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Do we have enough diversity of antibodies to overcome almost any antigen?
I always wonder about the capability of diversity of our antibodies. Do we have enough antibodies to fit to every kind of molecule? Wont't it be easier if our antibodies are like clay and can be molded to any form by antigens? Why to waste energy producing so many types of antibodies?
If some pathogen makes its antigens just like antibodies of our body, (I think) they won't ever be detected. So what would our body do?

As my answer is quite big I've highlighted the different regions I answer your question.
Intro and basic info
I take it you know how antibodies are made, but as a quick recap they're made by VDJ recombination of a limited but still quite numerous pool of genes which are recombined randomly, and then further recombination occurs by hypermutation of certain segments particularly in the regions that identify antigens.
What is Hypermutation?
Hypermutation occurs after the original antibody is made in order to perfect it. The same mechanism I talk about in moulding antigens below. It is exactly what it says: a high rate of mutation compared to that of the low rate in cells normally. When B cells are activated because they've met their antigen to which they respond (cognate antigen), they undergo somatic hypermutation. While the B cells undergo somatic hypermutation, the genes which code for the antibody are mutated so that the antibody binds to its cognate antigen with a different specificity. If it binds better the B cell gets to live, if it doesn't bind or it is worse then the B cell dies.
Moulding antigens
What we cannot do is the other way around. We can't recognise an antigen and then make an antibody to it, because recognising the antigen requires an antibody. What we can do is once we've recognised the antigen, then mould the antibody so it is a better fit. How we do this is by B cells mutating their antibodies and competing which binds better. However, B cells just don't have the knowledge to see an antigen and think a tyrosine residue at this position will be perfect to change my shape to this configuration - that's really complex stuff!
Do antibodies recognise every molecule?
Antibodies are made to essentially every antigen which is very costly in terms of energy as you mentioned. In fact, the number of genes that make antibodies are thought to be the perfect amount as to protect us without being too numerous so that it is not only too costly, but we have so many different antibodies the chance of ever finding the right B cell is so low we die before we manage. This is because of the way antibodies are mass produced, in the typical pathway of new antigens, firstly a T cell must recognise the antigen then B cells that produce an antibody that binds to the antigen (rarely in the same region, and may not even be to a protein antigen).
So these two paragraphs highlight the limitations and answer your first question. Antibodies are so diverse that we can expect quite a few to recognise every pathogen, but not every single possible antigen will have a cognate antibody. Diversity without so much diversity that it becomes redundant. The second limitation is that antibodies will ideally not form if they recognise self (our own proteins etc.) Which leads on to your next question.
What if a pathogen makes antigens that look like our own proteins?
Autoantibodies are made but are typically non-pathogenic (i.e., they don't cause harm). Certain HLA/MHC polymorphisms that make us likely to form autoreactive T cells, also make us make autoreactive antibodies. Interestingly, this increases our risk of autoimmune diabetes but ALSO makes us more resistant to infection by HIV. This can be practically seen in the DQ8 polymorphism. This is a perfect example to illustrate the answer to your second question. Ideally, pathogens which have antigens similar to our own would not be detected. HIV wraps itself with an envelope of our own lipid membrane for this purpose, and the best neutralising antibodies are often self-reactive and therefore are those that failed elimination.
However even these pathogens are going to do something or make something that isn't something our cells usually do. This is how the body finds and targets cancer cells (in a way), they do things our own cells won't typically do like make the wrong proteins or wrong amounts etc. Thus cancer cells and pathogens can be targeted by our cells that find something that isn't self (CD8 cytotoxic/killer T cells). As for pathogens, we all make MHC/HLA which is unique to us and pathogens could never manage to invade and make the specific HLA/MHC that we do, so our body also targets missing HLA/MHC.

Wow !!! I really like your answer .....:)

Could you tell me what is hypermutation ?

Thank you! And yes, I've updated the answer to describe hypermutation briefly.

Loved your answer. But can you add a chapter about self tolerance and how CD8 cells recognize cells which produce wrong amounts of protein?

That's a question in it's own right @NeoDevlin, best imo to open a new question. It isn't as related to this question, if I come across it I shall answer it =]

I am not able to understand how mutating the gene for antibody and then giving the antibody a new specificity could be accomplished. Is this mutation random , if so, there cud be many combos which were harmful and most of the cells wud die.   Please help.

Yes, it is random and most die. But that's normal, some studies say up to 99% of B cells die. It just shows how important the immune system is that it is actually advantageous to be that wasteful.

The structure of a protein is largely dependent on what it is supposed to do. There is a little bit of wiggle room, but essentially, major changes in structure will also change the function of the protein.
This is why it would be difficult (though not entirely impossible) for a pathogen to successfully change all its surface antigens into close-enough mimics of the host antigens that the host immune response is completely evaded. Antibody CDRs are extremely sensitive, and a change in even a single amino acid of the epitope is often sufficient to trigger a full-blown immune response.
In addition, antibodies are only one of the many mechanisms (albeit a very important one) by which the immune system detects and eliminates invading pathogens, so even in the case of failure of the antibody system, T-cells and the innate immune system should generally be sufficient to initiate an immune response.


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Plasma cells and memory cells
What decides whether an activated B cell will get converted to plasma cell or memory B cell? Is it necessary that out of a mitotic division one will convert to memory B cell and the other to plasma cell?

A summary of what we know so far includes that for B cells to become plasma cells they need BLIMP-1. For memory cells CD40 engaging with CD40L on B cells is required. CD40 is expressed on Th cells and thus they are also necessary for memory cell development. Problem is though, it's really damn confusing after that. It really isn't known but if you're interested in this stuff consider reading this review which talks about memory cell differentiation and this which discusses plasma cell differentiation.
The image below helps (taken from this review)
PC = Plasma Cell, MBC = Memory B cell

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Is it possible to condition the body to reduce bruising?
I do combat sports, and in these sports there are a lot of hits that can cause bruising.
I've found that, over time, physical conditioning can reduce and/or eliminate the bruising to the point where even after hard impacts, there is no residual bruising.
However, I was under the impression that it is not possible to "condition" for reduced bruising since bruising is the result of ruptured capillaries, and you can't condition to not rupture blood vessels.
Can someone offer an explanation to why, with conditioning, it is possible to reduce/eliminate bruising?

Speculation: It may have to do with an increased capacity for repair. While you will still bruise from impact, the intensity and duration of the bruise are more limited due to a quicker/more efficient healing response.

Hi Leonardo. Thanks. What causes the increased capacity for repair? Is it increased blood flow?

healing, esp speed of repair would be dependent upon your genetics as well as your nutrition

Shigeta, genetics and nutrition has nothing to do with this topic. Please read the question.

@me2 nutrition has a lot to do with healing better actually as I have pointed out in my answer

Bruises are a type of hematoma of tissue in which capillaries and sometimes venules are damaged by trauma, allowing blood to seep, hemorrhage, or extravasate into the surrounding interstitial tissues (reference).  From what I read there seems to be two reasons why you notice a reduction in bruising.
The first would be because there is a deadening of nerve cells where they get used to the pain and eventually less sensitive. There could also be the development of some scar tissue from the bruising which has irregularly developed nerve endings leading to lesser stimulation. (reference 1 and reference 2)
The second reason could be because you yourself get stronger. The Wolff's law states that:

Bone in a healthy person or animal will adapt to the loads under which
  it is placed.1 If loading on a particular bone increases, the bone
  will remodel itself over time to become stronger to resist that sort
  of loading.2 The internal architecture of the trabeculae undergoes
  adaptive changes, followed by secondary changes to the external
  cortical portion of the bone,3 perhaps becoming thicker as a result (reference).

So, repeated stress on the bones of your face/hands should be make them stronger. I don't think your body can adapt to heal faster in an area from repeated bruising as most likely scar tissue will develop from repeated stress on the skin. You can however improve your nutrition and diet to help your body heal better (reference).

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How can I learn about how cloning works in nature (twins)?
I would like to learn about how the process of cloning works in nature - how are twins "created" after fertilization what genetic changes can occur in each of the twins.
Where should I start? What are some interesting books on the topic, as well as recent research papers (or just the most important research topics that I could use to start looking for more information)?

A good starting point would be figuring out whether you want to study monozygotic or dizygotic twins. Monozygotic will produce genetically identical twins. Dizygotic twins are siblings who do not share a genome as there are two eggs involved.

To learn about the process of how cloning works, you need to appreciate the underlying principles. A general bio textbook should suffice (most popular one is Alberts, where you should focus on chapter 21, but maybe read other chapters for background)
Nature Scitable is also a good source.
I'd discourage reading research papers at this stage, primary research paper are often very specialized, and reviews are aimed at other researchers in the field, that is unless you find one that is focused on communicating science to the public.


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Same 185th million grandfather?
I was watching a lecture by Richard Dawkins earlier today and he mentioned that “Your 185th million grandfather was a fish.” I started wondering about the following question,
Is it true that my 185th million grandfather is the same as your 185th million grandfather?
Now, I fully recognize that there are more generations in my family tree than in yours or vice-versa so the 185 million may not match up exactly. This is not the point of the question. Do Humans share a common ancestor substantially after the origin of life?

Yes, all currently living humans stem from one ancestor which was also hominid. Much further back, all life probably shares one ancestor.

All currently existent forms of life (and all their ancestors) are thought to be descended from a single life form known as LUCA (Last Universal Common Ancestor). Within those organisms, all organisms that share a common ancestor more recent than LUCA are said to be phylogenetically related. These organisms are (ideally - see note) grouped together by scientists into monophyletic taxa.
Therefore, ideally, each taxon represents a group of organisms that have descended from a single common ancestor, not shared by any other taxon. Taxa are defined at various levels including, but not limited to, Kingdom, Phylum, Class, Order, Family, Genus and Species, with organisms at each level having a more recent common ancestor than the ones preceding it. For example, for humans, a superficial phylogenetic classification would look somewhat like this:

Kingdom: Animalia (shares a common ancestor with all multicellular, eukaryotic, heterotrphic, motile organisms)
Phylum: Chordata (shares a common ancestor with all animals that possess a spinal cord)
Class: Mammalia (shares a common ancestor with all chordates that produce milk and are warm-blooded)
Order: Primates (shares a common ancestor with all monkey-like mammals)
Family: Hominidae (shares a common ancestor with all the great apes)
Genus: Homo (shares a common ancestor with relatively recent humanoid species)
Species: sapiens (shares a common ancestor with all humans)

As you can see, this means that all humans share a common ancestor with all other humans, but going further back, they also share a common ancestor with all primates, all mammmals and all vertebrates. Eventually, all animals share a common ancestor, and if you go as far back as LUCA, so does all life.
Note on taxonomy and phylogenetics: Many modern taxa are (to the best of our knowledge) monophyletic, meaning all organisms in a given taxon share a unique common ancestor. However, there remain several taxa that are paraphyletic, because they were described before modern genetic methods became available, or because no one has got down to reclassifying them or (in at least one case, reptiles and birds), because they are so widely used that changing the classification could (and probably would) cause a lot of confusion. So, when using taxonomic classifications to deduce phylogenetic relationships, a bit of caution must be exercised to ensure that the taxon one is talking about is indeed monophyletic.


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Autophagy in eukaryotic cells
What is autophagy? How and under which circumstances is it used by the cell? I believe The reason for autophagy is some kind of recycling, am I right? But why does it occur in infections?

Autophagy is a cellular process that is occurring all the time, but it can be elevated during times of need (see below).
In autophagy, cargo (can be anything - mostly macromolecules but also bacteria/viruses etc) is taken up by a lipid membrane which folds on itself to form an autophagosome, which is like a vesicle but have markers on it that makes it specialized in carrying out autophagy. These autophagosomes are then transported to, and merge with, lysosomes, releasing the cargo into the lysosome to be degraded. The broken down materials are then released back into the cytosol, where other processes can make use of them. That is the "some kind of recycling" you are referring to.
There are two types of autophagy - selective and general. In selective autophagy, receptors on the membrane of the autophagosome specifically selects for ligands (e.g. p62, ndp52 selects for ubiquinylated substrates, which usually marks molecules for degradation). In general autophagy, the uptake into the autophagosome is random.
So, you can think of general autophagy as maintaining a basic level of turnover - to ensure everything in the cell is not worn out; and selective autophagy as a response to specific ligands that needs to be degraded.
By this logic, autophagy activity increases during infection because those infectious agents, once gaining entry into the cell (either through phagocytosis or by forced entry), will need the autophagy machinery to transport it to the lysosome to be degraded. Interestingly, some bacteria actualy hi-jacks this process to ensure its survival in the cell. Here's a good review to get you started if you are interested.
Note that the proteasome also recycles macromolecules, although the things it can recycle is limited by size.

I like your answer. But in most sources I read there is a distinction between normal phagosomes which have one membrane layer and autophagosomes which have 2 to 3 membrane layers. Which is the only distinction I found so far.  Are there any other reasons to differentiate between these two processes?

Like I said, autophagosomes can take up any cargo - this includes other vesicles and phagosomes.
The autophagosome is double-membraned, so when it fuses with the lysosome, the inner membrane is 'released' into the lumen of the lysosome, whereas the outer membrane fuses with that of the lysosome. Thus, the outer membrane of the autophagosome would resemble more of the lysosomal membrane (and they do share similar markers and it's often hard to distinguish the two in microscopy). This is different from the the membrane of phagosomes, which originate from the plasma membrane.

Having said this, no one is sure as to the origins of the autophagosome membrane - where the lipids are sourced from.

To answer your question - you can distinguish the two processes as their place of origins, phagocytosis originates at the cell membrane and autophagy originates inside the cell. The phagocytotic process may feed into the autophagosomal process, although it may not be an requirement.
If you read the review I suggested, you'll appreciate that some bacteria that is taken in using phagosomes, break out of their phagosomes and replicate in the cell. This is when autophagy can come in and restrict their replication.
So I, a very crude distinction would be - phagocytosis outside, autophagy inside

Any papers by Daniel Klionsky and Beth Levine should definitely be used for reference, they are the two biggest names in the field today.


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Which hormones/factors affect Calcium absorption in the small intestine and its regulation?
I think the question is very broad and cannot find precise mechanisms.
I am not sure about the precise mechanisms of the regulation.
I think they are at least Vitamin D, diffusion and specific calcium channels: calbindins.
More specifically, calbindin-D9K and the basolateral calcium pump transport calcium from cell interior to extracellular space.
The calcium gradient should also be free, -2-6 mmol/l, in the lumen to allow diffusional calcium absorption from the interstitial space.
Similarly, free calcium concentration in the extracellular fluid of the lamina propria.
I think that the most important mechanism for this absorption is the electrochemical gradient of sodium across the epithelial cell boundary of the lumen, similarly as for carbohydrates.
To keep the extracellular space free from calcium, the NA/K-ATPase i.e. sodium pump has to work.
I did not find any hormones that affect the intestinal calcium absorption.
Which factors affect calcium absorption and its regulation?

Parathyroid hormone increases intestinal calcium absorption by increasing production of vitamin D, which in turn uses calbindin. It also enhances calcium reabsorption from the kidney and the release of calcium from bone.

Is there any other hormones or factors that affect the calcium absorption in the small intestine?

The only other hormone involved in calcium homeostasis that I know of is calcitonin and that not only plays a minor role but doesn't have intestinal involvement. If there are any other they would be very minor.

As @AndroidPenguin said Vit D3, calcitonin and parathyroid hormone are main hormone regulators. You can check this review. It talks about Sex hormones having indirect roles.


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Change in conditions of an ecosystem lead to change in organisms
Let's think about the slash and burn method and its effects on the ecosystem.
Cutting down trees that rise all the way up to the canopy would expose the plants at ground level to more light, so would change an abiotic factor so changes the conditions required for survival. These plants are not adapted to the high light intensity so would find it hard to survive and compete, through inter-species competition, with newly arrived plant species that are much more adapted to the extra light intensity.
Obviously this would cause a dramatic reduction in the numbers of the previous plant species and would result in migration of the animals due to lack of food, assuming they can't feed on the newly arrived plants, and a change in the food chain.
In what ways do this affect the local and regional ecosystem, and what problems could it produce (both from an ecosystem and human perspective)? These types of land-use changes are often seen as problematic in conservation biology (as "...a bad thing"). Wouldn't the new plant species bring in new animals that do feed on them and a new equilibrium be reached just with different species? Is it to do with the reduced biodiversity or danger of extinction of indigenous organisms?
As you have probably realized I don't exactly understand this topic perfectly and would appreciate any amendments or extra information to the paragraphs above.
Thanks in advance.

Just to be clear: is your question mainly on 1) if ecosystem change and (local) species extinction is a bad thing (a philosophical/ethical question) or 2) if your description of the process is correct (ie how ecosystems change from clearcutting, including longterm effects on biodiversity - that is, an ecological question)?

I guess a bit of both! To make it more clear I want to know why cutting down trees is bad in terms of the ecosystem. Also is the process correct?

The question is not answerable unless you define "bad"

Remembering back to my undergrad in conservation & ecology; the cutting down of large trees/plants will make space for young of those species to grow - see first line of 4th paragraph here: http://www.forestrycorporation.com.au/__data/assets/pdf_file/0009/233739/as20-in-a-rainforest.pdf

@user3760 I suggest an edit would help this question (it has 4 close votes already and I assume you don't want it closed) - instead of asking why slash and burn might be bad for the ecosystem, you could perhaps ask what the consequences of slash and burn are on the ecosystem? - The reason it is attracting close votes is probably because trying to define it as a "bad thing" is more philosophical than biological - being good or bad for the ecosystem is largely subjective to what you want to achieve from the ecosystem.

@GriffinEvo I agree that the phrasing of the question is problematic. However, from the perspective of conservation biology (arguably a part of biology) similar arguments are often used as shorthand, since the outcome of certain actions clearly go against the "goals" of conservation biology (which is interdisciplinary and has been described as a "crisis discipline"). Therefore, I can understand why a newcomer to the field can become confused. I have tried to edit the Q to remove some of the more subjective elements.

Thanks @fileunderwater it's a good question and I saw it was getting closed in the review and thought I could advise & help the question survive

I will try to provide a general answer, starting point and overview to this question, even though it is rather wide ranging and vague.
The biological process
If we start with your description of the process; you are correct that such a dramatic change in the environment as slash-and-burn agriculture will drastically change the living environments on the canopy floor (well, in the entire ecosystem).
To name a few, there will be changes in:

Light conditions, which will alter the competitive balance between plant species, where ones adapted to a closed canopy will disappear.
Moisture
Temperature (maximum, minimum and variance in temperature)
Nutrients The point of slash-and-burn agriculture is to provide a boost of nutrients for farming. However, the boost is short-lived and transient. Afterwards, you are usually left with a very nutrient poor soil, which is common in tropical forests. Tropical forests (where slash-and-burn is often used) are high in biomass, but most if it is bound in the standing biomass. When this is removed by clear-cutting, the natural cycling of nutrients is disrupted, and excess nutrients are leached out of the soil (Ricklefs, 2001).
Loss of host species This will lead to loss of primary consumers (specialists & generalists) feeding on them, and cascading effects into the ecosystem that depends on these.

All these changes and several others will dramatically modify the niche spaces and the competition between species in the forest patch, and most previous species will probably not be able to persist locally. New species will move in to fill the open niches, and over a (long) period of succession a new quasi-stable community will emerge. Due to the extremely high biodiversity in tropical forests it will almost certainly contain fewer species than the original community.
The question of whether the community will eventually return to its previous state (even if that will take an extremely long time), is a relatively open question, and also depends on the conditions at the specific site and if the spatial scale of the disturbance. The biggest issue for conservation biology is that these land-use changes generally happen at a large scale, so fragmentation of species habitats can lead to regional and even global extinction. Since many tropical species have small ranges and are not adapted to fragmented landscapes, many run the risk of going extinct. Therefore, even if the overall appearance of the original forest will return, it will contain a very different set of species. Land-use changes, even in the form of temporary slash-and-burn agriculture, also generally leads to continued/secondary exploitation of the area and seldom to restoration/regrowth (Meffe & Carroll, 1997).
I also want to point out that you are indirectly referring ("...new equilibrium be reached...") to the idea of a Balance of nature in ecosystems, which is largely seen as obsolete and incorrect. However, as shorthand or when referring to a dynamical equilibrium between multiple populations (with ongoing evolutionary change) it can be meaningful.
The philosophical issue
The question of whether an ecosystem change or extinction of species is "...a bad thing" is inherently philosophical and depends on human judgement. The philosophical foundations for conservation biology can be divided into instrumental values and intrinsic/inherent values. Instrumental values can then be subcategorized as services (pollination, water regulation), goods/resources, information (e.g. genetical info to be used in medical research), and esthetic/spiritual values. Intrinsic values refers to a specific value placed on species, ecosystems or evolutionary history due to its uniqueness and it is seen as independent of human needs and wants (although some argue that values independent of humans are impossible). Intrinsic values are also connected to the acknowledgement that organisms have interests and wants themselves (their own 'good'). Different people naturally weight these issues in different ways, and for some the short-term economical gains will weigh heavier. The long-term economic costs are potentially large, but less certain. From a strict biodiversity perspective (i.e. a species counting perspective), the change will certainly be negative, since the change in land-use will decrease diversity and probably lead to more 'trivial' species moving in. From the perspective of the original ecosystem (if it has a say) the change is per definition negative, since it will disappear.
The direct intrumental value of individual species are usually uncertain (irrespectivly of the direct rationales used), so the precautionary principle is often invoked to justify species conservation. Also, numerous examples exist of how aspects of biodiversity are related to human values (some recent examples are Garibaldi et al. 2013 and Gamfeldt et al. 2013), such as production or services, which can also be used to justify both conserving biodiversity or individual species. An example of ecosystem services from tropical environements can be seen in Ricketts (2004). However, sometimes functional diversity is emphasized which focus on preserving functional groups of species instead of 'general' biodiversity (i.e. specific species).

It's worth noting that there are sustainable and biodiverse agricultural systems that have been called "slash and burn" by outsiders. In many parts of the world, these managed successionary stages of "swidden-fallow" or "shifting cultivation" have created dynamic and resilient anthropogenic landscapes.
Hal Conklin's studies on Hanunóo agriculture are the classics in this field. For a good, general introduction try this powerpoint, which also notes that sustainable swiddening is closer in ecological impact to natural tree-fall disturbance, which usually has been taken to promote forest biodiversity (see Intermediate Disturbance Hypothesis).
This is not to say that there aren't forests undergoing slash and burn that are being permanently transformed, and in a direction of lower biodiversity and lower human utility (i.e. "bad"/"destruction"), or to say that all traditional agricultural systems are necessarily sustainable; only that under many of the biological and philosophical criteria that fileunderwater raises, there do exist sustainable and biologically rich human-biological systems that have been called 'slash-and-burn'.

True that slash-and-burn can be sustainable, and that lack of natural disturbances (e.g. fire in boreal forests) can also be a problem. However, I would be hesitant to hinge this on the intermediate distrubance hypothesis, since the whole concept has been strongly critizised in a fairly convincing way, see e.g. *Fox. 2013. The intermediate disturbance hypothesis should be abandoned. TREE*.

Yes, it is an interesting topic, expecially since the IDH has been a default fall-back to explain diversity patterns. There are a couple of other papers as well, but they are cited in the review. Look at the blog posts by Fox as well (IDH as a zombie idea) at dynamicecology.wordpress.com e.g. here and here


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Can songbirds mimic car alarm sounds?
A silly question. A few days ago I observed a very vocal bird with impressive vocal variety. It was rapidly switching from one tune to the next. After sometime I realized that the bird might be mimicking the 6-8 tone car alarm (the one that rapidly changes). Is this my imagination, or are birds really know to mimic/compete with car alarms?

You would be amazed at the vocal abilities of the lyrebird.  A car alarm is easy for them; they can mimic much more complicated sounds.
Here's a snippet from a David Attenborough BBC documentary on YouTube (which includes the car alarm example, among others).  They are so skilled, it's hard not to think this video is fake.

Thanks, that bird does imitate car alarm, but I was really surprised at the chainsaw sound


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Do nerve cells cause action potential in cardiac muscle?
I think the answer is no, but I am not 100% sure.
If it was yes, then the dendrite of the nerve cell should each time receive a stimulus causing Na+ channels to open, when the contraction happen.
Also, then it would mean that outside events could alter the function of hearth, which would be dangerous.
The heart has a special excitatory system and a contractile system - Sinoatrial node and Pacemaker cells, which control the action potentials in different portions of the heart.
So heart and primarily myocardium i.e. cardiac muscle can depolarise without any external influence with a slow, positive increase in voltage across the cell's membrane.
Do nerve cells cause action potential in cardiac muscle?

The vagus nerve controls heart rate. This is the best example of a direct nerve action potential impacting cardiac muscle, although one could argue the adrenaline system to be an indirect mechanism.
The vagus nerve is part of the parasympathetic system, it acts to decrease heart rate. Resting heart rate is maintained by permanent vagal stimulation/tone by the release of acetylcholine.

Heart cells will contract on their own without the presence of nervous tissue. If you place small pieces of fresh heart tissue in a Petri dish in a proper solution, they will contract on their own at a frequency somewhat slower than a regular heartbeat. But the pieces may contract independently of one another.
The purpose of stimulation from the vagus nerve is to act like an orchestra conductor causing the contractions of individual cells to act in a coordinated manner.

Can you provide any sources and/or data sets about your claims? It would be great to study basic ECG signals or similar things of such experiments.


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What are the allowed evolution operators (on protein encoding sequences)?
What are the evolution operators, meaning allowed actions on the DNA sequence that encodes a protein.
I assume all evolution of genes is a result of duplication errors. So an answer could look somewhat like this: duplication of gene into two identical ones, omitting of nucleotide, addition of nucleotide and so on.
And some followup questions:

Does this mean that originally there were very few genes and they were very short?
If so - how few? How short?

It is incorrect to assume that all evolution of proteins is a result of duplication errors. Sequences can be changed in situ as well.

Also, evolution does not really act on proteins but on genes.

@terdon and all other base sequences that have any biological function like regulatory elements. I'm not sure how this question could be answered as it seems to be based on some false premises.

@MadScientist yes, I mean that evolution acts at the nucleotide rather than the amino acid level but felt it would be better understood by the OP if I said "genes".

The question is simply what kind of errors does the DNA replication machine do (or other mechanism  with which evolution occurs). I called it protein sequences, but of course I mean the DNA that encodes a certain protein. I rephrased for clarity.

Your follow up questions are vague.

I think what @AP means is that this question doesn't have the clean answers you are looking for.

An old microbial geneticists' adage is: anything that can happen will happen, and you just need to find a way to select for what you are seeking.
A look at the Wikipedia page on mutation might be instructive.

Looks like this is what I've been looking for.

The most frequent mechanisms are

Intragenic mutations: when existing genes mutate modifying gene function.
Gene duplication: leads to related genes in a single cell. A gene duplicates and then as two copies are available, one is free to change
Segment shuffling: leads to hybridisation of different DNA segments.
Horizontal transfer is transfer of DNA from one cell to another
Transduction: infection of cells by viruses or other intracellular pathogens where their DNA can integrate into the genome

You are incorrect to say all evolution occurs due to duplication. Your follow up questions are too vague. Genes can become larger or smaller, but yes as they increase so does their diversity.

Can you please clarify the following:
What exactly are intragenic mutations? What exactly is their mechanism?
What is the mechanism for complete gene duplication and segment shuffling?
Why didn't you mention single nucleotide errors by the replication process?


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Are CoA and CoAS the same thing in a compound?
Is CoA-S-R the same as CoA-R, and is CH3C(=O)CoA the same as CH3C(=O)SCoA? Eg. Above is the compound on the right just coenzyme A or is it actually another compound and not just notation?

To understand the nomenclature here it is very helpful to think about how Coenzyme A works. It has a thiol group (-SH) which can form a thioester bond to an acyl group.
So the sulphur in "CoA-S-R" is part of the CoA, and in "CoA-R" the sulfur is just not explicitly named. Those two mean exactly the same thing: Coenzyme A linked to R via a thioester on the thiol group.
One specific variant that is very important in biology is acetyl CoA. The chemical formula you mentioned (CH3C(=O)CoA) is acetyl CoA, and here the same as above applies and the sulphur is explicitly mentioned in the second one and implied in the first one.


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Are there any bacteria, in our environment, able to break down nitrate under aerobic conditions?
Given a fix volume of water saturated with dissolved oxygen through aeration. Suppose that ammonium, Nitrosomonas, and Nitrobacter are always available in the water. We know that some of the ammonium will eventually be oxidized, by the bacteria, to nitrate. We also know that under anaerobic condition, some of the nitrate, through many steps, will be broken down into Nitrogen by denitrifying bacteria.
Question: Are there any bacteria, in our environment, able to break down nitrate under aerobic conditions? If there aren't, will the nitrate continue to accumulate?

My initial reaction upon reading this question was to think that the answer was: no, denitrification is a process in which nitrate is used in the absence of oxygen as an alternative electron acceptor. However I decided to check the literature, and I have discovered that there is, in fact, a lot of new evidence that many bacterial species may be able to use both of these electron acceptors simultaneously. This article is a good place to start if you want to find out more:

Chen & Strous (2013) Denitrification and aerobic respiration, hybrid electron transport chains and co-evolution. BBA Bioenergetics 1827: 136-144

This is a review which summarises the area from the point of view of bioenergetics, but most importantly for this question, includes a Table summarising the experimental evidence for the phenomenon.  Referring to this Table, they state:

It appears that in most cases, the evidence presented is not sufficient to support the conclusion that denitrification really proceeded in the presence of excess oxygen. It should be noted that the aerobic denitrification rates were much lower than the anaerobic denitrification rates measured for the same strain while aerobic respiration rates remain high. This implies that the major electron flow in the respiratory chain is towards complex IV rather than the NOx reductases, and that aerobic respiration is still the preferred pathway for growth. Apparently aerobic denitrification can be an auxiliary pathway next to aerobic respiration.

The last sentence answers the OP question.


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How is antibody production stopped?
Once clonal selection is done, B cells would start dividing and producing antibodies. So, after an antigen is eliminated, what stops the division of B cells and antibody production?

Upon activation plasma B cells upregulate death receptors as part of being activated. Presence of the antigen overcomes the death signal, thus the cell survives. When antigen is lost, the death signals overcome the survival signals as there is no antigen, so the B cell dies via apoptosis.
Memory B cells don't do this. They survive and continue to produce antibodies for years, although this slowly wanes. Antibodies have to be produced as antibody mediated immune mechanisms are extremely important for memory and the reason why a subsequent infection is cleared so rapidly. Furthermore for the example of HPV, antibodies induced by the vaccine prevent the virus even infecting cells (so called neutralising antibodies).

You are right to say that Plasma Cells are terminally differentiated, so they don't become the memory cells, or calm back down or anything. But all Plasma Cells are not the same, there are Short-Lived Plasma Cells (SLPCs) that are less specific, but arise rapidly after stimulation, and there are Long-Lived Plasma Cells (LLPCs) that come about later and have more specific antigen binding.
SLPCs are rapidly activated, but also rapidly lost. These are the cells that Android was talking about when s/he said that apoptotic programs are initiated as soon as cells become activated and are eventually eliminated by these mechanisms.
LLPCs are the cells that stay in your body for a much longer time (theoretically for life, but probably not practically unless you get hit by a bus in a couple of years). When you get a vaccination, these are the cells that produce antibody that can be detected in the blood for a number of years (what testing your antibody titer looks for). These cells are in pretty limited supply, so we know less about them. My guess is that they are not actively eliminated, but may become eliminated over time by other mechanisms (purposely undefined here).

My understanding of this question is: Antibodies are produced by plasma cells which are terminally-differentiated B cells. Maturation of B cells to plasma cells is stimulated by the presence of antigen (T cells, cytokines, etc. etc).
In the absence of antigen the existing plasma cells undergo apoptosis, and the maturation of the cognate B cells will not be stimulated, so no more plasma cells will be produced.
I have found it surprisingly difficult to find references in support of these statements, although there is a large literature on the suppression of apoptosis in memory B cells.

Alan, you might try Ralph Zinkernagel's review: http://www.ncbi.nlm.nih.gov/pubmed/24909054. I don't have full access to the article, but it appears that he summarizes work showing the half-life of various types of Plasma Cells. I'm not sure to what extent anyone has looked into the apoptosis pathway that may be involved in these cells particularly.  Klaus Rajewsky has done work assessing the half-life of naive B Cells. It's possible that he has a review somewhere that can point you in the right direction. Good luck - and please post anything useful you find here.


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Blood circulation and blood pressure in different tissues
The volume of blood coursing the blood circulation is approximately five litres. A typical vein will stretch about eight times as much as corresponding artery. Because veins have high capacitance, large changes in blood volume have little effect on arterial blood pressure.
If the volume rise or falls, the elastic walls stretch or recoil, changing the volume of blood thus blood pressure in the nervous system.
What else tissues can we consider?
I am interested in blood circulation and blood pressures in different tissues.

I don't understand what you're asking. Please clarify

I'm not sure I understand your question very well-maybe try and rephrase it? As another example, low blood pressure in the kidneys is sensed by the juxtaglomerular apparatus which secretes renin into the circulation. Renin converts angiotensinogen (released by the liver) into angiotensin I. Angiotensin I is then converted into angiotensin II by angiotensin converting enzyme (this is the target of anti-hypertensives called ACE inhibitors) secreted by the lungs. Angiotensin II is a potent vasoconstrictor which directly increases the blood pressure (and hence glomerular filtration rate).  Angiotensin II also causes the release of aldosterone which acts on the kidneys to re-absorb salt and water again all facilitating an increase in blood pressure. I hope I've answered your question, if not please edit the question so it very clear.

I think you are correct. I got the exercise as is in the title. I discussed in the exam about Centers in Brain and Receptors. Basoreceptors and vasomotor center, for instance. Should I include neural regulation of blood circulation to the exercise in the title? I think now no.

The diameter of the blood vessel affects the speed of the flow of blood. Blood flow slows down as it moves from arteries to arterioles and subsequently to the capillaries because the cross-sectional area in the capillary beds is much bigger than the arteries or any part of the circulatory system. Use this drug awareness forum to know more about this.

Although the question isn't very clear, I'm not sure that this answers it and does rather read like an advert.


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What are the differences between G+ and G- bacteria?
The distinction between Gram-positive and Gram-negative bacteria is based upon the Gram staining method, that reflects the bacterial wall physical properties.
However, this classification involves also a large number of differences between them. For example, the endospore formation usually occurs in Gram-positive bacteria and also the quorum sensing mechanism is different.
So what are those differences? Which of them are due to the cell wall thickness and membrane(s) composition and which instead to evolutionary divergences?

here's a partial answer... http://biology.stackexchange.com/questions/7118/what-are-gram-negative-and-positive-bacteria

I didn't know there were distinct differences between gram-positive and gram-negative bacteria when it came to quorum sensing, but it seems as though there are:

In gram negative bacteria, acyl-homoserine lactone type molecules serve as the main signalling molecules while lipid, peptide, and amino acid based signalling molecules infrequently serve as signalling molecules. Furthermore, in gram-negative bacteria, there is one well conserved mechanism for controlling quorum response. Gram-positive bacteria, on the other hand, use peptides or modified peptides as the primary means of signaling; and also differing from gram-negative bacteria, there are several different mechanisms found within the class which are used to gain quorum responses.

Source.
In G+ bacteria, the two main quorum sensing mechanisms are apparently as follows:

Two-component signal transduction, in which the peptide signal works by binding to a sensor protein, histidine kinase, located in the cell membrane of the bacterium. The activation of the histidine kinase leads to phosphorylation of response-regulating protein, and interaction with another regulatory protein facilitates transcriptional activation.
Internalization, in which the signal molecules are transported into the responder cell to interact with intracellular effectors.

G- bacteria on the other hand, synthesize autoinducers, effector molecules that can diffuse freely through the cell membrane and trigger cell response when a certain concentration threshold is reached. I do not know how or if these differences are related to cell wall structure.
When it comes to endospore formation, all I know of the difference between the two is that this is by far most common in gram-positive bacteria.


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Do Acyl Carrier Proteins and Conenzyme A have similar reactivity?
In terms of the reactions they undergo are they roughly equivalent groups?

The acyl groups ligated to CoA and to acyl carrier proteins are actually attached to the same group (a phosphopantetheine group) as shown below, and so have very similar reactivities (i.e. group transfer potentials).


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How does a virus take control over the host cell?
When the virus integrates its DNA with the hosts and enters the lytic pathway, do the viral proteins that produced destroy the cells DNA? Do they deactivate it? Also does the cell function in the same way as before?

A virus does not typically destroy its host's DNA. Rather, the virus makes the host cell express viral proteins at an elevated rate compared to the host's own proteins. This is usually achieved because the viral genome contains a strong constitutive promoter, possibly coupled to an enhancer sequence. The virus may also preferentially insert itself into transcriptionally active sections of the host DNA.
As I said earlier, expression of the host's own genes as a whole is not directly regulated by the virus, though specific genes may be up- or down-regulated (immune-system related genes are often primary targets). However, the host's genes will usually be expressed at a reduced level because of the resources being diverted to make virions.
Remember however, that the virus relies totally on the host's machinery to make viral proteins. So, anything that kills the cell before sufficient viral particles are assembled is going to be selected against. This doesn't mean that the cell is healthy though. A significant chunk of the cell's resources have been hijacked by the virus, and a virus infected cell is typically just limping along, clinging to life, as it were.
Depending on the virus, once sufficient virions have been assembled inside the cell, the virus may enter a lytic phase, where the cell literally bursts to release the virions into the surrounding environment to infect new cells. At this point, the cell is obviously dead.

"The virus may also preferentially insert itself into transcriptionally active sections of the host DNA." I'd be interested in reference, it doesn't sound familiar to me. Any text book should do.

"However, the host's genes will usually be expressed at a reduced level because of the resources being diverted to make virions." Is there some textbook page addressing this?

RE "So, anything that kills the cell before sufficient viral particles are assembled is going to be selected against." Very interesting, refering to the question which erroneously sees integration of DNA into host genome as a rule and not the exception: "selected FOR" then should be the integration of DNA into the genome, as well as replication of virus by live replication of the host. Interestingly, it does not at all seem clear in science that integration into DNA depends on or is made possible by  the cell dividing.  "Transcriptionally active" : with the intention to divide, to cross-over?


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

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

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

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

I'm not certain of the accuracy of these tests because dog breeds aren't commonly genotyped. I'm not certain if there is a central database of dog breed genotyping, or if there is, whether they have significant sample size to accurately assign a breed.

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

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


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Structure of adenoids
I am not sure this question belongs in biology, but I can't find a more suitable stack exchange site, feel free to delete it if this doesn't fit here.
Also, this question is going to be slightly gross, just a warning, but I promise it comes to a point.
I have read that the adenoids have a texture to them but, unlike say the palatine tonsils, they don't have crypts.
Last year my palatine tonsils became fairly badly infected and had to be removed over the summer. Before the surgery, I discovered I could reach back to the tonsils with my tongue, enabling me to remove the tonsil stones that built up. Gross, I know, but I believe it actually did make the infection noticeably better. After the surgery, and after the area had healed, I resumed discovering the back of my throat and, eventually, up the nasal cavity, all the way to the back of the nasal septum, which means I can reach the Eustachian tubes, adenoids, and posterior nares. If that sounds impossible, I assure you, it is perfectly achievable, and only mildly uncomfortable. With my tongue I can feel the texture of the adenoids but, more toward the posterior nares, this texture changes and resembles folds or crypts like I remember the texture of the palatine tonsils. Three times, always in the morning after waking up, I have discovered debris in this region strongly resembling tonsil stones but green instead of off white. The mucus, however, is always clear.

My question has several parts:

What are these crypts? Are they even crypts at all? Are they part of the adenoids?
Why can I not find mention to these structures in any diagrams or medical articles?
Why can I not find mention to tonsil stone like debris except in the palatine tonsils? I am quite convinced that, if these are not tonsil stones of a sort, they are closely related.

The proportions of diagrams and cross sections of the nasal cavity all seem wildly different. Some of them are just blatantly wrong, depicting, for example, the Eustachian tubes coming from the roof of the nasal cavity instead of the sides. It has been very difficult to find good information on any of this. I am not even sure if I am referring to the region correctly. By nasal cavity, I mean everything between the back of the throat and the posterior nares, although I am aware the nasal cavity includes the region all the way up to the anterior nares as well.
This is the only picture I can find that shows the nasal septum.

This is a better diagram of the rest of the structures. The pharyngeal tonsils are the adenoids.

I would say that this question is borderline to medical advice (which is not allowed at SE Biology), especially since it is so closely related to your personal experiences. Have you discussed this with your doctor? Either way, I think it would be useful if you could post a diagram of the pharynx and nasal cavity to make your question more clear. I would also consider rephrasing it to get the question more up-front and general, with less personal details.

Well I can't seem to separate out the personal details as it's kinda hard to explain to someone what you feel in your adenoids with you tongue without a back-story! I'm not looking for medical advice. I've already had a doctor look at my adenoids. He said everything was fine but I'm afraid there wasn't time to discuss the finer points of tonsil structure. I'm looking for a good explanation or reference to medical literature that doesn't completely suck like most seems to. I've only seen one cross section of the head that shows the back of the nasal septum! What an omission!

@BigEndian: I've tried to cut out a sentence or two that was veering towards medical advice (the bit about the infection).  Perhaps you might consider putting a disclaimer near the start of the question saying that you've made some anatomical discoveries because of a medical condition, and you'd like to know more (and you've been to a doctor already who said your anatomy was normal). It's not at all necessary to have a disclaimer but someone might vote to close before they manage to read your comment, and I think that would be a mistake.

I'm impressed to stumble upon someone who can do that with his tongue. And mainly because I can do that myself!
Looking at the images and feeling with my tongue, this rugged area you mention is definitely too close to the nose to be the adenoids.
So I googled a bit (well, more like a lot) and I found this cool webpage which details that area.
http://www.theodora.com/anatomy/the_pharynx.html
and I found this snippet of text:

Above the pharyngeal tonsil, in the middle line, an irregular
  flask-shaped depression of the mucous membrane sometimes extends up as
  far as the basilar process of the occipital bone; it is known as the
  pharyngeal bursa.

I've found stones in my tonsils but never in my adenoids. What I've sometimes found was dried mucus adhered to it when waking up in the morning.
I believe those stones might be rests of food (which can't really get up there).
Maybe this green mucus you found was just dried mucus? Maybe a little infection on a particular day?
I hope you get the answer, since it's passed a quite long time since you asked :)

Well that's a heck of a lot more than I could find. Thanks.


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Transcription factor binding site located in intron
I have noticed that some TF binding sites are located in the introns of the genes.
I am puzzled about whether the TF only binds to DNA in the initiation stage of transcription and will detach during transcription. (I am thinking if the TF bind to the sense strand, it will block the PoLII for transcription, thus they should be removed.)
Many thanks in advance.

As Armatus said TF can remain bound without an effect.
There are some alternative explanations:

Promoters need not be always upstream to the Transcription Start Site (TSS). There are promoters called Downstream Promoter Elements that are actually downstream to TSS.
There can be alternate TSS within the introns
TF bound to intron may regulate elongation or splicing rather than initiation. [Elongation can also be regulated especially when a gene is poised for expression. RNApolymerase stalling is a well known phenomenon and is affected by epigenetic marks. Since splicing happens co-transcriptionally there can be DNA marks that affect the process. Although it has not been shown whether such a thing happens, but Intron-Exon boundaries are known to have a distinct nucleosomal pattern.{1, 2, 3}]

Hi, Thanks for pointing out the papers. I will read them carefully

Even in a quiescent state, DNA is bound to a lot of proteins. It is not a lone double-helix of DNA with an occasional protein attaching here or there. Rather, it is tightly wrapped around histones, which themselves have other proteins attaching and detaching constantly. Repair enzymes are always whizzing about and fixing the random damage that occurs in DNA naturally, and transcription factors may be sitting on the DNA for a while and then diffusing away again without doing anything. There are probably more proteins around that I've forgotten.
As you can see, the nucleus, DNA and in general the cell interior are extremely crowded spaces, and for transcription to happen it takes more than just removing some TFs attached to intronic sequences. Histones need to be modified to repel each other and make space. Ultimately, all proteins will need to detach for a short time when RNA polymerase comes through. If they don't, polymerase will stall until they move away, or it may simply fall off, producing an incomplete RNA fragment which will be degraded quickly. Another polymerase will come along soon enough and produce a new transcript if the promotor is still in a permissive state.

Hi,Armatus,Thanks for the detailed explanation! I didn't know nucleus is such a crowed place. I am wondering if the detach process of TF from DNA can be visualized under single molecular microscope.

Microscopy at such resolutions is possible using atomic force microscopy and transmission electron microscopy, but both of these are extremely complex procedures and require the sample to be fixed - i.e. dead.

I see, so it is not possible to observe in vivo. Thanks again~


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Polymorphism in cnidarians?
To me, the phenomenon of polymorphism in cnidarians is particularly troubling. I gather that it essentially refers to existence of various different forms or  kinds of individuals, i.e. zooids and polyps in one species. But when we refer to the cnidarian Physalia, as an animal, aren't we actually referring to a colony of individuals? Physalia consists of several "entities" including gastrozooids, dactylozooids, and the float, and since each of these is a distinct "organism", therefore is what we refer to by saying Physalia is actually a colony of phenotypically distinct forms of the same species?
Therefore, can "animals" like Physalia or Gorgonia or Pennatula be thought of actually as "colony-beings" which always contain several individuals in group?

It seems like your question might contain two separate and linked issues, both of which are perhaps equally confusing and equally interesting. They're both really discussion questions in a sense, but they've also both been dealt with in the literature in thoughtful ways, so here's a stab at an "answer".
Issue One: how does your species concept deal with polymorphism?
This may depend on which species concept you're using. And, to some extent, the choice of which species concept you use depends on what kind of organism you're dealing with (for instance, organisms that reproduce asexually have a whole different set of issues and challenge several species concepts).
Various papers by Kevin de Queiroz deal very well with species concepts. In 'The General Lineage Concept of Species'  (which is also summarized on this page), he argues that although there are many different species concepts that can be better applied to different situations, they all share the basic tenet of defining a "segment of a population-level lineage". In other words, each concept is attempting to put a continuum into slightly different categorical bins, but they all recognize the existence of the same continuum (the lineage). (Also see his 'Species Concepts and Species Delimitation'.)
I think most species concepts have no trouble dealing with polymorphism because the different morphs are all part of the same lineage, that is, "a series of entities forming a single line of direct ancestry and descent" (de Queiroz 1999).

Issue Two: how does your concept of the individual organism deal with colonialism?
In 'Does Biology Need an Organism Concept?'  Pepper and Herron make a similar point to that of de Queiroz. They argue that multiple definitions (concepts) exist, and that these concepts all attempt to categorically bin what is in fact a continuum. Like de Quieroz, they argue that most definitions recognize the same underlying continuum, and that the difference is in the categorical bins.
In the case of the organism concept, this continuum is based on two criteria: increasing genetic homogeneity, and increasing physiological integration.
So, for instance you could have two organism concepts (in the picture below, lighter yellow and darker yellow) that agree that Physalia falls in the same location along these axes, but disagree on exactly where to draw the boundary between their "multiple organisms / colony" zone (yellow), and their "individual organism" zone (white).

I'll finally get to my point, paraphrasing both de Queiroz and Pepper and Herron. For both concepts of the species and of the organism, arguing about whether one concept is better than another is endless (especially on a site that aims at answers rather than discussion). However, recognizing that there are different concepts, understanding that what these concepts do is to bin the same continuum in different ways, and being clear about which concept you decide to use is very useful.

The easiest way to understand this, in my opinion, is to think in social insects. In the ants, for example, there are polymorphisms, since the workers don't have the same phenotype as the queen or the soldiers. Also, one could argue that the whole colony is a massive metaorganism or superorganism, formed by the summation of all the individual ants.
As in an ant colony, in the case of Physalia, each one of the zooids have a fully formed body (cnidarians have a distinct body plan, consisting of a sac-like digestive system with a mouth crowned by tentacles, two embriologycal layers, etc.) and thus each zooid should be considered to be different individuals. In Physalia, the zooids are physically attached, but that's no different than siamese twins, who aren't usually considered to be only one organism.

While refering to an animal say Physalia, we refer to its massive type colony, containing many zooids. Among the zooids, a large cup shaped float is seen, which is bright blue in color and remains above sea water normally. On the undersurface of float many gastroaooids, gonozooids and dactylozooids are present. The colony thus shows a high degree of polymorphism.
This is all I know and thus the reasoning seems to be absolutely correct...

Perhaps consider finding and adding in a reference or two.


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What flying insect is this?

Found in Russia. Approx. 7 cm.

possible duplicate of What is this insect?

Out of curiosity, have you observed many more of them this year than normal? I live in the south of France and this year we have had a huge invasion of these things.

@terdon, more than normal, yes. I don't remember that I've ever seen this thing flew into my flat. But this time I've seen even three during one week.

I have ~10 in my kitchen every night this past month. Weird, someone in the duplicate thread suggested it might be because of the particularly long winter this year.

This is Crane fly, of the Tipulidae family. They don't bite humans, adults feed on nectar. Larvae prefer moist environments such as wet soil or decomposing vegetable matter and can consume roots and vegetation, damaging plants. Among others, bats and some Coleoptera are its predators.
Further informations can be found in the Wikipedia article linked above.

As a complement to Mattia Rovetta's answer, notice that this insect has only 2 wings, while insects typically have four.
Like flies and mosquitoes, these are Diptera: the hind wings have evolved into a stucture called "Haltere", and one of these small halteres can be seen on your upper photo.
The wikipedia page about halters is illustrated by a Crane Fly photo (as of June 2013), which is quite similar to your insect, but might be of a different species, if I judge by the fact that yours has a dark spot on the wing.

It is indeed a crane fly and there are >15000 species worldwide. Also see answers to this question: What is this insect?.


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Sewall Wright for dunces
[This is one more post in my growing "X for dummies/idiots/morons/etc." series.]
I've been enjoying Provine's The origins of theoretical population genetics for the last couple of days, but I must confess that I find his description (on pp 127-8) of the logic behind Sewall Wright's (and W. Castle's) selection experiments with "hooded rats" about as clear as if it had been chiseled in Linear A...
Which is really bumming me out, because I'd love to understand these experiments.
Does anyone know where I can find a description of these experiments aimed at those with only a very limited grasp of classical genetics?  (I took a graduate-level genetics class a billion years ago, and I did not find it easy.)

I think there might be several places to read a description of these experiments, but they are discussed extensively in a book by historian-philosopher Lindley Darden, entitled "Theory Change in Science: Strategies from Mendelian Genetics", parts of which are available online.  See p. 112 of Darden's book for references to other accounts of these experiments by historians E.A. Carlson (1966) and W. Provine (1988).
Everyone knows what Castle did but his aims have been obscured by "Synthesis Historiography" (i.e. making things turn out right for Ernst Mayr and his homies).
What Castle did was to breed rats in the laboratory and implement selection on coat patterns, with such success that he has able to get a large seemingly continuous range of forms. Imagine breeding oreos, with one line of selection of darker forms, and one of lighter, and achieving the success of getting both pure-black or pure-white oreos, and then lining up all the oreos from black to white to show the continuous range of forms.
The story that we hear from people like Wright and Provine is that this proved that selection can work on continuous variation, an idea that the "mutationists" allegedly rejected, paving the way for acceptance of Darwinism.
Yet, while the experiments may have helped one version of Darwinism, they also represented the dying gasps of another form of Darwinism-- the form that Darwin proposed and Castle was (partially) defending.
You can get an inkling of this from p. 143 of Provine's book, where you will find a curious confession, made in passing.  Provine is explaining why Pearson did not want to publish Fisher's famous 1918 paper.  He writes "Pearson claimed, and Darwin would probably have agreed, that the continuous variations in a pure line were heritable and that continued selection in a pure line should be effective."
Why would Pearson believe-- 17 years after the rediscovery of Mendelian inheritance-- that the environmental variations in Johannsen's pure lines were suitable material for selection?  The reason is that this is what Darwin believed, and Pearson was a follower of Darwin.  Darwin's "indefinite variability", the fuel for modification in his theory of "natural selection", described in Ch. 1 of the OOS, is clearly a description of environmental variation-- it is always present and emerges anew every generation in response to "conditions of life" (see Winther, 2000).  Darwin knew about "definite" single variations or "sports", which could be inherited perfectly (whereas indefinite variations were inherited by blending), but he didn't think they were important for evolution.  Darwin bet on the wrong horse, as Johannsen showed in 1903.
Pearson, Castle, and others defended Darwin's original view well into the 20th century.  They were not satisfied with the idea that selection merely sorted out stable Mendelian factors that undergo rare mutations.  Instead, they held out hope that there was some other form of heredity, or that the Mendelian units were squishy and underwent continuous shifts in potency under conditions of selection.  Thus Castle and Phillips in 1914 argued that "the unit character for hooded pattern is itself variable"
Muller, Sturtevant and others from Morgan's lab disagreed, arguing instead that there were simply various Mendelian modifying factors in the background affecting coat color.  There was a long-running dispute over the proper genetic interpretation of Castle's results.  If you want a very clear statement of the dispute, go to a 1916 article by Jennings, p. 287:

"Castle finds that in rats he can, by selection, gradually increase
  of decrease the amount of colour in the coat, passing by continuous
  stages from one extreme to the other.  As to this, he holds two main
  points:

The change is an actual change in the hereditary characteristics of the stock; not a mere result of the recombination of Mendelian
  factors.  This is the general and fundamental point at issue.
More specifically, he holds it to be an actual change in a single unit factor; this single factor changes its grade in a continuous and
  quantitative manner.

On the other side, the critics of these views
  maintain that the changes shown are not actual alterations in the
  hereditary constitution at all, but are mere results of recombinations
  of Mendelian factors.  And specifically, they find a complete
  explanation of such results as those of Castle in the hypothesis of
  multiple modifying factors."

A few years later in 1919, Castle recanted his earlier view and accepted the multifactorial theory (the development of which is described by Kyung-Man Kim, cited below).
And finally, the idea that the "mutationists" rejected selection on quantitative variation is mistaken.  What the mutationists rejected was selection on non-heritable environmental variations.  Johannsen's 1903 results were revolutionary because scientists at the time understood that they refuted Darwin's theory.  We don't "get" this today because "Darwinism" has been redefined to disentangle "natural selection" from Darwin's errant views of heredity-- see Jean Gayon's "Darwinism's Struggle for Survival" for more explanation.
References
Kim K-M. 1994. Explaining scientific consensus : the case of Mendelian genetics New York: Guilford Press. xxiv, 239 p. p.
Gayon J. 1998. Darwinism's Struggle for Survival: Heredity andthe Hypothesis of Natural Selection Cambridge, UK: Cambridge University Press.
Winther RG. 2000. Darwin on Variation and Heredity. Journal of the History of Biology 33:425-55.

I don't have access to Provine's book, and I can't describe the details of the hooded rat experiments, but here is an attempt to explain the importance of the work.
Darwin published “Origin of Species” in 1859. He proposed that modern species were all descended from ancestral species, and that evolution proceeded by natural selection. He believed that evolution proceeded gradually by an accretion of small changes (gradualism). The origins of hereditary change were, of course, unknown to Darwin.
Mendel’s work (published in 1865) was rediscovered in 1900, and gave rise to a school of thought referred to as mutationism.  Mutationist theories emphasised the importance of single factor changes with large effects, and placed these “leaps forward” at the centre of the mechanism for the generation of new species. This was in contrast to the biometricians who argued, in the Darwinian tradition, that natural selection acted on populations in which there was continuous variation. Extreme mutationists believed that continuous variation within a species had no relevance to the evolution of new species. Their view was that within a species most genes were fixed (100% wild-type allele), and that only mutations could create new species (‘hopeful monsters’). T.H. Morgan, for example, was a strong proponent of the mutationist theory, so this wasn't some minor controversy.
Sewall Wright joined the laboratory of W.E.Castle as an assistant in 1912, when he was 23. Starting with black and white hooded rats (white rats with black ‘hoods’) they instigated breeding programmes and showed that they could progress gradually, through a number of generations, towards all white or all black rats. The importance of this work was that it demonstrated that there was underlying genetic variation within this strain of rats that could be acted upon by selection (selective breeding) resulting in  gradual changes in coat colour. This provided strong evidence for the gradualist school.
By the 1930s the modern synthesis began to emerge, which combined mutationist and gradualist ideas: natural selection acts upon populations (gene frequencies etc.) but mutation provides the raw material that creates new variations in the population. Key to the acceptance of the modern synthesis was the development of a mathematical treatment of population genetics. This led to the current view of phenotypic  traits influenced by multiple loci, with natural populations harbouring genetic variability which can be acted upon by selective forces. We have all accepted this and so of course it is difficult to think ourselves into the controversies that existed in genetics at the beginning of the twentieth century.
Here is an article in which Sewall Wright refers briefly to his work with Castle, placing it in historical context. It also describes subsequent work with guinea pigs. This is a quotation from the article which underscores what I have written:

From assisting Prof. Castle, I learned at firsthand the efficacy of mass selection in changing permanently a character subject merely to quantitative variability. Because of this and a distaste for miracles in science, I started with full acceptance of Darwin's contention that evolution depends mainly on quantitative variability rather than on favorable major mutations. Thus, I have assumed that species are typically heteroallelic in tens of thousands of loci in which the leading alleles differ only slightly in effect, a situation that is maintained in a continually shifting state of near-equilibrium by the opposing pressures of recurrent mutation, diffusion and weak selection. Only a few loci at any time can show fairly rapid changes in allelic frequencies from strong selection.

Thanks for this summary (BTW, the first half of Provine's book is a chronicle of the biometrician/mutationist battle), the link, and the quote by Wright.  His is a clarity of understanding that we seem to have lost somehow.

@kjo So, you could have probably written this better yourself! Hopefully it will help other readers of your question and maybe you'll get the answer that you are looking for. I agree about clarity - it reminds me of the writing of AD Hershey, a "founding father" in a later generation of geneticists.


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What is a good Microbiology atlas for Bacteriology as online version?
I am looking for a online atlas for Bacteriology, the cost does not matter.
I have been searching SpringerLink, and Amazon but no good online version found.
What is a good atlas for Bacteriology as a online version?

Not sure what you are exactly looking for? If you change the question or comment I can update my answer...
NCBI's taxonomy site has a listing of bacteria.  Encyclopedia of life is also great.
Then there's UCSC's microbial genome browser.
Biocyc is  great reference for bacterial genes.  to get into E coli, which is the model bacterium there's Port Eco featuring 130 E coli genomes.
Am Soc Micro has an excellent E coli/ Salmonella site based on their classic reference - you have to pay for access though.

Thank you very much! The http://eol.org/ is outstanding resource for the basic course of Microbiology.

Ah glad I could help you find what you wanted! :)


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Why are males more likely than females to have autism spectrum disorder?
The male to female ratio in autism spectrum disorder is around 4:1. However it seems ASD is not a simple X-linked disorder.
Then how is it possible males are more susceptible than females, if the causal genes are located in autosomes?

Could you maybe add some background, e.g. references on the incidence of autism spectrum disorders?

Sure, I will do this later when I come to school

As the father of two sons with diagnoses of ASD, I think that it is best to think in terms of an extended spectrum which encompasses 'normal' people. We are all somewhere on this spectrum, but there is a threshold zone around where we cross from "normal" to "diagnosable as ASD". Now, if the distribution of spectral position for males is displaced towards the ASD end of the spectrum relative to females (because of some aspect underlying "normal' maleness, such as testosterone levels) then any genetic variation which pushes someone towards the ASD end of the spectrum by some fixed amount will tend to push more males over the threshold than females.

That is an interesting idea.  Do you know if there's a database of scores on an ASD questionnaire, for the general population so that we could verify it?  Simon Baron-Cohen's tests come to mind, but I'm not sure if they've looked at the distribution of scores.

Dear Alan, thanks for sharing the point. I hope the genetics study in the future can explain the mystery.

Nice thinking @alan-boyd, I wonder would it be nice to see a study correlating "manliness traits" with ASD test scores?

This spectrum that leads to autism on the far right tail is probably the empathising-systemizing trait, which shows half a standard deviation mean difference between man and women. This difference in mean pretty exactly results in the 4:1 ratio in a normal distribution, if you look at the right tail that corresponds to the autism incidence rate.

Males are more likely to develop ASD, but affected females tend to be more severely impaired. Why this occurs is an area of active research.
However, to address your question, there is a study suggesting that mutations on the X-chromosome account for about 1% of ASD and intellectual disability cases.  This clearly doesn't explain everything, but it's a start.  It might suggest that there are other X-linked loci involved. IIRC, ASD is one of those disorders that can be caused by many different combinations of (relatively rare) mutations, so it's hard to identify the genetic causes by GWAS.

hi, thanks a lot for the explanation. Another question came to my mind is that the one copy of X chromosome will be silenced (please correct me if I am wrong),so does the X chromosome which carry mutation always be deactivated?

I'm not expert on the topic, but whenever males more predominately have a condition than females, it might point to a sex-linked (recessive) trait. Males have one X chromosome, while females have two. This means that a male only needs one copy of a gene to have a condition (inherited from their mother), while females need two X chromosomes to be inherited to have the condition (mother and father).

Being a Special Education Trainer at ACCEL Centre, I have done some research regarding this topic, but haven’t found a shred of full-proof evidence to support this theory.
Well, first of all, autism is a sensory integration disorder showing visible signs of speech delays and communication difficulty with others.
The main reason that causes autism spectrum is still not known and various researches are still in progress, together with erratic proof that men/women ratio ranges between 2:1 and 16:1.
One probable factor is a diagnostic bias, suggesting that females obtain autism diagnoses later in life as compared to males, indicating that it is harder to spot.
Signs of autism spectrum also look different in females. They have fewer restricted interests and repetitive behaviors and may have socially acceptable interests.
References:

https://www.autism.org.uk/about/what-is/gender.aspx
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4164392/
https://www.spectrumnews.org/news/autisms-sex-ratio-explained/

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


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Breaking of fats
There is a question I encountered.
Why is fat harder to digest ?
A) It has ester bonds.
B) It is not easily soluble in water.
Which is the most appropriate answer?

Not everything in biology is black or white (in fact, almost everything is gray). A combination of these factors and others play a role in the observation.

I think that the main reason (but probably not the only one) is because fats are hydrophobic, while the environment of the digestive tract is aqueous. Most of the fats in the diet are triglyceride and in hydrophilic environment they form globules. Triglycerides must be hydrolysed to be absorbed by the duodenum and this work is done by pancreatic lipase, that is a water soluble enzyme and can only hydrolyse the esteric bonds at the surface of fat globules.
Therefore, during the digestion amphipathic molecules such as bile salts and phospholipids emulsify those droplets in smaller ones, increasing the surface area where lipases, together with colipase can digest.

Fats are not metabolized in the digestive tract.  The metabolic pathways that break down and utilize fat turn fats into glycerol which is much easier to obtain from carbohydrates.

My Lehninger principles of biochemistry says that "products of lipase action [(monoacylglycerols, diacylglycerols, free fatty acids and glycerol)] diffuse into the epithelial cells lining the intestinal surface".
Is this incorrect or maybe I didn't explain myself well? I omitted this last part of the process because I thought that it was superfluous.

You might be right. I'd thought that the question is about metabolizing for energy.


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How do viroids propagate to other hosts?
As viroids are simply non-encapsidated non-coding RNA molecules, it is difficult to imagine a mechanism for their continual infection, other than horizontal transfer which doesn't seem to be the case.
Is there a working theory on how viroids propagate and continually infect hosts?

Viroids are commonly thought of as remnants from the "RNA world" since they are composed of only RNA and have ribozyme activity.
Viroids can be considered as plant parasites of the transcriptional machinery of the organelles (nucleus or chloroplast), since they are non-coding and they replicate by RNA–RNA transcription (in a rolling cycle mode).
Viroids infect the epidermis of their hosts after mechanical damage of the plant cell wall. After entry to the first cell layers, viroids initiate replication in the nucleus or in the chloroplast and then are transported to neighbouring cells, reaching the vascular tissues and virtually all plant tissues.

The transmission of viroids is both "natural" and human-driven. Viroids are mostly transmitted via mechanical methods by contaminated machinery and tools, pruning, and other mechanic argricultural techniques. Transmission also occurs through infected seed and pollen, they don't have important natural vectors from the animal kingdom. Also contact between adjacent plants can be another (inefficient) way to transmit viriods.
I have found a reference here for further informations. It isn't open access but it is possible to watch an abundant Google preview.


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Are there beneficial genetic mutations identified by consumer DNA genotyping?
I'm looking at services like 23andme, and see that they identify a wide variety of genetic-based risks, like predisposition to diseases, hair loss, cancer, etc.
Are there a more "positive" DNA analysis outcomes out there? Like increased strength, cheerfulness(resistance to depression), etc?

First of all, I think it is, to a large extent, the way you perceive it. Instead of cancer-causing allele and hair-loss allele, you can think of them as cancer-protection and great-hair alleles. If you don't have disease alleles, that means that in some sense you have "life-extending" genes! Sounds much better, doesn't it?
Second of all, most funding for research is directed at disease so it is not surprising that most of the scientific knowledge is regarding this type of genetic variation.

Lactase persistence is a recent mutation which enables the people who have it to drink and digest milk as adults, while the default state has people unable to digest milk after childhood.
There is also a loci for muscle performance. People either have fast-twitch or slow-twitch preference, which affects your sprinting vs long-distance ability. Which one is "better"? It depends!


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How is consciousness linked to the brain?
Could the brain be working without consciousness? Does the brain interact with consciousness? Alternately, is it that consciousness can't really control the brain, and you only have the impression that you make the decisions, but your brain does.
If the answer to the last question is yes, it is impossible to know if someone else has a consciousness? Even if he doesn't, he'll say he does, because the brain thinks he does.
We can't be made only from matter. If we would, we'd be a mix of chemicals interacting with each other. What makes us be aware of our feelings, what we think, and our 5 senses?
When and how is consciousnesses created?

Unfortunately, although this is a very well researched area in neuroscience, I think we do not know the answer yet. Anyway good question! I would slightly edit it, however, to make it a bit more "biological" and a bit less phylosophical

Note that consciousness and mechanicism are not mutually exclusives. We, at the same time, can be both conscious and mere chemicals. Because this question lie at the limit between philosopy and biology I suggest you to search at http://philosophy.stackexchange.com/, for example here and here. Good question, though.

"A mix of chemicals interacting with each other" is a great way to describe organisms.

@Someone Great question. One point I'd make though is that 'We can't be made only from matter' is a statement that makes assumptions about the nature of matter. Matter is not like Lego. From what I remember from my uni physics courses, matter is actually pretty weird... i.e. non-intuitive. At least on the smallest scales.

A non-subjective definition of consciousness is needed first . I would go with "a created system that decides pro-activity and is given freedom to think for itself "


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Which texts are good for beginners to understand evolution on the genetic scope?
Are there good texts to study the evolution, how it works, and how mutations and changes lead to evolution of the organism ?
And how does the information increase through the long time using mutations and other mechanisms?
Can you recommend specific texts?

what level are you looking for; popular science for the general public, high school level, undergraduate, graduate in graphic design, graduate in evolutionary genetics? you say beginner but beginner at what level?

having looked at your profile I see you are a high school student, I'd suggest heading towards Dawkins' popular science texts first, then Ridley's evolution for some finer detail.

Books on my shelf right now (I'm an evolutionary genetics grad student)...
Entry level:
Evolution - Mark Ridley (not Matt Ridley)
A primer of ecological genetics - Connor & Hartl
Intermediate:
Elements of evolutionary genetics -  Charlesworth & Charlesworth
Advanced:
Principles of Population genetics - Hartl & Clark
Introduction to quantitative genetics - Falconer & Mackay
Further basic/popular-science books include R Dawkins' Selfish Gene/The Extended Phenotype/The Greatest Show on Earth and of course The Origin of Species by Darwin

Adding to previous answers. For basic textbooks I've been happy with (earlier editions of):

Evolution, Futuyma
Genetics: From Genes to Genomes, Hartwell et al.

EDIT:
I should also mention the free pdf book Theoretical Evolutionary Genetics by Joe Felsenstein, with latest update from 2013. He uses it for a course in population gentics. So far, I have only browsed it myself. It is fairly math-heavy, but I thought that it could be of general interest.


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Can the excessive consumption of mineral water lead to kidney stones or other health issues?
I heard that drinking too much mineral (bottled) water could lead to problems such as kidney stones because of the high amount of minerals in it. Is it true? If so, what is considered to be excessive?

I suffer from calcium oxalate stones.  My doctor pointed me to this study:
http://www.ncbi.nlm.nih.gov/pubmed/9096270
tl;dr;  For calcium oxalate, drinking Mineral Water high in Calcium and Magnesium may reduce the risk of forming stones.

It is unlikely that drinking too much mineral water will cause kidney stones. One of the chief causes of kidney stones is dehydration. I can't imagine the calcium content of mineral water could be that high as to cause kidney stones (please correct me if I'm wrong) unless you drink ridiculous amount by which stage you will probably start to have electrolyte abnormalities and perhaps seizures.
Consumption of excessive amount of water can cause various health issues (even life threatening). These include seizures, rhythm disturbances in the heart (all usually secondary to acute electrolyte imbalance in the blood).
I've never come across drinking too much mineral water as a cause for kidney stones-most people who get kidney stones usually aren't drinking enough water. The more water you take (in moderation), the less the likelihood for stone formation in your kidneys.


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Deep diving in mammals
Mammals like seals often dive and can remain under water for more than 70 minutes.
How do seals know when is it the time to come up?

I imagine that their breathing is controlled in the same way as ours. During a dive, oxygen will be used up and carbon dioxide will be produced, dissolving in the blood as bicarbonate and tending to decrease the pH of the blood.
Peripheral chemoreceptors in the circulatory system detect all of these changes and signal the need to breathe. This would tell the seal that it is time to head for the surface.
Diving mammals have various adaptations for prolonged diving, most importantly large reservoirs of blood containing haemoglobin which is oxygenated before a dive, as well as high concentrations of myoglobin in muscle which can also act as an oxygen reservoir.

Check this article in the today's issue of science. Was going through the TOC just before I looked at this question. It is about how myoglobin is more efficient in deep divers. Reinforcing the fact in the last statement of Alan's answer.


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E. coli, risk of infection?
There has been a warning about E. coli contaminated water in South Florida. Now I'm wondering are there empirical data or historic cases which show a correlation between E.coli levels in tap water and risk of infection in the population drinking this water. Which pathogens, that could be transmitted through tap water, are common in this area?

This falls within personal medical advice which is off topic as per the FAQ. If you can remove the references to yourself (can a glass washed with warm E coli contaminated water pose a health risk, or better yet, what is the max temperature at which infectious E coli survive), it might be answered, but it's still borderline.

You will know shortly. ;-)

@dd3 Ok as changed it.

I think there has been something of a misunderstanding here between E. coli and the risk of an infection. Normally E.coli is no pathogen, you have a lot of them in your intestines. The measuring of E. coli in tap water and food is a normal procedure to find faecal contamination, since E.coli is easy to grow. But there are other pathogens you have to worry about like Salmonella, Enterococcus, Cholera and also some E.coli. But it is to expensive to test for every possible pathogen. I'm trying to change you question, to what I think you want to know.

@NeoDevlin Your comment above would make the best answer currrently. Unfourtunately, there's no "Not a comment; Should be an answer instead." flag!

The maximum temperature for E. coli to survive is dependent on the strain. E. coli from warm areas can easily survive 45 °C and more. The minimum number of E. coli to ingest in order to become ill is also dependent on the strain. Whether you become ill at all is also dependent on the strain. You harbor many billions of E. coli in your digestive tract without becoming ill, so without further information on the released strain, it's really hard to tell.
One of the suggestions from the WHO Guidelines for drinking water quality is to boil the water in order to desinfect it.

One textbook of microbiology suggests that the infectious dose of a specific strain of enterotoxigenic E. coli in adults would be $10^{8}$ cells. Keep in mind that infective dose will vary with species and strain, as well as the health, age and immune-status of the individual ingesting the bacteria. Children, elderly and ill people will generally be affected by a lower infective dose. This does also not consider how well the bacteria can colonize the gastrointestinal system. It is possible for minimal numbers of pathogenic E. coli to colonize in the gut, and only after growing to a infectious level, being to exert pathogenic effects.


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What is the relationship between UV wavelength and penetration depth into human skin?
Some background - Some recent research has strongly suggested that UVA penetration into the skin is far more dangerous than UVB, a very good example is this paper by Agar et al. (2004).
My query is, is there a measure that relates the UV wavelength with the penetration depth into human skin?  Related, is the answer to this related to skin types?
(I understand that this may be migrated to Biology.SE).

Yeah, this seems much better off on Bio.SE. Could you first clarify what you mean by "measure" here? (i'll migrate afterwards)

No worries, what I am need of a measure is more of a relationship between penetration depth into the skin and incident UV radiation.

Solar UV radiation is broadly classified as UV- A,B and C (Decreasing order of wavelengths). Penetrating ability of UV is a not a direct function of its wavelength; lesser the wavelength lesser is the penetrating ability (But higher is the energy: a direct function of wavelength). Penetration ability is dependent on scattering and absorption. Most biomolecules in the skin, including melanin and proteins absorb at around 220-300nm range. Plus, scattering (esp Rayleigh scattering) is inversely proportional to wavelength.
Since UV B has higher energy compared to UV A, the former is more toxic to the cells. But a little UV B also does some good; conversion 7-dehydrocholesterol to Vitamin D. UV A doesn't have sufficient energy to directly cause DNA damage  but it can give rise to free radicals and cause DNA damage indirectly.
The paper that you mentioned says that the tissue that they studied has more of UV A mediated lesions. This could be because of higher availability of UV A to the cells. Ozone filters out a major chunk of UV B and C and melanin does little more. If these mechanisms didn't exist then high energy UVs would have burnt us.
To summarize, the inherent order of toxicity is C > B > A
References:

http://www.uio.no/studier/emner/matnat/fys/FYS3610/h04/undervisningsmateriale/Moan7.pdf
http://www.nature.com/jid/journal/v77/n1/abs/5615637a.html