text:
What does "chlorophyll photosynthesis peak" mean in relation to photon wavelength?
When reading about how green / leafy plants work,
I saw that they have chlorophyll A & B, which allow the plant to use the energy from light by capturing and transforming.
When reading about Chlorophyll, I saw some charts showing "peak points" for each type for light wavelengths. Apparently, each chlorophyll type has both peak points.
Since from further reading I learn that plants can use all the light in the visible spectrum for photosynthesis, I'm wondering (my questions >>):

What do "peak points" of wavelength correspond to / stand for?
How does light peaking in red spectrum (say around 630nm) differ to (or affect plants) compared to light in red spectrum peaking at 680nm (which I gather is Chlorophyll A peak-ish)?
When same amount of radiant flux is projected to leaves on different wavelengths, one far from a chlorophyll peak the other near, which one gives more energy to plant and why?

possible duplicate of What types of light can't a plant photosynthesize in?

I don't think it's a duplicate as the current question is quite specifically on the two peaks in the absorption spectra in chlorophyll.

First thing to note is that the absorption spectrum of chlorophyll A and chlorophyll B is similar but not the same. The reason for the appearance of absorption spectra is because the light is composed of photons of light.  Different photon has different  oscillation frequency and energy. The essence of Chlorophyll absorption is absorbing photons. After chlorophyll absorption of a photon, the electron transition from the ground state to the excited state, and get water electronic from the water cause decomposition. Only phonton that has resonant vibration frequency with electrons, and can meet the energy requirements of electronic transitions in order to be absorbed by chlorophyll. The Photon energy of different wavelengths of light is different. This is also the reason of different wavelengths of light affect chlorophyll light absorption.
Simply explain the absorption spectrum:

280 ~ 315nm  has small effect of plant morphology and physiological processes
315 ~ 400nnm absorption rate is small, impact the photoperiod, prevent stem elongation
400 ~ 520nm (blue) Absorption ratio of of chlorophyll and carotenoid in this light is maximum, it has the greatest impact on photosynthesis
520 ~ 610nm absorption rate is not high
610 ~ 720nm (red) low absorption rate.  It has a significant effect on photosynthesis and light cycle effect of  chlorophyll.
720 ~ 1000nm Low absorption rate, stimulate cell elongation, impact of flowering and seed germination
1000nm converted into heat

p.s. white light is a mixture of light

Hi @meateatingbunny, +1 on rephrasing and simplifying please. Also, can you please make 3 points to answer three parts of my question? Would greatly appreciate it! Thanks.

@meateatingbunny - why do you say that 610 ~ 720nm absorption rate low when all charts show differently? What do you mean, can you please explain?

Lets start with the absorption spectrum first (image from the Wikipedia page in chlorophyll):

What you see in the figure is the absorption of light thoughout the visible spectrum by chlorophyll a (blue) and b (red). The higher the peaks get, the higher the absorption is. What we can see, is that chlorophyll absorbs light roughly until 500 nanometers (nm) and from 620 nm. The light between this is not absorbed, but reflected. This is the green light and the reason why leafs are green. Above 700 nm the light is reflecxcted again, this is the reason why green leafs are visible white in infrared photography.
The peaking of the both chlorophylls ensures that light of the wavelength can be used efficiently for photosynthesis. Since leafs contain both chlorophylls, this gives a wider range for energy absorption than with only one. Additionally both absorption maxima are far enough from each other to prevent one chlorophyll from "stealing" light from the other.
The light closer located to the peak transmits more energy because it will absorbed better. The closer you get to the maxima of the absorption curves, the higher the absorption and the energy transfer will be.

What do "peak points" of wavelength correspond to / stand for?

The peak points of chlorophyll and their correspondence to the action spectrum indicate that the Chlorophylls play a major role in photosynthesis, it is also clear that chlorophyll isn't the only chemical involved in light harvesting and that other antenna pigments are utilized.
As mentioned in Chris' answer chlorophylls (plural) absorb and reflect light to a various degree at different frequencies, as explained on webpage in the link that was provided (in the section photosynthesis).
From Wikipedia's Chlorophyll webpage, "Measurement of chlorophyll content" section:

"In 90% acetone-water, the peak absorption wavelengths of chlorophyll a are 430 nm and 664 nm; peaks for chlorophyll b are 460 nm and 647 nm; chlorophyll c has a few isomers, peaks for c$_1$ are 442 nm and 630 nm; peaks for chlorophyll c$_2$ are 444 nm and 630 nm; variety c$_3$ is recently discovered; peaks for chlorophyll d are 401 nm, 455 nm and 696 nm;" chlorophyll f (also a newer discovery than information offered on Wikipedia) absorbs at 720nm - making it the most red-shifted chlorophyll to date.

Notice that chlorophyll A's Soret peak provides the greatest rate of growth. Blue light also affects phototropism more than red. Different wavelengths affect the plant differently, some cause growth while other wavelengths regulate bending, even seed development.
Here's an image from cell.us's webpage: "Action Spectrum Green Plants":

Note that plants reflect infrared light beyond 700nm, that is why they appear white (instead of black) in the right side infrared photograph:

Click to zoom

How does light peaking in red spectrum (say around 630nm) differ to (or affect plants) compared to light in red spectrum peaking at 680nm (which I gather is Chlorophyll A peak-ish)?

Chlorophyll b simply expands the range of usable light available to the plant.

When same amount of radiant flux is projected to leaves on different wavelengths, one far from a chlorophyll peak the other near, which one gives more energy to plant and why?

Light frequencies closest to one of the peaks has the most affect on growth, as you can see from the action spectrum blue light is more energetic than red and even mid-band (green) light has a small but significant effect on growth. Because green light is not absorbed some is reflected and some passes through the upper leaves to the lower shaded leaves.
Plants use light inefficiently because it isn't a limiting factor in its growth, instead CO$_2$ is.


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Does physical exercise following lack of sleep increase the risk of sudden cardiac death (SCD)?
Is there any scientific evidence supporting the hypothesis that physical exercise following lack of sleep increases the risk of sudden cardiac death (SCD)?
The only relevant research I could find is: Reddy PR, Reinier K, Singh T, et al. Physical activity as a trigger of sudden cardiac arrest: The Oregon Sudden Unexpected Death Study. International journal of cardiology 2009;131(3):345-349. doi:10.1016/j.ijcard.2007.10.024. However, it only points out that 5% of the SCD cases in the sample took place during vigorous physical activity, which does not directly answer my question.
I am not a biology professional, so please pardon me for any misunderstanding, and, when possible and reasonable, please avoid using too many biological jargons in the answer.

The closest I found: Acute sleep deprivation is associated with increased QT dispersion in healthy young adults. A surrogate endpoint, but a plausible one given that long QT is one of the more common causes of SCD during exercise. Research in the general population using the endpoint of SCD itself is nearly always retrospective and plagued by reporting bias.

I am probably not the best person to answer this, but I know of someone who had heart issues while training for a marathon while working long hours as a white collar worker. He also had trouble falling asleep a lot, even if he was feeling tired. This was probably because he was so pumped up at the time. He told me that sleep exercises helped him though..

Sleep is an important aspect of our life. Sleep disorders are acute due to their effects in physiological and mental health of a person.Sleep occupies nearly 30% of our daily life and people were gradually decreasing the sleep time in order to adjust their busy schedule. According to the United States National Sleep Foundation, adults need to sleep 7-9 hours each night. The decrease in sleep time contribute mostly towards cardiovascular disease, including hypertension, coronary artery disease(CAD),risk of arrhythmia, stroke etc.
The circadian and dirurnal rhythms influence the neural circulatory control causing the changes in heart rate, vascular tone and blood pressure. The REM(Rapid Eye Movement)sleep and nonREM sleep affects the cardiovascular system. Researchers found it important that normal sleep is a complex and dynamic process with profound effects on cardiovascular homeostasis.
Insufficient sleep is a stress stimulator that acts through the sympathetic nervous system elicit changes in blood pressure, heart rate and barroreflex setpoint.
Sleep deprivation is a state of having less or no sleep which is a major reason for cardiovascular diseases.Which may cause
Inflammation
Cardiovascular disease is mainly driven by atherothrombosis, which is an inflammatory process. Increased levels of C-reactive protein(CRP) and interleukin-6(IL6) have been implicated as the predictors of cardiovascular disease risk.Both CRP and IL6 have been found elevated in both totally and partially sleep-deprived subjects.Inflammatory cells such as monocytes and neutrophils were also found to be elevated during acute sleep deprivation, supporting that sleep deprivation is an inflammatory process.
Endothelial Dysfunction
Endothelial Dysfunction has been reported after a combination of sleep deprivation and stress, also increased heart rate, blood pressure are reported in sleep deprived subjects may result in Endothelial Dysfunction.
Hypertension and Stress
Hyper tension and stress hormones are released by the body when lack of sleep occurs, this results in elevated bloop pressure and may lead to CAD.
CardioArtery Disease
The American Cancer Society , the Almeda County study and Partinen also showed an increased risk of CAD in subjects who reported sleeping 4-6 hours a day.
Diabetes Mellitus(DM)
Diabetes Mellitus is a major risk factor for CAD and it has been underlined from several studies across past decades that sleeplessness can result in DM.

A sudden cardiac death is highly probable for a person who follows increased physical exercise and decreased sleep durations. For a sleep deprived person the risk of cardiac diseases are so high, then for some one who spend lot of time exercising can cause chronic cardiac problems. Physical exercise and over training can cause more stress hormones and increased heart rates, these factors along with prolonged sleep deprivation can cause serious cardiac diseases or even sudden cardiac death.

Levels of cortisol (the "stress" hormone) are elevated for long periods of time.
The body spends more time in a catabolic state than an anabolic state (perhaps as a result of elevated cortisol levels).
Excessive strain to the nervous system during training.
http://en.wikipedia.org/wiki/Overtraining

References

Critical Care Nursing: Synergy for Optimal Outcomes - Roberta Kaplow
Sleep Deprivation and Disease: Effects on the Body, Brain and Behavior - Matt T. Bianchi

You've brought in some interesting theoretical reasons why one might wonder about an association between sleep deprivation and SCD, but to my knowledge this research has been either 1) in chronic sleep deprivation (CAD, DM, HTN) or 2) in acute sleep deprivation using surrogate endpoints (cytokines, HTN - though the latter is certainly a good surrogate). To conclude that A sudden cardiac death is highly probable... for the OPs scenario of exercise after acute sleep deprivation seems like a leap.

@Susan:I have edited to "prolonged sleep deprivation", I personally know cases of SCD due to heavy exercise and lack of sleep. I have claimed that "highly probable" not always possible. So its really a highly risk situation for a person following these appetites. Thank you for your valuable suggestions.

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How can I purify RNA after gel electrophoresis to remove residual acrylamide?
I sometimes use denaturing gel electrophoresis on a preparative scale to purify RNA produced by in vitro transcription. The major issue with this is that the sample after extraction from the gel still contains significant amounts of acrylamide, or acrylamide oligomers/polymers.
Exchanging the buffer using Vivaspins doesn't reliably remove it, precipitating the RNA also only reduces the amount, but can't remove the acrylamide entirely.
In some cases the acrylamide doesn't interfere much with the later experiments, but there are some experiments that won't work with acrylamide in the sample.
What are the options to purify the RNA after gel electrophoresis that would reliable eliminate acrylamide from the sample? Preferably they should be simple and fast, not something like a full FPLC/HPLC run.

May I ask why you need to purify your in vitro transcribed RNA? I've been making mRNA by IVT and have gotten good results without any purification beyond phenol:chloroform extraction and isopropanol precipitation.

@user137 I use the RNA itself for NMR experiments, I need it in a different buffer and without the DNA and protein to get good quality spectra. And anything else that is still in there will likely overlap some of the signals of the RNA.

How much RNA do you need for NMR? I've always heard that NMR needs a lot of material for good signal.

@user137 Depending on what exactly you want to do you need about 0.2-1.0 mM protein or RNA in your sample in a volume of 300-500 microliters. And for many experiments you also need it 13C and/or 15N-labeled.

@MadScientist Maybe I did my math wrong, but 500uL of 1mM of my mRNA (1860 bases) would be 300mg of RNA. Even if 300uL of 0.2mM would be about 36mg RNA. With a good in vitro transcription reaction I can get 200ug of RNA. Obviously a short RNA would need a lot less mass for the same molarity.

@user137 The RNA you would investigate with NMR is usually around 15-150 nt long, you don't see much with NMR for anything larger. And we simply do the in vitro transcriptions on a larger scale, typically around 10-30 ml. RNA is also almost always measured in Shigemi tubes, so the volume is 300 ul, and while 1 mM concentration is ideal, but you can't always get that much.

If you don't want acrylamide in your preparation, don't use it, as you will always have some carry-over in the solution. And you will not get rid of it completely, as it at least partly co-precipitated with the nucleic acids (it's used as a co-precipitation agent for this purpose).
I think the best solution is to use chromatography, either size-exclusion or charged resins. See these two papers for more information:

Large-scale preparation and purification of polyacrylamide-free RNA
oligonucleotides
Rapid, non-denaturing RNA purification using weak anion-exchange fast
performance liquid chromatography

We also use chromatographic methods, but gel purification has certain advantages like better resolution. I don't need to get rid of acrylamide completely, reducing it significantly below the RNA concentration would be sufficient.

Gel is easier and faster, chromatography has a better resolution and takes longer. Now you have to choose what is more important...

I suspect if there would be any residual unpolymerized acrylamide after the run. Heating should decompose acrylamide to gaseous products (ammonia, hydrogen and carbon monoxide). Seehere. I am not sure about thermal decomposition though (no solid reference).

authors: Аня Пахомова

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What would be “Sternum-Intermediate” distance?
I've asked this question on the English Language & Usage board, not being entirely sure whether this question is strictly medical, or just English knowledge suffices to answer.
Do note I am no native speaker, hence I am afraid to misinterpret the possibly obvious thing.
In an article written by Wheat et al Engineernig for Life - Kinect Report the authors use the scanning device to calcuate distances on the human body.
The measured distances are: Sternum-Intermediate, Inter-nipple and Sternum-nipple (see Table 3.). The latter two are obvious. The first one, however, not so much. Unfortunately, the authors do not provide a definition, probably assuming it is clear to the reader.
What would be the Sternum-Intermediate? Is this the sternum's length or is "Intermediate" some specific body part?

The article states:

Markers (blue stickers, approximately 1 cm in diameter) were attached
  to a point approximating the suprasternal notch and an intermediate
  position on the dorsal aspect of the left breast. The position of
  these markers and the two nipples of the model were extracted from the
  point cloud scan of the breast model through manual digitising using
  Meshlab...Three straight line distances were analysed (1. internipple,
  2. sternum-to-right nipple and 3. sternum-to-intermediate marker).

One can infer that the sternum-intermediate distance is from the sternum to the intermediate marker on the dorsal aspect of the left breast. It is not, I believe, a widely measured anatomical distance, rather one 'invented' for the purposes of the study.


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Possible moth identification
There's a flying insect being caught indoors today in Sydney Australia. Before it is being caught, it basically flies like a moth. However googling of Tinea pellionella and other cloth moths does not suggest it is a cloth moth as hair is missing from its very small sized head.
It is also known to be very common every year when spring approaches in australia
To assist identification, the bug was caught in a plastic jar to allow multiple angles of it to be photographed

Measured body length (not including long antennae): 1.1 cm
Color: Brown an golden brown with lustre
Legs: 6 (front pair very short, middle pair is forked, hind legs have some golden brown feathery structure)
Head is black, very small and have no hair

Here one can easily see the hindlegs are covered by some bristle like golden brown feathery structures, and also its shiny golden segmented abdomen

The camera is not fast enough to capture it unblur when it is flying, but the few moments when it opened its wings can be seen here extracted from a video

And these are our best shots using the iphone camera in capturing its flight with its wings fully opened.

Is this a type of moth, is it a pest or is it neutral. What is the species?

It is a moth, so belongs to the order of Lepidoptera, and to the unoffical suborder of microlepidoptera. These are notoriously difficult, even with good literature, which i'm not sure exists for Australia (European myself).

Do you find this similar?

That might be it, as the glossiness of the wings, the feathery ends and the colors patterns matches. Strangely, I don't seemed to see any of the two dark horizontal bands that is present in all other google images of the species (except mine and the photo shown in your link)

This is a Bogong Moth,the migration point was really helpful !!
They migrate in masses around the
 1. Victorian alps
 2. southern Australia (Sydney,Canberra)
 3. New Zealand..
Agrotis infusa,
These are pests which affect many plants,they're not neutral and they
Cause some attentive damage
More on this and the site which helped me


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Can your immune system's cells destroy you? (Critical thinking and Fictional sense)
In an imaginary sense, If you alone were replicated into 2 so that there should now be 2 of "you" (meaning you both have the same DNA). Then let's say one of you shrunk to the size of a bacteria, and was placed inside the other you (normal human size. Let's call this the actual you).
The question is how would your immune system affect the bacterial sized you in your own body?
Would white blood/T cells try to get rid of the smaller you?
If so, how? And could the smaller you die from this?

I'm voting to close this question as off-topic because this is not a biology question but something that belongs on World Building.

Placed where inside the body? The question basically canbe reduced if surface antigens can be auto-immunogenic when implanted. @NocTurn - if this last sentence still matches your intention, it will have a much better chance of being answered. The question has a fair bit of Sci-Fi content as of now. Good luck.

was this question answered?

The immune system recognizes patterns - incase of innate immunity and shapes - incase of active immunity.
I am making a few assumptions:

The Shrinking would result in a smaller version of "the person" - meaning he/she is a bacteria sized person capable of executing all actions that a human can do.
The shrunk person is placed inside the blood vessel or some place where the immune cells will have easy access.

Now, the answer would basically depend on two factors:

The pattern recognition: It is higly unlikely that the innate immunity would recognize anything that is so small - As the person himself is the size of bacteria, the pattern recognition would be unable to find the patterns.
The Shape recognition  - This might be able to identify a specific structure. The structure in question may be a whole cell or a cluster of cells or a hair follicle, etc... The epitopes on foreign organisms which are recognized by the active immunity are much smaller than the organism itself. Infact a single bacteria may have thousands of epitopes. The epitopes are usually proteins and what is recognized may be as small as 3 to 4 amino acid cluster. Thus this system has the potential to identify and eliminate the shrunk person.

The shrunk person will not be considered as "self" because on shrinking, the "self-shapes" don't apply anymore. Think of it as a glove specifically made for the hand of an adult. A child's hand will not fit into it. Likewise any change in size of proteins will eliminate all question of self and everything in that "new size" is considered foreign.

This is a very interesting question. As others have alluded to, the body generally recognises self and non-self. However, as with any biology it's not that simple. Even leaving aside autoimmune disorders, the body doesn't always attack non-self and doesn't always leave self alone. Think of a pregnancy - the foetus is non-self, and yet the body doesn't reject it. The same can be said for a whole host of molecules that enter the body, such as food or things breathed in (e.g. pollen).  For this reason, Charles Janeway put forward the infectious non-self theory. This postulated that the body had a degree of leniency towards non-self, and would only attack if the macrophages became activated. This is done through recognition of Pathogen Associated Molecular Patterns, or PAMPs, binding to Pattern Recognition Receptors, PRRs. These PRRs are receptors present on immune cell surfaces, though most relevantly on macrophage surfaces, and when they bind to PAMPs it sends a message to the cell that it's likely in contact with a pathogen (or at least there is likely a pathogen in the area somewhere). This causes activation, and starts an immune response.
However, it's also too simplistic to suggest that the immune system always leaves self alone, and in fact one of the key jobs of macrophages is to clean up self cells that are damaged, and undergoing apoptosis - programmed cell death. (You can read more on macrophages here and more on apoptosis/other methods of cell death here). Therefore Polly Matzinger put forward what is known as the "Danger Model". This basically speculates that in order for an immune response to occur, the body has to recognise certian molecules that are evolutionarily associated with danger. PAMPs would indeed count, but there could also be endogenous molecules such as HSPs - proteins produced when a cell is under duress through heat, pH, cold, irradiation, viral infection etc. This tells the immune cell that detects it that the body is in danger, and allows activation and mobilisation of an immune response.
So the question here is, would the body respond to a miniature version of yourself? That would depend on a number of factors:
Where in the body would you go? If you were to stay in the digestive tract, so get swallowed and 'passed through' the body, I would say it's very unlikely you would be attacked. The body has a high tolerance for places such as the gut, because it's constantly exposed to external and non-self molecules. If it were in the blood stream, it's more likely because you're more likely to come across immune cells.
How is this 'shrinkage' achieved? Growth comes in two ways, through increase in cell size and increase in cell number. Which of these are you reducing? Are the cells the same size, but there are many fewer of them (unlikely, especially given that the opening question specifies to bacterium size, which are many times smaller than human cells already) or do you have the same number of cells but each cell is shrunk to a much smaller size (given that the entire body is the size of a bacterium, each cell would have to be many times smaller than a bacterium). If the cells were the same size, or even a bacterium-sized each, then an immune response is much more likely. If the whole organism is the size of a bacterium, the cells are going to be far too small to elicit an immune response.
Are you causing danger signals? As mentioned above, if no danger signals are present then it's unlikely an immune response will be launched regardless of anything else. Provided you're not killing or injuring cells, the body will pretty much ignore you.
I would say you wouldn't be attacked if you shrunk down as far as you've suggested. Everything would be too small for the body to recognise. However, if you didn't shrink down nearly as far, so your cells remained a size the body could recognise, and then started blundering about causing all manner of danger signals around you, the body may pick up some of your antigen and launch a response against you. On the other hand, the body is likely to have become tolerant to your antigens so even if this was the case, a full immune response is unlikely.

How does the body know you is you?
There's two forms of immunity: innate and adaptive.
Innate
The innate immune system is the first line of defence that basically works on pattern recognition. "If I see these chemicals, they're usually bacteria/fungi/viruses, so I'm going to kill anything with these chemicals." Little you wouldn't have any of these chemicals unless of course the fact is our body is covered in bacteria which might be recognised (were the chemicals big enough to be recognised). Then they also try to kill things when they're worried somethings causing damage. So if they see that the area is inflamed because little you accidentally broke something, they might come and gobble you up because they're extra activated by the inflammation.
Adaptive
As for the adaptive immune system, this looks for certain markers and can identify specific bacteria and things that aren't us. There's these proteins on cells called MHC (a.k.a HLA). Our body cells are covered in OUR ones and everyone has different ones (unless you're an identical twin). So in little you's case as long as those proteins were there, the body would think you're okay.

Its impossible to happend, why worried about it? Maybe you`re writing a fiction book. I cant answered using biological arguments because this is fiction.

This is actually the best answer so far.

When your body develops, immune system learns which tissues are foreign and which are innate. So usually immune system does not attack host's cells. Opposite case is autoimmune diseases. Immune system does that by addressing surface proteins of cells. Only foreign cells, never presented before, cause response.
If you think that large-you immune system will not attack large-you cells, then you should agree that large-you immune system will not attack small-you. Except, maybe, for bacteria that are on the skin on small-you and now sitting in blood stream of large-you.
The question boils down to: why my cells are not attacked by my immune system? Answer: because in healthy animals it discriminates host vs invaders due to memory of immune system.


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How Do White Blood Cells Learn? Or Do They?
So I get the concept that a vaccine is a weakened form of a virus so that the body can "learn" to fight it and make a person immune to that disease, but how exactly does this learning take place? What learns? The white blood cells? Do they have their own database or something and do they go from cell to cell informing them of what they learned? I read that they only last around 5 to 7 days so that means there's constantly new white blood cells that also need this information for all diseases ever encountered. How does this work? Thanks!

See: quorum sensing and controversial study about Electromagnetic Signals from Bacterial DNA where it indicates a "wireless" version of intercellular communication which was found in bacterial communities, so it could be similar for white blood cells.

So while some kind of a biological database might have been an evolutionary option, the way we evolved is different from this. Rather than 'planning' what diseases could be recognized in the environment and recording this, our bone marrow constantly pumps out naive B and T cells that have a randomized receptor on them. The effect of this is that every new B and T cell that your bone marrow makes will recognize a unique, random protein sequence, and you will have billions of these cells floating around in your blood circulation at any given time. These cells however will only float around in circulation for a short period of time before dying and being replaced by other cells with new random sequence receptors.
When you get a vaccination, you are injecting in specific protein sequences from a specific pathogen. As these injected protein sequences circulate through your blood they will eventually bump into a B or T cell that has a receptor that recognizes them. When this happens, the B or T cell will now start to divide and give rise to long lasting memory cells that express the exact same receptor and will therefore recognize the exact same protein sequence again in the future. These cells will float around in your blood for most of your life and make you 'immune' to the recognized pathogen. When you get reinfected with the same pathogen or the pathogen to which you were vaccinated these memory cells will rapidly divide upon recognition of the pathogen and give rise to a large number of effector cells that eliminate the pathogen before it can 'make you sick'.
What is really cool about this is that because each T or B cell carries on it a receptor that recognizes a random protein sequence, you currently have in you B and T cells that would recognize a protein that does not even exist on Earth, but might exist on Mars or somewhere else in the Universe. This makes our immune system quite valuable because any protein that nature creates for all of time anywhere in the universe will still be recognizable by our immune systems.

Thanks for the answer! Can you clarify how the memory remains if the B and T cells only last for a short while and would then be replaced by randomized ones from the bone marrow? I presume they must reproduce as well, but if they're reproducing while the marrow is making random ones, wouldn't the population be hard to manage?

So the recognition remains because of specific cells called memory B and T cells. These are almost identical to all of the naive short lived B and T cells but they last for most of your lifetime if not all of your lifetime. So they do not need to reproduce until you get reinfected with the pathogen. So typically these memory cells will be present in low numbers and just wait in the blood for 80 years, and then every time you get exposed to the pathogen they recognize they rapidly produce millions of new cells with the identical receptor to eliminate the pathogen. Make sense?

Ahh, so the "naive" B and T cells are short-lived, but if they come into contact with a protein befitting them they will create a "memory" B or T cell and those permanently remain?

Correct. The idea is that if a naive cell doesn't come into contact with and recognize a protein within a short while then it might not recognize a pathogen in your environment (or a protein sequence that even exists for that matter) and is eliminated so your blood doesn't just become a sludge full of too many cells. But when a naive cell does come into contact with and recognizes a protein it will produce a small population of memory cells that are very long lived so that they will be able to rapidly respond the next time you come into contact with the pathogen.

The B/T cell receptor is not only recognizing proteins, it is recognizing antigens in general. Most of these are proteins, but they don't have necessarily to be proteins.

There is also a subsystem to eliminate B cells that recognize "self" (which includes food).  Obviously it's not good for the immune system to go after "self" molecules.  And that's exactly what does happen in auto-immune diseases: the "identify self" subsystem glitches.

Right, I think a really good answer should cover clonal deletion and affinity maturation. The first explains why you aren't immune to "self" and the second is an important part element in making the polymorphic immune system even better.

Basically the adaptive immunity responds to shapes of the antigen, rather than sequence.

This is all also very relevant information. It's true that antigen recognition is far more complex that just the amino acid sequence of a protein. And yes many other compounds can show positive binding to the TCR/BCR especially some carbohydrates and lipids, though in those of these cases recognition is not straight forward, and other proteins must be available for this to occur.

As for the shape of the antigen determining binding to the TCR/BCR. In a sense this is correct in that the 'shape' of the receptor fits the 'shape' of the antigen, but to those without an in-depth biochemistry background this may be a bit misleading, because you could make an identically shaped molecule with vastly different charge distribution that would have no reactivity to the receptor. So because of this I find it easier to just explain it as the amino acid sequence determining binding. But all good points.

Recognition by peptide sequence applies much more to TCRs than antibodies.

If this is the case, how do some vaccines last longer than others?

@canadianer TCRs are structurally similar to immunoglobulin. AFAIK TCR recognize the shape of the peptide presented by the Antigen Presenting Cells. Am I wrong? The point about charge never occurred to me, although now thinking retrospectively it is obvious!

@Eric that would be an excellent question to ask separately

@CRags All receptors recognize shape insofar as it is defined by the spatial arrangement of atoms and electron distribution in a molecule. TCRs recognize short peptides that are proteolytically generated from larger proteins and presented on MHC. Although some local folding is expected, the peptides are pretty linear and are not in the native configuration found in the original protein. That is what I meant by recognizing peptide sequences. A BCR recognizes amino acids by their arrangement in the tertiary structure without any requirement for them being close in the primary sequence.

@Eric, some vaccines last longer due to mutations of the disease. The flu, for example, is different every year so the previous vaccination does very little for the new strain. I can only guess Tetanus must also mutate then but at a much slower rate or something. I'm not the biologist though so as CRags indicated, it's a good question to ask separately :-)

Afaik. TCR binds only to MHC1, so it won't recognize what you inject in a vaccine. Most of the vaccines are B cell vaccines. Creating T cell vaccines is much harder and it is bleeding edge science.


text:
What is the maximal insert length for PCR based homologous recombination in S. cerevisae
I would like to insert a 6 kbp construct, which I have on a plasmid into the genome of S. cerevisiae. This plasmid was originally constructed to integrate at the HIS locus via homologous recombination after transformation with the plasmid. The problem is that the strain I would like to use is HIS-Δ0, so the complete HIS-ORF has been deleted so that the plasmid will not insert via homologous recombination.
My question is now whether I can still insert my construct into the genome via PCR based homologous recombination, by amplifying the region of interest on the plasmid with primers which have a homology to the genomic sequence where I would like to insert my construct. I am afraid that 6 kbp are too much to transform yeast cells efficiently. Does anyone have experience with such long inserts?
thanks for your help,
Jannis

Are you having trouble with the amplification or the transformation?

No, I have not even tried yet. I am just worried that the homologous recombination will not work with such a long insert and I wanted to know if other people have done similar tranformations before.


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Why reference genome is a reference?
I have heard that a reference genome such as humans is generated by randomly choosing samples from a group of donors. But why do we call the DNA sequence generated as a reference? Why should we believe those few samples can represent all humans, from which we need to align with?

Good question. It is a quirk of history - the initial genome sequencing work was WAY too expensive and WAY too laborious to even contemplate sequencing multiple genomes. Thus, an initial genome (later extended to a couple of genomes) was used as a "reference".
However, technological advances mean we can sequence genomes for under $1000 in a day now. Thus, the advent of things such as the 1000 genomes project (http://en.wikipedia.org/wiki/1000_Genomes_Project).

Having said that, as the answer below points out, the variation between humans is tiny compared to the overall similarities. Thus, a "reference" can be generated from a sample of one or few.

The main reason is because the genetic differences between individuals of the same species are tiny. For the vast majority of studies, they can simply be ignored.
Differences between individuals are usually (not always, but mostly) differences in SNP genotypes. These are single nucleotide differences which, while they can have phenotypic effect, don't really affect the ability of sequences to align. Sequence alignment software is designed to be able to deal with such small differences. For example, consider these two random sequences:
>seq1
ACCTTGCATCGGATCGAATTCGCGTTAGCGATCG
>seq2
GCCTAGCATCGGACCGAATTCCCGTTAGCAATCG

If we align them, we will get:
seq1            ACCTTGCATCGGATCGAATTCGCGTTAGCGATCG
seq2            GCCTAGCATCGGACCGAATTCCCGTTAGCAATCG
                 *** ******** ******* ******* ****

As you can see, despite the small differences in sequence, the two can be aligned very well. The same is true when you look at real data. My haemoglobin gene, for example, will align perfectly well against both yours and the one in the reference genome. In fact, they will almost certainly be identical or, at best, have a couple of different residues.
So, when doing work that is not about studying specific polymorphisms, we need a representative genome. Anyone's will do, unless they have a particularly serious mutation such as a chromosomal translocation.

To put some number, the average homology between human genomes is approx. 99.5%. As @terdon described, this relatively high homology (i.e. ~2,850,000,000 base pairs out of the total 3,000,000,000bp of the human genome will be identical) allows to align any human sequence to this so-called reference. This is of course in the scenario of no major chromosomal translocation, which usually leads to diseases.

@vajra78 it probably never will actually. These differences are irrelevant for most studies. You almost never care about individual genotypes, not unless this is a medical issue involving a specific individual. The point here is alignment and that is not affected by such small changes. Studies at the species level (looking at evolution or genetic regulation etc) rarely, if ever, need to take into account the intra-species variation.

Reference genomes do not accurately represent the set of genes of any single person.it is created by fragments of various donors, which when built,is used as a template for creating the real genome. Though we will find All humans are 99.9 per cent identical and, of that tiny 0.1 per cent difference the reference genome might not be 100% identical to the real genome.Every reference genome con be sequenced again and the gaps can be reduced each time. We can reach a point where we can say that the accuracy is high enough to be used as a reference platform for constructing the real genome

The same question sticked in my mind a month ago. Even @terdon gave an explanatory answer, I want to make a small contribution.
When I asked similar question on seqanswers *, one of users gave the link of the study Ashley Lab in Stanford. They generated the "Synthetic major allele human reference genomes".  (1)
They combined the current reference sequence (in that time it was hg19), with the 1000Genomes data of variants with high allele frequencies. This combination creates three different reference genome of three human population (YRI, CEU and CHBJPT).
This synthetic reference sequences represents the variants that are highly seen in these population. It is possible to download these genomes from their page.

Dewey FE, et. al. (2011) Phased whole-genome genetic risk in a family
  quartet using a major allele reference sequence. PLoS Genetics 7(9):
  e1002280. http://dx.doi.org/10.1371/journal.pgen.1002280


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What's cosmic VCF?
The popular MuTect variant tool:

http://archive.broadinstitute.org/cancer/cga/mutect_run

has the following VCF option:

--cosmic < comic.vcf >

Q: What is this cosmic VCF file? What's the purpose of the file?

VCF is an abbreviation for Variant Call Format. It is a file format for SNPs.
COSMIC stands for Catalogue Of Somatic Mutations In Cancer. It is a database.
Have a look at the links for more information.
A COSMIC VCF is likely just a file in VCF format file containing data coming from the COSMIC data base.

Without looking at any mutect docs and how it might use this, the COSMIC VCF would refer to a VCF from the cosmic database http://cancer.sanger.ac.uk/cosmic/


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

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

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

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

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

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

@TheNightman Maybe you can post a new answer?

No problem I'll post it in a minute.


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About tomatoes pigments, why red tomatoes rather than yellow ones
How the first tomatoes (yellow) that arrived in Europe turned from yellow to red ?
I know the yellow pigment is xantophylle and the red one is lycopene, but my question is, was it an adaptation of the plant to new soil conditions, temperatures or insects ? Or just a natural random mutation like, and it probably already happened in America ?
Bonus question:
Why did Europeans stopped to eat yellow tomates, and prefered red ones, was It because they though the fruit color was aphrodisiac ? And now why do even American tomatoes are red.
(They were called pommodoro in Italian, pomme d'or or pomme d'amour in French, " mala aurea " in Latin, and " love apple" in English.)

Probably due to a natural genetic mutation amplified by human cultural preferences and selective breeding practices.
Europeans may have preferentially selected and cultivated the red varieties for a few reasons:

The red colour was novel and visually striking compared to
yellow/orange fruits more common in Europe.
There was a belief that the deeper red colour indicated more ripeness.
Different (arguably better?) flavour – yellow = less acidic + milder.
Some cultures associated the vibrant red colour with love/fertility,
lending to names like the French "pomme d'amour”.

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


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Why would a snake try to swallow itself?
On Youtube, there is a video where a veterinarian has to take care of a snake who swallowed its tail, like trying to swallow itself.
The man didn't seem surprised about this behaviour.
https://m.youtube.com/watch?v=puKevC5boFg
I guess it's a pathologic behaviour, but do you know what can be the causes ?

I'd guess more of a reflexive behaviour than pathologic.

Read this: https://www.petmd.com/reptile/conditions/behavioral/ouroboros-snake-bites-its-own-tail

Towards the end, when snakes are ill, they will bite themselves ... I’ve seen rattle snakes go into convolutions and bite their own bodies.

Another explanation could be due to stress. Cramped enclosures that restrict movement lead the snake to become confused and unable to distinguish its tail from prey.

When kept in small containment, the snake is unable to stretch out fully and may think that its tail is that of another snake.

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


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How do birds avoid mid-air collision?
Across from me there is a large flick of Pigeons and Ravens that like to nest on the roof. They swoop and dive and fly all over. Sometimes the whole flock lifts off at once. My question is, how do they avoid running into each other? Certainly they can't see every bird around them, can they?

I think, the reason would be the same as, when flocks of birds like starlings, etc. do not run into each other while making patterns. They can un-group and regroup with complete harmony. So, maybe the concept behaves the same with different types of birds as well. Or, maybe they have some kind of natural radio wave signaling due to which they are capable of preventing flying into each other.

They can't see all the birds that are around them as some are hidden behind the others. However, I don't think there is anything so extraordinary; they watch around, have good reflexes and can change direction very abruptly. There is no need for some kind of special sensing abilities to explain bird flocks.
3 simple rules
One can simulate a flock of birds with 3 simples rules:

Adapt your speed on the speed of the other agents

$$\overrightarrow v_{i,1} = \frac{1}{K_L}\sum_j^K\overrightarrow v_j (t) - \overrightarrow v_i(t)$$
, where $K_L$ is the number of birds in the Large area of perception, $\overrightarrow v_j (t)$ is the speed of a given bird in the large area of perception and $\overrightarrow v_i (t)$ is the speed of the focal individual.

Attraction

$$\overrightarrow v_{i,2} = \frac{1}{K_L}\sum_j^K\overrightarrow p_j (t) - \overrightarrow p_i(t)$$
, where $\overrightarrow p_i(t)$ and $\overrightarrow p_j(t)$ are the positions of the focal bird and of a bird present in the large area of perceptio, respectively.

Repulsion

$$\overrightarrow v_{i,3} = -\frac{1}{K_s}\sum_j^K\overrightarrow p_j (t) - \overrightarrow p_i(t)$$
, where $K_s$ is the number of birds present in the Small area of perception.
Then, to update the speed of the birds you just sum up those 3 contributions:
$$\overrightarrow v_i(t+1) =  \overrightarrow v_i(t) + \overrightarrow v_{i,1} + \overrightarrow v_{i,2} + \overrightarrow v_{i,3}$$
see boids for more information.
My point in descrbing this algorithm is that you can get the emergent behaviour of a bird flock out of very simple rules.
Bird Collision
If birds don't often collide each others (what I assume but honestly I don't know much), note that it is estimated that 100 millions birds that die every year after colliding a window (see here). Birds also collide with power lines (ref) and wind turbines (ref).

When they are flying together as a flock, they anticipate the flock's behavior and react accordingly. earthsky.org/earth/how-do-flocking-birds-move-in-unison
And when they are just flying around, but not in a flock, the concept is the same as how we humans don't collide into each other when we are walking. Although birds fly faster, they also see farther
(eagles and other birds of prey can see four to five times farther than the average human can), which means that they have a longer distance to react.

But how about when they fly together? They're really close as they fly.

When they are flying together as a flock, they anticipate the flock's behavior and react accordingly. http://earthsky.org/earth/how-do-flocking-birds-move-in-unison

@YvonneLiew I think the flying together part answers the question better, you should edit your answer to include that citation.

Schooling and flocking behavior is actually very interesting stuff. The real answer- many of the things mentioned already (speed of processing, good reflexes) but there's still much to be found out. Computer analysis is helping enormously, and also helping to create robot flocks. Here's an article of scientists finding out more. Unfortunately, that article's from 2009, but I also read about it in "Complexity: a guided tour". Anyone have something more updated?
some neat flocking robots- there are many other similar projects lately

Sitting in stadium full of thousands of people looking around we notice that just about everyone is in our line of sight.  Flocks of birds also always seem to follow a pattern involving maintaining this global line of sight.  Even as the flock is flying straight ahead, changing direction, taking off or landing the the individual birds seem to move and adjust the pattern to maintain this line of sight to the maximum possible.  The seem to follow this logic even while on the ground pecking grain.

Can you add some references to this claim?


text:
Is each generation getting older?
So we know that our sperm and egg cells get set aside relatively early so that they aren't going through unnecessary cell divisions and causing DNA damage or telomere shortening, but since each new generation starts from one cell each generation has germ cells that have divided more than the previous generation's germ cells.
So, does this have an effect on age?
Is a second generation baby technically older than a first generation baby due to these extra cell divisions, or is telomerase and DNA repair able to keep each generation at the same relative life span?

In germ cells telomerase enzyme is active and elongates telomeres, so youngsters are not born older than their parents due to telomeres.
Still, they do receive mutations, accumulated by their parents' germ-line cells, i.e. eggs and sperm. Most of the mutations occur upon division of the cell. Egg cells don't undergo many divisions - they are created in the course of embryonic development of a woman and then are spent one-by-one. At the same time, precursors of sperm cells divide constantly, thus accumulating mutations at a constant rate.
Got no time to look for a hyperlink, but I read that no matter what is the age of the mother, she gives 15 new single-nucleotide mutations on average to her offspring. Father gives about 10 mutations for each year of his life after reaching puberty, historically 70 on average. Out of those mutations most are neutral or silent (due to genetic code degeneracy), but on average ~1/70 leads to a change in aminoacid sequence of some protein, usually harmful.
So, although babies don't get older, but alas, they get uglier as generations pass :( Natural selection is what saves us from deterioration, so that the weakest are sentenced to childlessness.
EDIT:
Added a couple of hyperlinks as requested: decay of cognitive indicators of children with parent's age:
http://journals.plos.org/plosmedicine/article?id=10.1371/journal.pmed.1000040
Another link: drosophila simulation of middle-class neighborhood (MCN) population, where each family has exactly 2 children, son and daughter, and no natural selection pressure is applied: such population rapidly deteriorates with fitness in wilderness decreasing by 2% per generation:
http://www.ncbi.nlm.nih.gov/pubmed/9371795

Can you reference "they get uglier as generations pass"?

@MarchHo added a couple of links to papers about the rate of deterioration of population without natural selection and about negative effect of father's age on child's IQ. I mean that in absence of natural selection, we accumulate the spontaneous mutations in our genetic material and over generations get weaker and weaker.


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Do our belly buttons consist of scar tissue?
I read an interesting post on Facebook the other day saying that we all have a visible scar since birth - our belly button. This got me thinking (and research for me only found results regarding belly button piercing) is the belly button made up of scar tissue?
I seem to recall that there are some stem cells still within the umbilical cord (which is why doctors tell you to spend the money to have it saved (I think)) so I was wondering if scar tissue closed the hole left by our cut umbilical cord, or if the stem cells divided to produce normal skin tissue.

According to Wikipedia they are scar tissue.

@canadianeradianer I'd like something more definitive than Wikipedia that can be changed by anyone (like when the lunar eclipse said that the moon would blow up)

I think the question hinges on the definition of scar tissue and the histology of the navel tissue. Given that the navel is not a functional organ, other than as a locus for piercings, I think finding a conclusive scientific answer is next to impossible.

@SolarLunix I'm sure you are, which is why I didn't post an answer. Just thought you might like to know.

The place where the cord was cut do not stay with us - it falls in a week +- after the birth, while the umbilicus is the only visible natural scar formed by natural processes, not by gynecologists:

Multiple sources say the umbilicus has a scar tissue in it.

After birth the umbilicus is the only naturally formed visible scar on
  the body.

Br J Plast Surg. 1998 Oct;51(7):538-41. Umbilicosculpture: a concept revisited.

Umbilicus is a scar, which is the place of the previous merger of the
  fetus with the umbilical cord.


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How long does it take unused antibodies to clear the system?
Say you have the flu and a normal immune system. Now you're all better but your antibody level is still elevated. How long does it take for those antibody levels to go back to a base value?

This is quite broad since there are many different classes and subclasses and each has a different half life which ranges from hours to weeks.

Wouldn't nearly all major classes of antibodies have about the same life expectancy? @canadianer

No. Very generally, you can find numbers like 3 weeks for IgG, 1 week for IgM and IgA, 3 days for IgD and 2 days for IgE. Also, these isotypes differ vastly in serum concentration and are expressed at different times.

@canadianer - your comment basically answers the question. So perhaps it is not so broad? Further, to discard issues with initial Ab concentrations the Q may be focused on half-life and perhaps the Q could go for IgG alone, or another Ab type typical of the Flu to narrow it down further?

@AliceD The question really is about more than antibody half lives and there are many factors that could contribute. Actually, I can imagine some study would have answered it by measuring antibody titre over time, so I have retracted my close vote.

I agree that this question may be broader than a simple half-life question in theory, however, I think that it is still basically a half-life question. For instance, does the presence of the virus (using the flu example) contribute to opsionization and clearance? Possibly, but this would be variable and difficult to generalize about.
The question has been asked in a number of ways (for endogenous / exogenous antibody). For simplicity, Mankarious et al examined transferred antibody in IVIG therapy and found, "For total IgG, the half-life found was 25.8 days; for IgG1 it was 29.7 days; for IgG2 it was 26.9 days; and for IgG3 it was 15.7 days." - an answer in line with that proposed by canadianer, above.


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Had there been a non-flying pterosaur?
Since there are non-flying birds and secondary non-flying insects, it is reasonable to assume there were also non-flying pterosaurs.

Well, according to this source there are no flightless bats, so it isn't an absolute that all flying clades have flightless members:
https://pterosaurheresies.wordpress.com/2011/07/21/meet-the-first-flightless-pterosaur-sos-2428/

Everyone knows about the various flightless birds: the penguin, the dodo, the ostrich… the list goes on. There are no flightless bats. And no one has ever discovered a flightless pterosaur… until now.

But the short answer to your question is: no confirmed flightless pterosaur fossil seems to have been discovered so far.
The longer answer is: from what I can tell no pterosaur has been found that was clearly flightless, but pterosaur flight isn't well-understood in the first place so there is debate as to how and whether some specimens could have flown. It seems to be the consensus so far that they did fly however (based on the lack of mention of flightlessness on the Wikipedia page, and the last paper I link to in this answer is fairly convincing).
As far as not finding flightless specimen, the above link claims to have found one but the source is not reputable and I found no confirmation of it elsewhere (Wikipedia confirms, and I'm usually all about Wikipedia but here the page has all the hallmarks of having been written by the same person who wrote the blog). The same author argues a large pterosaur is flightless here, but their arguments are quite poor compared to others made in the field and they seem again to be the only ones making them.
Here is a post from Tetrapod Zoology in 2008 imagining what a flightless pterosaur might be like, and also claiming none have been found:

Long-time readers will know that I am an unashamed fan of both speculative zoology, and of Dougal Dixon’s hypothetical ‘alternative’ animals. Inspired by a comment made here in August by Jenny Islander, I have been having a re-think about the possible evolution of flightless pterosaurs: the fossil record gives no indication that such animals ever existed, and maybe they didn’t, but that hasn’t stopped people from speculating.

A similar quote from the 2004 book "Posture, Locomotion, and Paleoecology of Pterosaurs":

So far, there is no example of flightless pterosaurs.

The Wikipedia page for pterosaurs makes it clear how hard it is to figure out how pterosaurs flew.
Here is one of the main arguments that the largest pterosaur Quetzalcoatlus northropi was flightless

The estimated mass for the largest pterosaur known, Quetzalcoatlus northropi, exceeds the previous highest estimates by more than 100%, and it is argued that this extremely large pterosaur is better interpreted as a secondarily flightless form.

And an argument that the largest pterosaurs would have been flightless based on a comparison to modern oceangoing birds:

Our result therefore casts doubt on the flying ability of large, extinct pterosaurs. The largest extant soarer, the wandering albatross, weighs about 12 kg, which might be a pragmatic limit to maintain a safety margin for sustainable flight and to survive in a variable environment.

This paper summarizes the debates and argues against those assessments (the whole paper is worth reading actually):

While the conclusions on giant pterosaur flight by Chatterjee and Templin [19], Sato et al. [17], Henderson [25] and other workers using avian analogues for pterosaurs are not without merit, we find that they leave themselves open to criticism by not considering alternative data sources when making inferences about the palaeobiology of extinct animals. Giant pterosaur anatomy, functional morphology and, in the case of Pteranodon at least, sedimentary context all indicate that they were flighted animals and, likewise, clear anatomical distinctions between birds and pterosaurs indicate that only basic mechanical details can be treated interchangeably.

+1 for skepticism about the pterosaur heresies, which is "wrong in just about every detail ... It’s just bad science"

Two more flightless pterosaurs have been discovered.
Alcione is a flightless nycotosaur.
http://reptileevolution.com/nyctosaurusUNSM.htm
PIN 2585/4 a flightless unnamed anurognathid
http://reptileevolution.com/jeholopterus-CAG.htm

Can you provide peer-reviewed evidence here for flightlessness here, rather than just links to your own webpage.

Sorry, but no. A ms. describing one were rejected because I had not seen the specimen recently, after I had seen it a year earlier. That bogus rejection was only one of the reasons why I decided to start the web page. All the data is there for anyone to judge the validity of the reconstructions.


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Do we need to drink less water in humid weather than in dry weather?
From my understanding, humid weather means that the air has a lot of water in it. Therefore, someone who lives in this kind of weather would be hydrating himself just by breathing.
Does that mean that, to stay hydrated, one needs to drink less water in humid weather than in dry weather?
Of couse, I know that humid weathers are usually hotter, which accelerates dehydration. But in this case, let's assume the temperature is independent of the humidity of the air.

I think it depends.  At least from personal experience, I seem to need more water in dry cold than humid.  And in hot, humid weather, I seem to lose more water by sweating simply because the humidity makes the cooling process less efficient than it would be in dry air at the same temperature.

@jamesqf You seem to lose more water in moist weather but actually you lose more in dry weather.

You don't get hydrated by breathing moist air. That may at best hydrate your respiratory tract. You should drink more water in dry weather because the body gets dehydrated more.
Humid weather is not hotter, it just feels more uncomfortable. But dry heat is actually more harmful, because it dehydrates you (not in the sense of extreme heat).

It all sounds plausible, but do you have references to back this up? Particularly, when I am hiking in humid Florida or Maryland I drink many liters of water a day. The thing is that sweat doesn't evaporate and it seems the body is simply only heating up. In dry heat, however, sweating is way more efficient as evaporative cooling is always more efficient in dry climates, such as in most parts of Australia. When I hike in Australia, I do not particularly drink more, on the contrary even, in similar temperatures. Anecdotal stuff, but still something to contemplate about, perhaps.

@AliceD I didn't see any reference. I'll look up; I am not sure if there is actually some review on this. At very high temperatures moist heat would be more damaging (because of specific heat of water) but drinking water per se just hydrates your body. I don't think it has a direct role in bringing down temperature unless of course you are drinking cold water.  This is all based on the physics of it. I'll look for a reference.

Not referenced, but MIT indicates it is unclear which climate makes you sweat more, http://engineering.mit.edu/ask/why-do-we-sweat-more-high-humidity

@AliceD You do apparently sweat more in humid climate because the water doesn't get evaporated. Dehydration is more in dry clmate.

Yes exactly my point: perspiring equals dehydration. The question then becomes, due to the inefficiency of perspiring in humid envrionments whether you perspire more in humidity, or whether it only seems so because it won't evaporate.

@AliceD You apparently sweat more because the sweat doesn't evaporate. The principle is similar to osmosis if you see. You may notice that though humid heat is uncomfortable, there are less incidences of heat strokes and heat cramps (anecdotal).

@WYSIWYG If I get you right, you're saying that we perspire the same in dry and humid weather. If that's so, then why does dry heat dehydrate us more than humid heat? Shouldn't they dehydrate us the same?

@Zenadix dehydration is not just because of perspiration. You would get dehydrated if you are in a dry atmosphere. Heat increases the evaporation rate. After a particular limit of dehydration perspiration reduces (see this article) but dehydration nonetheless happens. Imagine keeping a tomato in a dry condition versus keeping in moist condition. Tomato doesn't perspire but will nonetheless be dehydrated in the dry condition. I'll add this point to the answer in a while.

First of all, we sweat as a method of normalizing/reducing our body temperature caused by the situ temperature, outside of our bodies. This mechanism, is primarily completed with thanks to the Eccrine sweat glands - those that cover the greatest majority of the body and hence, are the most essential in this context.
Sweating is classed as 'evaporative heat loss' so, the correct conditions have to apply in order for the mechanism to effectively occur.
Humidity: The common perception is that we sweat less in hot and humid conditions since, "the sweat just sits there", inferring that we are perspiring at a slower rate. However, it's the complete opposite. This is because, in the stated environmental conditions, the ambient water vapor pressure is greater and resultantly, the body needs to increase the area effected by perspiration -- the sweat rate increases -- thus to match the same effect that you'd experience in hot, dry conditions. The affinity for the evaporation product to attach to molecules in the air is less due, to there being more water molecules already present in the air. It's a bit like how water in cells moves from areas of high potential to low water potential.
Dry:
The body can more efficiently cool itself in this environment. This is due to fact that dry air has a greater affinity for water molecules so, the sweat will evaporate quicker. Additionally, this has a knock-on affect on salivary glands and furtherly, the humidity of your essential respiratory organ, the lungs - causing dryness. This is very prevalent when breathing heavily e.g. in exercise.
This is very similar to hygroscopy.
To conclude, you need to drink more water in hot, humid environment than the contrary.
If my answer is too "generalized"; i apologize.
Citations:

Eccrine sweating
Jay Hoffman in Physiological Aspects of Sport Training and Performance


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Trisomy 21 and Down syndrome
Can Down syndrome occur without trisomy 21 in the karyotype of an individual? Or vice versa can a person have trisomy 21 while unaffected by Down syndrome?

First question: No, all Down Syndrome patients have a inappropriate duplication of part or all of chromosome 21.
Second Question: More complicated.  The phenotype can vary in severity depending how much much of chromosome is duplicated, whether it is duplicated and stuck onto the end of chromosome 14 (translocation vs. non-disjunction).  Lastly, a rare form of this event is defined by incomplete penetrance or mosaicism of cells that contain duplication.  Short Answer: No, In rare cases, a carrier can pass on trisomy 21 without being affected themselves but they themselves are a "balanced carrier" and don't have extra chromosome 21 material. See last paragraph below from the NIH and this quote from the Mayo Clinic:

When translocations are inherited, the mother or father has some rearranged genetic material, but no extra genetic material — this means he or she is a balanced carrier. A balanced carrier has no signs or symptoms of Down syndrome, but he or she can pass the translocation on to children, causing extra genetic material from chromosome 21

Types of Down Syndrome details from: NIH Down Syndrome Information Page

Research shows that three types of chromosomal changes can lead to Down syndrome.
Complete trisomy 21. In this case, an error during the formation of the egg or the sperm results in either one having an extra chromosome. So after the egg and sperm unite, the resulting cells will also have three copies of chromosome 21. The complete extra copy of chromosome 21 is in all of the person's cells—or a complete trisomy. Complete trisomy 21 is the cause of about 95% of Down syndrome cases.1,2,3
Mosaic trisomy 21. Not every cell in the body is exactly the same. In about 1% of Down syndrome cases, most of the cells in the body have the extra chromosome, but some of them don't. This is called "mosaicism." Mosaic trisomy 21 can occur when the error in cell division takes place early in development but after a normal egg and sperm unite. It can also occur early in development when some cells lose an extra chromosome 21 that was present at conception. The symptoms of someone with mosaic trisomy 21 may vary from those of someone with complete trisomy 21 or translocation trisomy 21, depending on how many cells have the extra chromosome.1,2
Translocation trisomy 21. In this type of chromosomal change, only part of an extra copy of chromosome 21 is in the cells. The extra part of the chromosome gets "stuck" to another chromosome and gets transmitted into other cells as the cells divide. This type of change causes about 4% of Down syndrome cases. There are no distinct cognitive or medical differences between people with translocation trisomy 21 and those with complete trisomy 21.
Sometimes, a parent who does not have Down syndrome may carry a translocation in chromosome 21 that can be passed on to children and cause Down syndrome. Studying the parents’ chromosomes can reveal whether this is the cause of the syndrome. A genetic counsellor can assist families affected by translocation trisomy 21 in understanding the risk of Down syndrome in future pregnancies.1,2,3

Added EDIT:

Also important to note that people can have trisomy 21 develop in somatic cells spontaneously, later in life without having most of the effects of DS. But this can significantly predispose to leukemias shown here, which is an interesting area of study.  Thanks to @The Nightman.

@user5034361 Great!  Welcome to Biology!

What is xsome? I don't think it is a standard term for chromosome. I edited all instances. (When I google "xsome" I get hits about threesomes and foursomes :D)

Thanks WYSIWYG, its holdover shorthand notation from a professor of cell biology I had 25 years ago!  Some habits are hard to break. Sorry for the confusion.  Good catch on the British spelling of counsellor.  Odd that the NIH info page didn't catch that, but since it is a direct quote, probably not good to change.

Also important to note that people can have trisomy 21 develop in somatic cells spontaneously, later in life, and this can predispose to leukemias. 'http://download.springer.com/static/pdf/94/art%253A10.1007%252Fs00431-014-2430-3.pdf?originUrl=http%3A%2F%2Flink.springer.com%2Farticle%2F10.1007%2Fs00431-014-2430-3&token2=exp=1445874867~acl=%2Fstatic%2Fpdf%2F94%2Fart%25253A10.1007%25252Fs00431-014-2430-3.pdf%3ForiginUrl%3Dhttp%253A%252F%252Flink.springer.com%252Farticle%252F10.1007%252Fs00431-014-2430-3*~hmac=170badd7df784094a3e026e183dbda9936a844a8add14ad5640fd6b7bb690032'


text:
What is the normal blood water content
What is the normal water volume per 1 L of blood, and how much deviation from that norm causes dehydration or hyponatremia?

The human blood contains about 45% of erythrocytes and 54.3% of plasma by volume. The plasma contains about 92% water, while the erythrocytes, about 64% by weight.
The blood is slightly less than 80% water.
Dehydration occurs when water intake is insufficient to replace free water lost due to normal physiologic processes (like sweating, urination etc). Hyponatremia is low sodium concentration in the blood. Usually, the Sodium and water concentrations in blood are regulated independently. Hyponatremia can be caused by intake of to much water, which reduces the sodium concentration.
References: The sodium, potassium, and water contents of red blood cells of healthy human adults by L J Beilin, G J Knight, A D Munro-Faure, and J Anderson, J Clin Invest. 1966 Nov; 45(11): 1817–1825.


text:
Why is wind cold for humans?
Coming out of the pool the other day, I felt very cold because I was wet and the wind picked up. My idea is that a "cold" feeling should be associated with low temperatures, but it's indeed wrong.
Why do we perceive wind at a farely normal temperature as cold?

Evaporation of water..

So why would it be worse if I'm wet?

@SolarLunix I got what you mean, but still it is not clear how a bigger evaporated mass of water should cause my body temperature to fall or give me the perception of this happening

Is your question why does wind feel cold or why do we feel cold when we're wet?

I'm voting to close this question as off-topic because it is about physics

You don't just feel colder, you ARE colder, or at least your skin is.  It's not just a human thing: hygroscopes & wet bulb thermometers use the same phenomenon to measure humidity & dew point, evaporative coolers use it to cool homes, refrigerators & air conditioners use it with other refrigerants than water...

Whatever this question inclosed for, I just wish to raise attention that this should not be closed because it is physics. It is psychophysics and sensory systems deal with physical stimuli.

@AliceD: But it's not about sensory systems, really.  That is, the perception of cold is not some sort of illusion: the temperature receptors in the skin are accurately reporting a lower temperature due to increased evaporation.  A thermometer on the skin would report the same thing.

@jamesqf - exactly my point. That is why it should not be closed, as this question is exactly borderline Biology. If one asks what the wavelengths are recognized by the retinal photoreceptors, it is also not closed because it is physics.

@AliceD: True enough, and I wasn't suggesting it be closed.  It's just that there are really two separate questions implied here: 1) How do we sense temperature? and 2) Why does evaporation cause cooling?  Now if the OP wants to know the answer to #2, that's a physics question.  But if s/he's more interested in how temperature is perceived, that's a biology question.  (Just as explaining how photoreceptors work gets us into chemistry.)

the question is based on a false premise (that the air temperature alone determines the temperature experienced) see also: http://meta.biology.stackexchange.com/questions/3111/not-all-questions-featuring-something-biological-are-biology-questions?cb=1 your question could easily be reformated as "why does something cool down more quickly when wetted or blown on?" which is a physics question

One important point that you might not be considering is the heat of vaporization.
You may be aware that while it normally takes 4.18 J (1 calorie) of heat to raise 1 gram of water 1 °C, it takes around 2250 J of heat to raise 1 g of water from liquid at 99.5 °C to gas at 100.5 °C, due to the energy needed to go from a liquid to a gas. - What you may not know is that the enthalpy of vaporization isn't limited to vaporization at the boiling point. Any conversion of water to water vapor requires heat of vaporization, though exactly how much is temperature dependant.
So when water evaporates, it cools things much more than one might expect from the "average" energy (or even statistically above average energy) a water molecule may have in the liquid state - several hundred times more. All this is driven by the entropic benefits of having water molecules in the gaseous state rather than the liquid state.
Wind makes the process more efficient because it removes the water-vapor laden air, unbalancing the equilibrium of the process in favor of further evaporation. More water makes it more efficient (to a point), because there's more water to evaporate and the rate of evaporation increases, increasing the removal of heat.
This is not just a physiological perception effect - one can actually measure the temperature drop when water evaporates. Evaporative coolers make use of this effect, and traditional wet-bulb hygrometers (psychrometers) use exactly this effect to measure the humidity -- in some cases you can get a temperature differential of 20 °C or more between a dry bulb thermometer and a wet bulb thermometer.
There is a small perceptual effect in that the evaporative cooling is happening on your skin, where a large number of temperature receptors are located. Therefore, your skin (and temperature receptors) feel a cooling effect even if your core temperature doesn't change detectably. Local cooling produces a larger temperature change than might be expected if you calculated for a whole-body heat change.

This is what I wanted. Love it! Thank you very much!

"takes around 2250 J of heat to raise 1 g of water from liquid at 99.5 °C to gas at 100.5 °C" wow! very new to me.

This phenomena has nothing to do with any different kinds of receptors.
When we are wet, we have lots of water on our surface. The evaporation of water causes cooling.
Blowing wind tends to make evaporation faster. So, even if wind blows at normal temperature, we feel cold. If we are not wet, there is some water on our body surface. This water is low in quantity as compared  to when we are wet. So, we feel less cooling this time.
Also, water has high specific heat i.e. it doesen't change temperature very easily. So,even on a warm day, we don't feel the heat if we are soaked.

It is not clear to me as why water evaporation should cause cooling. Could you please explain this point more thoroughly? Thank you.

The surface molecules can escape out only if they have energy high enough. So, if they leave the surface, some energy is lost. this loss causes cooling.

Change in Energy = Change in Mass * Specific Heat * Change in Temperature. In this case, the energy is high in comparison to mass. So loss of 1 molecule can't compensate the loss of energy so there is slight change in temperature. Effective movement of lots of water molecules result in cooling

At normal conditions, there are equal no. of water molecules leaving and arriving at the surface. So, no change in temp. at normal conditions.

The equation that you cite is an experimental law valid in macroscopic systems which have fixed mass, mixing these results with microscopic analysis often leads to discrepancies. Of course one high energy molecule is lost, but it is also one that required more energy for its temperature to be maintained.

As other answers and comments have stated the reason that you feel cooler when the wind is blowing (wind chill factor often gets talked about on the news) is because evaporation is speed up by the wind. The reason that this evaporation causes cooling (explained in more detail here) is because when water evaporates, that water takes its energy with it. That energy loss to you is in the form of heat, thus making you feel colder.
However, there is a little bit more to it than that. If you look on How stuff works - windchill factor they go onto to talk about how the process of convection is what makes you feel cooler. What's happening is you're actually warming the air around your body up, and as the wind blows it's wisking that nice warm air away from your body replacing it with much colder air. The faster the wind blows, the faster your warm air is taken away from your body. When the wind blows fast the molecules around you move away from you faster so you have less time to heat them.
How Stuff Works says this about convection:

Convection - Convection is a property of liquids and gases. It occurs
  because when a liquid or gas gets hot, it tends to rise above the rest
  of the body of liquid or gas. So, if you have a hot bowl of soup on
  the table, it heats a layer of air surrounding the bowl. That layer
  then rises because it is hotter than the surrounding air. Cold air
  fills in the space left by the rising hot air. This new cold air then
  heats up and rises, and the cycle repeats. It is possible to speed up
  convection -- that is why you blow on hot soup to cool it down. If it
  weren't for convection your soup would stay hot a lot longer, because
  it turns out that air is a pretty poor heat conductor.

So while evaporation plays a minor roll, it's most likely because you're no longer able to heat up the air around you as efficiently when the wind blows all that nice warm air away.

The distribution of the speed of the molecules is Maxwellian, and the variance should not be very significant, meaning that the molecule speed should not vary consistently from the average speed. At least, not enough to modify the average temperature by many degrees. Am I wrong?

The thing is that it won't modify the average temperature very significantly, but it will make it feel slightly colder. It's really about perception. We may not see a significant change in actual temperature, but we can feel the small difference. (Like some of us are freezing at 71F but feel perfect at 72F - that one degree F difference (which is only a fraction of a degree C) makes a huge difference in how we feel). @bharb

I wouldn't call the sensation of being hit by a strong wind a feeling of slight change in temperature. It can be quite drastic, depending on the speed of the wind.

@bharb I've changed my answer.


text:
Structure of Cell
Are cells spheres or ovals/circles bound by phospholipidbilayer?
If they are spherical how are we able to see the nucleus through the phospholipid bilayer under a microscope?

It will largely depend on the type of cell!

Are guard cells spherical (completely bound by phospholipidbilayer)?

Many cells are spherical, but there is some variation.  Curiously, bright light often travels through all the structures of a cell.  In order to see things, the easiest way is to add some stain, which binds up to specific parts of the cell.  That way you can see the nucleus.  If you use dimmer light, or some other technique (eg cross polarization), you can sometimes see some structure as darker patches, but cells are translucent.

Not exactly.  That is a stereotype of cells.  Muscle cells are not round nor oval, but rather elongated rods.  If you were to look up epithelia cells, you can quickly see that cells are grouped based on their physical characteristics; simple (round/oval & single layer), columnar, and cuboidal to name a few.  Cells come in many shapes and sizes.  As Hans stated, stains are vital in viewing cellular components.  There is a diverse amount of stains used - which all carry a purpose and benefit in a specific application.

As MG_MD already pointed out, cells come in all shapes and sizes.
Take for example this image of a neuron. The central cell body contains the nucleus and is surrounded by a network of extensions called neurites which form neural networks. The extensions and the cell body have been stained fluorescently to make the cytoskeleton visible:

photo credit: ZEISS Microscopy/flickr (CC by SA 2.0)
The reason why we are able to see inside them is because the plasma membrane (a phospholipid bilayer) is transparent. Check out this website for some nice movies of cells moving under the microscope. In the left of these movie (keratocytes) you can clearly see that the cells have a bulge where the nucleus is which is surrounded by a flat so called lamellipodium giving the cell and overall "fried-egg"-like shape.
The only time when most cell types are rounded is during cell division. This is to make sure that the cells divide evenly and each daughter cell gets an exact copy of the DNA.


text:
Does RNA serve as the genetic material of some plants and animals along with viruses?
My teacher mentioned that some plants and animals have RNA as genetic material but did not substantiate his statement  with examples. I'm wondering if it is so?
I have searched the internet but have found no such information.

There are no animals or plants with RNA genomes. There was a mistaken belief in the 1920s that plant genetic material was RNA whereas animals had DNA, but this was finally disproved by JN Davidson in the 1940s.


text:
What does differentiation of B-cell mean?
Does differentiation of B lymphocytes mean the formation of plasma cells and memory cells by matured B lymphocytes?

Immature B lymphocytes mature into either plasma cells or memory cells. If a B cell is mature, that means it's already a memory or plasma cell.

Could you cite some references?


text:
What is meant by topographic barrier?
There are three types of barriers, physical , climatic and biological barriers that can prevent the dispersal of organisms.
Topographic barrier falls in the category of physical barrier but exactly what should be considered as topographic barriers is not clear to me.
The source from which I actually came across the term says that mountain range is a topographic barrier like the Himalayan range separating the North-asian fauna (partly Palearctic fauna) from the Oriental fauna. But what else falls under topographic barriers is my question?

Topograhpy refers to earth's physical features and a topographic barrier refers to physical features that prevent free movement from one position to another. As GForce pointed out, whether or not something is a barrier can depend heavily on the animal in question. A long, wide canyon can be a barrier for squirrels, but not for birds.
Think of topographic as referring to features on a map, which is a type of topological graph.

Whether something is considered a topographic barrier for an organism depends on the species being considered and its ability to traverse the terrain from one side of the barrier to the other. There's no blanket classification of what is considered a topographic barrier and what isn't.
For example, a certain mountain range may be a topographic gradient to a salamander (due to limited food, extreme weather conditions, etc.), but these same mountains might not be for a brown bear.


text:
Identification of brown film inside a plastic water bottle
What could this film be at the base of a plastic water bottle?

Also observed one around the neck.

Is it possible to you to see them in a microscope?-No.They were inside.

I did understand what you said. No, it is not possible to view the film under microscope.

It could be algae or bacteria film, but also ironoxide.


text:
Usage of the terms: Enhancer, Upstream activating sequence and Downstream activating sequence
From wikipedia

An upstream activating sequence or upstream activation sequence (UAS) is a cis-acting regulatory sequence. It is distinct from the promoter and increases the expression of a neighbouring gene.

Again,

In genetics, an enhancer is a short (50-1500 bp) region of DNA that can be bound by proteins (activators) to increase the likelihood that transcription of a particular gene will occur.

I find no difference between them, are they synonymous ?

Due to its essential role in activating transcription, the upstream activating sequence is often considered to be analogous to the function of the enhancer in multicellular eukaryotes.

There appears to exist another kind of regulatory sequence, downstream activating element.I think it's another synonym for enhancer located downstream the transcription start site.


text:
Why do Indian Major Carps spawn in running water?
I think running water serves as a cue necessary for hypothalamus to release GnRH into hypophyseal portal system which initiates a cascade of hormone actions ultimately leading to release of gametes.
I have looked up in Internet with no results. I guess no work has actually been done to discover the reason. But as it's an assumption I would like to here from anybody more specialised.

Some fish spawn in running water for a simple reason: There eggs need oxygen and survival rate will be low under hypoxic conditions. Running water has a much lower change of becoming hypoxic than standing water, so that is why many fish spawn in running water. Some fish of standing water, like sticklebacks, wave fresh water over the eggs to achieve the same.
How they sense oxygen level is another matter. In fish, the neuroepithelial cells (NEC) have been implicated as the major oxygen sensing cells. See wikipedia above and specifically this if.you want to know more.


text:
What is open complex in E.coli DNA replication?

The E.coli DnaB helicase is essential for replication initiation from the chromosomal origin of replication ( oriC ) and is present in vivo as a protein complex with six monomers of the DnaC ATPase protein and six ATP molecules (Wickner and Hurwitz, 1975; Lanka and Schuster, 1983). DNA replication initiation at oriC begins with binding of multiple molecules of the bacterial DnaA initiator protein to a 9 bp repeats (DnaA boxes). This binding promotes destabilization of nearby AT-rich sequences, resulting in unwinding of the DNA double helix and the formation of an open complex.

I looked up in DNA Replication by Arthur Kornberg, Tania A. Baker (the authors who probably coined this term), Google and Google.Scholar but didn't stumble upon any definition.
What is it actually?

The sentence itself is actually the definition of open complex: It is the structure that is created once the DNA double helix is unwinded due to the DnaA proteins.

This binding promotes destabilization of nearby AT-rich sequences,
  resulting in unwinding of the DNA double helix and the formation of an
  open complex.

I have also found a papera co-authored by Arthur Kornberg himself where the authors self-define "open complex" as well:

Three tandem repeats of a 13-mer in the AT-rich region are essential
  to the unique replication origin of E. coli and of remotely related
  Enterobacteriaceae. These iterated sequences are identified by
  deletion analysis and sensitivities to endonucleases as the site for
  initial duplex opening by the initiator dnaA protein. This “open
  complex” requires ATP and 38% for optimum formation and stability.

There are several papersb,c that use "open complex" in the same way.
References:
a David Bramhill, Arthur Kornberg, Duplex opening by dnaA protein at novel sequences in initiation of replication at the origin of the E. coli chromosome, Cell, Volume 52, Issue 5, 1988, Pages 743-755, ISSN 0092-8674, http://dx.doi.org/10.1016/0092-8674(88)90412-6.
(http://www.sciencedirect.com/science/article/pii/0092867488904126)
b Ozaki, Shogo, et al. "A common mechanism for the ATP-DnaA-dependent formation of open complexes at the replication origin." Journal of Biological Chemistry 283.13 (2008): 8351-8362. (http://www.jbc.org/content/283/13/8351.full)
c Mukhopadhyay, Gauranga, et al. "Open-complex formation by the host initiator, DnaA, at the origin of P1 plasmid replication." The EMBO journal 12.12 (1993): 4547. (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC413885/)

Thank you. Hope you don't mind if I take some time to respond to your entry.

An open complex is the complex of RNA polymerase and one DNA strand (antisense strand). Whereas closed strand means that RNA ploymerase is attached to both strands of the DNA.
Procedure: RNA Polymerase first creates the closed compex.
Then open complex is created when the double stranded DNA is separated to two strands.

I saw this term used in transcription too. But I'm interested in replication solely.


text:
I brought a hibernating yellow jacket queen into my house accidentally. What will happen?
There was apparently a hibernating yellow jacket queen in my stack of firewood outside.  An hour or so after bringing in the firewood, we saw the queen fly off into the house, where we can't find her.
What will happen?  Will she lay her eggs and start a nest somewhere in our house?  Will she just find somewhere and go back to sleep?

I'd just sell the house and move as quickly as you can... ;)

lol, that doesn't seem like too bad of an idea at the moment :-)

She will likely die somewhere unseen in the house, probably by a window. She won't dive bomb anyone, though, if that's what you're worried about. We used to find a dead queen every year in our old house. Never understood why.

Well; if mostly your house is sanitized; poor queen will die somewhere in the house. Queens are not "designed" to attack; so I wouldn't have worried about it if I were you........Only, I couldn't get my eyes closed at night :D.

Yellow jacket is a very general term, that covers a wide variety of species with different biologies. Can you be more specific?