sounds in my throat.
After trying to stop the serous inflammation again, I heard them without managing to stop serous inflammation in both nostrils at the same time.
How is the control of Cough and Runny nose regulated by the autonomic nervous system?
Probably, some parallelism there.
Processes going on regulating Cough and Runny nose

reflex from medulla oblongata
sympaticus and parasympaticus (not sure about these)
possible parallelism of irritated cough and runny nose control

From my experience (and what my kids doctors told me) most of the coughing connected with a cold (especially the sort which occurs at night when you lay down) comes from the mucus which is coming from the sinuses and is moving around due to the changed body position and thus causing problems.

@Chris That is different story. Moving mucose in the nose between nostrils and completely relieve of runny nose (you do not feel anymore the serous inflammation process at all).

To add to your idea of a link between cough and runny nose: Codein binds to opioidreceptors. A runny nose is known to be one of the early symptoms of opioid withdrawal.

Skymninge mentioned opioidreceptors and the withdrawal symptom of opiods as a runny nose: codein binds to opioidreceptors.
I think now that the cough can trigger runny nose.
I breathed with empty nose some 15 minutes.
Then, I had a deep dry cough and right after it a stuffy nose.
I really felt this time the negative gradient at the level of kidneys and also posteriorly.
I do not know how this kind of pain was felt, I think, near or on the kidneys.
I do not understand the effects of deep dry coughs.
They seem to be linked to several processes and locations in the body.
After this deep dry cough, I did some abdominal breathes and this way massaging the lymphatic circulation systemically, the stuffy nose disappeared.
My thorax is opposite of astonic person (say if you remember the name in Propedeutics).
This can be a restricting factor in the circulation of the lymph.
My conjecture is that the people with big chests (opposite of astonic) need to concentrate more on abdominal breathing such that to keep out of stuffy noses.
Restricted lymphatic circulation causes less wastes returned to the blood circulation.
Thus, accumulation of bacteria in the larynges which increases the risk of a dry cough.
Good lymphatic circulation ensures that bacteria is not congested in the larynx.
So cough seems to be a mechanism to start a runny nose.
This all is finely regulated.
There are several receptors in the body.
The deep cough however seems to be linked to a reflex which causes a runny nose.
Some studies about opiates and respiratory activity

The effects of opiates on the respiratory activity of thoracic motoneurones in the anaesthetized and decerebrate rabbit.


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conservation of C-peptide sequence in the guinea pig
Where can I compare the C-peptide sequence of guinea pig with human or mouse?
I am also interested in finding whether the guinea pig has insulin 1 and 2 to know whether I could use an anti-C-peptide 1 and 2?

Dou you want to compare protein or DNA sequences?

I would like to compare the protein sequence (amino acid sequence) to know wether I could use anti C-peptide that reacts for human to detected  C-peptide or proinsulin in guinea pig pancreas

Do a BLASTP with the human and mouse protein sequences to ascertain similarity between the sequences

and where can I find the protein sequence? is there a database?

The NCBI Nucleotide database can be used to search for coding sequences (mRNA and translated protein) of genes. You need to enter the name of the gene (INS) or protein (insulin) and then species (use either the common name, "guinea pig" or the scientific name, "Cavla porcellus").
Filter the results to show you only mRNA coding sequences (sometimes abbreviated as "complete CDS"). These entries are annotated with the regions that account for the signal peptide, mature peptide(s) and prodomain(s). In your case, the full proinsulin is annotated as mature peptide and the B and A chains. The C peptide connects the A and B chains, located between the only two dibasic sites (R55R56 and K88R89).
Another useful database is the UniProt Protein Knowledge Base which presents similar information in a slightly more graphical presentation. Here is guinea pig insulin in this database.
If you happen to compile a whole list of C-peptide domains from other mammals, then you can use an alignment tool like ClustalOmega to align the peptide sequences to look for commonalities.
As for guinea pigs, there is only a single insulin gene (like most mammals). Only mice and rats have a two gene insulin system, Ins1 and Ins2. Generally speaking, there is poor conservation of the C peptide domain across mammals, in part because it only serves to link the A and B chains together to form the necessary disulfide bridges.
If you are wondering whether an anti-guinea pig antibody will cross react with another species' epitope, that information is listed on the antibody specification sheet under species cross-reactivity. Some antibodies are more cross-reactive than others, and you will need to refer to the specific manufacturer's information to be sure.

Wang S, Wei W, Zheng Y, Hou J, Dou Y, et al. (2012) The Role of Insulin C-Peptide in the Coevolution Analyses of the Insulin Signaling Pathway: A Hint for Its Functions. PLoS ONE 7(12): e52847. doi:10.1371/journal.pone.0052847 A note on this paper, I would not take the conclusions that C-peptide has a physiological role in intracellular or endocrine signalling because it is still quite a controversial issue. I used this article because it was open access and to demonstrate in Figure 1 the variability of the C-peptide domain across selected mammals.


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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


text:
Defining: Evolutionary (quantitative) Genetics and Population Genetics
How do we define the fields that are Evolutionary (quantitative) genetics and population genetics. What set these two fields apart? Can you try to provide definitions?
To my intuitive understanding, I'd tend to think that population genetics is a subfield of evolutionary genetics.

According to Hartl & Clark on population genetics:

"Population genetics deals with Mendel's laws and other genetic
  principles as they apply to entire populations of organisms.... also
  includes the study of the various forces that result in evolutionary
  changes in species through time."

According to Conner & Hartl also on population genetics:

"Population genetics is the study of naturally occurring genetic
  differences between organisms; these differences are called genetic
  variation. Genetic variation is important because it is the raw
  material for evolution... to understand the purview of population
  genetics, we need to have a better understanding of populations and
  genetic variation"

According to Conner & Hartl on quantitative genetics:

"Most phenotypic traits do not fall in to distinct categories, but
  rather are continuously distributed... These traits are called
  quantitative or metric traits because they need to be measured not
  just scored."

According to Falconer & Mackay on quantitative genetics (my personal favourite book on quant gen, which spends the first 5 chapters going through population genetics):

"Quantitative genetics is concerned with the inheritance of those
  differences between individuals that of degree rather than of kind,
  quantitative rather than qualitative.... It is nevertheless a basic
  premise of quantitative genetics that the inheritance of quantitative
  differences depends on genes subject to the same laws of transmission
  and having the same general properties as the genes whose transmission
  and properties are displayed by qualitative differences.
  Quantitative genetics is therefore an extension of Mendelian genetics, resting squarely on Mendelian principles as its
  foundation."

Personally I would say that evolution is inescapably a population genetics process and (virtually) no study of it can be done without some understanding of population genetic principles. Many evolutionary genetics problems can be best dealt with using quantitative methods, and quantitative genetics is an extension of population genetic principles. Population genetics relies on selection, drift, mutation and gene flow - these are all key quantitative genetics.
Population genetics study focuses then on the four basic principles above from a (simplified) Mendelian view, while quantitative genetics deals with more realistic evolutionary genetic phenomena by allowing for, and assessing, genetic variance from many loci influenced by additivity, dominance, and environmental factors. Both fields are studies of evolutionary genetics, population genetics can be studied whilst ignoring quantitative genetics, but quantitative genetics relies on population genetics principles so I would call it an extension of - but not sub-field - of population genetics.


text:
Topology of closed circular DNA

Why are covalently closed circular plasmid DNAs naturally found in an underwound state ?

Is it because this makes it easier for the DNA replication machinery to access and unwind DNA ? Or is it because underwound state is energetically more favourable than an overwound state ?

DNA is not always negatively supercoiled naturally. It is important to keep in mind that different regions of topologically constrained DNA can have different supercoiling values. For example, the action of unwinding DNA for transcription or replication introduces positive supercoils ahead of the polymerase and negative supercoils behind it.
Additionally, supercoiling is present in DNA normally. Supercoiling is the result of more or less twist in a DNA helix, which is most stable when it has ~10.5 bp/turn (for B-DNA). Supercoiling allows under- or overwound DNA to return to its most stable twist. Negative supercoiling is the result of underwound DNA. Underwound DNA is not thremodynamically favourable and will actually lower the melting point of DNA (the point where strand separation occurs). This can be compensated by introducing supercoils but it is also important for processes such transcription, which require ssDNA. Negative supercoils and ssDNA can be thought of as interchangeable. Negative supercoils are also used to package DNA around histones in eukaryotes and archaea. On the other hand, positive supercoiling is the result of overwound DNA (also not thermodynamically favourable) and will increase the melting point of DNA. Positive supercoiling is often found in thermophiles which live at higher temperatures and need to prevent their DNA from melting excessively. It has also been suggested that positive supercoiling can play a role in regulation of gene expression (by inhibiting promoter melting). Organisms like to keep an approximately constant amount of supercoiling in their DNA for the above reasons; this is called the superhelical density and is characteristic of different classes of organisms.


text:
Book Recommendation: Complex Traits and Complex Genetic Architecture
I am looking for a book (or any good source of information) that offers an in-depth discussion and models about the evolution and analysis of complex traits and complex genetic architecture. Do you have any suggestions?
I'd define complex traits as those traits whose variance in the population is explained by quite a lot of various genetic loci and environmental factors.

You might like "The mathematical theory of selection, recombination, and mutation" by R Bürger

Lynch and Walsh's Genetics and Analysis of Quantitative Traits (http://www.sinauer.com/genetics-and-analysis-of-quantitative-traits.html) is pretty comprehensive (if not necessarily comprehensible).

Suggestions:
Evolutionary Genetics : Concepts and Case Studies: Concepts and Case Studies
Edited by Lexington Charles W. Fox Department of Entomology University of Kentucky, Faculty of Life Sciences University of Manchester Jason B. Wolf Lecturer
The mathematical theory of selection, recombination, and mutation
by R Bürger (as suggested by @rg255 in the comments)
Lynch and Walsh's Genetics and Analysis of Quantitative Traits
(as suggested by @kmm in the comments)
PS: Do tell us if you found a better one.


text:
With an excess supply of nutrients, in how much time will the number of algae cells double in full sun?
I am growing algae in a container in my roof. It gets sunlight for the whole day as there are no clouds nowadays in my area. There is no lack of nutrients as I am constantly adding water mixed with organic waste. The dirt visible in the photos is from manure, which I added as fertilizer.
The water has become green and algae is deposited on top covering almost all of the surface area. There are no threads, so it is not filamentous.
Since there are probably several species of algae in it which I don't know, please tell me the doubling time of most common species.
Also, is there anything I can do to hasten the production of cells?
Below are pictures of the culture, as asked for.

I think it is possible to answer this question.

Please go through the articles http://www.marine.csiro.au/microalgae/methods/Growth%20rate.htm and http://eprints.cmfri.org.in/400/1/Article_09.pdf

I am presuming this a Blue Green Algae(BGA) Identify your algae
Growth rate for N1, N2 biomass at t1 and t2 time respectively, can be give as,
Growth rate:   $K'$ = $\ln \frac{(N_2 / N_1)}{(t_2 - t_1)}$

(source: csiro.au)
So, by this equation it is easy to calculate the doubling time of your algae.

For BGA normal doubling time is 6-8 hours.$^2$
Source:

http://www.marine.csiro.au/microalgae/methods/Growth%20rate.htm
https://sites.google.com/site/biomonstaaar/algae

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text:
Standard curve for real time
When performing a standard curve for some new primers to test for fold change, is it necessary to run the standard curve? I mean, in case your experiment has several genotypes for the same ecotype background, with correspondent control and treatments, must I run the standard curves for all this scenarios, or rather may I pick, just to say a random genotype of treated ones, see that it R=0.99 is or higher and efficiency 2?
It is in order to not to waste material.

Do the standard curve once for each primer pair to determine efficiencies. You can use the efficiency values for any number of replicates with any template.
I think we have somewhat discussed this issue in your previous post.

sorry to disturb but then if i get an efficiency value using control tissue, this values may be used for treatments, isn´t it?

yep.. the efficiency is just the property of the primer and its template DNA..


text:
Can a virophage potentially be used to cure a viral disease?
Wikipedia states "Virophages are satellite viruses that inhibit or impair the reproduction of the auxiliary virus."
Is it theoretically possible for a virophage that doesn't hurt the human body to attach itself to a more serious virus like the AIDS virus for example and be used to wipe out the virus, or at least inhibit it's reproduction?  I'm completely ignorant of the virophage relationship, so feel free to inform me as needed.

There are few enough virophages occurring in nature that I don't know if there's a clear and compelling case for them being potentially therapeutic.
In principle however, the answer is yes, though they may suffer from the same problems that bacteriophage treatments have suffered during their history - difficulty in preparation, extreme species specificity, and fairly daunting regulatory hurdles. While viral diseases don't have the "Or we could just use antibiotics, which work" out which made bacteriophages less popular, as far as I know there's not been a suggestion of widespread virophages against human pathogens.

In theory it should be possible, though this approach seems to be limited by the nature of the virophages known today. They seem to "infect" (this is actually wrong, since they take use of some of the proteins produced by the mama virus and do not infect these viruses) only very big DNA viruses.
This article (which is interesting to read in this context) talks about 400nm for the mimivirus, which is quite a lot. The problem is that many of the viruses which are interesting are fast mutating RNA viruses like HIV and the Ebola virus.


text:
What is a lip? (upper lip and lower lip)
Everyone knows what a lip is but I'm asking from a technical and anatomical standpoint.
Actually what we call "lip" is "vermilion" in medical terminology. But I want to ask if my understanding is right or not regarding to surface anatomy of the lip.
Lip consists of two parts called upper lip and lower lip. And upper lip and lower lip consists of two parts: skin (cutaneous) part and vermilion part  (vermilion is a special kind of skin also but we do not call it skin).
Thus:
Lip = upper lip (upper cutaneous lip + upper vermilion) + lower lip (lower cutaneous lip + lower vermilion)
This is a diagram that depicts the upper lip portion:

Source: http://elementsofmorphology.nih.gov/anatomy-oral.shtml

Questions:
Am I right so far? Did I miss any points?
Is the term "upper lip" ever used for the skin (cutaneous) part only? (especially in surgical terminology and reconstruction surgeries)
Are the "upper cutaneous lip" and "lower cutaneous lip" terms established terms in medicine? Are there any other names or latin names for those?  (I also see the usage of "cutaneous upper lip" and "cutaneous lower lip")

Don’t forget the part of the inside of lip where the skin texture changes to smooth wet surface. In cosmetic procedures this is call the wet - dry border.

Source

The upper lip extends from the base of the nose superiorly to the nasolabial folds laterally and to the free edge of the vermilion border inferiorly. The lower lip extends from the superior free vermilion edge superiorly, to the commissures laterally, and to the mandible inferiorly. Around the circumferential vermilion-skin border, a fine line of pale skin accentuates the color difference between the vermilion and normal skin. Along the upper vermilion-skin border, 2 paramedian elevations of the vermilion form the Cupid bow. Two raised vertical columns of tissue form a midline depression called the philtrum. The philtrum is located between the paramedian elevations of the vermilion and the columella above. The labiomental crease passes horizontally in an inverted U-shape across the lower lip, which intraorally corresponds to the depth of the gingivolabial sulcus.

This includes vermilion as well. Dont forget the mucous part inside mouth.

This whole is lip.
As for upper cutaneous lip or cutaneous upper lip, it wont matter, both are same and are used interchangeably. And quite frequently
used is upper cutaneous lip.
As for latinisation, you can use labium for lip, no such specific word for upper or lower lip, is know to me. But, you can try superior cutaneous labium and inferior cutaneous labium, if you want.


text:
how does DNA and RNA work
How do the DNA modules tell the cell what to do?

Since this is pretty broad, have you tried looking it up in the Wikipedia and then ask some more specific questions? This stuff fills a few pages in biology books and probably no one wants to write this down here...

This question is too broad (and also a bit poorly defined). I will try to give few concepts to help you in your exploration of wikipedia articles. If then you have more specific question, we'll be delighted to help you answering them.
In very short...
The genetic information contained in DNA in coded through codons, which are series of three base pairs, there are 4 different base pairs, namely, A,T,C,G. Therefore, there are $4^4 = 64$  but these 64 codons codes for only 20 amino acids (in most species). By analogy you may consider a base pair as a letter, a codon as a word (all words are made of 3 letters) and genes are sentences. But many words are synonymous. The genetic code is said to be redundant.
DNA is a double stranded molecule, which splits in two around a coding region so that a RNA molecule can be created by copying the DNA template. This process is called transcription. This RNA is called pre mRNA. It is then spliced to become a mRNA (messenger RNA). The mRNA exit the nucleus. Two rRNA (ribosomial) RNA (which forms the so called ribosome) attach to the mRNA and tRNA (transfer RNA) will recognize the RNA sequence and paste amino-acids the ones to the others according to RNA sequence. This process is called translation. The molecule that is constructed is a polypetpide (a protein).
The quantity of proteins that are produced can be regulated by various mechanisms at different "moments": pre-transcription, pre-translation, post-translation.

Great answer Remi.  Along these lines, I wanted to impart an important concept to understand as you read.  Most proteins become either enzymes or structural components in the body.  The key to conceptualizing the DNA-->RNA-->protein process is this: shape determines function.   A strand of DNA is a template for which the Amino Acid (AA) subunits will be strung together in a chain.  That chain will fold into a complex shape.  The shape is determined by the interactions between the different amino acids.  Each AA has unique effects, causing the chain to twist, bend, loop, link together, etc.

Once the AA chain is done bending, it's a shape that is pretty much unique to that protein.  For enzymes: the shape of the enzyme determines what it can do, how it interacts with molecules, and where it can go in the body.  Shape is everything.  For structural components, shape is everything too.  Think of an engine - the shape of each component is critical to its ability to function.  Because the order of Amino Acids in the chain causes it to form a specific shape, that is why the DNA sequence is a template for the protein's shape - and ultimately, its function.

I agree with Chris that this is way too broad a question.  But if you want a very broad answer...
DNA is a long molecule consisting of a sequence of 4 different subunits.  The sequence of those subunits determines the shape of the DNA, and its shape determined how it interacts with other molecules, based on their shapes.
Computer code doesn't work like that at all, so I think you need to really strongly question your premise that knowing anything about computers is going to tell you much about biology.


text:
What is the difference between vegetable and animal fats?
I often hear from many people saying to waiters - "Please, don't put oil to salad". They probably believe the fat from vegetables has the same impact on the weight as an "animal" fat (meat, eggs, butter).
My questions are -

Are these two types of fat have equal influence considering their converting to fat tissue in humans?
What are the pathways for conversion of vegetable oil fats to adipose tissue storage, in humans?
If one eats $X$ grams of either saturated or unsaturated fats, will they (in equal conditions) gain equal weight ($Y$ grams) in both the cases ?

There is a subtle difference between oils and fats- oils are generally unsaturated (Carbon-Carbon double bonds) whereas fats are saturated (all single bonds).

Are these two types of fat have equal influence considering their converting to fat tissue in humans?

No. There are some kinds of fatty acids that are synthesized only by plants (Essential fatty acids). However, these can be obtained indirectly from animal sources such as fish.
Fats have multiple roles- not just storage. They are also critical for making up the cell membrane.

What are the converting pathways for vegetable oil fats to adipose tissue in humans?

The fatty acids in oils are absorbed in the intestine and esterified (wit glycerol) to form triglycerides. Then, they are incoporated in lipoprotein complexes. There are different types of lipoproteins- VLDL (Very Low Density Lipoprotein), LDL (Low Density Lipoprotein) and HDL (High Density Lipoprotein) which have different sizes and compositions.
When lipoprotein comes in contact with lipoprotein lipase in capillaries, the free fatty acids are liberated from trigycerides, which is taken up by adipose tissue.
The fats stored in adipose tissue depends on diet. This has been studied in rabbit but similar principles may apply to humans too. Fats can also be synthesized in the body. It is always saturated fat and is synthesized by the fatty acid synthase complex. The starting substance is Acetyl-CoA which is produced during catabolism of both carbohydrates and fats.

if one eat Y of 2 meal if saturated and unsaturated fats, he/she (in equal conditions) will gain X gram if they were saturated fat and Z in a case of unsaturated fats?

By principles of mass balance, if both have equal rates of absorption and degradation then there will be equal gain. According to this study, absorption rate of unsaturated fats is higher. In that case if you eat $X$ grams of both types then the absorbed amount should be $Y_{sat}$ < $Y_{unsat}$
I am not sure about the degradation rates but I think it is higher for saturated fats because unsaturated has to be reduced to saturated before metabolizing via $\beta$-oxidation. Determining the exact steady state values will be tricky without a mathematical model.
NOTE: Dont confuse this with body weight gain (in the sense of obesity); it is a complex phenomenon. You have to consider a lot of things when predicting weight gain.

Do you know any answer to question if one eat Y of fats,  he/she (in equal conditions) will gain X gram if they were saturated fat and Z gram if they were polyunsaturated fats?

Gaining in the sense ?

Weight i mean - are these two types of fat similar considering weight gain

weight gain is a complex issue. it is not that straightforward. I added an answer to that question but it is in the sense of amount absorbed in the body.


text:
Can Serous inflammation on pleura pulmonalis cause dry cough and runny nouse?
I am interested in the mechanism between the dry cough and runny nose (serous inflammation) here.
I started to think how Acute respiratory viral infection is causing the dry cough.
The serous membrane, pleura pulmonalis, connects diaphragma to pars basalis pulmonalis.
It can be the source of the serous inflammatory response spreading to the nose probably.
There must be some source of inflammatory responses such that reflex arches can use them fast, thinking physically.
Assume medication Montelukast (stop asthmatic symptoms), codeine (to stop irritated dry cough) Flixotide (with Montelukast).
Assume that there is a diaphragm press on pars basalis pulmonalis.
Assume you breath mostly by abdomen 15 minutes in the supine position.
Assume opposite-astonic person in thorax.
You then feel that you exhale too much - the serous membrane pushing on pars basalis pulmonalis - serous inflammatory response in pleura pulmanalis.
The breathing process moves thoracic muscles and thoracic cavity gets shortly extended only little.
Negative tensor on lungs i.e. the volume of the lungs is getting smaller.
Consequently, a cough reflex arch and sympaticus start a deep dry cough to protect lungs.
Characteristics of the pathway against Acute respiratory viral infection

serous inflammation on pleura pulmonalis
serous membrane pleura pulmonalis presses on pars basalis pulmonalis
negative tensor on lungs
cough reflex arch and sympaticus
dry cough
positive gradient on the pleura spreads inflammatory response through the surrounding lymphatic system is sensed as dry in larynx
negative gradient is sensed on the nasal mucosa membranes as serous inflammation (runny nose)

Can the serous inflammation of plera pulmonalis cause a deep dry cough and runny nose?
The cause of this inflammatory response can then be Acute viral respiratory infection in some part of the lungs.

If serous inflammation produces a large amount of serous fluid this leads to lung compression and limitation of respiratory movement. This, as you said produces dry cough by means of reflex arch.
However lung compression leads to alveolar collapse or atelectasis through pleural effusion. After atelectasis, pneumonia can develop quickly as a complication.
And nasal congestion is a symptom of pneumonia. Also if pneumonia develops, the cough, initially dry and reflex, will turn to cough with mucus expectoration.
Cough stimulates nasal congestion when it brings up mucus from the lungs and extends the alveolar inflammation up to the nose by taking and concentrating all the bacteria in the upper airway (pharynx and larynx bacteria gets in the nasal sinuses) - and in case of bacterial pneumonia mucus also contains the etiologic agent of that pneumonia (so not only from the upper airway).

Thank you for your clear and logical answer! I think the atelectasis which I just described above is caused due to lack of movement in the supine position. Change of position seems to be its best way of prevention. That is a logical. Medically inhibited, cough can start again by atelectasis. Atelectasis is a respond to the congestion in the lungs. Atelectasis seems to be tied to the reflex arch because Codeine blocks the cough center.

@Masi Yes, change of position and deep breathing are the best ways to prevent atelectasis (and also treat atelectasis without airway blockage).


text:
Does increased physical activity increase the rate of cell division?
Ever since learning that the shortening of telomeres is linked to aging I've tried to figure out what causes cells to divide, and if it's possible to slow down the rate of cell division through life style changes.
How would, for example, increased or decreased metabolism affect the cell cycle? If we exercise a lot, would it tear on the cells in any way, forcing faster cell division?

My understanding is that telomeres are linked to cell senescence, which is not necessarily the same thing as organism senescence. So even if you could track down a method to slow cell division, it would more likely mess with organ function now rather than extend life.
Here's a nice summary of cell senescence: http://www.ncbi.nlm.nih.gov/books/NBK26877/#A3266
I did look into cell division in muscle, and new muscle cells come from satellite cells, rather than from mitotic division of currently active muscle cells.
Caloric restriction was the hot new way to live longer for a while, but studies in primates found that a sensible diet and good genetics have a bigger effect. Which is pretty much the T-shirt in medical science.
This question was asked last spring as well. Coincidence? Homework?

Metabolism does affect cell cycle. Stress is known to affect ageing.
Mitchell et al., (2014) report that there is a telomere shortening in kids who grow up in disadvantaged social environments.
Metabolism and stress are known to affect longevity and general health. After much research on genomic associations of diabetes, people have come to the conclusion that physical exercise helps.
Physical exercise is also known to stimulate neurogenesis in the hippocampus; the causes are not well understood (van Praag, 2008).
There are more of such reports. If you search you'll find.

Little occupied now- so couldn't post a more elaborate answer.


text:
Modern research or study on patterns in nerve signals
I am trying to find any recent study on pattern recognition in nerve signals. It does not really matter the part of the body where the research is focused on. It can be anything from studying activity of one group of nerves to signals coming from an entire limb.
I was only able to find old (1996) research, which could be much more complete with the modern advancements in computing and manufacturing of micro-instruments. Here is an example of an old paper.
P.S. I am generally looking for information on how nerve signals differ within multiple subjects of same specie. For example, how would nerve response to a stimuli differ for two mice from same offspring and how will they differ from it's parents.

what kind of a pattern do you want to find; what do you mean by signal ?

@WYSIWYG some kind of logical sequence of neural activity caused by the stimulus. For example I would want to know if applying hot/cold object to skin of both right and left limbs would cause the sensory neuron to send the same or similar signal (electrical impulse) to the spinal cord. Would it be possible to identify what happened with the limb, having access to part or all of the electrical activity in central and peripheral neural systems, even theoretically. Is it possible to learn what each impulse is about and if it is, should you learn anew for every new body or signals are universal?

I meant what will you capture: Voltage changes ?

@WYSIWYG Yes, it would be synaptic potential.

You might want to read about event related potentials (recorded by EEG) or event related fields (recorder by MEG). The idea is simple:
1) Pick some stimulus, e.g. a person touching the hand of a subject. Pick another stimulus, e.g. the subject seeing a person touching the hand of another subject. Record EEG/MEG.
2) Repeat each condition for at least few hundred times. Throw away bad data, and average the repetitions. You do the averaging because the signal-to-noise ratio is low in all non-invasive electrical measurements, and the signals are always riddled with movement, cardiac, and eye-blink artefacts.
3) Compare the conditions in each sensor. Rest is statistics, though not very easy.
Actually, the experiment above would be about mirror neurons, a relatively hot topic in neuroscience. (See e.g. recent issue from Nature)
The more general situation is that using pattern recognition/machine learning algorithms to study brain signals is already a standard thing to do. There are for example graduate/undergraduate programs in computational neuroscience.
If you would study some other signal (e.g. measure from a hand, leg), they are going to dull. Very dull. Mostly because then you have 1 time-series, instead of several hundreds of time-series to analyse.

For example I would want to know if applying hot/cold object to skin of both right and left limbs would cause the sensory neuron to send the same or similar signal (electrical impulse) to the spinal cord.

This you could too study with the event related fields/potentials.

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Can oncogenesis happen without apoptosis pathway being affected?
Has there ever been incidences of one or more cancerous cells having all it's cell-death pathways and apoptosis mechanisms intact and functional?

Are any apoptosis mechanisms in a cell that are not functioning or suppressed or damaged a typical sign of a cancerous cell?

Could something be used to cause a mutation in a cancer cell that is 'noticeable' to the immune system?

Usually the cell death mechanisms are overridden and therefore oncogenesis. The pathway components themselves are not mutated. One classical case I can cite is that of Ras-oncogene. See this article for details. Usually the survival/growth signals (MAP-kinase) are activated with simultaneous inactivation of apoptotic regulators (Akt-pathway). A mutation of MAP-kinase component ERK can also cause cancer but apoptosis is nonetheless supressed because of the interconnections of these tow pathways in the gene regulatory network.
Whereas in the case of tumor suppressors, the cause of cancer is genomic instability and failure to initiate apoptosis.

This is pretty unlikely, since one of the most important steps for cancer cells is to shut off apoptosis and proteins which control it (like p53, BCL2 and so on). Cancer cells (especially when they are genetically unstable) acquire so much mutations and misregulations, that these would otherwise trigger apoptosis which would result in the removal of the cell.
This can look like the following (figure taken from here), when you compare normal and cancer cell:

quite a complete figure.. i like it..

Thanks. It is a slightly different perspective to your figure.

Does a pre-cancerous cell shut off apoptosis and the proteins that control it before it becomes a cancer cell or is it the case a cancer cell shuts off apoptosis mechanisms after it is already cancerous?

Usually apoptosis is affected in a later stage of oncogenesis. However, in case of DNA damage induced oncogenesis, there is a failure to initiate apoptosis when the DNA is damaged and not repaired. In this case the signal has not yet reached the apoptotic pathway. This ensues genomic instability which may further lead to uncontrolled growth i.e cancer (as you can imagine, to grow and multiply maximally is the first instinct of any lifeform)

Is there some way to detect if a cells apoptosis mechanisms have been shut down or made to malfunction? If so could this be a way to detect if a cell is cancerous?

@user128932 You could do a genome analysis and search for inactivating mutations. Since there is more than one way to activated apoptosis, this usually happens only in cells which have already gone down the cancer path.

Is there a less involved method then genome analysis to see if a cell has had its apoptosis mechanisms 'turned off'? If cancer cells are immortal-like can they withstand many types of viruses or harmful bacteria or phagocytes?

If a cell sample has only cells with no apoptosis mechanisms but it has not been determined if they are cancerous ; if some process can induce cellular growth that would not occur if the cells were not cancerous would this show this cell culture has no apoptosis mechanisms?

Can a cell with no apoptosis mechanism spontaneously reproduce in conditions it shouldn't be able?

@user128932 Sorry, but I don't understand your last question. You want to know if cells without apoptosis can divide?

My question on Nov 2 at 3:48 ; yes , can a cell without any apoptosis mechanisms divide , given it is in a 'situation'(possibly artificially induced) were it shouldn't be able to divide?

Again, cancer cells are an example. Disabled apoptosis is not uncommon, this mechanism is used to evade apoptosis.

If a cell has a lot of mutations yet it can still function would this make any apoptosis mechanism not 'work'?

This depends on the specific mutation itself.

So some types of mutated cells can still have all its apoptosis mechanisms working? What kind of mutation can cause an apoptosis mechanism to malfunction?

@201044 Can you please stop asking questions in the comments and open a new question instead?

@201044 First: Perpetual questions in the comments are not liked. Then: You ask questions, so you need to decide if you want to know more or not. I am not going to open a question for this.

I don't repeat the same question over and over again; that would be a perpetual question. Why argue about 'meta-biology' stack exchange issues  or other syntax or 'administrative' issues when I have asked relevant questions even in the comments. If this bother's you people just ignore it. Don't make a separate issue out of it.

The original question was ; have there been  any examples of active cancer cells with an apoptosis mechanism that is functioning?


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Why do Bee stings cause swelling?
Why is it that when a bee stings, a little area around it gets swelled?
I think it is some sort of defense mechanism of the body.  But how does it help?

Not exactly the answer, but interesting- I used to swell a lot from bee stings, like my whole foot and half way up my shin if i stood on a bee. Used to freak me out. Then I started working for a bee keeper during summers.
After 10 or so stings I would no longer swell. Non-specific immune responses by then I gather. But the first few stings at the beginning of every season would swell pretty good. I sometimes would try to get those first stings intentionally in places like on the back of my arm or somewhere more convenient than getting swollen fingers. Pretty cool that the body adapts like that

Bee, or other insect stings/bites, will cause a reaction to occur due to chemicals being released from your immune system.  This can result in anywhere from a small bump to anaphylaxis, which can be life-threatening if not treated right away.

From Southern Cross Medical Library:

An anaphylactic reaction occurs when the body's antibodies respond to the insect venom by releasing chemicals such as histamine and serotonin that trigger the allergic reaction.

Whatever the reaction, it is correct to say that the reaction to an insect sting/bite is a defense mechanism of the body.  An interesting study done by Stanford University School of Medicine was done and discusses these immune mechanisms:

Innate immune responses occur in subjects exposed to a foreign substance, such as a pathogen or a toxic material like venom, for the first time. [...] Immune cells called mast cells, which reside in most of the body’s tissues, are poised to unleash signals that turn on defense responses when a pathogen or toxin intrudes.  Prior immunization is not required for these types of innate immune responses, nor is the development of specific antibodies. In contrast, during an adaptive immune response, the immune system creates antibodies that can recognize the toxin or pathogen that is invading the animal’s system. Adaptive immunity is typically a faster, more specified and more effective form of defense than innate immunity, the research team explained.

More explanation of the non-specific immune response:

If a bee stings you, the presence of the bee venom triggers a nonspecific immune response. White blood cells arrive first on the scene to rid the body of bee venom antigens. As war wages between antigens and white blood cells, battle signs may appear on the affected skin. Inflammation (redness, swelling, heat, and pain) results as the body wards off invaders.

If the body detects an antigen that it previously met, a specific immune response occurs. In this response, the body has been trained to recognize and neutralize a familiar specific antigen; its immune system "remembers" the antigen. Such systemic (not restricted to the initial infection site) immunity enables a faster, longer lasting immune response than does a nonspecific response.

Therefore, these reactions to bee stings and other foreign toxins help us to better develop our immune system to protect against potential future encounters with these insects.

is the swelling only characteristic of the non-specific immune response? Does the immune system react differently to second and subsequent bee stings?

There is some information at this site http://bindaree.com.au/hints/bee-stings/ that states: In a non-allergic person, many stings can be sustained without threat to life, and repeated stings produce a tolerance or immunity resulting in a gradual decrease in reaction severity. This is due to the body’s production of appropriate antibody which neutralises the toxin subsequently injected.


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Function of the Auricle in heart
What is the function of the auricles (conical appendages through the atria) present in the heart?
Do they have any other function than increasing the volume of blood the heart can hold?

The left auricle is a decompression chamber when atrial blood pressure is high (in systole or in some pathological conditions) [1, 2]. Some research claims it also plays a role in cardiac regeneration because it contains cardiac progenitor cells [3].
Probably the right auricle has less important function; also there are fewer studies about it.

References:

Al-Saady NM, Obel OA, Camm AJ. Left atrial appendage: structure, function, and role in thromboembolism. Heart. 1999 Nov;82(5):547-54. PubMed PMID: 10525506.
Bansal M, Kasliwal RR. Echocardiography for left atrial appendage structure and function. Indian Heart J. 2012 Jul 27;64(5):469-75. doi: 10.1016/j.ihj.2012.07.020. PubMed PMID: 23102384.
Leinonen JV, Emanuelov AK, Platt Y, Helman Y, Feinberg Y, Lotan C, Beeri R. Left atrial appendages from adult hearts contain a reservoir of diverse cardiac progenitor cells. PLoS ONE. 2013 Mar 12;8(3):e59228. doi: 10.1371/journal.pone.0059228. PubMed PMID: 23555001.


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How do I tell whether a mass spectrum was made with ESI or MALDI?
I was working through a previous exam and came across the following question (with reference to the picture shown below):

"What MS ionization method was employed (MALDI or ESI)?"

I cannot seem to find the answer, so I'm guessing it is not possible to tell, but if there is a way to see which one was used, please enlighten me.

It is probably ESI because, as already mentioned, ESI produces multiply charged precursors while Maldi would generally produce fewer charge states and +1 most frequently. But, you can not say that MALDI wont give  multiply charged ions. So from just this picture you can not say for certain but can only make a guess.

I am not an expert in this topic but from what I have heard ESI generates multiply charged ions but MALDI usually does't. It is possible to find multiply charged species in the spectrum.

They all have a charge of four it seems to me? (Assume one Da mass difference, and then divide by .25, the m/z difference.) Is that how you are able to tell it comes from ESI, namely that they have a charge of four, not one? If you confirm I will upvote and accept your answer.

I was not actually looking at the spectrum that you attached.. I answered that in general ESi produces multiply charged ions. But when you commented, I noticed the spectrum and it seems that these are +4 charged ions of different molecules/peptides. Nothing else fits that neatly

This is the isotopic cluster of an ion, so chemically it should be of one kind of molecule/peptide and not multiple. Yes the analyte is in a charge state of 4, so most likely it would come from a an ESI.


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Image formation
I have learnt that the brain provides a perception of image due to previous memory and experience. Then how does a blind person attain vision after cornea replacement?

Note: Questions of neuroscience are not off-topic on biology.SE but they are also on topic on CognitiveScience.SE. If you don't get a satisfying answer here, you may want to give a try later on on this other site.


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Do RNA molecules bind each other?
I have a question, maybe a naive one.
Let's assume that we isolated some RNA from a tissue. Do RNA molecules can bind each other if they have the complementary sequence? I know that some small RNA molecules can bind other RNAs and regulate them but I do not know it is possible in this case? It is like 2 different mRNA can bind each other or not?

The difference between RNA and DNA is rather small, and both can form a double-helix structure. So if you had two sequences of RNA complementary to each other they would basepair and form a helix.
There were also some ideas to use this for therapeutic purposes, antisense RNA, an RNA oligo complementary to a messenger RNA, can theoretically be used to silence gene expression by base-pairing to the mRNA.

Thanks. But do they need to be completely complementary or not? And during the experiments, is there a way to prevent this issue?

@golgicik Not completely, a certain amount of mismatches would be tolerated. There are various programs to calculate the likely secondary structure of RNA like MFold or the Vienna RNA package you could use to predict the structure of your specific RNA.

Thanks @Mad Scientist. I think 2-ME would prevent it, right?

@golgicik 2'-OMe doesn't really affect base-pairing, it's a modification of the ribose.

I mean 2-Mercaptoethanol.

Would ME prevent secondary structure? I think at reasonable concentrations it would have little effect and it's not used (as far as I know) as a denaturant.

@golgicik 2-ME doesn't denature secondary structures. It is a reducing agent that reduces disulphide bonds in proteins. Urea will denature RNAs just like it does  proteins.

@golgicik for hybridizing two RNA strands you can use UNAfold. However, it doesn't compute it for RNAs longer than 500nt. Also, in RNA G can form a wobble base pair with U

@MadScientist answer is very good. I just want to add a detail that could not fit in a comment.
Double stranded RNA is nothing exceptional. You can see an RNA strand that binds to its antisense in tRNA and in RNAi for example.
tRNA

RNAi


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About a mechanical aid to the heart
I saw a news story a few years ago (I think) about a girl with a poor heart having a device implant that took over only some of the functioning of her heart ( I think they called it a piggy-back device , or something like that). The extraordinary thing is that it not only helped her live but all the heart functions started to improve. It was as if giving part of the heart a chance to 'rest'  allowed the whole heart to improve. If this procedure works could it be applied to other organs? Could a Piggy-Back device be made for the liver taking over only some of its functions for instance?  Could such a thing help the liver functions to 'regenerate'?

The function of heart is just to pump blood and nothing else. Though, it is a vital organ, its functions are limited. The device that you are talking about is a battery powered mechanical pump that performs the same function as heart.
Liver, however has a more complex function. One of its function is to synthesize and secrete certain molecules. A small artificial device cannot do that (you would need a bioreactor !!!).
We still haven't developed and artificial cell. Perhaps a consortium of bacteria can do some of the liver's functions but to culture them in right proportions and implant them without the risk of infection or their elimination is almost impossible as of now. You can clearly see that there are too many steps to be optimized.

There was a news story about a device that took over some of a young girl's heart functioning and the girl's heart did improve. It was not  a heart pump that took over all its functions.

if you can then please post a link to that story.

See this, tell me which one are you talking about ?
All artificial hearts do nothing but pump. Even the real heart has no other function.
Or do you mean the pacemaker (that is for controlling arrythmic beating)

@user128932 - you can have an implanted assistive device that helps by pumping some of, but not the entire, volume of blood. These are used by patients (and I assume this young girl is one) whose hearts can still pump blood on their own, but for whatever reason are unable to do it under optimal conditions (low pressure and/or low volume caused by incomplete chamber contraction/expansion, backflow from issues like leaky valves, etc.).

Yes , this (I think ) was it , an implanted assistive device. The news story even said the young girl's heart improved in function. Could there be an implanted assistive device for the lungs? Thank you MattDMo

I heard cows and salmon and sheep have been cloned ; so if they can clone a large animal can they clone a cell? Can a liver cell be cloned or would it have problems with longevity like the sheep did? Could blood be cloned?


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evolution and mutation of microrganisms against medicines?
I presume microorganisms would have very short life span and they would multiply more creating millions of their kind. Is it really a threat to consider when we use anibiotics and other stuff more making these creatures becoming resilient to the medicines. On the other hand bodies becoming dependent on the medicine making us weaker .we clean our office spaces homes etc with bleaching agents, acids killing microorganisms and thus making our body unaware of these and letting these organisms survive and create more deadly strains.
I believe there are examples like malaria microbes becoming resistant to quinine perhaps many more.  If someone tries not to take medicines when he suffers from common cold and small fevers and let the body fight but is it right to do so considering that mecines are available and one should take them.
There is an article also published today.

A few throughts about this: Microorganisms have a short life span but they replicate very fast with a short generation time. So this create vast amounts of "offsprings" with some mutations naturally occurring. Due to this large numbers the chance of developing resistances is much higher than for slowly replicating species.
This is especially true, when the selection pressure is high, as this is the case when you treat with drugs which usually kill these microbes efficiently. When people are not taking these drugs (antibiotics for example) according to the necessary scheme, the concentration of the drug in the body is lower than necessary to kill of all microorganisms. This leads to the survival of microorganisms which are a bit adapted to survive the drug and so on.
The real problem are people who are not following their treatment regime necessary and thus causing resistancies. A case for this is tuberculosis. Regarding taking medication: Always take them when necessary and leave them out when not. A simple cold for example can not be treated antibiotics since it is viral, the secondary middle ear infection usually can.

Great answer.  I'll add that there is debate in medical circles (especially primary care) whether to treat mild ear infections (without hearing alterations) with antibiotics at all, since statistical analyses are showing that the vast majority resolve on their own naturally without treatment (source: UpToDate, PubMed) and the more antibiotics are used, the more resistance develops.

Also, there used to be widespread overuse of antibiotics for upper respiratory infections when most URI are viral, sinus infections are usually secondary to viral and far more rare than people think, and (similar to ear infections) frequently resolve on their own (sources same). Overuse of antibiotics has caused resistance, as discussed.  We're causing bacterial evolution right in front of our eyes.  Look up MRSA, VRE, and multi-drug resistant organisms (MDRO).  It's scary to wonder how close we could be to an epidemic of bacteria resistant to everything we currently have!


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Do birds have navels?
This picture shows the development inside a bird egg:

This shows the connection of the embryo to the yolk sac.  Does this mean birds have navels?  And if so, what happens to the umbilical cord once the bird hatches?

All animals develop in this way, whether they are oviparous (developing in an egg) or viviparous (developing inside their mother, or live-birth).
From Wild Birds Unlimited:

All mammals have navels or belly buttons where the umbilical cord distributes nutrients between a mother and her fetus. After birth, the umbilical cord is cut and a scar develops on the abdomen where the hole closes.
Of course avians or birds hatch from eggs which are virtually self-contained life-support systems that only require warmth and oxygen to develop properly. Instead of an umbilical cord scar, birds have yolk sac scars at hatching. This is where the chick embryo is attached to the yolk sac. But don’t look for any bird belly button rings. The scars usually heal and become virtually invisible.

As for their umbilical cord, it looks like it falls off when the chick hatches if it is not fully absorbed along with the yolk sac, along with everything else contained in the egg (although there is not a lot of material left within the egg by the time the chick is ready to hatch).

Inside a bird's egg there is a tiny cord that connects the developing embryo to the yolk sac. When the egg cracks open, the hatchling does in fact have a miniscule residual scar where the cord was.

I doubt it falls off, the sources I looked up say that the whole yolk sac goes inside the bird's body.

You are right about the yolk sac! http://msucares.com/poultry/reproductions/poultry_chicks_embryo.html - However, it says that when they are born some residual umbilical cord tissue is still attached to the chick.  http://www.justcockatiels.net/assist-hatches.html  There are sometimes problems with the yolk sac being absorbed as well, so this could be related.

The first sentence is a fragment and doesn't make any sense. If you remove the parenthetical expressions, it reads: "All animals that develop in this way, whether they are oviparous or viviparous." Did you mean to say more?

How obnoxious of me.  'That' was removed.


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Enzyme kinetics
I can't understand how to study enzyme kinetics. Say I have a lipase and want to study the kinetics of this lipase using a fluorogenic substrate, how would I do this? From what I understand I would use a 96 or so well plate and in each increase the amount of substrate or increase the amount of enzyme and use a fluorescence microscope or a spectrophotometer?

A basic biochemistry textbook (or Google) will be very useful in answering this.

I'm going to try to lay out some basic definitions here in as plain language as I can find.
Its difficult to study enzymes when they are outside the cell, where they may behave quite differently in different contexts.  We categorize a given enzyme in its class by kcat, Km and by mechanism (the sort of reaction they catalyze.
kcat is sort of a maximum velocity of the enzyme - when there is a lot of substrate around - what is the rate of catalysis.  Ideally there will be zero product present.
Km is sort of the inverse affinity of the enzyme for its substrate, but at half the maximum velocity of the reaction.
The mechanism, which has a couple of definition basically asks how many substrates are bound and in what order, which products are released and in what order, and any intermediates in the reaction which might appear, and in what order.

e.g.: A -> A* -> B* -> B
  A + B -> C + D

I say 'sort of' because you might never see an enzyme operate at maximum rate in living cells.  Substrates are usually rate controlled there - they only have enough of any given compound as they need.
The context that all of these numbers and designations are used is often taxonomical - that is to say you can categorize and sort, and describe what the enzyme does.  In practice large differences in the numbers can describe how useful one enzyme is over another, but it doesn't necessarily tell you how an enzyme will definitely behave in vivo or entirely how it will work in an industrial application.  Its just a start.


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What is most simple eukaryotic genome?
Expressed in number of Base Pairs or Bytes, about how large is the simplest eukaryotic genome?
How much of this is 'junk-DNA' (non-coding)?

what do you mean by "most simple DNA molecule"?

you can synthesize DNA of any length, from 1 bp on up, so this question is kind of meaningless...

True.. but I implied that I wanted to know about the shortest naturally occurring DNA in eukaryotic cells.

Information content in mathematical sense?

I have to agree with @MattDMo, this question is meaningless in its current state (which is why I downvoted it and voted to close it). The problem would be much better if you were to clarify a few things. For example, what do you mean by "most simple DNA molecule"? Are you using the term "information" in the vernacular sense or in the theoretical sense? And if by "exists today" you really meant, "naturally occurring in eukaryotic cells", then it's better to say what you really mean. Addressing these concerns will help us as a community address your question meaningfully.

In case you were unaware, you can (and are encouraged!) go back and edit the text of your original question. We're not trying to condemn you for the way you asked the question, just providing suggestions for how you can clarify and improve the question, for your benefit and ours.

Hey @AndreasHartmann I've edited your question - hope this helps - feel free to change it again... thought this might help.  Most biologists don't think in terms of information content, which is not well defined beyond the 'one base = 2 bits' chestnut.

When you say genome, what exactly do you mean? All of the chromosomes? Biggest chromosome? Does mitochondrial or plastid DNA count? Do plasmids count?

How do you define simplicity? Because of what was discovered by the field of epigenetics, it is very difficult to figure out the exact entropy of a genome. @shigeta 's "times 2" model is only relevant for storage of sequence in a computer, not actual organisms.

You should edit your question to ask for the smallest eukaryotic genome, and maybe also ask for how compactness (% of coding sequence - junk DNA is a very obsolete term) varies with length. Everything else should be a separate question (which you can formulate after pondering your answers).

You asked about eukaryotes. The genome of the yeast Saccharomyces cerevisiae is 12.2 Mb.
The genome of the smallest free-living eukaryote, Ostreococcus tauri (a unicellular green alga) is 12.6 Mb
There are smaller eukaryotic genomes, but these are not free-living organisms they are intracellular parasites.

I'd be interested in some detail about why Saccharomyces is not 'free-living' and maybe a reference for what the smaller genomes are?

@Shigeta the question was ambiguous, and my answer didn't help. O. tauri is physically (i.e. cell size) the smallest free-living eukaryote. See http://en.wikipedia.org/wiki/List_of_sequenced_eukaryotic_genomes for some genomes of obligate intracellular parasites such as Cryptosporidium.

According to this:
http://users.rcn.com/jkimball.ma.ultranet/BiologyPages/G/GenomeSizes.html
The shortest DNA of a individually living cell is that of Mycoplasma genitalium at about 580000 base pairs. -But it's not eucariotic!

...but M. genitalium is not a eukaryote!