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How to correctly and accurately identify a few species of trees from their leaves?
I want to identify a tree from one of the 12 species listed based on observing their branch and leaves. Is there quick and neat way to do it?
Red Oak, White Oak, Red Maple, Striped Maple, Tulip Poplar, Black Cherry, White Pine, Virginia Pine, Dogwood, Hickory Species, Sourwood and Cucumber Magnolia.
Thank you!

Yes. Get examples of each tree (or Google), then memorize their structure and features. It's quite easy...

Becoming familiar with the leaves and bark of various trees really is the best way of identifying them, even if you just know it's an oak tree, for example, but not what kind, as all oaks have the same basic leaf structure. Learning to identify the subtypes just takes a little more work.

@MattDMo I understand, but that should be so obvious of a method as to not warrant a question, at least not in a day and age of Google. Say I was going on a trip to the American Southwest and I wanted to be able to identify the different types of Cacti, I'd do a few Google searches. I think we need to start a stack for questions on how to do basic queries. There is only one thing that I can think of that would warrant that, and it is if the OP is in a country that censors sites such as Google, etc. What we take for granted in Western countries cannot be taken for granted elsewhere.

@AMR let's discuss this more in chat - it's not really pertinent to this question.

This online key (and app) can probably help you: Arbor Day Foundation: What Tree Is That?

@MattDMo actually oaks have wildly different leaf structures.  See *Q. phellos, Q. nigra, and Q. Michauxii as examples. However many oak species found in the Appalachians and surrounding  southeastern and mid Atlantic piedmont (where the OP is certainly located) do typically have a fairly standard 'shape'  (though not to a novice)

A good first step is to pay attention to common differences between tree structure:

Alternate vs. Opposite structure

MADHORSE = your common eastern US opposite-leaved trees are Maple, Ash, Dogwood, and Horsechestnut (AKA buckeye).

Simple vs. compound leaves

Toothed ("entire") vs. untoothed leaves

Lobed vs. unlobed leaves

Differences in texture, hairiness, & color of leaves

both b/w species and b/w top/bottom of leaves of the same species

Generally when you come across a new tree in Eastern N. America I'd recommend going through these steps:

Is it alternate or opposite?
Is it simple or compound?
Is it toothed, doubly-toothed, or smooth along the edge?

If you can answer yes to (any or all of) those questions you typically SIGNIFICANTLY reduce your options.
You also want to make sure you're aware of large variations in some species (especially oaks and hickories). One good example is the difference in shape, texture, and color of sun leaves vs. shade leaves of many species.
Importantly, paying attention to WHERE the tree is located (and what else is growing around it) as this can really help narrow your choices. You'll also start recognizing common cohabitants of certain habitats.
Finally, don't be afraid to use your many senses (smelling, feeling and even tasting) -- though get to know poison ivy well before you start licking plants!!

Ok, now for some useful hints:

Red Oak = stereotypical oak shape (i.e., pinnately lobed), smooth on both side of leaf, lobes are not deep. You'll find 'spikes' at the end of each lobe. Bark looks like it has vertical shiny stripes.

White Oak = rounded SMOOTH lobes. Bark light grey/white with flaking appearance when mature

Red Maple = OPPOSITE. Leaves serrated (toothed). Smooth grey bark (with few low-hanging branches)

Sugar Maple = OPPOSITE. Leaves NOT serrated. Smooth whiter grey bark.

Striped Maple = OPPOSITE. Maple-like shape, but with rounded/butt-shaped (cordate) base. Bark = very striped in appearance.

Tulip Poplar = Leaf-shape looks like a tulip flower. Tree tall and straight.

Black Cherry = Oval/round leaves with fine single-toothing along edge. Tuft of brown/white fur along mid-rib on underside of leaf. Bark = horizontal striping due to lenticels; gets flaky when mature. Bark/twigs have strong bad smell when scratched (cyanide).

White Pine = 5 relatively long wispy needles per cluster.

Virginia Pine = 3 Short, dense needles per cluster.  Bark has cornflake appearance.

Dogwood = OPPOSITE. round leaf with deep ribbing veins and drip tip. Leaves often look to be growing in pairs. If you pull a leaf apart carefully, you'll find some thin tissues dangling between the halves. The bark is cobblestone (mosaic bumpy) and the shape of the tree is typically flat-umbrella-esque.

Hickory Species = VERY DIFFICULT TO TELL SPECIES APART (though I can give you a bunch of hints to help). Fairly easy to tell apart from other species, though. Is ALTERNATE + COMPOUND with generally 5-9 leaflets per leaf. (unlike ash = opposite/compound or walnut = compound with MANY leaflets). Leaves often carry some odor and large seeds can be found nearby

Sourwood = Long, oval, tiny-toothed leaves that have strong sunken midrib and thin leaf texture. Tastes very sour. Bark is dark and ridged, and trunks very rarely grow straight (so look for crooked or leaning trees!).

Cucumber Magnolia = Look for LARGE, strongly veined leaves that are often drooping. Look for circular ring (stipule scar) beneath leaf petiole base.

Old post, but this is a ridiculous resource.


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Since nature highly favors the pyranose forme of Ribose, what explains the fact we find it in the form of furanose in DNA and RNA?
I read in my notes that relative abundance of ribopyranose represents about 80% of all ribose in solution (including the alpha and beta anomeres).
I'm curious as to why evolution favored the use of the least abundant conformation for DNA and RNA.
Do we have enzymes that convert pyranose to furanose in order to achieve this? or are we just using the furanose?
Thank you,
Pierre-Eric

Because the ribose in RNA is a component of a nucleotide and is not a molecule unto itself. It has the 5' phosphates and 1' nitrogenous bases attached, and those functional groups will alter the conformation of the ribose in the nucleotide.

But then, my question should be read like this:
Is the cell using ribofuranose or ribopyranose  in the synthesis of nucleosides?
and if it is the latter, how.... or when is it converted?
or even... does the cell synthesize nucleosides at all? Or do we simply use the one we get from digestion of food?
If we do get it all from digestion, then wherever the nucleosides are formed in the foodchain, wether it is in bacterias or protozoas...
How does it go from pyranose to furanose (if the pyranose are used), and why are the furanose used and not the pyranose if it is the other way around?

Look at your textbook for the De Novo Purine Nucleotide synthesis. You do not start with ribose you start with 5-Phosphoribosyl-1-pyrophosphate and its precursor is ribose 5-phosphate. The 1,3-diaxial interactions of a C5 phosphate group likely pushes the molecule into favoring the furanose form as the negativity of the phosphate and the lone pairs on the ring oxygen are likely not very happy that next to each other to assume the pyranose conformation.

Can you provide a link to the reference that says that pyranose structure is more abundant? That may be true but I am not too sure about it.

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Effect of cellular phone towers on human health
We live in world of mobiles, tablets, PCs and other electronic gadgets. We are continuously exposed to radio frequencies and other cellular frequencies. Generally, all of these waves are very low energy / long wavelength (which makes them non-inonizing). This makes them less probable agents to cause any health problems.
I have been searching for potential effect of cellular phone towers on human health. Towers will emit large number of such waves due to our daily usage of electronic devices. The International Agency for Research on Cancer (IARC) has reported cumulative radiofrequencies are categorized as class 2B (possibly carcinogenic to humans). Does this mean people living near cellular phone towers are more prone to health hazards?
I was searching for scientific reports to support or deny any claim made here. I checked the FDA website for guidelines:

Under the law, FDA does not review the safety of radiation-emitting consumer products such as cell phones and similar wireless devices before they can be sold, as it does with new drugs or medical devices.... FDA shares regulatory responsibilities for cell phones with the Federal Communications Commission (FCC)

However, the FCC guidelines state:

The FDA, which has primary jurisdiction for investigating mobile phone safety, has stated that it cannot rule out the possibility of risk

And there are lot of other links to other organizations. I couldn't find any citing of scientific paper. This, again, made me confused as to whether cellular phone towers are safe for people living around them? How does the 'non-thermal' effect of this radiation work? There are few reports (like this and this) which I found but they didn't seem convincing.

I suggest using Google scholar search to find a review paper which will summarise studies done in the area before. If you want to save time you can answer your question by reading the abstract and the conclusion. Good luck!

Well.. I don't know why you tagged this question with [tag:cancer]. Microwaves can have some harmful effects but carcinogenesis is not one of them. MW do not have enough energy to cause electronic transitions that can cause DNA damage or produce free radicals.

Possible duplicate of http://biology.stackexchange.com/q/36394/3340

@WYSIWYG I used cancer tag because only health hazard I was able to find with reliable source is "possibly carcinogenic" remark from IARC (as mentioned in question). Also I know that companies requires NOC (No objection certificate) from radiologist or radio oncologist.

Possible duplicate of http://biology.stackexchange.com/q/39422/3340 as well

C'mon, how is that duplicate? There discussion is about different kinds of radiations.

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Does the human body metabolize what it smells, even in trace amounts?
I conjectured to a friend that some small amount of anything we smell is likely metabolized by the body. He disagreed. My thinking is that, if you are smelling something, some portion of molecules are being sensed by the olfactory tissue and some portion is taken into the lungs. Of the portion taken into the lungs, some portion is exhaled and some portion remains. I didn't propose a mechanism for the part that "remains" at the time, but it seems reasonable that some of it gets caught in mucus, some of which is then swallowed.
Obviously, a very, very small portion of whatever we're smelling would go through this process if my conjecture is even correct. For context, we were discussing people who have elected to restrict their diets for ethical or similar reasons. I was comparing what I proposed to when food products are labeled with "may contain trace amounts" due to "shared equipment".
So I guess my questions are these: was I right in my guess, and if so, was the mechanism correct or not?

Olfaction is the result of the neuronal impulse of ligand / receptor binding. To smell something requires 1) Specificity between the receptor and the ligand, 2) Concentration of the ligand molecule, and 3)The receptors that are on the surface of neurons in the olfactory bulb.
As for metabolize, then you need to be much more specific in defining what you are considering metabolism. Is the molecule broken down further; does it pass into the cells directly; does it need to be the unaltered molecule to qualify as metabolizing the molecule that you sensed as a smell.
The majority of our mucus in our airways is moved to the digestive tract as the result of ciliated epithelial cells "sweeping" the mucus and everything trapped in it to our esophagus, where it goes into the stomach and is digested. It is hard to say whether or not the molecules that you detect as smell are reactive, and if they are, whether or not they would chemically react with something else before it got to your stomach.
Also the volatile chemicals which you sense as an odor, aren't necessarily what would constitute the substance that they emanated from. So I would probably argue against your conjecture that someone who decides to be vegetarian or who has a peanut allergy is metabolizing something just because they inhaled it. It is likely the proteins in a peanut that cause an allergy, and that is not what you are inhaling, and as for the vegetarian, I think the justification is that it would be the protein that constitutes the consumption of a meat and not the molecules that come from the cooked or uncooked tissue.
If you want to broaden what you are calling metabolize, then you would only need to look at inhaled medicines such as corticosteroids or compounds to bronchodilate, to make a case for the fact that you are metabolizing what you inhale.

Thanks, @AMR. Can you clarify what you mean about volatile chemicals not constituting what they emanated from? Also, are you saying that the stuff we smell is non-nutrative and non-caloric? And since the precise context of the discussion was where an ethical vegan draws lines, can we define metabolism as breaking down the molecule and using its components? I apologize for any casual or incorrectly used language. I'm rather far afield of my discipline here. I appreciate the interest in such facile and impractical question.

What I meant by volatile chemicals are just chemicals that easily enter the gas phase are the molecules we are smelling. This article might clarify a bit, though if you are interested further I would suggest a Google Scholar search of Volatile Compounds in Food. https://en.wikipedia.org/wiki/Volatile_organic_compound To the extent they may not be used by the body as an energy source then you may or may not want to classify them as a undergoing metabolic processing. To the extent that they initiate a cellular response, i.e. the olfactory nerve impulse, then they do initiate a metabolic process.

I also think that an ethical vegan needs to draw the line at their choice of what they ingest and not inhale. If they are claiming that their right to be a vegan is being violated because they have to inhale compounds from animal products, then they are going overboard, in my opinion. And if they are arguing that they are vegan even if they inhale compounds from animals, then I would say that their argument is valid. The difference between what we inhale and what we ingest are very different things, which is why municipalities have a much easier time passing no smoking laws than soda taxes.

In the end, you are really defining the terms of the debate, my suggestion was that you clarify what your terms and conditions are. Like I said, inhaled medicines can even go as far as to turn on or turn off the transcription of genes in your cells, which is a metabolic process of the cell, so you need to specify the rules in order to get a definitive answer.

It sounds like, basically, the chemicals that enter the gas phase during cooking are VOCs and cannot be used as an energy source, though they might have other effects. So I'm going with I was wrong! This really was a hypothetical debate, since I wasn't suggesting people not breath in restaurants. Thanks again!


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"Antibiotic resistance" equivalent in archaea for selection during cloning
I'm beginning to work with halophilic archaea and I'm trying to figure out a good way to select for cells that have taken up a plasmid.  Obviously, one can't use antibiotic resistance since they are not bacteria.
Is there anything equivalent I could use for + selection in cloning experiment for halophilic archaea? Usually I would use NeoR and Neo plates but that won't work...

Obviously, one can't use antibiotic resistance since they are not bacteria.

This is not so obvious. Some common antibiotics are active against archaea.1 The Halohandbook, an indispensable document for the propagation and transformation of Halobacteria, includes a list of selectable markers and their concomitant plasmids:

NovR, MevR, and TmR are genes conferring resistance to novobiocin, mevinolin, and trimethoprim, respectively.

Usually I would use NeoR and Neo plates but that won't work...

Without knowing the specific organism you are trying to clone, we can't know if neomycin resistance will work as a selectable marker. Indeed, the bacterial neomycin resistance gene Neo (encoding aminoglycoside-O-phosphotransferase) can be utilized by mammalian cells to reduce aminoglycoside toxicity2, so it's not a huge logical jump to assume that archaea could similarly use Neo.  If you are working with Methanococcus, you can take advantage of vectors encoding aminoglycoside phosphotransferases native to Methanococcus voltae to select for neomycin resistance.3

References

Khelaifia S, Drancourt M. Susceptibility of archaea to antimicrobial agents: applications to clinical microbiology. Clin Microbiol Infect. 2012 Sep;18(9):841-8.
Dulon D, Ryan AF. The bacterial Neo gene confers neomycin resistance to mammalian cochlear hair cells. Neuroreport. 1999 Apr 26;10(6):1189-93.
Argyle JL, Tumbula DL, Leigh JA. Neomycin resistance as a selectable marker in Methanococcus maripaludis. Appl Environ Microbiol. 1996 Nov;62(11):4233-7.

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Will moths evolve to become blue if we paint walls in blue?
I know dark moths are more frequent than white moths when the environment is full of dirty (dark) walls/trees; it is a consequence of natural selection. Will moths evolve to become blue if walls/trees are painted in blue?

There were a few languages issues in your post. I rewrote it (Note, btw that english is not my mother tongue). Feel free to roll back if you don't like my edits. Note that my edits will likely make future readers think you have a better understanding of evolutionary processes that you actually do.

I think the question was poorly formulated (mainly for language issues) and is quite introductory but I think it can still be answered. I don't vote to close.

Note that the following answer is an over simplification. For example, I don't consider cases of balancing selection.
What is Natural Selection?
Definition
Natural selection is the process that yield to a change in allele (≈variant of a gene) at a given locus (=position on a chromosome) frequency in a population due to a differential in fitness (≈reproductive success) between individuals carrying the different alleles.
What Natural selection does
By selecting some alleles over others, natural selection ultimately causes a decrease in the genetic variance to the extreme point where only the beneficial allele is left in the population. Of course, in the absence of genetic variance (that is if there is only one allele at a given locus), natural selection cannot act.
Where does genetic variance come from then?
If natural selection decreases genetic variance, how come there is some genetic variance left in population then. The answer is mutations.
Will the moth population become blue if you pain all walls (or trees) in blue?
Intro
The moths could vary from white to dark because there is genetic variance for the level of pigmentation in their population.
Note of course that for the blue variant to be beneficial (=to have a higher fitness) when the walls are painted in blue, you will need predators (as the moth colour evolve first as a camouflage to hide from predators) and you will need to assume that it is not too costly to produce the blue pigments.
If there is no "blue" allele
If there is a few alleles coding for being blue, then if you paint walls in blue, you will see a change in the frequency of blue individuals in the population just as we saw changes in the frequency of white/black individuals in the population.
If there are "blue" alleles
If there is no allele coding for being blue in the population, then you will need to wait for a mutation (or a series of mutations) to give the ability to produce blue pigments. This may take a very long time (can be approximated by a sum of exponential distribution) with parameters that depend on the exact developmental processes of the moth.
Why down votes and close votes
I think (but I might miss the some reasons) you receive them because...

there are a few english mistakes and that makes the question a bit difficult to understand. I tried to fix that issue.
The question is quite introductory and I think that having a look at an introductory course to evolutionary biology (such as Understanding Evolution for example) will help you.


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Insect identification, Chennai, India
Could someone tell me what the species of this beautiful insect is? Location: Chennai, India.

Thank you!

To me, it looks like a Lepidoptera from the Sphingidae family (Hawk moths). It is similar to species in Hemaris and might belong to this genus.
One similar species from this genus (found in India) is Hemaris tityus, but the moth in your picture doesn't look exactly like this particular species. Another similar species is Hemaris saundersii, which is found in and around India.

(Hemaris tityus, pic from wikipedia)

Thank you. I will try to find the exact species by going through Wikipedia. Thanks again!

As suggested by @fileunderwater this moth belongs to the Sphingidae. It is Cephonodes hylas the Coffee bee hawkmoth, aka the pellucid hawk moth or Coffee clearwing. It is a largely distributed moth, found from the Middle east to Autralia.
Glass wings are not very common among butterflies. Research has shown that the glass wings of this species act like a sort of invisibility cloak, as explained in this article and this blog

https://en.m.wikipedia.org/wiki/Cephonodes_hylas


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Insect ID, Maharashtra, India
could someone please identify this insect? This photograph was taken in the Western Ghats of Maharashtra, India, near the town of Mahabaleshwar. Hemiptera was about as far as I could get using other online guides.
Thanks!

This is a Coleoptera (beetle), not a Hemiptera (true bug). The tarsal formula and overall shape to me suggests Meloidae.

Due to its coloration, shape and tarsal formula (5-5-4) I think that a Meloidae(Blister beetle) of the Pyrota genus is likely. You can see several examples of species in this genus from a basic google search. Meloidae has about 2500 species world-wide though, and there might be similar species in other genera. Here is an example of Pyrota bilineata, just for comparison.

(picture from http://bugguide.net/node/view/918423/bgpage)
You probably need somebody more knowledgeable on Indian beetles for a proper species determination though, but hopefully my suggestions can serve as a starting point.

Thank you! That looks very similar to the one in my photograph! Could the difference in the colour of the thorax and legs be attributed to gender or maturity?

@user19271 I don't think that your species is the same as the one in the picture I attached (P. bilineata) - the shape of the head and the thorax coloration is completely different. I only included it to show that your beetle is similar to the Pyrota genus.

@user19271 So, for the record, I don't think my answer should be "accepted", since it doesn't include a likely species ID.

@fileunderwater Often, ID to species level is impossible with insects, even by experts, certainly based on only photographs. So why shouldn't the answer not be accepted?


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Reading and Understanding profile bands in DNA Fingerprinting
I have very limited knowledge when it comes to DNA fingerprinting. I know about the technique gel electrophoresis and how everything is carried out. But I don't know how to read the result or understand that. Can anyone please explain me how to read the result  [profile of bands]?
Because of my lack of knowledge, I can't solve problems like this one.
Please explain me using this one so that I can get a clear idea about DNA profiling. This seems like home-work problem but the thing is I want to understand the technique of restriction mapping by reading the result of restriction digestion on electrophoresis and my intention is to understand the topic. Please Help.

And I can't describe how I tried to solve this question because I don't have any kind of knowledge about this technique [Restriction Mapping] so my efforts are very silly to mention and I have improper way of approach to this as I don't know how to do the Restriction Mapping.
But I am given the answer which I tried to make sense by working on it but I just couldn't help it. It seems easy after seeing the Map but I don't get the relation between the profile of bands and the Map so if I am given a different problem I will fail to come up with a reasonable answer.

What I am trying to say is, by seeing this map and working on it I get to agree that this is the correct mapping for the data given but I have some doubts, like, why we keep 3Kb distance between BamHI and EcoRI sites. Working out in some another way will end up with wrong answer. How these inticacies are understood? By reading the profile of bands [data given] right? So that's what I am asking for you to explain to me. I don't know anything about it.
Thank you always.

This is homework, one way or another. Please let us know what you tried to solve your problems and exactly what the bottle neck is.

Homework questions are off-topic on Biology unless you have shown your attempt at an answer. For more information see our homework policy.

@MattDMo I would let this question go. As you can see from my description of how to go from the gels to a restriction maps, these types of HW are extremely difficult if you don't have a really good handle on what you are doing.

@AliceD I remember getting this pretty easily in school and then I would have a line of my classmates asking me to explain how to solve these. These are not trivial problems and they are not something that you can look up, and unless can work it out, it is very easy not to even know where to begin. I would cut the OP some slack. This is probably one of the harder Molecular Bio questions that can be asked at the undergraduate level.

@AMR, after edits this question is great. No worries. I retracted my vote and +1'd

The answer below should give you the logic behind how to work through these problems and answer the questions. I edited it to try and be as complete as possible as to how I thought through the solution and the steps you should take to determine the plasmid map from the restriction digest. These are very difficult questions, the best thing to do is to practice them, and they will become easier to solve.

How you would determine the plasmid map from just the restriction digest data
The thought process behind doing this is a bit involved.

From the question you are told that the Gene is 8kb and does not contain an EcoRI site inside of the gene

I say not inside because the ends of the gene were made with EcoRI cuts, but digesting in EcoRI will only produce the 8kb fragment of the gene

The vector is 6kb and you know that they have EcoRI sites at either end, but you are not told what other cut sites there are.
When you digest the plasmid in BamHI you get 3 fragments, meaning that your plasmid has 3 BamHI sites somewhere in it.
You know that your total plasmid size is 14kb (easiest way to know is just look and see that they tell you that there is an 8kb gene and a 6kb vector). Looking at the Double Restriction Digest, you can see that the five fragments add up to 14kb, which implies that there are only one of each fragment in the plasmid, and they are produced by 5 separate cuts.

This is an important piece of information because this tells you that you do not have 2 fragments of the same size making up different parts of the plasmid.
Remember that when you do a restriction digest on a circular piece of DNA, the number of fragment you get equals the number of cuts (restriction sites) in the plasmid. So because there were 5 fragments, you have 5 separate restriction sites
From the Double Digest data, you also know that the smallest fragment of DNA that you have is 1kb and the largest is 4kb.

Since the 4kb site is common to both the BamHI only and the the Double Digest, as since you do not have a 0.5kb or 1.5kb fragment (the remainders if the Double Digest 4kb fragment had been produced from the 4.5kb or 5.5kb fragments in the BamHI digest) in the Double Digest, you know that the 4kb fragment is the same in both the BamHI digest and the Double Digest, and is produced by 2 BamHI cuts.

You can now work on roughly placing where the 4kb fragment should be in the map.
If you try to place that 4kb fragment in the vector, then you would either generate a 2kb fragment, or something less than 2kb and a very small fragment.
Since you do not have a 2kb fragment or fragments smaller than 1kb, you know that it cannot be in the vector region. Also in order to get a 2kb fragment from the 6kb vector the 4kb fragment would have needed to be cut once with EcoRI and from the description, above, we worked out that the 4kb fragment is produced by two BamHI cuts
It could have been that the vector was 1kb + 4kb + 1kb, however from point 4 you determined that you only had one of each fragment, so you can't have two 1kb fragments.

All of that tells you that it has to be in the 8kb gene portion, though you need some more information to determine exactly where.

Remember that you do know that the 4kb fragment was produced by 2 BamHI cuts, which means that it cannot be at the very end of the gene region, as that would require it to be cut once with EcoRI
This also tells you that you have at least two BamHI cut sights in the gene.

What I would do here is draw two circles, the first having an 8kb arc and a 6kb arc, then draw second circle and make three cuts in it.

From 6 we worked out that the 4kb piece will overlap somewhere in the 8kb area, that it cannot be at an end and that there need to be 2 BamHI restriction sites within the gene.
You also have to consider the 4.5kb and 5.5kb parts from the BamHI digest. Since 4kb plus either of those two are greater than 8kb, then you know that the cut that separates 4.5kb from 5.5kb will be somewhere in the 6kb vector. This is how you know that the third BamHI site is in the vector.

Now that you have determine that the 4kb fragment is in the gene you can start to work out the other pieces.
You had 2 fragments from the BamHI digest that were 5.5kb and 4.5kb and in the double digest you have fragments that are 1.0kb, 2.5kb, 3.0kb, and 3.5kb.

Since you have already determine that that 4kb piece is the same for both digests, then at this point you can tell yourself that the 1.0kb and 3.5kb fragments made up the 4.5kb fragments and the 2.5kb and 3.0kb fragments made up the 5.5kb fragment.

Since you know that there has to be two EcoRI cuts that make the 6kb fragment, you are going to need two fragments that add up to 6kb.

The only way to get this with the four fragments that you have from the double digest is with the 2.5kb piece and the 3.5 kb piece.
So you have now determined the exact position of one of the BamHI cut sites. It is in the Vector, 2.5kb from one of the EcoRI sites and 3.5kb from the other EcoRI sites.

Now that you determined where one of the sites is, you know that the 2.5kb fragment was paired with the 3.0kb fragment, so this tells you that there is a BamHI site 3kb away from the EcoRI site in the Gene.
From there you can connect the 4.0kb piece to the end of the 3.0kb piece because you know that the 3.5kb piece has to be attached to the 1kb piece and cannot be attached to the 3kb piece.
All that is left is to close the circle. You know that you have 1.0kb more of the gene that needs to be place and this will connect the 7.0kb that you determine of the gene in step 11 to the 3.5kb fragment in the vector. You have that 1.0kb fragment, and that is the one.

So that is how you determine how to construct the plasmid map from the restriction digests.
What the distances between the cut sites tell you
The cut sites are determined by the sequence of the DNA that the Restriction Enzyme recognizes.

EcoRI recognizes GAATTC
BamHI recognizes GGATCC

You will notice that these are palindromic sequences, so 5'-GAATTC-3' is 3'-CTTAAG-5' on the complimentary strand.
All that the distances are telling you is that in the areas in between the cut sites, the sequences GAATTC and GGATCC do not appear. If they did, then the Restriction Endonuclease would recognize that position and cut the DNA, and you would have an additional cut site at that location.
Assuming that you were given the plasmid map, this should be the answer.
The answer should be C. The 1kb and 3kb fragments are the DNA fragments from the gene that are generated from the EcoRI / BamHI digest. So one end of the fragment was produced with EcoRI and the other end of the fragment was produced with BamHI
The 4kb fragment is the result of BamHI restriction alone. So both ends of the fragment were produced by BamHI so it cannot be the answer to a fragment produced by EcoRI / BamHI restriction.
If they are saying that they also want answer A as well, then their question is very poorly worded, in my opinion.

The short answer:
After the Eco digest, you have two pieces, (which means a single cut) one 6 kb which is all vector, one 8 kb, which is all gene.  Then you digest those with another enzyme, but the pieces that came from the vector should add up to 6, and the pieces that came from the gene should add up to 8.  The 2.5 and 3.5 long pieces must be the cut up vector, the rest must be the cut up gene.  There is no other way to group pieces of those lengths into 6 kb and 8 kb parent fragments.
To find the order of them all:
Basically, you have the 5 smaller fragments, and you want to put them in the right linear order, like this:
enzyme - DNA of some size - enzyme - DNA of some size - enzyme ...etc.
We know that there is 6 kb Eco RI fragment, and THEN we cut with Bam, so there have to be Bam fragments that add up to 6, and the rest will add up to 8.  In this set that HAS to be the 3.5 and 2.5 which are part of the 6kb fragment that you get when cutting with Eco alone.  So we know part of the sequence :
Eco - 2.5 kb - Bam - 3.5 kb - Eco - ??? Bam ??? Bam ??? Eco
Since there are only two, order doesn't matter.
Now, if the 4.0 kb fragment was adjacent to the 3.5 kb fragment, the result of cutting that with Bam alone would be 7 kb.  There is no fragment that size, so that's not right.  Same with the 3.0 kb fragment.  So, it must be the 1.0 kb fragment, because that would yield the 4.5 kb fragment that we do see.
Eco - 2.5 kb - Bam - 3.5 - Eco - 1.0 - Bam ??? Bam ??? Eco
Again, if the 4.0 were adjacent to the 2.5 kb fragment, the Bam alone digest would have a 6.5 kb fragment, which it doesn't.  So the 4.0 fragment must be in the middle, with the 3.0 fragment adjacent to the 2.5 fragment, which yields the 5.5 kb digestion Bam alone digestion product that we observe.
Eco - 2.5 kb - Bam - 3.5 kb - Eco - 1.0 kb - Bam - 4.0 kb - Bam - 3.0 kb - Eco

You cannot assume the 2.5 and 3.5kb fragments make up the 6kb fragment right away. You have to get to it by a process of elimination that rules out the 4kb and 2 X 1kb fragments from being a possibility.

We know the whole vector is 14 kb.  We know the 5 fragments visible add up to 14.  Therefore, there is only one fragment of each size.

Your answer makes the point without explaining how you get there. You can't make the assumption without ruling out the 4kb and 1kb two times first. You did that as a matter of course, because you are familiar with how to do it. Someone who doesn't understand needs that explained to them. You also don't mention that there are 5 fragments that add up to 14kb in the initial part of your answer and you can't assume that the OP will have picked up on that or understand the significance.

The other answer already existed when I wrote mine, and it lays out why each band must represent only a single fragment of that size.


text:
Can we change one's genome into the genome of somebody else
If I (grown-up individual and not just an egg after fertilization) wanted your exact genome, would we be able with today's technology to change my genome into yours?

Do you mean if all genetic material in a grown-up person can be modified?

No, that would be practically impossible with modern technology. The explanation is pretty lengthy, but do you have specific questions or a certain method you were thinking of that could be more concretely addressed?

that my friend is what we call a future breakthrough and will happen centuries in the future

@Tusky - The future doesn't necessarily mean centuries from now... the future is also tomorrow ; )

@gstestso I am trying to save your posts today $\ddot \smile$. I rewrote your post to clarify it. It still is a very introductory question but at least it gets rid of the feeling it gave that your question mixed philosophy and science (the definition of a "person" goes way beyond its DNA and the question of identity is a question of philosophy not biology). Feel free to roll back if you don't like my edits.

@Gstestso If you think your question has been answered (which is my feeling), then please check the answer you prefer below (same for your other posts). Thanks

There are 3.72x1013 (37 trillion) cells in the average adult human body. It would be essentially impossible to target every single cell just to change a single base pair, let alone the massive genetic and epigenetic changes that would be necessary to change someone into a clone of another.

I am going to go one step further than Matt and say it would be impossible even if we had the technology.
And here is why.
Lymphocytes, B-Cells and T-cells, through V-J and V-D-J joining actually recombine their DNA as they are maturing, they cut out long stretches of DNA, so each and every one of those cells has regions of DNA that are different from every other cell in your body.
Then even when they get selected and go through clonal expansion those regions of DNA go through a process called somatic hypermutation which deletes and replaces nucleotides in the hyper variable regions of those genes, in the hopes of making them better binders.
So you would then have to account for every single one of those unique genomes, and the only way to do that would be to destroy the cells, so in the Biological equivalent of the Heisenberg uncertainty principle, the act of observing effects the outcome because you would be changing the other person as well. So you will never ever be able take on the complete genetic make-up of someone else.


text:
What dangers would the wireless transmission of power through microwaves pose to living organisms?
If we were one day able to harness the power of "wireless electricity", and INTEGRATE it into society, what disadvantages and/or dangers to living organisms would become relevant at that point? To my understanding, the power would be transmitted through microwaves, which may or may not be correct.
The example I will use in regards to "wireless electricity", would be... The transmission of power from one source to another without the need for power cords, or power lines.
One such instance, according to "http://phys.org/news/2015-03-japan-space-scientists-wireless-energy.html", states "The idea, said the JAXA spokesman, would be for microwave-transmitting solar satellites—which would have sunlight-gathering panels and antennae—to be set up about 36,000 kilometres (22,300 miles) from the earth."

Perhaps my question should be reformulated to, what are the immediate and long term effects, if any, of microwaves on living organisms? Although I'm sure this has already been asked. Even more specifically, If some day in the future, this wireless power transfer was integrated and power lines/ electrical cords became obsolete and these microwaves were abundant, could it cause damage to living things?

Whether wireless power transfer is safe depends on the type of power transfer. Inductive coupling is generally safe, but only works across small distances (i.e., millimeters to centimeters). The other option is far-field or radiative technology, where either visible light (from lasers) or microwaves are used. The latter has not been applied much, some uses have been found in space technology. Their safety in general will depend mainly on the power being transmitted. For example, a laser can be destructive if it is powerful enough.
I will focus on inductive coupling, because it is not only safe, it is commonplace. The prime example being cochlear implants. Cochlear implants are basically electrode arrays implanted in the inner ear to directly electrically stimulate the auditory nerve in deaf people where the hair cells have degenerated (or were never there). The implant is powered by an external battery worn behind the ear. It is coupled to a head-worn external coil that wirelessly transfers the power needed to drive the implant to an internal, surgically implanted coil. I'm not entirely sure about the exact numbers, but more than 100,000 folks around the globe have received one or two cochlear implants.

Cochlear implant showing the external and internal coil to transcranially transmit power to the implant.Source: Extreme Technology
Very similar technology is used in retinal implants. Retinal implants electrically stimulate the degenerate retina to [partly] restore vision in the blind. For example, the Argus II deploys an external coil mounted on a pair of glasses that wirelessly couples to a surgically implanted coil in the eye to power the implant. Being newer technology, there are not more than two hundred or so people implanted worldwide as we speak, but this number will definitely sore in the near future, all, or at least many relying on wireless power transfer.

Schematic of the Argus II retinal prosthesis showing the wireless link. Source: Ars Technica.
These examples may not be exhaustive. For example, transcranial magnetic stimulation of the brain is another example of wireless energy transfer across the skull, making use of magnetic induction to stimulate the cortex. However, these examples do show that medical bionics is already making use of wireless power transmission technology.

Very intriguing perspective! I never would have considered this. Thanks!

@marcbally - Thanks :-) It's not exactly what you're after, but it's just my 2-cents worth. I'm not familiar with microwave technology. Perhaps others are.

Yes, I posted this in physics first. They immediately shot me down saying it was an environmental or politics question. It's very abstract and hypothetical so I'm open to all kinds of input

@marcbally - yes it is certainly a question prone to close votes. I just happen to be in bionics and it's very relevant stuff from an engineering point of view.


text:
How heavy are all foreign microorganisms in and on the human body?
I define "foreign microorganism" as a microorganism which is not produced
by the human body (not antibodies or leukocytes) including bacteria, viruses, fungi, biofilm aggregates or small lifeforms independent if they are benign or hostile.
Let's say I have currently a weight of exactly 100 kg. How much of it consists of organisms not belonging to me?

Maybe a good definition of "foreign microorganism" could be: a microorganism with a different DNA from the human host?

Edit: Matters Arising
In this Nature News article, Scientists bust myth that our bodies have more bacteria than human cells, and in the bioRxiv pre-print article, Revised estimates for the number of human and bacteria cells in the body, a new estimate of the ratio of microbial cells on the human body to human cells that make up the body has been revised down to close to 1-to-1, with there being slightly more microbial cells to human cells.
It should be noted that near 90% of the human cells taken into account were red blood cells and platelets.

- Revised estimates for the number of human and bacteria cells in the body, Sender et.al. bioRxiv preprint.  doi: http://dx.doi.org/10.1101/036103
Note: Preprint articles have not been refereed. The information in them is subject to change, may not pass review, and in the end my not be accepted for publication.

Readers should therefore be aware that articles on bioRxiv have not been finalized by authors, might contain errors, and report information that has not yet been accepted or endorsed in any way by the scientific or medical community.
- bioRxiv.org: What is an unrefereed preprint?

Original Post

The human body contains trillions of microorganisms — outnumbering human cells by 10 to 1. Because of their small size, however, microorganisms make up only about 1 to 3 percent of the body's mass (in a 200-pound adult, that’s 2 to 6 pounds of bacteria), but play a vital role in human health.

From: NIH Human Microbiome Project defines normal bacterial makeup of the body
Additional Information on Microbiome and Obesity
From Cell
Altering the Intestinal Microbiota during a Critical Developmental Window Has Lasting Metabolic Consequences
From The American Journal of Gastroenterology Supplements (a Nature Press Journal)
Disclaimer

This article was published as part of a supplement sponsored by the Gi Health Foundation, a nonprofit 501(c)(3) educational organization dedicated to increasing awareness of the effect of gastrointestinal disorders in the United States. The foundation's goal is to provide health professionals with the most current education and information on gastrointestinal health.

Impact of the Gut Microbiota on the Development of Obesity: Current Concepts

That not only is surprising, but gives also more interesting information. That they are outnumbering our cells by a factor of 10 is astonishing to say the least, so by looking how that is possible I was surprised how diverse the size of human cells is.

Yep... It makes you start to question whether humans actually are just transportation units for the microorganisms... Look at some of the studies that have looked at how the microbiome affects thought processes.

Nuts! And there for a brief moment I had a perfect scapegoat! "It's not ME, Doc - it's my microorganisms! THEY'RE why I'm overweight!!". Yeah...if only... :-(

@BobJarvis, They may still give you an out. http://www.nature.com/ajgsup/journal/v1/n1/full/ajgsup20125a.html

@ThorstenS. I expanded my answer to your question. While not technically an answer to your question, the gut microbiome can affect weight in more ways than just adding their own mass; they can alter metabolism and can contribute to your weight and body mass, either positively or adversely.

@AMR - ah, but the article you cite seems to be suggesting that being overweight is still, somehow, my fault - as if my diet and activity levels might in some way affect my metabolism. Feh! Clearly flawed research, as it does not align with my knowledge-free opinions. Why, this paper would imply that the consumption of dietary staples such as french fries and pizza would negatively affect me! What nonsense!! But on the other hand, reading it made me depressed - I think I'll go eat a dozen donuts to make myself feel better. Thanks!

The paper on cell ratios has now been published in peer-reviewed form: http://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.1002533

authors: Bob Jarvis - Слава Україні


text:
Why do we blow when we're out of breath?
When people are out of breath from exercising, instead of breathing normally they partially obstruct their expirations by blowing out instead of breathing out.
Why is this?
EDIT: This photo illustrates what I'm referring to.

I'm not sure I understand your question. You have to breathe out in order to breathe in again…

I don't. I start panting. This is opinion based I guess.

@canadianer: You don't understand the difference between blowing and breathing out normally?

Why did 'AliceD' mark this question as 'unclear what [I'm] asking', when her comment shows that she understood the question perfectly? I give up. No one is capable of answering, or, it seems, even understanding my simple question.

@EmmaV, after a while, thinking about it, I now understand what you are asking. Alice is clearly saying that the answer(s) would be opinion based and thus not constructive and hence put a block on any further answers. In my opinion based answer, I would say I do that so the strong air flow does not go through my teeth because it gives me a strange feeling when it goes through my teeth... Like others, I think the question could have been better expressed.

@EmmaV Do you mean why do we typically exhale harder than inhale after strenuous exercise?

What is the difference between blowing out and breathing out?

Trying to rephrase the question
If I understand the question (and what you missunderstand) correctly, I think one could rephrase the post as
When one spends some time under water and come back to the surface, one usually breath out and then breath in. This is surprising to me because I would expect the person to be out of air and therefore wouldn't need to breath out before breathing in.
Let me know if I failed to understand your question and misunderstandings
Answer
We don't incorporate the air we breath in our lungs. We only use the molecules of oxygen $O_2$ from the air (which takes ~20% of the total volume). This molecule goes in the blood, reach the cells and react with sugar to produce energy. The waster of this reaction is another molecule $CO_2$ that needs to be exhaled through the lungs.
So, really the volume and of air that we have in our lungs doesn't vary much (It actually increase a little bit as we had some carbons). Only the composition of the air that we have in our lungs changes. After some time, we need to renew this air and for this purpose we first need to breath out the air that is contain a high density of $CO_2$ before breathing in.
This is why when sticking the head out of the water many people first breath out and then breath in. Note, however that one can breath out all its air underwater and then only has to breath in when back at the surface.
EDIT
Are you asking why do we contract our lips during sport?
If yes, I think it very much depend from one person to another. There is probably no physiological advantage/disadvantage at doing so and it probably is just a consequence of expressing pain on our face.

That's not what I mean. When people are out of breath, they breath more heavily than normal, but instead of expiring gently as normal, they 'blow'. By this I mean they partially close their mouth so that there's a small opening and blow through it, often making thier cheeks bulge. Inspirations are still normal, albeit deeper. Here's an image I found quickly: http://watchfit.com/wp-content/uploads/2015/07/xshortness-of-breath-during-exercise_1-1024x682.jpeg.pagespeed.ic.qrPeKJuXUm.jpg

Your comment seems very unrelated to your post...but ok. I tried to answer to what might be your question (still unclear to me) in an edit in my answer above.

My comment is an elaboration on my question. I'm not asking why we contract our lips during sport. I personally 'blow' when out of breath because a rapid expiration when out of breath is uncomfortable. This is doubtless why others do it too. I thought that there must be a physiological explanation for it.

Well you blow to make room to breath in again, isn't it? Or you just stop inhaling altogether?!

I find it hard to believe that someone with a PhD genuinely can't understand my question, and is confusing blowing with normal expiration. Does one 'breathe' up a balloon? I make a point of always phrasing my questions as simply as possible in order to accommodate non-native English speakers, and I'm really at a loss as to how this question could possibly be any simpler to understand.

To clarify: I'm not saying people stop expiring when they're out of breath. Why would I say that? It's idiotic. I'm saying that when people are out of breath, they expire by blowing instead of expiring by breathing out normally, as a person at rest does.

Note also btw that I don't have a PhD (yet) as I am currently a PhD student. I'll delete my answer once I'll understand your question (and will then try to suggest an edit to your post).

I am not sure what is this difference between blowing and breathing out. Is it specific to the lips position or to the amount of air flowing through the mouth (or something else)?

It puzzling that my last comment has enabled you to understand my question, since the comment is essentially the same as the question. The difference between blowing and breathing out is obvious. Do both, and you'll notice the difference. Blowing is more forceful than normal breathing, and the mouth is made smaller.

And so is you question, why do we need to inhale and exhale more air when we are exercising?

You're not serious, surely. The reason why we breathe more when exercising is taught in Junior school. How is this relevant anyway?

So what is the point that interest you about blowing if it is not related to the amount of air? Is it the position of the lips?

I will soon give up trying to understand your question. It is the job of the OP to make its question easy to understand and it appears that we all struggle with yours.

No offense intended, but you might as well give up now. Stop wasting your time. It's impossible for this question to be any clearer, and yet it is still ostensibly beyond everyone's comprehension. Thanks for your efforts anyway.


text:
How do we sneeze?
When a stimulus triggers the sneezing pathway, known as the trigenimal nerve network, how do the droplets from a sneeze get created within the nose? What affects the size of these droplets?

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


text:
Is there a good easy protocol for extracting proteins (enzymes) from fungal mycelium?
I quantify the enzyme (polygalacturanase) activity by DNSA method. To determine endo-polygalacturonase activity I'm searching for a good easy enzyme extracting method. Any suggestions for a suitable buffer?

Production, Purification, and Characterization of Polygalacturonase from Mucor circinelloides ITCC 6025. The authors use a sephacryl S-100 gel filtration column (chromatography), followed by enzyme activity assay and SDS-PAGE.


text:
Nucleoside analogs that cause mutation
I'm confused with this explanation in my book:
2-aminopurine is incorporated into DNA in place of adenine but can pair with cytosine, so an AT pair becomes a CG pair.
This sentence seems odd to me. It says that adenine is replaced with 2-aminopurine, but can pair with cytosine. And the AT pair turns to CG pair. Does it mean that 2-aminopurine substitute adenine, and then it works like cytosine to bind with guanine?? Because 'AT pair becomes CG'. But it says 'but can pair with cytosine', which one is going to bind with cytosine??
I've Googled on this but couldn't reach to a clear explanation about this. Can someone please explain to me how this analog works or rephrase the sentence in my book? Thank you.
The book that I'm referring is Microbiology: an introduction 10th ed. By tortora, funke and case. Page 229.

Welcome. If you could give the title, edition, and page of the book you are using, someone on the site may have it and can reference it. Without seeing everything else in the chapter, I am going to take a stab that Aminopurine basepairs with cytosine, then when the DNA repair mechanism finds aminopurine in the DNA, it will cut it out. When it does that its template will be the C, and it will replace aminopurine with a G.

Such a mutation can also occur when the DNA is replicated. http://biology.stackexchange.com/questions/26022/gt-transversion-vs-tg-transversion

I am not sure if this will help to clarify Base pairing and mutagenesis: observation of a protonated base pair between 2-aminopurine and cytosine in an oligonucleotide by proton NMR.

Thanks for the links but those are beyond what I'm learning now.

If you feed bacteria 2-aminopurine then at some low rate it gets incorporated into into the DNA instead of adenine during DNA replication. In other words there will be a base pair between thymidine and 2-aminopurine.
Two things could happen:

DNA repair could detect the unusual base and attempt to correct. If the 2-aminopurine is excised then adenine will be inserted--no mutation. If, however the thymidine is excised then sometimes a cytidine will be inserted. This gets resolved below.
During the next cell division the replication machinery will sometimes incorporate a dC across from the 2-aminopurine. Then in the following cell-division a dG will be incorporated across from the C, so what used to be an A-T base pair has become a G-C base pair (eventually).

Oh!! @mdperry, I've got it!!!! Thank you so much!! And I've 2 questions. I'm wondering if that cytosine form a complementary pair with guanine, then what about 2-aminopurine, since it's a semi conservative replication, we shouldn't leave 2-aminopurine hanging there correct? Would it pair with a new cytosine again?

And another question. This tortora text said that 5-bromouracil would pair with cytosine (if it's not being fixed by DNA pol) but what the Brock's book said it actually binds with guanine. Which one is correct? Or 5-bromouracil actually capable of pairing with both of them?

@Theresa Re: fate of nucleoside analogs incorporated into DNA, I don't actually know how long the modified base persists, but I have read papers where one entire strand was labeled, and the analogs could be detected 10 or 20 cell divisions later. If I understand correctly, the 2-AP can form base pairs with either dT or dC in subsequent rounds of DNA replication.

Re: BUdR (bromouridine deoxyribose--that is what you are referring to?) I am not familiar with all the details, but off the top of my head, you would not expect to find U in DNA, only in RNA (ordinarily). Since T pairs with A in DNA, it follows that U pairs with A in RNA. In RNA double-stranded regions rU can also form base pairs with rG, as long as the Br atom does not disrupt this U=G pairing I would naively assume that dU (and by extension Br-dU) can base pair with dG. A dU=dC base pair would be quite unusual since they are both smaller, pyrimidines.


text:
What are the metabolic concerns associated with hard water?
If humans can maintain a consistent blood pH, then what problems does alkalized water cause us?
Why is it recommended that we filter and boil hard water? Is the issue that hard water can affect the pH of our blood?

Could you add where you have gotten this advice? I have lived in many regions with pretty hard water, and never came across it. The only reason I could envisage is to improve the water's taste...

@Gerhard I don't remember, it is the conventional wisdom.

It might help mentioning where you are from, if you say that it's "conventional wisdom" :)

@Gerhard it isn't matter, filters are sold all over the world.

I don't know this area, but found a recent review http://www.ncbi.nlm.nih.gov/pubmed/24049611 on epidemiological studies on hard water. It seems there are no conclusive data showing a health risk. Water hardness will definitely not affect your blood pH, which is carefully regulated by buffering systems. I think the reason most people install water softeners is because higher salt content can in the long run damage pipes, valves, dishwashers etc.

@RS: no problem if you would like to keep your location a secret. It's just that I had never heard of such a claim neither in the south of Germany nor in England and was curious - and thought that there might be something more behind the recommendation than just the hardness of the water, which might depend on your location. And yes, water filters are on sale here, too, but exclusively to improve the taste of tea and coffee :)

Right now, there is no evidence shows hard water can cause any healthy problem.
Previously people were concerned about the high mineral content, such as calcium and magnesium, may cause disease such like cardiovascular disease.
But from the report World Health Organization published in 2003 Hardness in Drinking-water, it says "Although a number of epidemiological studies have shown a statistically significant inverse relationship between the hardness of drinking-water and cardiovascular disease, the available data are inadequate to permit the conclusion that the association is causal. No health-based guideline value for water hardness is proposed."
And the United States National Research Council thinks hard water can supply the calcium and magnesium ions that dietary need. Hard Water Hardness Calcium Magnesium Water Corrosion Mineral Scale
And at the same time, I have to say the filters cannot directly work for hard water because ions cannot be isolate by filter. We can filter the precipitation after boil the water. Boiled water is better because tap water may contain microbes in some country, that will be harm for our health. And also you don't want to feel some "precipitation" while you drinking water. That's it.
For my personal view, I prefer soft water because it tastes a little bit sweet.

Ions can be isolated and removed by filters.  That's the exact premise of reverse osmosis for water purification. They don't work as well for hard water over time because scale can build up on the filter and drop it's efficiency faster than expected.


text:
What happens to H+ when Glycerate 3-Phosphate is converted to Triose Phosphate?
The conversion from Glycerate 3-Phosphate to Triose Phosphate requires:
$ATP \rightarrow ADP + P_i$
$NADPH \rightarrow NADP + H^+$
So what happens to the $H^+$?
Is it in-effect "recycled" back to the Light Dependent reaction.

The H+ is used for the photophosphorylation part, in which the H+ is pumped.. so yes, you are correct...

First off, I believe you have the production/consumption of the proton off, at least for the reaction with NADPH. Most reactions with NAD(P)H go like NADPH + H+ + (oxidized compound) --> NAD(P)+ + (reduced compound). In fact, in most reaction mechanisms the hydrogen that's actually on the NADPH is ends up covalently bonded to the reduced compound.
That said, acid-base reactions are some of the fastest reactions that can occur in the cell. The cellular environment is pH buffered, so any excess H+ ions would be rapidly taken up by the excess of buffering agents which are floating around in the cell. Likewise, when a hydrogen ion is needed in a reaction, it's pulled from the general pool of free hydrogen ions, and it is rapidly replaced from that same pool of buffering agents. As a consequence of this, it normally doesn't make much sense to talk about where hydrogen ions flow in the cell - there's just a general hydrogen ion pool which supplies and takes up any hydrogen ions that are needed/produced by the reactions in the cell.
The big exception to this is where hydrogen ion movement is restricted by things like membranes. The TCA cycle and the light-dependent reactions of photosynthesis being major examples of this. In those situations hydrogen ions are pumped across the membrane during the reaction, and there is a distinction between hydrogen ions "inside" and "outside" the membrane. But there isn't any distinction between any of the hydrogens on one particular side of the membrane.
The light independent reactions of the Calvin cycle, though, happen within the chloroplast stroma and don't pump hydrogen ions across the membrane. So the hydrogen ions generated/consumed by these reactions go into/come from the general stromal pool of hydrogen ions. Here they can be used by any reaction that requires/generates hydrogen ions - a major one of these would be the light-dependent reactions, which take hydrogen ions from the stroma and pump them to the lumen (and then release them back to capture the energy for phosphorylation). But the hydrogen atoms from the Calvin cycle enzymes aren't in any way "earmarked" for the light dependent reactions.


text:
What is meant by "the degree to which a gene is expressed" in an individual?
Here is an excerpt from a text that I was reading,

Here is an example of microarray data. The idea is to take a group of
  different individuals and for each of them, you measure how much they
  do or do not express a certain gene. Technically, you measure how much
  certain genes are expressed. The colors in the graph, like red, green,
  grey etc. show the degree to which different individuals do or do not
  have a specific gene.

The data they are talking about is this:

But a gene is either expressed or not expressed right? It's one allele is expressed or another allele is expressed, or yet another one is expressed. It is a discrete thing.
Then what is meant by the extent or the degree to which the gene is expressed? Can a gene be expressed more in certain individuals and less in others? Please explain with example.

It is true that a gene is either being expressed, or not being expressed. However, the degree to which a gene is expressed can vary tremendously. "Degree of expression" basically means the number of times the gene is read by the transcription machinery, which (generally) correlates to the number of copies of mRNA present in the cell, which (generally) correlates with the number of protein molecules being translated. Essentially, the degree of expression of a gene corresponds to how much of the gene's product is being produced. (Of course, this being biology, things aren't always quite as simple as that, but this is the general trend.)
Here's an example. All nucleated cells express housekeeping genes that are required for the normal function of the cells. These are often involved in maintaining metabolism in the cell, sensing and processing nutrients, maintaining the cell's structure and shape, etc. These genes are expressed to a very high degree, meaning they are always "on" and being transcribed. On the other hand, there are many many genes that are not needed in "normal" situations, and are only turned on at certain points in development, during pathology, during a certain point of the cell cycle, or other similar situations. These genes have a very low degree of expression, and in fact may be turned off altogether in some cells.
So, the degree of expression can be described as the rate at which the gene is being transcribed. In a study like the one illustrated in your question, the number of copies of each gene's mRNA in the cell is quantitated, and compared to the expression of a housekeeping gene that should have the same degree of expression regardless of the sample. The relative amounts of each mRNA are then compared among individuals, and scored accordingly. This numerical score is then turned into a color for the purposes of generating the heatmap image.


text:
When does meiosis occur in flowering plants?
At what point does meiosis occur during the development of a flower?

Wikipedia says when the plant(anther) is growing for pollen at least, sorry if that is vague though, https://en.wikipedia.org/wiki/Microspore#Angiosperms

In pollen-mother cell and Megaspore mother cell, it happens.

Meiosis before pollen formation could be studied in anthers of flower-buds, with aceto-carmine staining

In case of male gametophyte (in angiosperms), meiosis ends before the formation of the pollen tetrads which in turn marks the end of cell division in anthers and petals (Li and Johnston, 1999). However, the same study reveals that the relative timing of pollen tetrad formation with respect to floral development (abbreviated as RAFT), varies between different plants. Despite the variation, they seem to form three clusters with mean RAFT at 0.45, 0.62 and 0.73.
In case of the female gametophyte, the megasporogenesis happens inside the ovule (Yadegari and Drews, 2004). Therefore, ovule should have formed before the onset of meiosis. I could not find a detailed study on the timing of the megasporogenesis.


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Is there a database of cell images?
We're working on an algorithm for processing images of cells, similar to but much more basic than Cell Profiler, and we are looking for a large database of cell images to test our software. Can anyone point us in the right direction? We found the Cell Image Library immediately, but it seems almost empty.

Possible duplicate of What are good sources of free-to-use images and diagrams and http://biology.stackexchange.com/questions/38774/open-database-of-medical-images and dataset of microscopic images before and after staining

The ATCC website has a bunch of images of cells in culture.

@AMR those are not duplicate questions. I vote to leave open as it looks like a valid question to me.

@AliceD That is your call, but all three have links to cell image libraries. The point of flagging as a duplicate question is also to show where a simple search of the stack would have yielded acceptable answers to the question. Answer in first link leads to Wellcome Images which has a large set of cellular images of all types. The second link had this comment https://www.nlm.nih.gov/NIHbmic/nih_data_sharing_repositories.html and the third is pretty much an identical question, with the sole exception that they did not specify it was for bioinformatics.

@AMR - admittedly, I didn't check the answers in your links, but then, as far as I understand SE's policy, I don't think questions should be closed because the answers are out there as sidelong answers posted to unrelated questions. If that would be so, a great many questions could be marked as duplicate.

There is a yearly contest on cell tracking organized by the IEEE International Symposium on Biomedical Imaging, and the associated data sets are freely available.
See for example: http://www.celltrackingchallenge.net/

I've actually answered my own question. The creators of Cell Profiler mentioned a database of biological images which they used to benchmark their software, and it appears to be available at http://www.broadinstitute.org/bbbc/


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How do antibiotics create drug-resistant strains
I've heard for years that low-level use of antibiotics causes the spread of drug-resistant strains of bacteria, but the explanations always fall short.  I understand mutations and natural selection, and that a bacterium can randomly mutate into one that is more resistant to the antibiotic than the wild-type.  I understand that the antibiotics kill off the less resistant strains and leave the more resistant ones, but those more resistant strains would be there even without the antibiotic use, right?
Do the more resistant bacteria compete somehow with the less resistant ones and the antibiotics kill off the competition?
(Edited: previously used the terms "strong" and "weak" which apparently have unintended connotations, and was unclear about the role of mutation).

The last part of your question is confusing. Can you reword your question and talk about mutants and wild-type instead of "strong" and "weak"? Those are value-laden words, and may not even apply to the populations you're talking about.

Resistance to an antibiotic doesn't make it "strong"; it makes it resistant to an antibiotic. If it happens to take hold in a wound, it will flourish no better than a wild-type bacteria, but it will survive exposure to the antibiotic, that's all.

Resistant strains might have been there but they would not have been in a position to outcompete the nonresistants without selection, for the reasons I gave in my answer. If you properly treat bacterial infections long enough and at a high enough dose with a combination of drugs, and have a patient with a functioning immune system, then the adaptive immune response should be able to clear the infection. When we didn't allow that to happen, or we gave antibiotics for viruses, we selected for the resistant mutants, and the adaptive response wasn't able to target and clear them.

There is no such thing as a "stronger" or "weaker" strain until the bacteria are treated with antibiotics.
It is true that potentially antibiotic-resistant mutants will still occur whether or not treated with antibiotics.
However, the mutants would not be "stronger" without the antibiotic use, so there is no selective pressure for them to survive to any greater degree than the wild-type. Without the antibiotic, something else will kill that mutant bacteria, meaning that the mutation ultimately did not make it any stronger.

All things being equal, in an environment without the selective pressure of the antibiotic, then the non-resistant wild-type will have a growth advantage.
EDIT

The events of random mutation and the attendant natural selection in the presence of a given antibiotic provide ample opportunity for the advent of the resistance phenotype. It is interesting to note that the survival cost to the microorganism in the evolution of drug resistance is high as it is highly dependent on the environment in which it happens to exist momentarily. One could envision that in the case of a plasmid-borne resistance factor, the organism must synthesise the additional genetic material and the protein that it encodes. However, this energy cost factor may be affected by the nutritional limits of the environment in which the organism finds itself. Furthermore, alterations of chromosomal genes encoding the targets for antibacterials may present the opportunity for the selection of resistance to antibiotics. However, such modifications may jeopardise the normal function of the gene products and make the organism that carries them less fit in the wild, or diminish or lose the capacity to survive in the absence of the antibiotic. Numerous studies indicate that genetic adaptation by secondary mutations elsewhere in the genome and natural selection reduces this ‘cost’ to the organism in several generations of growth, such that the cost is either reduced or eliminated entirely. Indeed, recent studies suggest that a progression of bacterial resistance to given noxious agents involves a sequence mechanism that renders the organism increasingly resistant to the agent, but nevertheless at a cost to its survival fitness

-Martins, A., Spengler, G., Molnár, J. and Amaral, L. 2014. Bacterial Antibiotic Resistance. eLS.
In order to truly grant resistance to an antibiotic, the bacterium needs to be expressing the enzyme the confers resistance constitutively so that it can react to the antibiotic when the cell comes in contact with the antibiotic. If the bacterium has to wait until it encounters the antibiotic to start expressing the resistance gene, then the bacterium will likely be killed before it has a chance to produce the protein that will protect it. This is especially true for antibiotics that target the bacterial ribosomes to prevent protein synthesis.
The result is that the bacterium has to use energy to produce the enzyme. It also has to maintain that gene either on a plasmid or incorporated in a very small genome. That again means the resistant cell needs more energy for replication, and likely a bit more time to divide. That may seem trivial, but if the nonresistants can divide every 20 minutes while it might take the resistants 25 or 30 minutes, the resistant bacteria will be out competed by the nonresistant bacteria, for the simple fact that the nonresistants are using less energy to survive and replicate and they are doing it faster, so the will have more descendants.
Another thing that you need to realize is that a lot of times the use of antibiotics only holds a bacterial infection in check until our adaptive immune system can be raised and respond to the infection. So not completing a course of antibiotics means that during the period of time that the antibiotic was used the resistant bacteria had a growth advantage over the nonresistant bacteria.
If you stop taking the antibiotic before the immune system can clear the infection completely, then both types of bacteria will begin to divide again, and there will be more of the resistant bacteria than there will be nonresistant, so they will contribute more descendants to the reemerging infection.
Another problem is that the more resistant bacteria there are the more of a chance there is that they can pass on that resistance gene to bacteria that didn't have it before. Now when you go back on the antibiotic, less and less of the bacteria in the infection will be affected, and you will get uncontrolled growth of the infection. There is a point where your immune system either is overwhelmed and cannot respond, the toxicity level from endo and exo toxins produced by the bacteria makes you very sick, or your immune response responds too strongly and does significant damage to your own tissue trying to fight off the bacteria.

"All things being equal, in an environment without the selective pressure of the antibiotic, then the non-resistant wild-type will have a growth advantage." Do you have a source for this? CA (community associated)-MRSA has mostly replaced HA (hospital associated)-MSRA because their doubling time is much less, giving them a competitive advantage over even "feral" SA unrelated to their methicillin resistance.

@anongoodnurse Your example is of an already resistant, already highly virulent strain of bacteria, and that is not what I am describing. I am describing how you go from a situation where the majority of the organisms are non-resistant and then through the incorrect use of antibiotics, you give rise to strains that have resistance.

Must it be incorrect use? What about correct use? All I'm asking for is a source to back up your claims. If you don't have one (or more), it's just opinion.

@anongoodnurse I also looked at several papers on CA-MRSA, and non them mentioned anything about a growth rate advantage due to replication speed. They have different virulence factors, and are more adept at causing infections in otherwise health people, and the prevalence of these infections has increased dramatically in comparison to HA, but non mentioned the rate at which they replicate.

@anongoodnurse Incorrect usage was the bases of the OPs question.

@anongoodnurse Edit to show source that supports my experimental observations.

How does low-level translate to incorrect usage? (I assumed lower dose, not incorrect.) Note the great difference in the possibilities they state and the certainties with which you frame your answer. I can easily accept the paper's hypotheses. You state it as if it's a known fact. The fact that you restricted antibiotic use to incorrect use shows a certain frame of reference which is restrictive, not open. "... my experimental observations." Are you doing microbiological research?

@anongoodnurse Yes.

@anongoodnurse I translated low-level use to be at amounts below minimum inhibitory concentration or incomplete treatment, and much of the first part of my answer, while factually accurate, was geared more towards correcting the OP's misconception that nonresistant = weaker. The advantage that resistants enjoy goes away when there is no selective pressure, because better breeders win out. Once established, as with MRSA and the other superbugs, they will be the predominant strain, because they have survived countless generations of selection that WTs did not. Their competition was wiped out.

I see a lot of explanation of how low-level use of antibiotics makes the ratio of resistant to non-resistant climb, but I don't see anything that would explain the absolute population of resistant going up or, more to the point, more people being infected with the resistant strain, because of the antibiotic use.

@user170733 Vertical Gene transfer. If, in a selective environment, the resistant strain is able to pass on its genes through replication, the larger the population gets in relation to non-resistants. Horizontal Gene Transfer. Resistant Bacteria, either the same species or entirely different ones are able to transfer the resistance gene, either by Transformation, Transduction, or Conjugation. Without antibiotics, there is no selective pressure, so the energy cost outweighs the benefit of resistance. With selection, the resistance gene(s) can be maintained...

@user170733 So now, because of decades of antibiotic use that was insufficient to kill off resistant strains, either below MIC, incomplete treatment, or from immunocompromised people that did not have an immune cyst that could fight the resistant bacteria, we have more resistant strains, and the rest is down to probability. More resistant strains = a higher probability that that is what will infect you.

@user170733 The issue isn't so much that antibiotics were used, it is that they were not used in high enough doses, for long enough periods of time and were often used as mono-therapies, instead of combination therapies that attack the bacteria multiple ways, making it less likely, at least initially, that you will have any bacterium will be resistant to all of the drugs, which is what we see now, because one drug didn't kill them, so the survivors are mostly killed by the second, but there are some that survive because they develop resistance to the second drug as well, and on and on.

@AMR - "I also looked at several papers on CA-MRSA, and non them mentioned anything about a growth rate advantage due to replication speed." Seriously? It's everywhere (it's a very hot topic.) Makes it difficult to comprehend your statements...

@anongoodnurse The paper only has a comparison between CA and HA. I tried to find the reference, but it was from a book (peer-review?) that I wasn't able to track down. You are giving one example, and when it comes to bacteria, I have learned never say never, but that doesn't change the fact that sub minimum inhibitory concentrations that reduce the competition for resistant strains is one of the driving forces in their emergence and prevalence. I provided you with a peer-reviewed link that backs that up, which you are not satisfied with. You got your downvote, let it go at that.

@anongoodnurse If that isn't enough, then please feel free to raise an edit to suggest the changes you would like to see, or submit your own answer to the question.


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How do we sneeze? - Part 2
Here is the second part of my question about how we sneeze. How are the sneeze droplets propelled at such a fast speed? I have heard sneeze travels at 100 mph. How is this possible?


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How does the sticky ends of foreign gene bind with its counterpart in the plasmid DNA if positions are not matching?
Consider  a foreign gene with recognition sequence as GAATTC  for EcoR1. Now suppose that it is being cut at two palindromic sequence  to form sticky ends.
Here the sticky ends are formed such that its position is parallel to each other around the axis of DNA.
The plasmid DNA has a recognition sequence and is  being cut at a  site and as obvious would be  cut with the sticky  ends as  counterparts. If we join the foreign DNA to this vector DNA the problem of combining the DNA arises. How will we cope with this problem  or if I am going wrong can someone tell me where?

I am having trouble understanding your question. Inserting a fragment of DNA into a plasmid is pretty standard procedure, especially if the restriction sites are the same, just cut, purify, mix, and ligate. Can you clarify where you don't understand?

@user137 Let us consider a two dimensional case for this where the DNA is represented by two parallel lines where only one of the lines extended represents the strand with two sticky ends.In the plasmid DNA this would not be the case as the sticky ends are counterparts therefore opposite to each other at the site where it is cut off.This position of sticky ends of the plasmid DNA is not allowing the combination of sticky ends of the foreign DNA.

A drawing would help I guess. I can't visualize the issue.

yeah it would certainly help.But I have some complications in doing so.I am not able to upload the image.I hope some symbols would help.

Now as shown above the question is how would one be able to make the recombinant when the position of sticky ends of both the the plasmid DNA and of the foreign DNA are located in different positions such that when combined only one of the sticky ends gets its complementary while the other doesn't gets it.Think of it in 3 dimensional view, no such change is being observed.

Instead of the ridiculous characters, try and use standard molecular biological notation. Sticky ends will either be a 5' overhang or a 3' overhang. EcoRI cuts between the G and the A and produces a 5' overhang of 5'-AATT...-3'. And what do you mean by "parallel to each other around the axis of DNA" If you are saying that your target gene has two EcoRI sites that flank it then the cut at the 3' end will still produce a 5'-AATT...-3' overhang, but on the complementary strand. If you cut your plasmid with EcoRI then it will pair complementary to those ends.

In the Google search engine I entered "ligation of sticky ends"; then I selected the "Images" tab. Here is the first result, which addresses your question exactly:

This originates from this website:
AddGene
Based on your question it sounds like you understand the basic rules of forming Watson-Crick base pairs; but your diagram and question omits the innate polarity of the sugar-phosphate backbone in DNA and RNA. The convention in depicting double-stranded DNA is that the "top" strand (sometimes referred to as "Watson") is written in the 5'-to-3' direction, reading from left to right. Since the two DNA strands are anti-parallel, it follows that the "bottom" strand (maybe nobody refers to it as "Crick" any longer?) is written in the 3'-to-5' direction -- if you are reading from left to right.  If you want to decode the biological information encoded in the bottom strand then you need to read it from right to left.
This is a long-winded way of saying that I usually note the 5' and 3'-ends on a drawing of DNA to emphasize this, and if I can figure out how to do so I will update the image.
Here is a slightly better version from Google:

Which is from this site: A WordPress Blog

my question is different.Now consider the one Watson strand of some foreign DNA. As one move from 5' end  we get the sticky end 5'-AATT.After some locations let the sticky end start again as 5'-TTAA.Now when we combine this foreign DNA piece to the plasmid DNA it is not necessary that the sticky ends of foreign DNA just fall above their complimentary cut counterparts of the plasmid DNA to complete the helical structure.

You may be confused about palindromic DNA sequences. Perhaps the simplest explanation is this: The Eco RI enzyme recognizes and cuts this double-stranded sequence: 5'-GAATTC-3' This sequence is the same on the top strand AND on the bottom strand--if you read the sequence in the 5'-to-3' direction. All of the sticky ends generated after digestion will have the sequence 5'-AATT-3', and will therefore form Watson-Crick base pairs with each other. There is no such thing as a 5'-TTAA-3' sticky end generated by Eco RI. That would require a completely different enzyme.

Assume this is your plasmid (N-Ñ denotes any complementary pair):

And you have an insert which has EcoRI site at its 5' end.
When you do an EcoRI digestion of the insert and the plasmid you'll get these products.

Digested insert:

Digested vector

During ligation, insert will pair with the vector in this manner (black is the vector and blue is the insert):

If you now want to ligate the other end you can use the HindIII site. However, if you have same restriction sites on both the ends (for instance EcoRI) of the insert then you will get two ligated products which will have opposite orientations of the insert.
I hope this clarifies your doubt.

let us take a plastic model of DNA with sticky ends which are also complentary.I take another foreign plastic model of DNA with varying lengths which also have same sticky ends to combine with the former one.Now every length of DNA may not combine with it because of different orientation? We cannot twist it forcefully to combine.

@Sikander I can't really understand what you mean. Are you saying that there is a ssDNA region but only the first few residues are sticky. Ligation would happen only in the situation I mentioned above. You can draw a diagram to illustrate what you are asking. Use powerpoint to make a diagram, save the diagram as a picture and then post it in the question.

In a test tube, where you have added two different pieces of DNA--with complementary sticky ends, if the DNA fragments are too short to circularize--like your plastic model, then what happens is that you form random multimers of the fragments, that all get ligated in a line. Eventually, when their cumulative length allows the two free ends to reach around and find each other, you will achieve intramolecular circularization.  This can all be assayed be gel electrophoresis and electron microscopy.

@mdperry yeah! that is the possible answer  I was looking for.You mean that there are many foreign fragments which will linearly combine till they get such orientation that their sticky ends are able to combine with their complementary in vector DNA.

@Sikander Yeah they can form multimers. Typically you should get a distribution of number of multimeric repeats. It also depends on concentration. In any case it would be great if you can add an illustration in your question to clarify the exact point that you are interested in.


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Two 20 million yr old fossils of Hummingbirds found "The amazing thing about the fossil is that it's essentially a modern hummingbird
does this only mean that the Hummingbird is perfect in creation and needs no change to survive?
http://news.bbc.co.uk/2/hi/science/nature/3691169.stm

Please add references/links to your claim.

The report does not say "exactly identical". The BBC news feature say the fossils "show many striking resemblances to modern hummingbird groups". The primary article (http://www.sciencemag.org/content/304/5672/861.full) says that the extinct species "is of essentially modern appearance and exhibits morphological specializations toward nectarivory and hovering flight". Your premise is wrong.

Nothing puts a biologist off as quickly as a phrase like "perfect in creation". Biology is a mess; see this xkcd to see what I'm talking about.

Hummingbirds were not created, they evolved.
Ancestors of a modern species need not be that morphologically different from their progeny, even over a time span of millions of years. And organism will fill a niche based on its fitness to survive in the niche.
If there are strong selective pressures in the environment to maintain the traits that we see today, even over a 20 million year time horizon, those traits will be preserved. That means that any variation that may have occurred, that does not confer a survival or a reproductive advantage, will be lost to the traits that are selected for.
You then also have the idea of coevolution. If a particular flower that produces nectar that the hummingbirds relied on as their only source of food, could only be pollenated by the hummingbirds, then they would also rely on the hummingbirds. The success of each organism relied upon the success of the other. So the adaptation that made the hummingbird successful at feeding from that plant also made the plant a better breeder, so as both succeeded, but both relied on specific traits of the other, then they both put pressure on each other to stay relatively the same.
Add to that, if the niche was such that the hummingbirds didn't have a significant threat from predators and the plant didn't have parasites or other invasive species that would kill it off, and no other plants in that niche evolved as a food source for the hummingbirds, then there really is very little selective pressure for change, and the traits of both can be maintained for long periods of time.


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Why isn't the biological niche occupied by whales instead occupied by fishes?
As by the title. Why aren't there many more, and larger, whale shark like creatures instead of the great mammalian swimmers? I'd assume fish have a benefit in doing the whole "being under water" thing on virtue of not having to get to the surface to breathe ever so often. Seems it's not that big of a benefit, but I still assume there must be something else about mammals that makes them good at being large swimmers and divers?

Is the question "why are marine mammals larger (on average) than marine fishes?"

Air breathing is a much more efficient method of obtaining oxygen than filtration through gils. The greater the depth, the less dissolved oxygen there is in the water, so larger, gilled creatures will not get enough oxygen to maintain metabolism. Large marine mammals that can take in massive quantities of air at the surface and hold their breath for extended periods of time while diving to great depths have the advantage here.

@AMR that seems to answer my question, why not make an answer out of it?

The "niche" of whales comprises much more than just being big. I would actually argue that this is just a byproduct of the marine lifestyle, since endotherms need to maintain their body temperature which is easier when you're big (lower surface/volume ratio). Some reasons for whales being very successful are:
1) Higher oxygen use efficiency:
AMR already mentioned the advantages of the mammal metabolism in the terms of oxygen intake. This allows whales to forage in great depths. Note that no fish could withstand such rapid pressure changes, since they need to dynamically adapt their swim bladder.
2) Intelligence:
Mammals are much more intelligent and therefore have access to resources that are not available for most other marine animals. E.g. hunting in groups requires a fair amount of intelligence and is much more efficient than hunting alone.
3) Acces to cold environments:
In contrast to fish, mammals can maintain high activity regardless of the ambient temperature. This gives them almost exclusive access to highly productive ecosystems like the antarctic and southern oceans.
4) Echolocation:
Toothed whales including dolphins use echolocation to communicate and sense objects. This is a very powerful ability for locating and tracking prey.


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What is this Sacrificial Reproductive Strategy Called?
The reproductive strategy of salmon is 'suicidal'. Before breeding the males metamorph permanently into a form suited for the breeding season but unsuited for survival. The females devote so much of their biomass to producing eggs that they do not survive long after spawning.
Does such a breeding strategy have a name? Where the parents die shortly after breeding, or indeed during the mating process. I'm sure the latter, more specialised, case could only occur in particularly simple organisms (think polyps, think deep sea). But does there exist an organism which as part of its reproductive strategy, after breeding, devote such a portion of its biomass into the production of eggs that it literally dissolves into  cloud of spawn?

It is called Semelparity.
From wikipedia:

Semelparity and iteroparity refer to the reproductive strategy of an organism. A species is considered semelparous if it is characterized by a single reproductive episode before death, and iteroparous if it is characterized by multiple reproductive cycles over the course of its lifetime.

You see semelparity as suicidal but it is more interesting to generalize survival after reproduction in all kind of species and ask why would an individual survive if it won't reproduce anymore anyway?
Why would an individual survive if it won't reproduce anymore?
From an evolutionary point of view, there is no point to keep living after the reproductive age. You will note a few interesting exceptions to the rule though, including Homo sapiens, where the female keep living relatively long after her reproductive age. Of course, modern medicine is part of the explanation but we tend to think that modern medicine alone is not sufficient. Another explanation is based on kin selection and is called the grandmother hypothesis. In consequence, semelparous species die right after reproduction.
Evolution of semelparity/ieroparity
I don't think this point can be summarized in a few words. In consequence, I will just invite you to have a look at wikipedia for an introduction on the subject.
How common is semelparity?
Iteroparity is more common. However it would be wrong to think semelparity is extremely rare or that it exists only in salmon species (in plural).
In invertebrates, Many insects (butterflies, cicadas, and mayflies) are semelparous as well as some arachnids and moluscs (some squids and octopus). In vertebrates, semelparity is rarer, but there are some frogs (i.e. gladiator frog), fishes (smelt, capelin), lizards (i.e. Labord's chameleon) and marsupials (such as the famous opossum). Finally there are semelparous plants (some agave and some bamboos). In unicellular species (and some multicellular species, such as some trees for example), the concept of semelparity/iteroparity may well not apply easily and depend on a philosophical discussion of the identity of an individual.

Thanks for the answer. I am surprised that I used to know this word. To me semelparity is a suicidal, not merely because the organism dies afterwards, but because the nature of the strategy ensures it CANNOT survive afterwards.


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What happened to this seashell?
We found this seashell on a Mediterranean beach in the south of France. While most of the shells we found were quite intact, this one caught our attention.
It is light and littered with tiny holes, and thicker than other shells we found.
Is this due to erosion in the water? How did the shell look like before the ocean changed it? Was the shell simply exposed to the water for a longer time?

I'd say that the holes were made by animals. I know some mollusks can make holes on rocks, for instance https://en.wikipedia.org/wiki/Pholadidae
But in the case of this shell, the animals must be much smaller.

The holes are probably caused by one of a family of parasitic sponges.  The holes, as you'd expect, kill the oyster, and the sponge then takes up residence in the shell. A number of species of this family live in the Mediterranean, with Cliona apparently being the most common genus (e.g. Cliona celata and C. viridis).  Images of oyster shells after a Cliona infestation can be seen here and here; these images are more dramatic than the one you found, but show the same general pattern.

Very fascinating, thank you very much for explaining!