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Why do I need a flu shot every year, while many other vaccinations last years or even a lifetime?
Is it a viral vs. bacterial thing?
Is there just more variety among types of flu than other diseases, so that this year's vaccines don't cover next year's flu?

The flu virus changes rapidly so that the current vaccine doesn't work against the new strains.
The way vaccines work is that they teach our immune system what to look out for. The vaccine contains bits of the virus but in a form that can't cause a proper infection, the body learns what to look for and next time before the virus can really get going the immune system kills it off first.
In the case of flu, every year it looks different enough that the targeting mechanisms of our body don't recognise it. Flu being a RNA virus frequently mutates until it is slightly different. This is called antigenic drift, the changing of the antigens or the parts our body recognises.
On top of that there's lots and lots of types of the influenza virus, that can not only infect humans but others which affect other animals. Occasionally the virus might combine with a random other strain making it completely new: an animal flu and human flu hybrid. These are the epidemics of swine or avian flu etc. This recombination is called antigenic shift.
So each year scientists predict which viruses will affect us this coming year and grow them ready for vaccines. Of course there's some of the old virus floating around looking for someone to infect, but those infected can't be infected by it again if the immune system is working.

Thank you! Looking based on your answer at the wikipedia page for RNA viruses I see that polio and measles are also RNA viruses. Why don't they mutate as quickly as the flu? Or is there just less biodiversity among those viruses than the flu?

HPV is a DNA virus that mutates at the same rate as our DNA. In comparison, there's the viruses you mentioned that mutate slowly and HIV another RNA virus that mutates so fast every couple of copies has a mutation. RNA itself is less stable, so RNA viruses mutate. However the real mutation rate is all about the error checking of the enzyme. HIV has no error checking basically and doesn't care. Increased mutations means more variability and immune escape but more non-functional virus particles. Too much or too little is a bad thing.

OK, I think I understand. The influenza virus does less error checking than some other RNA viruses and so it mutates faster. Is that right?

Yup! The scientific term for this is that the polymerases lack proofreading.

Would also add the influenza virus has strains that infect many animal species, ranging from humans, birds, pigs, horses, seals,
whales, camels. Should two influenza strains infect the same cell, they can swap parts of it genomes. This allows the influenza virus to very rapid change. Much higher than polio and measles which only inflect humans.

What you call influenza isn't a specific virus which is always the same, but a virus that has numerous different strains. Flu virus is constantly alive on this planet, and there are numerous different types, such as the ones which infect humans, the ones that infect birds, and occasionally a virus that mutates to infect humans although it shouldn't as it infects birds only.
Viruses evolve very quickly. The strain of flu virus which was rampant last year definitely won't be the one to look out for this year. What scientists are doing is a very difficult job - they're tracking the progress of different flu virus strains and trying to make an educated guess about the strain or strains which might spread the most during the flu season. And then they come up with a flu vaccine which is a mix that targets the several strains that were identified as being the biggest threat.
It's a hit or miss kind of thing, and it's quite possible that the scientists get it wrong, or not necessarily wrong, but something happens in the virus evolution process that renders this year's vaccine useless.
Also, it's possible to get a flu vaccine and still get flu - if you happen to come in contact with a strain that wasn't targeted by the vaccine. Viruses evolve very very quickly, so vaccine isn't failsafe, virus can evolve in some other person, you come in contact with the virus and get infected despite being vaccined against the original strain.

I hear you that viruses evolve very quickly. It's interesting that the combination of viruses we call "influenza" seems to change so much more quickly than polio and measles (see comments on @AndroidPenguin's answer above).


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Bacterial Conjugation/Horizontal Gene Transfer -- how does the plasmid exchange work?
So according to a PPT I'm reading, bacterial conjugation works by the two bacteria joining pili and exchanging plasmids. So how exactly do the plasmids get across the gap? If I understand this correctly, the pili are little hair-like things on the outside of the bacteria -- so unless the plasmids were actually able to somehow be pushed through the pili, there would be gap. Right?
The only other possibility I can think of would be that the membranes fused or something like that. But that comes with it's own whole set of problems.
How does this work?
Thanks!
evamvid

The donor cell retracts it pilus upon contact with another cell and both cells form a pore between the two cells, which allows the transfer of DNA.
Take a look at the image, I think this makes it clearer (from the Wikipedia article on Pili):

This has even be seen in an electron microscope:

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

sort: votes


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Can animals absorb atmospheric sulfur?
This is a follow up to this previous question:
In biosynthesis of cysteine and methionine, where does the sulfur come from?
Can animals use gaesous H2S in the atmosphere, say for instance from a sulfur rich hot springs, to aquire sulfur?

No, they can not do this. We don't have the enzymes to metabolize H2S, besides that, it is highly toxic. H2S can be used by some bacteria and archea (so called lithotrophic bacteria), but they are relatively rare.
Sulfur is reduced by plants, which take it up in the form of sulfates and subsequently reduce it to form different sulphur compounds. Animals are dependent on the uptake of sulphur from plant sources, as the sulphur containing amino acids are essential (meaning the cannot be synthesized by themself). The pathway is relatively complex. The image below is from the Wikipedia article on Sulphur assimilation, which I can also recommend, if you want to know all the details.

Geat reference, thanks so much. But one comment, I read somwhere that gaseous H2S in the atmosphere was highly correlated with reduced blood pressure.

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How do wild animals get rabies?
I can see the chain of spreading disease: Humans usually get rabies from domestic animals, those usually get it from wild animals, wild animals in their turn get from the other wild animals and here I'm stuck. Well, so where do wild animals get it from initially?
I know that rabies is a virus and it needs warm-blooded animals to live out. Also according to Wikipedia once an animal is effected it lasts, let's say, no longer than for 2 weeks.
In other words, does it mean that there is a constant population of rabid animals that exists in order to pass this virus from one animal to another every 2 week on the average?

Such viruses have a natural host, which might get sick, but is usually not killed by the virus. From there, the virus can get zoonotic (jump over species barriers) and infect other animals when it comes to contact. For Rabies the reservoir hosts are different, for the US these are bats, skunks and racoons. For more details, have a look on this PDF.
Another example for this is the SARS virus (a corona virus) which most likely lives in bats naturally and has jumped from there onto birds and from there infected humans.

Thank you very much for this PDF. The only section I found which explains virus origin is "Mechanisms of Attachment". Still I'm not sure I get it, could you rephrase it in layman's terms?

@dVaffection For example, ticks can carry lime disease, they're not affected by it but can still pass it on to you. Similarly mosquitoes and malaria. The latter is explained nicely in wikipedia. You can have a similar situation with viruses, that's what Chris means by "natural host".

@terdon Also "Natural hosts" are referred as reservoirs - I totally get it. But somehow those animals get this virus in the first place and this virus stems from somewhere!

@dVaffection that one is the age old question of the chicken and the egg, not really within the scope of this site :) Anyway, many viruses can survive outside a host (for a given value of "survive") so some can be airborne and picked up by the host that way.

Or host and reservoir come in contact somehow and transmit the virus. It is only present for some time in the intermediate host (and will either kill him or simply leave him) before the virus gets either transmitted to another (probably better) host or the spreading stops here.

I wonder what is the reason a virus strives to find a host? My guess so it can replicate itself. Am I right here?

@terdon As far as I understand virus of rabies if transmitted only through saliva.

@dVaffection no, you're anthropomorphising, a virus doesn't "strive" to find a host any more than an Oxygen strives to find two Hydrogens to make water. We are at the frontier between life and chemistry here.

Well, so from your words I may infer that a virus (rabies in this case) is just a poison scattered all over the earth which animals pick up on occasion. And this virus has no any intention to hit any animal but this is just a way it exists?!

A virus has a host for which it fits. If it doesn't meet this host, nothing will happen and over time it will be deactivated. It is a bit more than a poison though, since it can replicate (given the right conditions) and spread. But outside its host viruses are not alive.


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Is it possible to elicit transient gene silencing by using virus induced gene silencing (VIGS) in plants?
I am looking for a molecular tech' which could result in transient gene silencing in plants. The objective is to not make transgenic plant, but to use these tech' to silence a gene of interest for a short time. From my limited knowledge, I found that virus induced gene silencing (VIGS) may be an option, I wonder how easy and how long such silencing last? Is there any alternative method?
I don't have any candidate gene to be silenced at this moment, but the tissue will be flower. so it would be nice if the protocol works for flower.
Thank you in advance

I haven't worked on alpha viruses since my first rotation in grad-school, but an important question that needs to be answered is when are you infecting the plant? If try to infect fully formed flowers you might have a hard time getting effective silencing across the whole tissue.

Virus induced gene silencing (VIGS) is definitely an option.
The ease of using VIGS depends on a lot of factors. Current VIGS vectors have limited host ranges. Depending on the species of plant that you are working with, there may or may not be suitable, pre-made VIGS vectors available and published techniques for using them. Many of the VIGS vectors that are available may be limited in terms of which tissues they can infect. Working with the vectors themselves requires that you have some way to propagate them and some way of getting them into your target plants (for example Biolistics, Agrobacterium or direct application of infectious virus).
There have been a number of VIGS vectors developed over the years, capable of infecting a diversity of plant species. Modified Tobacco mosaic virus (TMV) and Tobacco rattle virus (TRV) are two common VIGS vectors used for silencing in a variety of plants. TRV in particular is known to have a very wide host range. If your species doesn't fall within or even near the documented host range of available vectors it may be worth just trying a few different ones. Or, you could always isolate a virus specific to your target plant and build you're own. What fun!
The length of time that silencing will last is difficult to predict. In my experience, it will typically last a few weeks. But this may vary depending on a number of host factors and the VIGS vector used.
One potential alternative would be to just use Agrobacterium. It could be combined with a recombinase system to satisfy your condition of transience. To build such a system you could insert you're silencing construct into a binary vector. By including an inducible recombinase sequence adjacent to your silencing construct sequence and by flanking both of these with the recombinases recognition sequences, you would be able to remove inserted DNA at some point down the road after transforming the plant.
Again, depending on which species and variety of plant you're working on, this could require some trial and error as there may not be published techniques for Agro mediated transformation of you're target plant.
While Agro mediated transformation may not quite be what you're looking for in terms of transient silencing, it may be sufficient for a proof of concept.


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From a purely biological perspective, how does an optimal human diet look?
There is hardly any subject as contested in the media as what humans should eat. Usually, such discussions are devoid of actual scientific reasoning, though they all claim to be backed by scientific studies (typically without naming those studies). The colorful spectrum of suggestions ranges from eating only bananas, to avoiding "refined" sugars and red meats, to avoiding meat altogether, to eating as much meat as possible etc. Clearly, many of them are completely contradictory.
From a purely biological, evidence-based perspective, how does an optimal human diet look? In particular, I'm interested in the following questions:

Is there a single diet that can be recommended to all humans, regardless of lifestyle, which only needs to be scaled in quantity (i.e. more physically active people should eat more of it) but not content?
Excluding diseases, does the optimal diet for an individual depend not only on their lifestyle but also on their genetic makeup?
Knowing nothing about their genetic makeup and living an average industrialized-society lifestyle, what is the best guess for what a human should eat?

Answers should be backed by solid reasoning and (ideally) references to verified (meta-)studies published in actual scientific journals supporting the claim. It seems strange to have to ask such a question, as one might expect it to have been answered thousands of times already, and of course it has, but the answers vary so wildly that I suspect I'm being fed hogwash mostly.

Is this question just a coincidence? See new topic at BioSE Meta: http://meta.biology.stackexchange.com/questions/556/policy-on-health-questions

I think you should refine your question, and split it into subquestions. This is really broad, and there are lots of diets out there. You should also define what you mean with optimal (what is the "target"?), since this could refer to e.g. keeping a healthy weight, nutritional balance, life span etc. Different diets may be optimal for different targets. Without a clear definition of a target, this question borders on primarily opinion-based ("what is the best...?").

No, there isn't a single diet that can be recommended from a biological perspective.
The most popular diet from a pseudo-scientific perspective is the Paleo diet, saying we should eat what our ancestors in the Paleolithic were eating, but it makes a mistake of forgetting that our metabolism has evolved since then. There are also numerous other flaws in the Paleo diet but I won't go through them all.
The most notable example to use here would be dairy products, as we're among the few species that can drink milk at adult age. Drinking milk as an adult isn't normal, and yet we evolved the ability to do so. Some individuals can't drink milk, same goes for consuming gluten, nuts, and several other things, but the species as a whole can consume all of the above. Some people must avoid certain foods because of their individual genetic makeup though. Most evolved to process gluten and this ability is greatly responsible for the fact that there are 7 billion of us now. If you read an article "gluten is bad", remember that gluten grew the human race and without it at least a third of the world's population would die through starvation. If you read an article about the Paleo diet, remember we wouldn't be here if the agricultural revolution didn't happen.
The correct answer would be - humans can consume everything that isn't toxic and provides them with energy. We're very capable omnivores, which is probably one of the reasons why we've done so well as a species. In other words, you won't die from eating processed sugar. There are healthier and less healthy foods, but none will kill you.
You are correct, there are numerous answers (or attempts to answer) to this question, and the way the research is concluded definitely doesn't help. Research is mostly conducted through polls designed to prove the scientist's original unverified claim, and virtually no research is conducted on the biological level, e.g. what happens to the body when you consume a certain carbohydrate. The whole field became pseudoscientific. The "food pyramid" is...pretty much wrong.
Body needs proteins, body needs carbohydrates, body needs fat. You could come up with a vague answer if you eliminate the foods that body doesn't need, such as processed sugars, but it's still energy and you won't die from consuming it.
There is no scientific research that consumation of any food, or elimination of any food, affects life span. Meaning, there's no differential survival rate depending on what you eat.
To put things in perspective, imagine a lion preoccupied with attempting to answer whether it would be better for his body to eat an antilope or a gazelle. 10.000 calories is 10.000 calories and if he eats either he'll live another day.

If by "the body needs carbohydrates" you mean carbohydrates in the diet, then I disagree. We can make all of the carbohydrates that we need from other nutrients (unless you class ascorbate as a carbohydrate). This is in contrast to both fatty acids and amino acids, for which there are dietary essential species.

I agree with you, I was just making a different point so this error slipped through. Thanks for pointing it out.


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What makes the amide bond the lowest energy pathway?
I've reading about proteomics and how it can be used with mass spectrometry to sequence digested peptides.
Reading this paper the author states (in box 2):

peptide fragmentation induced by collisions with residual gas, and
  bond breakage mainly occurs through the lowest energy pathways - that
  is, cleavage of the amide bonds

Why is cleavage predominately at the amide bond? What makes the amide bond the lowest energy pathway?

This question is probably better suited to Chemistry.SE

@MattDMo While this is a chemistry question, it is also about biologically important molecules, so it is still on-topic here.

@MadScientist Even though it is about a biological relevant molecule the principle behind this question is chemistry. Note that this is not about peptide formation and degradation in-vivo; it is about collision induced decay (nothing biological here).


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What is the minimum length required for a circular DNA ligation?
What is the minimum length of a DNA molecule for the ends to come in close enough contact that they can ligate. Assume there are free divalent cations in solution. Does anyone have any idea?

I stumbled across this paper demonstrating it is between 150-200 base pairs.
DNA flexibility studied by covalent closure of short fragments into circles
D Shore, J Langowski, and R L Baldwin
PNAS 1981 78 (8) 4833-4837
http://www.pnas.org/content/78/8/4833.full.pdf

good source - ligation still occurs at 126 bp but much less efficiently... at some point there, the DNA is too stiff to flop around and join in the ligase catalytic site.

Yes, and in the last sentence the authors suggest that the exact number of base pairs will become important at these lengths: "If the number of bp in the DNA fragment is not an integral multiple of the helix repeat,then the need to twist the DNA helix in order to make strand ends meet may [make ligation difficult] for sizes less than 500bp."


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Why only water in liquid form is essential to live?
My question is:-
Only liquid water supports almost every living organism's metabolism, neither the vapour nor the condensed form of water does so. What is the chemical & the biological reason behind this fact?

Because we depend on dissolved molecules, nutrients, minerals and so on. This is neither possible in solid (frozen) nor in gaseous water. Besides that, the temperatures necessary to have water either frozen or liquid are not really life promoting.

@Chris Just a minor correction, dissolved solutes may be present in solid form, forming a solid solution. Otherwise, the arguments are perfectly valid.

Ok, I wasn't thinking about this, but I think this doesn't play a role for life.

@SatwikPasani.. There is no fluidity in solid "solutions". Reactions that happen in a solid state will be extremely local and all the diffusion effects (including morphogenesis) will not occur. Rigid solid microdomains are important to maintain structure but there should be an appropriate solvent that can sustain the multitude of biochemical reactions.

A layman's view of the problem :
Let's assume that water in liquid form was not necessary and organisms could survive on solid or gaseous water. What would some of the difficulties be to sustain such a life form?
Solid Form of water

How would the organism move without breaking or tearing itself apart? How would essential substances be transported from one part to another of the organism body?

Gaseous form

What would be the size of the organism? Gas has a much bigger volume than water.
In order to transport nutrient molecules within the a gaseous body, a huge air pressure needs to be generated. Also, how will gravity be overcome while transporting these molecules? A lot of energy will be required to maintain such pressures.

I guess nature (which always takes an optimal path) asked such questions and found that water in it's liquid form was the most suited to support life on Earth.
It need not be water alone. Other liquids may be able to support life as well. Only, we haven't discovered them yet. But whatever the substance, it's liquid form would seem to be an optimal solution for life.

Organisms evolve to fit the environment they are in and all of earths organisms have a typical body temperature of above 0C and 100C, the freezing and boiling points of water respectively. So water at this temperature is liquid and we have evolved to carry out reactions at this temperature and use water as the solution for many reactions.
But why couldn't we have just done the same for water as a gas or a solid. Well as a gas it takes up a much larger volume, phenomenally higher and therefore we would either need to be massive or use high pressures. Additionally, containing reactions that carried out at this temperature with probably huge releases of energy is incredibly difficult. As a solid it is difficult to mobilise. As we dissolve essentially all of our bodies nutrients in water, or use the hydrophobic properties of fats to mobilise lipid soluble things, it would be incompatible with life. We rely very strongly on the ability of water to flow. Solids can't.
An interesting question is why water and not another liquid?

This is because of the physico-chemical properties of water. It can form hydrogen bonds with itself, making sure it will not be gaseous before reaching 100°C (under normal pressure). H2S for example, which is relatively similar when looking at the atoms from which it is build, melts at -85.7°C and boils at -60.2°C. Water is also capable of dissolving a lot of other substances, it is not acidic or reactive (though it can take part in reactions), which makes it the perfect substance for the basis of life.

What about alcohols?

Lower alcohols could work, but we have the same problems here with melting/boiling points and the solubility of substances. An alcohol based life form would of course rely on other molecules, but it would still be difficult.


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Drosophila Crosses
I have 2 transgenic lines of Drosophila. I would like to cross them and get both transgene in the same fly. To start this cross, does it matter which fly is female or male? Or as long as the female is virgin, it does not matter?

flies aren't my field of expertise, but you probably would want to verify by PCR that any crosses were homozygous in any case.

Ah no, I have certain markers for it. So thats not a big problem. I am asking a really silly question probably.

As long as none of your genes are X-linked and you use virgins it shouldn't matter and you'd get the same proportion of double homozygotes. You may want to perform a reciprocal cross (https://en.wikipedia.org/wiki/Reciprocal_cross) if you don't know what chromosome these genes are on (though flybase.org is useful too).


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What are these white areas of coronary thrombosis?
Please, see the picture where the areas (1,2,3) look little yellow:

I think these areas are fat, platelets and/or air.
I think 3 is fat/platelets while 1 is air/platelets.
There also exists white thrombosis, which can explain something here.
However, I do not it is that because those white areas do not contain thrombocytes or leucocytes (not sure, since I have no more closer picture; probably you can see it from this).
I think at the moment that these white areas are endothelium-lined spaces.
However, I am not sure about (3).
What can these three areas be in the coronary thrombosis?

Low density lipoproteins can be taken up by the macrophages under a number of circumstances (typically high circulating levels is the most important). These macrophages are called foam cells. The macrophage can then die and deposit this cholesterol and fatty material onto a vessel wall in the context of atherosclerosis. Additionally tissue damage as a result of release of damaging chemicals from the macrophage can induce an inflammatory response recruiting more macrophages (worsening the problem in a cyclical manner) and result in fibrosis and platelet activation. I think this would cause the white stuff you point to.
In summary I think you're right, it's a combination of fat, cholesterol, fibrotic tissue and platelets. 3 is more likely macrophages and platelets whilst 1 and 2 are more likely a combination of all the above.

Thank you for your answer! I completely missed the term "foam cells".


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What is the fastest marine mammal?
When I did a research, most of the sources say that orca is one of the fastest. But I could not find a source that says it is actually the fastest.
Some sources say that Dall's porpoises rival orcas in speed. And there are other kinds of porpoises and dolphins that comes into question.
Is there any scientific research with measurements? Or does anyone have any detailed knowledge about this topic?
(Also it would be nice to know top 10 fastest marine mammals, so the question becomes: what are the fastest marine mammals?)
Note: This scientific research might be difficult to conduct also so you can explain the situation as well.

This article by R. Aiden Martin doesn't have citations, but is a great read with a lot of detail on observations and mechanics of animals moving in water. If you trust the numbers the author gives, the top 10 marine mammals in terms of speed (in mph = 1.6 km/h) are:

Dall's Porpoise (Phocaenoides dalli), leaping   34.5 mph
Killer Whale (Orcinus orca)  34.5 mph
Shortfin Pilot Whale (Globicephala macrorhynchus)   30.4 mph
Blue Whale (Balaenopterus musculus) 29.76 mph
Fin Whale (Balaenoptera physalus)   25.42 mph
California Sea Lion (Zalophus californianus)    25 mph
Pacific Spotted Dolphin (Stenella attenuata)    24.7 mph
Common Dolphin (Delphinus delphis)  23.6 mph
Bottlenose Dolphin (Tursiops truncatus) 17 mph
Pacific Whitesided Dolphin (Lagenorhynchus obliquidens) 17 mph

As noted in the article, higher estimates of speed for, for instance, the common dolphin may be in fact records of them 'surfing' on the bow wave of boats (not propelling themselves through the water).

It's interesting that the common dolphin is 23.6mp/h here, and 39mp/h in @jarlemag's answer. I have a feeling the fastest marine mammal might depend on who is the observer and how the measurement is made!

According to the MarineBio conservation society, the fastest marine mammal is the Common Dolphin, with a top speed of 64 km/h. That places it just above the Zebra on the Wikipedia list of fastest mammals. (I wasn't able to find a primary source for this immediately, so take it with a pinch of salt.)

Thanks. I don't know how I missed that. It would be nice to find out top 10 also.

Interesting factoid! Incidentally this is dwarfed by the fastest fish. The sail fish for example can get up to 110km/h!

Dall's porpoise and orca are the two fastest cetacean species (whales, dolphins, and porpoise), but Dall's porpoise reach those speeds during shorter sprints while orca can sustain those speeds over longer durations.  Dall's porpoise are known for their "rooster tail" splash as they sprint to approach a ship to bow-ride.  The speeds provided by Oreotrephes look reliable as they are similar to speeds described in the Encyclopedia of Marine Mammals (Editors W.F. Perrin, B. Wursig, J.G.M. Thewissen, 2002).  Some of the speed research on smaller dolphins comes from systematic studies of trained dolphins while values for wild animals come from radio-tagged animals, theodolite tracking, or measurements of boat speeds for ships traveling at a similar speed to whales.

Hi and welcome to Bio.SE. Thanks for posting. However, please provide support/citations for your claims. Unsupported posts (or posts mentioning but not fully citing sources) come across as opinions and are best reserved for comments. We have high expectations of good answers on this site to help avoid the spread of misinformation. Please consider revising your answer to provide some sort of support to attract more positive attention and to better (and more accurately) inform our future visitors. Thanks!

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Is a stab wound to the back lethal?
How deadly is a stab in the back?
Video games, movies, and other fiction would have us believe that a backstab against a foe with a modestly-sized blade leads to immediate and certain death, having a 100% success rate and causing death virtually instantaneously.  How close is this to reality?  How does the lethality of a puncture wound to the back compare to such wounds delivered to other areas of the body?  What is the primary target in such an attack in terms of internal organs, and what variables effect its projected success?

It depends on a lot of factors like the size of the blade, where you stab etc.. I would think that a stab through the heart would mean instantaneous death..

Check out the sources of Wikipedia article: the mortality rate is up to 4%.
The main causes of "immediate" death in penetrating trauma are shock (low blood pressure due to external/internal hemorrhage, especially arterial hemorrhage), pneumothorax, penetrating heart injury (with resultant hemopericardium) and other less frequent causes.
The same causes account for "later" lethal case plus some specific causes like infections, emboly etc.
The overall mortality rate of stab wounds is far from 100%, and according to different studies is between 1% to 4%, but rarely more. The morbidity depends on depth of wound, place of injury, overall health status etc, thus multifactorial analysis is required to get an overall image of the penetrating wounds of the body.
Some sources:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2627025/ -
 (4.3% mortality in stab wounds to the anterior abdomen, back, and flank).
http://www.ncbi.nlm.nih.gov/pubmed/3798182 - the mortality in back/flank stab wounds was 1.3%.

I think there is a possibility for significant selection bias in those studies as they only include patients who made it to hospital alive

@RoryM You are right about the "selection". However, it is very rare occasion  to see an isolated back stab wound on autopsy as a cause of prehospital death, thus even if this bias were extremely significant, the mortality rate could not exceed 15%....


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Resources for interesting facts about biology
Are there resources for interesting or fun facts about biology, for example:

fastest animal/bird/insect
largest organ in human body
largest virus
largest genome
largest de novo synthesized genome
largest protein
longest experiment done so far
most expensive experiment done so far
biggest discovery by luck
...

You get the idea. It would be nice if these is a curated "database" for all these interesting facts that might be fascinating to lay people as well.

Well I think that jarlemag's answer is pretty good and important for the community. Too bad that others can't post other sources if they stumble upon them. I actually disagree that the answer will be opinion-based, as I would expect people to provide resources, not what they would consider to be "fun or important". If you have any suggestions how to change my question to reflect this, let me know.

Whether you find the content interesting or not I can't say, but you might want to check out the BioNumbers database. It has a category for "Amazing bionumbers" and a "BioNumber of the Month" section.

That's cool! Yeah, that's what I am talking about. And this is not just for me, but for the community. So whatever I don't find interesting, I am sure others will :) Your 'BioNumbers" link is not working.


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Do animals follow tactics?
Are animals able to plan hunts, give tasks if they do it in groups and fulfil it adapted to the current situation? Do they use unique tactics for special circumstances (e.g. based on experiences)  or they just act from instincts?

the size of the animal's brain is a factor here I think.  ants vs wolves and dolphins are a spectrum of scenarios in the ability to plan I'm sure.

Do some research on wolves hunting. They certainly have tactics that change depending on the prey that they're hunting, the terrain, danger posed by other members of the prey's herd or family (if any), etc. They're very capable of learning, and use fairly complex communications. They run in packs, live with their mother for a number of years, and have a rather involved family structure that allows for the passing on of behaviors learned from previous generations. It would be difficult to tease out exactly which behaviors are instinctual, and which are learned, but you could say the same of humans as well.


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Is Natural Selection like a Copy Editor?
I am stuck on a Homework Question. It says:

Evaluate the following statement: “Natural selection works like a copy
  editor; it works only with
  what is already present in a population.” (Note: Copy editors check
  written material before it is set into type, to correct errors in
  spelling, grammar, usage, and style.)

I thick that Natural Selection is not like a Copy editor because:
Natural Selection has no set direction, which means it does not decide on anything. A weak organism might be able to survive by luck. While a copy editor knows the mistakes and eliminates them instantly.
Can I get some help on this. Thanks!

If I had to compare natural selection to a job in the publishing industry, I'd say it's more like a commissioning editor -- that is, the guy who decides what to accept and what to throw in the garbage bin.

Thats good but its not answering the question. Is natural selection like a copy editor or not?

It not my question. Its part of my Homework.

Since this is a homework question, regardless of wheteher its a good one or not, you're supposed to give some indication that you have tried to answer it on your own. Maybe you should list how you think it is similar and how you think it is different.

Is natural selection like a copy editor?

Is a railway car like a weasel?
Honestly, I don't think that's a very good question.  The only reasonable answer is, put briefly, "In some ways it is, and in some ways it isn't."
It also doesn't really help that the "statement" the homework exercise asks you to to evaluate is actually two statements, and they're not really equivalent.  (Real copy editors don't just "work only with what is already present," at least not in the same sense as natural selection does.)  Sorry if that seems unhelpful, but that's how I see it.

OK, let me expand on that a bit:
Evolution, in the Darwinian sense, can be broadly described as the interaction of three processes: inheritance, mutation and selection.
Of those three processes, mutation is the one that produces novel innovation, by occasionally producing new alleles that did not exist in the parent population.  It is, however, a blind innovator — the novel genotypes produced by mutation are essentially random, and no more likely to be advantageous to the organisms carrying them than one would expect by change (i.e. not very likely at all).
Selection, whether natural or artificial, is what happens when the organisms carrying the diverse genomes produced by mutation end up competing for survival and reproductive opportunities against each other and against their environment.  It acts on the diversity generated and replenished by mutation, favoring those mutations that happen to confer a survival advantage.
Finally, inheritance ensures that the beneficial alleles generated by mutation and filtered by selection get passed on to successive generations, allowing them to spread in the population and to be further modified by successive mutations.  In a sense, inheritance and mutation can be seen as opposite sides of the same coin: the more faithfully genes are inherited, the less mutations there are.  Yet both are necessary for evolution; an organism that never mutates obviously could not evolve, but neither could one that mutated so much that all of its genes were totally scrambled in each generation.
Of course, this whole process is stochastic in nature — even the best adapted individual may die without offspring due to simple bad luck, just as even a maladapted individual may get lucky and prosper.  But over generations, there is nonetheless a statistical tendency for individuals carrying certain alleles, or combinations of them, to be more fecund than others, and those will be the alleles that will eventually come to dominate the population (assuming they're not it turn displaced by even more successful mutants).
Thus, I would personally say that, of these three components of evolution, (natural) selection indeed "works only with what is already present in a population."  However, it's not really like a copy editor, since it does not seek to "correct errors" in the genome; it's more akin to a slush reader, who just sorts the incoming texts into ones to keep and ones to throw away.


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The distance the electromagnetic field of the heart can be detected
A very smart friend of mine seems to get taken in by junk science. He started telling me last night that the electromagnetic field of the heart can be detected beyond 30 feet. What is the actual distance? Thank you.

what is the detector? seriously in a vacuum with the right equipment i'm sure it could be quite a long distance.

I heard such anecdotes from electrical engineering friends. Their circuit was so sensitive that you would see your own heart beat on the oscilloscope just in the vicinity. I don't know what the exact distance was. Perhaps you could as this Q at EE.SE http://electronics.stackexchange.com/ ?

The EM field strength falls off as the inverse square of the distance (even in space). The heart operates on mV and mA voltages/currents. I wonder if this is detectable beyond 5 meters using a nearly-ideal detector. 30 feet sounds really far.

In 2010 there was a brief note in LiveScience on a system developed at U. Sussex which detected heartbeats at 1 meter. That was apparently good 4 years ago.

The electomagnetic field of the heart actually changes with emotions so there is no fixed range as such (reference). It could also change with temperature and other external magnetic disturbances (reference). The heart generates the largest electromagnetic field in the body which is up to 50 mV/m, and that of the brain and other vital organs up to 5 mV/m. Here is a paper on the exposure of human beings to electromagnetic waves (reference). This paper details some of the current medical treatments focusing on the electromagnetic fields (reference).

In your first sentence I think you mean "changes with emotions." The E-field falls off as the inverse square of the distance so it loses strength rapidly. There is certainly a range even with an ideal detector.

@daniel yes it is "changes with emotions".. thank you for pointing that out.


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Can pulmonary infarction be asymptomatic?
I think it can because there are many parts in lungs.
Like for some COPD patients.
However, I am not sure if COPD patients can have infarction.
Lungs have parallel circulation.
Red infarct is possible there.
Blood can flow there.
One symptom should be at least pain.
So now, I think no asymptomatic possible.
But still, I am not sure.
Can pulmonary infarction be asymptomatic?

No. Based on experience. Lungs are very active organs.


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Functioning of BRCA2
I know that BRCA2 interacts with RAD51 to repair DNA damage.
But how exactly does it function ? What are the other proteins that interact with it ?

I'm just skimming through it now, but this 2011 review in Nature Reviews Cancer looks like it has everything you could possibly want to know about the BRCA1/BRCA2 pathway. If you don't have access to the journal, the first page of this Google search should have a PDF link to Researchgate down near the bottom, or you can try this direct link.
I apologize for the "link-only" answer, but there is a ton of info in the paper, and it would be rather difficult to summarize it in just a few paragraphs. This is a rather broad question, so perhaps you could read through the review and references, and if you still have specific questions about the pathways or interactions you can ask another question.

I agree with you, this paper offers a very good overview.

Here is an image of BRCA2 and RAD51 oriented.( I produced this using PyMOL!)
The chocolate coloured part is some BRCA repeats. You can see how BRCA repeats and RAD51 are oriented. Here, the association is shown only for one of the 7 subunits of RAD51
The exact mechanism in brief :
.

BRCA2 binds to RAD51 subunits within the ring via BRC repeat mimicry of the RAD51 polymerization motif.

2.BRC repeats disassembles the ring.
3.The RAD51:BRCA2 comple is recruited to a DNA double strand break.
4.BRCA2 helps displace a protective protein, Replication protein A- RPA, and binds the primary ssDNA substrate by its B folds.
5.It loads RAD51 onto DNA. The handoff reaction might be facilitated by attraction of DNA by the positively charged BRC repeat helical arches.The BRCA2 helix-turn-helix domain(red) at the end of the tower may bind dsDNA in cis at the ssDNA/dsDNA intra-DNA junction (3) or in trans to the dsDNA that later serves as the homologous DNA template (6) and the positively charged arch may also help to attract the dsDNA template.
Source : Yang etal. 2002 , Shin et al 2003
Thanks to Nicholas Provert for teaching me basics of PyMOL on Coursera.


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Gibson assembly using NeBuilder
I am supposed to construct a plasmid that contains features from two other plasmids.
My strategy is to generate three fragments form the two other plasmids. I was encouraged to try Gibson assembly, so I went to NeBuilder entered my sequences and got I list of primers with overhangs and ordered them… But now I am I bit unsure about the linearization of the backbone and insert into that fragment.
In NeBuilder you can choose "by sequence position" in for the insert in the backbone the description reads “Entering the sequence positions of the bases immediately flanking the insert site. Primers for inverse PCR terminating at these endpoints will be calculated automatically”.
Does anyone have experience using NeBuilder? i am completely unfamiliar with inverse PCR ?
also my regular software package Geneious is unable to comprehend the two primers for the inverse PCR reaction


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What is the difference between fibrogenesis and fibrosis?
Fibrosis is the formation of excess fibrous connective tissue in an organ or tissue in a reparative or reactive process.
I used the word "fibrogenesis" as the outcome of acute inflammation (healing).
My colleges use the word "fibrosis".
The fibrogenesis seems to be used with the emphasises of the genetic part.
What is the difference between fibrogenesis and fibrosis?

As a note, the suffix -genesis refers to the development or production of something, while the suffix -osis can be roughly translated as '...a current state of...' something.

I would say fibrosis represents an abnormal accumulation of fibrous tissue usually collagen fibres. Where as fibrogenesis is the process of formation of fibrous tissues be it collagen, reticulin, elastic, oxytalan..


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How quickly is antibiotic resistance lost?
I would imagine the bacterial genome is highly conserved and limited in its space, but maybe I am wrong.
If you were to take a strain of antibiotic resistant bacteria and kept them isolated, but fed well and so forth, how long would it take for them to lose their resistance? A year? A decade? 100 years? 1000 years? At some point it seems like that trait would disappear, but I have no feeling for how long. Please support your answer with a relevant citation.
EDIT:
My purpose is simple: I am thinking about a strategy for dealing with antibiotic resistance. If we were to ban them across the entire world (could be impossible) how long would we need to wait before they would be usable again. If it was a matter of years, then we could almost do a rotation of existing antibiotics (if we had enough) because I would rather not live in post-antiobitic world.

Is this a homework question, by any chance?

@MattDMo it is not.

Related/duplicate: Can antibiotic resistant bacteria compete with normal one in an antibiotic free environment?
related: What causes the development of antibiotic-resistant strains of bacteria?

Antibiotic resistances in bacteria is commonly encoded by extrachromosomal DNA, the plasmids. These are circular pieces of DNA, which are much smaller than the hosts genome and which replicate independently from it. See the image from the Wikipedia:

These plasmids can be transfered between different bacterial cells, which then also get resistant. Plasmids are divided between daughter cells, when the parent cell divides. One of the few exceptions seems to be Mycobacterium tuberculosis, which does not seem to carry plasmids but also develops resistances. It has been hypothesized that they contain extrachromosomal single-stranded DNA ("Does Mycobacterium tuberculosis have plasmids?")
Regarding your question: Plasmids which carry antibiotic resistances will only disappear, when the antibiotic is not seen for a while, since the cells, which don't carry it, have a growth advantage over cells who are still carriers (since they save the energy of forming the plasmid). However, these resistance plasmids are nothing new, evolutionary speaking. They appeared as a countermeasure against fungal toxins.
In the lab, bacterial strains loose plasmids within a few days, when not kept under selection pressure according to my experience. There are a few paper who looked into it:

Natural selection, infectious transfer and the existence conditions
for bacterial plasmids.
The persistence of parasitic plasmids.
The evolution of plasmid-carried antibiotic resistance

Lab strains of E. coli have been in use for many decades now. They have all retained a large number of genes encoding subunits of the flagellar apparatus and the chemotaxis system which confer absolutely no advantage under normal culture conditions. I conclude from this that the selective advantage conferred by losing "unused" genes must be very weak.
Also, most antibiotic resistance is encoded on plasmids. As @Chris points out, these can be lost easily.

I would expect bacterial DNA to have some natural decay rate over generations, so I find it very interesting they do maintain these "vestigial" genes; is it possible they are actively conserved?

No.  DNA doesn't "decay".  It changes.

In general terms entropy is the decay of order. So call it what you will, the question remains of its rate. If you wrote a message that wasn't vital for the organism to survive, over time it will become corrupted unless every DNA replication is 100% efficient.

@sciencenewbie Under standard culture conditions (37C rich medium) they aren't expressed, and it is difficult to conceive of a selective advantage under conditions in which it is unnecessary to move towards nutrients. But some weak selective pressure can't be ruled out I guess.

@swbarnes2 It is called information theory and can be applied anywhere. You are not going to win me over by coming across in a hostile tone.

I agree with Alan that chromosomal traits wont get lost easily as seen with the commonly used strains. I would add a point that the likelihood of loss of a gene depends on its cost..

If you were to take antibiotic resistant bacteria and kept them
  isolated, but fed well and so forth, how long would it take for them
  "forget" their resistance?

It's not a matter of "forgetting".  Bacteria are resistant if their DNA is such that it gives them a biology that renders the antibiotic non-lethal.
You put a resistant bacteria in glycerol stocks, you can freeze them for years, maybe longer, and when you revive the population, and get it growing again, the resulting population will still be resistant.
Also, when we talk about bacteria, or any kind of evolution, single organisms don't change their DNA.  Populations change their proportion of different alleles.  Any allele might drift out of a population, and if the resistance-granting mutation is deleterious, natural selection might speed that along, but not all resistance-granting alleles are deleterious enough for that.  If a resistance-granting allele is survival neutral in the absence of the antibiotic, or another mutation somewhere else restores the bacterias' survivability absent antibiotic to what the sensitive genotype's fitness is, the resistance-granting allele might not drift out of the population for a long time.

I'm not talking about putting resistant bacteria in glycerol stocks and freezing them, I'm curious about keeping them multiplying in a petri dish. Finally, I use "forgetting" not in a technical sense, but a figurative.
The allele must eventually be lost, but I would like some sense of how long until it is lost.

" I'm curious about keeping them multiplying in a petri dish."  So you are talking about a population, not an individual.  If you abandon that distinction, nothing makes any sense.  "The allele must eventually be lost"  You can get strep resistance in TB through GidB deletions.  You want to believe that a population descended from a deletion mutant will forget a deletion?

So in a trillion years without the presence of any antibiotic, will that allele still be there in a population? I would be surprised if so. I don't care if it is a day, or a billion years, but I want a sense of how long. Saying it will never be lost makes no sense to me.

swbarnes2 and @sciencenewbie I'll remind you both of our community guidelines: http://biology.stackexchange.com/help/behavior

@swbarnes2 You assume too much. I am not a creationist. I believe in the theory of evolution. I don't understand why you believe it is okay to treat people like this.


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NaCl role in CTAB - DNA complex in DNA extraction
I have a question about the role of NaCl in the DNA extraction process. So for NaCl concentrations under 0.5M, CTAB and DNA molecules can create complexes.
In those concentrations, proteins and other hydrocarbons are still soluble in water except the DNA-CTAB complex. If we raise the concentration of NaCl then the complex of CTAB-DNA will be soluble to water too. Correct me if I'm wrong until now.
So I don't understand something. Why do we use NaCl?
Let's assume that we don't add NaCl. Will the CTAB create complex with DNA or not? As I read CTAB creates ionic bonds with DNA (phosphate groups). So in this situation (without NaCl) CTAB must be able to create complex with DNA too.
So why did we use NaCl? Just to keep proteins and other hydrocarbons soluble in the water or there is something else that NaCl helps in this complex creation?

NaCl provides Na+ ions that will block negative charge from phosphates on DNA. Negatively charged phosphates on DNA cause molecules to repel each other. The Na+ ions will form an ionic bond with the negatively charged phosphates on the DNA, neutralizing the negative charges and allowing the DNA molecules to come together

CTAB forms insoluble complexes with nucleic acids and can be used to selectively precipitate them from solutions, see this reference:

The isolation of bacterial nucleic acids using cetyltrimethylammonium
bromide (Cetavlon)

When you add NaCl in a concentration between 0.4 - 0.7M, the nucleic acids stay in solution, while polysaccharides and other substances, which may interfere with the DNA preparation do not. See this paper: "Rapid isolation of high molecular weight plant DNA."


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Evolutionary rationale behind migration proteins
Tumor cells are able to migrate due to specific migration proteins.
What is their evolutionary origin?
Or are they simply deregulated?

This would be a very long answer but just to give you some hints, the migrational mechanisms are already there and the cancerous cells makes use of them to metastasise. So in short its deregulation. What is under selection pressure tho are cancerous cells themselves to constantly change and evade cellular fail safes which kill (apoptosis) uncontrollably replicating cells. You can find out about this here (http://www.nature.com/onc/journal/v22/n42/abs/1206757a.html)


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Can a carnivorous animal consume plants with no adverse effects?
While I know that in nature, carnivorous animals are poorly suited to eat plants (largely due to having sharp teeth, not grinding teeth, as far as I know), I was wondering if, in an emergency situation such as imminent starvation, could a carnivorous animal such as a wolf survive solely on plant life, maybe requiring it to be ground up before hand? Could an herbivore survive on meat, if the meat was prepared in a manner that would allow the herbivore to eat it? Would a wild animal voluntarily consume food that it is not suited for if it would stave off certain death, or would it require force feeding or training?
Also, I am interested in the other side of this question: if an animal cannot safely consume food outside of its normal diet (carnivore eating plants, herbivores consuming meat), what negative effects would this action have on the animal?
Just a note, this is purely a hypothetical question, and I am only asking out of curiosity. I am in no way planning on doing this, nor do I advise anyone else doing this if there is a high chance of it harming the animal.

Yes we are omnivores, but before hominid specie developed the capacity to cook meat the meat was eaten raw, and before they had the capacity to come up with ideas - like tools for hunting they ate a plant based diet. I agree with the fact that we are omnivores now, thousands of years later, after all the mutations in our body took place, but we do tend to fall into the herbivorous part of omnivores, so our diet should be 80% plants - 20% meat. Anything more than that puts us at risk for developing arterosclerosis. And dont even get me started on the fact that people consume way to much animal

What do you mean by a "diet contradicts an animal's biology"? Contradiction is the logical opposition of two facts, e.g., "it is day" and "it is night" contradict each other. But I find it meaningless to talk about a diet (which is a list of food) contradicting a "biology" where you probably meant "physiology" and which is the dynamical system consisting of a single living individual (the cat or human) in your example. Note that "herbivore", "omnivore" and "carnivore" are human constructs, just as the classification of living beings into "species", neither represents a airtight category presen

This is kind of a weird/trick question.  How long do you want the animal to live?  If the lifespan is shortened or compromised does that fit....   Obligate carnivores (cats, dogs) do eat plant material.  In the wild cats mainly eat grass to get rid of hairballs.  Cats are more impacted by phytotoxins than dogs.  However, both, are extremely vulnerable to compounds that don't bother humans (xanthines like theobromine, caffine, compounds in garlic, onions, broccoli, mushrooms).  Cats can't convert plant fats into what they need (we can) as a result they can go blind if they don't get the animal fats they need.  Likewise, herbivores will suffer increased cancer, heart disease, renal failure from diets with animal fats / protein.  Your mention of "wolf" is interesting because there is a South American wolf that supplements its diet with a tomato relative (called something like "fruit for wolves" in Spanish).  This is probably only "good" for it in that it keeps the wolf from otherwise starving.  I don't know that it has a strong deleterious effect (probably not, but it could be more sensitive to trace alkaloids in the fruit) but it could hurt it in a minor way.

Hi! Welcome to the site. It would improve your answer if you add some references for the information you provide.

"fruit for wolves": http://en.wikipedia.org/wiki/Solanum_lycocarpum

unable to synthesize taurine from other sources (as herbavores and omnivores can)  "For instance, cats require that their protein needs be met primarily by animal rather than plant sources, especially to supply adequate taurine, an amino acid which cats do not synthesize well for themselves." http://www.felineconstipation.org/prevention.html

let me know what exactly you want references for.  I was not directly quoting anything from any peer reviewed pub if that's what you want

Hi! It's not necessary to include references from peer reviewed research papers if your references are "reliable"

I think that the distinction between carnivores and herbivores contains a gray area with a spectrum of omnivores in-between. Bears are placed in the order of carnivores, but are definitely truly omnivores see link. However, if you give them a choice between a salmon and blueberries, it's quite clear what will be devoured first. That's why it's a carnivore. The answer by @Dan S clearly shows that not all creatures may be in the spectrum. For example, domestic cats are indeed quite carnivorous and would not touch plant material. On the other hand, now we are talking pets (the SE where this question apparently came from) - dogs are truly omnivores despite being categorized as carnivorous.

I'm pretty sure humans are herbivores, and we've been doing fine on meat.  Not as fine as we could without meat.  There are just extra illnesses to watch out for like what was listed above: heart disease, kidney failure, cancer, strokes.  These illnesses could occur on a natural diet as well, so if there are already precautions in place for these things, the animal should still live a happy life (maybe cut short by some years).
Animals eating diets that aren't suited for them is not as rare as you might think.  As I stated above, it seems likely that the natural diet for humans is (or at one point was) herbivorous.  We have had several mutations over the years that have assisted us in being able to eat meat with less adverse effects: http://www.wsj.com/articles/SB10001424052702303933704577533271378820202.  So, admittedly, giving primates meat is probably worse than giving humans meat.  But at one point humans were eating meat without those mutations, and the human race still managed to survive.
We also tend to feed domesticated carnivores, such as cats, grains.  Cat genetics has not been studied as much as human genetics, so it is not certain whether cats have also evolved to better be able to handle a diet that is contradictory to their nature.  However, either way, a species going against its natural diet seems to be able to sustain a reasonable, though perhaps not optimal, life.
The situation may be different if a species was subsisting solely on a diet that is contradictory to its nature.  However, it has been done.  There are reportedly human communities (such as possibly the Inuit) who survive or have survived on meat-only diets: http://www.popsci.com/science/article/2011-04/fyi-what-would-happen-if-i-ate-nothing-meat.  Many people who feed their cats a vegan diet, with supplemented vitamins, report that their cats live longer.
If giving an animal food that contradicts their biology, it is important to alter in some way.  Humans face a high risk of contracting a food-borne illness if meat is not cooked properly, and grains in cat food are ground and mixed with the food.  If giving an animal only food that contradicts their biology, the food should be supplemented.  Cats can go blind without taurine, which is an amino acid that is created by animals and not plants.  Humans on a meat-only diet could get scurvy from lack of vitamin C (if eating cooked meat) and constipation from lack of fiber.

You may be sure, but you're still wrong :-)  Humans, like bears & wolves (and chimpanzees!), are omnivores, with the amount of meat in their diet varying by biology & opportunity.  Humans who eat a (non-supplemented) exclusively vegetarian diet can experience various nutrional deficiencies, just as those who eat an exclusively meat-based diet do.

Sure you maybe, but wrong you are. Humans are not herbivores. Humans are omnivores. We are descended for apes that had begun the evolution towards eating meat... cooked meat and cooked vegetables. It should be remembered that cooking was not invented by humans nor was mastery of fire or even stone tools. These were things our species grew up with. We are descended from a hominid species that had already mastered the three.


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Difference between inbreeding and interbreeding
Is inbreeding the same as interbreeding?
On this site interbreeding is defined as (http://www.thefreedictionary.com/interbreeding):

To breed with another kind or species; hybridize.
To breed within a narrow range or with closely related types or individuals; inbreed.

But I am sure that interbreeding is not the same as inbreeding. Inbreeding would be between genetically related members of a species and interbreeding would be between genetically un-related members of the same or different species.
after looking at wikepedia pages for both terms as well as searching the english oxford dictionar I am certain they are different

You are basically correct. Most common usage in my experience:
Inbreeding refers to sexual reproduction between genetically closely related individuals, within a species. Inbreeding will increase the relatedness between individuals in a population.
Interbreeding refers to reproduction with another species (or race), and is often used as a synonym to crossbreeding or hybridization (when referring to hybrid offspring from two different species/races/breeds, not DNA hybridization). This is also how 'Interbreeding' is defined in the Oxford English Dictionary. However, 'Interbreeding' is sometimes used just to signify that two individuals can breed and have viable offspring ("...these two individuals can interbreed..."), and under this usage this can also include/overlap with inbreeding.
The latter usage can be seen in the Species article in Encyclopædia Britannica, online:

Species, in biology, classification comprising related organisms that share common characteristics and are capable of interbreeding.
  ...
  Interbreeding only within the species is of great importance for evolution in that individuals of one species share a common gene pool that members of other species do not.

interbreeding is a process in which same kind of species are breed together such as(male and female)but outer breeding is a process in which different kind of species are breed together such as(means horse is a specie it will breed with bitch those are different species


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Data analysis of transcriptome sequencing data
I want to learn more about the data analysis and statistics on transcriptome sequencing data. I would like to read some important papers of the field and books and maybe some MOOCS, if they are available.
More precisely I have data of differentially expressed genes across different groups of individuals and I want to test, if the genes are more expressed in one group are the genes also more polymorphic?
Any ideas?

there are several tools available for this analysis. Tophat-Cufflinks is a popular combo that people use.
For analysis, again, there are several tools.

Are you studying a species that currently have its genome sequenced?

No, it does not have a published genome sequence, de novo transcriptome assemly was used and cuffdiff was used to get the information about differentially expressed genes between two treatments. Now I want to statistically test if the genes, that are more expressed in one treatment also exhibit more polymorphism. Also, the data is very overdispersed.

@PiretAvila. You would need different sample isolates (biological replicates) to study polymorphism.

Yes, I have many biological replicates for each treatment. So you see, my problem is not obtaining the data, but analyzing it. I have differential gene expression values for genes that were expressed differently in two treatments (log2(FPKMy/FPKMx)) and I know how many SNPs each of these genes have. I want to know if the genes that were more expressed in one treatment (log2(FPKMy/FPKMx) is positive), are they on average more polymorphic. What would be the best statistical method? I used GLM's (hurdle and zero inflated neg. bin.), since there are a lot of sites with no polymorphism.

Sorry for a late reply. I suggest that you can first see if multiple isoforms exist for the differentially expressed genes that you are interested in. If so then you can find out if there is difference in isoform expression. If the gene has no isoforms then relationship between SNP and expression has to be studied under same experimental conditions.


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How did the roar evolve from snort?
When Lions roar, or Dogs show aggression, they do that snort-roar thing. They're producing sound while inhaling. How did that come to be when all (?) other forms of sound involve exhaling?
Humans do produce sound while snoring, but that's merely a by-product of it.
And while people could very well speak by inhaling, they don't do that in their regular communication. Lions and Dogs do. Why/when did they decide that (inhaling sound production) was a better/more effective means of making sound?

Snoring involves generating sound while inhaling, and people can speak while inhaling as well.

@MattDMo Addressed your comment into my question


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How do cellphones calculate heart rate?
How do cellphones calculate heart rate ? I understand that the cameras there try to count undulation in blood flow, but is the method of calculation same as that of professional SpO2 monitors ?

I'm not sure this question is on topic here - it's about technology and apps. But assuming you mean how do apps like this one calculate HR. I believe it measures fluctuations in the colour of the skin (it will change as the quantity of blood varies in the capillaries with pulsing action) and it is simply a case of X beats in 10 seconds = 6*X bpm. SpO2 is a measure of oxygen saturation, not heart rate.

@GriffinEvo Thus us exactly how it is done. The "redness" of the skin changes with the heart rate and this is measured. See this reference. I would suggest you make it a real answer.

@GriffinEvo I was not sure where the question belonged, this looked the most relevant forum.

I asked a related question on Skeptics recently and was pointed to this work - it appears to be detecting changes in skin colour related to heart rate.

Wouldn't this work out only for people with a very fair complexion ??

@WYSIWYG: if you look at ~1:40 of the the Siggraph 2012 video you will see that the algorithm works for dark skin tones too.

@GriffinEvo I agree with Chris, try to make this into an answer. You can also incorporate information given by others.


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What is the blood ejection speed outward from human body vein?
At what height blood can eject from human vein ?
I see, sometime there is direct blood transfer from one person to patient.
So sometime blood bottle is kept at certain height and blood is transfered from person to upper bottle and then from that bottle to patient directly.
At what height blood can go ?
EDIT
For example, I had not mentioned before,
What would be the blood pressure outside from body after cutting certain nerve or vein or whatever which carries blood-speedily, when we go inside vacuum chamber ?
Consider any chamber where you will be able to remove air/atmosphere inside it and a person is provided with oxygen cylinder. Now what will be the blood ejection speed outward from the body ? At what height ? You will have to consider atmospheric pressure also when we leave normally on earth. So question is, at what height in vacuum (where there is no pressure from outside world) ?

I'm a little uncertain based on your title and wording, but are you asking how elevated a human donor has to be, vs. the recipient, for an unaided (no pump) blood transfusion?

@AtlLED At what height blood can go if one's vein got cut by knife or something ?

This question appears to be off-topic because even though it presents a biological scenario it is about basic principles of physics.

You can use Bernoulli's equation and the equation of continuity to measure velocity of blood from the cut site. Then add the effect of gravity of calculate the distance covered.

@WYSIWYG If people want to close, I have no objection.  I couldn't tell if it was on topic here because it needed to look up average venous pressure, but that's such an easy task, it doesn't on topic ether.  I had a hard time deciding whether or not I should answer. I'm at least willing to say it's not a good question, but not sure on close.

@AtlLED I edited my question.

@AtlLED.. There is no problem in answering.. In one or two instances I have answered and then closed the question. I guess the purpose of closing is to avoid long discussions and also to encourage the OP to ask the right question or ask elsewhere. I don't know if this is a right thing (to answer and close); I try to answer in the form of a hint.

@AmitG.. your question still has got very little to do with biology per se. It is more of fluid mechanics (just veins instead of the pipes). So I suggest that you reformat your question and ask in physicsSE.

This question appears to be off-topic because it is about physics.

Does this question have anything to do with needle "blow-out"?

No. This is random question as a curiosity. This question is related with Biology along with Physics. Doctor must be knowing what is the speed of flow of blood from the human body when injection is injected to take the blood from the body in the vacuum chamber. Normally we have atmospheric pressure on our body. Looking for answer in vacuum. I didn't understand why this question was closed. There must be some answer.

Ah, I'm afraid there are a near infinite number of variables that will make a general answer impossible.  Factors such as: age, sex, weight, which vein, additional damage, heart condition, cholesterol level, body position, body temperature, and how the vein was cut and exposed will all lead to different answers.
A general answer from someone with lots of trauma experience, not very far.  Rarely if ever greater than 10cm.  Veins just don't have the pressure that arteries do.

Central venous pressure is something like 5 mm of mercury.

@kmm I'm not so sure a chest/back wound required to expose the venae cavae would spurt, even at it's higher pressures.  You simply have to go through so much to get there that it seems unlikely.  Also at that point you almost assuredly have arterial if not aortic damage.  That average of 5mm for a healthy adult [caucasian] male at room temp has to pass a lot of tissue.  There are a lot of ways to get blood splatter, but neatly cutting through a vein isn't a particularly good one.

For a further point of clairification, the CVP is normaly limited to the blood pressure in the proximal SVC, not the more distal portions that would be more exposed to puncture.  The pressure change would make more of a pulsing uzze than big spirts.  If the punture was small enough to take full advantage of the pressure changes, you could get some distance from the body, but nothing like an artery.

Agreed. The OP was asking about veins, which have almost no pressure even where their pressure is highest.

@AtlLED I edited my question.


text:
Functioning of BCG vaccine
I  read (from Nature Volume507, S4–S7 (06 March 2014) :

For reasons that are poorly understood, BCG protects only infants; it
  is ineffective in older children and adults. Its efficacy also depends
  on latitude. BCG works better, and protects people at later ages,
  farther from the equator. Both effects may result from interfering
  exposure to noninfectious mycobacteria that are closely related to
  both BCG and TB. These bacteria are more abundant closer to the
  equator, and while infants are unlikely to have encountered them,
  children and adults have more exposure over time.

I am unable to understand the relation between exposure to noninfectious mycobacteria and lessening of efficacy of BCG vacccine. What exactly is the "interference" caused by the noninfectious mycobacteria ?

The exposure to environentally occurring Mycobacteria causes a immune response to these (mostly unspecific, since no real infections occur). It seems that immunizations with BCG in these individuals is causing either no, or only a very attenuated immune response
This is shown in this ("BCG-induced increase in interferon-gamma response to mycobacterial antigens and efficacy of BCG vaccination in Malawi and the UK: two randomised controlled studies.") in which individuals with a high environmental exposure to mycobycteria showed only a very small response to this vaccination. If this natural level of immunity is enough to produce immunity to tuberculosis is unknown (and can not be tested for obvious reasons).
Another possibility is that the natural occurring immunity blocks the vaccine strains so they get eliminated before they induce an immune response. See here.
This is called the masking theory,if you want to read further, have a look at this three reviews, they give a good overview over the field:

TB vaccines: progress and problems.
A novel TB vaccine; towards a strategy based on our understanding of
BCG failure.
The success and failure of BCG - implications for a novel
tuberculosis vaccine.


text:
Are there tools for automatically parsing glycan names into tree structures?
My colleague and I are working on a project involving data produced at a glycan microarray facility. The array data that came back to us were a list of glycan names (in IUPAC condensed format). We would like to parse the list of 610 names into the graphical representation of the glycan.
To clarify, I wanted to take a list of glycans, written in the IUPAC condensed nomenclature, and return an image for each glycan. Here, each image would be the "graph" representation (nodes + edges). Ideally, I would like to be able to write a Python script to get this done, so we wouldn't have to do this by hand.
Is this possible? If so, what tools are available to get this done?
Thank you!

I don't know if that answers your question or not.  I think code samples on text parsing would probably be off topic here, but I could refer you to some examples.  The key would be the second KEGG table.

@AtlLED, thank you for your effort in answering. Though your response didn't give me a direct solution to what I was looking for, it was helpful nonetheless, and I up voted it. Please see my clarification in the comment there. Thanks again!

Edit: C# Functions used in our system, slightly paired down for to simplfy
using Microsoft.VisualBasic;
using System;
using System.Collections;
using System.Collections.Generic;
using System.Data;
using System.Diagnostics;
using System.Web;
using System.Net;
using System.IO;
using System.Text.RegularExpressions;

public class KEGGCaller
{
    public object ReturnKEGGgif(string GlycanMonoCode, System.Web.HttpServerUtility HTTPUtilityHolder)
    {

        string CallURL = "http://www.genome.jp/dbget-bin/www_bfind_sub?dbkey=glycan&keywords=";
        string GlycanURL = HTTPUtilityHolder.HtmlEncode(GlycanMonoCode);
        WebClient wc = new WebClient();
        System.Drawing.Image GlycanGif = default(System.Drawing.Image);
        CallURL += GlycanURL + "&mode=bfind&max_hit=1";
        StreamReader reader = new StreamReader(wc.OpenRead(CallURL));
        string Gcode = FetchGcode(reader.ReadToEnd());
        if (Gcode == "Failed") {
            return 0;
        } else {
            System.Net.HttpWebRequest Request = default(System.Net.HttpWebRequest);
            System.Net.HttpWebResponse Response = default(System.Net.HttpWebResponse);
            Request = System.Net.WebRequest.Create("http://www.genome.jp/dbget-bin/www_bget?gl:" + Gcode + ".gif");
            Response = (System.Net.WebResponse)Request.GetResponse;
            if (Request.HaveResponse) {
                if (Response.StatusCode == HttpStatusCode.OK) {
                    GlycanGif = System.Drawing.Image.FromStream(Response.GetResponseStream);
                    return GlycanGif;
                } else {
                    return 2;
                }
            } else {
                return 1;
            }

        }

    }
    public object FetchGcode(string PageBlock)
    {
        string MatchURLString = "?gl:G\d\d\d\d\d";
        Match URLMatch = Regex.Match(PageBlock, MatchURLString);
        if (URLMatch.Success) {
            return Strings.Right(URLMatch.Value, 6);
        } else {
            return "Failed";
        }
    }

}

Remainder of the Answer
Biomodels.Net is a great resource to begin with and familiarize yourself with the field and get ideas of how to tackle your qualification needs.  We used it when we were doing drug screens.
More specifically for glycans, you're going to be looking at KEGG.  Then use KEGG draw for your visual application.  If you actually just want to parse them, here is the table on the monosaccharides used (most places).
Here's a better link right to the download in case you didn't find it.  The script we wrote was pretty simple, here is the basic logic.
Start with the monosaccharide code.
Call a single return of DBGET to GenomeNet pulling from KEGG Glycan.  For example:
(GlcNAc)6 (Man)3 (Asn)1
would be called:
 http://www.genome.jp/dbget-bin/www_bfind_sub?dbkey=glycan&keywords=%28GlcNAc%296+%28Man%293+%28Asn%291&mode=bfind&max_hit=1

Where http://www.genome.jp/dbget-bin/www_bfind_sub?dbkey=glycan&keywords= and &mode=bfind&max_hit=1 are going to be constant and the middle part is going to be your search.
You need to change your monosaccharide to standard URL ASCII Reference, concatenating each monosaccharide with a "+".  Thus (GlcNAc)6 (Man)3 (Asn)1 becomes %28GlcNAc%296+%28Man%293+%28Asn%291.
That will give you one hit with the link to your exact match if there is one.  There will be one link on the returned page in the format of http://www.genome.jp/dbget-bin/www_bget?gl:G#####, where G##### is your glycan number (in our example G00021).
Once you have the glycan number you're good to go.  All of the structure images can be found at:
http://www.genome.jp/Fig/glycan/G#####.gif
And then you just download your GIF.  The way we did our batches was to do each step for all the hits then move to the next step.
Hope that helps more.

Upvote because your answer was helpful, though I still couldn't figure out an answer to my problem. To clarify, I wanted to take a list of glycans, written in the IUPAC condensed nomenclature, and return an image for each glycan. Here, each image would be the "graph" representation (nodes + edges). I will update my original question to clarify that; in the meantime, do you know of any tool to do this? Thanks in advance!

Update: I tried KEGG Draw, but it doesn't accept glycan IUPAC names.

@ericmjl I was going to show some examples of short scripts used to call KEGG Draw, which is what I thought you would want.  If they're in IUPAC, I don't know a good way to get it graphics.  Have you asked them if they will give it to you in KEGG? Might be easy on the source side, or parsing then converting might be your only option.

Ah! I misunderstood, my apologies. Would you be kind enough to share that code?

@ericmjl are ok if they're not in Python?  KEGG is a Java program.  My Python is limited though I have a tech who's ok in it.  I'll check with my tech transfer and let you know.  Right now I'm looking for published ones, we can't be the only ones who needed to.

No problem, I can brush up on my Java (it's been 6 years since I last used it). Thank you very much!

@ericmjl actually what we have is in C# (I thought it was Java, just checked).  I added the logic of it to the answer, hope that helps.

@ericmjl I hope that points you in the right direction, maybe someone else will have a Python solution.  And there might be a way to go directly from IUPAC, I just don't know it.

I don't know if this works out for glycans but this tool converts IUPAC name to SMILES format. SMILES is a text based structure notation which can be converted to graphical structure.
You can also check these out:
http://www.openmolecules.org/name2structure
http://www.iupac.org/home/publications/e-resources/inchi.html
I am still not sure what you are really asking. It would be easy if you give a dummy example.

I tried it, but unfortunately, the tools do not work with the glycan IUPAC names that we have on hand. :-(

The CFG do not use consistent nomenclature for their glycan structures in the excel files they provide. It is human readable but not machine readable. So you'll have to curate their list first. I have bash scripts that do this.
We convert glycan array structures into CFG symbols
http://glycam.org/Pre-builtLibraries.jsp
You want to click on the cfglibs and maybe give it a few secs to load.
If you are still interested in doing this send in an email to glycam@gmail.com explaining what you would like and include my name "Oliver".


text:
What is the standing genetic variation?
I am reading this review. In the first part, the author introduces Standing Genetic Variation, described as:

STANDING GENETIC VARIATION Allelic variation that is currently
  segregating within a population; as opposed to alleles that appear by
  new mutation events

Does it mean that in adaptation the allelic variation is already present (not created by mutations) and in adaptation it prevails over the others?
Thanks

Standing genetic variation is when there is more than one allele at locus in the population at the time-point in question. When an allele goes to fixation there is no standing genetic variation at the locus until new mutations occur. Loci where alleles are not fixed are described as having standing genetic variation.

"Standing genetic variation: the presence of more than one allele at a locus in a
  population."

from Barrett and Schluter 2007


text:
If everybody DNA is different then how blood can match even with matching blood group?
We know that everybody's DNA pattern is different in the world. Then how can ´we transfer blood from one person to another person and this person can survive ?

A few components to my answer.

Red blood cells do not contain a nucleus, therefore, they do not harbour DNA.
The major determinant of blood compatibility is the blood antigen. There are only 4 types: O, A, B, AB. This is genetically encoded, and is expressed as a set of sugar coats on the blood cell membrane. However, the enzymes that encode for A or B should be identical from person to person.

I hope this gives you a preliminary answer to work off.

Because one's DNA doesn't have to exactly match another person at all 3 billion locations for the transfusion to be successful.  As it turns out, there are only a few proteins that determine whether a person's blood is a match to someone else's.  And as it turns out, in the vast majority of the human population, there are only three alleles of the ABO gene, and only two alleles for the Rh gene, and for the vast majority of cases, compatibility of those two proteins is all that you need.

It is critical for you to realize that one's DNA is not the determining factor when it comes to a blood transfusion. Rather, what you have to look at is the proteins being expressed by the DNA coding for blood-associated proteins, as it is these proteins that are the determinant of blood acception or rejection.In other words, the key question is whether or not the blood being transfused harbors antigens -- specific blood proteins associated with a given blood genotype like A & B -- that are foreign to the recipient.
Individuals that have type A blood express A-type antigens, but also house anti-B antibodies which specifically bind to blood with the B antigen. For a person with type A blood (AO or AA), transfusing either AB or A type blood would be dangerous. The RBC in both cases would house B antigens, which the recipient would respond to the transfusion by initiation an immune response against the blood.
I want to touch up one more time on your connection of DNA to rejection of blood. Please be careful with this as different DNA really does not mean much in this case OR in many other biological cases. You have to be much more specific and ask what is the DNA encoding, what is is transcribing and eventually translating and how that relates to the biological process in question. For blood type, although every individual has 'different' DNA, their DNA for blood type has 3 distinct alleles to consider --iO, iA and iB. These alleles are located only within a small region of a person's overall DNA and the difference are 3 discrete categories, as opposed to every person having a different allele and expressing a different protein. If every person different over this small segment of DNA, in the DNA coding for blood type, then indeed it would be possible for each person to make unique antigens and thus for all transfusions to be rejected.
However, since the differences  encompass only 3 allele types, people can only have a limited range of genotypes (aO, aa, bo, bb, ab, oo) which connect to only 4 distinct phenotypes (A, B, AB, O). So there is different in DNA, but the difference is defined and limited, so that overlap of genotypes between is possible and compatibility is quite common. So yes people differ in that DNA, but you have to ask if those differences are significant for a particular biological phenomenon.

Welcome to the site. I appreciate your effort in answering the question; it would be even better if you can make your answer more precise by avoiding repetition of previous answers.

Since the antigens are genetically encoded DNA IS  the determining factor when it comes to a blood transfusion. Just not all of it.


text:
Can P. falciparum and other malaria parasites be cultured and genetically engineered?
I'm not a parasitologist, and I was wondering about the current state of malaria research. For instance, is it possible to culture P. falciparum? Are there techniques for genetic manipulation, editing or transfection (analogous to in vitro cell culture) ? Are there any major limitations to studying these parasites in culture?

If you are interested in a very brief update on malaria vaccine research, see Vaccine Outlook pg.s5, 6 March 2014 Nature.

Yes it is possible to culture plasmodia but they don't grow in a simple constituted medium. Usually RPMI supplemented with serum and erythrocytes is used for growing plasmodia ex-vivo. This article discusses the issues related to plasmodial culture in detail. The authors say that sometimes a certain growth stage (in particular gametocyte) is lost on prolonged cultivation.
In the same paper it is discussed that the exo-erythrocytic (liver stage) plasmodia can be grown on cultured hepatoma cell lines.
Several transfection methods also exist. However, culturing is not a mandatory prerequisite for transfection. Usual methods like electroporation work for a wide spectrum of cell types (in-vivo electroporation is also becoming popular). You can refer to this article for a summary on different transfection methods for plasmodia.
A major limitation, in my opinion would be that the different life stages may not be reproduced in a single culture (as you can see that each stage thrives in a very different type of milieu).

I did a rotation in grad school in a malaria lab, and I seem to recall the PI saying (this was 10 years ago) that you can get a fairly homogenous population by timing when you infect the RBCs with the parasite. This way, they can get the reproducibility they need for multiple experiments.


text:
how do they identify different protein chains?
Can someone please explain how different protein chains occur exactly? I'm not talking about the side chain, but the protein chain which is typically labelled as A,B,C etc in the PDB. I'm curious as to how they are first found and what causes them? As far as I understand, the protein backbone could be in any of several conformations and each conformation has a label? Is that correct?

Chains are individual polypeptides that make up a multimeric protein complex.

I'm curious as to how they are first found and what causes them?

SDS-PAGE will resolve all the different chains (if they are different in molecular weight). Chains are products of translation (and some modifications such as clipping and/or other PTMs etc) and they assemble to form final protein complex.

As far as I understand, the protein backbone could be in any of
  several conformations and each conformation has a label? Is that
  correct?

Yes. The labels are assigned as per the reported conformation.

Is one chain more common than the other? What causes translation to
  produce different chains in this case? And finally, during the x-ray
  crystallography, how do they identify them when they grow the crystal?

There can be different kinds of multimers. There can be homomultimer or a heteromultimer or a multimer of this configuration $(XX)_2$-$(YY)_2$ (a heterodimer of homodimers- just one arbitrary case) etc.
Each chain is a polypeptide and is encoded by a distinct gene. It is possible that in a multimer there are more number of a certain chain than the other for e.g. $X_3$$Y$. This is not because $X$ is produced more then $Y$ but rather because of the way the multimer is assembled.
In X-ray crystallography you basically get the arrangement of atoms. You can also understand which atom is what and similarly the termini can be found out. In any case people don't just proceed to crystallography without understanding the subunits and other biochemical properties.

Is one chain more common than the other? What causes translation to produce different chains in this case? And finally, during the x-ray crystallography, how do they identify them when they grow the crystal? Thank you again for your help!

edited the answer

Awesome, this helps a lot. So to be clear, your heterodimer of homodimers, that would be something like two chain A's bonded to two chain B's? Could it be completely different proteins bonded together? Last question: Also, let's pick a particular structure, say 3GFT in the PDB. There are 6 chains there. Are all 6 in the structure forming an ABCDEF heterodimer? What would be an example of a homodimer (I assume the same chain would be labeled twice?) Thank you again!

Slight addendum, it seems that 3GFT is a monomer, so how do the 6 chains come into play?


text:
Activity of glucokinase
From Solomon et al, 2013 ACC Synthetic biology and from this video :

Here, there are 2 competing reactions for glucose - one with glk as enzyme and other with gdh as enzyme.
In the graph, y axis is gluconate yield and x axis is glk activity. Logically, as glk activity increases, gluconate yield should decrease.
This is the case for most of the graph. But why is there an increase in gluconate production initially(when glk activity is somewhere between 0.2 and 0.27 )?

Are you talking about this paper? Can you please either cite journal name, volume and page numbers or give the title? Solomon is not very specific.

See the horizontal standard deviation bars of first and second points: they overlap. The estimation process might be error prone.

This is one point which is questionable. For the others I will have to take a look on the paper first, but this has to wait for the moment. I'll do that later.

@Chris I have confirmed, this is the same paper as what you cite.

First of all lets have a look, what these guys want to accomplish: They want to use bacteria to make certain products. To do so, they want to exploit the bacterial metabolism at steps where no alternative pathways are available. One of these steps is the first step of glycolysis, when Glucose gets phosphorylated to glucose-6-phosphate (G6P). In bacteria the phosphorylation is done during the import of glucose into the cell by the "phosphoenolpyruvate (PEP):carbohydrate phosphotransferase system", which uses Phosphorenolpyruvate as a phosphate source. This has the disadvantage, that there is almost no free glucose inside the cell, but mostly G6P.
To overcome this problem, the group expressed alternative transporters (which transport glucose into the cell) and Glucokinase (Glk) to allow the cells to survive. This steps decoupled import and phosphorylation of the glucose and resulted in free glucose inside the cell. This free glucose can now be used by different proceses. It also allows glycolysis, since the Glk phosphorylates the glucose which then enters the glycolysis pathway. The Glk was put under different promoters to make different mutants in order to test how the different expression of Glk affects the cells viability.
To bring in another enzyme which also metabolizes glucose, they used glucose dehydrogenase (Gdh) which was expressed from a plasmid with a strong, IPTG inducible promoter. They then used different concentrations of IPTG to test the effect on the production of gluconate and cell viability (I am not going into this).

The figure above is figure 5 from the paper and shows the effect of the three different IPTG concentrations used to induce the expression of the Gdh. For 10 and 25uM IPTG the yield of gluconate is getting smaller, the higher the Glk activity gets. Only the smalled activity shows a lower yield. This is complete different for the highest concentration, but here the cells get probably messed up by the high expression of the Gdh (which also consumes a lot of energy).
In the paper they give no explanation or at least discuss the behaviour of the gluconate yield at the smallest Glk activity (I would like to read the reviewers comments on that). From the data I would expect a higher production. It is possible that the lower energy production (low amounts of G6P means little glycolysis) has negative side effects on the cells. It is also possible, that the Gdh is inhibited at lower Glk activities by some other substances in the cell. Gdh activity is for example inhibited by higher concentrations of nucleotidtriphosphates (ATP and so on), see here. Since Glk needs ATP as a cofactor it would be possible that the ATP concentration at lower Glk activities has a negative effect on the Gdh activity (my own speculation).
Or it is simply some artefact from the experiment. This has some points which can be critisized (I would like to see the reviewers comments here as well). First the error bars are pretty big, so this can also be somewhat different. In the text they mention that the data was acquired by

at least 2 parallel cultures in a representative experiment

I would expect some more repetitions (at least three independent experiments), which would make the data more reliable. Then (and this point is much more important) they can not measure the activity of Glk and Gdh in the same culture due to restrictions in the detection system. Glk activity measurements use a coupled system which in the end measure the concentration change in NADH, while Gdh uses NADPH as a co-factor. Both versions can not be differentiated by measuring a spectrum, so activity measurements of Glk can only take place in untransfected cells. Since the expression changes conditions in the cell (and we don't know how), I would expect at least some discussion about it, but it is missing.

You`re welcome. The paper was fun to read.